Search

Your search keyword '"Arda Halu"' showing total 89 results
Start Over Author "Arda Halu"
89 results on '"Arda Halu"'

1. Integrating pharmacogenomics and cheminformatics with diverse disease phenotypes for cell type-guided drug discovery

Author

Arda Halu, Sarvesh Chelvanambi, Julius L. Decano, Joan T. Matamalas, Mary Whelan, Takaharu Asano, Namitra Kalicharran, Sasha A. Singh, Joseph Loscalzo, and Masanori Aikawa

Subjects
Network pharmacology, Pharmacogenomics, Cheminformatics, Connectivity mapping, CMap, Cell type-specific, Medicine, Genetics, QH426-470
Abstract

Abstract Background Large-scale pharmacogenomic resources, such as the Connectivity Map (CMap), have greatly assisted computational drug discovery. However, despite their widespread use, CMap-based methods have thus far been agnostic to the biological activity of drugs as well as to the genomic effects of drugs in multiple disease contexts. Here, we present a network-based statistical approach, Pathopticon, that uses CMap to build cell type-specific gene-drug perturbation networks and integrates these networks with cheminformatic data and diverse disease phenotypes to prioritize drugs in a cell type-dependent manner. Methods We build cell type-specific gene-drug perturbation networks from CMap data using a statistical procedure we call Quantile-based Instance Z-score Consensus (QUIZ-C). Using these networks and a large-scale disease-gene network consisting of 569 disease signatures from the Enrichr database, we calculate Pathophenotypic Congruity Scores (PACOS) between input gene signatures and drug perturbation signatures and combine these scores with cheminformatic data from ChEMBL to prioritize drugs. We benchmark our approach by calculating area under the receiver operating characteristic curves (AUROC) for 73 gene sets from the Molecular Signatures Database (MSigDB) using target gene expression profiles from the Comparative Toxicogenomics Database (CTD). We validate the drugs predicted in our proofs-of-concept using real-time polymerase chain reaction (qPCR) experiments. Results Cell type-specific gene-drug perturbation networks built using QUIZ-C are topologically distinct, reflecting the biological uniqueness of the cell lines in CMap, and are enriched in known drug targets. Pathopticon demonstrates a better prediction performance than solely cheminformatic measures as well as state-of-the-art network and deep learning-based methods. Top predictions made by Pathopticon have high chemical structural diversity, suggesting their potential for building compound libraries. In proof-of-concept applications on vascular diseases, we demonstrate that Pathopticon helps guide in vitro experiments by identifying pathways that are potentially regulated by the predicted therapeutic candidates. Conclusions Our network-based analytical framework integrating pharmacogenomics and cheminformatics (available at https://github.com/r-duh/Pathopticon ) provides a feasible blueprint for a cell type-specific drug discovery and repositioning platform with broad implications for the efficiency and success of drug development.

Published
2025
Full Text
View/download PDF

2. Vitamin D constrains inflammation by modulating the expression of key genes on Chr17q12-21.1

Author

Ayse Kilic, Arda Halu, Margherita De Marzio, Enrico Maiorino, Melody G Duvall, Thayse Regina Bruggemann, Joselyn J Rojas Quintero, Robert Chase, Hooman Mirzakhani, Ayse Özge Sungur, Janine Koepke, Taiji Nakano, Hong Yong Peh, Nandini Krishnamoorthy, Raja-Elie Abdulnour, Katia Georgopoulos, Augusto A Litonjua, Marie Demay, Harald Renz, Bruce D Levy, and Scott T Weiss

Subjects
asthma, vitamin D receptor, inflammation, Medicine, Science, Biology (General), QH301-705.5
Abstract

Vitamin D possesses immunomodulatory functions and vitamin D deficiency has been associated with the rise in chronic inflammatory diseases, including asthma (Litonjua and Weiss, 2007). Vitamin D supplementation studies do not provide insight into the molecular genetic mechanisms of vitamin D-mediated immunoregulation. Here, we provide evidence for vitamin D regulation of two human chromosomal loci, Chr17q12-21.1 and Chr17q21.2, reliably associated with autoimmune and chronic inflammatory diseases. We demonstrate increased vitamin D receptor (Vdr) expression in mouse lung CD4+ Th2 cells, differential expression of Chr17q12-21.1 and Chr17q21.2 genes in Th2 cells based on vitamin D status and identify the IL-2/Stat5 pathway as a target of vitamin D signaling. Vitamin D deficiency caused severe lung inflammation after allergen challenge in mice that was prevented by long-term prenatal vitamin D supplementation. Mechanistically, vitamin D induced the expression of the Ikzf3-encoded protein Aiolos to suppress IL-2 signaling and ameliorate cytokine production in Th2 cells. These translational findings demonstrate mechanisms for the immune protective effect of vitamin D in allergic lung inflammation with a strong molecular genetic link to the regulation of both Chr17q12-21.1 and Chr17q21.2 genes and suggest further functional studies and interventional strategies for long-term prevention of asthma and other autoimmune disorders.

Published
2024
Full Text
View/download PDF

3. Identifying novel mechanisms of abdominal aortic aneurysm via unbiased proteomics and systems biology

Author

Stephanie Morgan, Lang Ho Lee, Arda Halu, Jessica S. Nicolau, Hideyuki Higashi, Anna H. Ha, Jennifer R. Wen, Alan Daugherty, Peter Libby, Scott J. Cameron, Doran Mix, Elena Aikawa, A. Phillip Owens, Sasha A. Singh, and Masanori Aikawa

Subjects
inflammation, thrombosis, network analysis, angiotensin II, elastase, mouse model, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

BackgroundAbdominal aortic aneurysm (AAA), characterized by a continued expansion of the aorta, leads to rupture if not surgically repaired. Mice aid the study of disease progression and its underlying mechanisms since sequential studies of aneurysm development are not feasible in humans. The present study used unbiased proteomics and systems biology to understand the molecular relationship between the mouse models of AAA and the human disease.Methods and resultsAortic tissues of developing and established aneurysms produced by either angiotensin II (AngII) infusion in Apoe−/− and Ldlr−/− mice or intraluminal elastase incubation in wildtype C57BL/6J mice were examined. Aortas were dissected free and separated into eight anatomical segments for proteomics in comparison to their appropriate controls. High-dimensional proteome cluster analyses identified site-specific protein signatures in the suprarenal segment for AngII-infused mice (159 for Apoe−/− and 158 for Ldlr−/−) and the infrarenal segment for elastase-incubated mice (173). Network analysis revealed a predominance of inflammatory and coagulation factors in developing aneurysms, and a predominance of fibrosis-related pathways in established aneurysms for both models. To further substantiate our discovery platform, proteomics was performed on human infrarenal aortic aneurysm tissues as well as aortic tissue collected from age-matched controls. Protein processing and inflammatory pathways, particularly neutrophil-associated inflammation, dominated the proteome of the human aneurysm abdominal tissue. Aneurysmal tissue from both mouse and human had inflammation, coagulation, and protein processing signatures, but differed in the prevalence of neutrophil-associated pathways, and erythrocyte and oxidative stress-dominated networks in the human aneurysms.ConclusionsIdentifying changes unique to each mouse model will help to contextualize model-specific findings. Focusing on shared proteins between mouse experimental models or between mouse and human tissues may help to better understand the mechanisms for AAA and establish molecular bases for novel therapies.

Published
2022
Full Text
View/download PDF

4. Robustness and lethality in multilayer biological molecular networks

Author

Xueming Liu, Enrico Maiorino, Arda Halu, Kimberly Glass, Rashmi B. Prasad, Joseph Loscalzo, Jianxi Gao, and Amitabh Sharma

Subjects
Science
Abstract

Robustness is a prominent feature of most biological systems, but most of the current efforts have been focused on studying homogeneous molecular networks. Here the authors propose a comprehensive framework for understanding how the interactions between genes, proteins, and metabolites contribute to the determinants of robustness.

Published
2020
Full Text
View/download PDF

5. Gene Expression Profiling Reveals the Shared and Distinct Transcriptional Signatures in Human Lung Epithelial Cells Infected With SARS-CoV-2, MERS-CoV, or SARS-CoV: Potential Implications in Cardiovascular Complications of COVID-19

Author

Prabhash Kumar Jha, Aatira Vijay, Arda Halu, Shizuka Uchida, and Masanori Aikawa

Subjects
SARS-CoV-2, SARS-CoV, MERS-CoV, COVID-19 and transcriptome analysis, cardiovasclar disease, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is the causative virus for the current global pandemic known as coronavirus disease 2019 (COVID-19). SARS-CoV-2 belongs to the family of single-stranded RNA viruses known as coronaviruses, including the MERS-CoV and SARS-CoV that cause Middle East respiratory syndrome (MERS) and severe acute respiratory syndrome (SARS), respectively. These coronaviruses are associated in the way that they cause mild to severe upper respiratory tract illness. This study has used an unbiased analysis of publicly available gene expression datasets from Gene Expression Omnibus to understand the shared and unique transcriptional signatures of human lung epithelial cells infected with SARS-CoV-2 relative to MERS-CoV or SARS-CoV. A major goal was to discover unique cellular responses to SARS-CoV-2 among these three coronaviruses. Analyzing differentially expressed genes (DEGs) shared by the three datasets led to a set of 17 genes, suggesting the lower expression of genes related to acute inflammatory response (TNF, IL32, IL1A, CXCL1, and CXCL3) in SARS-CoV-2. This subdued transcriptional response to SARS-CoV-2 may cause prolonged viral replication, leading to severe lung damage. Downstream analysis of unique DEGs of SARS-CoV-2 infection revealed changes in genes related to apoptosis (NRP1, FOXO1, TP53INP1, CSF2, and NLRP1), coagulation (F3, PROS1, ITGB3, and TFPI2), and vascular function (VAV3, TYMP, TCF4, and NR2F2), which may contribute to more systemic cardiovascular complications of COVID-19 than MERS and SARS. The study has uncovered a novel set of transcriptomic signatures unique to SARS-CoV-2 infection and shared by three coronaviruses, which may guide the initial efforts in the development of prognostic or therapeutic tools for COVID-19.

Published
2021
Full Text
View/download PDF

6. A Systems Approach to Refine Disease Taxonomy by Integrating Phenotypic and Molecular Networks

Author

Xuezhong Zhou, Lei Lei, Jun Liu, Arda Halu, Yingying Zhang, Bing Li, Zhili Guo, Guangming Liu, Changkai Sun, Joseph Loscalzo, Amitabh Sharma, and Zhong Wang

Subjects
Medicine, Medicine (General), R5-920
Abstract

The International Classification of Diseases (ICD) relies on clinical features and lags behind the current understanding of the molecular specificity of disease pathobiology, necessitating approaches that incorporate growing biomedical data for classifying diseases to meet the needs of precision medicine. Our analysis revealed that the heterogeneous molecular diversity of disease chapters and the blurred boundary between disease categories in ICD should be further investigated. Here, we propose a new classification of diseases (NCD) by developing an algorithm that predicts the additional categories of a disease by integrating multiple networks consisting of disease phenotypes and their molecular profiles. With statistical validations from phenotype-genotype associations and interactome networks, we demonstrate that NCD improves disease specificity owing to its overlapping categories and polyhierarchical structure. Furthermore, NCD captures the molecular diversity of diseases and defines clearer boundaries in terms of both phenotypic similarity and molecular associations, establishing a rational strategy to reform disease taxonomy. Keywords: Disease taxonomy, Network medicine, Disease phenotypes, Molecular profiles, Precision medicine

Published
2018
Full Text
View/download PDF

7. PARP9 and PARP14 cross-regulate macrophage activation via STAT1 ADP-ribosylation

Author

Hiroshi Iwata, Claudia Goettsch, Amitabh Sharma, Piero Ricchiuto, Wilson Wen Bin Goh, Arda Halu, Iwao Yamada, Hideo Yoshida, Takuya Hara, Mei Wei, Noriyuki Inoue, Daiju Fukuda, Alexander Mojcher, Peter C. Mattson, Albert-László Barabási, Mark Boothby, Elena Aikawa, Sasha A. Singh, and Masanori Aikawa

Subjects
Science
Abstract

Signalling pathways that mediate macrophage activation in disease are poorly understood. Here the authors show that inhibition of PARP9 and/or activation of PARP14 may attenuate macrophage-mediated vascular diseases, and also provide new insight into the development of effective therapies for other inflammatory disorders.

Published
2016
Full Text
View/download PDF

8. Context-enriched interactome powered by proteomics helps the identification of novel regulators of macrophage activation

Author

Arda Halu, Jian-Guo Wang, Hiroshi Iwata, Alexander Mojcher, Ana Luisa Abib, Sasha A Singh, Masanori Aikawa, and Amitabh Sharma

Subjects
macrophages, networks, cardiovascular, proteomics, Medicine, Science, Biology (General), QH301-705.5
Abstract

The role of pro-inflammatory macrophage activation in cardiovascular disease (CVD) is a complex one amenable to network approaches. While an indispensible tool for elucidating the molecular underpinnings of complex diseases including CVD, the interactome is limited in its utility as it is not specific to any cell type, experimental condition or disease state. We introduced context-specificity to the interactome by combining it with co-abundance networks derived from unbiased proteomics measurements from activated macrophage-like cells. Each macrophage phenotype contributed to certain regions of the interactome. Using a network proximity-based prioritization method on the combined network, we predicted potential regulators of macrophage activation. Prediction performance significantly increased with the addition of co-abundance edges, and the prioritized candidates captured inflammation, immunity and CVD signatures. Integrating the novel network topology with transcriptomics and proteomics revealed top candidate drivers of inflammation. In vitro loss-of-function experiments demonstrated the regulatory role of these proteins in pro-inflammatory signaling.

Published
2018
Full Text
View/download PDF

9. Multiplex PageRank.

Author

Arda Halu, Raúl J Mondragón, Pietro Panzarasa, and Ginestra Bianconi

Subjects
Medicine, Science
Abstract

Many complex systems can be described as multiplex networks in which the same nodes can interact with one another in different layers, thus forming a set of interacting and co-evolving networks. Examples of such multiplex systems are social networks where people are involved in different types of relationships and interact through various forms of communication media. The ranking of nodes in multiplex networks is one of the most pressing and challenging tasks that research on complex networks is currently facing. When pairs of nodes can be connected through multiple links and in multiple layers, the ranking of nodes should necessarily reflect the importance of nodes in one layer as well as their importance in other interdependent layers. In this paper, we draw on the idea of biased random walks to define the Multiplex PageRank centrality measure in which the effects of the interplay between networks on the centrality of nodes are directly taken into account. In particular, depending on the intensity of the interaction between layers, we define the Additive, Multiplicative, Combined, and Neutral versions of Multiplex PageRank, and show how each version reflects the extent to which the importance of a node in one layer affects the importance the node can gain in another layer. We discuss these measures and apply them to an online multiplex social network. Findings indicate that taking the multiplex nature of the network into account helps uncover the emergence of rankings of nodes that differ from the rankings obtained from one single layer. Results provide support in favor of the salience of multiplex centrality measures, like Multiplex PageRank, for assessing the prominence of nodes embedded in multiple interacting networks, and for shedding a new light on structural properties that would otherwise remain undetected if each of the interacting networks were analyzed in isolation.

Published
2013
Full Text
View/download PDF

10. Sortilin enhances fibrosis and calcification in aortic valve disease by inducing interstitial cell heterogeneity

Author

Farwah Iqbal, Florian Schlotter, Dakota Becker-Greene, Adrien Lupieri, Claudia Goettsch, Joshua D Hutcheson, Maximillian A Rogers, Shinsuke Itoh, Arda Halu, Lang Ho Lee, Mark C Blaser, Andrew K Mlynarchik, Sumihiko Hagita, Shiori Kuraoka, Hao Yu Chen, James C Engert, Livia S A Passos, Prabhash K Jha, Eric A Osborn, Farouc A Jaffer, Simon C Body, Simon C Robson, George Thanassoulis, Masanori Aikawa, Sasha A Singh, Abhijeet R Sonawane, and Elena Aikawa

Subjects
Cardiology and Cardiovascular Medicine
Abstract

AimsCalcific aortic valve disease (CAVD) is the most common valve disease, which consists of a chronic interplay of inflammation, fibrosis, and calcification. In this study, sortilin (SORT1) was identified as a novel key player in the pathophysiology of CAVD, and its role in the transformation of valvular interstitial cells (VICs) into pathological phenotypes is explored.Methods and resultsAn aortic valve (AV) wire injury (AVWI) mouse model with sortilin deficiency was used to determine the effects of sortilin on AV stenosis, fibrosis, and calcification. In vitro experiments employed human primary VICs cultured in osteogenic conditions for 7, 14, and 21 days; and processed for imaging, proteomics, and transcriptomics including single-cell RNA-sequencing (scRNA-seq). The AVWI mouse model showed reduced AV fibrosis, calcification, and stenosis in sortilin-deficient mice vs. littermate controls. Protein studies identified the transition of human VICs into a myofibroblast-like phenotype mediated by sortilin. Sortilin loss-of-function decreased in vitro VIC calcification. ScRNA-seq identified 12 differentially expressed cell clusters in human VIC samples, where a novel combined inflammatory myofibroblastic-osteogenic VIC (IMO-VIC) phenotype was detected with increased expression of SORT1, COL1A1, WNT5A, IL-6, and serum amyloid A1. VICs sequenced with sortilin deficiency showed decreased IMO-VIC phenotype.ConclusionSortilin promotes CAVD by mediating valvular fibrosis and calcification, and a newly identified phenotype (IMO-VIC). This is the first study to examine the role of sortilin in valvular calcification and it may render it a therapeutic target to inhibit IMO-VIC emergence by simultaneously reducing inflammation, fibrosis, and calcification, the three key pathological processes underlying CAVD.

Published
2023
Full Text
View/download PDF

11. Integrating pharmacogenomics and cheminformatics with diverse disease phenotypes for cell type-guided drug discovery

Author

Arda Halu, Julius L. Decano, Joan Matamalas, Mary Whelan, Takaharu Asano, Namitra Kalicharran, Sasha A. Singh, Joseph Loscalzo, and Masanori Aikawa

Abstract

Large-scale pharmacogenomic resources, such as the Connectivity Map (CMap), have greatly assisted computational drug discovery. However, despite their widespread use, CMap-based methods have thus far been agnostic to the biological activity of drugs, as well as to the genomic effects of drugs in multiple disease contexts. Here, we present a network-based statistical approach, Pathopticon, that uses CMap to build cell type-specific gene-drug perturbation networks and integrates these networks with cheminformatic data and diverse disease phenotypes for a nested prioritization of cell lines and drugs. Pathopticon demonstrates a better prediction performance than solely cheminformatic measures and state-of-the-art methods that rely exclusively on pharmacogenomic data. Top predictions made by Pathopticon have high chemical structural diversity, suggesting their potential for building compound libraries. In a proof-of-concept application on vein graft disease, we validate the predicted drugsin vitroand demonstrate that Pathopticon helps pinpoint the shared intermediate phenotypes targeted by each prediction. Overall, our analytical framework integrating pharmacogenomics and cheminformatics provides a feasible blueprint for a cell typespecific drug discovery and repositioning platform with broad implications for the efficiency and success of drug development.

Published
2022
Full Text
View/download PDF

12. Proprotein Convertase Subtilisin/Kexin 9 (PCSK9) Promotes Macrophage Activation via LDL Receptor-Independent Mechanisms

Author

Shunsuke Katsuki, Prabhash K. Jha, Adrien Lupieri, Toshiaki Nakano, Livia S.A. Passos, Maximillian A. Rogers, Dakota Becker-Greene, Thanh-Dat Le, Julius L. Decano, Lang Ho Lee, Gabriel C. Guimaraes, Ilyes Abdelhamid, Arda Halu, Alessandro Muscoloni, Carlo V. Cannistraci, Hideyuki Higashi, Hengmin Zhang, Amélie Vromman, Peter Libby, C. Keith Ozaki, Amitabh Sharma, Sasha A. Singh, Elena Aikawa, and Masanori Aikawa

Subjects
Lipoproteins, LDL, Mice, Cholesterol, Receptors, LDL, Physiology, Serine Endopeptidases, NF-kappa B, Animals, Subtilisins, Macrophage Activation, Proprotein Convertase 9, Cardiology and Cardiovascular Medicine
Abstract

Background: Activated macrophages contribute to the pathogenesis of vascular disease. Vein graft failure is a major clinical problem with limited therapeutic options. PCSK9 (proprotein convertase subtilisin/kexin 9) increases low-density lipoprotein (LDL)-cholesterol levels via LDL receptor (LDLR) degradation. The role of PCSK9 in macrophage activation and vein graft failure is largely unknown, especially through LDLR-independent mechanisms. This study aimed to explore a novel mechanism of macrophage activation and vein graft disease induced by circulating PCSK9 in an LDLR-independent fashion. Methods: We used Ldlr -/- mice to examine the LDLR-independent roles of circulating PCSK9 in experimental vein grafts. Adeno-associated virus (AAV) vector encoding a gain-of-function mutant of PCSK9 (rAAV8/D377Y-mPCSK9) induced hepatic PCSK9 overproduction. To explore novel inflammatory targets of PCSK9, we used systems biology in Ldlr -/- mouse macrophages. Results: In Ldlr -/- mice, AAV-PCSK9 increased circulating PCSK9, but did not change serum cholesterol and triglyceride levels. AAV-PCSK9 promoted vein graft lesion development when compared with control AAV. In vivo molecular imaging revealed that AAV-PCSK9 increased macrophage accumulation and matrix metalloproteinase activity associated with decreased fibrillar collagen, a molecular determinant of atherosclerotic plaque stability. AAV-PCSK9 induced mRNA expression of the pro-inflammatory mediators IL-1β (interleukin-1 beta), TNFα (tumor necrosis factor alpha), and MCP-1 (monocyte chemoattractant protein-1) in peritoneal macrophages underpinned by an in vitro analysis of Ldlr -/- mouse macrophages stimulated with endotoxin-free recombinant PCSK9. A combination of unbiased global transcriptomics and new network-based hyperedge entanglement prediction analysis identified the NF-κB (nuclear factor-kappa B) signaling molecules, lectin-like oxidized LOX-1 (LDL receptor-1), and SDC4 (syndecan-4) as potential PCSK9 targets mediating pro-inflammatory responses in macrophages. Conclusions: Circulating PCSK9 induces macrophage activation and vein graft lesion development via LDLR-independent mechanisms. PCSK9 may be a potential target for pharmacologic treatment for this unmet medical need.

Published
2022

13. Systems Approach to Discovery of Therapeutic Targets for Vein Graft Disease: PPARα Pivotally Regulates Metabolism, Activation, and Heterogeneity of Macrophages and Lesion Development

Author

Jianguo Wang, Sarvesh Chelvanambi, Andrew K. Mlynarchik, Lang H Lee, Peter Libby, Daniel G. Anderson, C. Keith Ozaki, Sasha A Singh, Shin Mukai, Arda Halu, Amitabh Sharma, Hengmin Zhang, Masanori Aikawa, Julius L. Decano, Joan T. Matamalas, Elena Aikawa, Jiao Qiao, and Caue Gasparotto A Bueno

Subjects
0303 health sciences, Pathology, medicine.medical_specialty, business.industry, Fistula, Systems biology, Inflammation, Metabolism, 030204 cardiovascular system & hematology, Proteomics, medicine.disease, Lesion, 03 medical and health sciences, 0302 clinical medicine, Physiology (medical), medicine, Macrophage, medicine.symptom, Cardiology and Cardiovascular Medicine, Vein graft disease, business, 030304 developmental biology
Abstract

Background: Vein graft failure remains a common clinical challenge. We applied a systems approach in mouse experiments to discover therapeutic targets for vein graft failure. Methods: Global proteomics and high-dimensional clustering on multiple vein graft tissues were used to identify potential pathogenic mechanisms. The PPARs (peroxisome proliferator-activated receptors) pathway served as an example to substantiate our discovery platform. In vivo mouse experiments with macrophage-targeted PPARα small interfering RNA, or the novel, selective activator pemafibrate demonstrate the role of PPARα in the development and inflammation of vein graft lesions. In vitro experiments further included metabolomic profiling, quantitative polymerase chain reaction, flow cytometry, metabolic assays, and single-cell RNA sequencing on primary human and mouse macrophages. Results: We identified changes in the vein graft proteome associated with immune responses, lipid metabolism regulated by the PPARs, fatty acid metabolism, matrix remodeling, and hematopoietic cell mobilization. PPARα agonism by pemafibrate retarded the development and inflammation of vein graft lesions in mice, whereas gene silencing worsened plaque formation. Pemafibrate also suppressed arteriovenous fistula lesion development. Metabolomics/lipidomics, functional metabolic assays, and single-cell analysis of cultured human macrophages revealed that PPARα modulates macrophage glycolysis, citrate metabolism, mitochondrial membrane sphingolipid metabolism, and heterogeneity. Conclusions: This study explored potential drivers of vein graft inflammation and identified PPARα as a novel potential pharmacological treatment for this unmet medical need.

Published
2021
Full Text
View/download PDF

14. Detecting and dissecting signaling crosstalk via the multilayer network integration of signaling and regulatory interactions

Author

Arda Halu, Seung Han Baek, Ian Lo, Leonardo Martini, Edwin K. Silverman, Scott T. Weiss, and Kimberly R. Glass

Abstract

The versatility of cellular response arises from the communication, or crosstalk, of signaling pathways in a complex network of signaling and transcriptional regulatory interactions. Understanding the various mechanisms underlying crosstalk on a global scale requires untargeted computational approaches. We present a network-based statistical approach, MuXTalk, that uses high-dimensional edges called multilinks to model the unique ways in which signaling and regulatory interactions can interface. We demonstrate that the signaling-regulatory interface is located primarily in the intermediary region between signaling pathways where crosstalk occurs, and that multilinks can differentiate between distinct signaling-transcriptional mechanisms. Using statistically over-represented multilinks as proxies of crosstalk, we predict crosstalk among 60 signaling pathways, expanding currently available crosstalk databases by more than five-fold. MuXTalk surpasses existing methods in terms of prediction performance, identifies additions to manual curation efforts, and pinpoints potential mediators of crosstalk for each prediction. Moreover, it accommodates the inherent context-dependence of crosstalk, allowing future applications to cell type- and disease-specific crosstalk.

Published
2022
Full Text
View/download PDF

15. Vitamin D constrains inflammation by modulating the expression of key genes on Chr17q12-21.1

Author

Ayşe Kılıç, Arda Halu, Margherita De Marzio, Enrico Maiorino, Melody G. Duvall, Thayse Brueggemann, Joselyn J. Rojas Quintero, Robert Chase, Hooman Mirzakhani, Ayse Özge Sungur, Janine Koepke, Taiji Nakano, Hong Yong Peh, Nandini Krishnamoorthy, Raja-Elie Abdulnour, Katia Georgopoulos, Augusto A. Litonjua, Marie B. Demay, Harald Renz, Bruce D. Levy, and Scott. T Weiss

Abstract

Vitamin D possesses immunomodulatory functions and vitamin D deficiency has been associated with the rise in chronic inflammatory diseases, including asthma (1). Vitamin D supplementation studies do not provide insight into the molecular genetic mechanisms of vitamin D mediated immunoregulation. Here we provide evidence for vitamin D regulation of two human chromosomal loci, Chr17q12-21.1 and Chr17q21.2, reliably associated with autoimmune and chronic inflammatory diseases (2–4). We demonstrate increased vitamin D receptor (VDR) expression in mouse lung CD4+ Th2 cells, differential expression of Chr17q12-21.1 and Chr17q21.2 genes in Th2 cells based on vitamin D status and identify the IL-2/Stat5 pathway as a target of vitamin D signaling. Vitamin D deficiency caused severe lung inflammation after allergen challenge in mice that was prevented by long term prenatal vitamin D supplementation. Mechanistically, vitamin D induced the expression of theIkzf3encoded protein Aiolos to suppress IL-2-signaling and ameliorate cytokine production in Th2 cells. These translational findings demonstrate mechanisms for the immune protective effect of vitamin D in allergic lung inflammation with a strong molecular genetic link to the regulation of both Chr17q12-21.1 and Chr17q21.2 genes and suggest further functional studies and interventional strategies for long-term prevention of asthma and other autoimmune disorders.One Sentence SummaryVitamin D regulates two human chromosomal loci, Chr17q12-21.1 and Chr17q21.2, that are associated with autoimmune and chronic inflammatory diseases.

Published
2022
Full Text
View/download PDF

16. Abstract 10223: Tissue-Entrapped Extracellular Vesicles Modulate Divergent Mechanisms of Cardiovascular Calcification

Author

Mark C Blaser, Fabrizio Buffolo, Arda Halu, Florian Schlotter, Hideyuki Higashi, Lorena Pantano Rubino, Louis A Saddic, Samantha Atkins, Maximillian Rogers, Tan Pham, Amelie Vromman, Eugenia Shvartz, Galina K Sukhova, Silvia MONTICONE, giovanni. camussi, Simon C Body, Tsuyoshi Kaneko, J Daniel D Muehlschlegel, Sasha A Singh, Masanori Aikawa, and Elena Aikawa

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Introduction: Fewer than 50% of patients develop vascular and valvular calcification, implying differential pathogenesis. Tissue-entrapped extracellular vesicles (EVs) are implicated in mineralization but their contents and functions are unstudied. We investigated entrapped EV cargoes in human cardiovascular disease. Methods: Human carotid endarterectomy specimens and stenotic aortic valves were obtained from 53 patients. Disease stage-specific proteomics was performed on whole tissue (non-diseased/fibrotic/calcified areas). Tissue EVs were enriched by gradient fractionation then underwent proteomics and miRNA-seq. miR targets were predicted by TargetScan, pathway analyses utilized BioCarta/KEGG/Reactome, and protein-protein interaction networks employed STRING. Results: Disease progression drove significant convergence (p Conclusions: This first comparative proteomics study of human valves and arteries finds shared EV functionality in both diseases. Using novel means to examine tissue EV molecular cargoes, we also reveal critical divergent tissue-specific roles for EVs in mediating cardiovascular disease.

Published
2021
Full Text
View/download PDF

17. Abstract 12316: Carnitine O-octanoyltransferase Inhibition Attenuates Human Aortic Valve Interstitial Cell Calcification by Correcting Energetic Mitochondrial State

Author

Takehito Okui, Masaya Iwashita, Maximillian A Rogers, Shiori Kuraoka, Arda Halu, Yoshikazu Sawada, Masanori Aikawa, Sasha A Singh, and Elena Aikawa

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Abstract

Background: Cardiovascular calcification is a critical pathology associated with increased cardiovascular risk, but there are no FDA-approved anti-calcification therapies. Through an unbiased screening approach, we previously identified carnitine O-octanoyltransferase (CROT) as a novel contributing factor to vascular calcification, but whether it can inhibit calcification in cardiac valves remains unknown. Here we investigated CROT-associated mechanisms of calcification in human valvular interstitial cells (VICs). Methods and Results: Human VICs were isolated from aortic valve leaflets of patients undergoing valve replacement surgeries at Brigham and Women’s Hospital, and cultured in osteogenic medium (OM) to induce calcification. OM increased CROT mRNA expression (1.83±0.41 fold-change; p99.9%; p Conclusions: CROT promotes calcification of human aortic VICs. CROT inhibition attenuates the calcification of VICs via correcting mitochondrial dysfunction induced by osteogenic environment. CROT inhibition is an attractive approach as a therapy for aortic valve calcification, a major unmet medical need.

Published
2021
Full Text
View/download PDF

21. CROT (Carnitine O-Octanoyltransferase) Is a Novel Contributing Factor in Vascular Calcification via Promoting Fatty Acid Metabolism and Mitochondrial Dysfunction

Author

Sasha A Singh, Ilyes Abdelhamid, Arda Halu, Shiori Kuraoka, Hideyuki Higashi, Samantha K. Atkins, Masanori Aikawa, Masaya Iwashita, Elena Aikawa, Maximillian A. Rogers, Takehito Okui, and Ashisha Ramsaroop

Subjects
Drug, Adult, Male, Proteomics, medicine.medical_specialty, Proteome, media_common.quotation_subject, Myocytes, Smooth Muscle, Mitochondrion, Muscle, Smooth, Vascular, Article, chemistry.chemical_compound, Osteogenesis, Internal medicine, Lipidomics, medicine, Myocyte, Animals, Humans, Vascular Calcification, Vascular calcification, Cells, Cultured, media_common, Mice, Knockout, Fatty acid metabolism, business.industry, Cholesterol, Fatty Acids, Middle Aged, Atherosclerosis, Fibrosis, Mitochondria, Mice, Inbred C57BL, Disease Models, Animal, Endocrinology, chemistry, Carnitine Acyltransferases, Receptors, LDL, Female, Cardiology and Cardiovascular Medicine, business, Energy Metabolism, Signal Transduction
Abstract

Objective: Vascular calcification is a critical pathology associated with increased cardiovascular event risk, but there are no Food and Drug Administration-approved anticalcific therapies. We hypothesized and validated that an unbiased screening approach would identify novel mediators of human vascular calcification. Approach and Results: We performed an unbiased quantitative proteomics and pathway network analysis that identified increased CROT (carnitine O-octanoyltransferase) in calcifying primary human coronary artery smooth muscle cells (SMCs). Additionally, human carotid artery atherosclerotic plaques contained increased immunoreactive CROT near calcified regions. CROT siRNA reduced fibrocalcific response in calcifying SMCs. In agreement, histidine 327 to alanine point mutation inactivated human CROT fatty acid metabolism enzymatic activity and suppressed SMC calcification. CROT siRNA suppressed type 1 collagen secretion, and restored mitochondrial proteome alterations, and suppressed mitochondrial fragmentation in calcifying SMCs. Lipidomics analysis of SMCs incubated with CROT siRNA revealed increased eicosapentaenoic acid, a vascular calcification inhibitor. CRISPR/Cas9-mediated Crot deficiency in LDL (low-density lipoprotein) receptor-deficient mice reduced aortic and carotid artery calcification without altering bone density or liver and plasma cholesterol and triglyceride concentrations. Conclusions: CROT is a novel contributing factor in vascular calcification via promoting fatty acid metabolism and mitochondrial dysfunction, as such CROT inhibition has strong potential as an antifibrocalcific therapy.

Published
2020

22. A disease-driver population within interstitial cells of human calcific aortic valves identified via single-cell and proteomic profiling

Author

Julius L. Decano, Yukio Iwamoto, Shinji Goto, Janey Y. Lee, Joan T. Matamalas, Arda Halu, Mark Blaser, Lang Ho Lee, Brett Pieper, Sarvesh Chelvanambi, Jessica Silva-Nicolau, Francesca Bartoli-Leonard, Hideyuki Higashi, Haruki Shibata, Payal Vyas, Jianguo Wang, Elena Gostjeva, Simon C. Body, Sasha A. Singh, Masanori Aikawa, and Elena Aikawa

Subjects
Proteomics, Extracellular Matrix Proteins, Osteogenesis, Aortic Valve, Animals, Calcinosis, Humans, Aortic Valve Stenosis, General Biochemistry, Genetics and Molecular Biology, Cells, Cultured
Abstract

Cellular heterogeneity of aortic valves complicates the mechanistic evaluation of the calcification processes in calcific aortic valve disease (CAVD), and animal disease models are lacking. In this study, we identify a disease-driver population (DDP) within valvular interstitial cells (VICs). Through stepwise single-cell analysis, phenotype-guided omic profiling, and network-based analysis, we characterize the DDP fingerprint as CD44

Published
2020
Full Text
View/download PDF

23. Annexin A1-dependent tethering promotes extracellular vesicle aggregation revealed with single-extracellular vesicle analysis

Author

Maximillian A. Rogers, Kristin Luther, Elena Aikawa, Mark C. Blaser, Elena Tsolaki, Fabrizio Buffolo, Peter Libby, Hideyuki Higashi, Simon C. Body, Sasha A Singh, Florian Schlotter, Samantha K. Atkins, Masanori Aikawa, Carlijn V. C. Bouten, Arda Halu, Lang H Lee, George G. Daaboul, Sergio Bertazzo, Biomedical Engineering, Cell-Matrix Interact. Cardiov. Tissue Reg., and ICMS Core

Subjects
0301 basic medicine, endocrine system, Microarray, education, SDG 3 – Goede gezondheid en welzijn, Proteomics, 03 medical and health sciences, 0302 clinical medicine, SDG 3 - Good Health and Well-being, Neutralizing antibody, Molecular Biology, Research Articles, Gene knockdown, Multidisciplinary, biology, Chemistry, Vesicle, SciAdv r-articles, Cell Biology, Extracellular vesicle, Microvesicles, Cell biology, 030104 developmental biology, biology.protein, 030217 neurology & neurosurgery, Research Article, Annexin A1
Abstract

Protein-mediated tethering of vesicles in the extracellular matrix contributes to microcalcification formation., Extracellular vesicles (EVs) including plasma membrane–derived microvesicles and endosomal-derived exosomes aggregate by unknown mechanisms, forming microcalcifications that promote cardiovascular disease, the leading cause of death worldwide. Here, we show a framework for assessing cell-independent EV mechanisms in disease by suggesting that annexin A1 (ANXA1)–dependent tethering induces EV aggregation and microcalcification. We present single-EV microarray, a method to distinguish microvesicles from exosomes and assess heterogeneity at a single-EV level. Single-EV microarray and proteomics revealed increased ANXA1 primarily on aggregating and calcifying microvesicles. ANXA1 vesicle aggregation was suppressed by calcium chelation, altering pH, or ANXA1 neutralizing antibody. ANXA1 knockdown attenuated EV aggregation and microcalcification formation in human cardiovascular cells and acellular three-dimensional collagen hydrogels. Our findings explain why microcalcifications are more prone to form in vulnerable regions of plaque, regulating critical cardiovascular pathology, and likely extend to other EV-associated diseases, including autoimmune and neurodegenerative diseases and cancer.

Published
2020

24. Conserved and Divergent Modulation of Calcification in Atherosclerosis and Aortic Valve Disease by Tissue Extracellular Vesicles

Author

Lorena Pantano, Tan H Pham, Giovanni Camussi, Florian Schlotter, Eugenia Shvartz, Hideyuki Higashi, Silvia Monticone, Fabrizio Buffolo, Louis A. Saddic, Samantha K. Atkins, Masanori Aikawa, Mark C. Blaser, Jochen D. Muehlschlegel, Simon C. Body, Sasha A Singh, Maximillian A. Rogers, Galina K. Sukhova, Elena Aikawa, and Arda Halu

Subjects
MAPK/ERK pathway, 0303 health sciences, Chemistry, Immunogold labelling, 030204 cardiovascular system & hematology, Proteomics, medicine.disease, 3. Good health, Cell biology, Extracellular matrix, Pathogenesis, 03 medical and health sciences, 0302 clinical medicine, Transcriptional regulation, medicine, Intracellular, 030304 developmental biology, Calcification
Abstract

BackgroundFewer than 50% of patients develop calcification of both atherosclerotic plaques and aortic valves, implying differential pathogenesis. While circulating extracellular vesicles (EVs) act as biomarkers of cardiovascular diseases, tissue-entrapped EVs associate with early mineralization, but their contents, function, and contributions to disease remain unknown.ResultsGlobal proteomics of human carotid artery endarterectomies and calcified aortic valves from a total of 27 donors/patients revealed significant over-representation of proteins with vesicle-associated pathways/ontologies common to both diseases. We exploited enzymatic digestion, serial (ultra)centrifugation and OptiPrep density-gradient separation to isolate EV populations from diseased arteries and valves. Mass spectrometry found 22 EV marker proteins to be highly enriched in the four least-dense OptiPrep fractions while extracellular matrix proteins predominated in denser fractions, as confirmed by CD63 immunogold electron microscopy and nanoparticle tracking analysis. Proteomics and miRNA-sequencing of OptiPrep-enriched tissue EVs quantified 1,104 proteins and 123 miR cargoes linked to 5,182 target genes. Pathway networks of proteins and miR targets common to artery and valve tissue EVs revealed a shared regulation of Rho GTPase and MAPK intracellular signaling cascades. 179 proteins and 5 miRs were significantly altered between artery and valve EVs; multi-omics integration determined that EVs differentially modulated cellular contraction and p53-mediated transcriptional regulation in diseased vascular vs. valvular tissue.ConclusionsOur findings delineate a strategy to isolate, purify, and study protein and RNA cargoes from EVs entrapped in fibrocalcific tissues. Multi-omics and network approaches implicated tissue-resident EVs in human cardiovascular disease.

Published
2020
Full Text
View/download PDF

25. XINA: A Workflow for the Integration of Multiplexed Proteomics Kinetics Data with Network Analysis

Author

Masanori Aikawa, Sasha A Singh, Hiroshi Iwata, Lang H Lee, Arda Halu, and Stephanie Morgan

Subjects
Proteomics, 0301 basic medicine, Computer science, In silico, Quantitative proteomics, Datasets as Topic, Computational biology, Biochemistry, Workflow, Bioconductor, 03 medical and health sciences, Animals, Humans, Protein Interaction Maps, KEGG, Cluster analysis, Cells, Cultured, 030102 biochemistry & molecular biology, Macrophages, General Chemistry, Kinetics, Identification (information), 030104 developmental biology, Software, Network analysis
Abstract

Quantitative proteomics experiments, using for instance isobaric tandem mass tagging approaches, are conducive to measuring changes in protein abundance over multiple time points in response to one or more conditions or stimulations. The aim is often to determine which proteins exhibit similar patterns within and across experimental conditions, since proteins with coabundance patterns may have common molecular functions related to a given stimulation. In order to facilitate the identification and analyses of coabundance patterns within and across conditions, we previously developed a software inspired by the isobaric mass tagging method itself. Specifically, multiple data sets are tagged in silico and combined for subsequent subgrouping into multiple clusters within a single output depicting the variation across all conditions, converting a typical inter-data-set comparison into an intra-data-set comparison. An updated version of our software, XINA, not only extracts coabundance profiles within and across experiments but also incorporates protein-protein interaction databases and integrative resources such as KEGG to infer interactors and molecular functions, respectively, and produces intuitive graphical outputs. In this report, we compare the kinetics profiles of >5600 unique proteins derived from three macrophage cell culture experiments and demonstrate through intuitive visualizations that XINA identifies key regulators of macrophage activation via their coabundance patterns.

Published
2018
Full Text
View/download PDF

26. Spatiotemporal Multi-Omics Mapping Generates a Molecular Atlas of the Aortic Valve and Reveals Networks Driving Disease

Author

Florian Schlotter, Lang H Lee, Payal Vyas, Masanori Aikawa, Jonathan G. Seidman, Hideyuki Higashi, Daniel M. DeLaughter, Amitabh Sharma, Simon C. Body, Christine E. Seidman, Elena Aikawa, Shinji Goto, Joseph Loscalzo, Sasha A Singh, Joshua D. Hutcheson, Arda Halu, Mark C. Blaser, Maximillian A. Rogers, and Tan Pham

Subjects
0301 basic medicine, Network medicine, Aortic valve, medicine.medical_specialty, Pharmacological therapy, business.industry, Atlas (topology), medicine.medical_treatment, Disease, 030204 cardiovascular system & hematology, medicine.disease, 03 medical and health sciences, Stenosis, 030104 developmental biology, 0302 clinical medicine, medicine.anatomical_structure, Valve replacement, Physiology (medical), Internal medicine, Cardiology, Medicine, Multi omics, Cardiology and Cardiovascular Medicine, business
Abstract

Background: No pharmacological therapy exists for calcific aortic valve disease (CAVD), which confers a dismal prognosis without invasive valve replacement. The search for therapeutics and early diagnostics is challenging because CAVD presents in multiple pathological stages. Moreover, it occurs in the context of a complex, multi-layered tissue architecture; a rich and abundant extracellular matrix phenotype; and a unique, highly plastic, and multipotent resident cell population. Methods: A total of 25 human stenotic aortic valves obtained from valve replacement surgeries were analyzed by multiple modalities, including transcriptomics and global unlabeled and label-based tandem-mass-tagged proteomics. Segmentation of valves into disease stage–specific samples was guided by near-infrared molecular imaging, and anatomic layer-specificity was facilitated by laser capture microdissection. Side-specific cell cultures were subjected to multiple calcifying stimuli, and their calcification potential and basal/stimulated proteomes were evaluated. Molecular (protein–protein) interaction networks were built, and their central proteins and disease associations were identified. Results: Global transcriptional and protein expression signatures differed between the nondiseased, fibrotic, and calcific stages of CAVD. Anatomic aortic valve microlayers exhibited unique proteome profiles that were maintained throughout disease progression and identified glial fibrillary acidic protein as a specific marker of valvular interstitial cells from the spongiosa layer. CAVD disease progression was marked by an emergence of smooth muscle cell activation, inflammation, and calcification-related pathways. Proteins overrepresented in the disease-prone fibrosa are functionally annotated to fibrosis and calcification pathways, and we found that in vitro, fibrosa-derived valvular interstitial cells demonstrated greater calcification potential than those from the ventricularis. These studies confirmed that the microlayer-specific proteome was preserved in cultured valvular interstitial cells, and that valvular interstitial cells exposed to alkaline phosphatase–dependent and alkaline phosphatase–independent calcifying stimuli had distinct proteome profiles, both of which overlapped with that of the whole tissue. Analysis of protein–protein interaction networks found a significant closeness to multiple inflammatory and fibrotic diseases. Conclusions: A spatially and temporally resolved multi-omics, and network and systems biology strategy identifies the first molecular regulatory networks in CAVD, a cardiac condition without a pharmacological cure, and describes a novel means of systematic disease ontology that is broadly applicable to comprehensive omics studies of cardiovascular diseases.

Published
2018
Full Text
View/download PDF

27. A Systems Approach to Refine Disease Taxonomy by Integrating Phenotypic and Molecular Networks

Author

Bing Li, Zhong Wang, Changkai Sun, Yingying Zhang, Xuezhong Zhou, Zhili Guo, Lei Lei, Guangming Liu, Arda Halu, Jun Liu, Amitabh Sharma, and Joseph Loscalzo

Subjects
0301 basic medicine, Network medicine, Genotype, Computer science, lcsh:Medicine, Disease, Computational biology, Disease taxonomy, Biology, computer.software_genre, Interactome, Models, Biological, General Biochemistry, Genetics and Molecular Biology, Disease phenotypes, 03 medical and health sciences, 0302 clinical medicine, Biomedical data, Similarity (psychology), Humans, Clinical phenotype, 030304 developmental biology, 0303 health sciences, Molecular profiles, lcsh:R5-920, Precision medicine, lcsh:R, General Medicine, Classification, Phenotype, 3. Good health, Molecular network, 030104 developmental biology, Editorial, 030220 oncology & carcinogenesis, Data mining, lcsh:Medicine (General), computer, Algorithms, Research Paper
Abstract

The International Classification of Diseases (ICD) relies on clinical features and lags behind the current understanding of the molecular specificity of disease pathobiology, necessitating approaches that incorporate growing biomedical data for classifying diseases to meet the needs of precision medicine. Our analysis revealed that the heterogeneous molecular diversity of disease chapters and the blurred boundary between disease categories in ICD should be further investigated. Here, we propose a new classification of diseases (NCD) by developing an algorithm that predicts the additional categories of a disease by integrating multiple networks consisting of disease phenotypes and their molecular profiles. With statistical validations from phenotype-genotype associations and interactome networks, we demonstrate that NCD improves disease specificity owing to its overlapping categories and polyhierarchical structure. Furthermore, NCD captures the molecular diversity of diseases and defines clearer boundaries in terms of both phenotypic similarity and molecular associations, establishing a rational strategy to reform disease taxonomy., Highlights • The International Classification of Diseases (ICD) lags behind the current molecular characteristics of disease. • We quantified the limitations (specificity and blurred boundary) of ICD with integrated phenotypic and molecular profiles. • An integrative disease network integrating phenotypic and genotypic profiles proposes a refined disease category framework. Disease taxonomy is one of the foundations of medical science and healthcare solutions. The most widely used disease taxonomy in clinical settings is the International Classification of Diseases (ICD), a system established >100 years ago and maintained by the World Health Organization to track disease incidence. It is well recognized that ICD, which is based on clinical observations, largely lags behind the molecular achievements of this medical big data era. We quantified the limitations of ICD using integrated phenotypic and molecular profiles and proposed a refined disease taxonomy with possible applications for precision medicine.

Published
2018

28. Regulation of Nuclear Receptor Interacting Protein 1 (NRIP1) Gene Expression in Response to Weight Loss and Exercise in Humans

Author

Erik Renström, Jiangming Sun, Yang De Marinis, Judit Domènech Omella, Amitabh Sharma, Martin Ridderstråle, Pradeep Bompada, Arda Halu, and Cheng Luan

Subjects
0301 basic medicine, Regulation of gene expression, medicine.medical_specialty, Nutrition and Dietetics, Endocrinology, Diabetes and Metabolism, Insulin, medicine.medical_treatment, Medicine (miscellaneous), Adipose tissue, Skeletal muscle, Biology, medicine.disease, 03 medical and health sciences, 030104 developmental biology, Endocrinology, medicine.anatomical_structure, Insulin resistance, Weight loss, Internal medicine, Gene expression, medicine, NRIP1, medicine.symptom
Abstract

Objective Nuclear receptor interacting protein 1 (NRIP1) is an important energy regulator, but few studies have addressed its role in humans. This study investigated adipose tissue and skeletal muscle NRIP1 gene expression and serum levels in response to weight loss and exercise in humans. Methods NRIP1 expression was measured by microarray and serum NRIP1 by ELISA and Western blotting. Skeletal muscle transcriptomes were analyzed from Gene Expression Omnibus databases. Network-based proximity analysis was performed on the proximity of NRIP1 interacting genes in the human interactome. Results In patients with obesity, adipose tissue NRIP1 mRNA expression increased during weight loss and weight maintenance and showed strong associations with metabolic markers and anthropometric parameters. Serum NRIP1 protein levels also increased after weight loss. In skeletal muscle, imposed rest increased NRIP1 expression by 80%, and strength training increased expression by ∼25% compared to baseline. Following rest, NRIP1 expression became sensitive to insulin stimulation. After re-training, NRIP1 expression decreased. Interactome analysis showed significant proximity of NRIP1 interacting partners to the obesity network/module. Conclusions NRIP1 gene expression and serum levels are strongly associated with metabolic states such as obesity, weight loss, different types of exercise, and peripheral tissue insulin resistance, potentially as a mediator of sedentary effects.

Published
2017
Full Text
View/download PDF

29. Target Discovery in Calcification Through Omics and Systems Approaches

Author

Masanori Aikawa, Elena Aikawa, Arda Halu, Mark C. Blaser, and Louis A. Saddic

Subjects
Network medicine, Cardiovascular calcification, Drug discovery, Systems biology, Proteome, Metabolome, Computational biology, Biology, Proteomics, Omics
Abstract

Aberrant mineralization of soft tissues is a widespread, complex, and often fatal condition that is strongly predictive of morbidity and mortality. Despite the success of the current pharmacological era in revolutionizing treatment options for a host of diseases, therapeutic approaches for calcification have lagged far behind. In this chapter, we move sequentially through efforts to assess how calcification affects the (epi)genome, transcriptome, proteome, and metabolome, with a particular focus on cardiovascular calcification – though we expand to other tissues, organs, or diseases when possible or necessary. We then describe how cutting-edge systems biology approaches are being applied to this treasure trove of data, in order to infer meaning, causality, and mechanistic insight. In particular, we highlight recent efforts to integrate data from multiple omics techniques and the application of network medicine as a means to visualize the complex interplay of perturbations detected by omics, identify novel molecular interactions, and prioritize drug targets for subsequent validation studies.

Published
2020
Full Text
View/download PDF

30. Multiorgan Systems Study Reveals Igfbp7 as a Suppressor of Gluconeogenesis after Gastric Bypass Surgery

Author

Andrew K. Mlynarchik, Jose-Luiz Figueiredo, Hengmin Zhang, Ken Mizuno, Anna H. Ha, Arda Halu, Iwao Yamada, Masanori Aikawa, Lang H Lee, Yukiyoshi Yamazaki, Sasha A Singh, Naoaki Arima, Jiao Qiao, Hideyuki Higashi, and Yusuke Sasaki

Subjects
Blood Glucose, Proteomics, medicine.medical_specialty, IGFBP7, Gastric Bypass, Carbohydrate metabolism, medicine.disease_cause, Biochemistry, Mice, Weight loss, Diabetes mellitus, Internal medicine, Medicine, Animals, Humans, Glycemic, business.industry, Gastric bypass surgery, Gluconeogenesis, nutritional and metabolic diseases, General Chemistry, medicine.disease, Insulin-Like Growth Factor Binding Proteins, Intestines, Endocrinology, Metabolic syndrome, medicine.symptom, Insulin Resistance, business
Abstract

Roux-en-Y gastric bypass (RYGB) surgery reduces weight in obese patients. A marked decrease in blood glucose levels occurs before weight loss; however, key molecules that improve the glycemic profile remain largely unknown. Using a murine RYGB surgery model, we performed multiorgan proteomics and bioinformatics to monitor the proteins and molecular pathways that change in this early glycemic response. Multiplexed proteomic kinetics data analysis revealed that the Roux limb, biliopancreatic limb, liver, and pancreas each exhibited unique temporal and molecular responses to the RYGB surgery. In addition, protein-protein network analysis indicated that the changes to the microbial environment in the intestine may play a crucial role in the beneficial effects of RYGB surgery. Furthermore, insulin-like growth factor binding protein 7 (Igfbp7) was identified as an early induced protein in the Roux limb. Known secretory properties of Igfbp7 prompted us to further investigate its role as a remote organ regulator of glucose metabolism. Igfbp7 overexpression decreased blood glucose levels in diet-induced obese mice and attenuated gluconeogenic gene expression in the liver. Secreted Igfbp7 appeared to mediate these beneficial effects. These results demonstrate that organs responded differentially to RYGB surgery and indicate that Igfbp7 may play an important role in improving blood glucose levels.

Published
2019

31. Robustness and lethality in multilayer biological molecular networks

Author

Xueming Liu, Enrico Maiorino, Jianxi Gao, Amitabh Sharma, Joseph Loscalzo, and Arda Halu

Subjects
Molecular network, Computer science, Robustness (computer science), Interaction network, Homogeneous, Gene regulatory network, Lethality, Computational biology, Gene, Biological network, Network model
Abstract

Robustness is a prominent feature of most biological systems. In a cell, the structure of the interactions between genes, proteins, and metabolites has a crucial role in maintaining the cell’s functionality and viability in presence of external perturbations and noise. Despite advances in characterizing the robustness of biological systems, most of the current efforts have been focused on studying homogeneous molecular networks in isolation, such as protein-protein or gene regulatory networks, neglecting the interactions among different molecular substrates. Here we propose a comprehensive framework for understanding how the interactions between genes, proteins and metabolites contribute to the determinants of robustness in a heterogeneous biological network. We integrate heterogeneous sources of data to construct a multilayer interaction network composed of a gene regulatory layer, and protein-protein interaction layer and a metabolic layer. We design a simulated perturbation process to characterize the contribution of each gene to the overall system’s robustness, defined as its influence over the global network. We find that highly influential genes are enriched in essential and cancer genes, confirming the central role of these genes in critical cellular processes. Further, we determine that the metabolic layer is more vulnerable to perturbations involving genes associated to metabolic diseases. By comparing the robustness of the network to multiple randomized network models, we find that the real network is comparably or more robust than expected in the random realizations. Finally, we analytically derive the expected robustness of multilayer biological networks starting from the degree distributions within or between layers. These results provide new insights into the non-trivial dynamics occurring in the cell after a genetic perturbation is applied, confirming the importance of including the coupling between different layers of interaction in models of complex biological systems.

Published
2019
Full Text
View/download PDF

33. ApoC-III is a novel inducer of calcification in human aortic valves

Author

Renata Caroline Costa de Freitas, Masanori Aikawa, Cayla N. Rodia, Frank M. Sacks, Hideyuki Higashi, Alison B. Kohan, Florian Schlotter, Michael D. Creager, Joshua D. Hutcheson, Arda Halu, Mark C. Blaser, Jennifer R. Wen, Allison B. Andraski, Elena Aikawa, Farwah Iqbal, Shiori Kuraoka, Sasha A Singh, Pin-Jou Wu, Simon C. Body, Maximillian A. Rogers, and Tan Pham

Subjects
RT, retention time, 0301 basic medicine, Apolipoprotein E, Aortic valve, Pathology, Apolipoprotein B, VICs, valvular interstitial cells, Biochemistry, Fibrosis, FACS, fluorescence-activated cell sorting, PRM, parallel reaction monitoring, AV, aortic valve, IL-6, interleukin-6, Cells, Cultured, apoB, apolipoprotein B, DMEM, Dulbecco's modified Eagle's medium, biology, C, calcific, Calcinosis, lp(a), lipoprotein(a), Lipoprotein(a), F, fibrotic, Mitochondria, αSMA, α-smooth muscle actin, NC, noncalcific, medicine.anatomical_structure, APOM, Aortic Valve, BMP, bone morphogenic protein, lipids (amino acids, peptides, and proteins), Aortic valve calcification, Research Article, medicine.medical_specialty, FDR, false discovery rate, NF, nonfibrotic, AS, aortic stenosis, PPI, protein–protein interaction, HDL, high-density lipoprotein, lipids, 03 medical and health sciences, FBS, fetal bovine serum, medicine, Humans, Molecular Biology, Inflammation, Apolipoprotein C-III, 030102 biochemistry & molecular biology, apoC-III, business.industry, fibrosis, Aortic Valve Stenosis, Cell Biology, medicine.disease, CAVD, calcific aortic valve disease, calcific aortic valve disease, 030104 developmental biology, PM, procalcifying media, DDA, data-dependent acquisition, biology.protein, LDL-C, low-density lipoprotein cholesterol, business, valvular interstitial cells, NM, normal media, Calcification
Abstract

Calcific aortic valve disease (CAVD) occurs when subpopulations of valve cells undergo specific differentiation pathways, promoting tissue fibrosis and calcification. Lipoprotein particles carry oxidized lipids that promote valvular disease, but low-density lipoprotein-lowering therapies have failed in clinical trials, and there are currently no pharmacological interventions available for this disease. Apolipoproteins are known promoters of atherosclerosis, but whether they possess pathogenic properties in CAVD is less clear. To search for a possible link, we assessed 12 apolipoproteins in nonfibrotic/noncalcific and fibrotic/calcific aortic valve tissues by proteomics and immunohistochemistry to understand if they were enriched in calcified areas. Eight apolipoproteins (apoA-I, apoA-II, apoA-IV, apoB, apoC-III, apoD, apoL-I, and apoM) were enriched in the calcific versus nonfibrotic/noncalcific tissues. Apo(a), apoB, apoC-III, apoE, and apoJ localized within the disease-prone fibrosa and colocalized with calcific regions as detected by immunohistochemistry. Circulating apoC-III on lipoprotein(a) is a potential biomarker of aortic stenosis incidence and progression, but whether apoC-III also induces aortic valve calcification is unknown. We found that apoC-III was increased in fibrotic and calcific tissues and observed within the calcification-prone fibrosa layer as well as around calcification. In addition, we showed that apoC-III induced calcification in primary human valvular cell cultures via a mitochondrial dysfunction/inflammation-mediated pathway. This study provides a first assessment of a broad array of apolipoproteins in CAVD tissues, demonstrates that specific apolipoproteins associate with valvular calcification, and implicates apoC-III as an active and modifiable driver of CAVD beyond its potential role as a biomarker.

Published
2021
Full Text
View/download PDF

34. Uremic toxin indoxyl sulfate promotes pro-inflammatory macrophage activation via the interplay of OATP2B1 and Dll4-Notch signaling: Potential mechanism for accelerated atherogenesis in chronic kidney disease

Author

Toshiaki Nakano, Lang H Lee, Takashi Maejima, Daniel G. Anderson, Rodrigo K. Kuromoto, Angelo S.T. Kum, Kevin J. Kauffman, Mario S. Boff, Takehiro Suzuki, Albert-László Barabási, Mingxian Chen, Hiroshi Iwata, Jon C. Aster, Masanori Aikawa, Hideyuki Higashi, Gabriel C. Guimaraes, Shunsuke Katsuki, Diego V.S. Pestana, Sasha A Singh, Julius L. Decano, Whitney S. Golden, Elena Aikawa, Amitabh Sharma, Arda Halu, and Massachusetts Institute of Technology. Institute for Medical Engineering & Science

Subjects
Male, Notch signaling pathway, Organic Anion Transporters, Inflammation, 030204 cardiovascular system & hematology, Article, Proinflammatory cytokine, 03 medical and health sciences, Mice, 0302 clinical medicine, Physiology (medical), Medicine, Macrophage, Animals, Humans, Risk factor, Renal Insufficiency, Chronic, Vascular Calcification, 030304 developmental biology, Adaptor Proteins, Signal Transducing, Toxins, Biological, Uremia, Mice, Knockout, 0303 health sciences, Receptors, Notch, business.industry, Macrophages, Calcium-Binding Proteins, Intracellular Signaling Peptides and Proteins, Membrane Proteins, Macrophage Activation, medicine.disease, Atherosclerosis, Plaque, Atherosclerotic, Disease Models, Animal, Phenotype, RAW 264.7 Cells, Receptors, LDL, Uremic toxins, Cancer research, Indoxyl Sulfate, Intercellular Signaling Peptides and Proteins, medicine.symptom, Inflammation Mediators, Cardiology and Cardiovascular Medicine, business, Indican, Kidney disease, Signal Transduction
Abstract

Background: Chronic kidney disease (CKD) increases cardiovascular risk. Underlying mechanisms, however, remain obscure. The uremic toxin indoxyl sulfate is an independent cardiovascular risk factor in CKD. We explored the potential impact of indoxyl sulfate on proinflammatory activation of macrophages and its underlying mechanisms. Methods: We examined in vitro the effects of clinically relevant concentrations of indoxyl sulfate on proinflammatory responses of macrophages and the roles of organic anion transporters and organic anion transporting polypeptides (OATPs). A systems approach, involving unbiased global proteomics, bioinformatics, and network analysis, then explored potential key pathways. To address the role of Delta-like 4 (Dll4) in indoxyl sulfate–induced macrophage activation and atherogenesis in CKD in vivo, we used 5/6 nephrectomy and Dll4 antibody in low-density lipoprotein receptor–deficient (Ldlr-/-) mice. To further determine the relative contribution of OATP2B1 or Dll4 to proinflammatory activation of macrophages and atherogenesis in vivo, we used siRNA delivered by macrophage-targeted lipid nanoparticles in mice. Results: We found that indoxyl sulfate–induced proinflammatory macrophage activation is mediated by its uptake through transporters, including OATP2B1, encoded by the SLCO2B1 gene. The global proteomics identified potential mechanisms, including Notch signaling and the ubiquitin-proteasome pathway, that mediate indoxyl sulfate-triggered proinflammatory macrophage activation. We chose the Notch pathway as an example of key candidates for validation of our target discovery platform and for further mechanistic studies. As predicted computationally, indoxyl sulfate triggered Notch signaling, which was preceded by the rapid induction of Dll4 protein. Dll4 induction may result from inhibition of the ubiquitin-proteasome pathway, via the deubiquitinating enzyme USP5. In mice, macrophage-targeted OATP2B1/Slco2b1 silencing and Dll4 antibody inhibited proinflammatory activation of peritoneal macrophages induced by indoxyl sulfate. In low-density lipoprotein receptor–deficient mice, Dll4 antibody abolished atherosclerotic lesion development accelerated in Ldlr-/- mice. Moreover, coadministration of indoxyl sulfate and OATP2B1/Slco2b1 or Dll4 siRNA encapsulated in macrophage-targeted lipid nanoparticles in Ldlr-/- mice suppressed lesion development. Conclusions: These results suggest that novel crosstalk between OATP2B1 and Dll4-Notch signaling in macrophages mediates indoxyl sulfate–induced vascular inflammation in CKD.

Published
2019

35. Exploring the cross-phenotype network region of disease modules reveals concordant and discordant pathways between chronic obstructive pulmonary disease and idiopathic pulmonary fibrosis

Author

Seung Han Baek, Gary M. Hunninghake, Michael H. Cho, Shikang Liu, Edwin K. Silverman, Amitabh Sharma, Brian D. Hobbs, and Arda Halu

Subjects
Glycation End Products, Advanced, Male, MAP Kinase Signaling System, Gene regulatory network, Genome-wide association study, Disease, Biology, Bioinformatics, 03 medical and health sciences, Idiopathic pulmonary fibrosis, Pulmonary Disease, Chronic Obstructive, 0302 clinical medicine, Genetics, medicine, Humans, Anaplastic Lymphoma Kinase, Gene Regulatory Networks, Molecular Biology, Gene, Lung, Genetics (clinical), 030304 developmental biology, 0303 health sciences, COPD, Telomere Homeostasis, General Medicine, respiratory system, medicine.disease, Phenotype, Idiopathic Pulmonary Fibrosis, respiratory tract diseases, Extracellular Matrix, medicine.anatomical_structure, 030228 respiratory system, Female, General Article, Genome-Wide Association Study
Abstract

Chronic obstructive pulmonary disease (COPD) and idiopathic pulmonary fibrosis (IPF) are two pathologically distinct chronic lung diseases that are associated with cigarette smoking. Genetic studies have identified shared loci for COPD and IPF, including several loci with opposite directions of effect. The existence of additional shared genetic loci, as well as potential shared pathobiological mechanisms between the two diseases at the molecular level, remains to be explored. Taking a network-based approach, we built disease modules for COPD and IPF using genome-wide association studies-implicated genes. The two disease modules displayed strong disease signals in an independent gene expression data set of COPD and IPF lung tissue and showed statistically significant overlap and network proximity, sharing 19 genes, including ARHGAP12 and BCHE. To uncover pathways at the intersection of COPD and IPF, we developed a metric, NetPathScore, which prioritizes the pathways of a disease by their network overlap with another disease. Applying NetPathScore to the COPD and IPF disease modules enabled the determination of concordant and discordant pathways between these diseases. Concordant pathways between COPD and IPF included extracellular matrix remodeling, Mitogen-activated protein kinase (MAPK) signaling and ALK pathways, whereas discordant pathways included advanced glycosylation end product receptor signaling and telomere maintenance and extension pathways. Overall, our findings reveal shared molecular interaction regions between COPD and IPF and shed light on the congruent and incongruent biological processes lying at the intersection of these two complex diseases.

Published
2018

37. Abstract 175: Dynamin-Related Protein 1 Regulates Proteostasis and Proprotein Convertase Subtilisin/Kexin Type 9 Secretion

Author

Florian Schlotter, Hideyuki Higashi, Elena Aikawa, Maximillian A. Rogers, Takehito Okui, Sasha A Singh, Stephanie Morgan, Lang H Lee, Lixiang Wang, Alan Daugherty, Masanori Aikawa, Masatoshi Nomura, Yukiyoshi Yamazaki, Joshua D. Hutcheson, Arda Halu, and Claudia Goettsch

Subjects
endocrine system, DNM1L, Proteostasis, Chemistry, PCSK9, Autophagy, Subtilisin, Kexin, Mitochondrial fission, Cardiology and Cardiovascular Medicine, Proprotein convertase, Cell biology
Abstract

Objective: Dysfunctional protein homeostasis (proteostasis) contributes to cardiovascular and metabolic disorders. We and others associated the mitochondrial fission protein, Dynamin-related protein 1 (DRP1) with cardiometabolic disease. Liver DRP1-deficiency reduces serum lipids and very-low density lipoprotein secretion in high-fat fed mice; whether DRP1 mediates these effects via proteostasis regulation is unknown. Approach and Results: Using mass spectrometry integrated with network analysis to map the human liver secretome, we found DRP1 associated with cardiovascular disease modules and lipid pathways. Electron microscopy revealed human liver DRP1 at mitochondria, cytosol, vesicles, endoplasmic reticulum (ER), and clustered at membrane tethered to ER exit sites. DRP1 small molecule inhibition (Mdivi-1) or CRISPR/Cas9-mediated DRP1 deletion in human liver cells, and Drp1 -liver deficiency in mice reduced autophagic flux without impairing the amino acid metabolome, or activating the autophagy inhibitor, mammalian target of rapamycin complex 1. DRP1 partially co-localized and co-immunoprecipitated with the ER trafficking and autophagy regulator, Syntaxin 17, in human liver tissue and cells. DRP1 inhibition reduced Proprotein convertase subtilisin/kexin type 9 (PCSK9) secretion in human liver cells and mice (-78.5%), and altered trafficking of the PCSK9-binding and ER maintenance chaperone, Glucose-regulated protein 94. Co-treating human liver cells with Mdivi-1 and proteasome inhibitor (MG132), non-transcriptionally increased intracellular PCSK9, while maintaining Mdivi-1-mediated reduced PCSK9 secretion. Conclusions: We propose a novel function of DRP1 in the regulation of proteostasis, wherein DRP1 may cluster, then tether and/or constrict nascent autophagy-associated membrane at the ER via its interaction with Syntaxin 17. DRP1 inhibition likely reduces lipoprotein and PCSK9 secretion in part by impairing autophagic flux leading to compensatory chaperone-mediated proteasomal degradation for ER maintenance. Proteostasis regulation and the cellular function of DRP1 is more complex than previously thought, potentially providing new avenues to therapeutically target cardiometabolic disease.

Published
2018
Full Text
View/download PDF

38. Abstract 608: Integrated Omics and Network Analysis Identify Drivers of Calcific Bicuspid Aortic Valve Disease

Author

Ron Blankstein, Elena Aikawa, Lívia Silva Araújo Passos, Wunan Zhou, Hideyuki Higashi, Sasha A Singh, Tan H Pham, Mark C. Blaser, Lang H Lee, Masanori Aikawa, Marcelo F. DiCarli, Maria do Rosário Conceição Moura Nunes, Simon C. Body, Amitabh Sharma, Arda Halu, and Florian Schlotter

Subjects
Aortic valve disease, medicine.medical_specialty, business.industry, Heart malformation, Disease, medicine.disease, Omics, Pharmacotherapy, Bicuspid aortic valve, Aortic valve stenosis, Internal medicine, medicine, Cardiology, Cardiology and Cardiovascular Medicine, business
Abstract

Objectives: Calcific aortic valve disease (CAVD) shares risk factors with atherosclerosis but has no pharmacotherapy. Bicuspid aortic valve (BAV) is the most common congenital cardiac defect (2% of humans), and individuals with BAVs acquire CAVD at a rate >15-25x of those with tricuspid aortic valves (TAVs). The causes and mechanisms of accelerated BAV-CAVD remain unclear. This study demonstrates the integrated transcriptome and proteome of BAV-CAVD. Methods: Quantification of gated chest CTs assessed aortic valve calcification. We performed transcriptomics using Illumina sequencing and global unlabeled proteomics by LC-MS/MS in a total of 55 human aortic valves (24 stenotic TAVs and 25 stenotic BAVs from valve replacement surgeries segmented into fibrotic and calcific portions, and 6 non-diseased aortic valves from heart transplants). Results: Calcific burden did not differ between BAVs and TAVs (Agatston score: p = 0.88), but BAV mineralization was significantly accelerated as BAVs underwent surgery 11.5±1.74 years earlier than TAVs (p < 0.01). Transcriptomics sequenced 11,223 genes and proteomics identified 1,798 proteins. Of these, 174 genes (fibrotic = 121, calcified = 53) and 98 proteins (fibrotic = 24, calcified = 74) were differentially expressed between BAV- and TAV-CAVD. Pathway analysis of proteins enriched in BAVs vs. TAVs found significant enhancement of iron metabolism and proteoglycan function in BAV-CAVD, while complement activation and collagen biosynthesis distinguished TAVs. When overrepresented proteins were mapped to the protein-protein interactome, network analysis identified disease stage- and valve type-specific subnetworks. While numerous protein-protein interactions existed between the fibrosis and calcification subnetworks of TAVs, a disconnection between these two pathological processes was identified in BAV subnetworks. Conclusions: Integrated multi-omics of CAVD stratified by disease stage and valve type identify unique contributors to BAV pathogenesis and shed light on molecular drivers of disease. Network analysis finds that while fibrocalcific responses are linked in TAVs, fibrosis and calcification may develop independently in BAVs, with vital implications for targeting of therapeutics.

Published
2018
Full Text
View/download PDF

39. Abstract 329: Systems-based Target Discovery Reveals PPARa as a Key Metabolic Regulator for Macrophage Activation in Vein Graft Disease

Author

Julius Decano, Peter Mattson, Andrew Mlynarchik, Sasha A Singh, Hideyuki Higashi, Jung Choi, Hengmin Zhang, Arda Halu, C. Keith Ozaki, Peter Libby, Elena Aikawa, Jiao Qiao, Michael Creager, Lang H Lee, Alexander Mojcher, Daniel G. Anderson, Jianguo Wang, and Masanori Aikawa

Subjects
Pathology, medicine.medical_specialty, business.industry, Regulator, Inflammation, Vein graft, Lesion, medicine, Macrophage, medicine.symptom, Cardiology and Cardiovascular Medicine, Vein graft disease, Limb loss, business
Abstract

Objectives: Vein graft (VG) failure rates after surgical bypass for PAD remain high, which can cause limb loss. Yet, the underlying mechanisms for VG lesion development remain obscure. We took a systems approach to explore key pathways in a mouse model. Approach and Results: We implanted the inferior vena cava into the left carotid artery of fat-fed Ldlr-/- mice and monitored lesion development up to 4 weeks post-surgery. Unbiased proteomic profiling followed by hierarchical clustering showed distinct clusters. One protein cluster is decreased in vein grafts with overt lesions (poor outcome) relative to the group of non-diseased veins devoid of lesions and vein grafts with minimal lesion (favorable outcome). Conversely, this can be viewed as increased in the “favorable” outcome group. Using the “favorable outcome” predominant protein cluster, network analysis and pathway enrichment identified PPARα pathway as a top-ranked key hub node with high betweeness centrality measure. This implies that PPARα may play a key regulatory role in limiting lesion severity. We examined whether network-based prediction of PPARα can also serve as a therapeutic target to attenuate the development of experimental VG lesions. A blinded in vivo loss-of-function study using PPARα siRNA encapsulated in macrophage-targeted lipid nanoparticles (LNP) demonstrated higher plaque volume as seen by 3D ultrasound and histologic morphometry in the test group (n=7) versus the control group (n=8). In contrast, a randomized drug study on another set of VG mice using the new PPARα-selective agonist pemafibrate demonstrated less plaque lesions and macrophage accumulation in the drug group (n=11) compared to the control group (n=11). In vitro validation studies (alongside loss-of-function) including high-throughput qPCR, single cell qPCR, CyTOF, ELISA, FACS, and metabolic assays all suggested that pemafibrate-induced PPARα activation promotes a phenotype shift of activated macrophages into a less inflammatory state through metabolic reprogramming. Conclusion: Systems-based target discovery on VG demonstrates that PPARα agonism reduces lesion development and inflammatory burden. Targeting this pathway might furnish a novel therapeutic option to prevent VG lesion development.

Published
2018
Full Text
View/download PDF

40. Abstract 663: Nuclear RSK1 Induces Pro-inflammatory Activation of Macrophages through STAT1 Phosphorylation at Ser727

Author

Masanori Aikawa, Jiao Qiao, Iwao Yamada, Elena Aikawa, Jianguo Wang, Lee Lang Ho, Hideyuki Higashi, Alexander Mojcher, Sasha A Singh, Julius L. Decano, Arda Halu, and Keishi Nihira

Subjects
Cell signaling, biology, Chemistry, medicine, biology.protein, Phosphorylation, Macrophage, Inflammation, STAT1, medicine.symptom, Cardiology and Cardiovascular Medicine, Nuclear translocation, Cell biology
Abstract

Objective: Maladaptive inflammatory responses involve macrophage activation by pro-inflammatory cytokines such as IFN-γ. Proteins that undergo nuclear translocation may regulate these processes. Approach and Results: To explore novel key regulators of macrophage activation, we performed quantitative proteomics to monitor protein translocation to the nuclei of human primary macrophages elicited with IFN-γ for 0, 10, 20, 30, or 60 min. Bioinformatics identified RSK1, a ribosomal protein kinase, as one of the candidates. We found that IFN-γ stimulation promotes RSK1 phosphorylation at Ser380. STAT1 is a key mediator of IFN-γ-triggered cellular responses. Mass spectrometry identified RSK1-mediated phosphorylation sites within STAT1, including Ser727. siRNA silencing of RSK1 attenuated STAT1 phosphorylation in IFN-γ-stimulated macrophages. In concert with these results, RSK1 silencing hindered IFN-γ-induced secretion of pro-inflammatory chemokines in human primary macrophages, such as CCL2/MCP-1, CCL7/MCP-3, and CCL8/MCP-2. Conclusion: We discovered that RSK1 nuclear translocation triggers STAT1 phosphorylation, resulting in pro-inflammatory activation of macrophages (Figure), a novel role for a ribosomal protein-associated kinase in nuclear signaling and inflammation.

Published
2018
Full Text
View/download PDF

41. Abstract 228: Multi-omics Mapping Generates a Molecular Atlas of the Aortic Valve and Reveals Networks Driving Disease

Author

Maximillian A. Rogers, Masanori Aikawa, Daniel M. DeLaughter, Simon C. Body, Sasha A Singh, Jonathan G. Seidman, Elena Aikawa, Joshua D. Hutcheson, Christine E. Seidman, Arda Halu, Shinji Goto, Florian Schlotter, Payal Vyas, Joseph Loscalzo, Hideyuki Higashi, Tan H Pham, Amitabh Sharma, Mark C. Blaser, and Lang H Lee

Subjects
Aortic valve disease, Aortic valve, medicine.medical_specialty, Pharmacological therapy, business.industry, medicine.medical_treatment, valvular heart disease, Disease, medicine.disease, medicine.anatomical_structure, Valve replacement, Internal medicine, Aortic valve stenosis, medicine, Cardiology, Multi omics, Cardiology and Cardiovascular Medicine, business
Abstract

Background: No pharmacological therapy exists for calcific aortic valve disease (CAVD), which confers a dismal prognosis without valve replacement. The search for therapeutics and early diagnostics is challenging since CAVD presents in multiple pathological stages. Methods: A total of 25 human stenotic aortic valves obtained from valve replacement surgery were analyzed by multiple modalities, including transcriptomics and global unlabeled and tandem-mass-tagged proteomics by liquid chromatography-mass spectrometry. Results: Global transcriptional and protein expression signatures differed between the non-diseased, fibrotic, and calcific stages of CAVD, with consistent trends in gene and protein expression across disease stages. Anatomical aortic valve microlayers exhibited unique proteome profiles that were maintained throughout disease progression, and revealed GFAP as a specific marker of valvular interstitial cells (VICs) from the spongiosa layer. CAVD disease progression was marked by an emergence of smooth muscle cell activation, inflammation, and calcification-related pathways. Proteins overrepresented in the disease-prone fibrosa are functionally annotated to fibrosis and calcification pathways, and we found that, in vitro , fibrosa-derived VICs demonstrated greater calcification potential than those from the ventricularis. These studies confirmed that the microlayer-specific proteome was preserved in cultured VICs, and that VICs exposed to TNAP-dependent and TNAP-independent calcifying stimuli had distinct proteome profiles, both of which overlapped with that of the whole tissue. Network analysis of protein-protein interaction networks found a significant closeness to multiple inflammatory and fibrotic diseases. Conclusions: A spatially- and temporally-resolved multi-omics and systems biology strategy identifies the first molecular regulatory networks in CAVD, a cardiac condition without a pharmacological cure, and describes a strategy for endophenotype characterization that is broadly applicable to comprehensive omics studies of cardiovascular diseases.

Published
2018
Full Text
View/download PDF

42. Abstract 708: Using Global Proteomics and Network Science to Explore Therapeutic Targets for Abdominal Aortic Aneurysm (AAA)

Author

Stephanie Morgan, Lang H Lee, Hideyuki Higashi, Alan Daugherty, Masanori Aikawa, Sasha A Singh, Arda Halu, and Elena Aikawa

Subjects
medicine.medical_specialty, business.industry, cardiovascular system, medicine, Radiology, Cardiology and Cardiovascular Medicine, medicine.disease, business, Proteomics, Abdominal aortic aneurysm
Abstract

Objective: To understand mechanisms critical to aneurysm development and identify potential therapeutic targets, we performed global proteomics and network analysis in mouse models of AAA. Methods and Results: AAAs were produced by luminal perfusion of the infrarenal aorta of C57BL/6 (wild-type) mice with elastase or subcutaneous infusion of angiotensin II (AngII) in Apoe-/- and Ldlr-/- mice (on congenic C57BL/6 background). Aortas were harvested at two intervals corresponding to developing or end-point aneurysm phenotypes that are specific to each model (n=3 for each procedure, interval, and genotype). Aortas were dissected into 8 segments spanning the arch to infrarenal portion, resulting in combined 288 aortic segments for label-free proteomics. Proteins were classified as significantly correlated to aneurysm according to their fold-change over control. Additional correlations were derived from a high-dimensional data analysis tool (“Xina”), developed in our laboratory, which enables clustering of proteins according to model, genotype, aortic region, and interval. Using our criteria, we identified lists of 159 proteins in the Apoe-/- and 158 proteins in the Ldlr-/- mice (AngII infused), and 173 proteins in wild-type mice (elastase perfused). Network analysis of these protein lists reveal commonalities between the models to include protein pathways related to protein translation, immune function, platelet activation, and extracellular matrix organization. Pathways enriched following AngII infusion included phagosome function and platelet aggregation, while pathways enriched in the elastase model included apoptosis, smooth muscle cell contraction, and Fc gamma R-mediated phagocytosis. Conclusion: Identification of pathways and proteins shared among these models may present master regulators of aneurysmal events and identify therapeutic targets. Conversely, identifying aneurysmal events unique to each model will provide valuable information regarding the model(s) chosen for use in a study and help contextualize model-specific findings.

Published
2018
Full Text
View/download PDF

43. Context-enriched interactome powered by proteomics helps the identification of novel regulators of macrophage activation

Author

Sasha A Singh, Ana Luisa Abib, Hiroshi Iwata, Arda Halu, Alexander Mojcher, Amitabh Sharma, Jianguo Wang, and Masanori Aikawa

Subjects
0301 basic medicine, Proteomics, QH301-705.5, Systems biology, Science, Computational biology, Plasma protein binding, Biology, Interactome, General Biochemistry, Genetics and Molecular Biology, Transcriptome, 03 medical and health sciences, Immunology and Inflammation, Humans, Protein Interaction Maps, Biology (General), Cells, Cultured, Regulation of gene expression, Inflammation, General Immunology and Microbiology, General Neuroscience, Macrophages, cardiovascular, Immunity, Reproducibility of Results, General Medicine, Macrophage Activation, Phenotype, 030104 developmental biology, Gene Expression Regulation, ROC Curve, Cardiovascular Diseases, networks, Medicine, Signal transduction, Protein Binding, Signal Transduction, Research Article, Computational and Systems Biology, Human
Abstract

The role of pro-inflammatory macrophage activation in cardiovascular disease (CVD) is a complex one amenable to network approaches. While an indispensible tool for elucidating the molecular underpinnings of complex diseases including CVD, the interactome is limited in its utility as it is not specific to any cell type, experimental condition or disease state. We introduced context-specificity to the interactome by combining it with co-abundance networks derived from unbiased proteomics measurements from activated macrophage-like cells. Each macrophage phenotype contributed to certain regions of the interactome. Using a network proximity-based prioritization method on the combined network, we predicted potential regulators of macrophage activation. Prediction performance significantly increased with the addition of co-abundance edges, and the prioritized candidates captured inflammation, immunity and CVD signatures. Integrating the novel network topology with transcriptomics and proteomics revealed top candidate drivers of inflammation. In vitro loss-of-function experiments demonstrated the regulatory role of these proteins in pro-inflammatory signaling., eLife digest When human cells or tissues are injured, the body triggers a response known as inflammation to repair the damage and protect itself from further harm. However, if the same issue keeps recurring, the tissues become inflamed for longer periods of time, which may ultimately lead to health problems. This is what could be happening in cardiovascular diseases, where long-term inflammation could damage the heart and blood vessels. Many different proteins interact with each other to control inflammation; gaining an insight into the nature of these interactions could help to pinpoint the role of each molecular actor. Researchers have used a combination of unbiased, large-scale experimental and computational approaches to develop the interactome, a map of the known interactions between all proteins in humans. However, interactions between proteins can change between cell types, or during disease. Here, Halu et al. aimed to refine the human interactome and identify new proteins involved in inflammation, especially in the context of cardiovascular disease. Cells called macrophages produce signals that trigger inflammation whey they detect damage in other cells or tissues. The experiments used a technique called proteomics to measure the amounts of all the proteins in human macrophages. Combining these data with the human interactome made it possible to predict new links between proteins known to have a role in inflammation and other proteins in the interactome. Further analysis using other sets of data from macrophages helped identify two new candidate proteins – GBP1 and WARS – that may promote inflammation. Halu et al. then used a genetic approach to deactivate the genes and decrease the levels of these two proteins in macrophages, which caused the signals that encourage inflammation to drop. These findings suggest that GBP1 and WARS regulate the activity of macrophages to promote inflammation. The two proteins could therefore be used as drug targets to treat cardiovascular diseases and other disorders linked to inflammation, but further studies will be needed to precisely dissect how GBP1 and WARS work in humans.

Published
2018

44. The Transcriptional Signature of Growth in Human Fetal Aortic Valve Development

Author

Joshua M. Gorham, Christine E. Seidman, Elena Aikawa, Danielle Gottlieb Sen, Abdur Razzaque, Arda Halu, Jonathan G. Seidman, and Jessica Hartnett

Subjects
0301 basic medicine, Pulmonary and Respiratory Medicine, Aortic valve, Cellular differentiation, 030204 cardiovascular system & hematology, In Vitro Techniques, Andrology, Fetal Development, 03 medical and health sciences, 0302 clinical medicine, Downregulation and upregulation, Medicine, Humans, Gene, Regulation of gene expression, Fetus, Extracellular Matrix Proteins, business.industry, Sequence Analysis, RNA, Gene Expression Profiling, Gene Expression Regulation, Developmental, Gene expression profiling, 030104 developmental biology, medicine.anatomical_structure, Aortic Valve, Surgery, Cardiology and Cardiovascular Medicine, business, Extracellular matrix organization
Abstract

Background In the second trimester of human fetal development, a tenfold increase in fetal size occurs while cardiac valves grow and retain their function. Patterns of transcription in normally growing human aortic valves are unknown. Methods Discarded human aortic valve samples were collected from the second trimester, 6 from early (14, 15, 17 weeks) and 6 from late (20, 21, 22 weeks) gestation. Network analysis of RNA sequencing data identified subnetworks of significantly increasing and decreasing transcripts. Subsequent cluster analysis identified patterns of transcription through the time course. Pathway enrichment analysis determined the predominant biological processes at each interval. Results We observed phasic transcription over the time course, including an early decrease in cell proliferation and developmental genes (14 to 15 weeks). Pattern specification, shear stress, and adaptive immune genes were induced early. Cell adhesion genes were increased from 14 to 20 weeks. A phase involving cell differentiation and apoptosis (17 to 20 weeks) was followed by downregulation of endothelial-to-mesenchymal transformation genes and then by increased extracellular matrix organization and stabilization (20 to 22 weeks). Conclusions We present a unique data set, comprehensively characterizing human valve development after valve primordia are formed, focusing on key processes displayed by normal aortic valves undergoing significant growth. We build a time course of genes and processes in second trimester fetal valve growth and observe the sequential regulation of gene clusters over time. Critical valve growth genes are potential targets for therapeutic intervention in congenital heart disease and have implications for regenerative medicine and tissue engineering.

Published
2018

45. Controllability in an islet specific regulatory network identifies the transcriptional factor NFATC4, which regulates Type 2 Diabetes associated genes

Author

João Fadista, Albert-László Barabási, Leif Groop, Jörg Menche, Edwin K. Silverman, Julius L. Decano, Marc Vidal, Rashmi B. Prasad, Marc Santolini, Arda Halu, Yang-Yu Liu, Scott T. Weiss, Megha Padi, Masanori Aikawa, Amitabh Sharma, and Joseph Loscalzo

Subjects
0301 basic medicine, Candidate gene, endocrine system, endocrine system diseases, Gene regulatory network, Computational biology, Biology, General Biochemistry, Genetics and Molecular Biology, Article, 03 medical and health sciences, 0302 clinical medicine, Drug Discovery, Gene expression, Gene silencing, Gene, lcsh:QH301-705.5, 030304 developmental biology, 0303 health sciences, Applied Mathematics, Computer Science Applications, 3. Good health, 030104 developmental biology, lcsh:Biology (General), Modeling and Simulation, Expression quantitative trait loci, Pancreatic islet transplantation, TCF7L2, 030217 neurology & neurosurgery
Abstract

Probing the dynamic control features of biological networks represents a new frontier in capturing the dysregulated pathways in complex diseases. Here, using patient samples obtained from a pancreatic islet transplantation program, we constructed a tissue-specific gene regulatory network and used the control centrality (Cc) concept to identify the high control centrality (HiCc) pathways, which might serve as key pathobiological pathways for Type 2 Diabetes (T2D). We found that HiCc pathway genes were significantly enriched with modest GWAS p-values in the DIAbetes Genetics Replication And Meta-analysis (DIAGRAM) study. We identified variants regulating gene expression (expression quantitative loci, eQTL) of HiCc pathway genes in islet samples. These eQTL genes showed higher levels of differential expression compared to non-eQTL genes in low, medium, and high glucose concentrations in rat islets. Among genes with highly significant eQTL evidence, NFATC4 belonged to four HiCc pathways. We asked if the expressions of T2D-associated candidate genes from GWAS and literature are regulated by Nfatc4 in rat islets. Extensive in vitro silencing of Nfatc4 in rat islet cells displayed reduced expression of 16, and increased expression of four putative downstream T2D genes. Overall, our approach uncovers the mechanistic connection of NFATC4 with downstream targets including a previously unknown one, TCF7L2, and establishes the HiCc pathways’ relationship to T2D., Network medicine: Identifying the controlling pathways of Type 2 Diabetes Genes that structurally control regulatory networks uncover the pathways driving complex diseases. Amitabh Sharma of Brigham and Women’s Hospital and his colleagues constructed a tissue-specific gene regulatory network derived from human pancreatic islets and determined the genes that control the network, using the concept of “control centrality.” Pathways with high control centrality were significantly more associated with Type 2 Diabetes (T2D) than pathways with lower control centrality, and harbored loci that significantly affected gene expression (eQTLs) related to glucose levels. In vitro knockdown of NFATC4, jointly identified by control centrality and eQTL analysis, verified its downstream influence on genes known to be associated with T2D. Controllability in biological networks may help us pinpoint influential pathways as well as key regulators of many other complex diseases.

Published
2017
Full Text
View/download PDF

46. Fine synchronization of the CMS muon drift-tube local trigger using cosmic rays

Author

Sergio F Novaes, Cecilia Elena Gerber, J. Haupt, Morgan Lethuillier, H. Postema, Yasar Onel, Albert Ferrando, D. Campi, G. Merino, A. Ranieri, Christopher Seez, S. Qazi, Olivier Devroede, Donato Creanza, Ada Solano, Yao Weng, John T Harvey, Umberto Dosselli, Stefano Colafranceschi, Alessandro Giassi, V. Radicci, Julian Bunn, C. Marchica, Y. Zheng, M. Bontenackels, Franco Gonella, Benjamin Stieger, Hyun-Chul Kim, Yurii Maravin, A. Makankin, Vladimir Gavrilov, I. Osborne, Gaetano-Marco Dallavalle, Maurizio Pierini, S. Baccaro, David Cussans, L. Berretta, Aleko Khukhunaishvili, Gabriella Pugliese, Salvatore Costa, A. Smoron, D. C. Miner, Stephen Sanders, Yong Ban, M. De Gruttola, R. Volpe, F. Odorici, Josef Hrubec, B. R. Drell, Salim Cerci, Markus Friedl, C. Diez Pardos, F. Calzolari, Daniel R Claes, M. Carleton, A. Furgeri, Mikko Voutilainen, M. Eichberger, Karl Gill, M. Bertani, D. J. Kong, K. Kastner, G. Cuscela, Robert Harr, Nancy Marinelli, S. Korjenevski, Andris Skuja, J. Vaughan, Nicola Pozzobon, D. Soroka, M. K. Daniel, F. Borcherding, Daniele Bonacorsi, Plamen Iaydjiev, M. Sowa, Gyorgy Bencze, Dimitri Bourilkov, S. Carrillo Moreno, Kevin Lannon, R. Stefanovitch, G. Della Ricca, C. N. Nguyen, E. B. Ziebarth, P. Trüb, G. Obrant, D. Bodin, Viktor Veszpremi, S. Y. Jun, D. Wenman, Aliaksandr Litomin, Z. Zinonos, Gianluca Petrillo, P. Siegrist, T. Schreiner, J. Frangenheim, B. Gomez Moreno, Dmytro Kovalskyi, Gyorgy Vesztergombi, Luca Malgeri, S. Slabospitsky, Batool Safarzadeh, Frank Jm Geurts, D. Liang, D. Vishnevskiy, Juliet Ritchie Patterson, S. Muzaffar, S. Di Vincenzo, S. Los, M. Jenkins, Thomas Bergauer, H. S. Chen, G. Lukhanin, Julie Malcles, Y. Fu, A. Solovey, H. Van Haevermaet, M. Zeise, I. Villella, Hannes Jung, Alexander Zhokin, Boaz Klima, D. Evans, Richard G Kellogg, Michael Tytgat, David Lange, Robin Erbacher, Wesley H Smith, V. Timciuc, S. Ravat, I. Gonzalez Caballero, Colin Bernet, Nadia Pastrone, R. Beuselinck, Sergey Shmatov, I. Crotty, V. Tancini, Boris Mangano, A. De Benedetti, R. Vasquez Sierra, Sebastian Naumann-Emme, Markus Stoye, Kai Yi, Harvey B Newman, Jeffrey Berryhill, Martijn Mulders, F. M. Farina, L. Barcellan, C. Baty, Ivica Puljak, Hans Reithler, Ben Bylsma, Carlos Willmott, Vladimir Mossolov, R. Godang, S. Esen, T. Toole, Roland Horisberger, Yuan Chao, Michele Arneodo, M. Baquero Ruiz, Guido Tonelli, T. Dupasquier, Roberto Tenchini, J. Weng, Seth Cooper, H. Held, Joao Varela, Leander Litov, A. Von Schultz Dratzig, M. Dzelalija, Jean-Pierre Merlo, Alexandre Zabi, M. Z. Mehta, A. M. Brett, O. Atramentov, Edmund Berry, Fabian Stockli, S. Sala, R. Bard, Guenakh Mitselmakher, H. Teng, F. Raffaelli, A. Madorsky, Joanne Cole, Othmane Bouhali, G. Broccolo, Tariq Aziz, A. Tumanov, M. Mazzucato, Anna Colaleo, Martti Raidal, Pamela Klabbers, S. A. Koay, I. Lazzizzera, Granville Ott, Louis Antonelli, Jordan Damgov, Dave M Newbold, Jessica Leonard, A. Anastassov, F. Chiumarulo, Jacobo Konigsberg, R. Gomez-Reino Garrido, P. Wertelaers, Daniele Fasanella, Stephane Perries, Dušan Jovanović, Zeljko Antunovic, Claudia-Elisabeth Wulz, Christoph Paus, A. Anisimov, A. Gresele, K. Nirunpong, S. S. Caiazza, G. Schwering, Paul Edmund Karchin, C. Zeidler, T. Liamsuwan, A. Macpherson, Vladimir Chekhovsky, Eija Tuominen, Luigi Fiore, Giovanna Selvaggi, T. Mäki, A. Moshaii, S. Chatrchyan, G. Szekely, X. Yang, Gabor Istvan Veres, David Mason, M. Marienfeld, Pablo Garcia-Abia, Luigi Moroni, Luca Lista, Alain Hervé, A. F. Osorio Oliveros, V. Kozhuharov, Ivan Vila, Sergey Troitsky, Vladimir Rekovic, Ian Shipsey, P. Verdier, Martino Margoni, Jochen Ott, M. Boldini, Costas Foudas, Devdatta Majumder, Dominique Gigi, I. Segoni, Peter Kreuzer, Wolfgang Waltenberger, Michael Albrow, S. Lukyanenko, Hamed Bakhshiansohi, Stephan Linn, Marguerite Tonjes, David Mark Raymond, Christophe Delaere, D. Soares, J. Caballero Bejar, J. A. Lopez Perez, M. Balazs, Hannes Sakulin, Piergiulio Lenzi, S. Kailas, A. Karneyeu, M. Kirn, Gregor Kasieczka, A. Pullia, A. Besson, W. D. Schlatter, G. Kaussen, Kisung Lee, P. Van Mechelen, Claude Amsler, W. Ahmed, Marko Dragicevic, Willard Johns, D. Druzhkin, Y. Choi, Nishu Nishu, C. D. Jones, M. Stettler, Aram Avetisyan, I. Diaz Merino, V. Tarakanov, T. Danielson, Paul Kyberd, Toyoko Orimoto, Luciano Romero, Bolek Wyslouch, Sergei Gleyzer, Maria Spiropulu, Andrea Venturi, Richard J. K. Taylor, P. Van Hove, Urs Langenegger, Andrea Petrucci, Piet Verwilligen, Stefan Spanier, K. Gunthoti, Vardan Khachatryan, Y. Gavrikov, C. C. Wang, M. Pernicka, James G Branson, Teng Ma, Keith Rose, Mingshui Chen, Nikita Beliy, V. E. Postoev, L. Sala, Viatcheslav Stolin, Victor Kim, Sarah Catherine Eno, G. Bauer, Minkyoo Choi, Alessio Bonato, G. Kozlov, Raffaello D'Alessandro, Frank Würthwein, W. Van Doninck, William John Womersley, Hans-Christian Kaestli, T. Kuhr, K. Tokesi, M. Giunta, Armando Lanaro, W. Dagenhart, A. Vedaee, Eric Wayne Vaandering, Vladimir Karjavin, F. Mariani, Tilman Rohe, Mia Tosi, Daniel Bloch, M. C. Sawley, M. H.G. Souza, Jose M Hernandez, S. Jaditz, Alan D. Lopez, Vivek Sharma, Lorenzo Foà, Slawek Tkaczyk, T. M. Aliev, Fabio Cossutti, H. Topakli, Andrei Sobol, Mariarosaria D'Alfonso, Mario Galanti, A. De Roeck, M. Binkley, Zoltan Szillasi, D. G. Phillips, J. Gruschke, Salvatore My, James Dolen, Tomas Lindén, Scott Thomas, Piero Giorgio Verdini, Manas Maity, A. Scheurer, D. Dammann, Marco Meschini, Prashant Shukla, Akram Khan, K. Lelas, A. Meyer, Nicolas Chanon, Helena Malbouisson, Andrey Vorobyev, Camelia Mironov, N. Bourgeois, V. Kozlov, Marcella Bona, Ilknur Hos, J. N. Butler, Alexandre Sakharov, Susan Gascon, M. Haguenauer, Mikhail Korzhik, M. Chamizo Llatas, Kerstin Borras, Freya Blekman, L. M. Edera, H. El Mamouni, Russell Richard Betts, N. Darmenov, T. R. Fernandez Perez Tomei, M. I. Asghar, Giovanni Polese, J. Nysten, Alexi Mestvirishvili, Ulrich Goerlach, Farida Fassi, Robert Hirosky, S. Gowdy, Jesus Marco, David Krofcheck, T. Sabonis, T. Le Grand, Konstantin Matchev, M. J. Ryan, David Petyt, A. Gomez, Xin Shi, Piero Giubilato, André Rosowsky, J. C. Marin, Anna Elliott-Peisert, Vuko Brigljevic, Bruno Wittmer, Joris Maes, Sho Maruyama, Franco Ligabue, D. Benedetti, Hugues Brun, A. Sytine, Pieter Everaerts, Roman Ryutin, Roberto Carlin, P. Tropea, D. Cebra, F. Mittermayr, Jonathan Hollar, Georgia Karapostoli, Willis Lin, Jean-Marie Brom, Z. Xue, N. Van Remortel, Steve Nahn, C. Lundstedt, Paolo Capiluppi, James Rohlf, Carlos Avila, F. De Guio, M. Kossov, Pierre Depasse, Y. Gotra, Giuseppe Benedetto Cerati, James D. Olsen, David S. Holmes, Sridhara Dasu, Emilio Meschi, Anirban Saha, Vyacheslav Klyukhin, Carlo Civinini, Gunther Roland, A. Satpathy, A. Ruiz Jimeno, M. A. Borgia, Darren Puigh, Vitaliano Ciulli, Apostolos Panagiotou, M. A. Afaq, N. Konovalova, M. Biasotto, S. Schmid, S. Natali, Chiara Mariotti, Ugur Akgun, Aytul Adiguzel, Andrey Uzunian, H. Park, Gui Nyun Kim, Alice Bean, Demetra Tsiakkouri, Lukas Vanelderen, D. Franci, Dennis Shpakov, Giuseppe Zito, David Michael Morse, U. Gebbert, Muhammad Imran Malik Awan, Ivan-Kresimir Furic, R. Brauer, Kai-Feng Chen, J. Bernardim, Ettore Focardi, J. Garberson, Viola Sordini, P. Jindal, Nikolay Bondar, S. Mueller, D. Martschei, Sergei Bitioukov, A. Artamonov, Daniela Bortoletto, Crisostomo Sciacca, Z. Xie, Richard D Field, Marco Pieri, M. H. Zoeller, Y. Ershov, M. Meneghelli, Paolo Lariccia, O. Koybasi, O. Oberst, P. Bellan, S. Oggero, Stefan Piperov, Pierre Piroué, L. Gross, Z. Geese, Jeannine Wagner-Kuhr, John Rander, F. Pellegrino, N. Santacruz, Balazs Ujvari, Yuri Musienko, Aaron Levine, D. Novak, F. Clemente, Lea Caminada, Rong-Shyang Lu, E. Hazen, A. C. Kraan, H. B. Rhee, Egidio Longo, Y. Guo, M. Oberegger, K. S. Sim, R. Romaniuk, Markus Merschmeyer, Arie Bodek, M. Gataullin, R. Stark, Jan Veverka, Frédéric Drouhin, Avishek Chatterjee, Mehmet Vergili, Alexander Tapper, Vyacheslav Krutelyov, Ricardo Eusebi, Suvadeep Bose, David Fehling, Peter Wagner, A. Lyonnet, Y. Mel'Nik, Ian R Tomalin, V. Delachenal, Edwin Antillon, Si-Jin Qian, Youn Roh, Barry Blumenfeld, J. Sibille, B. Camanzi, Giulio Pellegrini, P. D'Angelo, Lorenzo Visca, Pierluigi Paolucci, R. Loos, A. Trunov, V. Burtovoy, B. Klein, E. Marinova, Mustafa Numan Bakirci, Dong-Chul Son, Manoj Jha, Ozlem Kaya, A. K. Honma, Salvatore Rappoccio, H. Szczesny, V. D. Cafaro, C. Mavrommatis, T. Punz, D. Aisa, Hongfang Liu, P. Schieferdecker, H. Bergauer, C. Plager, Liliana Teodorescu, B. Gobbi, Richard Wigmans, Adolf Bornheim, Loukas Gouskos, J. Lee, R. Gonzalez Suarez, Andrey Gribushin, M. De La Calderón Barca Sanchez, Lalit Mohan Pant, A. Lopez Virto, I. Dafinei, L. Goscilo, Gian Mario Bilei, V. Cuplov, Pushpalatha C Bhat, L. Antunes Pedro, Wolfgang Adam, A. Kumar, K. J. Smith, G. Alampi, Josef Strauss, V. Panov, N. Amaglobeli, Isa Dumanoglu, Aaron Dominguez, John Michael Marraffino, J. Efron, J. Temple, Konstantinos Petridis, O. A. Grachov, A. A. Ocampo Rios, Giancarlo Mantovani, Carlo Battilana, L. Dobrzynski, Sezen Sekmen, Anna Teresa Meneguzzo, G. Faber, A. Sánchez Hernández, Vladimir Palichik, S. Lacaprara, A. Hahn, N. Manna, Francesco Navarria, P. Sharp, Magdalena Djordjevic, Rafael Marco, M. Searle, Hung T. Nguyen, Igor Sfiligoi, S. L. Bally, Martin Kirakosyan, J. D. Swain, A. Petrunin, Rupinder Kaur, J. D. Maillefaud, Theodoros Geralis, I. Churin, Andrea Rizzi, Dietrich Liko, Yen-Jie Lee, M. Benettoni, V. Kolosov, Burt Holzman, C. Diez Gonzalez, S. Frosali, P. Petiot, U. Pein, A. Flossdorf, G. Torromeo, G. Giurgiu, K. Goulianos, Regina Demina, L. Sabbatini, Igor Katkov, Joachim Mnich, Alexey Volkov, Christian Sander, Andrea Triossi, Christoph Schwick, Richard Lander, G. Petragnani, Raj Thilak Rajan, M. Aguilar-Benitez, C. Jarvis, Edward Allen Wenger, Roberto Sacchi, P. Bartalini, E. Anttila, G. Marian, Natascha Hörmann, R. Wilkinson, Tejinder Virdee, D. G. Cassel, Riccardo Paramatti, Andrea Giammanco, P. Q. Ribeiro, S. Tourneur, Ajit Kumar Mohanty, J.H. Wang, V. Kalagin, D. Pandoulas, Xavier Janssen, C. Pinto, Ken W Bell, U. Nauenberg, L. Wehrli, Elisabetta Gallo, Alin Titus Serban, Javier Santaolalla, M. Kirsch, Michaël Maes, Leonid Levchuk, Gino Bolla, A. Zachariadou, Wing To, Luca Scodellaro, Firdevs Duru, Y. Velikzhanin, S. Schael, Kalanand Mishra, Lawrence Sulak, R. Musenich, I. Svintradze, Andrzej Zuranski, A. Conde Garcia, G. Ball, E. Bartz, Michael Wlochal, J. P. Chatelain, Andréia Márcia Santos de Souza David, C. Markou, Marcos Cerrada, B. Neuherz, S. Rugovac, P. Martinez Ruiz del Arbol, R. Carroll, C. Jung, M. Davids, Y. Ge, G. Patay, Simone Gennai, R. Walton, Cosmin Dragoiu, Jing Liu, M. A. Strang, B. Marangelli, F. Bostock, K. Krajczar, L. J. Gutay, M. Gulmini, Yajun Mao, T. Schum, Mikhail Kirsanov, Maria Cepeda, Jorgen D'Hondt, Daniele Pedrini, Bradley Cox, Filip Thyssen, B. Fabbro, Maria Elena Pol, Giacomo Sguazzoni, Alan Campbell, J. Heyninck, A. Everett, Oliver Pooth, J. Whitmore, G. Roselli, D. V. Bandurin, Fotios Ptochos, D. Gerbaudo, I. Goitom, Riccardo Bellan, J. Alcaraz Maestre, V. Dero, D. Tsirigkas, A. Fedorov, Maciej Górski, L. I. Sarycheva, Anna Kropivnitskaya, B. K. Heltsley, P. de Barbaro, D. Sprenger, Alberto Santoro, Monika Grothe, Konrad Deiters, Anna Cimmino, J. Yelton, Suresh C Tonwar, Sylvie Braibant-Giacomelli, Ajit Mohapatra, A. M. Vinogradov, P. Sturm, K. Karafasoulis, G. Grégoire, Iban Jose Cabrillo, Kadri Ozdemir, E. A. Chen, C. M. Lei, Andrei Gritsan, Michael W. Anderson, S. De Visscher, T. Kelly, Michael L. Norman, A. Zampieri, Francesco Santanastasio, Stoyan Stoynev, Tongguang Cheng, Christian Veelken, R. De Granier Cassagnac, Jason Gilmore, Marco Paganoni, D. J. Summers, S. Bricola, J. Gronberg, G. Hilgers, Loic Quertenmont, Yu. Andreev, Markus Klute, M. Buehler, A. Markou, R. Moser, Gian Piero Siroli, E. J. Garcia-Solis, N. Lumb, M. Afaq, M. Aldaya Martin, T. De Tabarelli Fatis, G. Gomez Ceballos, Nikos Varelas, J. Chen, Helen F Heath, M. Cardaci, Felicitas Pauss, N. Siegrist, R. Wilken, Jeremy Mans, C. Yuste, C. Mesropian, W. Hintz, Alexander Toropin, R. Schmidt, Grigory Safronov, Virgil E Barnes, Andrew Beretvas, D. Toback, M. Jaworski, H. Castilla Valdez, Jan Steggemann, Krzysztof T. Pozniak, A. Ayhan, Matthias Ulrich Mozer, Massimiliano Chiorboli, A. Morelos Pineda, J. Alberdi, Claus Kleinwort, Alexander Savin, D. P. Eartly, Julia Thom, Finn Rebassoo, Y. Ma, N. Lacalamita, Christopher George Tully, Jae Yool Kim, J. Yarba, Eleni Petrakou, Frederic Jean Ronga, Y. J. Lei, K. Banicz, Z. Wan, Demetrios Loukas, Jorge Molina, Colin Jessop, J. P. Fernández Ramos, Joel Goldstein, L. Millischer, S. Hernath, M. Niegel, Jordan Nash, Sung Keun Park, Matteo Marone, Jie Zhang, Jozsef Molnar, S. Ryu, Taimoor Khurshid, C. Eggel, Oana Elena Vickey Boeriu, E. Orishchin, Francesca Romana Cavallo, C. Siamitros, V. E. Kuznetsov, Elizaveta Shabalina, B. Huckvale, Gregory Rakness, Jean-Louis Faure, B. C. MacEvoy, Claudio Grandi, K. H. Hoffmann, Mayda Velasco, Valery Zhukov, Christos Leonidopoulos, Francesca Nessi-Tedaldi, M. Pioppi, Efe Yazgan, Günter Flügge, M. Guerzoni, I. Filozova, Robert Clare, Patrizia Azzi, M. De Magrans Abril, Francesca Cavallari, Andrea Sciabà, Stefano Belforte, D. Tonoiu, Grzegorz Wrochna, J. Eugster, Christopher Hill, Kirti Ranjan, N. Almeida, K. Ueno, C. Genta, Henrik Jeldtoft Jensen, P. Kuchinsky, T. Speer, T. L. Watts, Alexander Nikitenko, Giuseppe Barbagli, Jasvinder A. Singh, S. W. Lin, M. Jindal, A. S. Yoon, W. Braunschweig, T. Anguelov, G. Govi, Lucia Silvestris, Neeti Parashar, R. Gokieli, Ijaz Hussain, Klaus Rabbertz, Sebastiano Albergo, G. Dughera, Tiziano Rovelli, Michal Bluj, Andrey Marinov, Tomasz Frueboes, A. Sedov, P. Zych, Patrick Nedelec, Matthias Edelhoff, A. M. Guler, P. Antipov, N. K. Mondal, R. K. Shivpuri, T. A. Bolton, Kenichi Hatakeyama, B. W. Kennedy, Petr Levchenko, Marco Costa, M. De Palma, Enrique Calvo, Hafeez R Hoorani, H. Arfaei, E. Widl, Rino Castaldi, D. Rousseau, Daniel John Karmgard, Manfred Jeitler, Fabrizio Palla, T. Signal, Alessio Ghezzi, J. Palinkas, M. Müntel, Daniel Treille, D. De Jesus Damiao, J. Schümann, T. M. Shaw, M. Nikolic, K. Sogut, T. Christiansen, Richard Vidal, A. Azman Gokce, S. Semenov, Matthias Kasemann, R. Rahmat, G.K. Mini, A. Meynet Cordonnier, N. Mohr, W. Badgett, Howard Baer, F. X. Gentit, Catherine Kirsty Mackay, R. Goudard, M. Favre, Salvatore Buontempo, Paul Avery, Salavat Abdullin, Ferhat Ozok, I. Vankov, Randy Ruchti, Joe Incandela, Ayse Polatoz, S. Cihangir, A. Petrosyan, R. Fereos, N. Smiljkovic, Viktor Savrin, Mitchell Wayne, Karol Bunkowski, P. Lobelle Pardo, Roger Rusack, Marc Dejardin, J. M. Vizan Garcia, Kati Lassila-Perini, R. A. Ofierzynski, L. Lueking, Petra Merkel, R. Zuyeuski, Pelin Kurt, Domenico Giordano, Andrey A. Khomich, Si Xie, Paolo Checchia, L. Barbone, Robert Stone, Frank Meier, S. Hänsel, P. G. Murray, J. G. Shiu, Georg Steinbrück, J. C. Williams, J. M. Kohli, Suzan Basegmez, V. Grishin, Barbara Clerbaux, E. Washington, P. Debbins, Marcello Maggi, Davide Piccolo, G. Papagni, A. Papageorgiou, Antonio Rossi, Sean Lynch, Pete Markowitz, A. Kayis Topaksu, Claudio Campagnari, Teppo Mäenpää, M. Heinrich, J. Imrek, Duong Nguyen, J. Lamb, A. K. Srivastava, Volker Adler, Matti J Kortelainen, M. Serin, P. Arce, K. V. Tsang, S. H. Chuang, G. Altenhöfer, Alexander Dermenev, E. Nikonov, L. Perchalla, Dario Menasce, Konstantinos Theofilatos, Sandor Czellar, Ryan Rivera, Manuel Giffels, G. Sidiropoulos, Nikolai Golubev, Dong Ho Moon, M. Gateau, H. Naves Sordo, Dipanwita Dutta, P. P. Trapani, Anders Ryd, Gavin Davies, M. Calloni, Nikolai Krasnikov, D. W. Jang, Igor Lokhtin, Alexei Safonov, Gianni Zumerle, Sami Lehti, Robert Cousins, Didar Dobur, A. Oulianov, S. Goy Lopez, C. Timlin, Kadir Ocalan, M. Zielinski, B. Mura, Austin Ball, I. D'Antone, E. Eskut, Daniel Teyssier, Robert M Brown, J. Hays, Pasquale Noli, U. Felzmann, N. Frank, Victor Perelygin, Alessandra Fanfani, P. E. Marage, Mika Huhtinen, Steve Schnetzer, A. Dolgopolov, F. P. Schilling, Kevin Klapoetke, Marco Bellato, G. Olesen, D. Ungaro, Nikola Godinovic, A. Piluso, Altan Cakir, J. Howell, D. Osborne, German Martinez, Cristina Botta, J. Duarte Campderros, Frixos A Triantis, Marcos Fernandez, S. Metson, Carlos Lourenco, Andrew Askew, I. Vodopiyanov, J. Ellison, X. T. Meng, C. Viviani, Johannes Hauk, M. Guerra Jordao, S. Ashby, R. Panero, G. Önengüt Gökbulut, Gero Flucke, Manfred Paulini, Thomas Hebbeker, Yang Yang, K. Abadjiev, P. Killewald, Victor Krychkine, Matthew Jones, G. Maron, Paolo Giacomelli, E. Norbeck, Alberto Messineo, J. S. Keller, Salvatore Nuzzo, S. Pathak, H. Jeong, Vincenzo Monaco, M. Massa, Cristina Tuve, S. Lusin, Eric Conte, David Barney, Stephanie Beauceron, Mark Raymond Adams, M. Cardenas Montes, Wolfgang Lohmann, Christopher Neu, Dirk Ryckbosch, P. Martins, Alexander Oh, Sharon Hagopian, Giorgia Mila, K. Gabathuler, W. Zabolotny, W. Bender, M. Vazquez Acosta, T. Whyntie, Antonio Tropiano, M. Franco, M. Hoch, Miroslav Finger, S. Arora, Borislav Pavlov, Sergey Vavilov, G. De Lentdecker, Mithat Kaya, B. Curé, John Perry Cumalat, J. Puzović, Paul Lecoq, Sunil Bansal, Pierre Lecomte, Suyong Choi, Etiennette Auffray, B. Arnold, S. Tolaini, Alexander Lanev, Valentin Sulimov, Maurizio Biasini, Serena Mattiazzo, Philip H Butler, Sa. Jain, Ta-Yung Ling, Janos Erö, Panagiotis Katsas, Csaba Hajdu, S. Heier, Alessandro Montanari, J. Klem, G. Pasztor, Pavel Bunin, A. Parenti, P. Allfrey, Michael S. Witherell, S. Khalatian, Ian Fisk, T. Yetkin, E. McCliment, Elliot Lipeles, Marta Felcini, Luc Pape, T. Kurca, Vassili Kachanov, Christopher Justus, M. A. Ferreira Dias, S. L. Zang, Marc Weber, F. Dal Corso, Paolo Meridiani, Aron Soha, A. Chandra, Zheng Wang, Wajid Ali Khan, E. Castro, Christoph Grab, Drew Baden, Florian Beaudette, M. Hansen, Andrew Kubik, Marcella Diemoz, A. York, V. Gaultney, E. Twedt, Edouard Boos, Dario Bisello, Pascal Paganini, Heiko Geenen, A. Bhatti, Giacinto Donvito, David Stickland, Andi Hektor, Ugo Gasparini, Veikko Karimäki, Silvia Ochesanu, M. Chan, Nicola Cavallo, S. Dos Santos, M. Chauvey, V. Patras, D. Hufnagel, Albert M. Sirunyan, Ingo Bloch, B. Ponzio, M. Bose, Vasken Hagopian, Peter Elmer, S. Bilmis, Philippe Bloch, C. De Oliveira Martins, Victor Golovtsov, R. Pintus, M. Freitas Ferreira, Guo-Ming Chen, A. H. Heering, C. Lazaridis, S. Reucroft, Arabella Martelli, Victoria Zhukova, Alan Garfinkel, Jozef Kaiser, Gregory Habib Hammad, Lorenzo Bianchini, S. Vanini, J. F. Pernot, R. Dabrowski, Sudhir Malik, S. Dambach, Maksym Titov, V. Pavlunin, Herbert Rohringer, Victor Zhiltsov, Marina Passaseo, H. Pieta, J. Ribnik, Federico Ferri, G. Maire, Ia Iashvili, Filip Moortgat, Konstantinos Kousouris, Roberto Guida, Monoranjan Guchait, Jean-Roch Vlimant, Igor Golutvin, Ariella Cattai, L. K. Gibbons, J. A. Bakken, N. Ratnikova, M. C. Lemaire, Brajesh C Choudhary, Paul David Luckey, Serguei Volkov, N. Ilina, J. P. Girod, M. Deniz, Thomas Schoerner-Sadenius, Khristian Kotov, Krzysztof Piotrzkowski, Ekaterina Kuznetsova, Stefano Marcellini, Georgios Daskalakis, Maiko Takahashi, Alessandra Romero, Sergei Gninenko, D. Reyes Romero, Antonio Branca, Jean-Charles Fontaine, G. Zilizi, P. Sonnek, Anton Dimitrov, A. Denisov, C. Y. Chien, Daniel Robert Marlow, J. M. Barcala, Werner Lustermann, Andromachi Tsirou, Tatiana Medvedeva, Matteo Pegoraro, U. Baur, Sudha Ahuja, J. S. Wood, Lloyd Stanley Durkin, Benigno Gobbo, Nikolai Gorbounov, Pietro Govoni, Vincenzo Innocente, Remi Chipaux, Th. Hermanns, M. Weinberger, M. Blanco Otano, Mani Tripathi, Maryam Zeinali, Patrick Jarry, N. De Filippis, C. R. Newsom, Giuseppe Antonio Pierro, Evgueni Vlasov, D. Maronde, Saewoong Bahk, B. Baldin, Ping Tan, Kurtis F Johnson, M. E. Mattson, R. Remington, Senka Duric, S. Petrushanko, M. Ronquest, Wolfgang Wagner, Luca Perrozzi, Manfred Krammer, Nikolai Shumeiko, Bora Akgun, Kevin Sung, B. Tali, Nicola Bacchetta, Attila Racz, Roberta Arcidiacono, Jonathan Fulcher, Zhenwei Yang, F. M. Stober, J. C. Yun, J. Olzem, J. Pivarski, Greg P Heath, James Alexander, A. Onnela, Lutz Feld, Tommaso Boccali, C. Rogan, Geoffrey Hall, Mikhail Dubinin, Konstanty Sumorok, Semiray Girgis, A. Knutsson, Sanjay Padhi, E. Delmeire, Wei Li, S. D. Worm, Roger Wolf, Yongsun Kim, Natale Demaria, Douglas Berry, M. Nervo, D. Volyanskyy, N. Dinu, Ioannis Papadopoulos, P. Fabbricatore, Igor Azhgirey, Frank Golf, James Letts, J. A. Ballin, Joshua Bendavid, Nicanor Colino, Yves Sirois, Muhammad Ahmad, Georgios Anagnostou, Melody A. Swartz, Maxwell Chertok, Vipin Bhatnagar, Danilo Piparo, Leonid Tourtchanovitch, Anatoli Pashenkov, Avto Kharchilava, Mikhail Ignatenko, Tapio Lampén, A.G. Volodko, V. Sekhri, K. Kaschube, M. Bedjidian, Danek Kotlinski, Denis Gelé, G. De Hamel Monchenault, Fabrizio Fabbri, Andrea Gaddi, R. Frühwirth, L. Lloret Iglesias, Waclaw Karpinski, Warren Clarida, Elena Tikhonenko, A. Korpela, J. Asaadi, Inkyu Park, J. Puerta Pelayo, V. Miccio, O. Gonzalez Lopez, Nicola Amapane, Matteo Sani, T. Kypreos, E. James, B. I. Abelev, Ramazan Sever, L. Masetti, D. A. Sanders, Tuure Tuuva, W. Guan, Christoph Schäfer, G. Kukartsev, M. Cwiok, L. Demortier, F. Simonetto, Phillip Russell Dudero, Suman Bala Beri, Rachel Yohay, Luigi Guiducci, Gregory R Snow, T. Grassi, L. Wilke, B. Scurlock, Igor Volobouev, Lev Dudko, Jeremy Andrea, M. Alidra, Jim Hanlon, I. M. Anghel, Suat Ozkorucuklu, M. Bonnett Del Alamo, Shahram Rahatlou, C. Saout, P. Kalavase, J. Chung, Frank Hartmann, Luciano Orsini, Lev Uvarov, Rainer Wallny, T. Karaman, Vasile Mihai Ghete, Claire Shepherd-Themistocleous, Alan Sill, R. Ralich, G. Debreczeni, J. W. Gary, David Stuart, Giorgio Maggi, A. Clemente, Luigi Benussi, B. Caponeri, Ahmet S. Ayan, Sergio P Ratti, Z. Chen, Clara Jorda, L. M. Lebolo, Mauro Emanuele Dinardo, Frank Chlebana, Jaap Velthuis, E. Babucci, Nhan Viet Tran, M. Feindt, Christof Roland, M. Eads, V. Maroussov, C. Fernandez Bedoya, Christoph Wissing, D. Pierluigi, N. Toth, Christoph Rosemann, Giovanni Organtini, Paolo Rumerio, S. De Fonseca Souza, J. Blaha, D. Lansket, Leonard Apanasevich, M. Vander Donckt, Andreas Nowack, M. Delia Negra, S. Guo, John Paul Chou, L. Servoli, Frans Meijers, Emanuela Barberis, Avraham Yagil, Nicolo Magini, A. Linn, Simon Kwan, Michael Dittmar, Vladimir Andreev, Paraskevas Sphicas, Antonis P. Papadakis, A. Aurisano, J. Slaunwhite, F. Ambroglini, G. Velichko, Frank Raupach, Silvia Miglioranzi, M. Hollingsworth, S. De Weirdt, Andreas Hinzmann, Alain Givernaud, L. Perera, Sarah Kate Boutle, C. P. Beetz, Marcin Konecki, Pierluigi Zotto, Hwi Dong Yoo, Ioannis Evangelou, Richard Cavanaugh, F. Nowak, P. Negri, N. Toniolo, Jan Troska, A. Golyash, P. Rossman, Robert Bainbridge, A. Solin, Wee Don Teo, Anton Taurok, D. Heydhausen, Stephanie Baffioni, S. K. Kataria, B. De La Cruz, Vivian O'Dell, S. Wu, Yetkin Yilmaz, Arda Halu, Kristian Harder, Lei Feng, Panagiotis Kokkas, R. P. Smith, G. Dirkes, Ivan Amos Cali, I. Lobov, Brian Paul Padley, Giovanni Petrucciani, Dawn Leslie, M. Padrta, S. Zub, G. Schott, A. K. Sanchez, V. Sytnik, J. Descamps, Lorenzo Uplegger, William T. Ford, C. Burgos Lazaro, A. Drozdetskiy, Aruna Nayak, D. Engh, F. A. Teischinger, Christian Autermann, E. Borsato, Paolo Spagnolo, Kenneth Bloom, B. C. Shen, Ketino Kaadze, J. Parsons, P. Verrecchia, M. Michelotto, Vincenzo Chiochia, J. Thomsen, L. Farnesini, J. Klukas, Sercan Sen, A. Lucaroni, Y. H. Chang, A. Heikkinen, P. Van Mulders, Marco Rovere, B. Heyburn, D. Sillou, M. Ohlerich, S. Rouhani, Daniel Denegri, Quentin Ingram, Hartmut Stadie, Chuan-Ming Liu, S. König, André Holzner, Otilia Militaru, Igor Vorobiev, Josef Hammer, K. Banzuzi, C. K. Lae, M. Boutemeur, Bernard Ille, G. Cerizza, Christian Hartl, S. Elgammal, Gervasio Gomez, S. Muhammad, Dinko Ferencek, Giovanni Franzoni, Vladimir Petrov, G. Landi, R. Frazier, Radia Redjimi, A. Inyakin, N. Roinishvili, D. Samyn, Predrag Milenovic, Lindsey Gray, Peter R Hobson, J. Robles, E. Alagoz, Norbert Neumeister, Durmus A. Demir, Paolo Petagna, M. Janulis, Dmitri Konstantinov, Oliver Gutsche, M. Bertoldi, P. Torre, Vladimir Epshteyn, G. Pierschel, Philip Baringer, Werner Sun, Nicholas Cripps, N. Bernardino Rodrigues, M. Demarteau, P. Baesso, Gregory Iles, S. B. Rew, Pierre Juillot, S. Vasil'Ev, Alicia Calderon, F. Palmonari, Arno Heister, M. De Mattia, Sandra Oliveros, Alfredo Gurrola, Jeremy Scott Werner, Gordon H. Hanson, H. Shahzad, K. Zhu, Alexander Schmidt, Lei Zhang, Amedeo Staiano, D.D. Reeder, C. Sanzeni, A. Zatzerklyany, Meenakshi Narain, Robert Schöfbeck, Peter Timothy Cox, C. Alhajar, A. Moggi, D. Deyrail, Alessandro Thea, Sunil Somalwar, N. Redaelli, Silvio César Sampaio, W. Bacchi, K. Arisaka, C. Thiebaux, J. J. Navarrete, Alberto Benvenuti, M. Giardoni, T. Klimkovich, Alexis Pompili, Panos A Razis, Steven R. Simon, John Gabriel Acosta, N. Sinanis, F. Gasparini, Ernesto Migliore, N. Ippolito, E. Luiggi Lopez, Hans-Jürgen Simonis, Philip Harris, J. Fernandez Menendez, Stephen Wimpenny, Henning Flacher, Dave Pellett, Horst Breuker, Joachim Baechler, J. Butt, R. Trentadue, Dan Green, Lars Sonnenschein, Sergey Kuleshov, W. T. Chen, Archana Sharma, Ijaz Ahmed, N. Djaoshvili, S. Sengupta, L. Tuura, A. Nappi, P. Limon, V. Roinishvili, Fabio Montecassiano, Victor Daniel Elvira, Simone Paoletti, E. A. Albayrak, H. Gamsizkan, E. Albert, George Stephans, Francisco Yumiceva, H. Mendez, Gaelle Boudoul, L. Wendland, Joao Seixas, Francisco Matorras, S. Banerjee, John A Coughlan, Ritva Kinnunen, C. Loizides, Petar Maksimovic, Roberto Dell'Orso, E. Di Marco, Sergey Troshin, Meng Wang, P. Raies, T. Maes, J. Silva, Pàl Hidas, Nikolaos Manthos, K. T. Flood, Martin Grunewald, J. Piedra Gomez, G. Sartisohn, Patrick Janot, B. Hegner, Saptaparna Bhattacharya, A. P. Singh, Subir Sarkar, Remigius K. Mommsen, T. Sobrier, N. I. Geddes, B. Kim, Alexis Kalogeropoulos, A. Garcia Raboso, Alexander Ledovskoy, Vincent J Smith, Michail Bachtis, Leonid Chtchipounov, P. Cushman, P. Biallass, E. Dusinberre, David D'Enterria, U. Berzano, B. L. Betev, E. Prettner, Laura Borrello, Willi Bertl, A. Kamenev, Ilya Kravchenko, N. Grant, Marta Ruspa, V. Kaftanovt, R. Kroeger, Attilio Santocchia, Z. Toteva, P. Petrov, J. Smith, F. Liu, Oleg Prokofyev, Wolfram Erdmann, Suchandra Dutta, Giuseppe Codispoti, H. S. Budd, M. Wingham, B. Ananthan, M. Matveev, S. A. Schmitz, I. V. Akin, Roko Plestina, Mario Pelliccioni, Laird Kramer, Andrey Korytov, Alexander Snigirev, N. Sonmez, Alessandro Vicini, Tulika Bose, J. E. Ramirez Vargas, Byung-Sik Hong, A. Kurenkov, M. Pimiä, Maike Brigitte Neuland, D. Martisiute, G. Williams, Gigi Rolandi, W. Hopkins, Thorsten Chwalek, Nikolay Terentyev, Michael Mooney, Alberto Orso Maria Iorio, P. Chang, Nicolo Cartiglia, L. Agostino, V. Chetluru, M. Fischler, V. Barashko, Christopher Brew, Eduardo De Moraes Gregores, Serguei Ganjour, J. Muelmenstaedt, Silvia Taroni, John H. Wickens, Ricky Egeland, Anne-Marie Magnan, S. Foulkes, Wagner Carvalho, Todd Adams, G. Lungu, M. Sobron Sanudo, Vladimir Korenkov, Wit Busza, Vyacheslav Valuev, Lothar At Bauerdick, Wei Wu, Andrey Pozdnyakov, Lovedeep Kaur Saini, Dezso Horvath, A. White, W. Dominik, Thomas Kress, B. Zhu, Filippo Bosi, G. Hahn, S. C. Kao, H. F. Hoffmann, I. Belotelov, Noemi Beni, F. Loddo, Jean Fay, Igor Dremin, Y. B. Hsiung, Abideh Jafari, Greg Landsberg, Nathan Mirman, David Lomidze, J. Babb, Anatoli Zarubin, James Russ, S. Hone, L. Bagby, Alessia Tricomi, Krzysztof Nawrocki, G. Derylo, James Wetzel, X. T. Huang, Andras Laszlo, G. Le Godec, W. Beaumont, Jean-Laurent Agram, L. Veillet, Maria Isabel Josa, Anthony Moeller, Jim Freeman, Edward Laird, S. M. Silva Do Amaral, Giovanni Abbiendi, Leonard Spiegel, David Miller, Robert Klanner, Sertac Ozturk, C. H. Rivetta, Stefano Argiro, J. M. Bauer, J. Gartner, R. N.C. Gray, Catherine Newman-Holmes, Nikolay Tyurin, F. Bechtel, P. Gupta, Geng-Yuan Jeng, G. Cirino, Jordan Tucker, J. Callner, Teresa Rodrigo, K. S. Grogg, J. Mulon, Igor Smirnov, J. Gonzalez Sanchez, L. M. Cremaldi, Teimuraz Lomtadze, M. Eppard, Burak Bilki, A. Garmash, J. Stilley, J. C. Sanabria, Jung-Hyun Kim, S. P. Singh, Andreas Pfeiffer, Kreso Kadija, J. Olson, Jeffrey Richman, Gilvan Alves, Denis Favart, Jaakko Härkönen, Z. P. Zhang, Kerstin Hoepfner, Richard Loveless, D. Onoprienko, M. Dyulendarova, T. Dupont, E. Wicklund, S. Aisa, Nicholas John Hadley, Robert M Harris, Jan Krolikowski, Luiz Mundim, A. Kopecky, Andrea Benaglia, Michael Hildreth, Ren-Yuan Zhu, Aristotelis Kyriakis, Pascal Vanlaer, Luciano Barone, Manjit Kaur, Richard Breedon, S. Paktinat Mehdiabadi, E. Daubie, Darin Acosta, Kristian Allan Hahn, Marcello Mannelli, H. Steininger, I. Emeliantchik, Cristina Biino, Ivan Mikulec, Pasquale Musella, Andrea Bocci, C. Munro, Marco Musich, J. Rodrigues Antunes, J. Swanson, V. Halyo, Duncan Carlsmith, Sam Harper, Jehad Mousa, W-S Hou, Karl Matthew Ecklund, Francesco Fiori, V. Lukanin, Philippe Busson, Duccio Abbaneo, Gianluca Cerminara, V. Litvine, Elizabeth Locci, A. Kapusi, K. Sudhakar, U. E. Surat, Y. Zhang, V. Buege, T. McCauley, J. E. Elias, Giuseppe Bagliesi, S. Zelepoukine, S. Won, Welathantri Gd Dharmaratna, A. B. Meyer, E. Skup, Ferenc Sikler, Dayong Wang, Gabriele Benelli, Nikolaos Rompotis, Mario Kadastik, S. Blyweert, Shashikant Dugad, Sangmin Lee, Tommaso Dorigo, Sandra Malvezzi, S. Kalinin, Pietro Faccioli, M. Yan, J. Jones, Eva Halkiadakis, Hamit Mermerkaya, D. H. Kim, Shuichi Kunori, M. A. Castro, Antonio Russo, A. Tikhonov, Jose Lazo-Flores, Paolo Azzurri, Erik Butz, S. Piccolomo, Günther Dissertori, S. A. Tupputi, Brian Bockelman, A. Kaminskiy, Ivan Reid, Songkyo Lee, M. Nespolo, L. Raposo, V. Sknar, Joao Pela, A. Vishnevskiy, R. Kelley, B. Checcucci, Ted Kolberg, B. Philipps, Laurent Mirabito, Steven Lowette, Dmitry Hits, Jorma Tuominiemi, Maria Cruz Fouz, S. Moccia, Amitabh Lath, Souvik Das, Pedrame Bargassa, E. Juska, Dave Dykstra, Joseph Lykken, Lucas Taylor, L. Lusito, Marco Cuffiani, Andrew Rose, Oliver Buchmuller, Vladimir Ryjov, B. A. Barnett, C. Martinez Rivero, Giorgio Apollinari, Ulf Behrens, Daniele Spiga, Piotr Traczyk, P. Sauerland, Claude Charlot, Burton Betchart, Teruki Kamon, Srecko Morovic, A. Singovsky, A. Ostaptchouk, E. Friis, David B. Cline, Erhan Gülmez, Kaori Maeshima, Martin Erdmann, J. A. Coarasa Perez, A. Oehler, K. Chung, T. Miceli, S. Erhan, J.C. Oller, L. Mucibello, Frank Glege, S. Ventura, Patricia McBride, Krzysztof Doroba, Jorge Luis Rodriguez, R. Briggs, Thomas Ferguson, I. Shreyber, Malte Renz, B. Pirollet, J. Mumford, David Colling, A. Gurtu, Jose Flix, D. Orbaker, Johannes Gutleber, M. Deliomeroglu, A. Bartoloni, Thomas Peiffer, Didier Contardo, M. Gastal, Matthias Schröder, Michael Schmitt, C. Jeong, Carlo Rovelli, David Jonathan Hofman, S. Stroiney, C. Hof, Fedor Ratnikov, Ezio Torassa, L. Rebane, A. Graziano, T. Miao, L. Castellana, K. Biery, I. Altsybeev, Harry Cheung, Peter Schleper, Zhen Hu, Keith Ulmer, W. Haj Ahmad, L. N. Vergili, Anita Topkar, Zoltan Laszlo Trocsanyi, J. Conway, D. Del Re, V. E. Bazterra, Gunter Quast, Aldo Penzo, T. Themel, D. R. Da Silva Di Calafiori, M. Hashemi, Andrea Castro, Vincent Lemaitre, E. A. De Wolf, R. Semenov, Davide Pagano, F. D. Ingram, Paul Baillon, D. Winn, V. Genchev, Artur Apresyan, Andrea Perrotta, V. Rapsevicius, I. De Magrans Abril, I. Marfin, S. Bolognesi, Marc Besancon, Wolfram Dietrich Zeuner, M. J. Miller, G. Fetchenhauer, Sergey Rusakov, David Futyan, Malgorzata Kazana, J. Cai, Katja Klein, P. Gartung, R. Trayanov, Junghwan Goh, A. Krokhotin, Livio Fanò, R. Vilar Cortabitarte, J. Suarez Gonzalez, M. Poettgens, C. Hackstein, Giuseppe Iaselli, P. Blüm, Y. Shcheglov, A. C. Le Bihan, A. Sourkov, Georgi Sultanov, Emine Gurpinar, S. Akimenko, S. Kossiakov, F. Feyzi, Roberto Covarelli, Petr Moisenz, David Ja Cockerill, Wolfgang Lange, T. Rommerskirchen, Gianni Masetti, Y. Shinde, Roberto Rossin, P. G. Ferreira Parracho, Alexander Ershov, C. Vander Velde, Sergio Cittolin, Julien Caudron, Jared Sturdy, Kerem Cankocak, Douglas Wright, I. Schmidt, S. Guragain, M. L. Miller, Erik Gottschalk, David Robert Wardrope, Yuriy Pakhotin, Harrison Prosper, Paolo Vitulo, William J Spalding, Jay Roberts, Stefano Bianco, Nicolas Schul, P. Silva, S. W. Li, A. Go, W. Tanenbaum, J. O. Lopez Berengueres, Yury Ivanov, R. Ranieri, Andre Sznajder, Hermine Katharina Wöhri, S. Y. Jung, Yuri Gershtein, A. Ronzhin, Giacomo Bruno, D. Colonna, David Cutts, Kevin Stenson, C. Regenfus, Stephen Robert Wagner, Sanghyeon Song, Amnon Harel, H. Esser, Emmanuelle Perez, Cristina Riccardi, Achim Stahl, G. P. Di Giovanni, Stephen Mrenna, V. Giordano, W. De Boer, H. Kluge, R. Adolphi, Laszlo Boldizsar, T. Bourrel, S. Conetti, A. Palma, Piotr Zalewski, D. Krpic, Leonardo Benucci, Marc Weinberg, J. H. Williams, S. Gollapinni, Vitaly Smirnov, J. Bos, G. De Robertis, D. Uhl, Nuno Leonardo, Wolfgang Funk, Marco Zanetti, M. Case, G. Dellacasa, Y. S. Chung, V. V. Mitsyn, Bryan Dahmes, H. Sauce, James Jackson, Helmut Vogel, B. Liu, Rainer Mankel, Eric Christian Chabert, Peicho Petkov, V. Oguri, Achille Petrilli, Chun-Hua Jiang, Tae Jeong Kim, M. Thomas, Michael Murray, Eric Cano, V. Makarenko, Sushil Chauhan, Kajari Mazumdar, A. Baud, Alexander Dierlamm, J. Marrouche, F. Romano, S. Popescu, M. Wensveen, M. M. Necchi, Genady Gavrilov, Marcus Hohlmann, V. Postolache, M. S. Rudolph, J. Warchol, D. Lazic, Carlos Florez, A. S. Muhammad, Marvin Johnson, A. C. Garcia-Bonilla, Jennifer S. Haas, I. Suzuki, F. Fedele, A. Delgado Peris, Michal Szleper, Philippe Gras, L. Berntzon, Michael Squires, J. St. John, D. Polic, Roberto Chierici, Chia-Ming Kuo, D. Bailleux, J. Draeger, Lubomir Dimitrov, C. A. Carrillo Montoya, Tony Wildish, G. Segneri, Arun Luthra, M. Mohammadi Najafabadi, J. Gu, Daniel Troendle, Panja-Riina Luukka, Roberto Salerno, Michael Wayne Arenton, Monique K. LeBourgeois, D. Uzun, T. Paul, James John Brooke, Stefka Stoykova, A. Nardulli, D. Hatton, Michele Selvaggi, Gulsen Onengut, Viktor Matveev, Olga Kodolova, M. Noy, Bora Isildak, Riccardo Travaglini, Himali Kalakhety, Yeng-Ming Tzeng, H. Pi, George Alverson, Benjamin Kreis, Matthieu Marionneau, Mehmet Zeyrek, J. F. de Trocóniz, Mark Pesaresi, Z. Szabó, Mario Jose Da Cunha Sargedas De Sousa, S. Wakefield, Shih-Fu Chang, Pavel Demin, Luca Martini, L. Tauscher, Umesh Joshi, Irina Vardanyan, Doris Eckstein, Achim Geiser, M. Duda, F. Dumitrache, K. Freudenreich, Javier Cuevas, O.V. Dvornikov, Marcello Abbrescia, Alison Lister, Kristjan Kannike, Stefano Mersi, C. Villanueva Munoz, O. Actis, K. Rossato, Francesco Pandolfi, A. Hunt, Z. J. Guo, Federica Fanzago, Viktor Konoplyanikov, Th. Müller, M. Mateev, Paul Sheldon, Yuichi Kubota, C. Noeding, S. Klimenko, A. T. Laasanen, B. Alver, R. Stringer, Philip Lawson, G. Perinic, D.A. Smolin, Otman Charaf, Jay Hauser, A. Vilela Pereira, Andrei Starodumov, G. Christian, Roberto Castello, Peter Robmann, I. Yaselli, D. Dattola, Richard Hall-Wilton, Elizabeth Sexton-Kennedy, Séverine Ovyn, Paolo Ronchese, Marc M Baarmand, Daniele Trocino, Silvia Maselli, Ali Fahim, Winston Ko, G. Walzel, Tiziano Camporesi, H. S. Bawa, Seema Sharma, E. Conti, D. Maletic, M. Schroeder, Renato Potenza, H. Gerwig, J. N. Bellinger, Guenter Eckerlin, G. Eulisse, D. Tornier, N. E. Adam, D. Oleynik, Kevin Burkett, Nural Akchurin, K. Gumus, L. Passamonti, M. Frey, P.E. Schlein, C.Y. Prescott, Martina Malberti, Dorian Kcira, M. Crawford, D. Andelin, P. Miné, A. Shchetkovskiy, Dieter Renker, Petar Adzic, D. Hirschbuehl, C. Ceron, Maria Margherita Obertino, J. Speck, A. Molinero, A. Liu, Michele Gallinaro, Alexey Golunov, Junquan Tao, Peter Wittich, Francesco Fabozzi, Y. Patois, Stefaan Tavernier, R. K. Choudhury, Gobinda Majumder, S. S. Vaurynovich, Romain Rougny, Stefano Ragazzi, Jane Nachtman, Chatrchyan, S., Khachatryan, V., Sirunyan, A. M., Adam, W., Arnold, B., Bergauer, H., Bergauer, T., Dragicevic, M., Eichberger, M., Eroe, J., Friedl, M., Fruehwirth, R., Ghete, V. M., Hammer, J., Haensel, S., Hoch, M., Hoermann, N., Hrubec, J., Jeitler, M., Kasieczka, G., Kastner, K., Krammer, M., Liko, D., de Abril I., Magran, Mikulec, I., Mittermayr, F., Neuherz, B., Oberegger, M., Padrta, M., Pernicka, M., Rohringer, H., Schmid, S., Schoefbeck, R., Schreiner, T., Stark, R., Steininger, H., Strauss, J., Taurok, A., Teischinger, F., Themel, T., Uhl, D., Wagner, P., Waltenberger, W., Walzel, G., Widl, E., Wulz, C. E., Chekhovsky, V., Dvornikov, O., Emeliantchik, I., Litomin, A., Makarenko, V., Marfin, I., Mossolov, V., Shumeiko, N., Solin, A., Stefanovitch, R., Gonzalez J., Suarez, Tikhonov, A., Fedorov, A., Karneyeu, A., Korzhik, M., Panov, V., Zuyeuski, R., Kuchinsky, P., Beaumont, W., Benucci, L., Cardaci, M., De Wolf, E. A., Delmeire, E., Druzhkin, D., Hashemi, M., Janssen, X., Maes, T., Mucibello, L., Ochesanu, S., Rougny, R., Selvaggi, M., Van Haevermaet, H., Van Mechelen, P., Van Remortel, N., Adler, V., Beauceron, S., Blyweert, S., D'Hondt, J., De Weirdt, S., Devroede, O., Heyninck, J., Kalogeropoulos, A., Maes, J., Maes, M., Mozer, M. U., Tavernier, S., Van Doninck, W., Van Mulders, P., Villella, I., Bouhali, O., Chabert, E. C., Charaf, O., Clerbaux, B., De Lentdecker, G., Dero, V., Elgammal, S., Gay, A. P. R., Hammad, G. H., Marage, P. E., Rugovac, S., Vander Velde, C., Vanlaer, P., Wickens, J., Grunewald, M., Klein, B., Marinov, A., Ryckbosch, D., Thyssen, F., Tytgat, M., Vanelderen, L., Verwilligen, P., Basegmez, S., Bruno, G., Caudron, J., Delaere, C., Demin, P., Favart, D., Giammanco, A., Gregoire, G., Lemaitre, V., Militaru, O., Ovyn, S., Piotrzkowski, K., Quertenmont, L., Schul, N., Beliy, N., Daubie, E., Alves, G. A., Pol, M. E., Souza, M. H. G., Carvalho, W., De Jesus Damiao, D., De Oliveira Martins, C., Fonseca De Souza, S., Mundim, L., Oguri, V., Santoro, A., Silva Do Amaral, S. M., Sznajder, A., Fernandez Perez Tomei, T. R., Ferreira Dias, M. A., Gregores, E. M., Novaes, S. F., Abadjiev, K., Anguelov, T., Damgov, J., Darmenov, N., Dimitrov, L., Genchev, V., Iaydjiev, P., Piperov, S., Stoykova, S., Sultanov, G., Trayanov, R., Vankov, I., Dimitrov, A., Dyulendarova, M., Kozhuharov, V., Litov, L., Marinova, E., Mateev, M., Pavlov, B., Petkov, P., Toteva, Z., Chen, G. M., Chen, H. S., Guan, W., Jiang, C. H., Liang, D., Liu, B., Meng, X., Tao, J., Wang, J., Wang, Z., Xue, Z., Zhang, Z., Ban, Y., Cai, J., Ge, Y., Guo, S., Hu, Z., Mao, Y., Qian, S. J., Teng, H., Zhu, B., Avila, C., Baquero Ruiz, M., Carrillo Montoya, C. A., Gomez, A., Gomez Moreno, B., Ocampo Rios, A. A., Osorio Oliveros, A. F., Reyes Romero, D., Sanabria, J. C., Godinovic, N., Lelas, K., Plestina, R., Polic, D., Puljak, I., Antunovic, Z., Dzelalija, M., Brigljevic, V., Duric, S., Kadija, K., Morovic, S., Fereos, R., Galanti, M., Mousa, J., Papadakis, A., Ptochos, F., Razis, P. A., Tsiakkouri, D., Zinonos, Z., Hektor, A., Kadastik, M., Kannike, K., Muentel, M., Raidal, M., Rebane, L., Anttila, E., Czellar, S., Harkonen, J., Heikkinen, A., Karimaki, V., Kinnunen, R., Klem, J., Kortelainen, M. J., Lampen, T., Lassila Perini, K., Lehti, S., Linden, T., Luukka, P., Maenpaa, T., Nysten, J., Tuominen, E., Tuominiemi, J., Ungaro, D., Wendland, L., Banzuzi, K., Korpela, A., Tuuva, T., Nedelec, P., Sillou, D., Besancon, M., Chipaux, R., Dejardin, M., Denegri, D., Descamps, J., Fabbro, B., Faure, J. L., Ferri, F., Ganjour, S., Gentit, F. X., Givernaud, A., Gras, P., de Monchenault G., Hamel, Jarry, P., Lemaire, M. C., Locci, E., Malcles, J., Marionneau, M., Millischer, L., Rander, J., Rosowsky, A., Rousseau, D., Titov, M., Verrecchia, P., Baffioni, S., Bianchini, L., Bluj, M., Busson, P., Charlot, C., Dobrzynski, L., de Cassagnac R., Granier, Haguenauer, M., Mine, P., Paganini, P., Sirois, Y., Thiebaux, C., Zabi, A., Agram, J. L., Besson, A., Bloch, D., Bodin, D., Brom, J. M., Conte, E., Drouhin, F., Fontaine, J. C., Gele, D., Goerlach, U., Gross, L., Juillot, P., Le Bihan, A. C., Patois, Y., Speck, J., Van Hove, P., Baty, C., Bedjidian, M., Blaha, J., Boudoul, G., Brun, H., Chanon, N., Chierici, R., Contardo, D., Depasse, P., Dupasquier, T., El Mamouni, H., Fassi, F., Fay, J., Gascon, S., Ille, B., Kurca, T., Le Grand, T., Lethuillier, M., Lumb, N., Mirabito, L., Perries, S., Vander Donckt, M., Verdier, P., Djaoshvili, N., Roinishvili, N., Roinishvili, V., Amaglobeli, N., Adolphi, R., Anagnostou, G., Brauer, R., Braunschweig, W., Edelhoff, M., Esser, H., Feld, L., Karpinski, W., Khomich, A., Klein, K., Mohr, N., Ostaptchouk, A., Pandoulas, D., Pierschel, G., Raupach, F., Schael, S., von Dratzig A., Schultz, Schwering, G., Sprenger, D., Thomas, M., Weber, M., Wittmer, B., Wlochal, M., Actis, O., Altenhoefer, G., Bender, W., Biallass, P., Erdmann, M., Fetchenhauer, G., Frangenheim, J., Hebbeker, T., Hilgers, G., Hinzmann, A., Hoepfner, K., Hof, C., Kirsch, M., Klimkovich, T., Kreuzer, P., Lanske, D., Merschmeyer, M., Meyer, A., Philipps, B., Pieta, H., Reithler, H., Schmitz, S. A., Sonnenschein, L., Sowa, M., Steggemann, J., Szczesny, H., Teyssier, D., Zeidler, C., Bontenackels, M., Davids, M., Duda, M., Fluegge, G., Geenen, H., Giffels, M., Ahmad W., Haj, Hermanns, T., Heydhausen, D., Kalinin, S., Kress, T., Linn, A., Nowack, A., Perchalla, L., Poettgens, M., Pooth, O., Sauerland, P., Stahl, A., Tornier, D., Zoeller, M. H., Martin M., Aldaya, Behrens, U., Borras, K., Campbell, A., Castro, E., Dammann, D., Eckerlin, G., Flossdorf, A., Flucke, G., Geiser, A., Hatton, D., Hauk, J., Jung, H., Kasemann, M., Katkov, I., Kleinwort, C., Kluge, H., Knutsson, A., Kuznetsova, E., Lange, W., Lohmann, W., Mankel, R., Marienfeld, M., Meyer, A. B., Miglioranzi, S., Mnich, J., Ohlerich, M., Olzem, J., Parenti, A., Rosemann, C., Schmidt, R., Schoerner Sadenius, T., Volyanskyy, D., Wissing, C., Zeuner, W. D., Autermann, C., Bechtel, F., Draeger, J., Eckstein, D., Gebbert, U., Kaschube, K., Kaussen, G., Klanner, R., Mura, B., Naumann Emme, S., Nowak, F., Pein, U., Sander, C., Schleper, P., Schum, T., Stadie, H., Steinbrueck, G., Thomsen, J., Wolf, R., Bauer, J., Bluem, P., Buege, V., Cakir, A., Chwalek, T., De Boer, W., Dierlamm, A., Dirkes, G., Feindt, M., Felzmann, U., Frey, M., Furgeri, A., Gruschke, J., Hackstein, C., Hartmann, F., Heier, S., Heinrich, M., Held, H., Hirschbuehl, D., Hoffmann, K. H., Honc, S., Jung, C., Kuhr, T., Liamsuwan, T., Martschei, D., Mueller, S., Mueller, T. h., Neuland, M. B., Niegel, M., Oberst, O., Oehler, A., Ott, J., Peiffer, T., Piparo, D., Quast, G., Rabbertz, K., Ratnikov, F., Ratnikova, N., Renz, M., Saout, C., Sartisohn, G., Scheurer, A., Schieferdecker, P., Schilling, F. P., Schott, G., Simonis, H. J., Stober, F. M., Sturm, P., Troendle, D., Trunov, A., Wagner, W., Wagner Kuhr, J., Zeise, M., Zhukov, V., Ziebarth, E. B., Daskalakis, G., Geralis, T., Karafasoulis, K., Kyriakis, A., Loukas, D., Markou, A., Markou, C., Mavrommatis, C., Petrakou, E., Zachariadou, A., Gouskos, L., Katsas, P., Panagiotou, A., Evangelou, I., Kokkas, P., Manthos, N., Papadopoulos, I., Patras, V., Triantis, F. A., Bencze, G., Boldizsar, L., Debreczeni, G., Hajdu, C., Hernath, S., Hidas, P., Horvath, D., Krajczar, K., Laszlo, A., Patay, G., Sikler, F., Toth, N., Vesztergombi, G., Beni, N., Christian, G., Imrek, J., Molnar, J., Novak, D., Palinkas, J., Szekely, G., Szillasi, Z., Tokesi, K., Veszpremi, V., Kapusi, A., Marian, G., Raics, P., Szabo, Z., Trocsanyi, Z. L., Ujvari, B., Zilizi, G., Bansal, S., Bawa, H. S., Beri, S. B., Bhatnagar, V., Jindal, M., Kaur, M., Kaur, R., Kohli, J. M., Mehta, M. Z., Nishu, N., Saini, L. K., Sharma, A., Singh, A., Singh, J. B., Singh, S. P., Ahuja, S., Arora, S., Bhattacharya, S., Chauhan, S., Choudhary, B. C., Gupta, P., Jain, S., Jha, M., Kumar, A., Ranjan, K., Shivpuri, R. K., Srivastava, A. K., Choudhury, R. K., Dutta, D., Kailas, S., Kataria, S. K., Mohanty, A. K., Pant, L. M., Shukla, P., Topkar, A., Aziz, T., Guchait, M., Gurtu, A., Maity, M., Majumder, D., Majumder, G., Mazumdar, K., Nayak, A., Saha, A., Sudhakar, K., Banerjee, S., Dugad, S., Mondal, N. K., Arfaei, H., Bakhshiansohi, H., Fahim, A., Jafari, A., Najafabadi M., Mohammadi, Moshaii, A., Mehdiabadi S., Paktinat, Rouhani, S., Safarzadeh, B., Zeinali, M., Felcini, M., Abbrescia, M., Barbone, L., Chiumarulo, F., Clemente, A., Colaleo, A., Creanza, D., Cuscela, G., De Filippis, N., De Palma, M., De Robertis, G., Donvito, G., Fedele, F., Fiore, L., Franco, M., Iaselli, G., Lacalamita, N., Loddo, F., Lusito, L., Maggi, G., Maggi, M., Manna, N., Marangelli, B., My, S., Natali, S., Nuzzo, S., Papagni, G., Piccolomo, S., Pierro, G. A., Pinto, C., Pompili, A., Pugliese, G., Rajan, R., Ranieri, A., Romano, F., Roselli, G., Selvaggi, G., Shinde, Y., Silvestris, L., Tupputi, S., Zito, G., Abbiendi, G., Bacchi, W., Benvenuti, A. C., Boldini, M., Bonacorsia, D., Braibant Giacomelli, S., Cafaro, V. D., Caiazza, S. S., Capiluppi, P., Castro, A., Cavallo, F. R., Codispoti, G., Cuffiani, M., D'Antone, I., Dallavalle, G. M., Fabbri, F., Fanfani, A., Fasanella, D., Giacomelli, P., Giordano, V., Giunta, M., Grandi, C., Guerzoni, M., Marcellini, S., Masetti, G., Montanari, A., Navarria, F. L., Odorici, F., Pellegrini, G., Perrotta, A., Rossi, A. M., Rovelli, T., Siroli, G., Torromeo, G., Travaglini, R., Albergo, S., Costa, S., Potenza, R., Tricomi, A., Tuve, C., Barbagli, G., Broccolo, G., Ciulli, V., Civinini, C., D'Alessandro, R., Focardi, E., Frosali, S., Gallo, E., Genta, C., Landi, G., Lenzi, P., Meschini, M., Paoletti, S., Sguazzoni, G., Tropiano, A., Benussi, L., Bertani, M., Bianco, S., Colafranceschi, S., Colonna, D., Giardoni, M., Passamonti, L., Piccolo, D., Pierluigi, D., Ponzio, B., Russo, A., Fabbricatore, P., Musenich, R., Benaglia, A., Calloni, M., Cerati, G. B., D'Angelo, P., De Guio, F., Farina, F. M., Ghezzi, A., Govoni, P., Malberti, M., Malvezzi, S., Martelli, A., Menasce, D., Miccio, V., Moroni, L., Negri, P., Paganoni, M., Pedrini, D., Pullia, A., Ragazzi, S., Redaelli, N., Sala, S., Salerno, R., de Fatis T., Tabarelli, Tancini, V., Taroni, S., Buontempo, S., Cavallo, N., Cimmino, A., De Gruttola, M., Fabozzi, F., Iorio, A. O. M., Lista, L., Lomidze, D., Noli, P., Paolucci, P., Sciacca, C., Azzi, P., Bacchetta, N., Barcellan, L., Bellan, P., Bellato, M., Benettoni, M., Biasotto, M., Bisello, D., Borsato, E., Branca, A., Carlin, R., Castellani, L., Checchia, P., Conti, E., Dal Corso, F., De Mattia, M., Dorigo, T., Dosselli, U., Fanzago, F., Gasparini, F., Gasparini, U., Giubilato, P., Gonella, F., Gresele, A., Gulmini, M., Kaminskiy, A., Lacaprara, S., Lazzizzera, I., Margoni, M., Maron, G., Mattiazzo, S., Mazzucato, M., Meneghelli, M., Meneguzzo, A. T., Michelotto, M., Montecassiano, F., Nespolo, M., Passaseo, M., Pegoraro, M., Perrozzi, L., Pozzobon, N., Ronchese, P., Simonetto, F., Toniolo, N., Torassa, E., Tosi, M., Triossi, A., Vanini, S., Ventura, S., Zotto, P., Zumerle, G., Baesso, P., Berzano, U., Bricola, S., Necchi, M. M., Pagano, D., Ratti, S. P., Riccardi, C., Torre, P., Vicini, A., Vitulo, P., Viviani, C., Aisa, D., Aisa, S., Babucci, E., Biasini, M., Bilei, G. M., Caponeri, B., Checcucci, B., Dinu, N., Fano, L., Farnesini, L., Lariccia, P., Lucaroni, A., Mantovani, G., Nappi, A., Piluso, A., Postolache, V., Santocchia, A., Servoli, L., Tonoiu, D., Vedaee, A., Volpe, R., Azzurri, P., Bagliesi, G., Bernardini, J., Berretta, L., Boccali, T., Bocci, A., Borrello, L., Bosi, F., Calzolari, Federico, Castaldi, R., Dell'Orso, R., Fiori, F., Foa, L., Gennai, S., Giassi, A., Kraan, A., Ligabue, Franco, Lomtadze, T., Mariani, F., Martini, L., Massa, M., Messineo, A., Moggi, A., Palla, F., Palmonari, F., Petragnani, G., Petrucciani, G., Raffaelli, F., Sarkar, S., Segneri, G., Serban, A. T., Spagnolo, P., Tenchini, R., Tolaini, S., Tonelli, G., Venturi, A., Verdini, P. G., Baccaro, S., Barone, L., Bartoloni, A., Cavallari, F., Dafinei, I., Del Re, D., Di Marco, E., Diemoz, M., Franci, D., Longo, E., Organtini, G., Palma, A., Pandolfi, F., Paramatti, R., Pellegrino, F., Rahatlou, S., Rovelli, C., Alampi, G., Amapane, N., Arcidiacono, R., Argiro, S., Arneodo, M., Biino, C., Borgia, M. A., Botta, C., Cartiglia, N., Castello, R., Cerminara, G., Costa, M., Dattola, D., Dellacasa, G., Demaria, N., Dughera, G., Dumitrache, F., Graziano, A., Mariotti, C., Marone, M., Maselli, S., Migliore, E., Mila, G., Monaco, V., Musich, M., Nervo, M., Obertino, M. M., Oggero, S., Panero, R., Pastrone, N., Pelliccioni, M., Romero, A., Ruspa, M., Sacchi, R., Solano, A., Staiano, A., Trapani, P. P., Trocino, D., Pereira A., Vilela, Visca, L., Zampieri, A., Ambroglini, F., Belforte, S., Cossutti, F., Della Ricca, G., Gobbo, B., Penzo, A., Chang, S., Chung, J., Kim, D. H., Kim, G. N., Kong, D. J., Park, H., Son, D. C., Bahk, S. Y., Song, S., Jung, S. Y., Hong, B., Kim, H., Kim, J. H., Lee, K. S., Moon, D. H., Park, S. K., Rhee, H. B., Sim, K. S., Kim, J., Choi, M., Hahn, G., Park, I. C., Choi, S., Choi, Y., Goh, J., Jeong, H., Kim, T. J., Lee, J., Lee, S., Janulis, M., Martisiute, D., Petrov, P., Sabonis, T., Castilla Valdez, H., Sanchez Hernandez, A., Carrillo Moreno, S., Morelos Pineda, A., Allfrey, P., Gray, R. N. C., Krofcheck, D., Rodrigues N., Bernardino, Butler, P. H., Signal, T., Williams, J. C., Ahmad, M., Ahmed, I., Ahmed, W., Asghar, M. I., Awan, M. I. M., Hoorani, H. R., Hussain, I., Khan, W. A., Khurshid, T., Muhammad, S., Qazi, S., Shahzad, H., Cwiok, M., Dabrowski, R., Dominik, W., Doroba, K., Konecki, M., Krolikowski, J., Pozniak, K., Romaniuk, R., Zabolotny, W., Zych, P., Frueboes, T., Gokieli, R., Goscilo, L., Gorski, M., Kazana, M., Nawrocki, K., Szleper, M., Wrochna, G., Zalewski, P., Almeida, N., Antunes Pedro, L., Bargassa, P., David, A., Faccioli, P., Ferreira Parracho, P. G., Freitas Ferreira, M., Gallinaro, M., Guerra Jordao, M., Martins, P., Mini, G., Musella, P., Pela, J., Raposo, L., Ribeiro, P. Q., Sampaio, S., Seixas, J., Silva, J., Silva, P., Soares, D., Sousa, M., Varela, J., Woehri, H. K., Altsybeev, I., Belotelov, I., Bunin, P., Ershov, Y., Filozova, I., Finger, M., Finger, M. J. r., Golunov, A., Golutvin, I., Gorbounov, N., Kalagin, V., Kamenev, A., Karjavin, V., Konoplyanikov, V., Korenkov, V., Kozlov, G., Kurenkov, A., Lanev, A., Makankin, A., Mitsyn, V. V., Moisenz, P., Nikonov, E., Oleynik, D., Palichik, V., Perelygin, V., Petrosyan, A., Semenov, R., Shmatov, S., Smirnov, V., Smolin, D., Tikho Nenko, E., Vasil'Ev, S., Vishnevskiy, A., Volodko, A., Zarubin, A., Zhiltsov, V., Bondar, N., Chtchipounov, L., Denisov, A., Gavrikov, Y., Gavrilov, G., Golovtsov, V., Ivanov, Y., Kim, V., Kozlov, V., Levchenko, P., Obrant, G., Orishchin, E., Petrunin, A., Shcheglov, Y., Shchetkovskiy, A., Sknar, V., Smirnov, I., Sulimov, V., Tarakanov, V., Uvarov, L., Vavilov, S., Velichko, G., Volkov, S., Vorobyev, A., Andreev, Y. u., Anisimov, A., Antipov, P., Dermenev, A., Gninenko, S., Golubev, N., Kirsanov, M., Krasnikov, N., Matveev, V., Pashenkov, A., Postoev, V. E., Solovey, A., Toropin, A., Troitsky, S., Baud, A., Epshteyn, V., Gavrilov, V., Ilina, N., Kaftanov, V., Kolosov, V., Kossov, M., Krokhotin, A., Kuleshov, S., Oulianov, A., Safronov, G., Semenov, S., Shreyber, I., Stolin, V., Vlasov, E., Zhokin, A., Boos, E., Dubinin, M., Dudko, L., Ershov, A., Gribushin, A., Klyukhin, V., Kodolova, O., Lokhtin, I., Petrushanko, S., Sarycheva, L., Savrin, V., Snigirev, A., Vardanyan, I., Dremin, I., Kirakosyan, M., Konovalova, N., Rusakov, S. V., Vinogradov, A., Akimenko, S., Artamonov, A., Azhgirey, I., Bitioukov, S., Burtovoy, V., Grishin, V., Kachanov, V., Konstantinov, D., Krychkine, V., Levine, A., Lobov, I., Lukanin, V., Mel'Nik, Y., Petrov, V., Ryutin, R., Slabospitsky, S., Sobol, A., Sytine, A., Tourtchanovitch, L., Troshin, S., Tyurin, N., Uzunian, A., Volkov, A., Adzic, P., Djordjevic, M., Jovanovic, D., Krpic, D., Maletic, D., Puzovic, J., Smiljkovic, N., Aguilar Benitez, M., Alberdi, J., Alcaraz Maestre, J., Arce, P., Barcala, J. M., Battilana, C., Burgos Lazaro, C., Caballero Bejar, J., Calvo, E., Cardenas Montes, M., Cepeda, M., Cerrada, M., Chamizo Llatas, M., Clemente, F., Colino, N., Daniel, M., De La Cruz, B., Delgado Peris, A., Diez Pardos, C., Fernandez Bedoya, C., Fernandez Ramos, J. P., Ferrando, A., Flix, J., Fouz, M. C., Garcia Abia, P., Garcia Bonilla, A. C., Gonzalez Lopez, O., Goy Lopez, S., Hernandez, J. M., Josa, M. I., Marin, J., Merino, G., Molina, J., Molinero, A., Navarrete, J. J., Oller, J. C., Puerta Pelayo, J., Romero, L., Santaolalla, J., Villanueva Munoz, C., Willmott, C., Yuste, C., Albajar, C., Blanco Otano, M., de Troconiz, J. F., Garcia Raboso, A., Lopez Berengueres, J. O., Cuevas, J., Fernandez Menendez, J., Gonzalez Caballero, I., Lloret Iglesias, L., Naves Sordo, H., Vizan Garcia, J. M., Cabrillo, I. J., Calderon, A., Chuang, S. H., Diaz Merino, I., Diez Gonzalez, C., Duarte Campderros, J., Fernandez, M., Gomez, G., Gonzalez Sanchez, J., Gonzalez Suarez, R., Jorda, C., Lobelle Pardo, P., Lopez Virto, A., Marco, J., Marco, R., Martinez Rivero, C., Martinez Ruiz del Arbol, P., Matorras, F., Rodrigo, T., Ruiz Jimeno, A., Scodellaro, L., Sobron Sanudo, M., Vila, I., Vilar Cortabitarte, R., Abbaneo, D., Albert, E., Alidra, M., Ashby, S., Auffray, E., Baechler, J., Baillon, P., Ball, A. H., Bally, S. L., Barney, D., Beaudette, F., Bellan, R., Benedetti, D., Benelli, G., Bernet, C., Bloch, P., Bolognesi, S., Bona, M., Bos, J., Bourgeois, N., Bourrel, T., Breuker, H., Bunkowski, K., Campi, D., Camporesi, T., Cano, E., Cattai, A., Chatelain, J. P., Chauvey, M., Christiansen, T., Perez J. A., Coarasa, Garcia A., Conde, Covarelli, R., Cure, B., De Roeck, A., Delachenal, V., Deyrail, D., Di Vincenzo, S., Dos Santos, S., Dupont, T., Edera, L. M., Elliott Peisert, A., Eppard, M., Favre, M., Frank, N., Funk, W., Gaddi, A., Gastal, M., Gateau, M., Gerwig, H., Gigi, D., Gill, K., Giordano, D., Girod, J. P., Glege, F., Garrido R., Gomez Reino, Goudard, R., Gowdy, S., Guida, R., Guiducci, L., Gutleber, J., Hansen, M., Hartl, C., Harvey, J., Hegner, B., Hoffmann, H. F., Holzner, A., Honma, A., Huhtinen, M., Innocente, V., Janot, P., Le Godec, G., Lecoq, P., Leonidopoulos, C., Loos, R., Lourenco, C., Lyonnet, A., Macpherson, A., Magini, N., Maillefaud, J. D., Maire, G., Maeki, T., Malgeri, L., Mannelli, M., Masetti, L., Meijers, F., Meridiani, P., Mersi, S., Meschi, E., Cordonnier A., Meynet, Moser, R., Mulders, M., Mulon, J., Noy, M., Oh, A., Olesen, G., Onnela, A., Orimoto, T., Orsini, L., Perez, E., Perinic, G., Pernot, J. F., Petagna, P., Petiot, P., Petrilli, A., Pfeiffer, A., Pierini, M., Pimiae, M., Pintus, R., Pirollet, B., Postema, H., Racz, A., Ravat, S., Rew, S. B., Antunes J., Rodrigue, Rolandi, Luigi, Rovere, M., Ryjov, V., Sakulin, H., Samyn, D., Sauce, H., Schaefer, C., Schlatter, W. D., Schroeder, M., Schwick, C., Sciaba, A., Segoni, I., Siegrist, N., Siegrist, P., Sinanis, N., Sobrier, T., Sphicas, P., Spiga, D., Spiropulu, M., Stoeckli, F., Traczyk, P., Tropea, P., Troska, J., Tsirou, A., Veillet, L., Veres, G. I., Voutilainen, M., Wertelaers, P., Zanetti, M., Bertl, W., Deiters, K., Erdmann, W., Gabathuler, K., Horisberger, R., Ingram, Q., Kaestli, H. C., Koenig, S., Kotlinski, D., Langenegger, U., Meier, F., Renker, D., Rohe, T., Sibille, J., Starodumov, A., Betev, B., Caminada, L., Chen, Z., Cittolin, S., Di Calafiori D. R., Da Silva, Dambach, S., Dissertori, G., Dittmar, M., Eggel, C., Eugster, J., Faber, G., Freudenreich, K., Grab, C., Herve, A., Hintz, W., Lecomte, P., Luckey, P. D., Lustermann, W., Marchica, C., Milenovic, P., Moortgat, F., Nardulli, A., Nessi Tedaldi, F., Pape, L., Pauss, F., Punz, T., Rizzi, A., Ronga, F. J., Sala, L., Sanchez, A. K., Sawley, M. C., Sordini, V., Stieger, B., Tauscher, L., Thea, A., Theofilatos, K., Treille, D., Trueb, P., Wehrli, L., Weng, J., Zelepoukine, S., Amsler, C., Chiochia, V., De Visscher, S., Regenfus, C., Robmann, P., Rommerskirchen, T., Schmidt, A., Tsirigkas, D., Wilke, L., Chang, Y. H., Chen, E. A., Chen, W. T., Go, A., Kuo, C. M., Li, S. W., Lin, W., Bartalini, P., Chang, P., Chao, Y., Chen, K. F., Hou, W. S., Hsiung, Y., Lei, Y. J., Lin, S. W., Lu, R. S., Schuemann, J., Shiu, J. G., Tzeng, Y. M., Ueno, K., Velikzhanin, Y., Wang, C. C., Wang, M., Adiguzel, A., Ayhan, A., Gokce A., Azman, Bakirci, M. N., Cerci, S., Dumanoglu, I., Eskut, E., Girgis, S., Gurpinar, E., Hos, I., Karaman, T., Topaksu A., Kayi, Kurt, P., Oenenguet, G., Goekbulut G., Oenenguet, Ozdemir, K., Ozturk, S., Polatoez, A., Sogut, K., Tali, B., Topakli, H., Uzun, D., Vergili, L. N., Vergili, M., Akin, I. V., Aliev, T., Bilmis, S., Deniz, M., Gamsizkan, H., Guler, A. M., Oecalan, K., Serin, M., Sever, R., Surat, U. E., Zeyrek, M., Deliomeroglu, M., Demir, D., Guelmez, E., Halu, A., Isildak, B., Kaya, M., Kaya, O., Ozkorucuklu, S., Sonmez, N., Levchuk, L., Lukyanenko, S., Soroka, D., Zub, S., Bostock, F., Brooke, J. J., Cheng, T. L., Cussans, D., Frazier, R., Goldstein, J., Grant, N., Heath, G. P., Heath, H. F., Hill, C., Huckvale, B., Jackson, J., Mackay, C. K., Metson, S., Newbold, D. M., Nirunpong, K., Smith, V. J., Velthuis, J., Walton, R., Bell, K. W., Brew, C., Brown, R. M., Camanzi, B., Cockerill, D. J. A., Coughlan, J. A., Geddes, N. I., Harder, K., Harper, S., Kennedy, B. W., Murray, P., Shepherd Themistocleous, C. H., Tomalin, I. R., Williams, J. H., Womersley, W. J., Worm, S. D., Bainbridge, R., Ball, G., Ballin, J., Beuselinck, R., Buchmuller, O., Colling, D., Cripps, N., Davies, G., Della Negra, M., Foudas, C., Fulcher, J., Futyan, D., Hall, G., Hays, J., Iles, G., Karapostoli, G., Macevoy, B. C., Magnan, A. M., Marrouche, J., Nash, J., Nikitenko, A., Papageorgiou, A., Pesaresi, M., Petridis, K., Pioppi, M., Raymond, D. M., Rompotis, N., Rose, A., Ryan, M. J., Seez, C., Sharp, P., Sidiropoulos, G., Stettler, M., Stoye, M., Takahashi, M., Tapper, A., Timlin, C., Tourneur, S., Acosta M., Vazquez, Virdee, T., Wakefield, S., Wardrope, D., Whyntie, T., Wingham, M., Cole, J. E., Goitom, I., Hobson, P. R., Khan, A., Kyberd, P., Leslie, D., Munro, C., Reid, I. D., Siamitros, C., Taylor, R., Teodorescu, L., Yaselli, I., Bose, T., Carleton, M., Hazen, E., Heering, A. H., Heister, A., St John, J., Lawson, P., Lazic, D., Osborne, D., Rohlf, J., Sulak, L., Wu, S., Andrea, J., Avetisyan, A., Chou, J. P., Cutts, D., Esen, S., Kukartsev, G., Landsberg, G., Narain, M., Nguyen, D., Speer, T., Tsang, K. V., Breedon, R., Sanchez M., Calderon De La Barca, Case, M., Cebra, D., Chertok, M., Conway, J., Cox, P. T., Dolen, J., Erbacher, R., Friis, E., Ko, W., Kopecky, A., Lander, R., Lister, A., Liu, H., Maruyama, S., Miceli, T., Nikolic, M., Pellett, D., Robles, J., Searle, M., Smith, J., Squires, M., Stilley, J., Tripathi, M., Sierra R., Vasquez, Veelken, C., Andreev, V., Arisaka, K., Cline, D., Cousins, R., Erhan, S., Hauser, J., Ignatenko, M., Jarvis, C., Mumford, J., Plager, C., Rakness, G., Schlein, P., Tucker, J., Valuev, V., Wallny, R., Yang, X., Babb, J., Bose, M., Chandra, A., Clare, R., Ellison, J. A., Gary, J. W., Hanson, G., Jeng, G. Y., Kao, S. C., Liu, F., Luthra, A., Nguyen, H., Pasztor, G., Satpathy, A., Shen, B. C., Stringer, R., Sturdy, J., Sytnik, V., Wilken, R., Wimpenny, S., Branson, J. G., Dusinberre, E., Evans, D., Golf, F., Kelley, R., Lebourgeois, M., Letts, J., Lipeles, E., Mangano, B., Muelmenstaedt, J., Norman, M., Padhi, S., Petrucci, A., Pi, H., Pieri, M., Ranieri, R., Sani, M., Sharma, V., Simon, S., Wuerthwein, F., Yagil, A., Campagnari, C., D'Alfonso, M., Danielson, T., Garberson, J., Incandela, J., Justus, C., Kalavase, P., Koay, S. A., Kovalskyi, D., Krutelyov, V., Lamb, J., Lowette, S., Pavlunin, V., Rebassoo, F., Ribnik, J., Richman, J., Rossin, R., Stuart, D., To, W., Vlimant, J. R., Witherell, M., Apresyan, A., Bornheim, A., Bunn, J., Chiorboli, M., Gataullin, M., Kcira, D., Litvine, V., Ma, Y., Newman, H. B., Rogan, C., Timciuc, V., Veverka, J., Wilkinson, R., Yang, Y., Zhang, L., Zhu, K., Zhu, R. Y., Akgun, B., Carroll, R., Ferguson, T., Jang, D. W., Jun, S. Y., Paulini, M., Russ, J., Terentyev, N., Vogel, H., Vorobiev, I., Cumalat, J. P., Dinardo, M. E., Drell, B. R., Ford, W. T., Heyburn, B., Lopez E., Luiggi, Nauenberg, U., Stenson, K., Ulmer, K., Wagner, S. R., Zang, S. L., Agostino, L., Alexander, J., Blekman, F., Cassel, D., Chatterjee, A., Das, S., Gibbons, L. K., Heltsley, B., Hopkins, W., Khukhunaishvili, A., Kreis, B., Kuznetsov, V., Patterson, J. R., Puigh, D., Ryd, A., Shi, X., Stroiney, S., Sun, W., Teo, W. D., Thom, J., Vaughan, J., Weng, Y., Wittich, P., Beetz, C. P., Cirino, G., Sanzeni, C., Winn, D., Abdullin, S., Afaq, M. A., Albrow, M., Ananthan, B., Apollinari, G., Atac, M., Badgett, W., Bagby, L., Bakken, J. A., Baldin, B., Banicz, K., Bauerdick, L. A. T., Beretvas, A., Berryhill, J., Bhat, P. C., Biery, K., Binkley, M., Bloch, I., Borcherding, F., Brett, A. M., Burkett, K., Butler, J. N., Chetluru, V., Cheung, H. W. K., Chlebana, F., Churin, I., Cihangir, S., Crawford, M., Dagenhart, W., Demarteau, M., Derylo, G., Dykstra, D., Eartly, D. P., Elias, J. E., Elvira, V. D., Feng, L., Fischler, M., Fisk, I., Foulkes, S., Freeman, J., Gartung, P., Gottschalk, E., Grassi, T., Green, D., Guo, Y., Gutsche, O., Hahn, A., Hanlon, J., Harris, R. M., Holzman, B., Howell, J., Hufnagel, D., James, E., Jensen, H., Johnson, M., Jones, C. D., Joshi, U., Juska, E., Kaiser, J., Klima, B., Kossiakov, S., Kousouris, K., Kwan, S., Lei, C. M., Limon, P., Perez J. A., Lopez, Los, S., Lueking, L., Lukhanin, G., Lusin, S., Lykken, J., Maeshima, K., Marraffino, J. M., Mason, D., Mcbride, P., Miao, T., Mishra, K., Moccia, S., Mommsen, R., Mrenna, S., Muhammad, A. S., Newman Holmes, C., Noeding, C., O'Dell, V., Prokofyev, O., Rivera, R., Rivetta, C. H., Ronzhin, A., Rossman, P., Ryu, S., Sekhri, V., Sexton Kennedy, E., Sfiligoi, I., Sharma, S., Shaw, T. M., Shpakov, D., Skup, E., Smith, R. P., Soha, A., Spalding, W. J., Spiegel, L., Suzuki, I., Tan, P., Tanenbaum, W., Tkaczyk, S., Trentadue, R., Uplegger, L., Vaandering, E. W., Vidal, R., Whitmore, J., Wicklund, E., Wu, W., Yarba, J., Yumiceva, F., Yun, J. C., Acosta, D., Avery, P., Barashko, V., Bourilkov, D., Chen, M., Di Giovanni, G. P., Dobur, D., Drozdetskiy, A., Field, R. D., Fu, Y., Furic, I. K., Gartner, J., Holmes, D., Kim, B., Klimenko, S., Konigsberg, J., Korytov, A., Kotov, K., Kropivnitskaya, A., Kypreos, T., Madorsky, A., Matchev, K., Mitselmakher, G., Pakhotin, Y., Gomez J., Piedra, Prescott, C., Rapsevicius, V., Remington, R., Schmitt, M., Scurlock, B., Wang, D., Yelton, J., Ceron, C., Gaultney, V., Kramer, L., Lebolo, L. M., Linn, S., Markowitz, P., Martinez, G., Rodriguez, J. L., Adams, T., Askew, A., Baer, H., Bertoldi, M., Chen, J., Dharmaratna, W. G. D., Gleyzer, S. V., Haas, J., Hagopian, S., Hagopian, V., Jenkins, M., Johnson, K. F., Prettner, E., Prosper, H., Sekmen, S., Baarmand, M. M., Guragain, S., Hohlmann, M., Kalakhety, H., Mermerkaya, H., Ralich, R., Vodopiyanov, I., Abelev, B., Adams, M. R., Anghel, I. M., Apanasevich, L., Bazterra, V. E., Betts, R. R., Callner, J., Castro, M. A., Cavanaugh, R., Dragoiu, C., Garcia Solis, E. J., Gerber, C. E., Hofman, D. J., Khalatian, S., Mironov, C., Shabalina, E., Smoron, A., Varelas, N., Akgun, U., Albayrak, E. A., Ayan, A. S., Bilki, B., Briggs, R., Cankocak, K., Chung, K., Clarida, W., Debbins, P., Duru, F., Ingram, F. D., Lae, C. K., Mccliment, E., Merlo, J. P., Mestvirishvili, A., Miller, M. J., Moeller, A., Nachtman, J., Newsom, C. R., Norbeck, E., Olson, J., Onel, Y., Ozok, F., Parsons, J., Schmidt, I., Sen, S., Wetzel, J., Yetkin, T., Yi, K., Barnett, B. A., Blumenfeld, B., Bonato, A., Chien, C. Y., Fehling, D., Giurgiu, G., Gritsan, A. V., Guo, Z. J., Maksimovic, P., Rappoccio, S., Swartz, M., Tran, N. V., Zhang, Y., Baringer, P., Bean, A., Grachov, O., Murray, M., Radicci, V., Sanders, S., Wood, J. S., Zhukova, V., Bandurin, D., Bolton, T., Kaadze, K., Liu, A., Maravin, Y., Onoprienko, D., Svintradze, I., Wan, Z., Gronberg, J., Hollar, J., Lange, D., Wright, D., Baden, D., Bard, R., Boutemeur, M., Eno, S. C., Ferencek, D., Hadley, N. J., Kellogg, R. G., Kirn, M., Kunori, S., Rossato, K., Rumerio, P., Santanastasio, F., Skuja, A., Temple, J., Tonjes, M. B., Tonwar, S. C., Toole, T., Twedt, E., Alver, B., Bauer, G., Bendavid, J., Busza, W., Butz, E., Cali, I. A., Chan, M., D'Enterria, D., Everaerts, P., Ceballos G., Gomez, Hahn, K. A., Harris, P., Jaditz, S., Kim, Y., Klute, M., Lee, Y. J., Li, W., Loizides, C., Ma, T., Miller, M., Nahn, S., Paus, C., Roland, C., Roland, G., Rudolph, M., Stephans, G., Sumorok, K., Sung, K., Vaurynovich, S., Wenger, E. A., Wyslouch, B., Xie, S., Yilmaz, Y., Yoon, A. S., Bailleux, D., Cooper, S. I., Cushman, P., Dahmes, B., De Benedetti, A., Dolgopolov, A., Dudero, P. R., Egeland, R., Franzoni, G., Haupt, J., Inyakin, A., Klapoetke, K., Kubota, Y., Mans, J., Mirman, N., Petyt, D., Rekovic, V., Rusack, R., Singovsky, A., Zhang, J., Cremaldi, L. M., Godang, R., Kroeger, R., Perera, L., Rahmat, R., Sanders, D. A., Sonnek, P., Summers, D., Bloom, K., Bockelman, B., Bose, S., Butt, J., Claes, D. R., Dominguez, A., Eads, M., Keller, J., Kelly, T., Kravchenko, I., Lazo Flores, J., Lundstedt, C., Malbouisson, H., Malik, S., Snow, G. R., Baur, U., Iashvili, I., Kharchilava, A., Smith, K., Strang, M., Alverson, G., Barberis, E., Boeriu, O., Eulisse, G., Govi, G., Mccauley, T., Musienko, Y., Muzaffar, S., Osborne, I., Paul, T., Reucroft, S., Swain, J., Taylor, L., Tuura, L., Anastassov, A., Gobbi, B., Kubik, A., Ofierzynski, R. A., Pozdnyakov, A., Stoynev, S., Velasco, M., Won, S., Antonelli, L., Berry, D., Hildreth, M., Jessop, C., Karmgard, D. J., Kolberg, T., Lannon, K., Lynch, S., Marinelli, N., Morse, D. M., Ruchti, R., Slaunwhite, J., Warchol, J., Wayne, M., Bylsma, B., Durkin, L. S., Gilmore, J., Gu, J., Killewald, P., Ling, T. Y., Williams, G., Adam, N., Berry, E., Elmer, P., Garmash, A., Gerbaudo, D., Halyo, V., Hunt, A., Jones, J., Laird, E., Marlow, D., Medvedeva, T., Mooney, M., Olsen, J., Piroue, P., Stickland, D., Tully, C., Werner, J. S., Wildish, T., Xie, Z., Zuranski, A., Acosta, J. G., Del Alamo M., Bonnett, Huang, X. T., Lopez, A., Mendez, H., Oliveros, S., Vargas J. E., Ramirez, Santacruz, N., Zatzerklyany, A., Alagoz, E., Antillon, E., Barnes, V. E., Bolla, G., Bortoletto, D., Everett, A., Garfinkel, A. F., Gecse, Z., Gutay, L., Ippolito, N., Jones, M., Koybasi, O., Laasanen, A. T., Leonardo, N., Liu, C., Maroussov, V., Merkel, P., Miller, D. H., Neumeister, N., Sedov, A., Shipsey, I., Yoo, H. D., Zheng, Y., Jindal, P., Parashar, N., Cuplov, V., Ecklund, K. M., Geurts, F. J. M., Liu, J. H., Maronde, D., Matveev, M., Padley, B. P., Redjimi, R., Roberts, J., Sabbatini, L., Tumanov, A., Betchart, B., Bodek, A., Budd, H., Chung, Y. S., de Barbaro, P., Demina, R., Flacher, H., Gotra, Y., Harel, A., Korjenevski, S., Miner, D. C., Orbaker, D., Petrillo, G., Vishnevskiy, D., Zielinski, M., Bhatti, A., Demortier, L., Goulianos, K., Hatakeyama, K., Lungu, G., Mesropian, C., Yan, M., Atramentov, O., Bartz, E., Gershtein, Y., Halkiadakis, E., Hits, D., Lath, A., Rose, K., Schnetzer, S., Somalwar, S., Stone, R., Thomas, S., Watts, T. L., Cerizza, G., Hollingsworth, M., Spanier, S., Yang, Z. C., York, A., Asaadi, J., Aurisano, A., Eusebi, R., Golyash, A., Gurrola, A., Kamon, T., Nguyen, C. N., Pivarski, J., Safonov, A., Sengupta, S., Toback, D., Weinberger, M., Akchurin, N., Berntzon, L., Gumus, K., Jeong, C., Lee, S. W., Popescu, S., Roh, Y., Sill, A., Volobouev, I., Washington, E., Wigmans, R., Yazgan, E., Engh, D., Florez, C., Johns, W., Pathak, S., Sheldon, P., Andelin, D., Arenton, M. W., Balazs, M., Boutle, S., Buehler, M., Conetti, S., Cox, B., Hirosky, R., Ledovskoy, A., Neu, C., Phillips D., Ii, Ronquest, M., Yohay, R., Gollapinni, S., Gunthoti, K., Harr, R., Karchin, P. E., Mattson, M., Sakharov, A., Anderson, M., Bachtis, M., Bellinger, J. N., Carlsmith, D., Crotty, I., Dasu, S., Dutta, S., Efron, J., Feyzi, F., Flood, K., Gray, L., Grogg, K. S., Grothe, M., Hall Wilton, R., Jaworski, M., Klabbers, P., Klukas, J., Lanaro, A., Lazaridis, C., Leonard, J., Loveless, R., de Abril M., Magran, Mohapatra, A., Ott, G., Polese, G., Reeder, D., Savin, A., Smith, W. H., Sourkov, A., Swanson, J., Weinberg, M., Wenman, D., Wensveen, M., White, A., V. KHACHATRYAN, A.M. SIRUNYAN, A. TUMASYAN, W. ADAM, T. BERGAUER, M. DRAGICEVIC, J. ER¨O, C. FABJAN, M. FRIEDL, R. FRUHWIRTH, V.M. GHETE, J. HAMMER, S. H¨ANSEL, C. HARTL, M. HOCH, N. H¨ORMANN, J. HRUBEC, M. JEITLER, G. KASIECZKA, W. KIESENHOFER, M. KRAMMER, D. LIKO, I. MIKULEC, M. PERNICKA, H. ROHRINGER, R. SCH¨OFBECK, J. STRAUSS, A. TAUROK, F. TEISCHINGER, W.WALTENBERGER, G.WALZEL, E.WIDL, C.-E.WULZ, V. MOSSOLOV, N. SHUMEIKO, J. SUAREZ GONZALEZ, L. BENUCCI, L. CEARD, E.A. DE WOLF, X. JANSSEN, T. MAES, L. MUCIBELLO, S. OCHESANU, B. ROLAND, R. ROUGNY, M. SELVAGGI, H. VAN HAEVERMAET, P. VAN MECHELEN, N. VAN REMORTEL, V. ADLER, S. BEAUCERON, S. BLYWEERT, J. D’HONDT, O. DEVROEDE, A. KALOGEROPOULOS, J. MAES, M. MAES, S. TAVERNIER, W. VAN DONINCK, P. VAN MULDERS, I. VILLELLA, E.C. CHABERT, O. CHARAF, B. CLERBAUX, G. DE LENTDECKER, V. DERO, A.P.R. GAY, G.H. HAMMAD, T. HREUS, P.E. MARAGE, C. VANDER VELDE, P. VANLAER, J.WICKENS, S. COSTANTINI, M. GRUNEWALD, B. KLEIN, A. MARINOV, D. RYCKBOSCH, F. THYSSEN, M. TYTGAT, L. VANELDEREN, P. VERWILLIGEN, S.WALSH, N. ZAGANIDIS, S. BASEGMEZ, G. BRUNO, J. CAUDRON, J. DE FAVEREAU DE JENERET, C. DELAERE, P. DEMIN, D. FAVART, A. GIAMMANCO, G. GR´EGOIRE, J. HOLLAR, V. LEMAITRE, O. MILITARU, S. OVYN, D. PAGANO, A. PIN, K. PIOTRZKOWSKI, L. QUERTENMONT, N. SCHUL, N. BELIY, T. CAEBERGS, E. DAUBIE, G.A. ALVES, D. DE JESUS DAMIAO, M.E. POL, M.H.G. SOUZA, W. CARVALHO, E.M. DA COSTA, C. DE OLIVEIRA MARTINS, S. FONSECA DE SOUZA, L. MUNDIM, H. NOGIMA, V. OGURI, J.M. OTALORA GOICOCHEA, W.L. PRADO DA SILVA, A. SANTORO, S.M. SILVA DO AMARAL, A. SZNAJDER, F. TORRES DA SILVA DE ARAUJO, F.A. DIAS, M.A.F. DIAS, T.R. FERNANDEZ PEREZ TOMEI, E. M. GREGORES, F. MARINHO, S.F. NOVAES, SANDRA S. PADULA, N. DARMENOV, L. DIMITROV, V. GENCHEV, P. IAYDJIEV, S. PIPEROV, M. RODOZOV, S. STOYKOVA, G. SULTANOV, V. TCHOLAKOV, R. TRAYANOV, I. VANKOV, M. DYULENDAROVA, R. HADJIISKA, V. KOZHUHAROV, L. LITOV, E. MARINOVA, M. MATEEV, B. PAVLOV, P. PETKOV, J.G. BIAN, G.M. CHEN, H.S. CHEN, C.H. JIANG, D. LIANG, S. LIANG, J. WANG, X. WANG, Z.WANG, M. YANG, J. ZANG, Z. ZHANG, Y. BAN, S. GUO, Z. HU, W. LI, Y. MAO, S.J. QIAN, H. TENG, B. ZHU, A. CABRERA, B. GOMEZ MORENO, A.A. OCAMPO RIOS, A.F. OSORIO OLIVEROS, J.C. SANABRIA, N. GODINOVIC, D. LELAS, K. LELAS, R. PLESTINA, D. POLIC, I. PULJAK, Z. ANTUNOVIC, M. DZELALIJA, V. BRIGLJEVIC, S. DURIC, K. KADIJA, S. MOROVIC, A. ATTIKIS, R. FEREOS, M. GALANTI, J. MOUSA, C. NICOLAOU, F. PTOCHOS, P.A. RAZIS, H. RYKACZEWSKI, Y. ASSRAN, M.A. MAHMOUD, A. HEKTOR, M. KADASTIK, K. KANNIKE, M. M¨UNTEL, M. RAIDAL, L. REBANE, V. AZZOLINI, P. EEROLA, S. CZELLAR, J. H¨ARK¨ONEN, A. HEIKKINEN, V. KARIM¨AKI, R. KINNUNEN, J. KLEM, M.J. KORTELAINEN, T. LAMP´EN, K. LASSILA-PERINI, S. LEHTI, T. LIND´EN, P. LUUKKA, T. M¨AENP¨A¨A, E. TUOMINEN, J. TUOMINIEMI, E. TUOVINEN, D. UNGARO, L.WENDLAND, K. BANZUZI, A. KORPELA, T. TUUVA, D. SILLOU, M. BESANCON, M. DEJARDIN, D. DENEGRI, J. DESCAMPS, B. FABBRO, J.L. FAURE, F. FERRI, S. GANJOUR, F.X. GENTIT, A. GIVERNAUD, P. GRAS, G. HAMEL DE MONCHENAULT, P. JARRY, E. LOCCI, J. MALCLES, M. MARIONNEAU, L. MILLISCHER, J. RANDER, A. ROSOWSKY, D. ROUSSEAU, M. TITOV, P. VERRECCHIA, S. BAFFIONI, L. BIANCHINI, M. BLUJ, C. BROUTIN, P. BUSSON, C. CHARLOT, L. DOBRZYNSKI, R. GRANIER DE CASSAGNAC, M. HAGUENAUER, P. MIN´E, C. MIRONOV, C. OCHANDO, P. PAGANINI, D. SABES, R. SALERNO, Y. SIROIS, C. THIEBAUX, A. ZABI, J.-L. AGRAM, A. BESSON, D. BLOCH, D. BODIN, J.-M. BROM, M. CARDACI, E. CONTE, F. DROUHIN, C. FERRO, J.-C. FONTAINE, D. GEL´E, U. GOERLACH, S. GREDER, P. JUILLOT, M. KARIM, A.-C. LE BIHAN, Y. MIKAMI, P. VAN HOVE, F. FASSI, D. MERCIER, C. BATY, N. BEAUPERE, M. BEDJIDIAN, O. BONDU, G. BOUDOUL, D. BOUMEDIENE, H. BRUN, N. CHANON, R. CHIERICI, D. CONTARDO, P. DEPASSE, H. EL MAMOUNI, A. FALKIEWICZ, J. FAY, S. GASCON, B. ILLE, T. KURCA, T. LE GRAND, M. LETHUILLIER, L. MIRABITO, S. PERRIES, V. SORDINI, S. TOSI, Y. TSCHUDI, P. VERDIER, H. XIAO, V. ROINISHVILI, G. ANAGNOSTOU, M. EDELHOFF, L. FELD, N. HERACLEOUS, O. HINDRICHS, R. JUSSEN, K. KLEIN, J. MERZ, N. MOHR, A. OSTAPCHUK, A. PERIEANU, F. RAUPACH, J. SAMMET, S. SCHAEL, D. SPRENGER, H. WEBER, M.WEBER, B.WITTMER, M. ATA, W. BENDER, M. ERDMANN, J. FRANGENHEIM, T. HEBBEKER, A. HINZMANN, K. HOEPFNER, C. HOF, T. KLIMKOVICH, D. KLINGEBIEL, P. KREUZER, D. LANSKEY, C. MAGASS, M. MERSCHMEYER, A. MEYER, P. PAPACZ, H. PIETA, H. REITHLER, S.A. SCHMITZ, L. SONNENSCHEIN, J. STEGGEMANN, D. TEYSSIER, M. BONTENACKELS, M. DAVIDS, M. DUDA, G. FL¨UGGE, H. GEENEN, M. GIFFELS, W. HAJ AHMAD, D. HEYDHAUSEN, T. KRESS, Y. KUESSEL, A. LINN, A. NOWACK, L. PERCHALLA, O. POOTH, J. RENNEFELD, P. SAUERLAND, A. STAHL, M. THOMAS, D. TORNIER, M.H. ZOELLER, M. ALDAYA MARTIN, W. BEHRENHOFF, U. BEHRENS, M. BERGHOLZ, K. BORRAS, A. CAMPBELL, E. CASTRO, D. DAMMANN, G. ECKERLIN, A. FLOSSDORF, G. FLUCKE, A. GEISER, I. GLUSHKOV, J. HAUK, H. JUNG, M. KASEMANN, I. KATKOV, P. KATSAS, C. KLEINWORT, H. KLUGE, A. KNUTSSON, D. KR¨ UCKER, E. KUZNETSOVA, W. LANGE, W. LOHMANN, R. MANKEL, M. MARIENFELD, I.-A. MELZER-PELLMANN, A.B. MEYER, J. MNICH, A. MUSSGILLER, J. OLZEM, A. PARENTI, A. RASPEREZA, A. RAVAL, R. SCHMIDT, T. SCHOERNER-SADENIUS, N. SEN, M. STEIN, J. TOMASZEWSKA, D. VOLYANSKYY, R.WALSH, C.WISSING, C. AUTERMANN, S. BOBROVSKYI, J. DRAEGER, D. ECKSTEIN, H. ENDERLE, U. GEBBERT, K. KASCHUBE, G. KAUSSEN, R. KLANNER, B. MURA, S. NAUMANN-EMME, F. NOWAK, N. PIETSCH, C. SANDER, H. SCHETTLER, P. SCHLEPER, M. SCHR¨ODER, T. SCHUM, J. SCHWANDT, A.K. SRIVASTAVA, H. STADIE, G. STEINBR¨UCK, J. THOMSEN, R.WOLF, J. BAUER, V. BUEGE, A. CAKIR, T. CHWALEK, D. DAEUWEL, W. DE BOER, A. DIERLAMM, G. DIRKES, M. FEINDT, J. GRUSCHKE, C. HACKSTEIN, F. HARTMANN, M. HEINRICH, H. HELD, K.H. HOFFMANN, S. HONC, T. KUHR, D. MARTSCHEI, S. MUELLER, TH. M¨ULLER, M.B. NEULAND, M. NIEGEL, O. OBERST, A. OEHLER, J. OTT, T. PEIFFER, D. PIPARO, G. QUAST, K. RABBERTZ, F. RATNIKOV, M. RENZ, A. SABELLEK, C. SAOUT, A. SCHEURER, P. SCHIEFERDECKER, F.-P. SCHILLING, G. SCHOTT, H.J. SIMONIS, F.M. STOBER, D. TROENDLE, J. WAGNER-KUHR, M. ZEISE, V. ZHUKOV, E.B. ZIEBARTH, G. DASKALAKIS, T. GERALIS, S. KESISOGLOU, A. KYRIAKIS, D. LOUKAS, I. MANOLAKOS, A. MARKOU, C. MARKOU, C. MAVROMMATIS, E. PETRAKOU, L. GOUSKOS, T. MERTZIMEKIS, A. PANAGIOTOU, I. EVANGELOU, P. KOKKAS, N. MANTHOS, I. PAPADOPOULOS, V. PATRAS, F.A. TRIANTIS, A. ARANYI, G. BENCZE, L. BOLDIZSAR, G. DEBRECZENI, C. HAJDU1, D. HORVATH, A. KAPUSI, K. KRAJCZAR1, A. LASZLO, F. SIKLER, G. VESZTERGOMBI1, N. BENI, J. MOLNAR, J. PALINKAS, Z. SZILLASI, V. VESZPREMI, P. RAICS, Z.L. TROCSANYI, B. UJVARI, S. BANSAL, S.B. BERI, V. BHATNAGAR, M. JINDAL, M. KAUR, J.M. KOHLI, M.Z. MEHTA, N. NISHU, L.K. SAINI, A. SHARMA, R. SHARMA, A.P. SINGH, J.B. SINGH, S.P. SINGH, S. AHUJA, S. BHATTACHARYA, S. CHAUHAN, B.C. CHOUDHARY, P. GUPTA, S. JAIN, A. KUMAR, R.K. SHIVPURI, R.K. CHOUDHURY, D. DUTTA, S. KAILAS, S.K. KATARIA, A.K. MOHANTY1, L.M. PANT, P. SHUKLA, P. SUGGISETTI, T. AZIZ, M. GUCHAIT, A. GURTU, M. MAITY, D. MAJUMDER, G. MAJUMDER, K. MAZUMDAR, G.B. MOHANTY, A. SAHA, K. SUDHAKAR, N.WICKRAMAGE, S. BANERJEE, S. DUGAD, N.K. MONDAL, H. ARFAEI, H. BAKHSHIANSOHI, S.M. ETESAMI, A. FAHIM, M. HASHEMI, A. JAFARI, M. KHAKZAD, A. MOHAMMADI, M. MOHAMMADI NAJAFABADI, S. PAKTINAT MEHDIABADI, B. SAFARZADEH, M. ZEINALI, M. ABBRESCIA, L. BARBONE, C. CALABRIA, A. COLALEO, D. CREANZA, N. DE FILIPPIS, M. DE PALMA, A. DIMITROV, F. FEDELE, L. FIORE, G. IASELLI, L. LUSITO, G. MAGGI, M. MAGGI, N. MANNA, B. MARANGELLI, S. MY, S. NUZZO, G.A. PIERRO, A. POMPILI, G. PUGLIESE, F. ROMANO, G. ROSELLI, G. SELVAGGI, L. SILVESTRIS, R. TRENTADUE, S. TUPPUTI, G. ZITO, G. ABBIENDI, A.C. BENVENUTI, D. BONACORSI, S. BRAIBANT, P. CAPILUPPI, A. CASTRO, F.R. CAVALLO, M. CUFFIANI, G.M. DALLAVALLE, F. FABBRI, A. FANFANI, D. FASANELLA, P. GIACOMELLI, M. GIUNTA, C. GRANDI, S. MARCELLINI, G. MASETTI, M. MENEGHELLI, A. MONTANARI, F.L. NAVARRIA, F. ODORICI, A. PERROTTA, A.M. ROSSI, T. ROVELLI, G. SIROLI, R. TRAVAGLINI, S. ALBERGO, G. CAPPELLO, M. CHIORBOLI, S. COSTA, A. TRICOMI, C. TUVE, G. BARBAGLI, G. BROCCOLO, V. CIULLI, C. CIVININI, R. D'ALESSANDRO, E. FOCARDI, S. FROSALI, E. GALLO, P. LENZI, M. MESCHINI, S. PAOLETTI, G. SGUAZZONI, A. TROPIANO, L. BENUSSI, S. BIANCO, S. COLAFRANCESCHI, D. PICCOLO, P. FABBRICATORE, R. MUSENICH, A. BENAGLIA, G.B. CERATI, F. DE GUIO, L. DI MATTEO, A. GHEZZI, P. GOVONI, M. MALBERTI, S. MALVEZZI, A. MARTELLI, A. MASSIRONI, D. MENASCE, V. MICCIO, L. MORONI, M. PAGANONI, D. PEDRINI, S. RAGAZZI, N. REDAELLI, S. SALA, T. TABARELLI DE FATIS, V. TANCINI, S. BUONTEMPO, C.A. CARRILLO MONTOYA, A. CIMMINO, A. DE COSA, M. DE GRUTTOLA, F. FABOZZI, A.O.M. IORIO, L. LISTA, P. NOLI, P. PAOLUCCI, P. AZZI, N. BACCHETTA, P. BELLAN, D. BISELLO, A. BRANCA, R. CARLIN, P. CHECCHIA, E. CONTI, M. DE MATTIA, T. DORIGO, U. DOSSELLI, F. FANZAGO, F. GASPARINI, U. GASPARINI, P. GIUBILATO, A. GRESELE, S. LACAPRARA, I. LAZZIZZERA, M. MARGONI, M. MAZZUCATO, A.T. MENEGUZZO, L. PERROZZI, N. POZZOBON, P. RONCHESE, F. SIMONETTO, E. TORASSA, M. TOSI, S. VANINI, P. ZOTTO, G. ZUMERLE, P. BAESSO, U. BERZANO, C. RICCARDI, P. TORRE, P. VITULO, C. VIVIANI, M. BIASINI, G.M. BILEI, B. CAPONERI, L. FAN`O, P. LARICCIA, A. LUCARONI, G. MANTOVANI, M. MENICHELLI, A. NAPPI, A. SANTOCCHIA, L. SERVOLI, S. TARONI, M. VALDATA, R. VOLPE, P. AZZURRI, G. BAGLIESI, J. BERNARDINI, T. BOCCALI, R. CASTALDI, R.T. D’AGNOLO, R. DELL’ORSO, F. FIORI, L. FO`A, A. GIASSI, A. KRAAN, F. LIGABUE, T. LOMTADZE, L. MARTINI, A. MESSINEO, F. PALLA, F. PALMONARI, S. SARKAR, G. SEGNERI, A.T. SERBAN, P. SPAGNOLO, R. TENCHINI, G. TONELLI, A. VENTURI, P.G. VERDINI, L. BARONE, F. CAVALLARI, D. DEL RE, E. DI MARCO, M. DIEMOZ, D. FRANCI, M. GRASSI, E. LONGO, G. ORGANTINI, A. PALMA, F. PANDOLFI, R. PARAMATTI, S. RAHATLOU, N. AMAPANE, R. ARCIDIACONO, S. ARGIRO, M. ARNEODO, C. BIINO, C. BOTTA, N. CARTIGLIA, R. CASTELLO, M. COSTA, N. DEMARIA, A. GRAZIANO, C. MARIOTTI, M. MARONE, S. MASELLI, E. MIGLIORE, G. MILA, V. MONACO, M. MUSICH, M.M. OBERTINO, N. PASTRONE, M. PELLICCIONI, A. ROMERO, M. RUSPA, R. SACCHI, V. SOLA, A. SOLANO, A. STAIANO, D. TROCINO, A. VILELA PEREIRA, F. AMBROGLINI, S. BELFORTE, F. COSSUTTI, G. DELLA RICCA, B. GOBBO, D. MONTANINO, A. PENZO, S.G. HEO, S. CHANG, J. CHUNG, D.H. KIM, G.N. KIM, J.E. KIM, D.J. KONG, H. PARK, D. SON, D.C. SON, Z.KIM, J.Y. KIM, S. SONG, S. CHOI, B. HONG, M. JO, H. KIM, J.H. KIM, T.J. KIM, K.S. LEE, D.H. MOON, S.K. PARK, H.B. RHEE, E. SEO, S. SHIN, K.S. SIM, M. CHOI, S. KANG, C. PARK, I.C. PARK, S. PARK, G. RYU, Y. CHOI, Y.K. CHOI, J. GOH, J. LEE, S. LEE, H. SEO, I. YU, M.J. BILINSKAS, I. GRIGELIONIS, M. JANULIS, D. MARTISIUTE, P. PETROV, T. SABONIS, H. CASTILLA VALDEZ, E. DE LA CRUZ BURELO, R. LOPEZ-FERNANDEZ, A. S´ANCHEZ HERN´ANDEZ, L.M. VILLASENOR-CENDEJAS, S. CARRILLO MORENO, F. VAZQUEZ VALENCIA, H.A. SALAZAR IBARGUEN, E. CASIMIRO LINARES, A. MORELOS PINEDA, M.A. REYES-SANTOS, P. ALLFREY, D. KROFCHECK, J. TAM, P.H. BUTLER, R. DOESBURG, H. SILVERWOOD, M. AHMAD, I. AHMED, M.I. ASGHAR, H.R. HOORANI, W.A. KHAN, T. KHURSHID, S. QAZI, M. CWIOK, W. DOMINIK, K. DOROBA, A. KALINOWSKI, M. KONECKI, J. KROLIKOWSKI, T. FRUEBOES, R. GOKIELI, M. G´ORSKI, M. KAZANA, K. NAWROCKI, M. SZLEPER, G. WROCHNA, P. ZALEWSKI, N. ALMEIDA, A. DAVID, P. FACCIOLI, P.G. FERREIRA PARRACHO, M. GALLINARO, P. MARTINS, G. MINI, P. MUSELLA, A. NAYAK, L. RAPOSO, P.Q. RIBEIRO, J. SEIXAS, P. SILVA, D. SOARES, J. VARELA, H.K.W¨OHRI, I. BELOTELOV, P. BUNIN, M. FINGER, M. FINGER JR., I. GOLUTVIN, A. KAMENEV, V. KARJAVIN, G. KOZLOV, A. LANEV, P. MOISENZ, V. PALICHIK, V. PERELYGIN, S. SHMATOV, V. SMIRNOV, A. VOLODKO, A. ZARUBIN, N. BONDAR, V. GOLOVTSOV, Y. IVANOV, V. KIM, P. LEVCHENKO, V. MURZIN, V. ORESHKIN, I. SMIRNOV, V. SULIMOV, L. UVAROV, S. VAVILOV, A. VOROBYEV, YU. ANDREEV, S. GNINENKO, N. GOLUBEV, M. KIRSANOV, N. KRASNIKOV, V. MATVEEV, A. PASHENKOV, A. TOROPIN, S. TROITSKY, V. EPSHTEYN, V. GAVRILOV, V. KAFTANOV, M. KOSSOV, A. KROKHOTIN, S. KULESHOV, N. LYCHKOVSKAYA, A. OULIANOV, G. SAFRONOV, S. SEMENOV, I. SHREYBER, V. STOLIN, E. VLASOV, A. ZHOKIN, E. BOOS, M. DUBININ, L. DUDKO, A. ERSHOV, A. GRIBUSHIN, O. KODOLOVA, I. LOKHTIN, S. OBRAZTSOV, S. PETRUSHANKO, L. SARYCHEVA, V. SAVRIN, A. SNIGIREV, V. ANDREEV, M. AZARKIN, I. DREMIN, M. KIRAKOSYAN, S.V. RUSAKOV, A. VINOGRADOV, I. AZHGIREY, S. BITIOUKOV, V. GRISHIN1, V. KACHANOV, D. KONSTANTINOV, V. KRYCHKINE, V. PETROV, R. RYUTIN, S. SLABOSPITSKY, A. SOBOL, L. TOURTCHANOVITCH, S. TROSHIN, N. TYURIN, A. UZUNIAN, A. VOLKOV, P. ADZIC, M. DJORDJEVIC, D. KRPIC, D. MALETIC, J. MILOSEVIC, J. PUZOVIC, M. AGUILAR-BENITEZ, J. ALCARAZ MAESTRE, P. ARCE, C. BATTILANA, E. CALVO, M. CEPEDA, M. CERRADA, N. COLINO, B. DE LA CRUZ, C. DIEZ PARDOS, C. FERNANDEZ BEDOYA, J.P. FERN´ANDEZ RAMOS, A. FERRANDO, J. FLIX, M.C. FOUZ, P. GARCIA-ABIA, O. GONZALEZ LOPEZ, S. GOY LOPEZ, J.M. HERNANDEZ, M.I. JOSA, G. MERINO, J. PUERTA PELAYO, I. REDONDO, L. ROMERO, J. SANTAOLALLA, C. WILLMOTT, C. ALBAJAR, G. CODISPOTI, J.F. DE TROC´ONIZ, J. CUEVAS, J. FERNANDEZ MENENDEZ, S. FOLGUERAS, I. GONZALEZ CABALLERO, L. LLORET IGLESIAS, J.M. VIZAN GARCIA, I.J. CABRILLO, A. CALDERON, M. CHAMIZO LLATAS, S.H. CHUANG, I. DIAZ MERINO, C. DIEZ GONZALEZ, J. DUARTE CAMPDERROS, M. FELCINI, M. FERNANDEZ, G. GOMEZ, J. GONZALEZ SANCHEZ, R. GONZALEZ SUAREZ, C. JORDA, P. LOBELLE PARDO, A. LOPEZ VIRTO, J. MARCO, R. MARCO, C. MARTINEZ RIVERO, F. MATORRAS, J. PIEDRA GOMEZ, T. RODRIGO, A. RUIZ JIMENO, L. SCODELLARO, M. SOBRON SANUDO, I. VILA, R. VILAR CORTABITARTE, D. ABBANEO, E. AUFFRAY, P. BAILLON, A.H. BALL, D. BARNEY, F. BEAUDETTE, A.J. BELL, D. BENEDETTI, C. BERNET, A.K. BHATTACHARYYA, W. BIALAS, P. BLOCH, A. BOCCI, S. BOLOGNESI, H. BREUKER, G. BRONA, K. BUNKOWSKI, T. CAMPORESI, E. CANO, A. CATTAI, G. CERMINARA, T. CHRISTIANSEN, J.A. COARASA PEREZ, R. COVARELLI, B. CUR´E, D. D’ENTERRIA, T. DAHMS, A. DE ROECK, A. ELLIOTT-PEISERT, W. FUNK, A. GADDI, S. GENNAI, G. GEORGIOU, H. GERWIG, D. GIGI, K. GILL, D. GIORDANO, F. GLEGE, R. GOMEZ-REINO GARRIDO, M. GOUZEVITCH, S. GOWDY, L. GUIDUCCI, M. HANSEN, J. HARVEY, J. HEGEMAN, B. HEGNER, C. HENDERSON, H.F. HOFFMANN, A. HONMA, V. INNOCENTE, P. JANOT, E. KARAVAKIS, P. LECOQ, C. LEONIDOPOULOS, C. LOURENC¸O, A. MACPHERSON, T. M¨AKI, L. MALGERI, M. MANNELLI, L. MASETTI, F. MEIJERS, S. MERSI, E. MESCHI, R. MOSER, M.U. MOZER, M. MULDERS, E. NESVOLD1, L. ORSINI, E. PEREZ, A. PETRILLI, A. PFEIFFER, M. PIERINI, M. PIMI¨A, G. POLESE, A. RACZ, G. ROLANDI, C. ROVELLI, M. ROVERE, H. SAKULIN, C. SCH¨AFER, C. SCHWICK, I. SEGONI, P. SIEGRIST, M. SIMON, P. SPHICAS, D. SPIGA, M. SPIROPULU, F. ST¨ OCKLI, M. STOYE, P. TROPEA, A. TSIROU, G.I. VERES, P. VICHOUDIS, M. VOUTILAINEN, W.D. ZEUNER, W. BERTL, K. DEITERS, W. ERDMANN, K. GABATHULER, R. HORISBERGER, Q. INGRAM, H.C. KAESTLI, S. K¨ONIG, D. KOTLINSKI, U. LANGENEGGER, F. MEIER, D. RENKER, T. ROHE, J. SIBILLE, A. STARODUMOV, L. CAMINADA, Z. CHEN, S. CITTOLIN, G. DISSERTORI, M. DITTMAR, J. EUGSTER, K. FREUDENREICH, C. GRAB, A. HERV´E, W. HINTZ, P. LECOMTE, W. LUSTERMANN, C. MARCHICA27, P. MARTINEZ RUIZ DEL ARBOL, P. MERIDIANI, P. MILENOVIC, F. MOORTGAT, A. NARDULLI, P. NEF, F. NESSI-TEDALDI, L. PAPE, F. PAUSS, T. PUNZ, A. RIZZI, F.J. RONGA, L. SALA, A.K. SANCHEZ, M.-C. SAWLEY, B. STIEGER, L. TAUSCHERY, A. THEA, K. THEOFILATOS, D. TREILLE, C. URSCHELER, R. WALLNY, M. WEBER, L. WEHRLI, J. WENG, E. AGUIL´ O, C. AMSLER, V. CHIOCHIA, S. DE VISSCHER, C. FAVARO, M. IVOVA RIKOVA, A. JAEGER, B. MILLAN MEJIAS, C. REGENFUS, P. ROBMANN, T. ROMMERSKIRCHEN, A. SCHMIDT, H. SNOEK, L.WILKE, Y.H. CHANG, K.H. CHEN, W.T. CHEN, S. DUTTA, A. GO, C.M. KUO, S.W. LI, W. LIN, M.H. LIU, Z.K. LIU, Y.J. LU, J.H.WU, S.S. YU, P. BARTALINI, P. CHANG, Y.W. CHANG, Y. CHAO, K.F. CHEN, W.-S. HOU, Y. HSIUNG, K.Y. KAO, Y.J. LEI, R.-S. LU, J.G. SHIU, Y.M. TZENG, M.WANG, J.T.WEI, A. ADIGUZEL, M.N. BAKIRCI, S. CERCI, Z. DEMIR, C. DOZEN, I. DUMANOGLU, E. ESKUT, S. GIRGIS, G. G¨OKBULUT, Y. G¨ ULER, E. GURPINAR, I. HOS, E.E. KANGAL, T. KARAMAN, A. KAYIS TOPAKSU, A. NART, G. O¨ NENGU¨ T, K. OZDEMIR, S. OZTURK, A. POLATO¨Z, K. SOGUT, B. TALI, H. TOPAKLI, D. UZUN, L.N. VERGILI, M. VERGILI, C. ZORBILMEZ, I.V. AKIN, T. ALIEV, S. BILMIS, M. DENIZ, H. GAMSIZKAN, A.M. GULER, K. OCALAN, A. OZPINECI, M. SERIN, R. SEVER, U.E. SURAT, E. YILDIRIM, M. ZEYREK, M. DELIOMEROGLU, D. DEMIR, E. GU¨LMEZ, A. HALU, B. ISILDAK, M. KAYA, O. KAYA, M. O¨ZBEK, S. OZKORUCUKLU, N. SONMEZ, L. LEVCHUK, P. BELL, F. BOSTOCK, J.J. BROOKE, T.L. CHENG, D. CUSSANS, R. FRAZIER, J. GOLDSTEIN, M. GRIMES, G.P. HEATH, H.F. HEATH, C. HILL, B. HUCKVALE, J. JACKSON, L. KRECZKO, S. METSON, D.M. NEWBOLD, K. NIRUNPONG, A. POLL, V.J. SMITH, S.WARD, L. BASSO, K.W. BELL, A. BELYAEV, C. BREW, R.M. BROWN, B. CAMANZI, D.J.A. COCKERILL, J.A. COUGHLAN, K. HARDER, S. HARPER, B.W. KENNEDY, E. OLAIYA, D. PETYT, B.C. RADBURN-SMITH, C.H. SHEPHERD-THEMISTOCLEOUS, I.R. TOMALIN, W.J.WOMERSLEY, S.D.WORM, R. BAINBRIDGE, G. BALL, J. BALLIN, R. BEUSELINCK, O. BUCHMULLER, D. COLLING, N. CRIPPS, M. CUTAJAR, G. DAVIES, M. DELLA NEGRA, C. FOUDAS, J. FULCHER, D. FUTYAN, A. GUNERATNE BRYER, G. HALL, Z. HATHERELL, J. HAYS, G. ILES, G. KARAPOSTOLI, L. LYONS, A.-M. MAGNAN, J. MARROUCHE, R. NANDI, J. NASH, A. NIKITENKO, A. PAPAGEORGIOU, M. PESARESI, K. PETRIDIS, M. PIOPPI, D.M. RAYMOND, N. ROMPOTIS, A. ROSE, M.J. RYAN, C. SEEZ, P. SHARP, A. SPARROW, A. TAPPER, S. TOURNEUR, M. VAZQUEZ ACOSTA, T. VIRDEE1, S.WAKEFIELD, D.WARDROPE, T. WHYNTIE, M. BARRETT, M. CHADWICK, J.E. COLE, P.R. HOBSON, A. KHAN, P. KYBERD, D. LESLIE, W. MARTIN, I.D. REID, L. TEODORESCU, K. HATAKEYAMA, T. BOSE, E. CARRERA JARRIN, A. CLOUGH, C. FANTASIA, A. HEISTER, J. ST. JOHN, P. LAWSON, D. LAZIC, J. ROHLF, L. SULAK, J. ANDREA, A. AVETISYAN, J.P. CHOU, D. CUTTS, S. ESEN, A. FERAPONTOV, U. HEINTZ, S. JABEEN, G. KUKARTSEV, G. LANDSBERG, M. NARAIN, D. NGUYEN, M. SEGALA, T. SPEER, K.V. TSANG, M.A. BORGIA, R. BREEDON, M. CALDERON DE LA BARCA SANCHEZ, D. CEBRA, M. CHERTOK, J. CONWAY, P.T. COX, J. DOLEN, R. ERBACHER, E. FRIIS, W. KO, A. KOPECKY, R. LANDER, H. LIU, S. MARUYAMA, T. MICELI, M. NIKOLIC, D. PELLETT, J. ROBLES, T. SCHWARZ, M. SEARLE, J. SMITH, M. SQUIRES, M. TRIPATHI, R. VASQUEZ SIERRA, C. VEELKEN, K. ARISAKA, D. CLINE, R. COUSINS, A. DEISHER, J. DURIS, S. ERHAN, C. FARRELL, J. HAUSER, M. IGNATENKO, C. JARVIS, C. PLAGER, G. RAKNESS, P. SCHLEIN, J. TUCKER, V. VALUEV, J. BABB, R. CLARE, J. ELLISON, J.W. GARY, F. GIORDANO, G. HANSON, G.Y. JENG, S.C. KAO, F. LIU, A. LUTHRA, H. NGUYEN, G. PASZTOR, A. SATPATHY, B.C. SHENY, R. STRINGER, J. STURDY, S. SUMOWIDAGDO, R.WILKEN, S.WIMPENNY, W. ANDREWS, J.G. BRANSON, E. DUSINBERRE, D. EVANS, F. GOLF, A. HOLZNER, R. KELLEY, M. LEBOURGEOIS, J. LETTS, B. MANGANO, J. MUELMENSTAEDT, S. PADHI, C. PALMER, G. PETRUCCIANI, H. PI, M. PIERI, R. RANIERI, M. SANI, V. SHARMA1, S. SIMON, Y. TU, A. VARTAK, F. W¨URTHWEIN, A. YAGIL, D. BARGE, R. BELLAN, C. CAMPAGNARI, M. D’ALFONSO, T. DANIELSON, P. GEFFERT, J. INCANDELA, C. JUSTUS, P. KALAVASE, S.A. KOAY, D. KOVALSKYI, V. KRUTELYOV, S. LOWETTE, N. MCCOLL, V. PAVLUNIN, F. REBASSOO, J. RIBNIK, J. RICHMAN, R. ROSSIN, D. STUART, W. TO, J.R. VLIMANT, M.WITHERELL, A. BORNHEIM, J. BUNN, Y. CHEN, M. GATAULLIN, D. KCIRA, V. LITVINE, Y. MA, A. MOTT, H.B. NEWMAN, C. ROGAN, K. SHIN, V. TIMCIUC, P. TRACZYK, J. VEVERKA, R.WILKINSON, Y. YANG, R.Y. ZHU, B. AKGUN, A. CALAMBA, R. CARROLL, T. FERGUSON, Y. IIYAMA, D.W. JANG, S.Y. JUN, Y.F. LIU, M. PAULINI, J. RUSS, N. TERENTYEV, H. VOGEL, I. VOROBIEV, J.P. CUMALAT, M.E. DINARDO, B.R. DRELL, C.J. EDELMAIER, W.T. FORD, B. HEYBURN, E. LUIGGI LOPEZ, U. NAUENBERG, J.G. SMITH, K. STENSON, K.A. ULMER, S.R.WAGNER, S.L. ZANG, L. AGOSTINO, J. ALEXANDER, F. BLEKMAN, A. CHATTERJEE, S. DAS, N. EGGERT, L.J. FIELDS, L.K. GIBBONS, B. HELTSLEY, K. HENRIKSSON, W. HOPKINS, A. KHUKHUNAISHVILI, B. KREIS, V. KUZNETSOV, Y. LIU, G. NICOLAS KAUFMAN, J.R. PATTERSON, D. PUIGH, D. RILEY, A. RYD, M. SAELIM, X. SHI, W. SUN, W.D. TEO, J. THOM, J. THOMPSON, J. VAUGHAN, Y.WENG, P.WITTICH, A. BISELLI, G. CIRINO, D. WINN, S. ABDULLIN, M. ALBROW, J. ANDERSON, G. APOLLINARI, M. ATAC, J.A. BAKKEN, L.A.T. BAUERDICK, A. BERETVAS, J. BERRYHILL, P.C. BHAT, I. BLOCH, F. BORCHERDING, K. BURKETT, J.N. BUTLER, V. CHETLURU, H.W.K. CHEUNG, F. CHLEBANA, S. CIHANGIR, M. DEMARTEAU, D.P. EARTLY, V.D. ELVIRA, I. FISK, J. FREEMAN, Y. GAO, E. GOTTSCHALK, D. GREEN, K. GUNTHOTI, O. GUTSCHE, A. HAHN, J. HANLON, R.M. HARRIS, J. HIRSCHAUER, E. JAMES, H. JENSEN, M. JOHNSON, U. JOSHI, R. KHATIWADA, B. KILMINSTER, B. KLIMA, K. KOUSOURIS, S. KUNORI, S. KWAN, P. LIMON, R. LIPTON, J. LYKKEN, K. MAESHIMA, J.M. MARRAFFINO, D. MASON, P. MCBRIDE, T. MCCAULEY, T. MIAO, K. MISHRA, S. MRENNA, Y. MUSIENKO, C. NEWMAN-HOLMES, V. O’DELL, S. POPESCU, R. PORDES, O. PROKOFYEV, N. SAOULIDOU, E. SEXTON-KENNEDY, S. SHARMA, A. SOHA, W.J. SPALDING, L. SPIEGEL, P. TAN, L. TAYLOR, S. TKACZYK, L. UPLEGGER, E.W. VAANDERING, R. VIDAL, J. WHITMORE, W. WU, F. YANG, F. YUMICEVA, J.C. YUN, D. ACOSTA, P. AVERY, D. BOURILKOV, M. CHEN, G.P. DI GIOVANNI, D. DOBUR, A. DROZDETSKIY, R.D. FIELD, M. FISHER, Y. FU, I.K. FURIC, J. GARTNER, S. GOLDBERG, B. KIM, S. KLIMENKO, J. KONIGSBERG, A. KORYTOV, K. KOTOV, A. KROPIVNITSKAYA, T. KYPREOS, K. MATCHEV, G. MITSELMAKHER, L. MUNIZ, Y. PAKHOTIN, M. PETTERSON, C. PRESCOTT, R. REMINGTON, M. SCHMITT, B. SCURLOCK, P. SELLERS, M. SNOWBALL, D.WANG, J. YELTON, M. ZAKARIA, C. CERON, V. GAULTNEY, L. KRAMER, L.M. LEBOLO, S. LINN, P. MARKOWITZ, G. MARTINEZ, D. MESA, J.L. RODRIGUEZ, T. ADAMS, A. ASKEW, J. BOCHENEK, J. CHEN, B. DIAMOND, S.V. GLEYZER, J. HAAS, S. HAGOPIAN, V. HAGOPIAN, M. JENKINS, K.F. JOHNSON, H. PROSPER, S. SEKMEN, V. VEERARAGHAVAN, M.M. BAARMAND, B. DORNEY, S. GURAGAIN, M. HOHLMANN, H. KALAKHETY, R. RALICH, I. VODOPIYANOV, M.R. ADAMS, I.M. ANGHEL, L. APANASEVICH, Y. BAI, V.E. BAZTERRA, R.R. BETTS, J. CALLNER, R. CAVANAUGH, C. DRAGOIU, E.J. GARCIA-SOLIS, C.E. GERBER, D.J. HOFMAN, S. KHALATYAN, F. LACROIX, C. O’BRIEN, E. SHABALINA, C. SILVESTRE, A. SMORON, D. STROM, N. VARELAS, U. AKGUN, E.A. ALBAYRAK, B. BILKI, K. CANKOCAK, W. CLARIDA, F. DURU, C.K. LAE, E. MCCLIMENT, J.-P. MERLO, H. MERMERKAYA, A. MESTVIRISHVILI, A. MOELLER, J. NACHTMAN, C.R. NEWSOM, E. NORBECK, J. OLSON, Y. ONEL, F. OZOK, S. SEN, J.WETZEL, T. YETKIN, K. YI, B.A. BARNETT, B. BLUMENFELD, A. BONATO, C. ESKEW, D. FEHLING, G. GIURGIU, A.V. GRITSAN, Z.J. GUO, G. HU, P. MAKSIMOVIC, S. RAPPOCCIO, M. SWARTZ, N.V. TRAN, A. WHITBECK, P. BARINGER, A. BEAN, G. BENELLI, O. GRACHOV, M. MURRAY, D. NOONAN, V. RADICCI, S. SANDERS, J.S.WOOD, V. ZHUKOVA, D. BANDURIN, T. BOLTON, I. CHAKABERIA, A. IVANOV, M. MAKOUSKI, Y. MARAVIN, S. SHRESTHA, I. SVINTRADZE, Z.WAN, J. GRONBERG, D. LANGE, D. WRIGHT, A. BADEN, M. BOUTEMEUR, S.C. ENO, D. FERENCEK, J.A. GOMEZ, N.J. HADLEY, R.G. KELLOGG, M. KIRN, Y. LU, A.C. MIGNEREY, K. ROSSATO, P. RUMERIO, F. SANTANASTASIO, A. SKUJA, J. TEMPLE, M.B. TONJES, S.C. TONWAR, E. TWEDT, B. ALVER, G. BAUER, J. BENDAVID, W. BUSZA, E. BUTZ, I.A. CALI, M. CHAN, V. DUTTA, P. EVERAERTS, G. GOMEZ CEBALLOS, M. GONCHAROV, K.A. HAHN, P. HARRIS, Y. KIM, M. KLUTE, Y.-J. LEE, C. LOIZIDES, P.D. LUCKEY, T. MA, S. NAHN, C. PAUS, C. ROLAND, G. ROLAND, M. RUDOLPH, G.S.F. STEPHANS, K. SUMOROK, K. SUNG, E.A. WENGER, B. WYSLOUCH, S. XIE, Y. YILMAZ, A.S. YOON, M. ZANETTI, P. COLE, S.I. COOPER, P. CUSHMAN, B. DAHMES, A. DE BENEDETTI, P.R. DUDERO, G. FRANZONI, J. HAUPT, K. KLAPOETKE, Y. KUBOTA, J. MANS, V. REKOVIC, R. RUSACK, M. SASSEVILLE, A. SINGOVSKY, L.M. CREMALDI, R. GODANG, R. KROEGER, L. PERERA, R. RAHMAT, D.A. SANDERS, D. SUMMERS, K. BLOOM, S. BOSE, J. BUTT, D.R. CLAES, A. DOMINGUEZ, M. EADS, J. KELLER, T. KELLY, I. KRAVCHENKO, J. LAZO-FLORES, C. LUNDSTEDT, H. MALBOUISSON, S. MALIK, G.R. SNOW, U. BAUR, A. GODSHALK, I. IASHVILI, A. KHARCHILAVA, K. SMITH, J. ZENNAMO, G. ALVERSON, E. BARBERIS, D. BAUMGARTEL, O. BOERIU, M. CHASCO, K. KAADZE, S. REUCROFT, J. SWAIN, D. WOOD, J. ZHANG, A. ANASTASSOV, A. KUBIK, N. ODELL, R.A. OFIERZYNSKI, B. POLLACK, A. POZDNYAKOV, S. STOYNEV, M. VELASCO, S.WON, L. ANTONELLI, D. BERRY, M. HILDRETH, C. JESSOP, D.J. KARMGARD, J. KOLB, T. KOLBERG, K. LANNON, W. LUO, S. LYNCH, N. MARINELLI, D.M. MORSE, T. PEARSON, R. RUCHTI, J. SLAUNWHITE, N. VALLS, J. WARCHOL, M.WAYNE, J. ZIEGLER, B. BYLSMA, L.S. DURKIN, J. GU, P. KILLEWALD, T.Y. LING, M. RODENBURG, G.WILLIAMS, N. ADAM, E. BERRY, P. ELMER, D. GERBAUDO, V. HALYO, P. HEBDA, A. HUNT, J. JONES, E. LAIRD, D. LOPES PEGNA, D. MARLOW, T. MEDVEDEVA, M. MOONEY, J. OLSEN, P. PIROU´E, H. SAKA, D. STICKLAND, C. TULLY, J.S.WERNER, A. ZURANSKI, J.G. ACOSTA, X.T. HUANG, A. LOPEZ, H. MENDEZ, S. OLIVEROS, J.E. RAMIREZ VARGAS, A. ZATSERKLYANIY, E. ALAGOZ, V.E. BARNES, G. BOLLA, L. BORRELLO, D. BORTOLETTO, A. EVERETT, A.F. GARFINKEL, Z. GECSE, L. GUTAY, M. JONES, O. KOYBASI, A.T. LAASANEN, N. LEONARDO, C. LIU, V. MAROUSSOV, M. MEIER, P. MERKEL, D.H. MILLER, N. NEUMEISTER, K. POTAMIANOS, I. SHIPSEY, D. SILVERS, A. SVYATKOVSKIY, H.D. YOO, J. ZABLOCKI, Y. ZHENG, P. JINDAL, N. PARASHAR, C. BOULAHOUACHE, V. CUPLOV, K.M. ECKLUND, F.J.M. GEURTS, J.H. LIU, J. MORALES, B.P. PADLEY, R. REDJIMI, J. ROBERTS, J. ZABEL, B. BETCHART, A. BODEK, Y.S. CHUNG, P. DE BARBARO, R. DEMINA, Y. ESHAQ, H. FLACHER, A. GARCIA- BELLIDO, P. GOLDENZWEIG, Y. GOTRA, J. HAN, A. HAREL, D.C. MINER, D. ORBAKER, G. PETRILLO, D. VISHNEVSKIY, M. ZIELINSKI, A. BHATTI, L. DEMORTIER, K. GOULIANOS, G. LUNGU, C. MESROPIAN, M. YAN, O. ATRAMENTOV, A. BARKER, D. DUGGAN, Y. GERSHTEIN, R. GRAY, E. HALKIADAKIS, D. HIDAS, D. HITS, A. LATH, S. PANWALKAR, R. PATEL, A. RICHARDS, K. ROSE, S. SCHNETZER, S. SOMALWAR, R. STONE, S. THOMAS, G. CERIZZA, M. HOLLINGSWORTH, S. SPANIER, Z.C. YANG, A. YORK, J. ASAADI, R. EUSEBI, J. GILMORE, A. GURROLA, T. KAMON, V. KHOTILOVICH, R. MONTALVO, C.N. NGUYEN, J. PIVARSKI, A. SAFONOV, S. SENGUPTA, A. TATARINOV, D. TOBACK, M.WEINBERGER, N. AKCHURIN, C. BARDAK, J. DAMGOV, C. JEONG, K. KOVITANGGOON, S.W. LEE, P. MANE, Y. ROH, A. SILL, I. VOLOBOUEV, R.WIGMANS, E. YAZGAN, E. APPELT, E. BROWNSON, D. ENGH, C. FLOREZ, W. GABELLA, W. JOHNS, P. KURT, C. MAGUIRE, A. MELO, P. SHELDON, J. VELKOVSKA, M.W. ARENTON, M. BALAZS, S. BOUTLE, M. BUEHLER, S. CONETTI, B. COX, B. FRANCIS, R. HIROSKY, A. LEDOVSKOY, C. LIN, C. NEU, T. PATEL, R. YOHAY, S. GOLLAPINNI, R. HARR, P.E. KARCHIN, V. LOGGINS, M. MATTSON, C. MILST`ENE, A. SAKHAROV, M. ANDERSON, M. BACHTIS, J.N. BELLINGER, D. CARLSMITH, S. DASU, J. EFRON, L. GRAY, K.S. GROGG, M. GROTHE, R. HALL-WILTON, M. HERNDON, P. KLABBERS, J. KLUKAS, A. LANARO, C. LAZARIDIS, J. LEONARD, J. LIU, D. LOMIDZE, R. LOVELESS, A. MOHAPATRA, W. PARKER, D. REEDER, I. ROSS, A. SAVIN, W.H. SMITH, J. SWANSON, M.WEINBERG, Laboratoire d'Annecy de Physique des Particules (LAPP/Laboratoire d'Annecy-le-Vieux de Physique des Particules), Centre National de la Recherche Scientifique (CNRS)-Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry])-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3), Institut de Recherches sur les lois Fondamentales de l'Univers (IRFU), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay, Laboratoire Leprince-Ringuet (LLR), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-École polytechnique (X)-Centre National de la Recherche Scientifique (CNRS), Département Recherches Subatomiques (DRS-IPHC), Institut Pluridisciplinaire Hubert Curien (IPHC), Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Centre National de la Recherche Scientifique (CNRS), Institut de Physique Nucléaire de Lyon (IPNL), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), CMS, Institut de Physique des 2 Infinis de Lyon (IP2I Lyon), Université de Lyon-Université de Lyon-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), CMS Collaboration, Yerevan Physics Institute, Institut für Hochenergiephysik der OeAW, National Centre for Particle and High Energy Physics, Research Institute for Nuclear Problems, Research Institute of Applied Physical Problems, Universiteit Antwerpen, Vrije Universiteit Brüssel, Université Libre de Bruxelles, Ghent University, Université Catholique de Louvain, Université de Mons, Centro Brasileiro de Pesquisas Físicas (CBPF), Universidade do Estado do Rio de Janeiro (UERJ), Universidade Estadual Paulista (Unesp), Institute for Nuclear Research and Nuclear Energy, University of Sofia, Institute of High Energy Physics, Peking University, Universidad de los Andes, Technical University of Split, University of Split, Institute Rudjer Boskovic, University of Cyprus, National Institute of Chemical Physics and Biophysics, Helsinki Institute of Physics, Lappeenranta University of Technology, IN2P3-CNRS, CEA/Saclay, CNRS/IN2P3, Institut de Physique Nucléaire de Lyon, Academy of Science, Tbilisi State University, I. Physikalisches Institut, III. Physikalisches Institut A, III Physikalisches Institut A, Deutsches Elektronen-Synchrotron, University of Hamburg, Institut für Experimentelle Kernphysik, Institute of Nuclear Physics Demokritos, University of Athens, University of Ioánnina, KFKI Research Institute for Particle and Nuclear Physics, Institute of Nuclear Research ATOMKI, University of Debrecen, Panjab University, University of Delhi, Bhabha Atomic Research Centre, Tata Institute of Fundamental Research - EHEP, Tata Institute of Fundamental Research - HECR, Institute for Studies in Theoretical Physics and Mathematics (IPM), University College Dublin, INFN Sezione di Bari, Università di Bari, Politecnico di Bari, INFN Sezione di Bologna, Universita di Bologna, INFN Sezione di Catania, Universita di Catania, INFN Sezione di Firenze, Universita di Firenze, INFN Laboratori Nazionali di Frascati, INFN Sezione di Genova, INFN Sezione di Milano-Biccoca, Universita di Milano-Bicocca, INFN Sezione di Napoli, Universita di Napoli Federico II, INFN Sezione di Padova, Universita di Padova, INFN Sezione di Pavia, Universita di Pavia, INFN Sezione di Perugia, Universita di Perugia, INFN Sezione di Pisa, Universita di Pisa, Scuola Normale Superiore di Pisa, INFN Sezione di Roma, Universita di Roma la Sapienza, INFN Sezione di Torino, Universita di Torino, Università Del Piemonte Orientale (Novara), INFN Sezione di Trieste, Universita di Trieste, Kyungpook National University, Wonkwang University, Chonnam National University, Konkuk University, Korea University, Seoul National University, University of Seoul, Sungkyunkwan University, Vilnius University, Centro de Investigacion y de Estudios Avanzados Del IPN, Universidad Iberoamericana, Universidad Autónoma de San Luis Potosí, University of Auckland, University of Canterbury, Quaid-I-Azam University, Institute of Experimental Physics, Soltan Institute for Nuclear Studies, Laboratório de Instrumentação e Física Experimental de Partículas (LIP), Joint Institute for Nuclear Research, Petersburg Nuclear Physics Institute, Institute for Nuclear Research, Institute for Theoretical and Experimental Physics (ITEP), Moscow State University, P.N. Lebedev Physical Institute, Institute for High Energy Physics, Vinca Institute of Nuclear Sciences, Centro de Investigaciones Energéticas Medioambientales y Tecnológicas (CIEMAT), Universidad Autónoma de Madrid, Universidad de Oviedo, CSIC-Universidad de Cantabria, European Organization for Nuclear Research, Paul Scherrer Institüt, ETH Zurich, Universität Zürich, National Central University, National Taiwan University (NTU), Cukurova University, Physics Department, Bogaziçi University, Kharkov Institute of Physics and Technology, University of Bristol, Rutherford Appleton Laboratory, University of London, Brunel University, Boston University, Brown University, University of California, Davis, University of California, Los Angeles, University of California, Riverside (UCR), University of California, San Diego, University of California, Santa Barbara, California Institute of Technology, Carnegie Mellon University, University of Colorado at Boulder, Cornell University, Fairfield University, Fermi National Accelerator Laboratory, University of Florida, Florida International University, Florida State University, Florida Institute of Technology, University of Illinois at Chicago (UIC), University of Iowa, Johns Hopkins University, University of Kansas (KU), Kansas State University, Lawrence Livermore National Laboratory, University of Maryland, Massachusetts Institute of Technology (MIT), University of Minnesota, University of Mississippi, University of Nebraska-Lincoln, State University of New York at Buffalo, Northeastern University, Northwestern University (NU), University of Notre Dame, Ohio State University, Princeton University, University of Puerto Rico, Purdue University, Purdue University Calumet, Rice University, University of Rochester, Rockefeller University, Rutgers, the State University of New Jersey, University of Tennessee, Texas AandM University, Texas Tech University, Vanderbilt University, University of Virginia (UVA), Wayne State University, University of Wisconsin, Universidade Federal do ABC (UFABC), University of Visva-Bharati, Universita' di Roma la Sapienza, Universita Delia Basilicata, Laboratoři Nazionali di Legnaro Dell' INFN, Universita di Trento, ENEA - Casaccia Research Center, Institute of Electronic Systems, University of Belgrade, Alstom Contracting, Paul Scherrer Institut, Mersin University, Izmir Institute of Technology, Kafkas University, Suleyman Demirel University, Ege University, Istanbul Technical University, Université Haute-Alsace, Centre de Calcul de i' Institut National de Physique Nucleaire et de Physique des Particules(IN2P3), Scuola Normale e Sezione Dell' INFN, Çukurova Üniversitesi, Fen-Edebiyat Fakültesi, Fizik Bölümü, DELLA RICCA, Giuseppe, TR1918, Demir, Durmuş Ali, Izmir Institute of Technology. Physics, Massachusetts Institute of Technology. Department of Physics, Massachusetts Institute of Technology. Department of Nuclear Science and Engineering, Massachusetts Institute of Technology. Laboratory for Nuclear Science, İYTE, Fen Fakültesi, Fizik Bölümü, Laboratoire d'Annecy de Physique des Particules (LAPP), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Savoie Mont Blanc (USMB [Université de Savoie] [Université de Chambéry])-Centre National de la Recherche Scientifique (CNRS), Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Université de Haute-Alsace (UHA) Mulhouse - Colmar (Université de Haute-Alsace (UHA))-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-École polytechnique (X)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3), Université de Strasbourg (UNISTRA)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3), Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de Physique Nucléaire et de Physique des Particules du CNRS (IN2P3)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS), and (ukupan broj autora: 2424)

Subjects
Drift tube, Compact Muon Solenoid, Physics - Instrumentation and Detectors, Trigger detetectors, Physics::Instrumentation and Detectors, Astrophysics::High Energy Astrophysical Phenomena, FOS: Physical sciences, Cosmic ray, Large Hadron Collider (LHC), 01 natural sciences, Arrival time, PARTICLE PHYSICS, LARGE HADRON COLLIDER, CMS, Nuclear physics, Drift Tube Local Trigger, 0103 physical sciences, Synchronization (computer science), ddc:610, [PHYS.PHYS.PHYS-INS-DET]Physics [physics]/Physics [physics]/Instrumentation and Detectors [physics.ins-det], Detectors and Experimental Techniques, 010306 general physics, Instrumentation, Mathematical Physics, Large detector systems for particle and astroparticle physics, Physics, Muon, Large Hadron Collider, 010308 nuclear & particles physics, Cosmic ray muons, Settore FIS/01 - Fisica Sperimentale, Instrumentation and Detectors (physics.ins-det), COSMIC RAYS, Cosmic Run At Four Tesla (CRAFT), ComputingMethodologies_DOCUMENTANDTEXTPROCESSING, LHC
Abstract

33 páginas, 12 figuras.-- Open Access.-- CMS Collaboration: et al., The CMS experiment uses self-triggering arrays of drift tubes in the barrel muon trigger to perform the identification of the correct bunch crossing. The identification is unique only if the trigger chain is correctly synchronized. In this paper, the synchronization performed during an extended cosmic ray run is described and the results are reported. The random arrival time of cosmic ray muons allowed several synchronization aspects to be studied and a simple method for the fine synchronization of the Drift Tube Local Trigger at LHC to be developed., Individuals have received support from the Marie-Curie IEF program (European Union); the Leventis Foundation; the A. P. Sloan Foundation; and the Alexander von Humboldt Foundation.

Published
2016
Full Text
View/download PDF

47. Systems Approach Identified PPARα as a Therapeutic Target for Vein Graft Disease: the Effects of the Specific Activator Pemafibrate on Macrophage Activation

Author

Hideyuki Higashi, Masanori Aikawa, Lang H Lee, Daniel G. Anderson, Hengmin Zhang, Peter Libby, Elena Aikawa, Keith C. Ozaki, Sasha A Singh, Julius L. Decano, Jianguo Wang, and Arda Halu

Subjects
Activator (genetics), business.industry, Internal Medicine, Cancer research, Medicine, General Medicine, Cardiology and Cardiovascular Medicine, Vein graft disease, business
Published
2018
Full Text
View/download PDF

48. Data-driven modeling of solar-powered urban microgrids

Author

Marta C. González, Antonio Scala, Abdulaziz Khiyami, Arda Halu, Massachusetts Institute of Technology. Department of Civil and Environmental Engineering, Halu, Arda, and Gonzalez, Marta C.

Subjects
Computer science, 020209 energy, Distributed computing, Context (language use), 02 engineering and technology, Electrical Power, solar PV, 01 natural sciences, 7. Clean energy, Electric power system, power systems, Electric Power Supplies, Robustness (computer science), 0103 physical sciences, 11. Sustainability, 0202 electrical engineering, electronic engineering, information engineering, Solar Energy, 010306 general physics, Resilience (network), resilience, Simulation, Research Articles, Multidisciplinary, distributed generation, business.industry, Photovoltaic system, SciAdv r-articles, complex networks, Complex network, Models, Theoretical, microgrid, 13. Climate action, Distributed generation, Microgrid, business, complex networkspower systemsmicrogridsolar PVdistributed generationresilience, Research Article
Abstract

Distributed generation takes center stage in today’s rapidly changing energy landscape. Particularly, locally matching demand and generation in the form of microgrids is becoming a promising alternative to the central distribution paradigm. Infrastructure networks have long been a major focus of complex networks research with their spatial considerations. We present a systemic study of solar-powered microgrids in the urban context, obeying real hourly consumption patterns and spatial constraints of the city. We propose a microgrid model and study its citywide implementation, identifying the self-sufficiency and temporal properties of microgrids. Using a simple optimization scheme, we find microgrid configurations that result in increased resilience under cost constraints. We characterize load-related failures solving power flows in the networks, and we show the robustness behavior of urban microgrids with respect to optimization using percolation methods. Our findings hint at the existence of an optimal balance between cost and robustness in urban microgrids., MIT-Portugal Program, King Abdulaziz City of Science and Technology (Saudia Arabia). Center for Complex Engineering Systems

Published
2015
Full Text
View/download PDF

49. Emergence of overlap in ensembles of spatial multiplexes and statistical mechanics of spatial interacting network ensembles

Author

Satyam Mukherjee, Ginestra Bianconi, and Arda Halu

Subjects
Social and Information Networks (cs.SI), FOS: Computer and information sciences, Structure (mathematical logic), Physics - Physics and Society, Theoretical computer science, Property (programming), Computer science, FOS: Physical sciences, Network structure, Computer Science - Social and Information Networks, Physics and Society (physics.soc-ph), Disordered Systems and Neural Networks (cond-mat.dis-nn), Statistical mechanics, Condensed Matter - Disordered Systems and Neural Networks, Space (mathematics), Range (mathematics), Null (SQL), Robustness (computer science)
Abstract

Spatial networks range from the brain networks, to transportation networks and infrastructures. Recently interacting and multiplex networks are attracting great attention because their dynamics and robustness cannot be understood without treating at the same time several networks. Here we present maximal entropy ensembles of spatial multiplex and spatial interacting networks that can be used in order to model spatial multilayer network structures and to build null models of real datasets. We show that spatial multiplex naturally develop a significant overlap of the links, a noticeable property of many multiplexes that can affect significantly the dynamics taking place on them. Additionally, we characterize ensembles of spatial interacting networks and we analyse the structure of interacting airport and railway networks in India, showing the effect of space in determining the link probability., Comment: (12 pages, 4 figures) for downloading data see URL http://sites.google.com/site/satyammukherjee/pubs

Published
2014
Full Text
View/download PDF

50. Multiplex PageRank

Author

Ginestra Bianconi, Pietro Panzarasa, Raul J. Mondragon, and Arda Halu

Subjects
FOS: Computer and information sciences, Physics - Physics and Society, Theoretical computer science, Computer science, Complex system, lcsh:Medicine, FOS: Physical sciences, Physics and Society (physics.soc-ph), Social Networking, law.invention, PageRank, law, Node (computer science), Humans, Multiplex, Layer (object-oriented design), lcsh:Science, Condensed Matter - Statistical Mechanics, Social and Information Networks (cs.SI), Multidisciplinary, Statistical Mechanics (cond-mat.stat-mech), lcsh:R, Brain, Social Support, Computer Science - Social and Information Networks, Weights and Measures, Complex network, Ranking, lcsh:Q, Centrality, Algorithms, Research Article
Abstract

Many complex systems can be described as multiplex networks in which the same nodes can interact with one another in different layers, thus forming a set of interacting and co-evolving networks. Examples of such multiplex systems are social networks where people are involved in different types of relationships and interact through various forms of communication media. The ranking of nodes in multiplex networks is one of the most pressing and challenging tasks that research on complex networks is currently facing. When pairs of nodes can be connected through multiple links and in multiple layers, the ranking of nodes should necessarily reflect the importance of nodes in one layer as well as their importance in other interdependent layers. In this paper, we draw on the idea of biased random walks to define the Multiplex PageRank centrality measure in which the effects of the interplay between networks on the centrality of nodes are directly taken into account. In particular, depending on the intensity of the interaction between layers, we define the Additive, Multiplicative, Combined, and Neutral versions of Multiplex PageRank, and show how each version reflects the extent to which the importance of a node in one layer affects the importance the node can gain in another layer. We discuss these measures and apply them to an online multiplex social network. Findings indicate that taking the multiplex nature of the network into account helps uncover the emergence of rankings of nodes that differ from the rankings obtained from one single layer. Results provide support in favor of the salience of multiplex centrality measures, like Multiplex PageRank, for assessing the prominence of nodes embedded in multiple interacting networks, and for shedding a new light on structural properties that would otherwise remain undetected if each of the interacting networks were analyzed in isolation., (16 pages, 6 figures)

Published
2013

Catalog

Books, media, physical & digital resources
See catalog results