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1. Multinational Study of the Efficacy and Safety of Humanized Anti-HER2 Monoclonal Antibody in Women Who Have HER2-Overexpressing Metastatic Breast Cancer That Has Progressed After Chemotherapy for Metastatic Disease

Author: Virginia Paton, Gracie Lieberman, Melody A. Cobleigh, Debasish Tripathy, Nicholas J. Robert, Charles L. Vogel, Louis Fehrenbacher, Janet M. Wolter, Steven Shak, Susy Scholl, and Dennis J. Slamon
Subjects: Adult, Oncology, medicine.medical_specialty, Pathology, Cancer Research, Time Factors, Heart Diseases, Receptor, ErbB-2, medicine.medical_treatment, Population, Breast Neoplasms, Humanized antibody, Loading dose, Disease-Free Survival, Trastuzumab, Internal medicine, Confidence Intervals, medicine, Humans, education, Aged, Aged, 80 and over, Chemotherapy, education.field_of_study, business.industry, Maintenance dose, Antibodies, Monoclonal, Middle Aged, medicine.disease, Metastatic breast cancer, Clinical trial, Multivariate Analysis, Disease Progression, Quality of Life, Female, business, medicine.drug
Abstract: PURPOSE Overexpression of the HER2 protein occurs in 25% to 30% of human breast cancers and leads to a particularly aggressive form of the disease. Efficacy and safety of recombinant humanized anti-HER2 monoclonal antibody as a single agent was evaluated in women with HER2-overexpressing metastatic breast cancer that had progressed after chemotherapy for metastatic disease. PATIENTS AND METHODS Two hundred twenty-two women, with HER2-overexpressing metastatic breast cancer that had progressed after one or two chemotherapy regimens, were enrolled. Patients received a loading dose of 4 mg/kg intravenously, followed by a 2-mg/kg maintenance dose at weekly intervals. RESULTS Study patients had advanced metastatic disease and had received extensive prior therapy. A blinded, independent response evaluation committee identified eight complete and 26 partial responses, for an objective response rate of 15% in the intent-to-treat population (95% confidence interval, 11% to 21%). The median duration of response was 9.1 months; the median duration of survival was 13 months. The most common adverse events, which occurred in approximately 40% of patients, were infusion-associated fever and/or chills that usually occurred only during the first infusion, and were of mild to moderate severity. These symptoms were treated successfully with acetaminophen and/or diphenhydramine. The most clinically significant adverse event was cardiac dysfunction, which occurred in 4.7% of patients. Only 1% of patients discontinued the study because of treatment-related adverse events. CONCLUSION Recombinant humanized anti-HER2 monoclonal antibody, administered as a single agent, produces durable objective responses and is well tolerated by women with HER2-overexpressing metastatic breast cancer that has progressed after chemotherapy for metastatic disease. Side effects that are commonly observed with chemotherapy, such as alopecia, mucositis, and neutropenia, are rarely seen.
Published: 2023
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2. WNT activity reveals context-specific genetic effects on gene regulation in neural progenitors

Author: Nana Matoba, Brandon D Le, Jordan M Valone, Justin M Wolter, Jessica Mory, Dan Liang, Nil Aygün, K Alaine Broadaway, Marielle L Bond, Karen L Mohlke, Mark J Zylka, Michael I Love, and Jason L Stein
Subjects: Article
Abstract: Gene regulatory effects in bulk-post mortem brain tissues are undetected at many non-coding brain trait-associated loci. We hypothesized that context-specific genetic variant function during stimulation of a developmental signaling pathway would explain additional regulatory mechanisms. We measured chromatin accessibility and gene expression following activation of the canonical Wnt pathway in primary human neural progenitors from 82 donors. TCF/LEF motifs, brain structure-, and neuropsychiatric disorder-associated variants were enriched within Wnt-responsive regulatory elements (REs). Genetically influenced REs were enriched in genomic regions under positive selection along the human lineage. Stimulation of the Wnt pathway increased the detection of genetically influenced REs/genes by 66.2%/52.7%, and led to the identification of 397 REs primed for effects on gene expression. Context-specific molecular quantitative trait loci increased brain-trait colocalizations by up to 70%, suggesting that genetic variant effects during early neurodevelopmental patterning lead to differences in adult brain and behavioral traits.
Published: 2023

3. MicroRNA-eQTLs in the developing human neocortex link miR-4707-3p expression to brain size

Author: Michael J. Lafferty, Nil Aygün, Niyanta K. Patel, Oleh Krupa, Dan Liang, Justin M. Wolter, Daniel H. Geschwind, Luis de la Torre-Ubieta, and Jason L. Stein
Subjects: General Immunology and Microbiology, General Neuroscience, General Medicine, General Biochemistry, Genetics and Molecular Biology
Abstract: Expression quantitative trait loci (eQTL) data have proven important for linking non-coding loci to protein-coding genes. But eQTL studies rarely measure microRNAs (miRNAs), small non-coding RNAs known to play a role in human brain development and neurogenesis. Here, we performed small-RNA sequencing across 212 mid-gestation human neocortical tissue samples, measured 907 expressed miRNAs, discovering 111 of which were novel, and identified 85 local-miRNA-eQTLs. Colocalization of miRNA-eQTLs with GWAS summary statistics yielded one robust colocalization of miR-4707-3p expression with educational attainment and brain size phenotypes, where the miRNA expression increasing allele was associated with decreased brain size. Exogenous expression of miR-4707-3p in primary human neural progenitor cells decreased expression of predicted targets and increased cell proliferation, indicating miR-4707-3p modulates progenitor gene regulation and cell fate decisions. Integrating miRNA-eQTLs with existing GWAS yielded evidence of a miRNA that may influence human brain size and function via modulation of neocortical brain development.
Published: 2023
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4. Author response: MicroRNA-eQTLs in the developing human neocortex link miR-4707-3p expression to brain size

Author: Michael J Lafferty, Nil Aygün, Niyanta K Patel, Oleh Krupa, Dan Liang, Justin M Wolter, Daniel H Geschwind, Luis de la Torre-Ubieta, and Jason L Stein
Published: 2022
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5. Cell-type-specific effects of genetic variation on chromatin accessibility during human neuronal differentiation

Author: Michael I. Love, Justin M. Wolter, Marianna Yusupova, Oleh Krupa, Michael J. Lafferty, Angela L. Elwell, Dan Liang, Kenan P. Courtney, Melanie E. Garrett, Felix A Kyere, Jason L. Stein, Nil Aygün, Daniel H. Geschwind, Luis de la Torre-Ubieta, Kerry E. Cheek, Gregory E. Crawford, and Allison E. Ashley-Koch
Subjects: 0301 basic medicine, Neurogenesis, Quantitative Trait Loci, Genome-wide association study, Quantitative trait locus, Biology, Genome, Article, 03 medical and health sciences, 0302 clinical medicine, Neural Stem Cells, Genetic variation, Humans, Genetic Predisposition to Disease, Regulatory Elements, Transcriptional, Allele, Neurons, Genetics, Regulation of gene expression, Mental Disorders, General Neuroscience, Gene Expression Regulation, Developmental, Genetic Variation, Cell Differentiation, Chromatin, 030104 developmental biology, Neuroscience, 030217 neurology & neurosurgery, Genome-Wide Association Study, Transcription Factors
Abstract: Common genetic risk for neuropsychiatric disorders is enriched in regulatory elements active during cortical neurogenesis. However, it remains poorly understood as to how these variants influence gene regulation. To model the functional impact of common genetic variation on the noncoding genome during human cortical development, we performed the assay for transposase accessible chromatin using sequencing (ATAC-seq) and analyzed chromatin accessibility quantitative trait loci (QTL) in cultured human neural progenitor cells and their differentiated neuronal progeny from 87 donors. We identified significant genetic effects on 988/1,839 neuron/progenitor regulatory elements, with highly cell-type and temporally specific effects. A subset (roughly 30%) of chromatin accessibility-QTL were also associated with changes in gene expression. Motif-disrupting alleles of transcriptional activators generally led to decreases in chromatin accessibility, whereas motif-disrupting alleles of repressors led to increases in chromatin accessibility. By integrating cell-type-specific chromatin accessibility-QTL and brain-relevant genome-wide association data, we were able to fine-map and identify regulatory mechanisms underlying noncoding neuropsychiatric disorder risk loci.
Published: 2021
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6. Cellular Genome-wide Association Study Identifies Common Genetic Variation Influencing Lithium-Induced Neural Progenitor Proliferation

Author: Justin M. Wolter, Brandon D. Le, Nana Matoba, Michael J. Lafferty, Nil Aygün, Dan Liang, Kenan Courtney, Juan Song, Joseph Piven, Mark J. Zylka, and Jason L. Stein
Subjects: Adult, Bipolar Disorder, GTP-Binding Proteins, Humans, Genetic Variation, Nuclear Proteins, Lithium, Biological Psychiatry, Article, Genome-Wide Association Study, Cell Proliferation
Abstract: BACKGROUND: Bipolar disorder is a highly heritable neuropsychiatric condition affecting more than 1% of the human population. Lithium salts are commonly prescribed as a mood stabilizer for individuals with bipolar disorder. Lithium is clinically effective in approximately half of treated individuals, and their genetic backgrounds are known to influence treatment outcomes. While the mechanism of lithium’s therapeutic action is unclear, it stimulates adult neural progenitor cell proliferation, similar to some antidepressant drugs. METHODS: To identify common genetic variants that modulate lithium-induced proliferation, we conducted an EdU incorporation assay in a library of 80 genotyped human neural progenitor cells treated with lithium. These data were used to perform a genome-wide association study to identify common genetic variants that influence lithium-induced neural progenitor cell proliferation. We manipulated the expression of a putatively causal gene using CRISPRi/a (clustered regularly interspaced short palindromic repeats interference/activation) constructs to experimentally verify lithium-induced proliferation effects. RESULTS: We identified a locus on chr3p21.1 associated with lithium-induced proliferation. This locus is also associated with bipolar disorder risk, schizophrenia risk, and interindividual differences in intelligence. We identified a single gene, GNL3, whose expression temporally increased in an allele-specific fashion following lithium treatment. Experimentally increasing the expression of GNL3 led to increased proliferation under baseline conditions, while experimentally decreasing GNL3 expression suppressed lithium-induced proliferation. CONCLUSIONS: Our experiments reveal that common genetic variation modulates lithium-induced neural progenitor proliferation and that GNL3 expression is necessary for the full proliferation-stimulating effects of lithium. These results suggest that performing genome-wide associations in genetically diverse human cell lines is a useful approach to discover context-specific pharmacogenomic effects.
Published: 2022

7. Fragment-Based Stabilizers of Protein-Protein Interactions through Imine-Based Tethering

Author: Laura Levy, M. Wolter, Torsten Hoffmann, Dario Valenti, Dimitrios Tzalis, Thorsten Genski, P.J. Cossar, Luc Brunsveld, Stanimira Hristeva, Christian Ottmann, Macro-Organic Chemistry, Chemical Biology, and ICMS Core
Subjects: Small Molecule Libraries/chemistry, Imines/chemistry, Imine, Fragment-based lead discovery, Chemie, Transcription Factor RelA/chemistry, Peptide, Plasma protein binding, imine chemistry, protein–protein interactions, 010402 general chemistry, 01 natural sciences, Catalysis, Protein–protein interaction, Small Molecule Libraries, chemistry.chemical_compound, Structure-Activity Relationship, Structure–activity relationship, chemistry.chemical_classification, Molecular Structure, 010405 organic chemistry, Chemistry, Drug discovery, Protein Stability, Communication, Transcription Factor RelA, 14-3-3 proteins, General Chemistry, Combinatorial chemistry, Communications, 0104 chemical sciences, Covalent bond, cooperative effects, Imines, fragment-based drug discovery, 14-3-3 Proteins/chemistry, Protein Binding
Abstract: Small‐molecule stabilization of protein–protein interactions (PPIs) is a promising concept in drug discovery, however the question how to identify or design chemical starting points in a “bottom‐up” approach is largely unanswered. We report a novel concept for identifying initial chemical matter for PPI stabilization based on imine‐forming fragments. The imine bond offers a covalent anchor for site‐directed fragment targeting, whereas its transient nature enables efficient analysis of structure–activity relationships. This bond enables fragment identification and optimisation using protein crystallography. We report novel fragments that bind specifically to a lysine at the PPI interface of the p65‐subunit‐derived peptide of NF‐κB with the adapter protein 14‐3‐3. Those fragments that subsequently establish contacts with the p65‐derived peptide, rather than with 14‐3‐3, efficiently stabilize the 14‐3‐3/p65 complex and offer novel starting points for molecular glues., A novel concept for optimizing orthosteric protein–protein interaction (PPI) stabilization is reported. Increasing interactions with the protein partner that contributes less to the composite binding pocket of the stabilizer (NF‐κB, red surface) results in increased stabilization, whereas further enhancing the interaction with the dominant partner protein (14‐3‐3, white surface) does not contribute to the stabilizing effect.
Published: 2020
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8. Interaction of an IκBα Peptide with 14-3-3

Author: M. Wolter, Tomas Obsil, Petr Herman, Federica Centorrino, Domenico Lentini Santo, Alice Ballone, Christian Ottmann, Chemical Biology, and ICMS Core
Subjects: chemistry.chemical_classification, Chemistry, General Chemical Engineering, Chemie, Tryptophan, Peptide, NF-κB, General Chemistry, Crystal structure, SDG 3 – Goede gezondheid en welzijn, Article, 3. Good health, IκBα, chemistry.chemical_compound, SDG 3 - Good Health and Well-being, Biochemistry, ddc:660, Enhancer, Transcription factor, QD1-999, Fluorescence anisotropy
Abstract: Inflammatory responses mediated by the transcription factor nuclear factor kappa-light-chain enhancer of activated B cells (NF-κB) play key roles in immunity, autoimmune diseases, and cancer. NF-κB is directly regulated through protein-protein interactions, including those with IκB and 14-3-3 proteins. These two important regulatory proteins have been reported to interact with each other, although little is known about this interaction. We analyzed the inhibitor of nuclear factor kappa B α (IκBα)/14-3-3σ interaction via a peptide/protein-based approach. Structural data were acquired via X-ray crystallography, while binding affinities were measured with fluorescence polarization assays and time-resolved tryptophan fluorescence. A high-resolution crystal structure (1.13 Å) of the uncommon 14-3-3 interaction motif of IκBα (IκBαpS63) in a complex with 14-3-3σ was evaluated. This motif harbors a tryptophan that makes this crystal structure the first one with such a residue visible in the electron density at that position. We used this tryptophan to determine the binding affinity of the unlabeled IκBα peptide to 14-3-3 via tryptophan fluorescence decay measurements. © CA extern
Published: 2020
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9. Development of the radiation and magnetic field tolerant DC/DC converter system for the ATLAS ITk Strip Detector

Author: M. Dyndał, K. Cieśla, W. Dąbrowski, E. Górnicki, K. Guguła, R. Kopeć, S. Koperny, A. Korba, D. Krzempek, E. Stanecka, P. Wiącek, and M. Wolter
Subjects: Instrumentation, Mathematical Physics
Abstract: The radiation and magnetic field tolerant step-down DC/DC converter system is developed to supply low-voltage power for the ATLAS ITk Strip Detector. The system is modular and consists of custom designed crates with embedded cooling plates, backplane, and DC/DC converter modules. Each converter module comprises two or four power channels. Each channel comprises a 48-to-11 V DC/DC converter, hardware overcurrent and overvoltage protection circuits, correction circuitry to compensate for voltage drops along the cables, and control and monitoring functionality based on the AMACStar chip. We present the design and performance of such a DC/DC converter system, including evaluation of its radiation tolerance.
Published: 2023
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10. Multi-omic profiling reveals the ataxia protein sacsin is required for integrin trafficking and synaptic organization

Author: Lisa E.L. Romano, Wen Yih Aw, Kathryn M. Hixson, Tatiana V. Novoselova, Tammy M. Havener, Stefanie Howell, Bonnie Taylor-Blake, Charlotte L. Hall, Lei Xing, Josh Beri, Suran Nethisinghe, Laura Perna, Abubakar Hatimy, Ginevra Chioccioli Altadonna, Lee M. Graves, Laura E. Herring, Anthony J. Hickey, Konstantinos Thalassinos, J. Paul Chapple, and Justin M. Wolter
Subjects: Mice, Integrins, Cerebellar Ataxia, Mutation, Animals, Ataxia, Heat-Shock Proteins, General Biochemistry, Genetics and Molecular Biology
Abstract: Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is a childhood-onset cerebellar ataxia caused by mutations in SACS, which encodes the protein sacsin. Cellular ARSACS phenotypes include mitochondrial dysfunction, intermediate filament disorganization, and progressive death of cerebellar Purkinje neurons. It is unclear why the loss of sacsin causes these deficits or why they manifest as cerebellar ataxia. Here, we perform multi-omic profiling in sacsin knockout (KO) cells and identify alterations in microtubule dynamics and mislocalization of focal adhesion (FA) proteins, including multiple integrins. Deficits in FA structure, signaling, and function can be rescued by targeting PTEN, a negative regulator of FA signaling. ARSACS mice possess mislocalization of ITGA1 in Purkinje neurons and synaptic disorganization in the deep cerebellar nucleus (DCN). The sacsin interactome reveals that sacsin regulates interactions between cytoskeletal and synaptic adhesion proteins. Our findings suggest that disrupted trafficking of synaptic adhesion proteins is a causal molecular deficit in ARSACS.
Published: 2022
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11. The ataxia protein sacsin is required for integrin trafficking and synaptic organization

Author: Anthony J. Hickey, Suran Nethisinghe, Abubakar Hatimy, Lei Xing, Charlotte L. Hall, Laura Perna, Wen Yih Aw, Stefanie D. Howell, Laura E. Herring, Tammy M. Havener, Josh Beri, Lee M. Graves, Ginevra Chioccioli Altadonna, Konstantinos Thalassinos, Justin M. Wolter, Kathryn M. Hixson, J. Paul Chapple, Lisa E.L. Romano, and Tatiana V. Novoselova
Subjects: Vesicular transport protein, Focal adhesion, Ataxia, biology, Cerebellar ataxia, Microtubule, Integrin, medicine, biology.protein, medicine.symptom, Cell adhesion, Intermediate filament, Cell biology
Abstract: Autosomal recessive spastic ataxia of Charlevoix-Saguenay (ARSACS) is caused by mutations in SACS, which manifest as a childhood-onset cerebellar ataxia. Cellular ARSACS phenotypes include mitochondrial dysfunction, intermediate filament (IF) disorganization, and loss of Purkinje neurons. It is unclear how the loss of SACS causes these deficits, or why they manifest as cerebellar ataxia. We employed a multi-omics approach to characterize molecular and cellular deficiencies in SACS knockout (KO) cells. We identified alterations in microtubule structure and dynamics, protein trafficking, and mislocalization of synaptic and focal adhesion proteins. Targeting PTEN, a negative regulator of focal adhesions, rescued several cellular phenotypes in SACS KO cells. We found sacsin interacts with proteins implicated in vesicle transport, including HSP proteins, and interactions between structural and cell adhesion proteins were diminished in SACS KO cells. In all, this study suggests that trafficking and localization of synaptic adhesion proteins is a causal molecular deficiency in ARSACS.
Published: 2021
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12. Estimation tools for reducing the impact of sampling and nonresponse errors in dual‐frame RDD telephone surveys

Author: Kirk M. Wolter, James A. Singleton, Meena Khare, Nadarajasundaram Ganesh, and Kennon R. Copeland
Subjects: Male, Statistics and Probability, Epidemiology, Computer science, Population, 01 natural sciences, Sampling Studies, 010104 statistics & probability, 03 medical and health sciences, 0302 clinical medicine, Phone, Statistics, Humans, 030212 general & internal medicine, Landline, 0101 mathematics, education, Sampling frame, education.field_of_study, Vaccination, Frame (networking), Infant, Sampling (statistics), Estimator, Health Surveys, United States, Telephone, Weighting, Research Design, Child, Preschool, Female, Centers for Disease Control and Prevention, U.S
Abstract: We discuss alternative estimators of the population total given a dual-frame random-digit-dial (RDD) telephone survey in which samples are selected from landline and cell phone sampling frames. The estimators are subject to sampling and nonsampling errors. To reduce sampling variability when an optimum balance of landline and cell phone samples is not feasible, we develop an application of shrinkage estimation. We demonstrate the implications for survey weighting of a differential nonresponse mechanism by telephone status. We illustrate these ideas using data from the National Immunization Survey-Child, a large dual-frame RDD telephone survey sponsored by the Centers for Disease Control and Prevention and conducted to measure the vaccination status of American children aged 19 to 35 months.
Published: 2019
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13. An Exploration of Chemical Properties Required for Cooperative Stabilization of the 14-3-3 Interaction with NF-κB-Utilizing a Reversible Covalent Tethering Approach

Author: Thorsten Genski, Dimitrios Tzalis, Torsten Hoffmann, P.J. Cossar, Stanimira Hristeva, Christian Ottmann, M. Wolter, Laura Levy, Dario Valenti, Luc Brunsveld, Chemical Biology, and ICMS Core
Subjects: Imine, Cooperativity, 01 natural sciences, Article, Small Molecule Libraries, 03 medical and health sciences, chemistry.chemical_compound, Structure-Activity Relationship, Drug Discovery, Escherichia coli, Structure–activity relationship, Molecule, 030304 developmental biology, 0303 health sciences, Molecular Structure, Tethering, Drug discovery, Chemistry, Escherichia coli Proteins, Transcription Factor RelA, Combinatorial chemistry, 0104 chemical sciences, 3. Good health, 010404 medicinal & biomolecular chemistry, 14-3-3 Proteins, Covalent bond, Benzaldehydes, Drug Design, Molecular Medicine, Stabilizer (chemistry), Protein Binding
Abstract: Protein-protein modulation has emerged as a proven approach to drug discovery. While significant progress has been gained in developing protein-protein interaction (PPI) inhibitors, the orthogonal approach of PPI stabilization lacks established methodologies for drug design. Here, we report the systematic ″bottom-up″ development of a reversible covalent PPI stabilizer. An imine bond was employed to anchor the stabilizer at the interface of the 14-3-3/p65 complex, leading to a molecular glue that elicited an 81-fold increase in complex stabilization. Utilizing protein crystallography and biophysical assays, we deconvoluted how chemical properties of a stabilizer translate to structural changes in the ternary 14-3-3/p65/molecular glue complex. Furthermore, we explore how this leads to high cooperativity and increased stability of the complex.
Published: 2021

14. Reversible Covalent Imine-Tethering for Selective Stabilization of 14-3-3 Hub Protein Interactions

Author: Christian Ottmann, Luc Brunsveld, Lars van Dijck, P.J. Cossar, Dario Valenti, M. Wolter, Laura M. Levy, Chemical Biology, Biomedical Engineering, and ICMS Core
Subjects: Models, Molecular, Imine, Cooperativity, 010402 general chemistry, 01 natural sciences, Biochemistry, Interactome, Catalysis, Article, chemistry.chemical_compound, Colloid and Surface Chemistry, Molecule, Humans, Ternary complex, Molecular Structure, Chemistry, Protein Stability, General Chemistry, 0104 chemical sciences, NIMA-Interacting Peptidylprolyl Isomerase, 14-3-3 Proteins, Covalent bond, PIN1, Biophysics, Phosphorylation, Imines
Abstract: The stabilization of protein complexes has emerged as a promising modality, expanding the number of entry points for novel therapeutic intervention. Targeting proteins that mediate protein-protein interactions (PPIs), such as hub proteins, is equally challenging and rewarding as they offer an intervention platform for a variety of diseases, due to their large interactome. 14-3-3 hub proteins bind phosphorylated motifs of their interaction partners in a conserved binding channel. The 14-3-3 PPI interface is consequently only diversified by its different interaction partners. Therefore, it is essential to consider, additionally to the potency, also the selectivity of stabilizer molecules. Targeting a lysine residue at the interface of the composite 14-3-3 complex, which can be targeted explicitly via aldimine-forming fragments, we studied the de novo design of PPI stabilizers under consideration of potential selectivity. By applying cooperativity analysis of ternary complex formation, we developed a reversible covalent molecular glue for the 14-3-3/Pin1 interaction. This small fragment led to a more than 250-fold stabilization of the 14-3-3/Pin1 interaction by selective interfacing with a unique tryptophan in Pin1. This study illustrates how cooperative complex formation drives selective PPI stabilization. Further, it highlights how specific interactions within a hub proteins interactome can be stabilized over other interactions with a common binding motif.
Published: 2021

15. ToxCast chemical library screen identifies diethanolamine as an activator of Wnt signaling

Author: Jason L. Stein, Mark J. Zylka, Jessica A. Jiménez, and Justin M. Wolter
Subjects: Valproic Acid, Brain development, Activator (genetics), Mutant, Wnt signaling pathway, Biology, Cell biology, Chemical library, chemistry.chemical_compound, chemistry, medicine, Progenitor cell, Gene, medicine.drug
Abstract: Numerous autism spectrum disorder (ASD) risk genes are associated with Wnt signaling, suggesting that brain development may be especially sensitive to genetic perturbation of this pathway. Additionally, valproic acid, which modulates Wnt signaling, increases risk for ASD when taken during pregnancy. We previously found that an autism-linked gain-of-function UBE3AT485A mutant construct hyperactivated canonical Wnt signaling, providing a genetic means to elevate Wnt signaling above baseline levels. To identify environmental use chemicals that enhance or suppress Wnt signaling, we screened the ToxCast Phase I and II libraries in cells expressing this autism linked UBE3AT485 gain-of-function mutant construct. Using structural comparisons, we identify classes of chemicals that stimulated Wnt signaling, including ethanolamines, as well as chemicals that inhibited Wnt signaling, such as agricultural pesticides, and synthetic hormone analogs. To prioritize chemicals for follow-up, we leveraged predicted human exposure data, and identified diethanolamine (DEA) as a chemical that both stimulates Wnt signaling in UBE3AT485A–transfected cells and has a high potential for prenatal exposure in humans. DEA also enhanced proliferation in two primary human neural progenitor cell lines. Overall, this study identifies chemicals with the potential for human exposure that influence Wnt signaling in human cells.
Published: 2021
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16. Selectivity via Cooperativity : Preferential Stabilization of the p65/14-3-3 Interaction with Semisynthetic Natural Products

Author: João Neves, Christian Ottmann, Sonja Srdanovic, M. Wolter, Nobuo Kato, Luc Brunsveld, Pim J. de Vink, Isabelle Landrieu, Yusuke Higuchi, Andrew J. Wilson, Eindhoven University of Technology [Eindhoven] (TU/e), Facteurs de Risque et Déterminants Moléculaires des Maladies liées au Vieillissement - U 1167 (RID-AGE), Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Université de Lille-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP), Biologie Structurale Intégrative (ERL 9002 - BSI ), Institut Pasteur de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre National de la Recherche Scientifique (CNRS), University of Leeds, Osaka University [Osaka], University of Duisburg-Essen, This research is supported by funding from the European Union through the TASPPI project (H2020-MSCA-ITN-2015, grant number 675179) and by the LabEx (Laboratory of Excellence) DISTALZ (ANR, ANR-11-LABX-009) and through The Netherlands Organization for Scientific Research (NWO) via VICI grant 016.150.366 and via Gravity Program 024.001.035. The NMR facilities were funded by the Nord Region Council, CNRS, Institut Pasteur de Lille, the European Community (ERDF), the French Ministry of Research, and the University of Lille. We acknowledge support for the NMR facilities from TGE RMN THC (CNRS, FR-3050) and FRABio (Univ. Lille, CNRS, FR-3688). This work was supported by the EPSRC (EP/N013573/1) and The Wellcome Trust (097827/Z/11/A)., ANR-11-LABX-0009,DISTALZ,Développement de stratégies innovantes pour une approche transdisciplinaire de la maladie d'Alzheime(2011), European Project: 675179,H2020,H2020-MSCA-ITN-2015,TASPPI(2016), Université de Lille, Réseau International des Instituts Pasteur (RIIP)-Réseau International des Instituts Pasteur (RIIP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Lille-Centre Hospitalier Régional Universitaire [Lille] (CHRU Lille), Chemical Biology, ICMS Core, and Universität Duisburg-Essen = University of Duisburg-Essen [Essen]
Subjects: Scaffold protein, Models, Molecular, Protein subunit, Chemie, Cooperativity, [CHIM.THER]Chemical Sciences/Medicinal Chemistry, 010402 general chemistry, 01 natural sciences, Biochemistry, Catalysis, Article, Protein–protein interaction, chemistry.chemical_compound, Colloid and Surface Chemistry, Humans, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biochemistry [q-bio.BM], ComputingMilieux_MISCELLANEOUS, Biological Products, Natural product, [SDV.BBM.BS]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Structural Biology [q-bio.BM], Drug discovery, NF-kappa B, Cooperative binding, General Chemistry, 0104 chemical sciences, [SDV.BBM.BC]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biomolecules [q-bio.BM], [SDV.BBM.BS]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Biomolecules [q-bio.BM], chemistry, 14-3-3 Proteins, Biophysics, Stabilizer (chemistry), Protein Binding
Abstract: International audience; Natural compounds are an important class of potent drug molecules including some retrospectively found to act as stabilizers of protein–protein interactions (PPIs). However, the design of synthetic PPI stabilizers remains an understudied approach. To date, there are limited examples where cooperativity has been utilized to guide the optimization of a PPI stabilizer. The 14-3-3 scaffold proteins provide an excellent platform to explore PPI stabilization because these proteins mediate several hundred PPIs, and a class of natural compounds, the fusicoccanes, are known to stabilize a subset of 14-3-3 protein interactions. 14-3-3 has been reported to negatively regulate the p65 subunit of the NF-κB transcription factor, which qualifies this protein complex as a potential target for drug discovery to control cell proliferation. Here, we report the high-resolution crystal structures of two 14-3-3 binding motifs of p65 in complex with 14-3-3. A semisynthetic natural product derivative, DP-005, binds to an interface pocket of the p65/14-3-3 complex and concomitantly stabilizes it. Cooperativity analyses of this interaction, and other disease relevant 14-3-3-PPIs, demonstrated selectivity of DP-005 for the p65/14-3-3 complex. The adaptation of a cooperative binding model provided a general approach to characterize stabilization and to assay for selectivity of PPI stabilizers.
Published: 2020
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17. Financial education of founders, is it important A case study of Jacobs Startup Competition

Author: Andreas Seebeck and Robin M. Wolter
Subjects: Management of Technology and Innovation, Strategy and Management, Business and International Management
Published: 2022
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18. 70.46 Tb/s Over 7,600 km and 71.65 Tb/s Over 6,970 km Transmission in C+L Band Using Coded Modulation With Hybrid Constellation Shaping and Nonlinearity Compensation

Author: Timothy E. Hammon, Gregory M. Wolter, Maxim Bolshtyansky, P.C. Corbett, Carl R. Davidson, Alexei N. Pilipetskii, Dmitri Foursa, W.W. Patterson, Hussam G. Batshon, Oleg V. Sinkin, M. Mazurczyk, Ding Wang, Jin-Xing Cai, and Milen Paskov
Subjects: Engineering, L band, business.industry, Amplifier, 02 engineering and technology, Polarization-division multiplexing, Filter (signal processing), Atomic and Molecular Physics, and Optics, 020210 optoelectronics & photonics, Signal-to-noise ratio, Transmission (telecommunications), Modulation, 0202 electrical engineering, electronic engineering, information engineering, Electronic engineering, Forward error correction, business
Abstract: We demonstrate 70.46 Tb/s transmission over 7,600 km and 71.65 Tb/s transmission over 6,970 km with C+L band EDFAs using a multidimensional coded modulation format with hybrid probabilistic and geometric constellation shaping. The proposed format (4D-PS-9/12-56APSK) is designed to approach Shannon limit and to improve the performance of nonlinearity compensation over conventional and probabilistically shaped 2-D formats. The receiver DSP uses multistage nonlinearity compensation that includes fast least-mean-square equalizer and generalized filter in addition to digital back propagation. The adaptive linear filters are aided by coded modulation decisions. We study the contribution of each algorithm and show an average total nonlinearity compensation benefit of 1.4 dBQ at the designed amplifier power.
Published: 2018
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19. The autism-linked UBE3A T485A mutant E3 ubiquitin ligase activates the Wnt/β-catenin pathway by inhibiting the proteasome

Author: Matthew P. Walker, Justin M. Wolter, Michael B. Major, Michael J. Emanuele, Mark J. Zylka, Jason J. Yi, Smita R. Paranjape, Rajarshi Choudhury, and Giulia Fragola
Subjects: 0301 basic medicine, HECT domain, Proteasome Endopeptidase Complex, congenital, hereditary, and neonatal diseases and abnormalities, Ubiquitin-Protein Ligases, Biology, Biochemistry, 03 medical and health sciences, Neurobiology, Humans, Autistic Disorder, Wnt Signaling Pathway, Molecular Biology, beta Catenin, Wnt signaling pathway, LRP6, LRP5, Cell Biology, Ubiquitin ligase, HEK293 Cells, 030104 developmental biology, Proteasome, Catenin, Mutation, biology.protein, Cancer research, Phosphorylation, Proteasome Inhibitors
Abstract: UBE3A is a HECT domain E3 ubiquitin ligase whose dysfunction is linked to autism, Angelman syndrome, and cancer. Recently, we characterized a de novo autism-linked UBE3A mutant (UBE3AT485A) that disrupts phosphorylation control of UBE3A activity. Through quantitative proteomics and reporter assays, we found that the UBE3AT485A protein ubiquitinates multiple proteasome subunits, reduces proteasome subunit abundance and activity, stabilizes nuclear β-catenin, and stimulates canonical Wnt signaling more effectively than wild-type UBE3A. We also found that UBE3AT485A activates Wnt signaling to a greater extent in cells with low levels of ongoing Wnt signaling, suggesting that cells with low basal Wnt activity are particularly vulnerable to UBE3AT485A mutation. Ligase-dead UBE3A did not stimulate Wnt pathway activation. Overexpression of several proteasome subunits reversed the effect of UBE3AT485A on Wnt signaling. We also observed that subunits that interact with UBE3A and affect Wnt signaling are located along one side of the 19S regulatory particle, indicating a previously unrecognized spatial organization to the proteasome. Altogether, our findings indicate that UBE3A regulates Wnt signaling in a cell context-dependent manner and that an autism-linked mutation exacerbates these signaling effects. Our study has broad implications for human disorders associated with UBE3A gain or loss of function and suggests that dysfunctional UBE3A might affect additional proteins and pathways that are sensitive to proteasome activity.
Published: 2017
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20. Testen Sie Ihr Fachwissen

Author: H. Juratli, M. Wolter, and W. Pfützner
Subjects: Dermatology
Published: 2017
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21. Cas9 gene therapy for Angelman syndrome traps Ube3a-ATS long non-coding RNA

Author: Justin M. Wolter, Baris Oztemiz, Hannah O. Bazick, James L. Krantz, Hanqian Mao, Giulia Fragola, Jeremy M. Simon, Jason L. Stein, and Mark J. Zylka
Subjects: 0301 basic medicine, Male, congenital, hereditary, and neonatal diseases and abnormalities, Ubiquitin-Protein Ligases, Genetic Vectors, Biology, Nervous System, Article, 03 medical and health sciences, Mice, 0302 clinical medicine, Neurodevelopmental disorder, Angelman syndrome, Ube3a-ATS, CRISPR-Associated Protein 9, medicine, UBE3A, Animals, Humans, Gene Silencing, Allele, Gene, Genetics, Gene Editing, Multidisciplinary, RNA, Genetic Therapy, Dependovirus, medicine.disease, Long non-coding RNA, Mice, Inbred C57BL, Disease Models, Animal, 030104 developmental biology, Phenotype, Paternal Inheritance, Female, RNA, Long Noncoding, Angelman Syndrome, CRISPR-Cas Systems, 030217 neurology & neurosurgery, RNA, Guide, Kinetoplastida
Abstract: Angelman syndrome (AS) is a severe neurodevelopmental disorder caused by a mutation or deletion of the maternally inherited UBE3A allele. In neurons, the paternally inherited UBE3A allele is silenced in cis by a long non-coding RNA called UBE3A-ATS. Here, as part of a systematic screen, we found that Cas9 can be used to activate ('unsilence') paternal Ube3a in cultured mouse and human neurons when targeted to Snord115 genes, which are small nucleolar RNAs that are clustered in the 3′ region of Ube3a-ATS. A short Cas9 variant and guide RNA that target about 75 Snord115 genes were packaged into an adeno-associated virus and administered to a mouse model of AS during the embryonic and early postnatal stages, when the therapeutic benefit of restoring Ube3a is predicted to be greatest1,2. This early treatment unsilenced paternal Ube3a throughout the brain for at least 17 months and rescued anatomical and behavioural phenotypes in AS mice. Genomic integration of the adeno-associated virus vector into Cas9 target sites caused premature termination of Ube3a-ATS at the vector-derived polyA cassette, or when integrated in the reverse orientation, by transcriptional collision with the vector-derived Cas9 transcript. Our study shows that targeted genomic integration of a gene therapy vector can restore the function of paternally inherited UBE3A throughout life, providing a path towards a disease-modifying treatment for a syndromic neurodevelopmental disorder. Genomic integration of an adeno-associated virus vector in a mouse model of Angelman syndrome unsilences paternal Ube3a and rescues anatomical and behavioural phenotypes, suggesting a pathway towards the treatment of this neurodevelopmental disorder.
Published: 2019

22. The effects of hypothetical behavioral interventions on the 13-year incidence of overweight/obesity in children and adolescents

Author: C. Börnhorst, I. Pigeot, S. De Henauw, A. Formisano, L. Lissner, D. Molnár, L. A. Moreno, M. Tornaritis, T. Veidebaum, T. Vrijkotte, V. Didelez, M. Wolters, and on behalf of the GrowH! consortium
Subjects: Causal inference, Childhood obesity, IDEFICS/I.Family cohort, Modifiable risk factor, Observational data, Parametric g-formula, Nutritional diseases. Deficiency diseases, RC620-627, Public aspects of medicine, RA1-1270
Abstract: Abstract Background In view of the high burden of childhood overweight/obesity (OW/OB), it is important to identify targets for interventions that may have the greatest effects on preventing OW/OB in early life. Using methods of causal inference, we studied the effects of sustained behavioral interventions on the long-term risk of developing OW/OB based on a large European cohort. Methods Our sample comprised 10 877 children aged 2 to
Published: 2023
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23. Evolutionary patterns of metazoan microRNAs reveal targeting principles in the let-7 and miR-10 families

Author: Victoria A. Godlove, Thuy-Duyen Nguyen, Alan Rawls, Alexander Linse, Marco Mangone, Kasuen Kotagama, Hoai Huang Thi Le, Alissa Lynch, and Justin M. Wolter
Subjects: 0301 basic medicine, Nematoda, Computational biology, Biology, Genome, Evolution, Molecular, Mice, 03 medical and health sciences, microRNA, Genetics, Animals, Humans, Degree of similarity, RNA, Messenger, Gene, Conserved Sequence, Phylogeny, Genetics (clinical), Sequence (medicine), Research, MicroRNAs, 030104 developmental biology, Gene Expression Regulation, Multigene Family, Nucleic Acid Conformation, Drosophila, Function (biology)
Abstract: MicroRNAs (miRNAs) regulate gene output by targeting degenerate elements in mRNAs and have undergone drastic expansions in higher metazoan genomes. The evolutionary advantage of maintaining copies of highly similar miRNAs is not well understood, nor is it clear what unique functions, if any, miRNA family members possess. Here, we study evolutionary patterns of metazoan miRNAs, focusing on the targeting preferences of the let-7 and miR-10 families. These studies reveal hotspots for sequence evolution with implications for targeting and secondary structure. High-throughput screening for functional targets reveals that each miRNA represses sites with distinct features and regulates a large number of genes with cooperative function in regulatory networks. Unexpectedly, given the high degree of similarity, single-nucleotide changes grant miRNA family members with distinct targeting preferences. Together, our data suggest complex functional relationships among miRNA duplications, novel expression patterns, sequence change, and the acquisition of new targets.
Published: 2016
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24. High-throughput screening and classification of chemicals and their effects on neuronal gene expression using RASL-seq

Author: Gabriela Salazar, Mark J. Zylka, Smita R. Paranjape, Justin M. Wolter, and Jeremy M. Simon
Subjects: 0301 basic medicine, Male, Topoisomerase Inhibitors, High-throughput screening, lcsh:Medicine, Computational biology, Biology, Article, Transcriptome, 03 medical and health sciences, Mice, 0302 clinical medicine, Chemical mixtures, Gene expression, medicine, Animals, Cluster Analysis, lcsh:Science, Gene, Cells, Cultured, Neurons, Chemical concentration, Multidisciplinary, Sequence Analysis, RNA, Neurodegeneration, lcsh:R, High-Throughput Nucleotide Sequencing, medicine.disease, Embryo, Mammalian, Mice, Inbred C57BL, 030104 developmental biology, Autism, lcsh:Q, Female, 030217 neurology & neurosurgery
Abstract: We previously used RNA-seq to identify chemicals whose effects on neuronal gene expression mimicked transcriptional signatures of autism, aging, and neurodegeneration. However, this approach was costly and time consuming, which limited our study to testing a single chemical concentration on mixed sex cortical neuron cultures. Here, we adapted a targeted transcriptomic method (RASL-seq, similar to TempO-seq) to interrogate changes in expression of a set of 56 signature genes in response to a library of 350 chemicals and chemical mixtures at four concentrations in male and female mouse neuronal cultures. This enabled us to replicate and expand our previous classifications, and show that transcriptional responses were largely equivalent between sexes. Overall, we found that RASL-seq can be used to accelerate the pace at which chemicals and mixtures that transcriptionally mimic autism and other neuropsychiatric diseases can be identified, and provides a cost-effective way to quantify gene expression with a panel of marker genes.
Published: 2018

25. Biophysical and structural insight into the USP8/14-3-3 interaction

Author: Federica Centorrino, M. Wolter, Alice Ballone, Christian Ottmann, and Chemical Biology
Subjects: 0301 basic medicine, Endopeptidases/chemistry, medicine.medical_treatment, ErbB Receptors/genetics, fluorescence polarization, Ubiquitin Thiolesterase/chemistry, Crystallography, X-Ray, 01 natural sciences, Biochemistry, Deubiquitinating enzyme, Pathogenesis, Structural Biology, Epidermal growth factor receptor, ubiquitin-specific protease 8, Crystallography, biology, medicine.diagnostic_test, Chemistry, 3. Good health, Cell biology, isothermal titration calorimetry, ErbB Receptors, Pituitary ACTH Hypersecretion/genetics, Ubiquitin Thiolesterase, Biologie, Deubiquitination, Protein Structure, Proteolysis, Biophysics, Quaternary, 03 medical and health sciences, Endopeptidases, Genetics, medicine, Humans, Pituitary ACTH Hypersecretion, Protein Structure, Quaternary, Molecular Biology, X-ray crystallography, Protease, Endosomal Sorting Complexes Required for Transport, 010405 organic chemistry, Isothermal titration calorimetry, Cell Biology, 0104 chemical sciences, 030104 developmental biology, 14-3-3 Proteins, biology.protein, X-Ray, 14-3-3 Proteins/chemistry, Endosomal Sorting Complexes Required for Transport/chemistry, Fluorescence anisotropy
Abstract: The ubiquitin-specific protease 8 (USP8)/14-3-3 protein-protein interaction has recently been shown to exert a significant role in the pathogenesis of Cushing's disease (CD). USP8 is a deubiquitinase that prevents epidermal growth factor receptor (EGFR) degradation. Impairment of 14-3-3 binding leads to a higher deubiquitination of EGFR and results in a higher EGFR signaling and an increased production of adrenocorticotropic hormone. Here we report the high-resolution crystal structure of the 14-3-3 binding motif of USP8 surrounding Ser718 in complex with 14-3-3ζ and characterize the interaction with fluorescence polarization and isothermal titration calorimetry. Furthermore, we analyze the effect of USP8 mutations identified in CD on binding to 14-3-3.
Published: 2018

26. Testing IEC 60870-5-104 and C37.118 Based Control Center Applications Using a Real Time Simulation Platform

Author: M. Wolter, Davood Babazadeh, Shoaib Ansari, E. Glende, and Sebastian Lehnhoff
Subjects: Computer science, Real-time simulation, Control (management), Center (algebra and category theory), IEC 60870-5, Simulation
Published: 2018
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27. Supervision Today!

Author: Stephen P. Robbins, David A. DeCenzo, Robert M. Wolter, Stephen P. Robbins, David A. DeCenzo, and Robert M. Wolter
Subjects: Supervision of employees
Abstract: This is the eBook of the printed book and may not include any media, website access codes, or print supplements that may come packaged with the bound book. This print textbook is available for students to rent for their classes. The Pearson print rental program provides students with affordable access to learning materials, so they come to class ready to succeed. For supervision, supervision management, and intro to management courses. Supervisory management skills for the contemporary workplace Known as one of the most effective books on supervising, Supervision Today! helps readers build their supervisory skills through real-life concepts, examples, and practice. It's lively, conversational tone and full-color design engages individuals and helps capture the responsibilities and challenges of a real supervisor's job. The text covers the essential and traditional elements of managing others with a strong focus on applied and practical skills, all with a user-friendly approach. The 9th Edition continues to be a rich resource that includes lots of examples and visual stimuli that make the concepts come alive. Concentrating on the traditional and evolving roles supervisors must embrace in the current work environment, the text includes new information on employee recognition programs, global diversity, teleworking, and more. With this, readers will have the opportunity to develop the skills needed to effectively supervise employees in their future careers.
Published: 2018

28. Using Auxiliary Sample Frame Information for Optimum Sampling of Rare Populations

Author: Robert Montgomery, Kirk M. Wolter, Xian Tao, Wei Zeng, Carla Black, Christina Dorell, Michael Davern, and Martin Barron
Subjects: education.field_of_study, age-targeted list, telephone surveys, Statistics, Population, cost model, Sampling (statistics), Estimator, Variance (accounting), optimum allocation, variance, HA1-4737, Stratified sampling, national immunization survey, Sample size determination, disproportionate stratification, rare population, Econometrics, Range (statistics), education, Sampling frame, Mathematics
Abstract: We investigate disproportionate stratified sampling as a possibly efficient method of surveying members of a rare domain in circumstances in which there is no acceptable list of members. In this work, we assume that information is available at the sampling stage to stratify the general-population sampling frame into high- and low-density strata. Under a fixed constraint on the variance of the estimator of the domain mean, we make the optimum allocation of sample size to the several strata and show that, in comparison to proportional allocation, the optimum allocation requires (a) a smaller total sample size but (b) a larger number of interviews of members of the rare domain. We illustrate the methods using information about American consumers maintained by market-research companies. Such companies are able to develop lists of households that are thought to have a defined attribute of interest, such as at least one resident in a user-specified age range. The lists are imperfect, with false positives and negatives. We apply an age-targeted list to the National Immunization Survey (NIS), conducted by the Centers for Disease Control and Prevention, which targets the relatively rare population of children age 19–35 months. The age-targeted list comprises the high-density stratum and the rest of the survey’s sampling frame comprises the low-density stratum. Given the optimum allocation, we demonstrate potential cost savings for the NIS in excess of ten percent.
Published: 2015
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29. Total Survey Error Assessment for Sociodemographic Subgroups in the 2012 U.S. National Immunization Survey

Author: Wei Zeng, Philip J. Smith, Vicki Pineau, Benjamin Skalland, James A. Singleton, Kirk M. Wolter, Zhen Zhao, David Yankey, and Meena Khare
Subjects: 010104 statistics & probability, Geography, Actuarial science, Environmental health, 05 social sciences, 050602 political science & public administration, Survey error, 0101 mathematics, Immunization (finance), 01 natural sciences, 0506 political science
Published: 2017
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30. Examining the Need to Complement Karol Wojtyła’s Ethical Personalism through an Ethics of Inner Responses, Fundamental Moral Attitudes, and Virtues

Author: Maria M. Wolter
Subjects: Philosophy, Personalism, Religious studies, Sociology, Social psychology, Complement (complexity), Epistemology
Published: 2013
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31. Supervision Today!, Global Edition

Author: Stephen P. Robbins, David A. DeCenzo, Robert M. Wolter, Stephen P. Robbins, David A. DeCenzo, and Robert M. Wolter
Abstract: Appropriate for Supervision, Supervision Management, and Intro to Management Fundamental Management Skills for the Contemporary Workplace Known as one of the most effective books on management, Supervision Today helps students build an understanding of supervising through real-life concepts, examples, and practice. It's lively, conversational tone and full-color design engages students and helps capture the reality and excitement of the supervisor's job. Using a “student-friendly” approach, Supervision Today covers the essential and traditional elements of managing others with a strong focus on applied and practical skills. The 8th Edition continues to be rich in instructional aids and experiential opportunities. Concentrating on the evolving roles supervisors must embrace in the current work environment, Supervision Today includes new information on employee engagement; sustainability; technological advances; work, life, and family balance; workplace diversity; supervising global teams; and more. The full text downloaded to your computer With eBooks you can: search for key concepts, words and phrases make highlights and notes as you study share your notes with friends eBooks are downloaded to your computer and accessible either offline through the Bookshelf (available as a free download), available online and also via the iPad and Android apps. Upon purchase, you'll gain instant access to this eBook. Time limit The eBooks products do not have an expiry date. You will continue to access your digital ebook products whilst you have your Bookshelf installed.
Published: 2015

32. Design and performance of the ABCD3TA ASIC for readout of silicon strip detectors in the ATLAS semiconductor tracker

Author: F. Campabadal, C. Fleta, M. Key, M. Lozano, C. Martinez, G. Pellegrini, J.M. Rafi, M. Ullan, L.G. Johansen, B. Mohn, O. Oye, A.O. Solberg, B. Stugu, A. Ciocio, R. Ely, V. Fadeyev, M. Gilchriese, C. Haber, J. Siegrist, H. Spieler, C. Vu, P.J. Bell, D.G. Charlton, J.D. Dowell, B.J. Gallop, R.J. Homer, P. Jovanovic, G. Mahout, T.J. McMahon, J.A. Wilson, A.J. Barr, J.R. Carter, M.J. Goodrick, J.C. Hill, C.G. Lester, M.A. Parker, D. Robinson, F. Anghinolfi, E. Chesi, P. Jarron, J. Kaplon, A. Macpherson, H. Pernegger, T. Pritchard, S. Roe, A. Rudge, P. Weilhammer, W. Bialas, W. Dabrowski, M. Dwuznik, B. Toczek, S. Koperny, P. Bruckman, S. Gadomski, E. Gornicki, P. Malecki, A. Moszczynski, E. Stanecka, R. Szczygiel, M. Turala, M. Wolter, L. Feld, C. Ketterer, J. Ludwig, J. Meinhardt, K. Runge, A.G. Clark, M. Donega, M. D’Onofrio, D. Ferrere, D. La Marra, D. Macina, M. Mangin-Brinet, B. Mikulec, A. Zsenei, R.L. Bates, A. Cheplakov, Y. Iwata, T. Ohsugi, Y. Ikegami, T. Kohriki, T. Kondo, S. Terada, N. Ujiie, Y. Unno, R. Takashima, P.P. Allport, A. Greenall, J.N. Jackson, T.J. Jones, N.A. Smith, G.A. Beck, A.A. Carter, J. Morris, J. Morin, V. Cindro, G. Kramberger, I. Mandić, M. Mikuž, I.P. Duerdoth, J.M. Foster, J. Pater, S.W. Snow, R.J. Thompson, T.M. Atkinson, B. Dick, F. Fares, G.F. Moorhead, G.N. Taylor, L. Andricek, S. Bethke, D. Hauff, J. Kudlaty, G. Lutz, H.-G. Moser, R. Nisius, R. Richter, J. Schieck, A-P. Colijn, T. Cornelissen, G.W. Gorfine, F.G. Hartjes, N.P. Hessey, P. de Jong, R. Kluit, E. Koffeman, A.J.M. Muijs, S.J.M. Peeters, B. van Eijk, I. Nakano, R. Tanaka, O. Dorholt, K.M. Danielsen, T. Huse, H. Sandaker, S. Stapnes, N. Kundu, R.B. Nickerson, A. Weidberg, J. Bohm, M. Mikestikova, J. Stastny, Z. Broklova, J. Broz, Z. Dolezal, P. Kodys, P. Kubik, P. Reznicek, V. Vorobel, I. Wilhelm, P. Cermák, D. Chren, T. Horazdovský, V. Linhart, S. Pospísil, M. Sinor, M. Solar, B. Sopko, I. Stekl, R.J. Apsimon, L.E. Batchelor, J.P. Bizzell, N.G. Falconer, M.J. French, M.D. Gibson, S.J. Haywood, R.M. Matson, S.J. McMahon, M. Morrissey, W.J. Murray, P.W. Phillips, M. Tyndel, E.G. Villani, D.P. Cosgrove, D.E. Dorfan, A.A. Grillo, S. Kachiguine, F. Rosenbaum, H.F.-W. Sadrozinski, A. Seiden, E. Spencer, M. Wilder, T. Akimoto, K. Hara, K. Tanizaki, N. Bingefors, R. Brenner, T. Ekelof, L. Eklund, J. Bernabeu, J.V. Civera, M.J. Costa, J. Fuster, C. Garcia, J.E. Garcia-Navarro, S. Gonzalez-Sevilla, C. Lacasta, G. Llosa, S. Marti-Garcia, P. Modesto, F.J. Sanchez, L. Sospedra, M. Vos, Clark, Allan Geoffrey, Donega, Mauro, D'Onofrio, Monica, Ferrere, Didier, La Marra, Daniel, Macina-Buono, Daniela, Mangin-Brinet, Mariane, Mikulec, Bettina, and Zsenei, Andras
Subjects: Nuclear and High Energy Physics, Physics::Instrumentation and Detectors, Pipeline (computing), ddc:500.2, Hardware_PERFORMANCEANDRELIABILITY, BiCMOS, Silicon strip detectors, Binary readout, Computer Science::Hardware Architecture, Tracking detectors, Radiation damage, Application-specific integrated circuit, Hardware_INTEGRATEDCIRCUITS, Instrumentation, Physics, Large Hadron Collider, business.industry, Application specific integrated circuits, ATLAS experiment, Detector, Front-end electronics, Chip, Quality assurance, Trackingdetectors, CMOS, business, Computer hardware
Abstract: The ABCD3TA is a 128-channel ASIC with binary architecture for the readout of silicon strip particle detectors in the Semiconductor Tracker of the ATLAS experiment at the Large Hadron Collider (LHC). The chip comprises fast front-end and amplitude discriminator circuits using bipolar devices, a binary pipeline for first level trigger latency, a second level derandomising buffer and data compression circuitry based on CMOS devices. It has been designed and fabricated in a BiCMOS radiation resistant process. Extensive testing of the ABCD3TA chips assembled into detector modules show that the design meets the specifications and maintains the required performance after irradiation up to a total ionising dose of 10 Mrad and a 1-MeV neutron equivalent fluence of 2×10 14 n/cm2, corresponding to 10 years of operation of the LHC at its design luminosity. Wafer screening and quality assurance procedures have been developed and implemented in large volume production to ensure that the chips assembled into modules meet the rigorous acceptance criteria. © 2005 Elsevier B.V. All rights reserved.
Published: 2016

33. Differential expression of conserved and novel microRNAs during tail regeneration in the lizard Anolis carolinensis

Author: Justin M. Wolter, Elizabeth Hutchins, Kenro Kusumi, Walter L. Eckalbar, and Marco Mangone
Subjects: 0301 basic medicine, Tail, Reptile, Biology, Transcriptome, 03 medical and health sciences, RNA interference, microRNA, Gene expression, Embryonic morphogenesis, Genetics, Regeneration, Animals, RNA, Messenger, Regulation of gene expression, MicroRNA sequencing, Regeneration (biology), Gene Expression Profiling, Brain, Computational Biology, High-Throughput Nucleotide Sequencing, Lizards, Molecular Sequence Annotation, Cell biology, MicroRNAs, 030104 developmental biology, Gene Ontology, Gene Expression Regulation, Organ Specificity, Lizard, Muscle, RNA Interference, Biotechnology, Research Article
Abstract: Background Lizards are evolutionarily the most closely related vertebrates to humans that can lose and regrow an entire appendage. Regeneration in lizards involves differential expression of hundreds of genes that regulate wound healing, musculoskeletal development, hormonal response, and embryonic morphogenesis. While microRNAs are able to regulate large groups of genes, their role in lizard regeneration has not been investigated. Results MicroRNA sequencing of green anole lizard (Anolis carolinensis) regenerating tail and associated tissues revealed 350 putative novel and 196 known microRNA precursors. Eleven microRNAs were differentially expressed between the regenerating tail tip and base during maximum outgrowth (25 days post autotomy), including miR-133a, miR-133b, and miR-206, which have been reported to regulate regeneration and stem cell proliferation in other model systems. Three putative novel differentially expressed microRNAs were identified in the regenerating tail tip. Conclusions Differentially expressed microRNAs were identified in the regenerating lizard tail, including known regulators of stem cell proliferation. The identification of 3 putative novel microRNAs suggests that regulatory networks, either conserved in vertebrates and previously uncharacterized or specific to lizards, are involved in regeneration. These findings suggest that differential regulation of microRNAs may play a role in coordinating the timing and expression of hundreds of genes involved in regeneration. Electronic supplementary material The online version of this article (doi:10.1186/s12864-016-2640-3) contains supplementary material, which is available to authorized users.
Published: 2016

34. Validating advanced driver assistance systems (ADAS) using comprehensive, loss-free in-vehicle measurements

Author: A. Fernandez, M. Wolter, Johannes Wagner, and Joachim Löchner
Subjects: Internal combustion engine, Computer science, Powertrain, Range (aeronautics), In vehicle, Advanced driver assistance systems, Premium segment, Gasoline, Automotive engineering, Line (electrical engineering)
Abstract: Mercedes-Benz introduced the first plug-in hybrid electric vehicles in 2014, starting with the S 500 e an externally rechargeable hybrid with 33 km electric range. Hereinafter, additional varieties with 4-cylinder and 6-cylinder gasoline engines were released out of a modularly technology kit, scaling the internal combustion engine and the electric powertrain in line with the vehicle segment. This way electric ranges of at least 30 km were realized both in the SUV and premium segment. This paper covers the essential characteristics of the modularly technology kit and the different plug-in hybrid powertrains as well as the electric range requirements of the different vehicles. It further illustrates the operating strategy of the Mercedes-Benz plug-in hybrid vehicles and its application. In doing so, the rule-based operating strategy is described based on the main aspects of a fuel-optimal hybrid operation.
Published: 2016
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35. More on the Extent of Undercoverage in RDD Telephone Surveys Due to the Omission of 0-Banks

Author: Jenny Kelly, Martin Barron, Xian Tao, Kirk M. Wolter, Robert Montgomery, Benjamin Skalland, Hee-Choon Shin, and James A. Singleton
Abstract: More on the Extent of Undercoverage in RDD Telephone Surveys Due to the Omission of 0-Banks
Published: 2010
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36. Frankfurter Dermatologentagung

Author: S. Pätzold, M. Wolter, and R. Kaufmann
Subjects: Dermatology
Published: 2009
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37. Ergebnisse der Aphakiekorrektur durch retroiridal fixierte Kunstlinse

Author: M Küchle and M Wolter-Roessler
Subjects: Pars plana, medicine.medical_specialty, Visual acuity, genetic structures, business.industry, medicine.medical_treatment, Retinal detachment, Vitrectomy, Cataract surgery, medicine.disease, Aphakia, eye diseases, Sclera, Surgery, Ophthalmology, medicine.anatomical_structure, medicine, sense organs, medicine.symptom, business, Hyphema
Abstract: BACKGROUND: We report the results of the secondary implantation of retroiridally fixated irisclaw-lenses (Artisan®) to correct aphakia. PATIENTS AND METHODS: This retrospective study included all eyes that had undergone outpatient implantation of an Artisan IOL by the senior author (MK) between July 2004 and January 2008. We analysed 48 eyes of 46 patients (27 female, 19 male) aged 17 to 87 years. Underlying conditions were: aphakia after congenital cataract or trauma (19 eyes), late luxation of a posterior chamber IOL (16 eyes), intraoperative zonulolysis during cataract surgery that did not allow PC IOL implantation (12 eyes, including 10 eyes with pseudoexfoliation and one eye with Marfan syndrome), anterior chamber IOL with corneal decompensation problems and recurrent hyphema (1 eye). Simultaneous surgical procedures included: anterior vitrectomy (48 eyes), pars plana vitrectomy (14 eyes), removal of PC IOL (16 eyes), removal of AC IOL (1 eye), and penetrating keratoplasty (1 eye). Mean follow-up was 14.3 months (range: 1 - 31 months). IOL power was calculated using the SRKT formula and an A constant of 116.7. RESULTS: Surgery was uneventful in all cases with safe enclavation of both IOL haptics. Mean postoperative refraction was 0 dpt. (range: -0.75 to + 1.0 dpt.), median postoperative visual acuity in Log-Mar was 0.2; compared to preoperative visual acuity (median 0.4 Log-Mar); all patients improved. Pre- and postoperative intraocular pressures were in the normal range in all eyes. Complications were few: one eye without patent iridotomy developed pupillary block glaucoma one day following surgery and was successfully treated by Nd:YAG iridotomy. One patient following blunt ocular trauma developed a retinal detachment with PVR 10 months following implantation of the Artisan IOL that was repaired uneventfully by pars plana vitrectomy with silicone oil instillation. In this case, the Artisan IOL was left in place. In two eyes, secondary trauma resulted in dislocation of one haptic of the Artisan IOL. In both of these cases, refixation of the Artisan IOL was easily performed by enclavation of the iris claw. In two patients cystoid macula oedema was observed. CONCLUSIONS: With correct indications the implantation of a retroiridally fixated IOL (Artisan®) is a safe and predictable method to correct aphakia and has become our method of choice instead of anterior chamber IOLs and sclera fixated IOLs.
Published: 2008
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38. TGFBI (BIGH3) gene mutations in German families: two novel mutations associated with unique clinical and histopathological findings

Author: Gernot I.W. Duncker, U G Froster, Thomas Reinhard, Claudia Auw-Haedrich, H E Völcker, I. Clausen, D P Schulze, Daniel F. Schorderet, F. Tost, W Heinritz, M Wolter-Roessler, Claudia Gruenauer-Kloevekorn, and E Weidle
Subjects: Adult, Male, Proband, Pathology, medicine.medical_specialty, DNA Mutational Analysis, Visual Acuity, Corneal dystrophy, Gene mutation, Biology, medicine.disease_cause, Young Adult, Cellular and Molecular Neuroscience, Transforming Growth Factor beta, Genotype, medicine, Humans, Genetic Predisposition to Disease, Gene, Corneal Dystrophies, Hereditary, Genetics, Extracellular Matrix Proteins, Mutation, Age Factors, medicine.disease, Phenotype, eye diseases, Sensory Systems, Pedigree, Ophthalmology, Female, TGFBI
Abstract: Background: To report the clinical, histopathological and immunohistochemical findings of two novel mutations within the TGFBI gene. Methods: The genotype of 41 affected members of 16 families and nine sporadic cases was investigated by direct sequencing of the TGFBI gene. Clinical, histological and immunohistochemical characteristics of corneal opacification were reported and compared with the coding region changes in the TGFBI gene. Results: A novel mutation Leu509Pro was detected in one family with a geographic pattern-like clinical phenotype. Histopathologically we found amyloid together with non-amyloid deposits and immunohistochemical staining of Keratoepithelin (KE) KE2 and KE15 antibodies. In two families and one sporadic case the novel mutation Gly623Arg with a late-onset, map-like corneal dystrophy was identified. Here amyloid and immunohistochemical staining of only KE2 antibodies occurred. Further, five already known mutations are reported: Arg124Cys Arg555Trp Arg124His His626Arg, Ala546Asp in 13 families and five sporadic cases of German origin. The underlying gene defect within the TBFBI gene was not identified in any of the four probands with Thiel–Behnke corneal dystrophy. Conclusions: The two novel mutations within the TGFBI gene add another two phenotypes with atypical immunohistochemical and histopathological features to those so far reported.
Published: 2008
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39. Multivariate analysis methods in physics

Author: M. Wolter
Subjects: Physics, Nuclear and High Energy Physics, Multivariate statistics, Multivariate analysis, Particle properties, Mathematical model, business.industry, Statistical learning, Statistical model, Machine learning, computer.software_genre, Artificial intelligence, business, computer, Selection (genetic algorithm)
Abstract: In this article, a review of multivariate methods based on statistical learning is given. Several popular multivariate methods useful in high-energy physics analysis are discussed. Selected examples from current research in particle physics are discussed, both from online trigger selection and from off-line analysis. In addition, statistical learning methods, not yet applied in particle physics, are presented and some new applications are suggested.
Published: 2007
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40. Search for contact interactions and large extra dimensions in dilepton events from pp collisions at sqrt[s]=7??TeV with the ATLAS detector

Author: G. Aad, T. Abajyan, B. Abbott, J. Abdallah, S. Abdel Khalek, A. Abdelalim, O. Abdinov, R. Aben, B. Abi, M. Abolins, O. AbouZeid, H. Abramowicz, H. Abreu, B. Acharya, L. Adamczyk, D. Adams, T. Addy, J. Adelman, S. Adomeit, P. Adragna, T. Adye, S. Aefsky, J. Aguilar Saavedra, M. Agustoni, M. Aharrouche, S. Ahlen, F. Ahles, A. Ahmad, M. Ahsan, G. Aielli, T. Åkesson, G. Akimoto, A. Akimov, M. Alam, J. Albert, S. Albrand, M. Aleksa, I. Aleksandrov, F. Alessandria, C. Alexa, G. Alexander, G. Alexandre, T. Alexopoulos, M. Alhroob, M. Aliev, G. Alimonti, J. Alison, B. Allbrooke, P. Allport, S. Allwood Spiers, J. Almond, A. Aloisio, R. Alon, A. Alonso, F. Alonso, A. Altheimer, B. Alvarez Gonzalez, M. Alviggi, K. Amako, C. Amelung, V. Ammosov, S. Amor Dos Santos, A. Amorim, N. Amram, C. Anastopoulos, L. Ancu, N. Andari, T. Andeen, C. Anders, G. Anders, K. Anderson, A. Andreazza, V. Andrei, M. L. Andrieux, X. Anduaga, S. Angelidakis, P. Anger, A. Angerami, F. Anghinolfi, A. Anisenkov, N. Anjos, A. Annovi, A. Antonaki, M. Antonelli, A. Antonov, J. Antos, F. Anulli, M. Aoki, S. Aoun, L. Aperio Bella, R. Apolle, G. Arabidze, I. Aracena, Y. Arai, A. Arce, S. Arfaoui, J. F. Arguin, S. Argyropoulos, E. Arik, M. Arik, A. Armbruster, O. Arnaez, V. Arnal, C. Arnault, A. Artamonov, G. Artoni, D. Arutinov, S. Asai, S. Ask, B. Åsman, L. Asquith, K. Assamagan, A. Astbury, M. Atkinson, B. Aubert, E. Auge, K. Augsten, M. Aurousseau, G. Avolio, R. Avramidou, D. Axen, G. Azuelos, Y. Azuma, M. Baak, G. Baccaglioni, C. Bacci, A. Bach, H. Bachacou, K. Bachas, M. Backes, M. Backhaus, J. Backus Mayes, E. Badescu, P. Bagnaia, S. Bahinipati, Y. Bai, D. Bailey, T. Bain, J. Baines, O. Baker, M. Baker, S. Baker, P. Balek, E. Banas, P. Banerjee, S.w. Banerjee, D. Banfi, A. Bangert, V. Bansal, H. Bansil, L. Barak, S. Baranov, A. Barbaro Galtieri, T. Barber, E. Barberio, D. Barberis, M. Barbero, D. Bardin, T. Barillari, M. Barisonzi, T. Barklow, N. Barlow, B. Barnett, R. Barnett, A. Baroncelli, G. 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Di Ciaccio, L. Di Ciaccio, C. Di Donato, A. Di Girolamo, B. Di Girolamo, S. Di Luise, A. Di Mattia, B. Di Micco, R. Di Nardo, A. Di Simone, M. Diaz, E. Diehl, J. Dietrich, T. Dietzsch, S. Diglio, K. Dindar Yagci, J. Dingfelder, F. Dinut, C. Dionisi, P. Dita, S. Dita, F. Dittus, F. Djama, T. Djobava, M. do Vale, A. Do Valle Wemans, T. Doan, M. Dobbs, D. Dobos, E. Dobson, J. Dodd, C. Doglioni, T. Doherty, Y. Doi, J. Dolejsi, I. Dolenc, Z. Dolezal, B. Dolgoshein, T. Dohmae, M. Donadelli, J. Donini, J. Dopke, A. Doria, A. Dos Anjos, A. Dotti, M. Dova, A. Doxiadis, A. Doyle, N. Dressnandt, M. Dris, J. Dubbert, S. Dube, E. Duchovni, G. Duckeck, D. Duda, A. Dudarev, F. Dudziak, M. Dührssen, I. Duerdoth, L. Duflot, M. A. Dufour, L. Duguid, M. Dunford, H. Duran Yildiz, R. Duxfield, M. Dwuznik, M. Düren, W. Ebenstein, J. Ebke, S. Eckweiler, K. Edmonds, W. Edson, C. Edwards, N. Edwards, W. Ehrenfeld, T. Eifert, G. Eigen, K. Einsweiler, E. Eisenhandler, T. Ekelof, M. El Kacimi, M. Ellert, S. Elles, F. Ellinghaus, K. Ellis, N. Ellis, J. Elmsheuser, M. Elsing, D. Emeliyanov, R. Engelmann, A. Engl, B. Epp, J. Erdmann, A. Ereditato, D. Eriksson, J. Ernst, M. Ernst, J. Ernwein, D. Errede, S. Errede, E. Ertel, M. Escalier, H. Esch, C. Escobar, X. Espinal Curull, B. Esposito, F. Etienne, A. Etienvre, E. Etzion, D. Evangelakou, H. Evans, C. Fabre, R. Fakhrutdinov, S. Falciano, Y. Fang, M. Fanti, A. Farbin, A. Farilla, J. Farley, T. Farooque, S. Farrell, S. Farrington, P. Farthouat, F. Fassi, P. Fassnacht, D. Fassouliotis, B. Fatholahzadeh, A. Favareto, L. Fayard, S. Fazio, R. Febbraro, P. Federic, O. Fedin, W. Fedorko, M. Fehling Kaschek, L. Feligioni, C. Feng, E. Feng, A. Fenyuk, J. Ferencei, W. Fernando, S. Ferrag, J. Ferrando, V. Ferrara, A. Ferrari, P. Ferrari, R. Ferrari, D. Ferreira de Lima, A. Ferrer, D. Ferrere, C. Ferretti, A. Ferretto Parodi, M. Fiascaris, F. Fiedler, A. Filipčič, F. Filthaut, M. Fincke Keeler, M. Fiolhais, L. Fiorini, A. Firan, G. Fischer, M. 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Pospisil, I. Potrap, C. Potter, G. Poulard, J. Poveda, V. Pozdnyakov, R. Prabhu, P. Pralavorio, A. Pranko, S. Prasad, R. Pravahan, S. Prell, K. Pretzl, D. Price, J. Price, L. Price, D. Prieur, M. Primavera, K. Prokofiev, F. Prokoshin, S. Protopopescu, J. Proudfoot, X. Prudent, M. Przybycien, H. Przysiezniak, S. Psoroula, E. Ptacek, E. Pueschel, J. Purdham, M. Purohit, P. Puzo, Y. Pylypchenko, J. Qian, A. Quadt, D. Quarrie, W. Quayle, F. Quinonez, M. Raa, V. Radeka, V. Radescu, P. Radloff, F. Ragusa, G. Rahal, A. Rahimi, D. Rahm, S. Rajagopalan, M. Rammensee, M. Ramme, A. Randle-Conde, K. Randrianarivony, F. Rauscher, T. Rave, M. Raymond, A. Read, D. Rebuzzi, A. Redelbach, G. Redlinger, R. Reece, K. Reeve, A. Reinsch, I. Reisinger, C. Rembser, Z. Ren, A. Renaud, M. Rescigno, S. Resconi, B. Resende, P. Reznicek, R. Rezvani, R. Richter, E. Richter-Wa, M. Ridel, M. Rijpstra, M. Rijssenbeek, A. Rimoldi, L. Rinaldi, R. Rio, I. Riu, G. Rivoltella, F. Rizatdinova, E. Rizvi, S. Robertson, A. Robichaud-Veronneau, D. Robinson, J. Robinson, A. Robson, J. Rocha de Lima, C. Roda, D. Roda Dos Santo, A. Roe, S. Roe, O. Røhne, S. Rolli, A. Romaniouk, M. Romano, G. Romeo, E. Romero Adam, N. Rompoti, L. Roo, E. Ro, S. Rosati, K. Rosbach, A. Rose, M. Rose, G. Rosenbaum, E. Rosenberg, P. Rosendahl, O. Rosenthal, L. Rosselet, V. Rossetti, E. Rossi, L. Rossi, M. Rotaru, I. Roth, J. Rothberg, D. Rousseau, C. Royon, A. Rozanov, Y. Rozen, X. Ruan, F. Rubbo, I. Rubinskiy, N. Ruckstuhl, V. Rud, C. Rudolph, G. Rudolph, F. Rühr, A. Ruiz-Martinez, L. Rumyantsev, Z. Rurikova, N. Rusakovich, A. Ruschke, J. Rutherfoord, P. Ruzicka, Y. Ryabov, M. Rybar, G. Rybkin, N. Ryder, A. Saavedra, I. Sadeh, H. Sadrozinski, R. Sadykov, F. Safai Tehrani, H. Sakamoto, G. Salamanna, A. Salamon, M. Saleem, D. Salek, D. Salihagic, A. Salnikov, J. Salt, B. Salvachua Ferrando, D. Salvatore, F. Salvatore, A. Salvucci, A. Salzburger, D. Sampsonidi, B. Samset, A. Sanchez, V. Sanchez Martinez, H. Sandaker, H. Sander, M. Sander, M. Sandhoff, T. Sandoval, C. Sandoval, R. Sandstroem, D. Sankey, A. Sansoni, C. Santamarina Rio, C. Santoni, R. Santonico, H. Santo, I. Santoyo Castillo, J. Saraiva, T. Sarangi, E. Sarkisyan-Grinbaum, B. Sarrazin, F. Sarri, G. Sartisohn, O. Sasaki, Y. Sasaki, N. Sasao, I. Satsounkevitch, G. Sauvage, E. Sauvan, J. Sauvan, P. Savard, V. Savinov, D. Savu, L. Sawyer, D. Saxon, J. Saxon, C. Sbarra, A. Sbrizzi, D. Scannicchio, M. Scarcella, J. Schaarschmidt, P. Schacht, D. Schaefer, U. Schäfer, A. Schaelicke, S. Schaepe, S. Schaetzel, A. Schaffer, D. Schaile, R. Schamberger, A. Schamov, V. Scharf, V. Schegelsky, D. Scheirich, M. Schernau, M. Scherzer, C. Schiavi, J. Schieck, M. Schioppa, S. Schlenker, E. Schmidt, K. Schmieden, C. Schmitt, S. Schmitt, B. Schneider, U. Schnoor, L. Schoeffel, A. Schoening, A. Schorlemmer, M. Schott, D. Schouten, J. Schovancova, M. Schram, C. Schroeder, N. Schroer, M. Schulten, J. Schulte, H.-C. Schultz-Coulon, H. Schulz, M. Schumacher, B. Schumm, Ph. Schune, C. Schwanenberger, A. Schwartzman, Ph. Schwegler, Ph. Schwemling, R. Schwienhorst, R. Schwierz, J. Schwindling, T. Schwindt, M. Schwoerer, F. Sciacca, G. Sciolla, W. Scott, J. Searcy, G. Sedov, E. Sedykh, S. Seidel, A. Seiden, F. Seifert, J. Seixa, G. Sekhniaidze, S. Sekula, K. Selbach, D. Seliverstov, B. Sellden, G. Seller, M. Seman, N. Semprini-Cesari, C. Serfon, L. Serin, L. Serkin, R. Seuster, H. Severini, A. Sfyrla, E. Shabalina, M. Shamim, L. Shan, J. Shank, Q. Shao, M. Shapiro, P. Shatalov, K. Shaw, D. Sherman, P. Sherwood, S. Shimizu, M. Shimojima, T. Shin, M. Shiyakova, A. Shmeleva, M. Shochet, D. Short, S. Shrestha, E. Shulga, M. Shupe, P. Sicho, A. Sidoti, F. Siegert, Dj. Sijacki, O. Silbert, J. Silva, Y. Silver, D. Silverstein, S. Silverstein, V. Simak, O. Simard, Lj. Simic, S. Simion, E. Simioni, B. Simmon, R. Simoniello, M. Simonyan, P. Sinervo, N. Sinev, V. Sipica, G. Siragusa, A. Sircar, A. Sisakyan, S. Sivoklokov, J. Sjölin, T. Sjursen, L. Skinnari, H. Skottowe, K. Skovpen, P. Skubic, M. Slater, T. Slavicek, K. Sliwa, V. Smakhtin, B. Smart, L. Smestad, S. Smirnov, Y. Smirnov, L. Smirnova, O. Smirnova, B. Smith, D. Smith, K. Smith, R. Smith, M. Smizanska, K. Smolek, A. Snesarev, S. Snow, J. Snow, S. Snyder, R. Sobie, J. Sodomka, A. Soffer, C. Solan, M. Solar, J. Solc, E. Soldatov, U. Soldevila, E. Solfaroli Camillocci, A. Solodkov, O. Solovyanov, V. Solovyev, N. Soni, V. Sopko, B. Sopko, M. Sosebee, R. Soualah, A. Soukharev, S. Spagnolo, F. Spanò, R. Spighi, G. Spigo, R. Spiwok, M. Spousta, T. Spreitzer, B. Spurlock, R. St. Deni, J. Stahlman, R. Stamen, E. Stanecka, R. Stanek, C. Stanescu, M. Stanescu-Bellu, M. Stanitzki, S. Stapne, E. Starchenko, J. Stark, P. Staroba, P. Starovoitov, R. Staszewski, A. Staude, P. Stavina, G. Steele, P. Steinbach, P. Steinberg, I. Stekl, B. Stelzer, H. Stelzer, O. Stelzer-Chilton, H. Stenzel, S. Stern, G. Stewart, J. Stilling, M. Stockton, K. Stoerig, G. Stoicea, S. Stonjek, P. Strachota, A. Stradling, A. Straessner, J. Strandberg, S. Strandberg, A. Strandlie, M. Strang, E. Strau, M. Strau, P. Strizenec, R. Ströhmer, D. Strom, J. Strong, R. Stroynowski, B. Stugu, I. Stumer, J. Stupak, P. Sturm, N. Style, D. Soh, D. Su, HS. Subramania, R. Subramaniam, A. Succurro, Y. Sugaya, C. Suhr, M. Suk, V. Sulin, S. Sultansoy, T. Sumida, X. Sun, J. Sundermann, K. Suruliz, G. Susinno, M. Sutton, Y. Suzuki, M. Svato, S. Swedish, I. Sykora, T. Sykora, J. Sánchez, D. Ta, K. Tackmann, A. Taffard, R. Tafirout, N. Taiblum, Y. Takahashi, H. Takai, R. Takashima, H. Takeda, T. Takeshita, Y. Takubo, M. Talby, A. Talyshev, M. Tamsett, K. Tan, J. Tanaka, R. Tanaka, S. Tanaka, A. Tanasijczuk, K. Tani, N. Tannoury, S. Tapprogge, D. Tardif, S. Tarem, F. Tarrade, G. Tartarelli, P. Ta, M. Tasevsky, E. Tassi, Y. Tayalati, C. Taylor, F. Taylor, G. Taylor, W. Taylor, M. Teinturier, F. Teischinger, M. Teixeira Dias Castanheira, P. Teixeira-Dia, K. Temming, H. Ten Kate, P. Teng, S. Terada, K. Terashi, J. Terron, M. Testa, R. Teuscher, J. Therhaag, T. Theveneaux-Pelzer, S. Thoma, J. Thoma, E. Thompson, P. Thompson, A. Thompson, L. Thomsen, E. Thomson, M. Thomson, W. Thong, R. Thun, F. Tian, M. Tibbett, T. Tic, V. Tikhomirov, Y. Tikhonov, S. Timoshenko, E. Tiouchichine, P. Tipton, S. Tisserant, T. Todorov, S. Todorova-Nova, B. Toggerson, J. Tojo, S. Tokár, K. Tokushuku, K. Tollefson, M. Tomoto, L. Tompkin, K. Tom, A. Tonoyan, C. Topfel, N. Topilin, E. Torrence, H. Torre, E. Torró Pastor, J. Toth, F. Touchard, D. Tovey, T. Trefzger, L. Tremblet, A. Tricoli, I. Trigger, S. Trincaz-Duvoid, M. Tripiana, N. Triplett, W. Trischuk, B. Trocmé, C. Troncon, M. Trottier-McDonald, P. True, M. Trzebinski, A. Trzupek, C. Tsaroucha, J. Tseng, M. Tsiakiri, P. Tsiareshka, D. Tsionou, G. Tsipoliti, S. Tsiskaridze, V. Tsiskaridze, E. Tskhadadze, I. Tsukerman, V. Tsulaia, J.-W. Tsung, S. Tsuno, D. Tsybychev, A. Tua, A. Tudorache, V. Tudorache, J. Tuggle, M. Turala, D. Turecek, I. Turk Cakir, E. Turlay, R. Turra, P. Tut, A. Tykhonov, M. Tylmad, M. Tyndel, G. Tzanako, K. Uchida, I. Ueda, R. Ueno, M. Ugland, M. Uhlenbrock, M. Uhrmacher, F. Ukegawa, G. Unal, A. Undru, G. Unel, Y. Unno, D. Urbaniec, P. Urquijo, G. Usai, M. Uslenghi, L. Vacavant, V. Vacek, B. Vachon, S. Vahsen, J. Valenta, S. Valentinetti, A. Valero, S. Valkar, E. Valladolid Gallego, S. Vallecorsa, J. Valls Ferrer, R. Van Berg, P. Van Der Deijl, R. van der Geer, H. van der Graaf, R. Van Der Leeuw, E. van der Poel, D. van der Ster, N. van Eldik, P. van Gemmeren, I. van Vulpen, M. Vanadia, W. Vandelli, A. Vaniachine, P. Vankov, F. Vannucci, R. Vari, E. Varne, T. Varol, D. Varoucha, A. Vartapetian, K. Varvell, V. Vassilakopoulo, F. Vazeille, T. Vazquez Schroeder, G. Vegni, J. Veillet, F. Veloso, R. Vene, S. Veneziano, A. Ventura, D. Ventura, M. Venturi, N. Venturi, V. Vercesi, M. Verducci, W. Verkerke, J. Vermeulen, A. Vest, M. Vetterli, I. Vichou, T. Vickey, O. Vickey Boeriu, G. Viehhauser, S. Viel, M. Villa, M. Villaplana Perez, E. Vilucchi, M. Vincter, E. Vinek, V. Vinogradov, M. Virchaux, J. Virzi, O. Vitell, M. Viti, I. Vivarelli, F. Vives Vaque, S. Vlacho, D. Vladoiu, M. Vlasak, A. Vogel, P. Vokac, G. Volpi, M. Volpi, G. Volpini, H. von der Schmitt, H. von Radziewski, E. von Toerne, V. Vorobel, V. Vorwerk, M. Vo, R. Vo, T. Vo, J. Vossebeld, N. Vranje, M. Vranjes Milosavljevic, V. Vrba, M. Vreeswijk, T. Vu Anh, R. Vuillermet, I. Vukotic, W. Wagner, P. Wagner, H. Wahlen, S. Wahrmund, J. Wakabayashi, S. Walch, J. Walder, R. Walker, W. Walkowiak, R. Wall, P. Waller, B. Walsh, C. Wang, H. Wang, J. Wang, R. Wang, S. Wang, T. Wang, A. Warburton, C. Ward, D. Wardrope, M. Warsinsky, A. Washbrook, C. Wasicki, I. Watanabe, P. Watkin, A. Watson, I. Watson, M. Watson, G. Watt, S. Watt, A. Waugh, B. Waugh, M. Weber, J. Webster, A. Weidberg, P. Weigell, J. Weingarten, C. Weiser, P. Well, T. Wenau, D. Wendland, Z. Weng, T. Wengler, S. Wenig, N. Werme, M. Werner, P. Werner, M. Werth, M. Wessel, J. Wetter, C. Weydert, K. Whalen, A. White, M. White, S. White, S. Whitehead, D. Whiteson, D. Whittington, F. Wicek, D. Wicke, F. Wicken, W. Wiedenmann, M. Wieler, P. Wienemann, C. Wiglesworth, L. Wiik-Fuch, P. Wijeratne, A. Wildauer, M. Wildt, I. Wilhelm, H. Wilken, J. Will, E. William, H. William, W. Willi, S. Willocq, J. Wilson, M. Wilson, A. Wilson, I. Wingerter-Seez, S. Winkelmann, F. Winklmeier, M. Wittgen, S. Wollstadt, M. Wolter, H. Wolter, W. Wong, G. Wooden, B. Wosiek, J. Wotschack, M. Woudstra, K. Wozniak, K. Wraight, M. Wright, B. Wrona, S. Wu, X. Wu, Y. Wu, E. Wulf, B. Wynne, S. Xella, M. Xiao, S. Xie, C. Xu, D. Xu, L. Xu, B. Yabsley, S. Yacoob, M. Yamada, H. Yamaguchi, A. Yamamoto, K. Yamamoto, S. Yamamoto, T. Yamamura, T. Yamanaka, T. Yamazaki, Y. Yamazaki, Z. Yan, H. Yang, U. Yang, Y. Yang, Z. Yang, S. Yanush, L. Yao, Y. Yao, Y. Yasu, G. Ybeles Smit, J. Ye, S. Ye, M. Yilmaz, R. Yoosoofmiya, K. Yorita, R. Yoshida, K. Yoshihara, C. Young, S. Youssef, D. Yu, J. Yu, L. Yuan, A. Yurkewicz, B. Zabinski, R. Zaidan, A. Zaitsev, Z. Zajacova, L. Zanello, D. Zanzi, A. Zaytsev, C. Zeitnitz, M. Zeman, A. Zemla, C. Zendler, O. Zenin, T. Ženiš, Z. Zinono, D. Zerwa, G. Zevi della Porta, D. Zhang, H. Zhang, J. Zhang, X. Zhang, Z. Zhang, L. Zhao, Z. Zhao, A. Zhemchugov, J. Zhong, B. Zhou, N. Zhou, Y. Zhou, C. Zhu, H. Zhu, J. Zhu, Y. Zhu, X. Zhuang, V. Zhuravlov, A. Zibell, D. Zieminska, N. Zimin, R. Zimmermann, S. Zimmermann, M. Ziolkowski, R. Zitoun, L. Živković, V. Zmouchko, G. Zobernig, A. Zoccoli, M. zur Nedden, V. Zutshi, and L. Zwalinski
Subjects: HADRON-HADRON COLLISIONS, High Energy Physics::Experiment, NEW PHYSICS
Abstract: A search for nonresonant new phenomena, originating from either contact interactions or large extra spatial dimensions, has been carried out using events with two isolated electrons or muons. These events, produced at the LHC in proton-proton collisions at √s=7 TeV, were recorded by the ATLAS detector. The data sample, collected throughout 2011, corresponds to an integrated luminosity of 4.9 and 5.0 fb-1 in the e+e- and μ+μ- channels, respectively. No significant deviations from the Standard Model expectation are observed. Using a Bayesian approach, 95% confidence level lower limits ranging from 9.0 to 13.9 TeV are placed on the energy scale of ℓℓqq contact interactions in the left-left isoscalar model. Lower limits ranging from 2.4 to 3.9 TeV are also set on the string scale in large extra dimension models. After combining these limits with results from a similar search in the diphoton channel, slightly more stringent limits are obtained.
Published: 2013

41. Detection of miRNA Targets in High-throughput Using the 3'LIFE Assay

Author: Kasuen Kotagama, Cody S. Babb, Justin M. Wolter, and Marco Mangone
Subjects: Genetics, General Immunology and Microbiology, General Chemical Engineering, General Neuroscience, High-Throughput Nucleotide Sequencing, Computational biology, Biology, Transfection, General Biochemistry, Genetics and Molecular Biology, Rapid identification, MicroRNAs, Identification (information), Mrna level, Luminescent Measurements, microRNA, Humans, RNA, Messenger, Instrumentation (computer programming), Luciferases, 3' Untranslated Regions, Molecular Biology, Throughput (business)
Abstract: Luminescent Identification of Functional Elements in 3’UTRs (3’LIFE) allows the rapid identification of targets of specific miRNAs within an array of hundreds of queried 3’UTRs. Target identification is based on the dual-luciferase assay, which detects binding at the mRNA level by measuring translational output, giving a functional readout of miRNA targeting. 3’LIFE uses non-proprietary buffers and reagents, and publically available reporter libraries, making genome-wide screens feasible and cost-effective. 3’LIFE can be performed either in a standard lab setting or scaled up using liquid handling robots and other high-throughput instrumentation. We illustrate the approach using a dataset of human 3’UTRs cloned in 96-well plates, and two test miRNAs, let-7c and miR-10b. We demonstrate how to perform DNA preparation, transfection, cell culture and luciferase assays in 96-well format, and provide tools for data analysis. In conclusion 3'LIFE is highly reproducible, rapid, systematic, and identifies high confidence targets.
Published: 2015
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42. Molekulargenetische und histopathologische Untersuchungen zur Genotyp-Phänotyp-Analyse bei Patienten mit TGFBI-gekoppelten Hornhautdystrophien

Author: F. Tost, C Auw-Haedrich, Claudia Grünauer-Kloevekorn, M Wolter-Roessler, Ursula G. Froster, H E Völcker, W Heinritz, S Braeutigam, Giw Duncker, and E Weidle
Subjects: Pathology, medicine.medical_specialty, Corneal dystrophy, Biology, medicine.disease, Phenotype, eye diseases, Ophthalmology, Exon, Molecular genetics, Genotype, medicine, Mutation testing, Missense mutation, TGFBI
Abstract: Purpose Different missense mutations in the TGFBI gene cause granular (Groenouw CDGG1, Avellino CDA, Reis-Bucklers CDB1) and lattice (Type I; Biber-Haab-Dimmer; CDL1) corneal dystrophies and, in some reports, corneal dystrophy Thiel-Behnke (CDB2). We report on the mutation spectrum and the genotype-phenotype correlations on the basis of clinical and histopathological examinations of 13 German families with TGFBI-linked corneal dystrophies. Methods In 31 patients with different corneal dystrophies, DNA was extracted from leukocytes of the peripheral blood and mutation analysis was performed by direct sequencing of the TGFBI gene. Clinical and histopathological findings were compared with the molecular genetic findings for genotype-phenotype correlations. Results In 6 patients (2 families/one single person) with clinical and histopathological CDL1 we found a Missense mutation Arg124Cys and in 7 patients (3 families/one single person) with clinical and histopathological CDA we found a Missense mutation Arg124His in the exon 4 of the TGFBI gene. In 12 patients (4 families/2 single persons) with clinical and histopathological CDGG1 we found a Missense mutation Arg555Trypt in the codon 12 of the TGFBI gene. In all five patients (1 family/4 single persons) with clinical and histopathological CDB2 we could not find any mutation in the TGFBI gene. In one patient with exceptional clinical and histopathological findings we found a Missense mutation Ala546Asp, which was reported before only twice in connection with polymorphous corneal amyloidosis. Conclusions In comparison of our clinical and histopathological findings and the molecular genetic results we found a strong genotype-phenotype correlation in patients with TGFBI-linked corneal dystrophies. Rare mutations can lead to exceptional clinical and histopathological findings which cannot be classified into the different groups of corneal dystrophies. In our patients with CDB2 we could not find any molecular genetic correlation to the TGFBI gene.
Published: 2006
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43. Silikathaltige Harnsteine im Klinikalltag

Author: M. Seehafer, M. Wolter, C. Helke, Matthias May, Bernd Hoschke, and K. Kubenz
Subjects: Gynecology, medicine.medical_specialty, business.industry, Urology, Medicine, business
Abstract: Eine Steinbildung in den ableitenden Harnwegen ist immer Folge einer Ubersattigung harnsteinbildener Substanzen und der damit verbundenen vermehrten Kristallisation. Neben den typischen Harnsteinen, bestehend aus Kalziumoxalat, anorganischen Phosphaten, Harnsaure oder Zystin, gibt es immer wieder Hinweise auf seltene Substanzklassen. Obwohl in der internationalen Literatur bereits >50 silikathaltige Steine dargestellt wurden, ist diese Steinentitat weiterhin relativ unbekannt. Insbesondere das Auftreten von Silikatsteinen ohne den medikamentosen Abusus von Magnesiumtrisilikat stellt eine absolute Raritat dar.
Published: 2005
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44. Molekulargenetische Analyse des BIGH3-Gens bei gittriger Hornhautdystrophie Typ I (Biber-Haab-Dimmer) und bei bröckliger Hornhautdystrophie Typ II (Avellino): Erlauben Hot Spots einen indirekten Mutationsnachweis?

Author: Claudia Grünauer-Kloevekorn, M Wolter-Roessler, E Weidle, Ursula G. Froster, S Bräutigam, Giw Duncker, and F. Tost
Subjects: Genetics, Ophthalmology, Restriction enzyme, Exon, Point mutation, Mutation testing, medicine, Missense mutation, Corneal dystrophy, Restriction digest, Biology, medicine.disease, Gene
Abstract: Background Mutations of the BIGH3 gene were delineated as the underlying gene defect for corneal dystrophy Lattice Type I (CDL1) and corneal dystrophy Avellino type (CDA) in families with different regional provenance. Missense mutations in exon 4 with single base pair substitution which result in amino acid alterations Arg124Cys (CDL1) and ARG124His are described as hot spots. We report on histopathological and molecular genetic investigations in 2 German families and a single patient with CDL1 and CDA. Method In 3 affected family members and 1 unaffected family member and in one single patient with CDL1 and in 3 affected family members and 1 unaffected family member of a family with CDA mutation analysis in exon 4 of BIGH3 gene by direct sequencing of genomic DNA from peripheral blood was performed. Histopathological examination of corneal tissue of both index patients was performed after penetrating keratoplasty. Results We revealed a heterozygous single base pair substitution 417C-->T in family A and patient B (CDL1) and a heterozygous single base pair substitution 418G-->A in family C (CDA). In all index patient's diagnosis was confirmed by histopathological examination of corneal tissue. The sequencing results were confirmed by restriction digestion with HpyCH4V (NEB; CDL1) restriction endonuclease site and AvaII (NEB; CDA) restriction endonuclease site. The heterozygous 417C-->T transition in family A and patient B alters the amino acid sequence from Arg124Cys while the heterozygous 418G-->A transition in family C alters the amino acid sequence from Arg124His in the keratoepithelin. Comment Codon 124 of the BIGH3 gene appears as a mutation hot spot also in German families with CDL1 and CDA. Indirect mutation analysis with restriction digestion is suggested as first step investigation in families with relevant corneal dystrophies. Direct sequencing of all exons is recommended as a second step if there are no results in restriction digestion.
Published: 2005
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45. Performance of unpassivated AlGaN/GaN/SiC HEMTs after short-term electrical bias stress

Author: A. Fox, Michel Marso, J. Bernat, Peter Kordos, P. Javorka, and M. Wolter
Subjects: Materials science, Passivation, business.industry, Transconductance, Biasing, High-electron-mobility transistor, Condensed Matter Physics, Electronic, Optical and Magnetic Materials, Stress (mechanics), Materials Chemistry, Optoelectronics, Metalorganic vapour phase epitaxy, Electrical and Electronic Engineering, business, Power density, Voltage
Abstract: Performance of unpassivated MOVPE grown AlGaN/GaN/SiC HEMTs under short-term electrical bias stress is reported. Insignificant degradation in DC and RF behaviour of prepared devices after 16 h stress at V D =21 V and V G =−2.5 V is observed. This can be demonstrated by a maximum drain current of 1.03 and 1.01 A/mm and a peak extrinsic transconductance of 233 and 225 mS/mm before and after bias stress, respectively. Consecutive drain voltage sweeps indicates on low current collapse in samples investigated. The RF characteristics show a decrease of the f max -to- f T ratio from 2.23 to 2.15 and the saturated output power density measured at 2 GHz from 3.60 to 3.53 W/mm after the devices were stressed. This result indicates that reliable AlGaN/GaN/SiC HEMTs without passivation can be prepared. However, additional studies are needed to understand if the material structure and/or the device processing is responsible for low current collapse and RF dispersion in these devices.
Published: 2004
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46. Investigation of traps in AlGaN/GaN HEMTs on silicon substrate

Author: P. Javorka, Hans Lüth, M. Wolter, J. Bernát, Michel Marso, Peter Kordos, and Reinhard Carius
Subjects: Materials science, Deep-level transient spectroscopy, Silicon, business.industry, Relaxation (NMR), chemistry.chemical_element, Heterojunction, Substrate (electronics), Trapping, Photoionization, chemistry, Optoelectronics, business, Spectroscopy
Abstract: Deep levels in AlGaN/GaN heterostructures are known to be responsible for trapping processes like current collapse or dispersion. In order to investigate these processes we performed different measurements on HEMTs fabricated with heterostructures grown on silicon substrate. First by photoionization spectroscopy we found three different traps with activation energies of about 2.1 eV, 2.9 eV and 3.2 eV. Secondly, the temperature dependent relaxation of the drain current was investigated by the backgating current deep level transient spectroscopy (DLTS) method. Hereby we detected majority and minority carrier traps in the GaN buffer at the energies EV + 0.41 eV and EC – 0.55 eV, respectively. The latter energy can be attributed to the well known “E2” level in GaN.
Published: 2003
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47. Influence of doping concentration on DC and RF performance of AlGaN/GaN HEMTs on silicon substrate

Author: Michel Marso, J. Bernat, A. Fox, Holger Kalisch, Peter Javorka, C. Schäfer, Michael Heuken, A. v. d. Hart, Peter Kordos, M. Wolter, Bernd Schineller, Rolf H. Jansen, Hans Lüth, and Y. Dikme
Subjects: Materials science, business.industry, Aluminium nitride, Doping, Transistor, Analytical chemistry, Heterojunction, Gallium nitride, High-electron-mobility transistor, Condensed Matter Physics, Electronic, Optical and Magnetic Materials, law.invention, chemistry.chemical_compound, chemistry, law, Hall effect, Optoelectronics, business, Leakage (electronics)
Abstract: AlGaN/GaN HEMTs with different carrier supply layers are fabricated on Si substrate, using MOVPE growth technique. The influence of the carrier supply doping concentration on the HEMT properties is investigated by Hall measurements and by electrical DC and RF characterisation of transistor devices. Hall mobility is found to decrease with increasing sheet concentration, while the gate leakage current increases. The device with the highest carrier supply doping concentration of 1019 cm−3 is provided with a GaN cap layer to reduce gate leakage. The transistors based on modulation doped layer structures show much higher DC performance than the undoped device. Best RF properties are obtained for a doping level of 5 × 1018 cm−3. High frequency measurements exhibit fT and fMAX values of 35 GHz and 37 GHz, respectively, for devices with 300 nm gate length. (© 2003 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim)
Published: 2003
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48. Mannose-binding lectin gene polymorphism predicts hospital admissions for COPD infections

Author: E M Anders, Kwun M. Fong, J. M. Wolter, G. C. Rabnott, S. T. Kim, Paul Zimmerman, A. M. Tunnicliffe, Annette Dent, Ian A. Yang, Janet G. Shaw, S. L. Seeney, and Joseph G. McCormack
Subjects: Adult, Male, Exacerbation, Immunology, Polymorphism (biology), chemical and pharmacologic phenomena, Biology, Mannose-Binding Lectin, Cystic fibrosis, Pulmonary Disease, Chronic Obstructive, Predictive Value of Tests, Genotype, Genetics, medicine, Humans, Genetic Predisposition to Disease, Genetics (clinical), Aged, Mannan-binding lectin, Aged, 80 and over, COPD, Polymorphism, Genetic, Respiratory infection, Middle Aged, bacterial infections and mycoses, medicine.disease, respiratory tract diseases, Hospitalization, Amino Acid Substitution, Female, Gene polymorphism
Abstract: Infection frequently causes exacerbations of chronic obstructive pulmonary disease (COPD). Mannose-binding lectin (MBL) is a pattern-recognition receptor that assists in clearing microorganisms. Polymorphisms in the MBL2 gene reduce serum MBL levels and are associated with risk of infection. We studied whether the MBL2 codon 54 B allele affected serum MBL levels, admissions for infective exacerbation in COPD and disease susceptibility. Polymorphism frequency was determined by PCR-RFLP in 200 COPD patients and 104 smokers with normal lung function. Serum MBL was measured as mannan-binding activity in a subgroup of 82 stable COPD patients. Frequency of COPD admissions for infective exacerbation was ascertained for a 2-year period. The MBL2 codon 54 B allele reduced serum MBL in COPD patients. In keeping, patients carrying the low MBL-producing B allele had increased risk of admission for infective exacerbation (OR 4.9, P(corrected)=0.011). No association of MBL2 genotype with susceptibility to COPD was detected. In COPD, serum MBL is regulated by polymorphism at codon 54 in its encoding gene. Low MBL-producing genotypes were associated with more frequent admissions to hospital with respiratory infection, suggesting that the MBL2 gene is disease-modifying in COPD. MBL2 genotype should be explored prospectively as a prognostic marker for infection risk in COPD.
Published: 2003
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49. Reliability of the Uncertified Ballots in the 2000 Presidential Election in Florida

Author: Joe Murphy, Whitney Moore, Kirk M. Wolter, Diana Jergovic, and Colm O'Muircheartaigh
Subjects: Statistics and Probability, Presidential system, Presidential election, General Mathematics, media_common.quotation_subject, ComputingMilieux_LEGALASPECTSOFCOMPUTING, Public administration, Supreme court, Consistency (negotiation), State (polity), Voting, Political science, Statistics, Probability and Uncertainty, Research center, Reliability (statistics), media_common
Abstract: Following one of the most closely contested elections in American history, a group of the nation's largest media organizations retained the National Opinion Research Center (NORC) to conduct an in-depth inventory of all uncounted ballots from the 2000 presidential race in Florida. This article describes the planning and implementation of the project and its resulting databases. The State of Florida employed three major voting systems for the election: two systems based on punch cards, and various optical scanning systems. We analyze and present statistics regarding the reliability of the various voting systems. Although none are perfect, we generally found optical scanning to be superior to the punch card systems. We summarize analyses of project databases conducted by the Media Group with respect to new vote totals that hypothetically might have been achieved had the U.S. Supreme Court not stopped the vote counting. We offer recommendations to policy makers for future elections.
Published: 2003
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50. Mammasonographische Dignitätskriterien unter besonderer Berücksichtigung der Tumorgröße

Author: K. L. Marquet, R. Stressig, W. Rath, P. Kozlowski, S. Handt, A. Funk, and M. Wolter
Subjects: medicine.medical_specialty, medicine.diagnostic_test, business.industry, Echogenicity, Retrospective cohort study, Malignancy, medicine.disease, Acoustic shadow, Palpation, Surgery, Breast cancer, Predictive value of tests, Medicine, Mammography, Radiology, Nuclear Medicine and imaging, Radiology, business
Abstract: Aim Ongoing technical progress has increased the accuracy of imaging in ultrasound mammography. Using a 10-MHz-transducer, eight different criteria of dignity were evaluated for validity, also with regard to the size of a tumor. Materials and methods Over a period of three years, 446 breast tumors were ultrasonographically examined by two experienced medical doctors. The study comprised only suspicious lesions detected by mammography and/or manual palpation. Diagnostic validity was quantified by means of sensitivity, specificity, positive and negative predictive value, as well as the ODDS-ratio. Results Ultrasound mammography demonstrated a sensitivity of 94.0 %, specificity of 91.4 %, positive predictive value of 95.9 %, and a negative predictive value of 99.1 %. Eight different sonographic criteria were validated separately. The most important signs of malignancy were (in descending order): a highly echogenic halo, spikes, jagged contour, posterior acoustic shadowing, and discontinuity of tissue structure. Features of benign disease were: smooth edge, posterior acoustic enhancement, displacement margin, bilateral acoustic shadowing and continuity of tissue structure. Furthermore, it appeared that the size of a tumor only had consequences on posterior shadowing (p = 0.017). All other features did not show significant variation in relation to tumor size. Conclusion We were able to prove that ultrasound mammography is an excellent medium for the differentiation of benign and malignant breast lesions, when precise indication criteria were adhered to, even in cases of small tumor size.
Published: 2003
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