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1. CIBRA identifies genomic alterations with a system-wide impact on tumor biology.

Author: Lakbir, Soufyan, Buranelli, Caterina, Meijer, Gerrit A, Heringa, Jaap, Fijneman, Remond J A, and Abeln, Sanne
Subjects: TRANSCRIPTOMES, METASTASIS, BIOMARKERS, BIOLOGY, GENOMICS
Abstract: Motivation Genomic instability is a hallmark of cancer, leading to many somatic alterations. Identifying which alterations have a system-wide impact is a challenging task. Nevertheless, this is an essential first step for prioritizing potential biomarkers. We developed CIBRA (Computational Identification of Biologically Relevant Alterations), a method that determines the system-wide impact of genomic alterations on tumor biology by integrating two distinct omics data types: one indicating genomic alterations (e.g. genomics), and another defining a system-wide expression response (e.g. transcriptomics). CIBRA was evaluated with genome-wide screens in 33 cancer types using primary and metastatic cancer data from the Cancer Genome Atlas and Hartwig Medical Foundation. Results We demonstrate the capability of CIBRA by successfully confirming the impact of point mutations in experimentally validated oncogenes and tumor suppressor genes (0.79 AUC). Surprisingly, many genes affected by structural variants were identified to have a strong system-wide impact (30.3%), suggesting that their role in cancer development has thus far been largely under-reported. Additionally, CIBRA can identify impact with only 10 cases and controls, providing a novel way to prioritize genomic alterations with a prominent role in cancer biology. Our findings demonstrate that CIBRA can identify cancer drivers by combining genomics and transcriptomics data. Moreover, our work shows an unexpected substantial system-wide impact of structural variants in cancer. Hence, CIBRA has the potential to preselect and refine current definitions of genomic alterations to derive more nuanced biomarkers for diagnostics, disease progression, and treatment response. Availability and implementation The R package CIBRA is available at https://github.com/AIT4LIFE-UU/CIBRA. [ABSTRACT FROM AUTHOR]
Published: 2024
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2. Exploratory Analysis of the Economically Justifiable Price of a Hypothetical RSV Vaccine for Older Adults in the Netherlands and the United Kingdom

Author: Zeevat, F, Luttjeboer, J, Paulissen, J H J, van der Schans, J, Beutels, P, Boersma, C, Postma, M J, Nair, Harish, Campbell, Harry, Openshaw, Peter, Beutels, Philippe, Bont, Louis, Pollard, Andrew, Molero, Eva, Martinon-Torres, Federico, Heikkinen, Terho, Meijer, Adam, Kølsen Fischer, Thea, van den Berge, Maarten, Giaquinto, Carlo, Kieffer, Alexia, Demont, Clarisse, Gallichan, Scott, Dormitzer, Philip, Leach, Amanda, Dillon, Laura, Aerssens, Jeroen, Rosen, Brian, RESCEU Investigators, Value, Affordability and Sustainability (VALUE), Real World Studies in PharmacoEpidemiology, -Genetics, -Economics and -Therapy (PEGET), and Microbes in Health and Disease (MHD)
Subjects: Rsv vaccine, business.industry, Cost effectiveness, Incidence (epidemiology), MEDLINE, The Netherlands, Exploratory analysis, United Kingdom, Vaccination, Infectious Diseases, Elderly, Older adults, Preventive intervention, Immunology and Allergy, Medicine, Cost-effectiveness, Human medicine, Respiratory Syncytial Virus, business, Biology, health care economics and organizations, RSV Vaccines, Demography
Abstract: Background In older adults, the burden of respiratory syncytial virus (RSV) resembles that of influenza and may even be considered worse due to the lack of preventive interventions. This study was performed to identify the available literature on RSV infection in older adults, and to provide updated exploratory results of the cost-effectiveness of a hypothetical RSV vaccine in the Netherlands and the United Kingdom. Methods A literature search was performed in Medline and EMBASE on 11 November 2019, which served as input for a static decision-tree model that was used to estimate the EJP, for an RSV vaccine applying different willingness-to-pay (WTP) thresholds. WTP thresholds applied were €20 000 and €50 000 per quality-adjusted life-year for the Netherlands, and £20 000 and £30 000 per quality-adjusted life-year for the United Kingdom. Analyses were—in line with country-specific guidelines—conducted from a societal perspective for the Netherlands and a third-party payer perspective for the United Kingdom. The robustness of the cost-effectiveness results was tested in sensitivity analysis. Results After screening the literature, 3 studies for the Netherlands and 6 for the United Kingdom remained to populate the country-specific models. In the base case analysis for the Netherlands (mean RSV incidence, 3.32%), justifiable vaccine prices of €16.38 and €50.03 were found, based on applying the lower and higher WTP thresholds, respectively. Similarly, for the United Kingdom (mean incidence, 7.13%), vaccine prices of £72.29 and £109.74 were found, respectively. Conclusion RSV vaccination may well be cost-effective in both the Netherlands and the United Kingdom, depending on the exact RSV incidence, vaccine effectiveness and price. However, sensitivity analysis showed that the results were robust based on varying the different parameter estimates and assumptions. With RSV vaccines reaching the final stages of development, a strong need exists for cost-effectiveness studies to understand economically justifiable pricing of the vaccine.
Published: 2022

3. Inactivation of the dimeric RappLS20 anti-repressor of the conjugation operon is mediated by peptide-induced tetramerization

Author: Juan Román Luque-Ortega, Wilfried J. J. Meijer, Andrés Miguel-Arribas, Isidro Crespo, Dirk Roeland Boer, Marc Malfois, Praveen K. Singh, Nerea Bernardo, Carlos Alfonso, Ministerio de Economía y Competitividad (España), Fundación Ramón Areces, Banco Santander, Crespo, Isidro, Miguel-Arribas, Andrés, Singh, Praveen Kumar, Alfonso, Carlos, Malfois, Marc, Meijer, Wilfried J. J., Boer, Roeland, Crespo, Isidro [0000-0001-7698-1720], Miguel-Arribas, Andrés [0000-0001-5679-9083], Singh, Praveen Kumar [0000-0002-0254-7400], Alfonso, Carlos [0000-0001-7165-4800], Malfois, Marc [0000-0001-5231-1896], Meijer, Wilfried J. J. [0000-0003-1842-0049], and Boer, Roeland [0000-0001-5949-6627]
Subjects: Cell signaling, AcademicSubjects/SCI00010, Operon, Effector, Bacterial conjugation, fungi, Repressor, Gene Expression Regulation, Bacterial, Biology, Cell biology, Tetratricopeptide, Quorum sensing, Bacterial Proteins, Structural Biology, Conjugation, Genetic, Trans-Activators, Genetics, Tetratricopeptide Repeat, Protein Multimerization, Signal transduction, Peptides, Promoter Regions, Genetic, Bacillus subtilis
Abstract: 15 p.-4 fig.-3 tab., Quorum sensing allows bacterial cells to communicate through the release of soluble signaling molecules into the surrounding medium. It plays a pivotal role in controlling bacterial conjugation in Gram-positive cells, a process that has tremendous impact on health. Intracellular regulatory proteins of the RRNPP family are common targets of these signaling molecules. The RRNPP family of gene regulators bind signaling molecules at their C-terminal domain (CTD), but have highly divergent functionalities at their N-terminal effector domains (NTD). This divergence is also reflected in the functional states of the proteins, and is highly interesting from an evolutionary perspective. RappLS20 is an RRNPP encoded on the Bacillus subtilis plasmid pLS20. It relieves the gene repression effectuated by RcopLS20 in the absence of the mature pLS20 signaling peptide Phr*pLS20. We report here an in-depth structural study of apo and Phr*pLS20-bound states of RappLS20 at various levels of atomic detail. We show that apo-RappLS20 is dimeric and that Phr*pLS20-bound Rap forms NTD-mediated tetramers. In addition, we show that RappLS20 binds RcopLS20 directly in the absence of Phr*pLS20 and that addition of Phr*pLS20 releases RcopLS20 from RappLS20. This allows RcopLS20 to bind the promotor region of crucial conjugation genes blocking their expression., Ministry of Economy and Competitiveness of the Spanish Government [BFU2016-75471-C2-1-P (AEI/FEDER,EU) to C.A., BIO2013-41489-P (AEI/FEDER, EU) to W.M. which also funded AM-A, BIO2016-77883-C2-2-P (AEI/FEDER, EU) to R.B., BIO2016-77883-C2-2-P(AEI/FEDER, EU) also supported N.B.]; ‘Fundación Ramón Areces’ and ‘Banco de Santander’ to the Centro de Biología Molecular ‘Severo Ochoa’.Funding for open access charge: Ministry of Economy and Competitiveness of the Spanish Government [BIO2016-77883-C2-1-P and BIO2016-77883-C2-2-P].
Published: 2020
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4. CombiFlow

Author: Jan Jacob Schuringa, Bauke de Boer, Andre B. Mulder, Nisha van der Meer, Shanna M. Hogeling, Roos Houtsma, Marije T. Nijk, Linde M. Morsink, Kees Meijer, Gerwin Huls, Carolien M. Woolthuis, Emanuele Ammatuna, Stem Cell Aging Leukemia and Lymphoma (SALL), and Guided Treatment in Optimal Selected Cancer Patients (GUTS)
Subjects: Cell, Interleukin-3 Receptor alpha Subunit, MINIMAL RESIDUAL DISEASE, Disease, Computational biology, ACUTE MYELOID-LEUKEMIA, Biology, RELAPSE, Somatic evolution in cancer, Clonal Evolution, Track disease, hemic and lymphatic diseases, medicine, Humans, In patient, TRANSCRIPTOMICS, HETEROGENEITY, RISK, CELL TRANSPLANTATION, Cell Membrane, Myeloid leukemia, Hematology, Clone Cells, Leukemia, Myeloid, Acute, medicine.anatomical_structure, Expression data, PROTEOMICS, Interleukin-3 receptor
Abstract: Acute myeloid leukemia (AML) often presents as an oligoclonal disease whereby multiple genetically distinct subclones can coexist within patients. Differences in signaling and drug sensitivity of such subclones complicate treatment and warrant tools to identify them and track disease progression. We previously identified >50 AML-specific plasma membrane (PM) proteins, and 7 of these (CD82, CD97, FLT3, IL1RAP, TIM3, CD25, and CD123) were implemented in routine diagnostics in patients with AML (n = 256) and myelodysplastic syndrome (n = 33). We developed a pipeline termed CombiFlow in which expression data of multiple PM markers is merged, allowing a principal component–based analysis to identify distinctive marker expression profiles and to generate single-cell t-distributed stochastic neighbor embedding landscapes to longitudinally track clonal evolution. Positivity for one or more of the markers after 2 courses of intensive chemotherapy predicted a shorter relapse-free survival, supporting a role for these markers in measurable residual disease (MRD) detection. CombiFlow also allowed the tracking of clonal evolution in paired diagnosis and relapse samples. Extending the panel to 36 AML-specific markers further refined the CombiFlow pipeline. In conclusion, CombiFlow provides a valuable tool in the diagnosis, MRD detection, clonal tracking, and understanding of clonal heterogeneity in AML.
Published: 2022
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5. Economic Burden and Health-Related Quality of Life of Respiratory Syncytial Virus and Influenza Infection in European Community-Dwelling Older Adults

Author: Mao, Zhuxin, Li, Xiao, Korsten, Koos, Bont, Louis, Butler, Christopher, Wildenbeest, Joanne, Coenen, Samuel, Hens, Niel, Bilcke, Joke, Beutels, Philippe, Nair, Harish, Campbell, Harry, Pollard, Andrew, Openshaw, Peter, Martinon-Torres, Federico, Heikkinen, Terho, Meijer, Adam, Fischer, Thea K, van den Berge, Maarten, Giaquinto, Carlo, Abram, Michael, Swanson, Kena, Rizkalla, Bishoy, Vernhes, Charlotte, Gallichan, Scott, Aerssens, Jeroen, Kumar, Veena, Molero, Eva, Coenen, Samuel/0000-0002-1238-8052, Mao, Zhuxin, Li, Xiao, Korsten, Koos, BONTE, Luis, Butler, Christopher, Wildenbeest, Joanne, COENEN, Samuel, HENS, Niel, Bilcke, Joke, Beutels, Philippe, and RESCEU Investigators
Subjects: Financial Stress, Respiratory Syncytial Virus Infections, elderly, cost, EQ5D, Influenza, Human, Humans, Immunology and Allergy, Biology, Aged, flu, RSV, Middle Aged, outpatients, health-related quality of life, Hospitalization, productivity loss, Infectious Diseases, Respiratory Syncytial Virus, Human, influenza, prospective study, Independent Living, Quality of Life, Human medicine, Respiratory Syncytial Virus, costproductivity loss, Human
Abstract: Background Respiratory syncytial virus (RSV) and influenza virus infections result in a considerable mortality and morbidity among the aging population globally. Influenza vaccination for older adults before the seasonal influenza epidemic has been evaluated to be cost-effective in many countries. Interventions against RSV in older adults are in the pipeline, and evaluating their cost-effectiveness is crucial for decision making. To inform such evaluations, our aim was to estimate average costs and health-related quality of life (HRQoL) in older adults with RSV and influenza infection. Methods The European RESCEU observational cohort study followed 1040 relatively healthy community-dwelling older adults aged 60 years and older during 2 consecutive winter seasons. Health care resource use and HRQoL were collected and analyzed during RSV episodes, and also during influenza episodes. Country-specific unit cost data were mainly obtained from national databases. Direct costs were estimated from a patient, health care provider, and health care payers’ perspective, whereas indirect costs were estimated from a societal perspective. Due to small sample size, no formal statistical comparisons were made. Results Thirty-six RSV and 60 influenza episodes were reported, including 1 hospitalization. Means (median; first-third quartile) of €26.4 (€5.5; 0–47.3) direct and €4.4 (€0; 0–0) indirect costs were reported per nonhospitalized RSV episode, and €42.5 (€36; 3.3–66.7) direct and €32.1 (€0; 0–0) indirect costs per nonhospitalized influenza episode. For RSV episodes, the utility value decreased from 0.896 (0.928; 0.854–0.953) to 0.801 (0.854; 0.712–0.937) from preseason to 1 week after symptom onset; for influenza, the change was from 0.872 (0.895; 0.828–0.953) to 0.664 (0.686; 0.574–0.797). Conclusions The average costs and HRQoL estimates of older adults treated outside the hospital can be used to inform the design of future studies and the decision making regarding interventions to prevent RSV infection in older adults. Larger studies are needed to provide better country-specific and complementary cost estimates and to allow for formal statistical comparison of costs between RSV and influenza. Clinical Trials Registration NCT03621930.
Published: 2022
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6. Cost-effectiveness of Respiratory Syncytial Virus Disease Prevention Strategies: Maternal Vaccine Versus Seasonal or Year-Round Monoclonal Antibody Program in Norwegian Children

Author: Li, Xiao, Bilcke, Joke, Vázquez Fernández, Liliana, Bont, Louis, Willem, Lander, Wisløff, Torbjørn, Jit, Mark, Beutels, Philippe, Nair, Harish, Campbell, Harry, Pollard, Andrew, Openshaw, Peter, Martinon-Torres, Federico, Heikkinen, Terho, Meijer, Adam, Fischer, Thea K, van den Berge, Maarten, Giaquinto, Carlo, Abram, Michael, Swanson, Kena, Rizkalla, Bishoy, Vernhes, Charlotte, Gallichan, Scott, Aerssens, Jeroen, Kumar, Veena, Molero, Eva, and REsp Syncytial Virus Consortium EU (RESCEU)
Subjects: Vaccines, Cost-Benefit Analysis, Infant, Newborn, Antibodies, Monoclonal, Infant, Respiratory Syncytial Virus Infections, Antibodies, Monoclonal, Humanized, Antiviral Agents, Communicable Diseases, Respiratory Syncytial Viruses, Infectious Diseases, Child, Preschool, Humans, Immunology and Allergy, Seasons, Human medicine, Child, Biology, Palivizumab
Abstract: Background Every winter, respiratory syncytial virus (RSV) disease results in thousands of cases in Norwegian children under 5 years of age. We aim to assess the RSV-related economic burden and the cost-effectiveness of upcoming RSV disease prevention strategies including year-round maternal immunization and year-round and seasonal monoclonal antibody (mAb) programs. Methods Epidemiological and cost data were obtained from Norwegian national registries, while quality-adjusted life-years (QALYs) lost and intervention characteristics were extracted from literature and phase 3 clinical trials. A static model was used and uncertainty was accounted for probabilistically. Value of information was used to assess decision uncertainty. Extensive scenario analyses were conducted, including accounting for long-term consequences of RSV disease. Results We estimate an annual average of 13 517 RSV cases and 1572 hospitalizations in children under 5, resulting in 79.6 million Norwegian kroner (~€8 million) treatment costs. At €51 per dose for all programs, a 4-month mAb program for neonates born in November to February is the cost-effective strategy for willingness to pay (WTP) values up to €40 000 per QALY gained. For higher WTP values, the longer 6-month mAb program that immunizes neonates from October to March becomes cost-effective. Sensitivity analyses show that year-round maternal immunization can become a cost-effective strategy if priced lower than mAb. Conclusions Assuming the same pricing, seasonal mAb programs are cost-effective over year-round programs in Norway. The timing and duration of the cost-effective seasonal program are sensitive to the pattern of the RSV season in a country, so continued RSV surveillance data are essential.
Published: 2022
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7. Implementation of Pericytes in Vascular Regeneration Strategies

Author: Marianne C. Verhaar, Christian G. M. van Dijk, Rafael Kramann, Elana Marianne Meijer, Caroline Cheng, Internal Medicine, and Cardiology
Subjects: Neovascularization, Pathologic, Tissue Engineering, Angiogenesis, Regeneration (biology), Biomedical Engineering, Cell Differentiation, Bioengineering, Biology, Biochemistry, Mural cell, Cell biology, Biomaterials, Vascular tissue engineering, Humans, Oxygen diffusion, Pericytes, Cell survival
Abstract: For the survival and integration of complex large-sized tissue-engineered (TE) organ constructs that exceed the maximal nutrients and oxygen diffusion distance required for cell survival, graft (pre)vascularization to ensure medium or blood supply is crucial. To achieve this, the morphology and functionality of the microcapillary bed should be mimicked by incorporating vascular cell populations, including endothelium and mural cells. Pericytes play a crucial role in microvascular function, blood vessel stability, angiogenesis, and blood pressure regulation. In addition, tissue-specific pericytes are important in maintaining specific functions in different organs, including vitamin A storage in the liver, renin production in the kidneys and maintenance of the blood-brain-barrier. Together with their multipotential differentiation capacity, this makes pericytes the preferred cell type for application in TE grafts. The use of a tissue-specific pericyte cell population that matches the TE organ may benefit organ function. In this review, we provide an overview of the literature for graft (pre)-vascularization strategies and highlight the possible advantages of using tissue-specific pericytes for specific TE organ grafts. Impact statement The use of a tissue-specific pericyte cell population that matches the tissue-engineered (TE) organ may benefit organ function. In this review, we provide an overview of the literature for graft (pre)vascularization strategies and highlight the possible advantages of using tissue-specific pericytes for specific TE organ grafts.
Published: 2022
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8. Demographic changes in Pleistocene sea turtles were driven by past sea level fluctuations affecting feeding habitat availability

Author: Sietske van der Wal, Tadzio Bervoets, Marjolijn J. A. Christianen, Mabel Nava, Leontine E. Becking, Jessica Berkel, Per J. Palsbøll, Melanie Meijer Zu Schlochtern, Martine Bérubé, Jurjan van der Zee, Genomics Research in Ecology & Evolution in Nature, Palsbøll lab, and Marine Biology
Subjects: Aquatic Ecology and Water Quality Management, Pleistocene, Population, Population Dynamics, Biodiversity, Biology, Onderz. Form. D, Aquaculture and Fisheries, demographic change, Genetics, Animals, Glacial period, education, skin and connective tissue diseases, Ecology, Evolution, Behavior and Systematics, Ecosystem, ddRAD sequencing, geography, education.field_of_study, geography.geographical_feature_category, WIMEK, Ecology, Coral Reefs, Aquacultuur en Visserij, fungi, Pleistocene sea turtles, Marine habitats, habitat availability, Coral reef, Aquatische Ecologie en Waterkwaliteitsbeheer, Turtles, Habitat destruction, Habitat, WIAS, sense organs, sea level change
Abstract: Pleistocene environmental changes are generally assumed to have dramatically affected species’ demography via changes in habitat availability, but this is challenging to investigate due to our limited knowledge of how Pleistocene ecosystems changed through time. Here, we tracked changes in shallow marine habitat availability resulting from Pleistocene sea level fluctuations throughout the last glacial cycle (120–14 thousand years ago; kya) and assessed correlations with past changes in genetic diversity inferred from genome-wide SNPs, obtained via ddRAD sequencing, in Caribbean hawksbill turtles, which feed in coral reefs commonly found in shallow tropical waters. We found sea level regression resulted in an average 75% reduction in shallow marine habitat availability during the last glacial cycle. Changes in shallow marine habitat availability correlated strongly with past changes in hawksbill turtle genetic diversity, which gradually declined to ~1/4th of present-day levels during the Last Glacial Maximum (LGM; 26–19 kya). Shallow marine habitat availability and genetic diversity rapidly increased after the LGM, signifying a population expansion in response to warming environmental conditions. Our results suggest a positive correlation between Pleistocene environmental changes, habitat availability and species’ demography, and that demographic changes in hawksbill turtles were potentially driven by feeding habitat availability. However, we also identified challenges associated with disentangling the potential environmental drivers of past demographic changes, which highlights the need for integrative approaches. Our conclusions underline the role of habitat availability on species’ demography and biodiversity, and that the consequences of ongoing habitat loss should not be underestimated.
Published: 2022
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9. Selective targeting BMP2 and 4 in SMAD4 negative esophageal adenocarcinoma inhibits tumor growth and aggressiveness in preclinical models

Author: Shulin, Li, Sanne J M, Hoefnagel, Matthew, Read, Sybren, Meijer, Mark I, van Berge Henegouwen, Suzanne S, Gisbertz, Elena, Bonora, David S H, Liu, Wayne A, Phillips, Silvia, Calpe, Ana C P, Correia, Maria D C, Sancho-Serra, Sandro, Mattioli, Kausilia K, Krishnadath, Surgery, CCA - Cancer biology and immunology, Esophageal Adenocarcinoma Study Group Europe (EACSGE), Graduate School, Amsterdam Gastroenterology Endocrinology Metabolism, Center of Experimental and Molecular Medicine, AII - Cancer immunology, Pathology, Gastroenterology and Hepatology, Li, Shulin, Hoefnagel, Sanne J M, Read, Matthew, Meijer, Sybren, van Berge Henegouwen, Mark I, Gisbertz, Suzanne S, Bonora, Elena, Liu, David S H, Phillips, Wayne A, Calpe, Silvia, Correia, Ana C P, Sancho-Serra, Maria D C, Mattioli, Sandro, and Krishnadath, Kausilia K
Subjects: Cancer Research, esophageal adenocarcinoma, Esophageal Neoplasms, anti-BMP antibodies, VHHs, BMP2, Bone Morphogenetic Protein 2, BMP4, Bone Morphogenetic Protein 4, Adenocarcinoma, SMAD4, Mice, Animals, Humans, Hedgehog Proteins, VHHs, Biology, Smad4 Protein, anti-BMP antibodies, VHH, Animal, General Medicine, Oncology, Molecular Medicine, anti-BMP antibodies, Human medicine, Hedgehog Protein, Human
Abstract: Purpose Abnormalities within the Sonic Hedgehog (SHH), Bone Morphogenetic Protein (BMP) and SMAD4 signalling pathways have been associated with the malignant behavior of esophageal adenocarcinoma (EAC). We recently developed two specific llama-derived antibodies (VHHs), C4C4 and C8C8, which target BMP4 and BMP2/4, respectively. Here we aimed to demonstrate the feasibility of the VHHs for the treatment of EAC and to elucidate its underlying mechanism. Methods Gene Set Enrichment Analysis (GSEA) was performed on a TCGA dataset, while expression of SHH, BMP2/4 and SMAD4 was validated in a cohort of EAC patients. The effects of the VHHs were tested on the recently established SMAD4(-) ISO76A primary EAC cell line and its counterpart SMAD4(+) ISO76A. In a patient-derived xenograft (PDX) model, the VHHs were evaluated for their ability to selectively target tumor cells and for their effects on tumor growth and survival. Results High expression of BMP2/4 was detected in all SMAD4 negative EACs. SHH upregulated BMP2/4 expression and induced p38 MAPK signaling in the SMAD4(-) ISO76A cells. Inhibition of BMP2/4 by VHHs decreased the aggressive and chemo-resistant phenotype of the SMAD4(-) ISO76A but not of the SMAD4(+) ISO76A cells. In the PDX model, in vivo imaging indicated that VHHs effectively targeted tumor cells. Both VHHs significantly inhibited tumor growth and acted synergistically with cisplatin. Furthermore, we found that C8C8 significantly improved survival of the mice. Conclusions Our data indicate that increased BMP2/4 expression triggers aggressive non-canonical BMP signaling in SMAD4 negative EAC. Inhibiting BMP2/4 decreases malignant behavior and improves survival. Therefore, VHHs directed against BMP2/4 hold promise for the treatment of SMAD4 negative EAC.
Published: 2022
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10. Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition) 1

Author: Klionsky, Daniel, Abdel-Aziz, Amal Kamal, Abdelfatah, Sara, Abdellatif, Mahmoud, Abdoli, Asghar, Abel, Steffen, Abeliovich, Hagai, Abildgaard, Marie, Abudu, Yakubu Princely, Acevedo-Arozena, Abraham, Adamopoulos, Iannis, Adeli, Khosrow, Adolph, Timon, Adornetto, Annagrazia, Aflaki, Elma, Agam, Galila, Agarwal, Anupam, Aggarwal, Bharat, Agnello, Maria, Agostinis, Patrizia, Agrewala, Javed, Agrotis, Alexander, Aguilar, Patricia, Ahmad, S Tariq, Ahmed, Zubair, Ahumada-Castro, Ulises, Aits, Sonja, Aizawa, Shu, Akkoc, Yunus, Akoumianaki, Tonia, Akpinar, Hafize Aysin, Al-Abd, Ahmed, Al-Akra, Lina, Al-Gharaibeh, Abeer, Alaoui-Jamali, Moulay, Alberti, Simon, Alcocer-Gómez, Elísabet, Alessandri, Cristiano, Ali, Muhammad, Alim Al-Bari, M Abdul, Aliwaini, Saeb, Alizadeh, Javad, Almacellas, Eugènia, Almasan, Alexandru, Alonso, Alicia, Alonso, Guillermo, Altan-Bonnet, Nihal, Altieri, Dario, Álvarez, Élida, Alves, Sara, Alves Da Costa, Cristine, Alzaharna, Mazen, Amadio, Marialaura, Amantini, Consuelo, Amaral, Cristina, Ambrosio, Susanna, Amer, Amal, Ammanathan, Veena, An, Zhenyi, Andersen, Stig, Andrabi, Shaida, Andrade-Silva, Magaiver, Andres, Allen, Angelini, Sabrina, Ann, David, Anozie, Uche, Ansari, Mohammad, Antas, Pedro, Antebi, Adam, Antón, Zuriñe, Anwar, Tahira, Apetoh, Lionel, Apostolova, Nadezda, Araki, Toshiyuki, Araki, Yasuhiro, Arasaki, Kohei, Araújo, Wagner, Araya, Jun, Arden, Catherine, Arévalo, Maria-Angeles, Arguelles, Sandro, Arias, Esperanza, Arikkath, Jyothi, Arimoto, Hirokazu, Ariosa, Aileen, Armstrong-James, Darius, Arnauné-Pelloquin, Laetitia, Aroca, Angeles, Arroyo, Daniela, Arsov, Ivica, Artero, Rubén, Asaro, Dalia Maria Lucia, Aschner, Michael, Ashrafizadeh, Milad, Ashur-Fabian, Osnat, Atanasov, Atanas, Au, Alicia, Auberger, Patrick, Auner, Holger, Aurelian, Laure, Autelli, Riccardo, Avagliano, Laura, Ávalos, Yenniffer, Aveic, Sanja, Aveleira, Célia Alexandra, Avin-Wittenberg, Tamar, Aydin, Yucel, Ayton, Scott, Ayyadevara, Srinivas, Azzopardi, Maria, Baba, Misuzu, Backer, Jonathan, Backues, Steven, Bae, Dong-Hun, Bae, Ok-Nam, Bae, Soo Han, Baehrecke, Eric, Baek, Ahruem, Baek, Seung-Hoon, Baek, Sung Hee, Bagetta, Giacinto, Bagniewska-Zadworna, Agnieszka, Bai, Hua, Bai, Jie, Bai, Xiyuan, Bai, Yidong, Bairagi, Nandadulal, Baksi, Shounak, Balbi, Teresa, Baldari, Cosima, Balduini, Walter, Ballabio, Andrea, Ballester, Maria, Balazadeh, Salma, Balzan, Rena, Bandopadhyay, Rina, Banerjee, Sreeparna, Banerjee, Sulagna, Bánréti, Ágnes, Bao, Yan, Baptista, Mauricio, Baracca, Alessandra, Barbati, Cristiana, Bargiela, Ariadna, Barilà, Daniela, Barlow, Peter, Barmada, Sami, Barreiro, Esther, Barreto, George, Bartek, Jiri, Bartel, Bonnie, Bartolome, Alberto, Barve, Gaurav, Basagoudanavar, Suresh, Bassham, Diane, Bast, Robert, Basu, Alakananda, Batoko, Henri, Batten, Isabella, Baulieu, Etienne, Baumgarner, Bradley, Bayry, Jagadeesh, Beale, Rupert, Beau, Isabelle, Beaumatin, Florian, Bechara, Luiz, Beck, George, Beers, Michael, Begun, Jakob, Behrends, Christian, Behrens, Georg, Bei, Roberto, Bejarano, Eloy, Bel, Shai, Behl, Christian, Belaid, Amine, Belgareh-Touzé, Naïma, Bellarosa, Cristina, Belleudi, Francesca, Belló Pérez, Melissa, Bello-Morales, Raquel, Beltran, Jackeline Soares de Oliveira, Beltran, Sebastián, Benbrook, Doris Mangiaracina, Bendorius, Mykolas, Benitez, Bruno, Benito-Cuesta, Irene, Bensalem, Julien, Berchtold, Martin, Berezowska, Sabina, Bergamaschi, Daniele, Bergami, Matteo, Bergmann, Andreas, Berliocchi, Laura, Berlioz-Torrent, Clarisse, Bernard, Amélie, Berthoux, Lionel, Besirli, Cagri, Besteiro, Sebastien, Betin, Virginie, Beyaert, Rudi, Bezbradica, Jelena, Bhaskar, Kiran, Bhatia-Kissova, Ingrid, Bhattacharya, Resham, Bhattacharya, Sujoy, Bhattacharyya, Shalmoli, Bhuiyan, Md Shenuarin, Bhutia, Sujit Kumar, Bi, Lanrong, Bi, Xiaolin, Biden, Trevor, Bijian, Krikor, Billes, Viktor, Binart, Nadine, Bincoletto, Claudia, Birgisdottir, Asa, Bjorkoy, Geir, Blanco, Gonzalo, Blas-Garcia, Ana, 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Anna, Hernández, Agustín, Hernandez, Carlos, Hernandez-Diaz, Sergio, Hernandez-Gea, Virginia, Herpin, Amaury, Herreros, Judit, Hervás, Javier, Hesselson, Daniel, Hetz, Claudio, Heussler, Volker, Higuchi, Yujiro, Hilfiker, Sabine, Hill, Joseph, Hlavacek, William, Ho, Emmanuel, Ho, Idy, Ho, Philip Wing-Lok, Ho, Shu-Leong, Ho, Wan Yun, Hobbs, G Aaron, Hochstrasser, Mark, Hoet, Peter, Hofius, Daniel, Hofman, Paul, Höhn, Annika, Holmberg, Carina, Hombrebueno, Jose, Yi-Ren Hong, Chang-Won Hong, Hooper, Lora, Hoppe, Thorsten, Horos, Rastislav, Hoshida, Yujin, Hsin, I-Lun, Hsu, Hsin-Yun, Hu, Bing, Hu, Dong, Hu, Li-Fang, Hu, Ming Chang, Hu, Ronggui, Hu, Wei, Hu, Yu-Chen, Hu, Zhuo-Wei, Hua, Fang, Hua, Jinlian, Hua, Yingqi, Huan, Chongmin, Huang, Canhua, Huang, Chuanshu, Huang, Chuanxin, Huang, Chunling, Huang, Haishan, Huang, Kun, Huang, Michael, Huang, Rui, Huang, Shan, Huang, Tianzhi, Huang, Xing, Huang, Yuxiang Jack, Huber, Tobias, Hubert, Virginie, Hubner, Christian, Hughes, Stephanie, 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Kazuyuki, Kuenen, Sabine, Kuerschner, Lars, Kukar, Thomas, Kumar, Ajay, Kumar, Ashok, Kumar, Deepak, Kumar, Dhiraj, Kumar, Sharad, Kume, Shinji, Kumsta, Caroline, Kundu, Chanakya, Kundu, Mondira, Kunnumakkara, Ajaikumar, Kurgan, Lukasz, Kutateladze, Tatiana, Kutlu, Ozlem, Kwak, SeongAe, Kwon, Ho Jeong, Kwon, Taeg Kyu, Kwon, Yong Tae, Kyrmizi, Irene, La Spada, Albert, Labonté, Patrick, Ladoire, Sylvain, Laface, Ilaria, Lafont, Frank, Lagace, Diane, Lahiri, Vikramjit, Lai, Zhibing, Laird, Angela, Lakkaraju, Aparna, Lamark, Trond, Lan, Sheng-Hui, Landajuela, Ane, Lane, Darius, Lane, Jon, Lang, Charles, Lange, Carsten, Langel, Ülo, Langer, Rupert, Lapaquette, Pierre, Laporte, Jocelyn, LaRusso, Nicholas, Lastres-Becker, Isabel, Lau, Wilson Chun Yu, Laurie, Gordon, Lavandero, Sergio, Law, Betty Yuen Kwan, Law, Helen Ka-wai, Layfield, Rob, Le, Weidong, Le Stunff, Herve, Leary, Alexandre, Lebrun, Jean-Jacques, Leck, Lionel, Leduc-Gaudet, Jean-Philippe, Lee, Changwook, Lee, Chung-Pei, Lee, Da-Hye, Lee, Edward, Lee, Erinna, Lee, Gyun Min, Lee, He-Jin, Lee, Heung Kyu, Lee, Jae Man, Lee, Jason, Lee, Jin-A, Lee, Joo-Yong, Lee, Jun Hee, Lee, Michael, Lee, Min Goo, Lee, Min Jae, Lee, Myung-Shik, Lee, Sang Yoon, Lee, Seung-Jae, Lee, Stella, Lee, Sung Bae, Lee, Won Hee, Lee, Ying-Ray, Lee, Yong-ho, Lee, Youngil, Lefebvre, Christophe, Legouis, Renaud, Lei, Yu, Lei, Yuchen, Leikin, Sergey, Leitinger, Gerd, Lemus, Leticia, Leng, Shuilong, Lenoir, Olivia, Lenz, Guido, Lenz, Heinz Josef, Lenzi, Paola, León, Yolanda, Leopoldino, Andréia, Leschczyk, Christoph, Leskelä, Stina, Letellier, Elisabeth, Leung, Chi-Ting, Leung, Po Sing, Leventhal, Jeremy, Levine, Beth, Lewis, Patrick, Ley, Klaus, Li, Bin, Li, Da-Qiang, Li, Jianming, Li, Jing, Li, Jiong, Li, Ke, Li, Liwu, Li, Mei, Li, Min, Li, Ming, Li, Mingchuan, Li, Pin-Lan, Li, Ming-Qing, Li, Qing, Li, Sheng, Li, Tiangang, Li, Wei, Li, Wenming, Li, Xue, Li, Yi-Ping, Li, Yuan, Li, Zhiqiang, Li, Zhiyong, Li, Zhiyuan, Lian, Jiqin, Liang, Chengyu, Liang, Qiangrong, Liang, Weicheng, Liang, Yongheng, Liang, YongTian, Liao, Guanghong, Liao, Lujian, Liao, Mingzhi, Liao, Yung-Feng, Librizzi, Mariangela, Lie, Pearl, Lilly, Mary, Lim, Hyunjung, Lima, Thania, Limana, Federica, Lin, Chao, Lin, Chih-Wen, Lin, Dar-Shong, Lin, Fu-Cheng, Lin, Jiandie, Lin, Kurt, Lin, Kwang-Huei, Lin, Liang-Tzung, LIN, Pei-Hui, Lin, Qiong, Lin, Shaofeng, Lin, Su-Ju, Lin, Wenyu, Lin, Xueying, Lin, Yao-Xin, Lin, Yee-Shin, Linden, Rafael, Lindner, Paula, Ling, Shuo-Chien, Lingor, Paul, Linnemann, Amelia, Liou, Yih-Cherng, Lipinski, Marta, Lipovšek, Saška, Lira, Vitor, Lisiak, Natalia, Liton, Paloma, Liu, Chao, Liu, Ching-Hsuan, Liu, Chun-Feng, Liu, Cui Hua, Liu, Fang, Liu, Hao, Liu, Hsiao-Sheng, Liu, Hua-feng, Liu, Huifang, Liu, Jia, Liu, Jing, Liu, Julia, Liu, Leyuan, Liu, Longhua, Liu, Meilian, Liu, Qin, Liu, Wei, Liu, Wende, Liu, Xiao-Hong, Liu, Xiaodong, Liu, Xingguo, Liu, Xu, Liu, Xuedong, Liu, Yanfen, Liu, Yang, Liu, Yueyang, Liu, Yule, Livingston, J Andrew, Lizard, Gerard, Lizcano, Jose, Ljubojevic-Holzer, Senka, LLeonart, Matilde, Llobet-Navàs, David, Llorente, Alicia, Lo, Chih Hung, Lobato-Márquez, Damián, Long, Qi, Long, Yun Chau, Loos, Ben, Loos, Julia, López, Manuela, López-Doménech, Guillermo, López-Guerrero, José Antonio, López-Jiménez, Ana, López-Pérez, Óscar, López-Valero, Israel, Lorenowicz, Magdalena, Lorente, Mar, Lorincz, Peter, Lossi, Laura, Lotersztajn, Sophie, Lovat, Penny, Lovell, Jonathan, Lovy, Alenka, Lőw, Péter, Lu, Guang, Lu, Haocheng, Lu, Jia-Hong, Lu, Jin-Jian, Lu, Mengji, Lu, Shuyan, Luciani, Alessandro, Lucocq, John, Ludovico, Paula, Luftig, Micah, Luhr, Morten, Luis-Ravelo, Diego, Lum, Julian, Luna-Dulcey, Liany, Lund, Anders, Lund, Viktor, Lünemann, Jan, Lüningschrör, Patrick, Luo, Honglin, Luo, Rongcan, Luo, Shouqing, Luo, Zhi, Luparello, Claudio, Lüscher, Bernhard, Luu, Luan, Lyakhovich, Alex, Lyamzaev, Konstantin, Lystad, Alf Håkon, Lytvynchuk, Lyubomyr, Ma, Alvin, Ma, Changle, Ma, Mengxiao, Ma, Ning-Fang, Ma, Quan-Hong, Ma, Xinliang, Ma, Yueyun, Ma, Zhenyi, MacDougald, Ormond, Macian, Fernando, MacIntosh, Gustavo, MacKeigan, Jeffrey, Macleod, Kay, Maday, Sandra, Madeo, Frank, Madesh, Muniswamy, Madl, Tobias, Madrigal-Matute, Julio, Maeda, Akiko, Maejima, Yasuhiro, Magarinos, Marta, Mahavadi, Poornima, Maiani, Emiliano, Maiese, Kenneth, Maiti, Panchanan, Maiuri, Maria Chiara, Majello, Barbara, Major, Michael, Makareeva, Elena, Malik, Fayaz, Mallilankaraman, Karthik, Malorni, Walter, Maloyan, Alina, Mammadova, Najiba, Man, Gene Chi Wai, Manai, Federico, Mancias, Joseph, Mandelkow, Eva-Maria, Mandell, Michael, Manfredi, Angelo, Manjili, Masoud, Manjithaya, Ravi, Manque, Patricio, Manshian, Bella, Manzano, Raquel, Manzoni, Claudia, Mao, Kai, Marchese, Cinzia, Marchetti, Sandrine, Marconi, Anna Maria, Marcucci, Fabrizio, Mardente, Stefania, Mareninova, Olga, Margeta, Marta, Mari, Muriel, Marinelli, Sara, Marinelli, Oliviero, Mariño, Guillermo, Mariotto, Sofia, Marshall, Richard, Marten, Mark, Martens, Sascha, Martin, Alexandre, Martin, Katie, Martin, Sara, Martin, Shaun, Martín-Segura, Adrián, Martín-Acebes, Miguel, Martin-Burriel, Inmaculada, Martin-Rincon, Marcos, Martin-Sanz, Paloma, Martina, José, Martinet, Wim, Martinez, Aitor, Martinez, Ana, Martinez, Jennifer, Martinez Velazquez, Moises, Martinez-Lopez, Nuria, Martinez-Vicente, Marta, Martins, Daniel, Martins, Joilson, Martins, Waleska, Martins-Marques, Tania, Marzetti, Emanuele, Masaldan, Shashank, Masclaux-Daubresse, Celine, Mashek, Douglas, Massa, Valentina, Massieu, Lourdes, Masson, Glenn, Masuelli, Laura, Masyuk, Anatoliy, Masyuk, Tetyana, Matarrese, Paola, Matheu, Ander, Matoba, Satoaki, Matsuzaki, Sachiko, Mattar, Pamela, Matte, Alessandro, Mattoscio, Domenico, Mauriz, José, Mauthe, Mario, Mauvezin, Caroline, Maverakis, Emanual, Maycotte, Paola, Mayer, Johanna, Mazzoccoli, Gianluigi, Mazzoni, Cristina, Mazzulli, Joseph, McCarty, Nami, Mcdonald, Christine, McGill, Mitchell, McKenna, Sharon, Mclaughlin, Bethann, McLoughlin, Fionn, McNiven, Mark, McWilliams, Thomas, Mechta-Grigoriou, Fatima, Medeiros, Tania Catarina, Medina, Diego, Megeney, Lynn, Megyeri, Klara, Mehrpour, Maryam, Mehta, Jawahar, Meijer, Alfred, Meijer, Annemarie, Mejlvang, Jakob, Meléndez, Alicia, Melk, Annette, Memisoglu, Gonen, Mendes, Alexandrina, Meng, Delong, Meng, Fei, Meng, Tian, Menna-Barreto, Rubem, Menon, Manoj, Mercer, Carol, Mercier, Anne, MERGNY, Jean-Louis, Merighi, Adalberto, Merkley, Seth, Merla, Giuseppe, Meske, Volker, Mestre, Ana Cecilia, Metur, Shree Padma, Meyer, Christian, Meyer, Hemmo, Mi, Wenyi, Mialet-Perez, Jeanne, Miao, Junying, Micale, Lucia, Miki, Yasuo, Milan, Enrico, Milczarek, Małgorzata, Miller, Dana, Miller, Samuel, Miller, Silke, Millward, Steven, Milosevic, Ira, Minina, Elena, Mirzaei, Hamed, Mirzaei, Hamid Reza, Mirzaei, Mehdi, Mishra, Amit, Mishra, Nandita, Mishra, Paras Kumar, Misirkic Marjanovic, Maja, Misasi, Roberta, Misra, Amit, Misso, Gabriella, Mitchell, Claire, Mitou, Geraldine, Miura, Tetsuji, Miyamoto, Shigeki, MIYAZAKI, Makoto, Miyazaki, Mitsunori, Miyazaki, Taiga, Miyazawa, Keisuke, Mizushima, Noboru, Mogensen, Trine, Mograbi, Baharia, Mohammadinejad, Reza, Mohamud, Yasir, Mohanty, Abhishek, Mohapatra, Sipra, Möhlmann, Torsten, Mohmmed, Asif, Moles, Anna, Moley, Kelle, Molinari, Maurizio, Mollace, Vincenzo, Møller, Andreas Buch, Mollereau, Bertrand, Mollinedo, Faustino, Montagna, Costanza, Monteiro, Mervyn, Montella, Andrea, Montes, L Ruth, Montico, Barbara, Mony, Vinod, Monzio Compagnoni, Giacomo, Moore, Michael, Moosavi, Mohammad, Mora, Ana, Mora, Marina, Morales-Alamo, David, Moratalla, Rosario, Moreira, Paula, Morelli, Elena, Moreno, Sandra, Moreno-Blas, Daniel, Moresi, Viviana, Morga, Benjamin, Morgan, Alwena, Morin, Fabrice, Morishita, Hideaki, Moritz, Orson, Moriyama, Mariko, Moriyasu, Yuji, Morleo, Manuela, Morselli, Eugenia, Moruno-Manchon, Jose, Moscat, Jorge, Mostowy, Serge, Motori, Elisa, Moura, Andrea 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Ney, Paul, Nezis, Ioannis, Ng, Charlene, Ng, Tzi Bun, Nguyen, Hang, Nguyen, Long, Ni, Hong-Min, Ní Cheallaigh, Clíona, Ni, Zhenhong, Nicolao, M Celeste, Nicoli, Francesco, Nieto-Diaz, Manuel, Nilsson, Per, Ning, Shunbin, Niranjan, Rituraj, Nishimune, Hiroshi, Niso-Santano, Mireia, Nixon, Ralph, Nobili, Annalisa, Nobrega, Clevio, Noda, Takeshi, Nogueira-Recalde, Uxía, Nolan, Trevor, Nombela, Ivan, Novak, Ivana, Novoa, Beatriz, Nozawa, Takashi, Nukina, Nobuyuki, Nussbaum-Krammer, Carmen, Nylandsted, Jesper, O'Donovan, Tracey, O'Leary, Seónadh, O'Rourke, Eyleen, O'Sullivan, Mary, O'Sullivan, Timothy, Oddo, Salvatore, Oehme, Ina, Ogawa, Michinaga, Ogier-Denis, Eric, Ogmundsdottir, Margret, Ogretmen, Besim, Oh, Goo Taeg, Oh, Seon-Hee, Oh, Young, Ohama, Takashi, Ohashi, Yohei, Ohmuraya, Masaki, Oikonomou, Vasileios, Ojha, Rani, Okamoto, Koji, Okazawa, Hitoshi, Oku, Masahide, Oliván, Sara, Oliveira, Jorge, Ollmann, Michael, Olzmann, James, Omari, Shakib, Omary, M Bishr, Önal, Gizem, Ondrej, 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Oliver, Schmitt, Roland, Schmidt, Stephen, Schmitz, Ingo, Schmukler, Eran, Schneider, Anja, Schneider, Bianca, Schober, Romana, Schoijet, Alejandra, Schott, Micah, Schramm, Michael, Schröder, Bernd, Schuh, Kai, Schüller, Christoph, Schulze, Ryan, Schürmanns, Lea, Schwamborn, Jens, Schwarten, Melanie, Scialo, Filippo, Sciarretta, Sebastiano, Scott, Melanie, Scotto, Kathleen, Scovassi, A Ivana, Scrima, Andrea, Scrivo, Aurora, Sebastian, David, Sebti, Salwa, Sedej, Simon, Segatori, Laura, Segev, Nava, Seglen, Per, Seiliez, Iban, Seki, Ekihiro, Selleck, Scott, Sellke, Frank, Selsby, Joshua, Sendtner, Michael, Senturk, Serif, Seranova, Elena, Sergi, Consolato, Serra-Moreno, Ruth, Sesaki, Hiromi, Settembre, Carmine, Setty, Subba Rao Gangi, Sgarbi, Gianluca, Sha, Ou, Shacka, John, Shah, Javeed, Shang, Dantong, Shao, Changshun, Shao, Feng, Sharbati, Soroush, Sharkey, Lisa, Sharma, Dipali, Sharma, Gaurav, Sharma, Kulbhushan, Sharma, Pawan, Sharma, Surendra, Shen, Han-Ming, Shen, Hongtao, Shen, Jiangang, Shen, Ming, Shen, Weili, Shen, Zheni, Sheng, Rui, Sheng, Zhi, Sheng, Zu-Hang, Shi, Jianjian, Shi, Xiaobing, Shi, Ying-Hong, Shiba-Fukushima, Kahori, Shieh, Jeng-Jer, Shimada, Yohta, Shimizu, Shigeomi, Shimozawa, Makoto, Shintani, Takahiro, Shoemaker, Christopher, Shojaei, Shahla, Shoji, Ikuo, Shravage, Bhupendra, Shridhar, Viji, Shu, Chih-Wen, Shu, Hong-Bing, Shui, Ke, Shukla, Arvind, Shutt, Timothy, Sica, Valentina, Siddiqui, Aleem, Sierra, Amanda, Sierra-Torre, Virginia, Signorelli, Santiago, Sil, Payel, Silva, Bruno, Silva, Johnatas, Silva-Pavez, Eduardo, Silvente-Poirot, Sandrine, Simmonds, Rachel, Simon, Anna Katharina, Simon, Hans-Uwe, Simons, Matias, Singh, Anurag, Singh, Lalit, Singh, Rajat, Singh, Shivendra, Singh, Shrawan, Singh, Sudha, Singh, Sunaina, Singh, Surinder Pal, Sinha, Debasish, Sinha, Rohit Anthony, Sinha, Sangita, Sirko, Agnieszka, Sirohi, Kapil, Sivridis, Efthimios, Skendros, Panagiotis, Skirycz, Aleksandra, Slaninová, Iva, Smaili, Soraya, Smertenko, Andrei, Smith, Matthew, Soenen, Stefaan, Sohn, Eun Jung, Sok, Sophia, Solaini, Giancarlo, Soldati, Thierry, Soleimanpour, Scott, Soler, Rosa, Solovchenko, Alexei, Somarelli, Jason, Sonawane, Avinash, Song, Fuyong, Song, Hyun Kyu, Song, Ju-Xian, Song, Kunhua, Song, Zhiyin, Soria, Leandro, Sorice, Maurizio, Soukas, Alexander, Soukup, Sandra-Fausia, Sousa, Diana, Sousa, Nadia, Spagnuolo, Paul, Spector, Stephen, Srinivas Bharath, M., St Clair, Daret, Stagni, Venturina, Staiano, Leopoldo, Stalnecker, Clint, Stankov, Metodi, Stathopulos, Peter, Stefan, Katja, Stefan, Sven Marcel, Stefanis, Leonidas, Steffan, Joan, Steinkasserer, Alexander, Stenmark, Harald, Sterneckert, Jared, Stevens, Craig, Stoka, Veronika, Storch, Stephan, Stork, Björn, Strappazzon, Flavie, Strohecker, Anne Marie, Stupack, Dwayne, Su, Huanxing, Su, Ling-Yan, Su, Longxiang, Suarez-Fontes, Ana, Subauste, Carlos, Subbian, Selvakumar, Subirada, Paula, Sudhandiran, Ganapasam, Sue, Carolyn, Sui, Xinbing, Summers, Corey, Sun, Guangchao, Sun, Jun, SUN, Kang, Sun, Meng-xiang, Sun, Qiming, Sun, Yi, Sun, Zhongjie, Sunahara, Karen, Sundberg, Eva, Susztak, Katalin, Sutovsky, Peter, Suzuki, Hidekazu, Sweeney, Gary, Symons, J David, Sze, Stephen Cho Wing, Szewczyk, Nathaniel, Tabęcka-Łonczynska, Anna, Tabolacci, Claudio, Tacke, Frank, Taegtmeyer, Heinrich, Tafani, Marco, Tagaya, Mitsuo, Tai, Haoran, Tait, Stephen, Takahashi, Yoshinori, Takats, Szabolcs, Talwar, Priti, Tam, Chit, Tam, Shing Yau, Tampellini, Davide, Tamura, Atsushi, Tan, Chong Teik, Tan, Eng-King, Tan, Ya-Qin, Tanaka, Masaki, Tanaka, Motomasa, Tang, Daolin, Tang, Jingfeng, Tang, Tie-Shan, Tanida, Isei, Tao, Zhipeng, Taouis, Mohammed, Tatenhorst, Lars, Tavernarakis, Nektarios, Taylor, Allen, Taylor, Gregory, Taylor, Joan, Tchetina, Elena, Tee, Andrew, Tegeder, Irmgard, Teis, David, Teixeira, Natercia, Teixeira-Clerc, Fatima, Tekirdag, Kumsal, Tencomnao, Tewin, Tenreiro, Sandra, Tepikin, Alexei, Testillano, Pilar, Tettamanti, Gianluca, Tharaux, Pierre-Louis, Thedieck, Kathrin, Thekkinghat, Arvind, Thellung, Stefano, Thinwa, Josephine, Thirumalaikumar, V.P., Thomas, Sufi Mary, Thomes, Paul, Thorburn, Andrew, Thukral, Lipi, Thum, Thomas, Thumm, Michael, Tian, Ling, Tichy, Ales, Till, Andreas, Timmerman, Vincent, Titorenko, Vladimir, Todi, Sokol, Todorova, Krassimira, Toivonen, Janne, Tomaipitinca, Luana, Tomar, Dhanendra, Tomas-Zapico, Cristina, Tomić, Sergej, Tong, Benjamin Chun-Kit, Tong, Chao, Tong, Xin, Tooze, Sharon, Torgersen, Maria, Torii, Satoru, Torres-López, Liliana, Torriglia, Alicia, Towers, Christina, Towns, Roberto, Toyokuni, Shinya, Trajkovic, Vladimir, Tramontano, Donatella, Tran, Quynh-Giao, Travassos, Leonardo, Trelford, Charles, Tremel, Shirley, Trougakos, Ioannis, Tsao, Betty, Tschan, Mario, Tse, Hung-Fat, Tse, Tak Fu, Tsugawa, Hitoshi, Tsvetkov, Andrey, Tumbarello, David, Tumtas, Yasin, Tuñón, María, Turcotte, Sandra, Turk, Boris, Turk, Vito, Turner, Bradley, Tuxworth, Richard, Tyler, Jessica, Tyutereva, Elena, Uchiyama, Yasuo, Ugun-Klusek, Aslihan, Uhlig, Holm, Ułamek-Kozioł, Marzena, Ulasov, Ilya, Umekawa, Midori, Ungermann, Christian, Unno, Rei, Urbe, Sylvie, Uribe-Carretero, Elisabet, Üstün, Suayib, Uversky, Vladimir, Vaccari, Thomas, Vaccaro, Maria, Vahsen, Björn, Vakifahmetoglu-Norberg, Helin, Valdor, Rut, Valente, Maria, Valko, Ayelén, Vallee, Richard, Valverde, Angela, Van Den Berghe, Greet, van der Veen, Stijn, Van Kaer, Luc, van Loosdregt, Jorg, van Wijk, Sjoerd, Vandenberghe, Wim, Vanhorebeek, Ilse, Vannier-Santos, Marcos, Vannini, Nicola, Vanrell, M Cristina, Vantaggiato, Chiara, Varano, Gabriele, Varela-Nieto, Isabel, Varga, Máté, Vasconcelos, M Helena, Vats, Somya, Vavvas, Demetrios, Vega-Naredo, Ignacio, Vega-Rubin-de-Celis, Silvia, Velasco, Guillermo, Velázquez, Ariadna, Vellai, Tibor, Vellenga, Edo, Velotti, Francesca, Verdier, Mireille, Verginis, Panayotis, Vergne, Isabelle, Verkade, Paul, Verma, Manish, Verstreken, Patrik, Vervliet, Tim, Vervoorts, Jörg, Vessoni, Alexandre, Victor, Victor, Vidal, Michel, Vidoni, Chiara, Vieira, Otilia, Vierstra, Richard, Viganó, Sonia, Vihinen, Helena, Vijayan, Vinoy, Vila, Miquel, Vilar, Marçal, Villalba, José, Villalobo, Antonio, Villarejo-Zori, Beatriz, Villarroya, Francesc, Villarroya, Joan, Vincent, Olivier, Vindis, Cecile, Viret, Christophe, Viscomi, Maria Teresa, Visnjic, Dora, Vitale, Ilio, Vocadlo, David, Voitsekhovskaja, Olga, Volonté, Cinzia, Volta, Mattia, Vomero, Marta, Von Haefen, Clarissa, Vooijs, Marc, Voos, Wolfgang, Vucicevic, Ljubica, Wade-Martins, Richard, Waguri, Satoshi, Waite, Kenrick, Wakatsuki, Shuji, Walker, David, Walker, Mark, Walker, Simon, Walter, Jochen, Wandosell, Francisco, Wang, Bo, Wang, Chao-Yung, Wang, Chen, Wang, Chenran, Wang, Chenwei, Wang, Cun-Yu, Wang, Dong, Wang, Fangyang, Wang, Feng, Wang, Fengming, Wang, Guansong, Wang, Han, Wang, Hao, Wang, Hexiang, Wang, Hong-Gang, Wang, Jianrong, Wang, Jigang, Wang, Jiou, Wang, Jundong, Wang, Kui, Wang, Lianrong, Wang, Liming, Wang, Maggie Haitian, Wang, Meiqing, Wang, Nanbu, Wang, PengWei, Wang, PeiPei, Wang, Ping, Wang, Qing Jun, Wang, Qing, Wang, Qing Kenneth, Wang, Qiong, Wang, Wen-Tao, Wang, Wuyang, Wang, Xinnan, Wang, Xuejun, Wang, Yan, Wang, Yanchang, Wang, Yanzhuang, Wang, Yen-Yun, Wang, Yihua, Wang, Yipeng, Wang, Yu, wang, yuqi, Wang, Zhe, Wang, Zhenyu, Wang, Zhouguang, Warnes, Gary, Warnsmann, Verena, Watada, Hirotaka, Watanabe, Eizo, Watchon, Maxinne, Wawrzyńska, Anna, Weaver, Timothy, Wegrzyn, Grzegorz, Wehman, Ann, Wei, Huafeng, Wei, Lei, Wei, Taotao, Wei, Yongjie, Weiergräber, Oliver, Weihl, Conrad, Weindl, Günther, Weiskirchen, Ralf, Wells, Alan, Wen, Runxia, Wen, Xin, Werner, Antonia, Weykopf, Beatrice, Wheatley, Sally, Whitton, J Lindsay, Whitworth, Alexander, Wiktorska, Katarzyna, Wildenberg, Manon, Wileman, Tom, Wilkinson, Simon, Willbold, Dieter, Williams, Brett, Williams, Robin, Williams, Roger, Williamson, Peter, Wilson, Richard, Winner, Beate, Winsor, Nathaniel, Witkin, Steven, Wodrich, Harald, Woehlbier, Ute, Wollert, Thomas, Wong, Esther, Wong, Jack Ho, Wong, Richard, Wong, Vincent Kam Wai, Wong, W Wei-Lynn, Wu, An-Guo, Wu, Chengbiao, Wu, Jian, Wu, Junfang, Wu, Kenneth, Wu, Min, Wu, Shan-Ying, Wu, Shengzhou, Wu, Shu-Yan, Wu, Shufang, Wu, William, Wu, Xiaohong, Wu, Xiaoqing, Wu, Yao-Wen, Wu, Yihua, Xavier, Ramnik, Xia, Hongguang, Xia, Lixin, Xia, Zhengyuan, Xiang, Ge, Xiang, Jin, Xiang, Mingliang, Xiang, Wei, Xiao, Bin, Xiao, Guozhi, Xiao, Hengyi, Xiao, Hong-tao, Xiao, Jian, Xiao, Lan, Xiao, Shi, Xiao, Yin, Xie, Baoming, Xie, Chuan-Ming, Xie, Min, Xie, Yuxiang, Xie, Zhiping, Xie, Zhonglin, Xilouri, Maria, Xu, Congfeng, Xu, En, Xu, Haoxing, Xu, Jing, Xu, Jinrong, Xu, Liang, Xu, Wen Wen, Xu, Xiulong, Xue, Yu, Yakhine-Diop, Sokhna, Yamaguchi, Masamitsu, Yamaguchi, Osamu, Yamamoto, Ai, Yamashina, Shunhei, Yan, Shengmin, Yan, Shian-Jang, Yan, Zhen, Yanagi, Yasuo, Yang, Chuanbin, Yang, Dun-Sheng, Yang, Huan, Yang, Huang-Tian, Yang, Hui, Yang, Jin-Ming, Yang, Jing, Yang, Jingyu, Yang, Ling, Yang, Liu, Yang, Ming, Yang, Pei-Ming, Yang, Qian, Yang, Seungwon, Yang, Shu, Yang, Shun-Fa, Yang, Wannian, Yang, Wei Yuan, Yang, Xiaoyong, Yang, Xuesong, Yang, Yi, Yang, Ying, Yao, Honghong, Yao, Shenggen, Yao, Xiaoqiang, Yao, Yong-Gang, Yao, Yong-Ming, Yasui, Takahiro, Yazdankhah, Meysam, Yen, Paul, Yi, Cong, Yin, Xiao-Ming, Yin, Yanhai, Yin, Zhangyuan, Yin, Ziyi, Ying, Meidan, Ying, Zheng, Yip, Calvin, Yiu, Stephanie Pei Tung, Yoo, Young, Yoshida, Kiyotsugu, Yoshii, Saori, Yoshimori, Tamotsu, Yousefi, Bahman, Yu, Boxuan, Yu, Haiyang, Yu, Jun, Yu, Li, Yu, Ming-Lung, Yu, Seong-Woon, Yu, Victor, Yu, W Haung, Yu, Zhengping, Yu, Zhou, Yuan, Junying, Yuan, Ling-Qing, Yuan, Shilin, Yuan, Shyng-Shiou, Yuan, Yanggang, Yuan, Zengqiang, Yue, Jianbo, Yue, Zhenyu, Yun, Jeanho, Yung, Raymond, Zacks, David, Zaffagnini, Gabriele, Zambelli, Vanessa, Zanella, Isabella, Zang, Qun, Zanivan, Sara, Zappavigna, Silvia, Zaragoza, Pilar, Zarbalis, Konstantinos, Zarebkohan, Amir, Zarrouk, Amira, Zeitlin, Scott, Zeng, Jialiu, Zeng, Ju-deng, Žerovnik, Eva, Zhan, Lixuan, Zhang, Bin, Zhang, Donna, Zhang, Hanlin, Zhang, Hong, Zhang, Honghe, Zhang, Huafeng, Zhang, Huaye, Zhang, Hui, Zhang, Hui-Ling, Zhang, Jianbin, Zhang, Jianhua, Zhang, Jing-Pu, Zhang, Kalin, Zhang, Leshuai, Zhang, Lin, Zhang, Lisheng, Zhang, Lu, Zhang, Luoying, Zhang, Menghuan, Zhang, Peng, Zhang, Sheng, Zhang, Wei, Zhang, Xiangnan, Zhang, Xiao-Wei, Zhang, Xiaolei, Zhang, Xiaoyan, Zhang, Xin, Zhang, Xinxin, Zhang, Xu Dong, Zhang, Yang, Zhang, Yanjin, Zhang, Yi, Zhang, Ying-Dong, Zhang, Yingmei, Zhang, Yuan-Yuan, Zhang, Yuchen, Zhang, Zhe, Zhang, Zhengguang, Zhang, Zhibing, Zhang, Zhihai, Zhang, Zhiyong, Zhang, Zili, Zhao, Haobin, Zhao, Lei, Zhao, Shuang, Zhao, Tongbiao, Zhao, Xiao-Fan, Zhao, Ying, Zhao, Yongchao, Zhao, Yongliang, Zhao, Yuting, Zheng, Guoping, Zheng, Kai, Zheng, Ling, Zheng, Shizhong, Zheng, Xi-Long, Zheng, Yi, Zheng, Zu-Guo, Zhivotovsky, Boris, Zhong, Qing, Zhou, Ao, Zhou, Ben, Zhou, Cefan, ZHOU, Gang, Zhou, Hao, Zhou, Hong, Zhou, Hongbo, Zhou, Jie, Zhou, Jing, Zhou, Jiyong, Zhou, Kailiang, Zhou, Rongjia, Zhou, Xu-jie, Zhou, Yanshuang, Zhou, Yinghong, Zhou, Yubin, Zhou, Zheng-Yu, Zhou, Zhou, Zhu, Binglin, Zhu, Changlian, Zhu, Guo-Qing, Zhu, Haining, Zhu, Hongxin, Zhu, Hua, Zhu, Wei-Guo, Zhu, Yanping, Zhu, Yushan, Zhuang, Haixia, Zhuang, Xiaohong, Zientara-Rytter, Katarzyna, Zimmermann, Christine, Ziviani, Elena, Zoladek, Teresa, Zong, Wei-Xing, Zorov, Dmitry, Zorzano, Antonio, Zou, Weiping, Zou, Zhen, Zou, Zhengzhi, Zuryn, Steven, Zwerschke, Werner, Brand-Saberi, Beate, Dong, X Charlie, Kenchappa, Chandra Shekar, Li, Zuguo, Lin, Yong, Oshima, Shigeru, Rong, Yueguang, Sluimer, Judith, Stallings, Christina, Tong, Chun-Kit, Ahmad, S. Tariq, Alim Al-Bari, M. Abdul, Bechara, Luiz R.G., Behrens, Georg M.N., Bhuiyan, Md. Shenuarin, Broaddus, V. Courtney, Buchan, J. Ross, Burón, M. Isabel, Carter, A. Brent, Chan, Matthew T.V., Choi, Augustine M.K., D’Adamo, Stefania, D’Amelio, Marcello, D’Arcangelo, Daniela, D’Lugos, Andrew, D’Orazi, Gabriella, De Meyer, Guido R.Y., Delpino, M. Victoria, Distler, Jörg H.W., Dixon, Ian M.C., Dobson, Renwick C.J., 2nd Dorn, Gerald, Eissa, N. Tony, Engelsen, Agnete S.T., Fairlie, W. Douglas, Ferreira, Julio C.B., H.B., Ranjitha, Hanson, Phyllis I., Hejtmancik, J. Fielding, Ho, Idy H.T., Hobbs, G. Aaron, Hoet, Peter H.M., Huang, Michael L.H., Iyer, Anand Krishnan V., Johnson, Gail V.W., Joosten, Leo A.B., Karim, Md. Razaul, Kaufmann, Stefan H.E., Ko, Ben C.B., Leck, Lionel Y.W., Lima, Thania R.R., Livingston, J. Andrew, Martin, Alexandre P.J., Montes, L. Ruth, Murphy, J. Patrick, Ng, Charlene C.W., Nicolao, M. Celeste, O’Donovan, Tracey, O’Leary, Seónadh, O’Rourke, Eyleen, O’Sullivan, Mary, O’Sullivan, Timothy, Omary, M. Bishr, Pereira, Gustavo J.S., Ratnayaka, J. Arjuna, Riazuddin, S. Amer, Rouschop, Kasper M.A., Sanderson, J. Thomas, Scaglione, K. Matthew, Schapira, Anthony H.V., Scovassi, A. Ivana, St. Clair, Daret, Sunahara, Karen K.S., Symons, J. David, Triola, Gemma, van Wijk, Sjoerd J.L., Vanrell, M. Cristina, Vasconcelos, M. Helena, Whitton, J. Lindsay, Williams, Robin S.B., Wong, W. Wei-Lynn, Wu, William K.K., Yakhine-Diop, Sokhna M.S., Yu, W. Haung, Zhang, Kalin Y.B., Dong, X. Charlie, Ain Shams University [ASU], Johannes Gutenberg - Universität Mainz = Johannes Gutenberg University [JGU], Medical University Graz, Centre de Recherche des Cordeliers [CRC (UMR_S_1138 / U1138)], Institut Pasteur d'Iran, Leibniz Institute of Plant Biochemistry [IPB], The University of Texas M.D. Anderson Cancer Center [Houston], Institut de pharmacologie moléculaire et cellulaire [IPMC], Lipides - Nutrition - Cancer [Dijon - U1231] [LNC], Centre méditerranéen de médecine moléculaire [C3M], Institut de Biologie Valrose [IBV], Petites Molécules de neuroprotection, neurorégénération et remyélinisation, Signalisation Hormonale, Physiopathologie Endocrinienne et Métabolique, Institut Cochin [IC UM3 (UMR 8104 / U1016)], Institut NeuroMyoGène [INMG], Paris-Centre de Recherche Cardiovasculaire [PARCC (UMR_S 970/ U970)], Marqueurs cardiovasculaires en situation de stress [MASCOT (UMR_S_942 / U942)], Institut de Recherche sur le Cancer et le Vieillissement [IRCAN], Centre de Recherche en Cancérologie de Marseille [CRCM], Centre for Integrative Biology - CBI [Inserm U964 - CNRS UMR7104 - IGBMC], Oncogenesis, Stress, Signaling [OSS], Institut Necker Enfants-Malades [INEM - UM 111 (UMR 8253 / U1151)], Institut de Biologie Intégrative de la Cellule [I2BC], Microbes, Intestin, Inflammation et Susceptibilité de l'Hôte [M2iSH], Centre de Recherches en Cancérologie de Toulouse [CRCT], Physiopathologie et traitement des maladies du foie, Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 [CIIL], Institut de Génétique et de Biologie Moléculaire et Cellulaire [IGBMC], Laboratoire Bio-PeroxIL. Biochimie du peroxysome, inflammation et métabolisme lipidique [Dijon] [BIO-PEROXIL], Centre de recherche sur l'Inflammation [CRI (UMR_S_1149 / ERL_8252 / U1149)], Unité de génétique et biologie des cancers [U830], Laboratoire d'Optique et Biosciences [LOB], Institut des Maladies Métaboliques et Casdiovasculaires [UPS/Inserm U1297 - I2MC], Différenciation et communication neuronale et neuroendocrine [DC2N], Institut de Recherche en Cancérologie de Montpellier [IRCM - U1194 Inserm - UM], Centre d'Immunologie de Marseille - Luminy [CIML], Physiopathologie et imagerie des troubles neurologiques [PhIND], Laboratory of Fundamental and Applied Bioenergetics = Laboratoire de bioénergétique fondamentale et appliquée [LBFA], Imagine - Institut des maladies génétiques (IHU) [Imagine - U1163], Institut Mondor de Recherche Biomédicale [IMRB], Franco-czech Laboratory for clinical research on obesity, University of Michigan [Ann Arbor], University of Michigan System, Institut de pharmacologie moléculaire et cellulaire (IPMC), Centre National de la Recherche Scientifique (CNRS)-Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-Université Côte d'Azur (UCA), Lipides - Nutrition - Cancer [Dijon - U1231] (LNC), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement, Centre méditerranéen de médecine moléculaire (C3M), Université Nice Sophia Antipolis (... - 2019) (UNS), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), Institut de Biologie Valrose (IBV), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA)-Centre National de la Recherche Scientifique (CNRS), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Sud - Paris 11 (UP11), Centre de Recherche des Cordeliers (CRC (UMR_S_1138 / U1138)), École pratique des hautes études (EPHE), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université de Paris (UP), Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM)-AP-HP Hôpital Bicêtre (Le Kremlin-Bicêtre), Nutrition, Métabolisme, Aquaculture (NuMéA), Université de Pau et des Pays de l'Adour (UPPA)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Institut Cochin (IC UM3 (UMR 8104 / U1016)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP), Institut NeuroMyoGène (INMG), Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Paris-Centre de Recherche Cardiovasculaire (PARCC - UMR-S U970), Hôpital Européen Georges Pompidou [APHP] (HEGP), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Institut de Recherche sur le Cancer et le Vieillissement (IRCAN), COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015 - 2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), Centre des Sciences du Goût et de l'Alimentation [Dijon] (CSGA), Université de Bourgogne (UB)-AgroSup Dijon - Institut National Supérieur des Sciences Agronomiques, de l'Alimentation et de l'Environnement-Centre National de la Recherche Scientifique (CNRS)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Université Bourgogne Franche-Comté [COMUE] (UBFC), Centre de Recherche en Cancérologie de Marseille (CRCM), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Aix Marseille Université (AMU), Centre for Integrative Biology - CBI (Inserm U964 - CNRS UMR7104 - IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institute of genetics and molecular and cellular biology-Centre National de la Recherche Scientifique (CNRS), Chemistry, Oncogenesis, Stress and Signaling (COSS), Université de Rennes 1 (UR1), Université de Rennes (UNIV-RENNES)-Université de Rennes (UNIV-RENNES)-CRLCC Eugène Marquis (CRLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut Necker Enfants-Malades (INEM - UM 111 (UMR 8253 / U1151)), Unité de Nutrition Humaine (UNH), Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Clermont Auvergne (UCA), Institut de Biologie Intégrative de la Cellule (I2BC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Microbes, Intestin, Inflammation et Susceptibilité de l'Hôte (M2iSH), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre de Recherche en Nutrition Humaine d'Auvergne (CRNH d'Auvergne)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Université Clermont Auvergne (UCA), Institut des Maladies Neurodégénératives [Bordeaux] (IMN), Université de Bordeaux (UB)-Centre National de la Recherche Scientifique (CNRS), Centre International de Recherche en Infectiologie - UMR (CIRI), École normale supérieure - Lyon (ENS Lyon)-Université Claude Bernard Lyon 1 (UCBL), Université de Lyon-Université de Lyon-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre de Recherches en Cancérologie de Toulouse (CRCT), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Laboratoire de Physiologie et Génomique des Poissons (LPGP), Structure Fédérative de Recherche en Biologie et Santé de Rennes ( Biosit : Biologie - Santé - Innovation Technologique )-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Hôpital Paul Brousse-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay, Centre d’Infection et d’Immunité de Lille - INSERM U 1019 - UMR 9017 - UMR 8204 (CIIL), 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 Hospitalier Régional Universitaire [Lille] (CHRU Lille)-Centre National de la Recherche Scientifique (CNRS), Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA), Laboratoire Bio-PeroxIL. Biochimie du peroxysome, inflammation et métabolisme lipidique [Dijon] (BIO-PEROXIL), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Bourgogne Franche-Comté [COMUE] (UBFC), Centre de recherche sur l'Inflammation (CRI (UMR_S_1149 / ERL_8252 / U1149)), Institut Jean-Pierre Bourgin (IJPB), AgroParisTech-Université Paris-Saclay-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE), Unité de génétique et biologie des cancers (U830), Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM), Laboratoire d'Optique et Biosciences (LOB), École polytechnique (X)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Différenciation et communication neuronale et neuroendocrine (DC2N), Université de Rouen Normandie (UNIROUEN), Normandie Université (NU)-Normandie Université (NU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Institut de Recherche en Cancérologie de Montpellier (IRCM - U1194 Inserm - UM), CRLCC Val d'Aurelle - Paul Lamarque-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM), Centre d'Immunologie de Marseille - Luminy (CIML), Aix Marseille Université (AMU)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie et imagerie des troubles neurologiques (PhIND), Université de Caen Normandie (UNICAEN), Laboratory of Fundamental and Applied Bioenergetics = Laboratoire de bioénergétique fondamentale et appliquée (LBFA), Université Grenoble Alpes (UGA)-Institut National de la Santé et de la Recherche Médicale (INSERM), Epithelial biology and disease - Liliane Bettencourt Chair of Developmental Biology (Equipe Inserm U1163), Imagine - Institut des maladies génétiques (IHU) (Imagine - U1163), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Paris (UP), Biomécanique cellulaire et respiratoire (BCR), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12)-Centre National de la Recherche Scientifique (CNRS), Charles University [Prague]-Institut National de la Santé et de la Recherche Médicale (INSERM), This work was supported by the National Institute of General Medical Sciences [GM131919]., Université Paris-Sud - Paris 11 (UP11)-Institut National de la Santé et de la Recherche Médicale (INSERM), Marqueurs cardiovasculaires en situation de stress (MASCOT (UMR_S_942 / U942)), Institut National de la Santé et de la Recherche Médicale (INSERM)-Groupe Hospitalier Saint Louis - Lariboisière - Fernand Widal [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Centre National de la Recherche Scientifique (CNRS)-Université de Paris (UP)-Université Sorbonne Paris Nord, Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Physiopathologie des Adaptations Nutritionnelles (PhAN), Université de Nantes (UN)-Institut National de la Recherche Agronomique (INRA), Département Plateforme (PF I2BC), Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS)-Commissariat à l'énergie atomique et aux énergies alternatives (CEA)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Institut Gustave Roussy (IGR), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO), Chinese Academy of Medical Sciences [Suzhou, Chine] (CAMS), Karolinska Institutet [Stockholm], Karolinska University Hospital [Stockholm], Department of Women's and Children's Health [Stockholm, Sweden], Centre National de la Recherche Scientifique (CNRS)-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), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Centre National de la Recherche Scientifique (CNRS)-Institut National de la Santé et de la Recherche Médicale (INSERM)-École polytechnique (X), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées, FHU OncoAge - Pathologies liées à l’âge [CHU Nice] (OncoAge), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA)-Institut de Pharmacologie Moléculaire et Cellulaire [UNIV Côte d'Azur] (UPMC), Institut Universitaire du Cancer de Toulouse - Oncopole (IUCT Oncopole - UMR 1037), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-CHU Toulouse [Toulouse]-Institut National de la Santé et de la Recherche Médicale (INSERM), Life Sciences Institute [Ann Arbor, MI, USA], University of Michigan System-University of Michigan System, European Institute of Oncology IRCCS [Milan, Italy] (EIO), Ain Shams University (ASU), Johannes Gutenberg - Universität Mainz = Johannes Gutenberg University (JGU), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Sorbonne Université (SU)-Université Paris Cité (UPCité), Réseau International des Instituts Pasteur (RIIP), Leibniz Institute of Plant Biochemistry (IPB), Hebrew University of Jerusalem, Université Nice Sophia Antipolis (1965 - 2019) (UNS), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), Université de Bourgogne (UB)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Institut Agro Dijon, Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro)-Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Côte d'Azur (UCA), COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-COMUE Université Côte d'Azur (2015-2019) (COMUE UCA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Côte d'Azur (UCA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité), Paris-Centre de Recherche Cardiovasculaire (PARCC (UMR_S 970/ U970)), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpitaux Universitaires Paris Ouest - Hôpitaux Universitaires Île de France Ouest (HUPO)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Cité (UPCité)-Université Sorbonne Paris Nord, Aix Marseille Université (AMU)-Institut Paoli-Calmettes, Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Fédération nationale des Centres de lutte contre le Cancer (FNCLCC)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Oncogenesis, Stress, Signaling (OSS), Institut des Maladies Métaboliques et Casdiovasculaires (UPS/Inserm U1297 - I2MC), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Grenoble Alpes (UGA), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris Cité (UPCité), Institut Mondor de Recherche Biomédicale (IMRB), Institut National de la Santé et de la Recherche Médicale (INSERM)-IFR10-Université Paris-Est Créteil Val-de-Marne - Paris 12 (UPEC UP12), Charles University [Prague] (CU)-Institut National de la Santé et de la Recherche Médicale (INSERM), Klionsky, D. J., Abdel-Aziz, A. K., Abdelfatah, S., Abdellatif, M., Abdoli, A., Abel, S., Abeliovich, H., Abildgaard, M. H., Abudu, Y. P., Acevedo-Arozena, A., Adamopoulos, I. E., Adeli, K., Adolph, T. E., Adornetto, A., Aflaki, E., Agam, G., Agarwal, A., Aggarwal, B. B., Agnello, M., Agostinis, P., Agrewala, J. N., Agrotis, A., Aguilar, P. V., Ahmad, S. T., Ahmed, Z. M., Ahumada-Castro, U., Aits, S., Aizawa, S., Akkoc, Y., Akoumianaki, T., Akpinar, H. A., Al-Abd, A. M., Al-Akra, L., Al-Gharaibeh, A., Alaoui-Jamali, M. A., Alberti, S., Alcocer-Gomez, E., Alessandri, C., Ali, M., Alim Al-Bari, M. A., Aliwaini, S., Alizadeh, J., Almacellas, E., Almasan, A., Alonso, A., Alonso, G. D., Altan-Bonnet, N., Altieri, D. C., Alvarez, E. M. C., Alves, S., Alves da Costa, C., Alzaharna, M. M., Amadio, M., Amantini, C., Amaral, C., Ambrosio, S., Amer, A. O., Ammanathan, V., An, Z., Andersen, S. U., Andrabi, S. A., Andrade-Silva, M., Andres, A. M., Angelini, S., Ann, D., Anozie, U. C., Ansari, M. 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T., Balduini, W., Ballabio, A., Ballester, M., Balazadeh, S., Balzan, R., Bandopadhyay, R., Banerjee, S., Banreti, A., Bao, Y., Baptista, M. S., Baracca, A., Barbati, C., Bargiela, A., Barila, D., Barlow, P. G., Barmada, S. J., Barreiro, E., Barreto, G. E., Bartek, J., Bartel, B., Bartolome, A., Barve, G. R., Basagoudanavar, S. H., Bassham, D. C., Bast, R. C., Basu, A., Batoko, H., Batten, I., Baulieu, E. E., Baumgarner, B. L., Bayry, J., Beale, R., Beau, I., Beaumatin, F., Bechara, L. R. G., Beck, G. R., Beers, M. F., Begun, J., Behrends, C., Behrens, G. M. N., Bei, R., Bejarano, E., Bel, S., Behl, C., Belaid, A., Belgareh-Touze, N., Bellarosa, C., Belleudi, F., Bello Perez, M., Bello-Morales, R., Beltran, J. S. D. O., Beltran, S., Benbrook, D. M., Bendorius, M., Benitez, B. A., Benito-Cuesta, I., Bensalem, J., Berchtold, M. W., Berezowska, S., Bergamaschi, D., Bergami, M., Bergmann, A., Berliocchi, L., Berlioz-Torrent, C., Bernard, A., Berthoux, L., Besirli, C. G., Besteiro, S., Betin, V. M., Beyaert, R., Bezbradica, J. S., Bhaskar, K., Bhatia-Kissova, I., Bhattacharya, R., Bhattacharya, S., Bhattacharyya, S., Bhuiyan, M. S., Bhutia, S. K., Bi, L., Bi, X., Biden, T. J., Bijian, K., Billes, V. A., Binart, N., Bincoletto, C., Birgisdottir, A. B., Bjorkoy, G., Blanco, G., Blas-Garcia, A., Blasiak, J., Blomgran, R., Blomgren, K., Blum, J. S., Boada-Romero, E., Boban, M., Boesze-Battaglia, K., Boeuf, P., Boland, B., Bomont, P., Bonaldo, P., Bonam, S. R., Bonfili, L., Bonifacino, J. S., Boone, B. A., Bootman, M. D., Bordi, M., Borner, C., Bornhauser, B. C., Borthakur, G., Bosch, J., Bose, S., Botana, L. M., Botas, J., Boulanger, C. M., Boulton, M. E., Bourdenx, M., Bourgeois, B., Bourke, N. M., Bousquet, G., Boya, P., Bozhkov, P. V., Bozi, L. H. M., Bozkurt, T. O., Brackney, D. E., Brandts, C. H., Braun, R. J., Braus, G. H., Bravo-Sagua, R., Bravo-San Pedro, J. M., Brest, P., Bringer, M. -A., Briones-Herrera, A., Broaddus, V. C., Brodersen, P., Brodsky, J. L., Brody, S. L., Bronson, P. G., Bronstein, J. M., Brown, C. N., Brown, R. E., Brum, P. C., Brumell, J. H., Brunetti-Pierri, N., Bruno, D., Bryson-Richardson, R. J., Bucci, C., Buchrieser, C., Bueno, M., Buitrago-Molina, L. E., Buraschi, S., Buch, S., Buchan, J. R., Buckingham, E. M., Budak, H., Budini, M., Bultynck, G., Burada, F., Burgoyne, J. R., Buron, M. I., Bustos, V., Buttner, S., Butturini, E., Byrd, A., Cabas, I., Cabrera-Benitez, S., Cadwell, K., Cai, J., Cai, L., Cai, Q., Cairo, M., Calbet, J. A., Caldwell, G. A., Caldwell, K. A., Call, J. A., Calvani, R., Calvo, A. C., Calvo-Rubio Barrera, M., Camara, N. O. S., Camonis, J. H., Camougrand, N., Campanella, M., Campbell, E. M., Campbell-Valois, F. -X., Campello, S., Campesi, I., Campos, J. C., Camuzard, O., Cancino, J., Candido de Almeida, D., Canesi, L., Caniggia, I., Canonico, B., Canti, C., Cao, B., Caraglia, M., Carames, B., Carchman, E. H., Cardenal-Munoz, E., Cardenas, C., Cardenas, L., Cardoso, S. M., Carew, J. S., Carle, G. F., Carleton, G., Carloni, S., Carmona-Gutierrez, D., Carneiro, L. A., Carnevali, O., Carosi, J. M., Carra, S., Carrier, A., Carrier, L., Carroll, B., Carter, A. B., Carvalho, A. N., Casanova, M., Casas, C., Casas, J., Cassioli, C., Castillo, E. F., Castillo, K., Castillo-Lluva, S., Castoldi, F., Castori, M., Castro, A. F., Castro-Caldas, M., Castro-Hernandez, J., Castro-Obregon, S., Catz, S. D., Cavadas, C., Cavaliere, F., Cavallini, G., Cavinato, M., Cayuela, M. L., Cebollada Rica, P., Cecarini, V., Cecconi, F., Cechowska-Pasko, M., Cenci, S., Ceperuelo-Mallafre, V., Cerqueira, J. J., Cerutti, J. M., Cervia, D., Cetintas, V. B., Cetrullo, S., Chae, H. -J., Chagin, A. S., Chai, C. -Y., Chakrabarti, G., Chakrabarti, O., Chakraborty, T., Chami, M., Chamilos, G., Chan, D. W., Chan, E. Y. W., Chan, E. D., Chan, H. Y. E., Chan, H. H., Chan, H., Chan, M. T. V., Chan, Y. S., Chandra, P. 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E., Chung, H., Chung, K. P., Chung, S., Chung, S. -H., Chung, Y. -L., Cianfanelli, V., Ciechomska, I. A., Cifuentes, M., Cinque, L., Cirak, S., Cirone, M., Clague, M. J., Clarke, R., Clementi, E., Coccia, E. M., Codogno, P., Cohen, E., Cohen, M. M., Colasanti, T., Colasuonno, F., Colbert, R. A., Colell, A., Colic, M., Coll, N. S., Collins, M. O., Colombo, M. I., Colon-Ramos, D. A., Combaret, L., Comincini, S., Cominetti, M. R., Consiglio, A., Conte, A., Conti, F., Contu, V. R., Cookson, M. R., Coombs, K. M., Coppens, I., Corasaniti, M. T., Corkery, D. P., Cordes, N., Cortese, K., Costa, M. D. C., Costantino, S., Costelli, P., Coto-Montes, A., Crack, P. J., Crespo, J. L., Criollo, A., Crippa, V., Cristofani, R., Csizmadia, T., Cuadrado, A., Cui, B., Cui, J., Cui, Y., Culetto, E., Cumino, A. C., Cybulsky, A. V., Czaja, M. J., Czuczwar, S. J., D'Adamo, S., D'Amelio, M., D'Arcangelo, D., D'Lugos, A. C., D'Orazi, G., da Silva, J. A., Dafsari, H. S., Dagda, R. 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P., Whitton, J. L., Whitworth, A. J., Wiktorska, K., Wildenberg, M. E., Wileman, T., Wilkinson, S., Willbold, D., Williams, B., Williams, R. S. B., Williams, R. L., Williamson, P. R., Wilson, R. A., Winner, B., Winsor, N. J., Witkin, S. S., Wodrich, H., Woehlbier, U., Wollert, T., Wong, E., Wong, J. H., Wong, R. W., Wong, V. K. W., Wong, W. W. -L., Wu, A. -G., Wu, C., Wu, J., Wu, K. K., Wu, M., Wu, S. -Y., Wu, S., Wu, W. K. K., Wu, X., Wu, Y. -W., Wu, Y., Xavier, R. J., Xia, H., Xia, L., Xia, Z., Xiang, G., Xiang, J., Xiang, M., Xiang, W., Xiao, B., Xiao, G., Xiao, H., Xiao, H. -T., Xiao, J., Xiao, L., Xiao, S., Xiao, Y., Xie, B., Xie, C. -M., Xie, M., Xie, Y., Xie, Z., Xilouri, M., Xu, C., Xu, E., Xu, H., Xu, J., Xu, L., Xu, W. W., Xu, X., Xue, Y., Yakhine-Diop, S. M. S., Yamaguchi, M., Yamaguchi, O., Yamamoto, A., Yamashina, S., Yan, S., Yan, S. -J., Yan, Z., Yanagi, Y., Yang, C., Yang, D. -S., Yang, H., Yang, H. -T., Yang, J. -M., Yang, J., Yang, L., Yang, M., Yang, P. -M., Yang, Q., Yang, S., Yang, S. -F., Yang, W., Yang, W. Y., Yang, X., Yang, Y., Yao, H., Yao, S., Yao, X., Yao, Y. -G., Yao, Y. -M., Yasui, T., Yazdankhah, M., Yen, P. M., Yi, C., Yin, X. -M., Yin, Y., Yin, Z., Ying, M., Ying, Z., Yip, C. K., Yiu, S. P. T., Yoo, Y. H., Yoshida, K., Yoshii, S. R., Yoshimori, T., Yousefi, B., Yu, B., Yu, H., Yu, J., Yu, L., Yu, M. -L., Yu, S. -W., Yu, V. C., Yu, W. H., Yu, Z., Yuan, J., Yuan, L. -Q., Yuan, S., Yuan, S. -S. F., Yuan, Y., Yuan, Z., Yue, J., Yue, Z., Yun, J., Yung, R. L., Zacks, D. N., Zaffagnini, G., Zambelli, V. O., Zanella, I., Zang, Q. S., Zanivan, S., Zappavigna, S., Zaragoza, P., Zarbalis, K. S., Zarebkohan, A., Zarrouk, A., Zeitlin, S. O., Zeng, J., Zeng, J. -D., Zerovnik, E., Zhan, L., Zhang, B., Zhang, D. D., Zhang, H., Zhang, H. -L., Zhang, J., Zhang, J. -P., Zhang, K. Y. B., Zhang, L. W., Zhang, L., Zhang, M., Zhang, P., Zhang, S., Zhang, W., Zhang, X., Zhang, X. -W., Zhang, X. D., Zhang, Y., Zhang, Y. -D., Zhang, Y. -Y., Zhang, Z., Zhao, H., Zhao, L., Zhao, S., Zhao, T., Zhao, X. -F., Zhao, Y., Zheng, G., Zheng, K., Zheng, L., Zheng, S., Zheng, X. -L., Zheng, Y., Zheng, Z. -G., Zhivotovsky, B., Zhong, Q., Zhou, A., Zhou, B., Zhou, C., Zhou, G., Zhou, H., Zhou, J., Zhou, K., Zhou, R., Zhou, X. -J., Zhou, Y., Zhou, Z. -Y., Zhou, Z., Zhu, B., Zhu, C., Zhu, G. -Q., Zhu, H., Zhu, W. -G., Zhu, Y., Zhuang, H., Zhuang, X., Zientara-Rytter, K., Zimmermann, C. M., Ziviani, E., Zoladek, T., Zong, W. -X., Zorov, D. B., Zorzano, A., Zou, W., Zou, Z., Zuryn, S., Zwerschke, W., Brand-Saberi, B., Dong, X. C., Kenchappa, C. S., Lin, Y., Oshima, S., Rong, Y., Sluimer, J. C., Stallings, C. L., Tong, C. -K., and Centre National de la Recherche Scientifique (CNRS)
Subjects: 0301 basic medicine, Programmed cell death, Settore BIO/06, Autophagosome, Autolysosome, [SDV]Life Sciences [q-bio], lnfectious Diseases and Global Health Radboud Institute for Molecular Life Sciences [Radboudumc 4], Autophagy-Related Proteins, Review, Computational biology, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, Biology, Settore MED/04, 03 medical and health sciences, stress, Chaperone-mediated autophagy, ddc:570, Autophagy, LC3, Animals, Humans, cancer, Settore BIO/10, flux, lysosome, macroautophagy, neurodegeneration, phagophore, vacuole, Set (psychology), Molecular Biology, 030102 biochemistry & molecular biology, business.industry, Interpretation (philosophy), Autophagosomes, Cell Biology, Multicellular organism, 030104 developmental biology, Knowledge base, Biological Assay, Lysosomes, business, Biomarkers, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract: Contains fulltext : 232759.pdf (Publisher’s version ) (Closed access) In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.
Published: 2021
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11. Contact With Young Children Increases the Risk of Respiratory Infection in Older Adults in Europe—the RESCEU Study

Author: Korsten, Koos, Adriaenssens, Niels, Coenen, Samuel, Butler, Chris C, Pirçon, Jean-Yves, Verheij, Theo J M, Bont, Louis J, Wildenbeest, Joanne G, Butler, Christopher, Verheij, Theo, Bont, Louis, Wildenbeest, Joanne, Nair, Harish, Campbell, Harry, Beutels, Philippe, Openshaw, Peter, Pollard, Andrew, Molero, Eva, Meijer, Adam, Fischer, Thea K, van den Berge, Maarten, Giaquinto, Carlo, Abram, Michael, Aerssens, Jeroen, Swanson, Kena, Gruselle, Olivier, Leach, Amanda, Stoszek, Sonia, Demont, Clarisse, Gallichan, Scott, Pavot, Vincent, Vernhes, Charlotte, Kumar, Veena, and RESCEU Investigators
Subjects: Europe, Infectious Diseases, Child, Preschool, Odds Ratio, Humans, Infant, Immunology and Allergy, Human medicine, Respiratory Tract Infections, Biology, Aged
Abstract: Background Knowledge about how older adults get a respiratory infection is crucial for planning preventive strategies. We aimed to determine how contact with young children living outside of the household affects the risk of acute respiratory tract infections (ARTI) in community-dwelling older adults. Methods This study is part of the European RESCEU older adult study. Weekly surveillance was performed to detect ARTI throughout 2 winter seasons (2017-2018, 2018-2019). Child exposure, defined as having regular contact with children under 5 living outside of the subject’s household, was assessed at baseline. The average attributable fraction was calculated to determine the fraction of ARTI explained by exposure to these children. Results We prospectively established that 597/1006 (59%) participants experienced at least 1 ARTI. Child exposure increased the risk of all-cause ARTI (adjusted odds ratio [aOR], 1.58; 95% confidence interval [CI], 1.21 -2.08; P = .001). This risk was highest in those with the most frequent contact (aOR, 1.80; 95% CI, 1.23-2.63; P = .003). The average attributable fraction of child exposure explaining ARTI was 10% (95% CI, 5%-15%). Conclusions One of 10 ARTI in community-dwelling older adults is attributable to exposure to preschool children living outside of the household. Clinical Trials Registration NCT03621930.
Published: 2021
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12. The NORMAN Suspect List Exchange (NORMAN-SLE): facilitating European and worldwide collaboration on suspect screening in high resolution mass spectrometry

Author: Mohammed Taha, Hiba, Aalizadeh, Reza, Alygizakis, Nikiforos, Antignac, Jean-Philippe, Arp, Hans Peter H, Bade, Richard, Baker, Nancy, Belova, Lidia, Bijlsma, Lubertus, Bolton, Evan E, Brack, Werner, Celma, Alberto, Chen, Wen-Ling, Cheng, Tiejun, Chirsir, Parviel, Čirka, Ľuboš, D'Agostino, Lisa A, Djoumbou Feunang, Yannick, Dulio, Valeria, Fischer, Stellan, Gago-Ferrero, Pablo, Galani, Aikaterini, Geueke, Birgit, Głowacka, Natalia, Glüge, Juliane, Groh, Ksenia, Grosse, Sylvia, Haglund, Peter, Hakkinen, Pertti J, Hale, Sarah E, Hernandez, Felix, Janssen, Elisabeth M-L, Jonkers, Tim, Kiefer, Karin, Kirchner, Michal, Koschorreck, Jan, Krauss, Martin, Krier, Jessy, Lamoree, Marja H, Letzel, Marion, Letzel, Thomas, Li, Qingliang, Little, James, Liu, Yanna, Lunderberg, David M, Martin, Jonathan W, McEachran, Andrew D, McLean, John A, Meier, Christiane, Meijer, Jeroen, Menger, Frank, Merino, Carla, Muncke, Jane, Muschket, Matthias, Neumann, Michael, Neveu, Vanessa, Ng, Kelsey, Oberacher, Herbert, O'Brien, Jake, Oswald, Peter, Oswaldova, Martina, Picache, Jaqueline A, Postigo, Cristina, Ramirez, Noelia, Reemtsma, Thorsten, Renaud, Justin, Rostkowski, Pawel, Rüdel, Heinz, Salek, Reza M, Samanipour, Saer, Scheringer, Martin, Schliebner, Ivo, Schulz, Wolfgang, Schulze, Tobias, Sengl, Manfred, Shoemaker, Benjamin A, Sims, Kerry, Singer, Heinz, Singh, Randolph R, Sumarah, Mark, Thiessen, Paul A, Thomas, Kevin V, Torres, Sonia, Trier, Xenia, van Wezel, Annemarie P, Vermeulen, Roel C H, Vlaanderen, Jelle J, von der Ohe, Peter C, Wang, Zhanyun, Williams, Antony J, Willighagen, Egon L, Wishart, David S, Zhang, Jian, Thomaidis, Nikolaos S, Hollender, Juliane, Slobodnik, Jaroslav, Schymanski, Emma L, IRAS OH Epidemiology Chemical Agents, Ministerio de Ciencia e Innovación (España), European Commission, E&H: Environmental Chemistry and Toxicology, AIMMS, Analytical Chemistry and Forensic Science (HIMS, FNWI), Freshwater and Marine Ecology (IBED, FNWI), Publica, IRAS OH Epidemiology Chemical Agents, Bioinformatica, and RS: NUTRIM - R1 - Obesity, diabetes and cardiovascular health
Subjects: High-resolution mass spectrometry, Environmental sciences & ecology [F08] [Life sciences], EMERGING CONTAMINANTS, STRATEGIES, PHARMACEUTICALS, DATABASE, TRANSFORMATION PRODUCTS, Suspect screening, High resolution mass spectrometry, Non-target screening, Open science, FAIR (Findable Accessible Interoperable Reusable) data, Data exchange, Cheminformatics, Exposomics, Environmental contaminants, Chemicals of emerging concern, Bioinformatik och systembiologi, CHEMICALS, NONTARGET, Biology, Bioinformatics and Systems Biology, Pollution, POLYFLUOROALKYL SUBSTANCES, Chemistry, Sciences de l'environnement & écologie [F08] [Sciences du vivant], WASTE-WATER EFFLUENTS, RISK-ASSESSMENT, SDG 6 - Clean Water and Sanitation
Abstract: Background: The NORMAN Association (https:// www. norman-netwo rk. com/) initiated the NORMAN Suspect List Exchange (NORMAN-SLE; https:// www. norman-netwo rk. com/ nds/ SLE/) in 2015, following the NORMAN collaborative trial on non-target screening of environmental water samples by mass spectrometry. Since then, this exchange of information on chemicals that are expected to occur in the environment, along with the accompanying expert knowledge and references, has become a valuable knowledge base for “suspect screening” lists. The NORMAN-SLE now serves as a FAIR (Findable, Accessible, Interoperable, Reusable) chemical information resource worldwide. Results: The NORMAN-SLE contains 99 separate suspect list collections (as of May 2022) from over 70 contributors around the world, totalling over 100,000 unique substances. The substance classes include per- and polyfluoroalkyl substances (PFAS), pharmaceuticals, pesticides, natural toxins, high production volume substances covered under the European REACH regulation (EC: 1272/2008), priority contaminants of emerging concern (CECs) and regulatory lists from NORMAN partners. Several lists focus on transformation products (TPs) and complex features detected in the environment with various levels of provenance and structural information. Each list is available for separate download. The merged, curated collection is also available as the NORMAN Substance Database (NORMAN SusDat). Both the NORMAN-SLE and NORMAN SusDat are integrated within the NORMAN Database System (NDS). The individual NORMAN-SLE lists receive digital object identifiers (DOIs) and traceable versioning via a Zenodo community (https:// zenodo. org/ commu nities/ norman-sle), with a total of > 40,000 unique views, > 50,000 unique downloads and 40 citations (May 2022). NORMAN-SLE content is progressively integrated into large open chemical databases such as PubChem (https:// pubch em. ncbi. nlm. nih. gov/) and the US EPA’s CompTox Chemicals Dashboard (https:// compt ox. epa. gov/ dashb oard/), enabling further access to these lists, along with the additional functionality and calculated properties these resources offer. PubChem has also integrated significant annotation content from the NORMAN-SLE, including a classification browser (https:// pubch em. ncbi. nlm. nih. gov/ class ifica tion/# hid= 101). Conclusions: The NORMAN-SLE offers a specialized service for hosting suspect screening lists of relevance for the environmental community in an open, FAIR manner that allows integration with other major chemical resources. These efforts foster the exchange of information between scientists and regulators, supporting the paradigm shift to the “one substance, one assessment” approach. New submissions are welcome via the contacts provided on the NORMAN-SLE website (https:// www. norman-netwo rk. com/ nds/ SLE/)., NORMAN Association, Luxembourg National Research Fund A18/BM/12341006, European Union's Horizon 2020 research and innovation programme 101036756, National Center for Biotechnology Information of the National Library of Medicine (NLM), National Institutes of Health (NIH), National Health and Medical Research Council (NHMRC) of Australia EL1 2009209, Australian Research Council DP190102476 Queensland Department of Health, Instituto de Salud Carlos III European Commission CP19/00060 European Union through Fondo Europeo de Desarrollo Regional (FEDER), Federal Ministry of Education & Research (BMBF) FKz: 02WRS1495 A/B/E, FWO 11G1821N, NIH via grant NIH NIGMS R01GM092218 NIH via grant NIH NCI 1R03CA222452-01, Vanderbilt Chemical Biology Interface training program 5T32GM065086-16, Netherlands Organization for Scientific Research (NWO) 15747, SOLUTIONS project (European Union's Seventh Framework Programme for research, technological development and demonstration) 603437, HBM4EU (European Union's Horizon 2020 research and innovation programme 733032, German Research Foundation (DFG) 441958208, NaToxAq (European Union's Horizon 2020 research and innovation programme under the Marie Sklodowska-Curie Grant 722493, German Federal Ministry for the Environment, Nature Conservation and Nuclear Safety (BMU) (FKZ) 3716 67 416 0, German Federal Ministry for the Environment, Nature Conservation, Nuclear Safety and Consumer Protection (BMUV) Project (FKZ) 3719 65 408 0, EU Cohesion Funds within the project Monitoring and assessment of water body status 310011A366, Swiss Federal Office for the Environment (FOEN), Canadian Institutes of Health Research (CIHR) Genome Canada, MAVA foundation, Valery Foundation, National Science Foundation (NSF) RUI-1306074 National Natural Science Foundation of China (NSFC) 22193051 21906177, China Postdoctoral Science Foundation 2019M650863, Environmental Protection Administration, Executive Yuan, R.O.C. Taiwan (Taiwan EPA) 108C002871, Swiss Federal Office for the Environment, United States Environmental Protection Agency, Center for Forestry Research & Experimentation (CIEF), European Commission 2019/040, Marie Sklodowska-Curie grant 859891 European Commission European Commission Joint Research Centre 308610 289511, Joint Programming Initiative FOODBALL 2014-17 MCIN/AEI RYC2020-028901-I, ESF investing in your future, August T Larsson Guest Researcher Programme from the Swedish University of Agricultural Sciences, German Federal Ministry of Education and Research within the RiSKWa program 02WRS1273 02WRS1354, RECETOX research infrastructure (the Czech Ministry of Education, Youth and Sports) LM2018121, CETOCOEN PLUS project CZ.02.1.01/0.0/0.0/15_ 003/0000469 CETOCOEN EXCELLENCE Teaming 2 project - Czech ministry of Education, Youth and Sports CZ.02.1.01/0.0/0.0/1 7_043/0009632
Published: 2022
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13. Characterisation of anal intraepithelial neoplasia and anal cancer in <scp>HIV</scp> ‐positive men by immunohistochemical markers p16, Ki‐67, <scp>HPV‐E4</scp> and <scp>DNA</scp> methylation markers

Author: Wim Quint, Alexander Kreuter, Jan M. Prins, Renske D.M. Steenbergen, Henry J. C. de Vries, Chris J.L.M. Meijer, Ramon P. van der Zee, Miekel M. van de Sandt, and Tamzin Cuming
Subjects: Cancer Research, Pathology, medicine.medical_specialty, biology, business.industry, Anal Squamous Cell Carcinoma, Cancer, Methylation, medicine.disease, Malignant transformation, Oncology, Ki-67, DNA methylation, biology.protein, Biomarker (medicine), Medicine, Anal cancer, business
Abstract: Human papillomavirus (HPV)-induced anal intraepithelial neoplasia (AIN, graded 1-3) is highly prevalent in HIV-positive (HIV+) men who have sex with men (MSM), but only a minority of lesions progresses to cancer. Our study aimed to characterise comprehensively anal tissue samples from a cross-sectional series (n = 104) of HIV+ MSM and longitudinal series (n = 40) of AIN2/3 progressing to cancer using different biomarkers. The cross-sectional series consisted of 8 normal, 26 AIN1, 45 AIN2, 15 AIN3 and 10 anal squamous cell carcinoma. Tissue sections were immunohistochemically (IHC) stained for p16 (viral transformation marker), Ki-67 (cellular proliferation marker) and HPV-E4 (viral production marker). We evaluated the expression of IHC markers and compared it with DNA methylation, a marker for malignant transformation. E4 positivity decreased, whereas p16 and Ki-67 scores and methylation marker positivity increased (P values
Published: 2021
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14. Characterizing the molecular etiology of arthrogryposis multiplex congenita in patients with <scp> LGI4 </scp> mutations

Author: Nina Kozar, Daniel G Booth, Dies Meijer, and Stephen Bradley
Subjects: Arthrogryposis, Genetics, Arthrogryposis multiplex congenita, Mutant, ADAM22, Nerve Tissue Proteins, Biology, Compound heterozygosity, Axons, Mice, Cellular and Molecular Neuroscience, nervous system, Neurology, Mutant protein, Mutation, Animals, Humans, Missense mutation, Schwann Cells, Gene, Loss function
Abstract: Disruption of axon-glia interactions in the peripheral nervous system has emerged as a major cause of arthrogryposis multiplex congenita (AMC), a condition characterized by multiple congenital postural abnormalities involving the major joints. Several genes crucially important to the biology of Schwann cells have now been implicated with AMC. One such gene is LGI4 which encodes a secreted glycoprotein. LGI4 is expressed and secreted by Schwann cells and binds its receptor ADAM22 on the axonal membrane to drive myelination. Homozygous mutations in LGI4 or ADAM22 results in severe congenital hypomyelination and joint contractures in mice. Recently bi-allelic LGI4 loss of function mutations has been described in three unrelated families with severe AMC. Two individuals in a fourth, non-consanguineous family were found to be compound heterozygous for two LGI4 missense mutations. It is not known how these missense mutations affect the biology of LGI4. Here we investigated whether these missense mutations affected the secretion of the protein, its ADAM22 binding capacity, or its myelination-promoting function. We demonstrate that the mutations largely affect the progression of the mutant protein through the endomembrane system resulting in severely reduced expression. Importantly, binding to ADAM22 and myelination-promoting activity appear largely unaffected, suggesting that treatment with chemical chaperones to improve secretion of the mutant proteins might prove beneficial.
Published: 2021
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15. Breakpoint characterization of a rare alpha 0 ‐thalassemia deletion using targeted locus amplification on genomic DNA

Author: Cornelis L. Harteveld, Stefan J. White, Emile de Meijer, Henk P. J. Buermans, and Quint P Hottentot
Subjects: thalassemia, TLA, Inverse polymerase chain reaction, Biochemistry (medical), Clinical Biochemistry, Breakpoint, Locus (genetics), Hematology, General Medicine, Computational biology, Biology, DNA sequencing, molecular diagnostics, genomic DNA, hemoglobinopathy, Multiplex ligation-dependent probe amplification, targeted sequencing, Primer (molecular biology), clinical genetics, Southern blot
Abstract: Introduction The high-sequence homology of the α-globin-gene cluster is responsible for microhomology-mediated recombination events during meiosis, resulting in a high density of deletion breakpoints within a 10 kb region. Commonly used deletion detection methods, such as multiplex ligation-dependent probe amplification (MLPA) and Southern blot, cannot exactly define the breakpoints. This typically requires long-range PCR, which is not always successful. Targeted locus amplification (TLA) is a targeted enrichment method that can be used to sequence up to 70 kb of neighboring DNA sequences without prior knowledge about the target site. Methods Genomic DNA (gDNA) TLA is a technique that folds isolated DNA, ensuring that adjacent loci are in a close spatial proximity. Subsequent digestion and religation form DNA circles that are amplified using fragment-specific inverse primers, creating a library that is suitable for Illumina sequencing. Results Here, we describe the characterization of a rare 16 771 bp deletion, utilizing gDNA TLA with a single inverse PCR primer set on one end of the breakpoint. Primers for breakpoint PCR were designed to confirm the deletion breakpoints and were consequently used to characterize the same deletion in 10 additional carriers sharing comparable hematologic data and similar MLPA results. Conclusions The gDNA TLA technology was successfully used to identify deletion breakpoints within the alpha-globin cluster. The deletion was described only once in an earlier study as the --gb , but as it was not registered correctly in the available databases, it was not initially recognized as such.
Published: 2021
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16. BRN2 is a non-canonical melanoma tumor-suppressor

Author: Pierre Sohier, Luis Sánchez-del-Campo, Nisamanee Charoenchon, Colin Kenny, Madeleine Le Coz, Colin R. Goding, Lionel Larue, Véronique Delmas, Valérie Petit, Alain Sarasin, Eiríkur Steingrímsson, Zackie Aktary, Jérémy H. Raymond, Dies Meijer, Franck Gesbert, Michael Hamm, Irwin Davidson, Robert A. Cornell, Laura Mosteo, Florian Rambow, Alfonso Bellacosa, Göran Jönsson, Marie Pouteaux, Martin Lauss, Signalisation normale et pathologique de l'embryon aux thérapies innovantes des cancers, Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Carver College of Medicine [Iowa City], University of Iowa [Iowa City], Stabilité Génétique et Oncogenèse (UMR 8200), Université Paris-Sud - Paris 11 (UP11)-Institut Gustave Roussy (IGR)-Centre National de la Recherche Scientifique (CNRS), Mahidol University [Bangkok], Fox Chase Cancer Center, University of Oxford [Oxford], Lund University [Lund], University of Edinburgh, University of Iceland [Reykjavik], Institut de Génétique et de Biologie Moléculaire et Cellulaire (IGBMC), Université de Strasbourg (UNISTRA)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS), Signalisation, radiobiologie et cancer, Institut Curie [Paris]-Institut National de la Santé et de la Recherche Médicale (INSERM)-Université Paris-Saclay-Centre National de la Recherche Scientifique (CNRS), Carver College of Medicine, University of Iowa, University of Oxford, and delmas, veronique
Subjects: 0301 basic medicine, Neuroblastoma RAS viral oncogene homolog, Skin Neoplasms, Carcinogenesis, [SDV]Life Sciences [q-bio], General Physics and Astronomy, Haploinsufficiency, Cohort Studies, Mice, Phosphatidylinositol 3-Kinases, 0302 clinical medicine, CDKN2A, Genes, Tumor Suppressor, RNA, Small Interfering, Melanoma, Multidisciplinary, biology, Microphthalmia-associated transcription factor, Immunohistochemistry, Gene Expression Regulation, Neoplastic, Mechanisms of disease, Gene Knockdown Techniques, 030220 oncology & carcinogenesis, Disease Progression, [SDV.BBM.GTP] Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], Proto-Oncogene Proteins B-raf, Chromatin Immunoprecipitation, DNA Copy Number Variations, Science, Mice, Transgenic, [SDV.CAN]Life Sciences [q-bio]/Cancer, Context (language use), Article, General Biochemistry, Genetics and Molecular Biology, 03 medical and health sciences, [SDV.CAN] Life Sciences [q-bio]/Cancer, Cell Line, Tumor, [SDV.BBM.GTP]Life Sciences [q-bio]/Biochemistry, Molecular Biology/Genomics [q-bio.GN], medicine, Animals, Humans, PTEN, Transcription factor, neoplasms, Cell Proliferation, Homeodomain Proteins, Microphthalmia-Associated Transcription Factor, POU domain, PTEN Phosphohydrolase, General Chemistry, Microarray Analysis, medicine.disease, Mice, Inbred C57BL, 030104 developmental biology, Mutation, POU Domain Factors, biology.protein, Cancer research, Gene expression
Abstract: While the major drivers of melanoma initiation, including activation of NRAS/BRAF and loss of PTEN or CDKN2A, have been identified, the role of key transcription factors that impose altered transcriptional states in response to deregulated signaling is not well understood. The POU domain transcription factor BRN2 is a key regulator of melanoma invasion, yet its role in melanoma initiation remains unknown. Here, in a BrafV600E PtenF/+ context, we show that BRN2 haplo-insufficiency promotes melanoma initiation and metastasis. However, metastatic colonization is less efficient in the absence of Brn2. Mechanistically, BRN2 directly induces PTEN expression and in consequence represses PI3K signaling. Moreover, MITF, a BRN2 target, represses PTEN transcription. Collectively, our results suggest that on a PTEN heterozygous background somatic deletion of one BRN2 allele and temporal regulation of the other allele elicits melanoma initiation and progression., The transcription factor BRN2 regulates melanoma migration and invasion, but its role during melanoma initiation is unclear. Here the authors show that BRN2 is a haplo-insufficient tumour suppressor that positively regulates PTEN expression and in the context of BRAF mutation and heterozygous PTEN, BRN2 loss promotes melanoma initiation and progression.
Published: 2021
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17. Nonergodicity in protective factors of resilience in athletes

Author: Georgios Michelakis, Ruud J. R. Den Hartigh, Simon Barisch, Nico W. Van Yperen, Yannick Hill, Rob R. Meijer, Motor learning & Performance, Developmental Psychology, Psychometrics and Statistics, and Sociology/ICS
Subjects: DYNAMICS, Social Psychology, biology, Athletes, Psychological intervention, Cognitive complexity, Physical Therapy, Sports Therapy and Rehabilitation, Sample (statistics), dynamical systems, PSYCHOLOGICAL RESILIENCE, biology.organism_classification, SPORT, Developmental psychology, Test (assessment), SYSTEMS, time series, Resilience (network), Construct (philosophy), Psychology, Level of analysis, complexity, generalizability, Applied Psychology, SCALE
Abstract: Resilience is a key construct to understand when athletes continue to perform optimally, or when they break down. Although there is consensus that resilience can be conceptualized as a dynamic process, it remains an open question whether studying such a process on a group level adequately represents the individuals within a given sample. As a first step to answer this question, we designed a diary study to test whether the statistics for repeated assessments of protective factors and resilience can be generalized from group-level trajectories to the individuals. By tracking resilience and the protective factors over 21 days in athletes, we found divergent patterns of group-level and individual-level statistics for the repeated assessments. This so-called "ergodicity problem" implies that the individual, rather than the group, should be placed at the level of analysis to avoid wrong conclusions and ineffective interventions on their resilience.
Published: 2021
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18. Chondroitin Sulfate Disaccharides in the Gas Phase: Differentiation and Conformational Constraints

Author: Gert von Helden, Rebecca L. Miller, Gerard Meijer, Kevin Pagel, Kim Greis, Jan Horlebein, Maike Lettow, and Márkó Grabarics
Subjects: Anions, Glycan, Carbohydrates, Disaccharide, Infrared spectroscopy, 010402 general chemistry, 01 natural sciences, Article, Dermatan sulfate, chemistry.chemical_compound, Sulfation, Computational chemistry, 0103 physical sciences, Molecule, Chondroitin, Chondroitin sulfate, Physical and Theoretical Chemistry, Ions, Energy, 010304 chemical physics, biology, 0104 chemical sciences, chemistry, biology.protein, 500 Naturwissenschaften und Mathematik::540 Chemie::540 Chemie und zugeordnete Wissenschaften, Molecular structure
Abstract: Glycosaminoglycans (GAGs) are a family of complex carbohydrates vital to all mammalian organisms and involved in numerous biological processes. Chondroitin and dermatan sulfate, an important class of GAGs, are linear macromolecules consisting of disaccharide building blocks of N-acetylgalactosamine and two different uronic acids. The varying degree and the site of sulfation render their characterization challenging. Here, we combine mass spectrometry with cryogenic infrared spectroscopy in the wavenumber range from 1000 to 1800 cm-1. Fingerprint spectra were recorded for a comprehensive set of disaccharides bearing all known motifs of sulfation. In addition, state-of-the-art quantum chemical calculations were performed to aid the understanding of the differences in the experimental fingerprint spectra. The results show that the degree and position of charged sulfate groups define the size of the conformational landscape in the gas phase. The detailed understanding of cryogenic infrared spectroscopy for acidic and often highly sulfated glycans may pave the way to utilize the technique in fragment-based sequencing approaches.
Published: 2021
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19. Classification of high‐grade cervical intraepithelial neoplasia by p16 ink4a , Ki‐67, <scp>HPV E4</scp> and <scp>FAM19A4</scp> / <scp>miR124</scp> ‐2 methylation status demonstrates considerable heterogeneity with potential consequences for management

Author: Renske D.M. Steenbergen, Johannes Berkhof, Mario Poljak, Maaike C G Bleeker, Frederique J Vink, Jesper Bonde, Peter Hillemanns, Chris J.L.M. Meijer, Stèfanie Dick, Daniëlle A M Heideman, Birgit L W Lissenberg-Witte, Arno Floore, K. U. Petry, Lise M.A. De Strooper, Anja Oštrbenk Valenčak, and Nienke E. van Trommel
Subjects: Cervical cancer, Oncology, Cancer Research, medicine.medical_specialty, biology, business.industry, HPV infection, Cancer, medicine.disease, Cervical intraepithelial neoplasia, female genital diseases and pregnancy complications, 3. Good health, 03 medical and health sciences, 0302 clinical medicine, 030220 oncology & carcinogenesis, Internal medicine, Ki-67, DNA methylation, High Grade Cervical Intraepithelial Neoplasia, medicine, biology.protein, Biomarker (medicine), business
Abstract: High-grade cervical intraepithelial neoplasia (CIN2 and CIN3) represent a heterogeneous disease with varying cancer progression risks. Biomarkers indicative for a productive human papillomavirus (HPV) infection (HPV E4) and a transforming HPV infection (p16ink4a , Ki-67 and host-cell DNA methylation), could provide guidance for clinical management in women with high-grade CIN. This study evaluates the cumulative score of immunohistochemical expression of p16ink4a (score 0 - 3) and Ki-67 (score 0 - 3), referred to as the 'immunoscore' (IS), in 262 CIN2 and 235 CIN3 lesions derived from 5 European cohorts in relation to immunohistochemical HPV E4 expression and FAM19A4/miR124-2 methylation in the corresponding cervical scrape. The immunoscore classification resulted in 30 lesions within IS group 0 - 2 (6.0%), 151 lesions within IS group 3 - 4 (30.4%) and 316 lesions within IS group 5 - 6 (63.6%). E4 expression decreased significantly from CIN2 to CIN3 (p
Published: 2021
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20. LMW cyclin E and its novel catalytic partner CDK5 are therapeutic targets and prognostic biomarkers in salivary gland cancers

Author: Tuyen Bui, Xiayu Rao, Natalie W. Fowlkes, Adel K. El-Naggar, Laurent Meijer, Jing Wang, Said Akli, Cansu Karakas, Khandan Keyomarsi, Amriti R. Lulla, Yoshitsugu Mitani, Kelly K. Hunt, and Min Jin Ha
Subjects: 0301 basic medicine, Genetically modified mouse, Cancer Research, Cyclin E, Article, Tumour biomarkers, 03 medical and health sciences, 0302 clinical medicine, Target identification, Medicine, Cancer models, Molecular Biology, RC254-282, Salivary gland, biology, business.industry, Cell growth, Cyclin-dependent kinase 2, food and beverages, Neoplasms. Tumors. Oncology. Including cancer and carcinogens, Oncogenes, Parotid gland, 030104 developmental biology, medicine.anatomical_structure, 030220 oncology & carcinogenesis, Cancer research, biology.protein, Biomarker (medicine), Immunohistochemistry, business
Abstract: Salivary gland cancers (SGCs) are rare yet aggressive malignancies with significant histological heterogeneity, which has made prediction of prognosis and development of targeted therapies challenging. In majority of patients, local recurrence and/or distant metastasis are common and systemic treatments have minimal impact on survival. Therefore, identification of novel targets for treatment that can also be used as predictors of recurrence for multiple histological subtypes of SGCs is an area of unmet need. In this study, we developed a novel transgenic mouse model of SGC, efficiently recapitulating the major histological subtype (adenocarcinomas of the parotid gland) of human SGC. CDK2 knock out (KO) mice crossed with MMTV-low molecular weight forms of cyclin E (LMW-E) mice generated the transgenic mouse models of SGC, which arise in the parotid region of the salivary gland, similar to the common site of origin seen in human SGCs. To identify the CDK2 independent catalytic partner(s) of LMW-E, we used LMW-E expressing cell lines in mass spectrometric analysis and subsequent biochemical validation in pull down assays. These studies revealed that in the absence of CDK2, LMW-E preferentially binds to CDK5. Molecular targeting of CDK5, using siRNA, resulted in inhibition of cell proliferation of human SGCs overexpressing LMW-E. We also provide clinical evidence of significant association of LMW-E/CDK5 co-expression and decreased recurrence free survival in human SGC. Immunohistochemical analysis of LMW-E and CDK5 in 424 patients representing each of the four major histological subtypes of human salivary cancers (Aci, AdCC, MEC, and SDC) revealed that LMW-E and CDK5 are concordantly (positive/positive or negative/negative) expressed in 70% of these patients. The co-expression of LMW-E/CDK5 (both positive) robustly predicts the likelihood of recurrence, regardless of the histological classification of these tumors. Collectively, our results suggest that CDK5 is a novel and targetable biomarker for the treatment of patients with SGC presenting with LMW-E overexpressing tumors.
Published: 2021

21. Temporal Variations in Respiratory Syncytial Virus Epidemics, by Virus Subtype, 4 Countries

Author: Ana Paula Rodrigues, Clarisse Demont, John Paget, Saverio Caini, Adam Meijer, Lisa Staadegaard, Cheryl Cohen, Sue Huang, and Jojanneke van Summeren
Subjects: Microbiology (medical), 2019-20 coronavirus outbreak, Coronavirus disease 2019 (COVID-19), Epidemiology, respiratory syncytial virus, viruses, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), 030231 tropical medicine, Respiratory Syncytial Virus Infections, Infectious and parasitic diseases, RC109-216, Biology, Temporal, epidemics, Virus, South Africa, 03 medical and health sciences, 0302 clinical medicine, Research Letter, Humans, 030212 general & internal medicine, Respiratory system, Portugal, the Netherlands, DNA Viruses, Infant, virus diseases, respiratory system, Virology, Temporal Variations in Respiratory Syncytial Virus Epidemics, by Virus Subtype, 4 Countries, Infectious Diseases, Respiratory Syncytial Virus, Human, surveillance, Medicine, New Zealand
Abstract: Temporal variation of respiratory syncytial virus (RSV) epidemics was recently reported to be determined by the dominant RSV subtype. However, when we repeated the analysis for 4 countries in the Northern and Southern Hemispheres, the dominant subtype did not seem to affect temporal variation of RSV epidemics.
Published: 2021
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22. A world‐wide analysis of reduced sensitivity to <scp>DMI</scp> fungicides in the banana pathogen Pseudocercospora fijiensis

Author: Chong, Pablo, Essoh, Josué Ngando, Arango Isaza, Rafael E., Keizer, Paul, Stergiopoulos, Ioannis, Seidl, Michael F., Guzman, Mauricio, Sandoval, Jorge, Verweij, Paul E., Scalliet, Gabriel, Sierotzski, Helge, de Lapeyre de Bellaire, Luc, Crous, Pedro W., Carlier, Jean, Cros, Sandrine, Meijer, Harold J.G., Peralta, Esther Lilia, Kema, Gert H.J., Sub Bioinformatics, Sub Molecular Microbiology, Theoretical Biology and Bioinformatics, Molecular Microbiology, Sub Bioinformatics, Sub Molecular Microbiology, Theoretical Biology and Bioinformatics, Molecular Microbiology, Westerdijk Fungal Biodiversity Institute - Evolutionary Phytopathology, Westerdijk Fungal Biodiversity Institute, Escuela Superior Politécnica del Litoral [Guayaquil] (ESPOL), Wageningen University and Research [Wageningen] (WUR), African Center for Research on Bananas and Plantains = Centre Africain de Recherches sur Bananiers et Plantains (CARBAP), Fonctionnement écologique et gestion durable des agrosystèmes bananiers et ananas (UR GECO), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad), Universidad Nacional de Colombia Sede Medellín, Corporacion para Investigaciones Biologicas (CIB), University of California [Davis] (UC Davis), University of California (UC), Utrecht University [Utrecht], Corporación Bananera Nacional (CORBANA), Radboud University Medical Center [Nijmegen], Syngenta AG Suisse, Westerdijk Fungal Biodiversity Institute [Utrecht] (WI), Royal Netherlands Academy of Arts and Sciences (KNAW), Biologie et Génétique des Interactions Plante-Parasite (UMR BGPI), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-Institut National de la Recherche Agronomique (INRA)-Centre international d'études supérieures en sciences agronomiques (Montpellier SupAgro)-Institut national d’études supérieures agronomiques de Montpellier (Montpellier SupAgro), Plant Health Institute of Montpellier (UMR PHIM), Centre de Coopération Internationale en Recherche Agronomique pour le Développement (Cirad)-Institut de Recherche pour le Développement (IRD)-Université de Montpellier (UM)-Institut National de Recherche pour l’Agriculture, l’Alimentation et l’Environnement (INRAE)-Institut Agro - Montpellier SupAgro, Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro)-Institut national d'enseignement supérieur pour l'agriculture, l'alimentation et l'environnement (Institut Agro), Ecuadorian government through the Secretaría de Educación Superior, Ciencia, Tecnología e Innovación (SENESCYT), Ecuadorian University, Escuela Superior Politécnica del Litoral (ESPOL), Centro de Investigaciones Biotecnológicas del Ecuador (CIBE) and Syngenta AG., Wageningen University and Research (WUR) banana program, Universidad National de Colombia, sede Medellín, Dutch Dioraphte Foundation, University of California, and Westerdijk Fungal Biodiversity Insitute [Utrecht] (WI)
Subjects: 0106 biological sciences, Integrated pest management, Black sigatoka, Philippines, H02 - Pesticides, Musa (bananes), Wiskundige en Statistische Methoden - Biometris, 01 natural sciences, chemistry.chemical_compound, Maladie des plantes, Pseudocercospora fijiensis, Cameroon, Pathogen, Research Articles, Fungicides, 2. Zero hunger, promoter insertions, Contrôle de maladies, palindrome, food and beverages, General Medicine, Plant disease, Propiconazole, Fungicide, Horticulture, Fongicide, Industrial, Maladie des raies noires, Martinique, Research Article, Costa Rica, Crop and Pasture Production, Environmental Science and Management, azoles, Pathologie végétale, Colombia, Biology, Biointeractions and Plant Health, Ascomycota, Mycosphaerella fijiensis, Epoxiconazole, Résistance aux fongicides, Mathematical and Statistical Methods - Biometris, H20 - Maladies des plantes, fungicide resistant, Musa, black Sigatoka, mutations, Laboratorium voor Phytopathologie, Fungicides, Industrial, [SDV.BV.PEP]Life Sciences [q-bio]/Vegetal Biology/Phytopathology and phytopharmacy, 010602 entomology, bananas, chemistry, cyp51, Insect Science, Laboratory of Phytopathology, EPS, Entomology, Agronomy and Crop Science, 010606 plant biology & botany
Abstract: BACKGROUND Pseudocercospora fijiensis is the causal agent of the black leaf streak disease (BLSD) of banana. Bananas are important global export commodities and a major staple food. Their susceptibility to BLSD pushes disease management towards excessive fungicide use, largely relying on multisite inhibitors and sterol demethylation inhibitors (DMIs). These fungicides are ubiquitous in plant disease control, targeting the CYP51 enzyme. We examined sensitivity to DMIs in P. fijiensis field isolates collected from various major banana production zones in Colombia, Costa Rica, Dominican Republic, Ecuador, the Philippines, Guadalupe, Martinique and Cameroon and determined the underlying genetic reasons for the observed phenotypes. RESULTS We observed a continuous range of sensitivity towards the DMI fungicides difenoconazole, epoxiconazole and propiconazole with clear cross‐sensitivity. Sequence analyses of PfCYP51 in 266 isolates showed 28 independent amino acid substitutions, nine of which correlated with reduced sensitivity to DMIs. In addition to the mutations, we observed up to six insertions in the Pfcyp51 promoter. Such promoter insertions contain repeated elements with a palindromic core and correlate with the enhanced expression of Pfcyp51 and hence with reduced DMI sensitivity. Wild‐type isolates from unsprayed bananas fields did not contain any promoter insertions. CONCLUSION The presented data significantly contribute to understanding of the evolution and global distribution of DMI resistance mechanisms in P. fijiensis field populations and facilitate the prediction of different DMI efficacy. The overall reduced DMI sensitivity calls for the deployment of a wider range of solutions for sustainable control of this major banana disease. © 2021 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry., Studies on Pseudocercospora fijiensis demethylation inhibitor (DMI) sensitivity shows that Pfcyp51 modulations correlated with fungicide resistance. The importance of amino acid substitutions at positions 137, 311, 378, 379 and 458–461 is strengthened by mathematical modelling. Changes in these positions compromise the three‐dimensional structure of the protein resulting in an affinity change. The presence of repeated elements and insertions in the promotor region of Pfcyp51 was also positively correlated with resistance to DMIs. © 2021 The Authors. Pest Management Science published by John Wiley & Sons Ltd on behalf of Society of Chemical Industry.
Published: 2021
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23. A unique small cell lung carcinoma disease progression model shows progressive accumulation of cancer stem cell properties and CD44 as a potential diagnostic marker

Author: Reinoud Gosens, Frank A.E. Kruyt, Coby Meijer, Win Sen Heng, Shiau-Chuen Cheah, Milind Pore, T. Jeroen N. Hiltermann, Translational Immunology Groningen (TRIGR), Molecular Pharmacology, Groningen Research Institute for Asthma and COPD (GRIAC), Guided Treatment in Optimal Selected Cancer Patients (GUTS), and Damage and Repair in Cancer Development and Cancer Treatment (DARE)
Subjects: 0301 basic medicine, Pulmonary and Respiratory Medicine, Cancer Research, Lung Neoplasms, Stem cell marker, Flow cytometry, 03 medical and health sciences, 0302 clinical medicine, SOX2, Cancer stem cell, Cell Line, Tumor, Humans, Medicine, medicine.diagnostic_test, biology, business.industry, CD44, Small Cell Lung Carcinoma, carbohydrates (lipids), Hyaluronan Receptors, 030104 developmental biology, Oncology, Cell culture, 030220 oncology & carcinogenesis, Disease Progression, Neoplastic Stem Cells, biology.protein, Cancer research, Stem cell, business
Abstract: OBJECTIVES: Cancer stem cells (CSCs) have been implicated in disease progression of aggressive cancers including small cell lung carcinoma (SCLC). Here, we have examined the possible contribution of CSCs to SCLC progression and aggressiveness.MATERIALS AND METHODS: GLC-14, GLC-16 and GLC-19 SCLC cell lines derived from one patient, representing increasing progressive stages of disease were used. CSC marker expressions was determined by RT-qPCR and western blotting analyses, and heterogeneity was studied by CSC marker expression by immunofluorescence microscopy and flow cytometry. Colony formation assays were used to assess stem cell properties and therapy sensitivity.RESULTS: Increasing expression of stem cell markers MYC, SOX2 and particularly CD44 were found in association with advancing disease. Single and overlapping expression of these markers indicated the presence of different CSC populations. The accumulation of more homogeneous double- and triple-positive CSC populations evolved with disease progression. Functional characterization of CSC properties affirmed higher proficiency of colony forming ability and increased resistance to γ-irradiation in GLC-16 and GLC-19 compared to GLC-14. GLC-19 colony formation was significantly inhibited by a human anti-CD44 antibody.CONCLUSION: The progressive increase of MYC, SOX2 and particularly CD44 expression that was accompanied with enhanced colony forming capacity and resistance in the in vitro GLC disease progression model, supports the potential clinical relevance of CSC populations in malignancy and disease relapse of SCLC.
Published: 2021
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24. IgE autoantibodies in serum and skin of non-bullous and bullous pemphigoid patients

Author: Hendri H. Pas, M. F. Jonkman, Aniek Lamberts, Barbara Horváth, Bernhard F. Gibbs, G. Di Zenzo, Nika Kotnik, Joost M. Meijer, Ulrike Raap, Gilles F. H. Diercks, Translational Immunology Groningen (TRIGR), and Microbes in Health and Disease (MHD)
Subjects: 0301 basic medicine, Pemphigoid, BP180, Enzyme-Linked Immunosorbent Assay, Dermatology, Immunofluorescence, Immunoglobulin E, Autoantigens, DISEASE, Autoimmune Diseases, COMPLEMENT, Pathogenesis, 030207 dermatology & venereal diseases, 03 medical and health sciences, 0302 clinical medicine, Pemphigoid, Bullous, Medicine, Humans, skin and connective tissue diseases, ELDERLY-PATIENTS, Dermoepidermal junction, Aged, Autoantibodies, medicine.diagnostic_test, biology, integumentary system, business.industry, Autoantibody, Non-Fibrillar Collagens, medicine.disease, ANTI-BP180, SEVERE FORM, Pemphigus, XVII COLLAGEN, 030104 developmental biology, Infectious Diseases, Immunology, BLISTER FORMATION, biology.protein, MAST-CELLS, Original Article, Bullous pemphigoid, business, DERMAL-EPIDERMAL JUNCTION
Abstract: Background Non‐bullous pemphigoid (NBP) is a pemphigoid variant which frequently resembles other pruritic skin diseases. In contrast with bullous pemphigoid (BP), blisters are absent. In BP, previous studies showed that IgE autoantibodies may be involved in its pathogenesis. IgE‐activated mast cells, basophils and eosinophils may participate in BP by inducing pruritus and possibly blister formation, although the differential role of IgE in NBP compared with BP has not yet been described. Objective To assess IgE in serum and skin of NBP and BP patients. Methods We examined total IgE and pemphigoid‐specific IgE in the serum of 68 NBP and 50 BP patients by enzyme‐linked immunosorbent assay (ELISA). Sera of 25 pemphigus patients and 25 elderly patients with pruritus were included as controls. Skin biopsies of 14 NBP and 14 BP patients with the highest IgE titres to NC16A were stained for IgE by immunofluorescence techniques. Results Total IgE was elevated in 63% of NBP and 60% of BP patients, and in 20% of pemphigus controls, as well as 60% of elderly controls. IgE ELISAs were more frequently positive in BP than in NBP (NC16A 18% vs. 9%, P = 0.139; BP230 34% vs. 22%, P = 0.149). IgE ELISAs for NC16A and BP230 were positive in 8% and 20% of elderly controls, respectively, while all pemphigus controls were negative. Two of 28 biopsies (7%; one NBP, one BP) showed linear IgE along the basement membrane zone, while in most biopsies (71% NBP; 86% BP) IgE was bound to dermal cells. Conclusion Since IgE was present in the serum and skin of both NBP and BP patients, this supports IgE‐dependent mechanisms common to both diseases, such as pruritus. However, it remains to be elucidated whether IgE contributes to blister formation in BP., Linked Commentary: I. Kortekaas Krohn. J Eur Acad Dermatol Venereol 2021; 35: 781–782. https://doi.org/10.1111/jdv.17164.
Published: 2021

25. Discovery of a new family of relaxases in Firmicutes bacteria

Author: César Gago-Córdoba, Gayetri Ramachandran, Ling Juan Wu, Isidro Crespo, Praveen K. Singh, Juan Román Luque-Ortega, Jian-An Hao, Wilfried J. J. Meijer, Andrés Miguel-Arribas, Roeland Boer, David Abia, Carlos Alfonso, Ministerio de Economía y Competitividad (España), Ministerio de Economía, Industria y Competitividad (España), Wellcome Trust, Ramachandran, Gayetri, Miguel-Arribas, Andrés, Abia, David, Crespo, Isidro, Gago-Córdoba, César, Alfonso, Carlos, Boer, Roeland, Meijer, Wilfried J. J., Ramachandran, Gayetri [0000-0002-3457-266X], Miguel-Arribas, Andrés [0000-0001-5679-9083], Abia, David [0000-0003-0401-7590], Crespo, Isidro [0000-0001-7698-1720], Gago-Córdoba, César [0000-0001-7470-4033], Alfonso, Carlos [0000-0001-7165-4800], Boer, Roeland [0000-0001-5949-6627], and Meijer, Wilfried J. J. [0000-0003-1842-0049]
Subjects: 0301 basic medicine, Cancer Research, Relaxases, Molecular biology, Sequence similarity searching, Antibiotic resistance, Bacillus-subtilis, Artificial Gene Amplification and Extension, Bacillus, Relaxase, Pathology and Laboratory Medicine, Polymerase Chain Reaction, Biochemistry, Database and Informatics Methods, Plasmid, Mobile Genetic Elements, Medicine and Health Sciences, Functional-characterization, Database Searching, Genetics (clinical), Genetics, Diversity, biology, Genomics, Horizontal gene transfer, Relaxosome, Protein database searches, Bacterial Pathogens, Polymerase chain reaction, Nucleic acids, Bacillus Subtilis, Experimental Organism Systems, Medical Microbiology, Conjugation, Genetic, Prokaryotic Models, Sequence databases, Pathogens, Sequence Analysis, Research Article, Plasmids, lcsh:QH426-470, Gene Transfer, Horizontal, Firmicutes, Bioinformatics, Forms of DNA, 030106 microbiology, PSI-BLAST, Sequence Databases, DNA, Single-Stranded, DNA construction, Plasmid construction, Research and Analysis Methods, Microbiology, Bacterial genetics, 03 medical and health sciences, Genetic Elements, Bacterial Proteins, Sequence Motif Analysis, Microbial Control, Drug Resistance, Bacterial, Humans, Amino Acid Sequence, Sequence Similarity Searching, Gene, Plasmid PLS20, Microbial Pathogens, Ecology, Evolution, Behavior and Systematics, Pharmacology, Endodeoxyribonucleases, Biology and life sciences, Bacteria, Organisms, DNA, biology.organism_classification, Antibiotic-resistance reservoir, Gastrointestinal Microbiome, lcsh:Genetics, Molecular biology techniques, Biological Databases, Antibiotic Resistance, Sequence motif analysis, Plasmid Construction, Replication origins, Microbiome, Antimicrobial Resistance
Abstract: 23 p.-5 fig.-2 tab., Antibiotic resistance is a serious global problem. Antibiotic resistance genes (ARG), which are widespread in environmental bacteria, can be transferred to pathogenic bacteria via horizontal gene transfer (HGT). Gut microbiomes are especially apt for the emergence and dissemination of ARG. Conjugation is the HGT route that is predominantly responsible for the spread of ARG. Little is known about conjugative elements of Gram-positive bacteria, including those of the phylum Firmicutes, which are abundantly present in gut microbiomes. A critical step in the conjugation process is the relaxase-mediated site-and strand-specific nick in the oriT region of the conjugative element. This generates a single-stranded DNA molecule that is transferred from the donor to the recipient cell via a connecting channel. Here we identified and characterized the relaxosome components oriT and the relaxase of the conjugative plasmid pLS20 of the Firmicute Bacillus subtilis. We show that the relaxase gene, named rel(LS20), is essential for conjugation, that it can function in trans and provide evidence that Tyr26 constitutes the active site residue. In vivo and in vitro analyses revealed that the oriT is located far upstream of the relaxase gene and that the nick site within oriT is located on the template strand of the conjugation genes. Surprisingly, the Rel(LS20) shows very limited similarity to known relaxases. However, more than 800 genes to which no function had been attributed so far are predicted to encode proteins showing significant similarity to RelLS20. Interestingly, these putative relaxases are encoded almost exclusively in Firmicutes bacteria. Thus, RelLS20 constitutes the prototype of a new family of relaxases. The identification of this novel relaxase family will have an important impact in different aspects of future research in the field of HGT in Gram-positive bacteria in general, and specifically in the phylum of Firmicutes, and in gut microbiome research., Work in the Meijer lab was funded by the Spanish government through grant Bio2013- 41489-P of the Ministry of Economy and Competitiveness, and through grant Bio2016- 77883-C2-1-P of the Ministry of Economy, Industry and Competitiveness; the former grant also funded AMA and CGC. The Spanish government also supported DRB, JRLO, and CA.DRB was funded by grant Bio2016-77883-C2-2-P of the Ministry of Economy, Industry and Competitiveness, and JRLO and CA were supported by grant BFU2014-52070-C2-2-P of the Ministry of Economy and Competitiveness to CA.LJW's work was supported by Wellcome Trust grant WT098374AIA to Jeff Errington.
Published: 2021

26. EIF2AK2 Missense Variants Associated with Early Onset Generalized Dystonia

Author: Lena Sagi-Dain, Martje G. Pauly, Chiung C. Chen, Niccolo E. Mencacci, Shey Lin Wu, Inge A. Meijer, Aida M. Bertoli-Avella, Krishna Kumar Kandaswamy, Steven J. Lubbe, Celeste Panteghini, Wim Mandemakers, Christine Klein, Nicolas Marotta, Katja Lohmann, Peter Bauer, Andrea A. Kühn, Baiba Lace, Vincenzo Bonifati, Tu Hsueh Yeh, Chin Song Lu, Miryam Carecchio, Antonio E. Elia, Christina Fevga, Yah Huei Wu-Chou, Yi Hsin Weng, Vera Tadic, Bradley Osterman, Marialuisa Quadri, Barbara Garavaglia, Simone Olgiati, Guido J. Breedveld, Jens Volkmann, Hsiu Chen Chang, Demy J.S. Kuipers, and Clinical Genetics
Subjects: 0301 basic medicine, Adult, Male, Adolescent, Mutation, Missense, Biology, White People, 03 medical and health sciences, symbols.namesake, Young Adult, eIF-2 Kinase, 0302 clinical medicine, Asian People, Genetic linkage, Exome Sequencing, medicine, Missense mutation, Humans, Age of Onset, Protein kinase A, Child, Exome, Research Articles, Dystonia, Sanger sequencing, Genetics, Kinase, Brain, Infant, Fibroblasts, Middle Aged, medicine.disease, Protein kinase R, Magnetic Resonance Imaging, Pedigree, 030104 developmental biology, Neurology, Dystonic Disorders, Child, Preschool, symbols, Female, Neurology (clinical), 030217 neurology & neurosurgery, Genome-Wide Association Study, Research Article
Abstract: Objective: The study was undertaken to identify a monogenic cause of early onset, generalized dystonia. Methods: Methods consisted of genome-wide linkage analysis, exome and Sanger sequencing, clinical neurological examination, brain magnetic resonance imaging, and protein expression studies in skin fibroblasts from patients. Results: We identified a heterozygous variant, c.388G>A, p.Gly130Arg, in the eukaryotic translation initiation factor 2 alpha kinase 2 (EIF2AK2) gene, segregating with early onset isolated generalized dystonia in 5 patients of a Taiwanese family. EIF2AK2 sequencing in 191 unrelated patients with unexplained dystonia yielded 2 unrelated Caucasian patients with an identical heterozygous c.388G>A, p.Gly130Arg variant, occurring de novo in one case, another patient carrying a different heterozygous variant, c.413G>C, p.Gly138Ala, and one last patient, born from consanguineous parents, carrying a third, homozygous variant c.95A>C, p.Asn32Thr. These 3 missense variants are absent from gnomAD, and are located in functional domains of the encoded protein. In 3 patients, additional neurological manifestations were present, including intellectual disability and spasticity. EIF2AK2 encodes a kinase (protein kinase R [PKR]) that phosphorylates eukaryotic translation initiation factor 2 alpha (eIF2α), which orchestrates the cellular stress response. Our expression studies showed abnormally enhanced activation of the cellular stress response, monitored by PKR-mediated phosphorylation of eIF2α, in fibroblasts from patients with EIF2AK2 variants. Intriguingly, PKR can also be regulated by PRKRA (protein interferon-inducible double-stranded RNA-dependent protein kinase activator A), the product of another gene causing monogenic dystonia. Interpretation: We identified EIF2AK2 variants implicated in early onset generalized dystonia, which can be dominantly or recessively inherited, or occur de novo. Our findings provide direct evidence for a key role of a dysfunctional eIF2α pathway in the pathogenesis of dystonia. ANN NEUROL 2021;89:485–497.
Published: 2021

27. Dose-Finding Study of a CEA-Targeting Agent, SGM-101, for Intraoperative Fluorescence Imaging of Colorectal Cancer

Author: Shadhvi S. Bhairosingh, Koen C.M.J. Peeters, Dennis P. Schaap, Kim S. de Valk, Charlotte E.S. Hoogstins, Denise E. Hilling, Bérénice Framery, Fabian A. Holman, Leonora S.F. Boogerd, Miranda Kusters, Maxime J M van der Valk, Françoise Cailler, Marion M. Deken, Jacobus Burggraaf, Ruben P J Meijer, Harm J. T. Rutten, Ingrid M C Kamerling, Alexander L. Vahrmeijer, Surgery, CCA - Imaging and biomarkers, and CCA - Cancer Treatment and quality of life
Subjects: Male, medicine.medical_specialty, Fluorescence-lifetime imaging microscopy, Colorectal cancer, medicine.medical_treatment, 03 medical and health sciences, 0302 clinical medicine, Carcinoembryonic antigen, Surgical oncology, Translational Research, medicine, Humans, Neoadjuvant therapy, Aged, Chemotherapy, biology, business.industry, Optical Imaging, Middle Aged, medicine.disease, Carcinoembryonic Antigen, Radiation therapy, Clinical trial, Oncology, 030220 oncology & carcinogenesis, biology.protein, Female, 030211 gastroenterology & hepatology, Surgery, Radiology, Neoplasm Recurrence, Local, Colorectal Neoplasms, business
Abstract: BackgroundCarcinoembryonic antigen is overexpressed in colorectal cancer (CRC), making it an optimal target for fluorescence imaging. A phase I/II study was designed to determine the optimal imaging dose of SGM-101 for intraoperative fluorescence imaging of primary and recurrent CRC.MethodsPatients were included and received a single dose of SGM-101 at least 24 h before surgery. Patients who received routine anticancer therapy (i.e., radiotherapy or chemotherapy) also were eligible. A dedicated near-infrared imaging system was used for real-time fluorescence imaging during surgery. Safety assessments were performed and SGM-101 efficacy was evaluated per dose level to determine the most optimal imaging dose.ResultsThirty-seven patients with CRC were included in the analysis. Fluorescence was visible in all primary and recurrent tumors. In seven patients, no fluorescence was seen; all were confirmed as pathological complete responses after neoadjuvant therapy. Two tumors showed false-positive fluorescence. In the 37 patients, a total of 97 lesions were excised. The highest mean intraoperative tumor-to-background ratio (TBR) of 1.9 (p = 0.019) was seen in the 10-mg dose. This dose showed a sensitivity of 96%, specificity of 63%, and negative predictive value of 94%. Nine patients (24%) had a surgical plan alteration based on fluorescence, with additional malignant lesions detected in six patients.ConclusionsThe optimal imaging dose was established at 10 mg 4 days before surgery. The results accentuate the potential of SGM-101 and designated a promising base for the multinational phase III study, which enrolled the first patients in June 2019.
Published: 2021
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28. A polygenic resilience score moderates the genetic risk for schizophrenia

Author: Hess, Jonathan L, Tylee, Daniel S, Mors, Ole, Duan, Jubao, Dudbridge, Frank, Duncanson, Audrey, Durmishi, Naser, Edkins, Sarah, Ehrenreich, Hannelore, Eichhammer, Peter, Eriksson, Johan, Escott-Price, Valentina, Esko, Tõnu, Nordentoft, Merete, Essioux, Laurent, Fanous, Ayman H, Farh, Kai-How, Farrell, Martilias S, Frank, Josef, Franke, Lude, Freedman, Robert, Freeman, Colin, Freimer, Nelson B, Friedl, Marion, Hougaard, David M, Friedman, Joseph I, Fromer, Menachem, Gejman, Pablo V, Genovese, Giulio, Georgieva, Lyudmila, Giannoulatou, Eleni, Giegling, Ina, Gill, Michael, Gillman, Matthew, Giusti-Rodríguez, Paola, Byberg-Grauholm, Jonas, Godard, Stephanie, Goldstein, Jacqueline I, Golimbet, Vera, Gopal, Srihari, Gratten, Jacob, Gray, Emma, Gurling, Hugh, Gwilliam, Rhian, de Haan, Lieuwe, Hall, Jeremy, Bækvad-Hansen, Marie, Hammer, Christian, Hammond, Naomi, Hamshere, Marian L, Hansen, Mark, Hansen, Thomas, Haroutunian, Vahram, Hartmann, Annette M, Hellenthal, Garrett, Henskens, Frans A, Herms, Stefan, Greenwood, Tiffany A, Hirschhorn, Joel N, Hoffmann, Per, Hofman, Andrea, Hollegaard, Mads V, Huang, Hailiang, Hultman, Christina M, Hunt, Sarah E, Ikeda, Masashi, Iwata, Nakao, Iyegbe, Conrad, Tsuang, Ming T, Jablensky, Assen V, Jankowski, Janusz, Jayakumar, Alagurevathi, Joa, Inge, Jönsson, Erik G, Julià, Antonio, Kähler, Anna K, Kahn, René S, Kalaydjieva, Luba, Karachanak-Yankova, Sena, Curtis, David, Karjalainen, Juha, Kavanagh, David, Keller, Matthew C, Kendler, Kenneth S, Kennedy, James L, Khrunin, Andrey, Kim, Yunjung, Kirov, George, Klovins, Janis, Knight, Jo, Steinberg, Stacy, Knowles, James A, Konte, Bettina, Kucinskas, Vaidutis, Kucinskiene, Zita Ausrele, Kuzelova-Ptackova, Hana, Langford, Cordelia, Laurent, Claudine, Lawrie, Stephen, Lee, S Hong, Lee, Phil, Sigurdsson, Engilbert, Lee, Jimmy, Legge, Sophie E, Lencz, Todd, Lerer, Bernard, Levinson, Douglas F, Lewis, Cathryn M, Li, Tao, Li, Qingqin S, Li, Miaoxin, Liang, Kung-Yee, Mattheisen, Manuel, Stefánsson, Hreinn, Liddle, Jennifer, Lieberman, Jeffrey, Limborska, Svetlana, Lin, Kuang, Linszen, Don H, Liu, Jianjun, Lönnqvist, Jouko, Loughland, Carmel M, Lubinski, Jan, Macek, Milan, Stefánsson, Kári, Magnusson, Patrik K E, Maher, Brion S, Maier, Wolfgang, Malhotra, Anil K, Mallet, Jacques, Markus, Hugh S, Marsal, Sara, Mata, Ignacio, Mathew, Christopher G, Mattingsdal, Morten, Edenberg, Howard J, McCann, Owen T, McCarley, Robert W, McCarroll, Steven A, McCarthy, Mark I, McDonald, Colm, McIntosh, Andrew M, McQuillin, Andrew, Meier, Sandra, Meijer, Carin J, Melegh, Bela, Holmans, Peter, Melle, Ingrid, Mesholam-Gately, Raquelle I, Metspalu, Andres, Michie, Patricia T, Milani, Lili, Milanova, Vihra, Mokrab, Younes, Moran, Jennifer L, Morris, Derek W, Mowry, Bryan J, Faraone, Stephen V, Müller-Myhsok, Bertram, Murphy, Kieran C, Murray, Robin M, Myin-Germeys, Inez, Neale, Benjamin M, Nelis, Mari, Nenadic, Igor, Nertney, Deborah A, Nestadt, Gerald, Nicodemus, Kristin K, Glatt, Stephen J, Nikitina-Zake, Liene, Nisenbaum, Laura, Nordin, Annelie, Nöthen, Markus M, O'Callaghan, Eadbhard, O'Donovan, Michael C, O'Dushlaine, Colm, O'Neill, F Anthony, Oh, Sang-Yun, Olincy, Ann, Adolfsson, Rolf, Olsen, Line, Ophoff, Roel A, Van Os, Jim, Owen, Michael J, Palmer, Colin N A, Palotie, Aarno, Pantelis, Christos, Papadimitriou, George N, Papiol, Sergi, Parkhomenko, Elena, Agartz, Ingrid, Pato, Michele T, Pato, Carlos N, Paunio, Tiina, Pearson, Richard, Cairns, Murray J, DeLisi, Lynn E, Gershon, Elliot S, Kelly, Brian J, Lam, Max, Norgren, Nina, Agerbo, Esben, Paciga, Sara A, Tooney, Paul A, Wu, Jing Qin, Pejovic-Milovancevic, Milica, Perkins, Diana O, Pers, Tune H, Petryshen, Tracey L, Pietiläinen, Olli, Pimm, Jonathan, Pirinen, Matti, Albus, Margot, Plomin, Robert, Pocklington, Andrew J, Posthuma, Danielle, Potter, Simon C, Powell, John, Price, Alkes, Pulver, Ann E, Purcell, Shaun M, Quested, Digby, Rasmussen, Henrik B, Consortium, Schizophrenia Working Group of the Psychiatric Genomics, Alexander, Madeline, Rautanen, Anna, Ravindrarajah, Radhi, Reichenberg, Abraham, Reimers, Mark A, Richards, Alexander L, Ricketts, Michelle, Rietschel, Marcella, Riley, Brien P, Ripke, Stephan, Roffman, Joshua L, Amin, Farooq, Roussos, Panos, Ruderfer, Douglas M, Rujescu, Dan, Salomaa, Veikko, Sanders, Alan R, Sawcer, Stephen J, Schall, Ulrich, Schubert, Christian R, Schulze, Thomas G, Schwab, Sibylle G, Andreassen, Ole A, Scolnick, Edward M, Scott, Rodney J, Seidman, Larry J, Sham, Pak C, Shi, Jianxin, Silagadze, Teimuraz, Silverman, Jeremy M, Sim, Kang, Sklar, Pamela, Arranz, Maria J, Slominsky, Petr, Smoller, Jordan W, So, Hon-Cheong, Söderman, Erik, Spencer, Chris C A, Clair, David St, Stahl, Eli A, Stogmann, Elisabeth, Strange, Amy, Straub, Richard E, Bacanu, Silviu A, Strengman, Eric, Strohmaier, Jana, Stroup, T Scott, Su, Zhan, Subramaniam, Mythily, Sullivan, Patrick F, Suvisaari, Jaana, Svrakic, Dragan M, Szatkiewicz, Jin P, Tashakkori-Ghanbaria, Avazeh, Bakker, Steven, Thirumalai, Srinivas, Toncheva, Draga, Tosato, Sarah, Trembath, Richard C, Veijola, Juha, Visscher, Peter M, Viswanathan, Ananth C, Vukcevic, Damjan, Waddington, John, Waller, Matthew, Band, Gavin, Walsh, Dermot, Walshe, Muriel, Walters, James T R, Wang, Qiang, Wang, Dai, Webb, Bradley T, Weinberger, Daniel R, Weisbrod, Matthias, Weiser, Mark, Wendland, Jens R, Barroso, Ines, Weston, Paul, Whittaker, Pamela, Widaa, Sara, Wiersma, Durk, Wildenauer, Dieter B, Williams, Stephanie, Williams, Nigel M, Witt, Stephanie H, Wolen, Aaron R, Wong, Emily H M, Begemann, Martin, Wood, Nicholas W, Wormley, Brandon K, Wray, Naomi R, Xi, Hualin Simon, Zai, Clement C, Zheng, Xuebin, Zimprich, Fritz, Bellenguez, Céline, Research, Lundbeck Foundation Initiative for Integrative Psychiatric, Belliveau, Richard A, Bender, Stephan, Bene, Judit, Bergen, Sarah E, Bevilacqua, Elizabeth, Bigdeli, Tim B, Black, Donald W, Blackburn, Hannah, Blackwell, Jenefer M, Blackwood, Douglas H R, Børglum, Anders D, Bramon, Elvira, Brown, Matthew A, Bruggeman, Richard, Buccola, Nancy G, Buckner, Randy L, Bulik-Sullivan, Brendan, Bumpstead, Suzannah J, Buxbaum, Joseph D, Byerley, William, Cahn, Wiepke, Als, Thomas D, Cai, Guiqing, Campion, Dominique, Cantor, Rita M, Carr, Vaughan J, Carrera, Noa, Casas, Juan P, Catts, Stanley V, Chambert, Kimberley D, Chan, Ronald Y L, Chan, Raymond C K, Grove, Jakob, Chen, Eric Y H, Cheng, Wei, Cheung, Eric F C, Chong, Siow Ann, Cichon, Sven, Cloninger, C Robert, Cohen, David, Cohen, Nadine, Collier, David A, Cormican, Paul, Werge, Thomas, Corvin, Aiden, Craddock, Nick, Crespo-Facorro, Benedicto, Crowley, James J, Daly, Mark J, Darvasi, Ariel, Davidson, Michael, Davis, Kenneth L, Degenhardt, Franziska, Del Favero, Jurgen, Mortensen, Preben Bo, Deloukas, Panos, Demontis, Ditte, Dikeos, Dimitris, Dinan, Timothy, Djurovic, Srdjan, Domenici, Enrico, Donnelly, Peter, Donohoe, Gary, Drapeau, Elodie, Dronov, Serge, Læknadeild (HÍ), Faculty of Medicine (UI), Heilbrigðisvísindasvið (HÍ), School of Health Sciences (UI), Háskóli Íslands, University of Iceland, Adult Psychiatry, ANS - Complex Trait Genetics, ANS - Mood, Anxiety, Psychosis, Stress & Sleep, APH - Mental Health, Hess, Jonathan L, Tylee, Daniel S, Mattheisen, Manuel, Borglum, Anders D, Glatt, Stephen J, Lee, Sand Hong, Schizophrenia Working Group of thePsychiatric Genomics Consortium, Lundbeck Foundation Initiative for Integrative Psychiatric Research (iPSYCH), Amsterdam Neuroscience - Complex Trait Genetics, Complex Trait Genetics, and Myin-Germeys, Inez
Subjects: Multifactorial Inheritance, Schizophrenia/genetics, Genome-wide association study, Disease, Medical and Health Sciences, 0302 clinical medicine, Risk Factors, schizophrenia, genetics, risk, 2.1 Biological and endogenous factors, genetics, polygenic score, Aetiology, genome wide association study, risk, Genetics, Psychiatry, 0303 health sciences, Schizophrenia Working Group of the Psychiatric Genomics Consortium, Genetic Predisposition to Disease/genetics, Single Nucleotide, Genomics, Biological Sciences, Serious Mental Illness, Polymorphism, Single Nucleotide/genetics, Penetrance, 3. Good health, Psychiatry and Mental health, Mental Health, Mendelian disease, Erfðarannsóknir, Life Sciences & Biomedicine, Single Nucleotide/genetics, Biochemistry & Molecular Biology, Schizophrenia (object-oriented programming), high risk, Biology, Polymorphism, Single Nucleotide, Article, 03 medical and health sciences, Cellular and Molecular Neuroscience, Geðklofi, Humans, Genetic Predisposition to Disease, ddc:610, Allele, Polymorphism, Resilience (network), Molecular Biology, resilience, Multifactorial Inheritance/genetics, Alleles, 030304 developmental biology, Science & Technology, Prevention, Human Genome, Psychology and Cognitive Sciences, Neurosciences, Brain Disorders, Lundbeck Foundation Initiative for Integrative Psychiatric Research, schizophrenia, Good Health and Well Being, Schizophrenia, Neurosciences & Neurology, 030217 neurology & neurosurgery, Genome-Wide Association Study
Abstract: Publisher's version (útgefin grein), Based on the discovery by the Resilience Project (Chen R. et al. Nat Biotechnol 34:531–538, 2016) of rare variants that confer resistance to Mendelian disease, and protective alleles for some complex diseases, we posited the existence of genetic variants that promote resilience to highly heritable polygenic disorders1,0 such as schizophrenia. Resilience has been traditionally viewed as a psychological construct, although our use of the term resilience refers to a different construct that directly relates to the Resilience Project, namely: heritable variation that promotes resistance to disease by reducing the penetrance of risk loci, wherein resilience and risk loci operate orthogonal to one another. In this study, we established a procedure to identify unaffected individuals with relatively high polygenic risk for schizophrenia, and contrasted them with risk-matched schizophrenia cases to generate the first known “polygenic resilience score” that represents the additive contributions to SZ resistance by variants that are distinct from risk loci. The resilience score was derived from data compiled by the Psychiatric Genomics Consortium, and replicated in three independent samples. This work establishes a generalizable framework for finding resilience variants for any complex, heritable disorder., SJG is supported by grants from the U.S. National Institutes of Health (5R01MH101519, 5R01AG054002), the Sidney R. Baer, Jr. Foundation, and NARSAD: The Brain & Behavior Research Foundation. SVF is supported by the K.G. Jebsen Centre for Research on Neuropsychiatric Disorders, University of Bergen, Bergen, Norway, the European Union’s Seventh Framework Programme for research, technological development and demonstration under grant agreement number 602805, the European Union’s Horizon 2020 research and innovation programme under grant agreement number 667302 and NIMH grants 5R01MH101519 and U01 MH109536-01. HJE is supported by grants from the U.S. National Institutes of Health (U10 AA008401; U01 MH109532). Statistical analyses were conducted on the Genetic Cluster Computer, which is financially supported by the Netherlands Scientific Organization (NOW; 480-05-003) along with a supplement from the Dutch Brain Foundation and VU University. The Danish iPSYCH (The Lundbeck Foundation Initiative for Integrative Psychiatric Research) and GEMS2 teams acknowledge funding from The Lundbeck Foundation (grant no R102-A9118 and R155-2014-1724), the Stanley Medical Research Institute, an Advanced Grant from the European Research Council (project no: 294838), the Danish Strategic Research Council and grants from Aarhus University to the iSEQ and CIRRAU centers. The Danish National Biobank resource at Statens Serum Institut was supported by the Novo Nordisk Foundation. Computational resources for handling and statistical analysis of iPSYCH data on the GenomeDK HPC facility were provided by the iSEQ center, Aarhus University, Denmark (grant to ADB).
Published: 2021
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29. Excess Deaths during Influenza and Coronavirus Disease and Infection-Fatality Rate for Severe Acute Respiratory Syndrome Coronavirus 2, the Netherlands

Author: Don Klinkenberg, Marit M A de Lange, Adam Meijer, Lenny Stoeldraijer, Wim van der Hoek, Anne C. Teirlinck, Liselotte van Asten, Carel Harmsen, Susan van den Hof, Jan van de Kassteele, and Arianne B van Gageldonk-Lafeber
Subjects: Epidemiology, coronavirus, lcsh:Medicine, Disease, mortality rate, medicine.disease_cause, excess deaths, 0302 clinical medicine, Case fatality rate, Medicine, 030212 general & internal medicine, Coronavirus, Netherlands, biology, seasonality, Mortality rate, Orthomyxoviridae, Excess Deaths during Influenza and Coronavirus Disease and Infection-Fatality Rate for Severe Acute Respiratory Syndrome Coronavirus 2, the Netherlands, Infectious Diseases, coronavirus disease, surveillance, Seasons, influenza, influenza viruses, severe acute respiratory syndrome coronavirus 2, Microbiology (medical), trends, medicine.medical_specialty, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), 030231 tropical medicine, epidemics, lcsh:Infectious and parasitic diseases, 03 medical and health sciences, respiratory infections, Influenza, Human, infection-fatality rate, Humans, viruses, lcsh:RC109-216, Disease burden, business.industry, SARS-CoV-2, Research, the Netherlands, lcsh:R, COVID-19, Seroepidemiologic Studies, biology.organism_classification, mortality, zoonoses, Emergency medicine, time series, business
Abstract: Since the 2009 influenza pandemic, the Netherlands has used a weekly death monitoring system to estimate deaths in excess of expectations. We present estimates of excess deaths during the ongoing coronavirus disease (COVID-19) epidemic and 10 previous influenza epidemics. Excess deaths per influenza epidemic averaged 4,000. The estimated 9,554 excess deaths (41% in excess) during the COVID-19 epidemic weeks 12-19 of 2020 appeared comparable to the 9,373 excess deaths (18%) during the severe influenza epidemic of 2017-18. However, these deaths occurred in a shorter time, had a higher peak, and were mitigated by nonpharmaceutical control measures. Excess deaths were 1.8-fold higher than reported laboratory-confirmed COVID-19 deaths (5,449). Based on excess deaths and preliminary results from seroepidemiologic studies, we estimated the infection-fatality rate to be 1%. Monitoring of excess deaths is crucial for timely estimates of disease burden for influenza and COVID-19. Our data complement laboratory-confirmed COVID-19 death reports and enable comparisons between epidemics.
Published: 2021

30. Niche separation of wetland birds revealed from airborne laser scanning

Author: Christiaan Meijer, Henk Sierdsema, Meiert W. Grootes, W. Daniel Kissling, Arie C. Seijmonsbergen, Zsófia Koma, Francesco Nattino, Ruud P. B. Foppen, and Theoretical and Computational Ecology (IBED, FNWI)
Subjects: Ecological niche, Great reed warbler, biology, Ecology, Animal Ecology and Physiology, Niche, Niche differentiation, biology.organism_classification, Warbler, Geography, Habitat, Acrocephalus, Ecology, Evolution, Behavior and Systematics, Eurasian reed warbler
Abstract: Numerous organisms depend on the physical structure of their habitats, but incorporating such information into ecological niche analyses has been limited by the lack of adequate data over broad spatial extents. The increasing availability of high-resolution measurements from country-wide airborne laser scanning (ALS) surveys – a light detection and ranging (LiDAR) technology – now provides unprecedented opportunities for characterizing habitat structure. Here, we use country-wide ALS data in combination with presence–absence observations of birds from a national monitoring scheme in the Netherlands to quantify niche filling, niche overlap and niche separation of three closely-related wetland birds (great reed warbler, Eurasian reed warbler and Savi's warbler). We developed a workflow to derive LiDAR metrics capturing different aspects of vertical and horizontal vegetation structure and used a principal component analysis (PCA), niche equivalency and niche similarity tests to analyse the fine-scale breeding habitat niches of these warbler species in the Netherlands. The widespread Eurasian reed warbler almost completely filled the available wetland habitat space (93%) whereas the two other species showed considerably less niche filling (64% and 74%, respectively). Substantial niche overlap occurred among all species, but each species occupied a distinct part of the habitat space. The great reed warbler mainly occurred in tall and vertically complex wetland vegetation and was absent in areas with large proportions of reedbeds. The Eurasian reed warbler occupied all parts of the wetland habitat space, whereas the Savi's warbler mainly occurred in large homogenous reedbeds with low vegetation height. Our results demonstrate that broad-scale ecological niche analyses can incorporate the fine-scale 3D habitat preference of species with unprecedented detail (e.g. 10 m resolution), and thus go much beyond quantifying the climate niche and 2D habitat information from land cover maps. This is important to identify habitat features and priorities for biodiversity conservation in wetlands and other habitats.
Published: 2021
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31. Omics analysis of educated platelets in cancer and benign disease of the pancreas

Author: Thomas Wurdinger, Thang V. Pham, Ilias Glogovitis, Giulia Mantini, Geert Kazemier, Connie R. Jimenez, Tessa Y S Le Large, Elisa Giovannetti, Rosita Paleckyte, Sjors G J G In 't Veld, Laura L. Meijer, Adam E Frampton, M. Capula, Danijela Koppers-Lalic, Sander R. Piersma, Luca Morelli, Medical oncology laboratory, Surgery, CCA - Imaging and biomarkers, Amsterdam Neuroscience - Neurodegeneration, Neurosurgery, and Amsterdam Gastroenterology Endocrinology Metabolism
Subjects: 0301 basic medicine, EXPRESSION, Gene expression, Liquid biopsy, MiRNAs, Omics integration, Pancreatic cancer, Platelets, Proteins, Regulatory mechanisms, Cancer Research, endocrine system diseases, CELL LUNG-CANCER, pancreatic cancer, Biology, lcsh:RC254-282, Article, 03 medical and health sciences, 0302 clinical medicine, Transcription (biology), ENRICHMENT ANALYSIS, POOR-PROGNOSIS, microRNA, medicine, 1112 Oncology and Carcinogenesis, MESSENGER-RNAS, Messenger RNA, Science & Technology, liquid biopsy, MICRORNA, METHYLATION, RNA, DNA, lcsh:Neoplasms. Tumors. Oncology. Including cancer and carcinogens, medicine.disease, proteins, digestive system diseases, 3. Good health, regulatory mechanisms, GENOME, 030104 developmental biology, TARGET, Oncology, omics integration, 030220 oncology & carcinogenesis, RNA splicing, platelets, miRNAs, Cancer research, gene expression, Life Sciences & Biomedicine
Abstract: Pancreatic ductal adenocarcinoma (PDAC) is traditionally associated with thrombocytosis/hypercoagulation and novel insights on platelet-PDAC &ldquo, dangerous liaisons&rdquo, are warranted. Here we performed an integrative omics study investigating the biological processes of mRNAs and expressed miRNAs, as well as proteins in PDAC blood platelets, using benign disease as a reference for inflammatory noise. Gene ontology mining revealed enrichment of RNA splicing, mRNA processing and translation initiation in miRNAs and proteins but depletion in RNA transcripts. Remarkably, correlation analyses revealed a negative regulation on SPARC transcription by isomiRs involved in cancer signaling, suggesting a specific &rdquo, education&rdquo, in PDAC platelets. Platelets of benign patients were enriched for non-templated additions of G nucleotides (#ntaG) miRNAs, while PDAC presented length variation on 3&prime, (lv3p) as the most frequent modification on miRNAs. Additionally, we provided an actionable repertoire of PDAC and benign platelet-ome to be exploited for future studies. In conclusion, our data show that platelets change their biological repertoire in patients with PDAC, through dysregulation of miRNAs and splicing factors, supporting the presence of de novo protein machinery that can &ldquo, educate&rdquo, the platelet. These novel findings could be further exploited for innovative liquid biopsies platforms as well as possible therapeutic targets.
Published: 2021
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32. LEDs Make It Resilient: Effects on Plant Growth and Defense

Author: M. Meisenburg, W. van Ieperen, J.J.A. van Loon, Marcel Dicke, M. Lazzarin, I.F. Kappers, A.R. van der Krol, Davy Meijer, and Leo F. M. Marcelis
Subjects: 0106 biological sciences, 0301 basic medicine, Integrated pest management, Plant growth, Light, media_common.quotation_subject, growth, Plant Development, Greenhouse, Context (language use), Plant Science, 01 natural sciences, 03 medical and health sciences, Quality (business), Laboratorium voor Plantenfysiologie, Laboratory of Entomology, plant–arthropod interactions, Lighting, Spectral composition, Plant secondary metabolism, media_common, photosynthesis, biology, LED, Horticulture & Product Physiology, Plants, biology.organism_classification, PE&RC, Laboratorium voor Entomologie, Crop Production, Light quality, defense, 030104 developmental biology, light spectra, light-emitting diode, Biochemical engineering, EPS, Tuinbouw & Productfysiologie, Laboratory of Plant Physiology, 010606 plant biology & botany
Abstract: Light spectral composition influences plant growth and metabolism, and has important consequences for interactions with plant-feeding arthropods and their natural enemies. In greenhouse horticulture, light spectral composition can be precisely manipulated by light-emitting diodes (LEDs), and LEDs are already used to optimize crop production and quality. However, because light quality also modulates plant secondary metabolism and defense, it is important to understand the underlying mechanisms in the context of the growth-defense trade-off. We review the effects of the spectral composition of supplemental light currently used, or potentially used, in greenhouse horticulture on the mechanisms underlying plant growth and defense. This information is important for exploring opportunities to optimize crop performance and pest management, and thus for developing resilient crop-production systems.
Published: 2021
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33. RNF43 mutation analysis in serrated polyposis, sporadic serrated polyps and Lynch syndrome polyps

Author: Fokko M. Nagengast, Femke Simmer, Tanya M. Bisseling, Gerrit A. Meijer, Lieke M. Koggel, Yasmijn van Herwaarden, Polat Dura, Nicoline Hoogerbrugge, Elisa Vink-Börger, and Iris D. Nagtegaal
Subjects: Male, 0301 basic medicine, Colorectal cancer, DNA Mutational Analysis, Germline, Cohort Studies, Tumours of the digestive tract Radboud Institute for Health Sciences [Radboudumc 14], Exon, 0302 clinical medicine, Tumours of the digestive tract Radboud Institute for Molecular Life Sciences [Radboudumc 14], somatic mutation, Wnt Signaling Pathway, Sanger sequencing, General Medicine, Middle Aged, serrated polyps, Lynch syndrome, 030220 oncology & carcinogenesis, Colonic Neoplasms, RNF43, symbols, Female, Microsatellite Instability, Original Article, Colorectal Neoplasms, Adult, Histology, Colon, Ubiquitin-Protein Ligases, Colonic Polyps, Biology, Pathology and Forensic Medicine, Frameshift mutation, Diagnosis, Differential, 03 medical and health sciences, symbols.namesake, Germline mutation, medicine, Humans, Molecular Biology, neoplasms, Aged, Original Articles, serrated polyposis syndrome, medicine.disease, Colorectal Neoplasms, Hereditary Nonpolyposis, digestive system diseases, 030104 developmental biology, Hyperplastic Polyp, Mutation, Cancer research
Abstract: Contains fulltext : 231699.pdf (Publisher’s version ) (Open Access) AIMS: RNF43 is suggested to be involved in the serrated pathway towards colorectal cancer and encodes a transmembrane Ring-type E3 ubiquitin ligase that negatively regulates the Wnt pathway. This study aimed to elucidate the role of RNF43 gene variants in serrated polyposis syndrome (SPS) and serrated polyps. METHODS AND RESULTS: Three cohorts were tested. The first cohort included germline DNA of 26 SPS patients tested for pathogenic variants in RNF43 by Sanger sequencing all exons. In the second cohort we tested somatic DNA for RNF43 mutations from sporadic serrated lesions: 25 hyperplastic polyps, 35 sessile serrated lesions and 38 traditional serrated adenomas (TSA). In the third cohort we investigated RNF43 mutations in 49 serrated polyps and 60 conventional adenomas from 40 patients with Lynch syndrome. No germline RNF43 pathogenic variants were detected in our SPS cohort. In sporadic colorectal lesions we detected RNF43 deleterious frameshift mutations in three TSA and one SSL. The RNF43 mutations in previously described homopolymeric hot-spots were detected in microsatellite-instable (MSI) polyps and the other RNF43 mutations in microsatellite-stable (MSS) serrated polyps. RNF43 hot-spot mutations were discovered in seven serrated polyps and 12 conventional adenomas from Lynch patients. CONCLUSION: Truncating germline RNF43 mutations are uncommon in SPS patients. Somatic mutations in RNF43 were found in sporadic TSA and SSL and both serrated polyps and adenomas from Lynch syndrome patients, suggesting that they do not develop early in the pathway to CRC and are not specific for serrated polyp subtypes.
Published: 2020
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34. The mTOR regulated RNA-binding protein LARP1 requires PABPC1 for guided mRNA interaction

Author: Joseph A. Waldron, Ania Wilczynska, Katherine Morris, Mark Stoneley, Kelvin Cain, Martin Bushell, Nour El Houda Benbahouche, Ewan M. Smith, Rebekah Jukes-Jones, Cameron Bell, Bruno D. Fonseca, Sarah P. Blagden, Carolyn Jones, Hedda A. Meijer, Sarah L. Gillen, Anne E. Willis, Tobias Schmidt, Willis, Anne [0000-0002-1470-8531], and Apollo - University of Cambridge Repository
Subjects: AcademicSubjects/SCI00010, Recombinant Fusion Proteins, Mutation, Missense, RNA-binding protein, Mechanistic Target of Rapamycin Complex 2, mTORC1, Mechanistic Target of Rapamycin Complex 1, Biology, Autoantigens, Poly(A)-Binding Protein I, 03 medical and health sciences, 0302 clinical medicine, PABPC1, Genes, Reporter, Polysome, RNA and RNA-protein complexes, Genetics, Protein biosynthesis, Humans, Point Mutation, RNA, Messenger, Naphthyridines, PI3K/AKT/mTOR pathway, 030304 developmental biology, 0303 health sciences, TOR Serine-Threonine Kinases, RNA-Binding Proteins, LARP1, Cell biology, Gene Expression Regulation, Ribonucleoproteins, Polyribosomes, Protein Biosynthesis, Mutagenesis, Site-Directed, RNA Interference, 5' Untranslated Regions, 030217 neurology & neurosurgery, HeLa Cells
Abstract: The mammalian target of rapamycin (mTOR) is a critical regulator of cell growth, integrating multiple signalling cues and pathways. Key among the downstream activities of mTOR is the control of the protein synthesis machinery. This is achieved, in part, via the co-ordinated regulation of mRNAs that contain a terminal oligopyrimidine tract (TOP) at their 5′ends, although the mechanisms by which this occurs downstream of mTOR signalling are still unclear. We used RNA-binding protein (RBP) capture to identify changes in the protein-RNA interaction landscape following mTOR inhibition. Upon mTOR inhibition, the binding of LARP1 to a number of mRNAs, including TOP-containing mRNAs, increased. Importantly, non-TOP-containing mRNAs bound by LARP1 are in a translationally-repressed state, even under control conditions. The mRNA interactome of the LARP1-associated protein PABPC1 was found to have a high degree of overlap with that of LARP1 and our data show that PABPC1 is required for the association of LARP1 with its specific mRNA targets. Finally, we demonstrate that mRNAs, including those encoding proteins critical for cell growth and survival, are translationally repressed when bound by both LARP1 and PABPC1.
Published: 2020
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35. Behavior Genetics Association 50th Annual Meeting Abstracts

Author: Liisa Keltikangas-Järvinen, Juulia Jylhävä, Silvia Alemany, Meike Bartels, Timo E. Strandberg, Rosie M. Walker, Marina Vafeiadi, Olivier F. Colins, Yunzhang Wang, Michael Deuschle, Geòrgia Escaramís, Bart M. L. Baselmans, Lea Sirignano, Marieke Klein, David L. Corcoran, Marian J. Bakermans-Kranenburg, Barbara Franke, Christine M. Freitag, Peter J. Roetman, Aranzazu Fernandez-Rivas, Jari Lahti, Khadeeja Ismail, Estelle Lowry, Matthew Suderman, Eilis Hannon, Archie Campbell, Mark Adams, Christian Hakulinen, Jaakko Kaprio, Olli T. Raitakari, Mandy Meijer, Kerstin Konrad, Eero Vuoksimaa, Dorret I. Boomsma, Katri Räikkönen, Marinus H. van IJzendoorn, Sylvain Sebert, Stewart W. Morris, Leanne K. Küpers, Tellervo Korhonen, Jenny van Dongen, Kristine B. Gutzkow, Gareth E. Davies, Robert Vermeiren, Karen Sugden, Rosa H. Mulder, Elisabeth B. Binder, Andrew M. McIntosh, Eva Corpeleijn, Priyanka Parmar, Avshalom Caspi, Kathryn L. Evans, Jonathan D. Hafferty, Terrie E. Moffitt, Stephanie H. Witt, Tabea Send, Lude Franke, Marc Jan Bonder, Nancy L. Pedersen, Andreas G. Chiocchetti, Caroline L Relton, Richie Poulton, Harold Snieder, Jorunn Evandt, Henning Tiemeier, Jordi Sunyer, Juan R. González, Amaia Hervás, Lannie Ligthart, Terho Lehtimäki, Ágnes Vetró, Regina Grazuleviciene, Pashupati P. Mishra, Fabian Streit, Louise Arseneault, Janine F. Felix, Jonathan Mill, Martine Vrijheid, Fiona A. Hagenbeek, Sara Hägg, Josef Frank, Miina Ollikainen, Darina Czamara, Rick Jansen, Marjo-Riitta Järvelin, Dennis van der Meer, Cornelis Kluft, and Hill F. Ip
Subjects: Aggression, Computational biology, Epigenome, Biology, medicine.disease, Broad spectrum, Abstracts, Meta-analysis, DNA methylation, Genetics, medicine, Dementia, Epigenetics, medicine.symptom, Genetics (clinical), Ecology, Evolution, Behavior and Systematics
Published: 2020

36. Disentangling the multiple effects of stream drying and riparian canopy cover on the trophic ecology of a highly threatened fish

Author: Angus R. McIntosh, Helen J. Warburton, and Christopher G. Meijer
Subjects: Canopy, geography, geography.geographical_feature_category, biology, Ecology, Galaxiidae, Ecology (disciplines), Climate change, Aquatic Science, biology.organism_classification, Invasive species, Threatened species, Environmental science, Riparian zone, Trophic level
Published: 2020
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37. Tenascin C Plasma Levels in Critically Ill Patients with or Without Sepsis

Author: Marcus J. Schultz, Tom van der Poll, Olaf L. Cremer, Mariska T. Meijer, Fabrice Uhel, Graduate School, Center of Experimental and Molecular Medicine, Intensive Care Medicine, AII - Infectious diseases, Infectious diseases, ACS - Diabetes & metabolism, ACS - Pulmonary hypertension & thrombosis, and ACS - Microcirculation
Subjects: Male, medicine.medical_specialty, Critical Illness, 030204 cardiovascular system & hematology, Critical Care and Intensive Care Medicine, Severity of Illness Index, Sepsis, 03 medical and health sciences, 0302 clinical medicine, Immune system, Internal medicine, Humans, Medicine, Aged, biology, business.industry, Tenascin C, Tenascin, 030208 emergency & critical care medicine, Plasma levels, Middle Aged, medicine.disease, musculoskeletal system, Intensive Care Units, Pneumonia, Case-Control Studies, Emergency Medicine, biology.protein, Biomarker (medicine), Female, Observational study, business, Biomarkers, Abdominal surgery
Abstract: Tenascin C (TNC) is an extracellular matrix protein able to modulate the immune response. Knowledge regarding its role during sepsis and general critical illness is still limited. We here assessed the temporal dynamics of plasma TNC during sepsis and nonseptic critical illness, its capacity to predict patient outcome, and its specificity toward infection. TNC plasma concentrations were measured in 895 consecutive sepsis patients on ICU admission, day 2 and 4 thereafter, and, in a subset, before ICU discharge. To assess TNC diagnostic value, we compared patients with abdominal sepsis (N = 143) to noninfectious abdominal surgery controls (N = 98), and patients with severe community-acquired pneumonia (CAP, N = 227) to patients whose CAP diagnosis was retrospectively refuted (no-CAP controls, N = 70). Plasma TNC levels were persistently elevated in sepsis patients compared with healthy volunteers throughout the ICU stay. TNC levels varied by the site of infection and increased with the number of organs failing. Association of TNC levels with 30-day mortality could be wholly attributed to differences in disease severity. Noninfectious ICU patients also showed elevated TNC levels, albeit with different temporal dynamics. Although admission TNC was higher in CAP than in no-CAP patients, it performed poorly in distinguishing the 2 groups.TNC plasma levels are persistently elevated during sepsis and nonseptic critical illness. In sepsis patients, they are reflective of disease severity more than independent predictors of mortality. Despite higher levels in patients with infection compared with noninfectious controls, TNC does not perform sufficiently to be used as a standalone biomarker discriminating sepsis from noninfectious critical illness.
Published: 2020

38. Predominance of influenza virus A(H3N2) 3C.2a1b and A(H1N1)pdm09 6B.1A5A genetic subclades in the WHO European Region, 2018–2019

Author: Melidou, Angeliki, Hungnes, Olav, Pereyaslov, Dmitriy, Adlhoch, Cornelia, Segaloff, Hannah, Robesyn, Emmanuel, Penttinen, Pasi, Olsen, Sonja J., Redlberger-Fritz, Monika, Popow-Kraupp, Therese, Hasibra, Iris, Simaku, Artan, Thomas, Isabelle, Barbezange, Cyril, Dedeić-Ljubović, Amela, Rodić-Vukmir, Nina, Korsun, Neli, Angenova, Svetla, Draženović, Vladimir, Koliou, Maria, Pieridou, Despo, Havlickova, Martina, Nagy, Alexander, Trebbien, Ramona, Galiano, Monica, Thompson, Catherine, Ikonen, Niina, Haveri, Anu, Behillil, Sylvie, Enouf, Vincent, Valette, Martine, Lina, Bruno, Gavashelidze, Mari, Machablishvili, Ann, Gioula, Georgia, Exindari, Maria, Kossyvakis, Athanasios, Mentis, Andreas, Dürrwald, Ralf, Zsuzsanna, Molnar, Monika, Rozsa, Löve, Arthur, Erna, Gudrun, Dunford, Linda, Fitzpatrick, Sarah, Castrucci, Maria Rita, Puzelli, Simona, Sagymbay, Altynay, Nussupbayeva, Gaukhar, Zamjatina, Natalija, Pakarna, Gatis, Griskevičius, Algirdas, Skrickiene, Asta, Fournier, Guillaume, Mossong, Joel, Melillo, Jackie, Zahra, Graziella, Meijer, Adam, Fouchier, Ron, McCaughey, Conall, O'Doherty, Mark, Bragstad, Karoline, Guiomar, Raquel, Pechirra, Pedro, Apostol, Mariana, Alina, Druc, Lazar, Mihaela, Maria, Cherciu Carmen, Komissarov, Andrey, Burtseva, Elena, Gunson, Rory N., Shepherd, Samantha, Tichá, Elena, Staronova, Edita, Prosenc, Katarina, Berginc, Nataša, Pozo, Francisco, Casas, Inmaculada, Brytting, Mia, Wiman, Åsa, Gonçalves, Ana Rita, Demchyshyna, Iryna, Mironenko, Alla, Moore, Catherine, Cottrell, Simon, and European Region influenza surveillance network
Subjects: Influenzavirus A, Infecções Respiratórias, viruses, 030231 tropical medicine, Hemagglutinin Glycoproteins, Influenza Virus, Biology, World Health Organization, Virus, Antigenic, 03 medical and health sciences, Influenza A Virus, H1N1 Subtype, 0302 clinical medicine, Vaccine strain, Genetic, Antigen, Influenza, Human, Humans, 030212 general & internal medicine, Clade, Phylogeny, chemistry.chemical_classification, Surveillance, General Veterinary, General Immunology and Microbiology, Influenza A Virus, H3N2 Subtype, Public Health, Environmental and Occupational Health, Subclade, European region, Virology, A h1n1 pdm09, Influenza, Amino acid, Europe, Infectious Diseases, chemistry, Influenza Vaccines, RNA, Viral, Molecular Medicine, Vaccine
Abstract: Network authors: Portugal - Raquel Guiomar, Pedro Pechirra, National Influenza Reference Laboratory, Infectious Diseases Department, National Institute of Health Dr. Ricardo Jorge, Lisbon, Portugal Background: The 2018/2019 influenza season in the WHO European Region was dominated by influenza A (H1N1)pdm09 and (H3N2) viruses, with very few influenza B viruses detected. Methods: Countries in the European Region reported virus characterization data to The European Surveillance System for weeks 40/2018 to 20/2019. These virus antigenic and genetic characterization and haemagglutinin (HA) sequence data were analysed to describe and assess circulating viruses relative to the 2018/2019 vaccine virus components for the northern hemisphere. Results: Thirty countries reported 4776 viruses characterized genetically and 3311 viruses antigenically. All genetically characterized A(H1N1)pdm09 viruses fell in subclade 6B.1A, of which 90% carried the amino acid substitution S183P in the HA gene. Antigenic data indicated that circulating A(H1N1)pdm09 viruses were similar to the 2018/2019 vaccine virus. Genetic data showed that A(H3N2) viruses mostly fell in clade 3C.2a (75%) and 90% of which were subclade 3C.2a1b. A lower proportion fell in clade 3C.3a (23%) and were antigenically distinct from the vaccine virus. All B/Victoria viruses belonged to clade 1A; 30% carried a double amino acid deletion in HA and were genetically and antigenically similar to the vaccine virus component, while 55% carried a triple amino acid deletion or no deletion in HA; these were antigenically distinct from each other and from the vaccine component. All B/Yamagata viruses belonged to clade 3 and were antigenically similar to the virus component in the quadrivalent vaccine for 2018/2019. Conclusions: A simultaneous circulation of genetically and antigenically diverse A(H3N2) and B/Victoria viruses was observed and represented a challenge to vaccine strain selection. Highlights: Co-circulation of different clades/subclades of influenza A viruses in 2018/2019 in the Region; Most circulating A(H1N1)pdm09 viruses (6B.1A) carried S183P in hemagglutinin; Genetically heterogeneous A(H3N2) viruses, with co-circulation of clades 3C.2a and 3C.3a; Antigenically distinct A(H3N2) clade 3C.3a viruses were increasingly detected until 02/2019 and then decreased; Co-circulation of genetically and antigenically diverse A(H3N2) strains challenges vaccine strain selection. info:eu-repo/semantics/publishedVersion
Published: 2020
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39. Effects of a Hypercaloric and Hypocaloric Diet on Insulin-Induced Microvascular Recruitment, Glucose Uptake, and Lipolysis in Healthy Lean Men

Author: Etto C. Eringa, Erik H. Serné, Jorn Woerdeman, Mireille J. Serlie, Anna L. Emanuel, Mark H. H. Kramer, Rick I. Meijer, Daniël H. van Raalte, Michaela Diamant, Fysiologie, RS: Carim - H08 Experimental atrial fibrillation, Internal medicine, ACS - Diabetes & metabolism, Amsterdam Gastroenterology Endocrinology Metabolism, VU University medical center, Physiology, ACS - Microcirculation, and Endocrinology
Subjects: Blood Glucose, Male, obesity, Time Factors, muscle, Glucose uptake, medicine.medical_treatment, Adipose tissue, perfusion imaging, 030204 cardiovascular system & hematology, Weight Gain, adipose-tissue, in-vivo, MIXED MEAL, 0302 clinical medicine, insulin resistance, Insulin, Adiposity, dysfunction, biology, Healthy Volunteers, adipose tissue, Vasodilation, Arterioles, medicine.anatomical_structure, medicine.symptom, Cardiology and Cardiovascular Medicine, Adult, medicine.medical_specialty, Adolescent, endothelium, microcirculation, 030209 endocrinology & metabolism, Inflammation, perfusion, resistance, Young Adult, 03 medical and health sciences, Insulin resistance, INFLAMMATION, Internal medicine, Weight Loss, medicine, Humans, Lipolysis, Muscle, Skeletal, Caloric Restriction, business.industry, Skeletal muscle, medicine.disease, sensitivity, Insulin receptor, Endocrinology, Case-Control Studies, biology.protein, lipolysis, Energy Intake, business, diet
Abstract: Objective: In mice fed a high-fat diet, impairment of insulin signaling in endothelium is an early phenomenon that precedes decreased insulin sensitivity of skeletal muscle, adipose tissue, and liver. We assessed in humans whether short-term overfeeding affects insulin-induced microvascular recruitment in skeletal muscle and adipose tissue before changes occur in glucose uptake and lipolysis. Approach and Results: Fifteen healthy males underwent a hypercaloric and subsequent hypocaloric diet intervention. Before, during, and after the hypercaloric diet, and upon return to baseline weight, all participants underwent (1) a hyperinsulinemic-euglycemic clamp to determine insulin-induced glucose uptake and suppression of lipolysis (2) contrast-enhanced ultrasonography to measure insulin-induced microvascular recruitment in skeletal muscle and adipose tissue. In addition, we assessed insulin-induced vasodilation of isolated skeletal muscle resistance arteries by pressure myography after the hypercaloric diet in study participants and controls (n=5). The hypercaloric diet increased body weight (3.5 kg; P P P =0.041) and decreased the ratio between skeletal muscle and adipose tissue microvascular blood volume during hyperinsulinemia ( P =0.019). Insulin-induced vasodilation of isolated skeletal muscle arterioles was significantly lower in participants compared with controls ( P Conclusions: In lean men, short-term overfeeding reduces insulin-induced vasodilation of skeletal muscle resistance arteries and shifts the distribution of tissue perfusion during hyperinsulinemia from skeletal muscle to adipose tissue without affecting glucose uptake and lipolysis. Registration: URL: https://www.clinicaltrials.gov . Unique identifier: NCT02628301.
Published: 2020
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40. von Willebrand Factor and Factor VIII Clearance in Perioperative Hemophilia A Patients

Author: Moort, I. van, Bukkems, L.H., Heijdra, J.M., Schutgens, R.E.G., Laros-van Gorkom, B.A.P., Nieuwenhuizen, L., Meer, F.J.M. van der, Fijnvandraat, K., Ypma, P., Maat, M.P.M. de, Leebeek, F.G., Meijer, K., Eikenboom, J., Mathot, R.A.A., Cnossen, M.H., OPTI-CLOT Study Grp, Graduate School, Pharmacy, Paediatric Haematology, Amsterdam Reproduction & Development (AR&D), ACS - Pulmonary hypertension & thrombosis, Amsterdam Gastroenterology Endocrinology Metabolism, Real World Studies in PharmacoEpidemiology, -Genetics, -Economics and -Therapy (PEGET), Pediatrics, and Hematology
Subjects: Male, 0301 basic medicine, Vascular damage Radboud Institute for Health Sciences [Radboudumc 16], Blood Loss, Surgical, 030204 cardiovascular system & hematology, von Willebrand factor, Gastroenterology, Hemostatics, DISEASE, surgery, 0302 clinical medicine, Interquartile range, hemic and lymphatic diseases, Drug Dosage Calculations, Netherlands, linear mixed effect modeling, biology, HALF-LIFE, Hematology, Middle Aged, Treatment Outcome, factor VIII, cardiovascular system, hemophilia A, circulatory and respiratory physiology, Adult, medicine.medical_specialty, congenital, hereditary, and neonatal diseases and abnormalities, Metabolic Clearance Rate, Postoperative Hemorrhage, Drug Administration Schedule, Perioperative Care, 03 medical and health sciences, All institutes and research themes of the Radboud University Medical Center, Antigen, Von Willebrand factor, Internal medicine, medicine, Humans, In patient, Blood type, business.industry, FACTOR PROPEPTIDE, Perioperative, MODEL, 030104 developmental biology, Glycoprotein Ib, Mixed effects, biology.protein, postsurgical bleeding, business
Abstract: Background von Willebrand factor (VWF) is crucial for optimal dosing of factor VIII (FVIII) concentrate in hemophilia A patients as it protects FVIII from premature clearance. To date, it is unknown how VWF behaves and what its impact is on FVIII clearance in the perioperative setting. Aim To investigate VWF kinetics (VWF antigen [VWF:Ag]), VWF glycoprotein Ib binding (VWF:GPIbM), and VWF propeptide (VWFpp) in severe and moderate perioperative hemophilia A patients included in the randomized controlled perioperative OPTI-CLOT trial. Methods Linear mixed effects modeling was applied to analyze VWF kinetics. One-way and two-way analyses of variance were used to investigate perioperative VWFpp/VWF:Ag ratios and associations with surgical bleeding. Results Fifty-nine patients with median age of 48.8 years (interquartile range: 34.8–60.0) were included. VWF:Ag and VWF:GPIbM increased significantly postoperatively. Blood type non-O or medium risk surgery were associated with higher VWF:Ag and VWF:GPIbM levels compared with blood type O and low risk surgery. VWFpp/VWF:Ag was significantly higher immediately after surgery than 32 to 57 hours after surgery (p Conclusion VWF:Ag and VWF:GPIbM levels increase postoperatively, most significantly in patients with blood type non-O or medium risk surgery. Lower VWF antigen levels did not lead to clinically relevant higher FVIII clearance. VWF:Ag or VWF:GPIbM levels were not associated with perioperative hemorrhage.
Published: 2020
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41. Effects of biocontrol bacteria and earthworms on Aphanomyces euteiches root-rot and growth of peas (Pisum sativum) studied in a pot experiment

Author: Johan Meijer, Jan Lagerlöf, Fredrik Heyman, and Fredrick O. Ayuke
Subjects: 0106 biological sciences, biology, Soil biology, Biological pest control, food and beverages, Soil Science, Bacillus, 04 agricultural and veterinary sciences, biology.organism_classification, complex mixtures, 01 natural sciences, Plant disease, Sativum, Botany, 040103 agronomy & agriculture, Root rot, 0401 agriculture, forestry, and fisheries, Aphanomyces euteiches, Agronomy and Crop Science, Lumbricus terrestris, 010606 plant biology & botany
Abstract: The role of below-ground interactions between microbial biocontrol agents and soil fauna for combatting soil-borne plant diseases have not been studied sufficiently. This study tested the hypothesi...
Published: 2020
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42. Glucocorticoid Sexual Dimorphism in Metabolism: Dissecting the Role of Sex Hormones

Author: Onno C. Meijer, Alberto M. Pereira, and Jan Kroon
Subjects: Male, medicine.medical_specialty, Endocrinology, Diabetes and Metabolism, medicine.medical_treatment, 030209 endocrinology & metabolism, Steroid, 03 medical and health sciences, 0302 clinical medicine, Endocrinology, Sex hormone-binding globulin, Internal medicine, medicine, Animals, Humans, Cushing Syndrome, Glucocorticoids, Sex Characteristics, biology, Estrogens, Metabolism, Sexual dimorphism, Crosstalk (biology), Steroid hormone, Androgens, biology.protein, Female, hormones, hormone substitutes, and hormone antagonists, Glucocorticoid, Signal Transduction, Hormone, medicine.drug
Abstract: Glucocorticoids are steroid hormones that are of pivotal importance in human physiology. Glucocorticoid signaling is complex in nature and dependent on many interacting factors. As glucocorticoids exhibit sexually dimorphic effects on several key processes including in metabolism, crosstalk with the sex steroid hormones (androgens and estrogens) is relevant. In this review, we highlight the state-of-the-art knowledge on glucocorticoid sexual dimorphism and sex hormone crosstalk. We include current insight in the molecular mechanisms that underlie nuclear steroid receptor crosstalk, and sex hormone effects on glucocorticoid metabolism. Finally, we show how these findings translate to humans exposed to excess glucocorticoid signaling, and we propose future avenues in the emerging field of steroid hormone crosstalk.
Published: 2020
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43. Conservation of Rhodococcus equi (Magnusson 1923) Goodfellow and Alderson 1977 and rejection of Rhodococcus hoagii (Morse 1912) Kämpfer et al. 2014

Author: Mariela Scortti, José A. Vázquez-Boland, and Wim G. Meijer
Subjects: biology, Corynebacterium, Zoology, General Medicine, biology.organism_classification, Morse code, Microbiology, Nomen dubium, law.invention, Taxon, Type (biology), law, Principle of Priority, Rhodococcus equi, Rhodococcus, Ecology, Evolution, Behavior and Systematics
Abstract: A recent taxonomic study confirmed the synonymy of Rhodococcus equi (Magnusson 1923) Goodfellow and Alderson 1977 and Corynebacterium hoagii (Morse 1912) Eberson 1918. As a result, both R. equi and C. hoagii were reclassified as Rhodococcus hoagii comb. nov. in application of the principle of priority of the Prokaryotic Code. Because R. equi is a well-known animal and zoonotic human pathogen, and a bacterial name solidly established in the veterinary and medical literature, we and others argued that the nomenclatural change may cause error and confusion and be potentially perilous. We have now additionally found that the nomenclatural type of the basonym C. hoagii , ATCC 7005T, does not correspond with the original description of the species C. hoagii in the early literature. Its inclusion as the C. hoagii type on the Approved Lists 1980 results in a change in the characters of the taxon and in C. hoagii designating two different bacteria. Moreover, ATCC 7005, the only strain in circulation under the name C. hoagii , does not have a well documented history; it is unclear why it was deposited as C. hoagii and a possible mix-up with a Corynebacterium ( Rhodococcus ) equi isolate is a reasonable assumption. We therefore request the rejection of Rhodococcus hoagii as a nomen ambiguum, nomen dubium and nomen perplexum in addition to nomen periculosum, and conservation of the name Rhodococcus equi , according to Rules 56ab of the Code.
Published: 2020
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44. Tetranychus evansi spider mite populations suppress tomato defenses to varying degrees

Author: Martijn Egas, Tomas T. Meijer, Merijn R. Kant, Bram Knegt, E. Toby Kiers, Animal Ecology, and Evolutionary and Population Biology (IBED, FNWI)
Subjects: 0106 biological sciences, herbivore offense, jasmonate reporter, Zoology, Biology, medicine.disease_cause, 010603 evolutionary biology, 01 natural sciences, Predation, biotic interactions, 03 medical and health sciences, chemistry.chemical_compound, Solanum lycopersicum, Spider mite, lcsh:QH540-549.5, Infestation, Plant defense against herbivory, medicine, Plant–herbivore interactions, Ecology, Evolution, Behavior and Systematics, 030304 developmental biology, Nature and Landscape Conservation, Original Research, SDG 15 - Life on Land, 0303 health sciences, Herbivore, Ecology, Jasmonic acid, fungi, food and beverages, biology.organism_classification, chemistry, intraspecific variation, PEST analysis, lcsh:Ecology, Solanum
Abstract: Plant defense suppression is an offensive strategy of herbivores, in which they manipulate plant physiological processes to increase their performance. Paradoxically, defense suppression does not always benefit the defense‐suppressing herbivores, because lowered plant defenses can also enhance the performance of competing herbivores and can expose herbivores to increased predation. Suppression of plant defense may therefore entail considerable ecological costs depending on the presence of competitors and natural enemies in a community. Hence, we hypothesize that the optimal magnitude of suppression differs among locations. To investigate this, we studied defense suppression across populations of Tetranychus evansi spider mites, a herbivore from South America that is an invasive pest of solanaceous plants including cultivated tomato, Solanum lycopersicum, in other parts of the world. We measured the level of expression of defense marker genes in tomato plants after infestation with mites from eleven different T. evansi populations. These populations were chosen across a range of native (South American) and non‐native (other continents) environments and from different host plant species. We found significant variation at three out of four defense marker genes, demonstrating that T. evansi populations suppress jasmonic acid‐ and salicylic acid‐dependent plant signaling pathways to varying degrees. While we found no indication that this variation in defense suppression was explained by differences in host plant species, invasive populations tended to suppress plant defense to a smaller extent than native populations. This may reflect either the genetic lineage of T. evansi—as all invasive populations we studied belong to one linage and both native populations to another—or the absence of specialized natural enemies in invasive T. evansi populations., Suppression of plant defenses by herbivores promotes herbivore performance, but may also increase competition and predation. We hypothesize that biotic interactions with competitors and natural enemies shape the costs and benefits of defense suppression, and found significant variation in the magnitude of defense suppression among eleven populations of the defense‐suppressing spider mite Tetranychus evansi, ranging from Brazil to Japan. Invasive populations tended to suppress plant defense to a smaller extent than native populations, and we speculate that this may reflect the absence of specialized natural enemies in invasive T. evansi populations.
Published: 2020
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45. Accelerated growth of orbital schwannomas during pregnancy does not correlate with sex hormone- or growth factor receptor status

Author: Robert M. Verdijk, Niels Meijer, Dion Paridaens, and G. J. Hötte
Subjects: Adult, Pathology, medicine.medical_specialty, Exophthalmos, medicine.drug_class, Receptor expression, Young Adult, 03 medical and health sciences, 0302 clinical medicine, Sex hormone-binding globulin, Growth factor receptor, Pregnancy, medicine, Humans, Receptors, Growth Factor, Gonadal Steroid Hormones, 030223 otorhinolaryngology, biology, business.industry, Androgen, medicine.disease, Androgen receptor, Ophthalmology, Estrogen, 030221 ophthalmology & optometry, biology.protein, Orbital Neoplasms, Female, medicine.symptom, business, Neurilemmoma
Abstract: Purpose: Until now, three cases of growth of an orbital schwannoma during pregnancy have been published. We aim to provide additional insight in the effect of pregnancy on orbital schwannomas. Methods: We present two additional cases of accelerated growth of orbital schwannomas during pregnancy and investigate receptor expression profiles for estrogen, progesterone, androgen, VEGF, EGF, FGF, PDGF-Rβ and ki-67 in the two pregnant cases and six non-pregnant cases. Results: Case 1: A 26-year-old woman developed unilateral exophthalmos during pregnancy, with normal visual acuity and ocular motility. During a subsequent pregnancy, again the exophthalmos progressed. MRI showed a mass suggestive of schwannoma. After delivery, resection of the lesion was performed through an anterior approach. Pathology confirmed schwannoma. The expression profile was positive for estrogen- and FGF receptors and ki-67, but negative for progesterone-, androgen- and other growth factor receptors. Case 2: A 24-year-old woman presented with diplopia and unilateral pain during pregnancy. She had normal visual acuity, but a mild exophthalmos and elevation deficit. MRI revealed an extraconal mass suggestive of schwannoma. After delivery, resection was performed through an anterior approach. Pathology confirmed the diagnosis. The expression profile was positive for ki-67, but negative for sex hormone- and growth factor receptors. In the six non-pregnant cases the expression profiles varied, with only one subject showing a strong expression of estrogen-, progesterone- and androgen receptors. Conclusions: Orbital schwannomas can experience growth during pregnancy. The underlying mechanism remains unclear as hormone- and growth factor expression profiles show no correlation to the pregnant state.
Published: 2020
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46. Deficiency in the autophagy modulator Dram1 exacerbates pyroptotic cell death of Mycobacteria-infected macrophages

Author: Rui Zhang, Annemarie H. Meijer, Vincenzo Torraca, Gabriel Forn-Cuní, Monica Varela, and Michiel van der Vaart
Subjects: Cell death, Cancer Research, Programmed cell death, Immunology, Mycobacterium Infections, Nontuberculous, Article, Cellular and Molecular Neuroscience, 03 medical and health sciences, 0302 clinical medicine, Phagosome maturation, Autophagy, Pyroptosis, Animals, Humans, Tuberculosis, lcsh:QH573-671, Zebrafish, Caspase, 030304 developmental biology, 0303 health sciences, Gene knockdown, biology, lcsh:Cytology, Macrophages, Membrane Proteins, Cell Biology, biology.organism_classification, 3. Good health, Cell biology, 030220 oncology & carcinogenesis, biology.protein, Infection, 030217 neurology & neurosurgery, Intracellular
Abstract: DNA damage regulated autophagy modulator 1 (DRAM1) is a stress-inducible regulator of autophagy and cell death. DRAM1 has been implicated in cancer, myocardial infarction, and infectious diseases, but the molecular and cellular functions of this transmembrane protein remain poorly understood. Previously, we have proposed DRAM1 as a host resistance factor for tuberculosis (TB) and a potential target for host-directed anti-infective therapies. In this study, we generated a zebrafish dram1 mutant and investigated its loss-of-function effects during Mycobacterium marinum (Mm) infection, a widely used model in TB research. In agreement with previous knockdown analysis, dram1 mutation increased the susceptibility of zebrafish larvae to Mm infection. RNA sequencing revealed major effects of Dram1 deficiency on metabolic, immune response, and cell death pathways during Mm infection, and only minor effects on proteinase and metabolic pathways were found under uninfected conditions. Furthermore, unchallenged dram1 mutants did not display overt autophagic defects, but autophagic targeting of Mm was reduced in the absence of Dram1. The phagocytic ability of macrophages in dram1 mutants was unaffected, but acidification of Mm-containing vesicles was strongly reduced, indicating that Dram1 is required for phagosome maturation. By in vivo imaging, we observed that Dram1-deficient macrophages fail to restrict Mm during early stages of infection. The resulting increase in bacterial burden could be reverted by knockdown of inflammatory caspase a (caspa) and gasdermin Eb (gsdmeb), demonstrating pyroptosis as the mechanism underlying premature cell death of Mm-infected macrophages in dram1 mutants. Collectively, these data demonstrate that dissemination of mycobacterial infection in zebrafish larvae is promoted in the absence of Dram1 due to reduced maturation of mycobacteria-containing vesicles, failed intracellular containment, and consequent pyroptotic death of infected macrophages. These results provide new evidence that Dram1 plays a central role in host resistance to intracellular infection, acting at the crossroad of autophagy and cell death.
Published: 2020
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47. Micellar antibiotics of bacillus

Author: Wilfried J. J. Meijer, William T. Ferreira, Karolina Bakun, Mateusz Hess, Sisareuth Tan, Loredana Baccigalupi, Simon M. Cutting, Mikhail Soloviev, James R. G. Adams, Ezio Ricca, Enrico Ferrari, Alain Brisson, María Teresa Rejas, Huynh A. Hong, Hannah Wood, Medical Research Council (UK), Ministerio de Economía y Competitividad (España), Ferreira, W. T., Hong, H. A., Hess, M., Adams, J. R. G., Wood, H., Bakun, K., Tan, S., Baccigalupi, L., Ferrari, E., Brisson, A., Ricca, E., Rejas, M. T., Meijer, W. J. J., Soloviev, M., and Cutting, S. M.
Subjects: medicine.drug_class, Antibiotics, Pharmaceutical Science, Bacillus, Bacillus subtilis, Bacillus velezensi, Micelle, Article, Microbiology, chemistry.chemical_compound, Pharmacy and materia medica, Chlorotetaine, Bacillus velezensis, medicine, biology, Chemistry, Lipopeptide, Biosurfactant, Antimicrobial, biology.organism_classification, C510 Applied Microbiology, RS1-441, Drug delivery, Bacteria
Abstract: Members of the Bacillus genus, particularly the “Bacillus subtilis group”, are known to produce amphipathic lipopeptides with biosurfactant activity. This includes the surfactins, fengycins and iturins that have been associated with antibacterial, antifungal, and anti-viral properties. We have screened a large collection of Bacillus, isolated from human, animal, estuarine water and soil samples and found that the most potent lipopeptide producers are members of the species Bacillus velezensis. B. velezensis lipopeptides exhibited anti-bacterial activity which was localised on the surface of both vegetative cells and spores. Interestingly, lipopeptide micelles (6–10 nm diameter) were detectable in strains exhibiting the highest levels of activity. Micelles were stable (heat and gastric stable) and shown to entrap other antimicrobials produced by the host bacterium (exampled here was the dipeptide antibiotic chlorotetaine). Commercially acquired lipopeptides did not exhibit similar levels of inhibitory activity and we suspect that micelle formation may relate to the particular isomeric forms produced by individual bacteria. Using naturally produced micelle formulations we demonstrated that they could entrap antimicrobial compounds (e.g., clindamycin, vancomycin and resveratrol). Micellar incorporation of antibiotics increased activity. Bacillus is a prolific producer of antimicrobials, and this phenomenon could be exploited naturally to augment antimicrobial activity. From an applied perspective, the ability to readily produce Bacillus micelles and formulate with drugs enables a possible strategy for enhanced drug delivery., Medical Research Council (MR/R026262/1) to SMCand the Ministry of Economy and Competitiveness of the Spanish Government PID2019_108778GB_C21 (AEI/FEDER, EU)
Published: 2021

48. Spatial and temporal assessment of crack cocaine use in 13 European cities through wastewater-based epidemiology

Author: Ruud Steenbeek, Erik Emke, Dennis Vughs, João Matias, Tim Boogaerts, Sara Castiglioni, Marina Campos-Mañas, Adrian Covaci, Pim de Voogt, Thomas ter Laak, Félix Hernández, Noelia Salgueiro-González, Wim G. Meijer, Mario J. Dias, Susana Simões, Alexander L.N. van Nuijs, Lubertus Bijlsma, and Frederic Béen
Subjects: crack cocaine, Wastewater-Based Epidemiological Monitoring, Environmental Engineering, temporal variability, Wastewater, Pollution, wastewater-based epidemiology, Chemistry, Cocaine, Environmental Chemistry, Crack Cocaine, Humans, spatial variability, HILIC, Cities, Biology, Waste Management and Disposal, Biomarkers
Abstract: Already in early 2000s, concerns have been growing in the EU about increasing use of cocaine and it is estimated that below 1 % of the population administer the drug by smoking crack cocaine. New available data suggests an increase in the use of crack cocaine and an increase in the number of crack cocaine users entering treatment has been reported in several European countries. Robust estimations of crack cocaine use are however not available yet. The use of crack cocaine has long been associated with severe adverse socio-economic conditions as well as mental health problems, such as suicide ideation and depression. The aim of this study was to assess spatial trends in population-normalized mass loads of crack cocaine biomarkers (i.e., anhydroecgonine and anhydroecgonine methyl ester) in 13 European cities in six countries (the Netherlands, Belgium, Ireland, Portugal, Spain and Italy). Furthermore, temporal trends over a five-year period were evaluated through the analysis of historic samples collected in the Netherlands. Finally, the stability of the crack cocaine biomarkers in wastewater was investigated through batch experiments. The samples were analyzed with a new developed and validated hydrophilic interaction liquid chromatography coupled to mass spectrometry method. Targeted crack cocaine biomarkers were found in all cities. Also, crack cocaine biomarker was detected in wastewater from 2017 to 2021 in the Netherlands, but no significance between the years were found. With respect to biomarker in-sample stability, AEME was found to be stable in wastewater. This study assessed crack cocaine use for the first time on a broad scale, both temporal and in cities across Europe, with wastewater-based epidemiology and it shows the importance of wastewater analysis to monitor community loads of crack cocaine use.
Published: 2022

49. Von Willebrand disease type 2M: Correlation between genotype and phenotype

Author: Annet Simons, Paul P. T. Brons, Frank W.G. Leebeek, Daniëlle Meijer, Selene C M Schoormans, Britta A P Laros-van Gorkom, Waander L. van Heerde, Sandy Krouwel, Laurens Nieuwenhuizen, Dominique P M S M Maas, Nicole M. A. Blijlevens, Saskia E M Schols, Ferdows Atiq, and Hematology
Subjects: medicine.medical_specialty, congenital, hereditary, and neonatal diseases and abnormalities, biology, business.industry, Mucocutaneous zone, Vascular damage Radboud Institute for Health Sciences [Radboudumc 16], Hematology, Rare cancers Radboud Institute for Molecular Life Sciences [Radboudumc 9], medicine.disease, Gastroenterology, Cancer development and immune defence Radboud Institute for Health Sciences [Radboudumc 2], Genotype-phenotype distinction, Von Willebrand factor, Antigen, Hemostasis, Internal medicine, hemic and lymphatic diseases, Genotype, medicine, biology.protein, Von Willebrand disease, business, Genotyping, Rare cancers Radboud Institute for Health Sciences [Radboudumc 9], circulatory and respiratory physiology
Abstract: Contains fulltext : 248232.pdf (Publisher’s version ) (Open Access) BACKGROUND: An appropriate clinical diagnosis of von Willebrand disease (VWD) can be challenging because of a variable bleeding pattern and laboratory phenotype. Genotyping is a powerful diagnostic tool and may have an essential role in the diagnostic field of VWD. OBJECTIVES: To unravel the clinical and laboratory heterogeneity of genetically confirmed VWD type 2M patients and to investigate their relationship. METHODS: Patients with a confirmed VWD type 2M genetic variant in the A1 or A3 domain of von Willebrand factor (VWF) and normal or only slightly aberrant VWF multimers were selected from all subjects genotyped at the Radboud university medical center because of a high suspicion of VWD. Bleeding scores and laboratory results were analyzed. RESULTS: Fifty patients had a clinically relevant genetic variant in the A1 domain. Median bleeding score was 5. Compared with the nationwide Willebrand in the Netherlands study type 2 cohort, bleeding after surgery or delivery was reported more frequently and mucocutaneous bleedings less frequently. Median VWF activity/VWF antigen (VWF:Act/VWF:Ag) ratio was 0.32, whereas VWF collagen binding activity/VWF antigen (VWF:CB/VWF:Ag) ratio was 0.80. Variants in the A3 domain were only found in two patients with low to normal VWF:Act/VWF:Ag ratios (0.45, 1.03) and low VWF:CB/VWF:Ag ratios (0.45, 0.63). CONCLUSION: Genetically confirmed VWD type 2M patients have a relatively mild clinical phenotype, except for bleeding after surgery and delivery. Laboratory phenotype is variable and depends on the underlying genetic variant. Addition of genotyping to the current phenotypic characterization may improve diagnosis and classification of VWD.
Published: 2022

50. HI-NESS: a family of genetically encoded DNA labels based on a bacterial nucleoid-associated protein

Author: Patrick Voskamp, Daphne E. C. Boer, Monica Varela Alvarez, Martijn S. Luijsterburg, Fatema-Zahra M Rashid, Frédéric Crémazy, Daan J.W. Brocken, Thomas S Shimizu, Joachim Goedhart, Remus T. Dame, Annemarie H. Meijer, Michiel van der Vaart, Eike K. Mahlandt, Anneloes Blok, Bram Henneman, and Molecular Cytology (SILS, FNWI)
Subjects: DNA Replication, DNA, Bacterial, AcademicSubjects/SCI00010, DNA damage, Genetic Vectors, Gene Expression, Biology, Genome, Cell Line, chemistry.chemical_compound, Narese/3, Bacterial Proteins, Transcription (biology), Genetics, Animals, Cloning, Molecular, Fluorescent Dyes, Staining and Labeling, Chromosome, Bacterial nucleoid, Cell biology, Chromatin, DNA-Binding Proteins, Microscopy, Fluorescence, chemistry, Nucleic acid, Methods Online, Biological Assay, DNA
Abstract: The interplay between three-dimensional chromosome organisation and genomic processes such as replication and transcription necessitates in vivo studies of chromosome dynamics. Fluorescent organic dyes are often used for chromosome labelling in vivo. The mode of binding of these dyes to DNA cause its distortion, elongation, and partial unwinding. The structural changes induce DNA damage and interfere with the binding dynamics of chromatin-associated proteins, consequently perturbing gene expression, genome replication, and cell cycle progression. We have developed a minimally-perturbing, genetically encoded fluorescent DNA label consisting of a (photo-switchable) fluorescent protein fused to the DNA-binding domain of H-NS — a bacterial nucleoid-associated protein. We show that this DNA label, abbreviated as HI-NESS (H-NS-based indicator for nucleic acid stainings), is minimally-perturbing to genomic processes and labels chromosomes in eukaryotic cells in culture, and in zebrafish embryos with preferential binding to AT-rich chromatin.
Published: 2022

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