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1دورية أكاديمية
المؤلفون: Joseph M Replogle, Jessica L Bonnar, Angela N Pogson, Christina R Liem, Nolan K Maier, Yufang Ding, Baylee J Russell, Xingren Wang, Kun Leng, Alina Guna, Thomas M Norman, Ryan A Pak, Daniel M Ramos, Michael E Ward, Luke A Gilbert, Martin Kampmann, Jonathan S Weissman, Marco Jost
المصدر: eLife, Vol 11 (2022)
مصطلحات موضوعية: CRISPR, CRISPR interference, genetic screen, functional genomics, knockdown, Medicine, Science, Biology (General), QH301-705.5
الوصف: CRISPR interference (CRISPRi) enables programmable, reversible, and titratable repression of gene expression (knockdown) in mammalian cells. Initial CRISPRi-mediated genetic screens have showcased the potential to address basic questions in cell biology, genetics, and biotechnology, but wider deployment of CRISPRi screening has been constrained by the large size of single guide RNA (sgRNA) libraries and challenges in generating cell models with consistent CRISPRi-mediated knockdown. Here, we present next-generation CRISPRi sgRNA libraries and effector expression constructs that enable strong and consistent knockdown across mammalian cell models. First, we combine empirical sgRNA selection with a dual-sgRNA library design to generate an ultra-compact (1–3 elements per gene), highly active CRISPRi sgRNA library. Next, we compare CRISPRi effectors to show that the recently published Zim3-dCas9 provides an excellent balance between strong on-target knockdown and minimal non-specific effects on cell growth or the transcriptome. Finally, we engineer a suite of cell lines with stable expression of Zim3-dCas9 and robust on-target knockdown. Our results and publicly available reagents establish best practices for CRISPRi genetic screening.
وصف الملف: electronic resource
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2دورية أكاديمية
المؤلفون: Smriti Parashar, Ravi Chidambaram, Shuliang Chen, Christina R Liem, Eric Griffis, Gerard G Lambert, Nathan C Shaner, Matthew Wortham, Jesse C Hay, Susan Ferro-Novick
المصدر: eLife, Vol 10 (2021)
مصطلحات موضوعية: ER-phagy, protein quality control, misfolded prohormones, SEC24C, Lunapark, ER structure, Medicine, Science, Biology (General), QH301-705.5
الوصف: The endoplasmic reticulum (ER) is composed of sheets and tubules. Here we report that the COPII coat subunit, SEC24C, works with the long form of the tubular ER-phagy receptor, RTN3, to target dominant-interfering mutant proinsulin Akita puncta to lysosomes. When the delivery of Akita puncta to lysosomes was disrupted, large puncta accumulated in the ER. Unexpectedly, photobleach analysis indicated that Akita puncta behaved as condensates and not aggregates, as previously suggested. Akita puncta enlarged when either RTN3 or SEC24C were depleted, or when ER sheets were proliferated by either knocking out Lunapark or overexpressing CLIMP63. Other ER-phagy substrates that are segregated into tubules behaved like Akita, while a substrate (type I procollagen) that is degraded by the ER-phagy sheets receptor, FAM134B, did not. Conversely, when ER tubules were augmented in Lunapark knock-out cells by overexpressing reticulons, ER-phagy increased and the number of large Akita puncta was reduced. Our findings imply that segregating cargoes into tubules has two beneficial roles. First, it localizes mutant misfolded proteins, the receptor, and SEC24C to the same ER domain. Second, physically restraining condensates within tubules, before they undergo ER-phagy, prevents them from enlarging and impacting cell health.
وصف الملف: electronic resource
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3دورية أكاديمية
المؤلفون: Sandra Elizabeth Torres, Ciara M Gallagher, Lars Plate, Meghna Gupta, Christina R Liem, Xiaoyan Guo, Ruilin Tian, Robert M Stroud, Martin Kampmann, Jonathan S Weissman, Peter Walter
المصدر: eLife, Vol 8 (2019)
مصطلحات موضوعية: unfolded protein response, proteostasis, small molecule inhibition, Medicine, Science, Biology (General), QH301-705.5
الوصف: The unfolded protein response (UPR) detects and restores deficits in the endoplasmic reticulum (ER) protein folding capacity. Ceapins specifically inhibit the UPR sensor ATF6α, an ER-tethered transcription factor, by retaining it at the ER through an unknown mechanism. Our genome-wide CRISPR interference (CRISPRi) screen reveals that Ceapins function is completely dependent on the ABCD3 peroxisomal transporter. Proteomics studies establish that ABCD3 physically associates with ER-resident ATF6α in cells and in vitro in a Ceapin-dependent manner. Ceapins induce the neomorphic association of ER and peroxisomes by directly tethering the cytosolic domain of ATF6α to ABCD3’s transmembrane regions without inhibiting or depending on ABCD3 transporter activity. Thus, our studies reveal that Ceapins function by chemical-induced misdirection which explains their remarkable specificity and opens up new mechanistic routes for drug development and synthetic biology.
وصف الملف: electronic resource
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المؤلفون: Angela N Pogson, Jessica L Bonnar, Joseph M Replogle, Christina R Liem, Nolan K Maier, Yufang Ding, Baylee J Russell, Xingren Wang, Kun Leng, Alina Guna, Thomas M Norman, Ryan A Pak, Daniel M Ramos, Michael E Ward, Luke A Gilbert, Martin Kampmann, Jonathan S Weissman, Marco Jost
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::9e7d2d97d229edac14829d4e3858e296Test
https://doi.org/10.7554/elife.81856.sa2Test -
5
المؤلفون: Joseph M. Replogle, Jessica L. Bonnar, Angela N. Pogson, Christina R. Liem, Nolan K. Maier, Yufang Ding, Baylee J. Russell, Xingren Wang, Kun Leng, Alina Guna, Thomas M. Norman, Ryan A. Pak, Daniel M. Ramos, Michael E. Ward, Luke A. Gilbert, Martin Kampmann, Jonathan S. Weissman, Marco Jost
مصطلحات موضوعية: General Immunology and Microbiology, General Neuroscience, General Medicine, General Biochemistry, Genetics and Molecular Biology
الوصف: CRISPR interference (CRISPRi) enables programmable, reversible, and titratable repression of gene expression (knockdown) in mammalian cells. Initial CRISPRi-mediated genetic screens have showcased the potential to address basic questions in cell biology, genetics, and biotechnology, but wider deployment of CRISPRi screening has been constrained by the large size of single guide RNA (sgRNA) libraries and challenges in generating cell models with consistent CRISPRi-mediated knockdown. Here, we present next-generation CRISPRi sgRNA libraries and effector expression constructs that enable strong and consistent knockdown across mammalian cell models. First, we combine empirical sgRNA selection with a dual-sgRNA library design to generate an ultra-compact (1-3 elements per gene), highly active CRISPRi sgRNA library. Next, we rigorously compare CRISPRi effectors to show that the recently published Zim3-dCas9 provides the best balance between strong on-target knockdown and minimal nonspecific effects on cell growth or the transcriptome. Finally, we engineer a suite of cell lines with stable expression of Zim3-dCas9 and robust on-target knockdown. Our results and publicly available reagents establish best practices for CRISPRi genetic screening.
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::9fdf7ca55256386579b422055fd4e823Test
https://doi.org/10.1101/2022.07.13.499814Test -
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المؤلفون: Bhairavi Tolani, Anna Celli, Yanmin Yao, Yong Zi Tan, Richard Fetter, Christina R. Liem, Adam J. de Smith, Thamiya Vasanthakumar, Paola Bisignano, Adam D. Cotton, Ian B. Seiple, John L. Rubinstein, Marco Jost, Jonathan S. Weissman
المصدر: Nature biotechnology, vol 40, iss 12
مصطلحات موضوعية: Vacuolar Proton-Translocating ATPases, Tumor, Biomedical Engineering, Bioengineering, Antineoplastic Agents, Applied Microbiology and Biotechnology, Cell Line, Colo-Rectal Cancer, Proto-Oncogene Proteins p21(ras), Mice, Cell Line, Tumor, Neoplasms, Mutation, ras Proteins, Molecular Medicine, Humans, Animals, Digestive Diseases, Biotechnology, Cancer
الوصف: Mutations in Ras family proteins are implicated in 33% of human cancers, but direct pharmacological inhibition of Ras mutants remains challenging. As an alternative to direct inhibition, we screened for sensitivities in Ras-mutant cells and discovered 249C as a Ras-mutant selective cytotoxic agent with nanomolar potency against a spectrum of Ras-mutant cancers. 249C binds to vacuolar (V)-ATPase with nanomolar affinity and inhibits its activity, preventing lysosomal acidification and inhibiting autophagy and macropinocytosis pathways that several Ras-driven cancers rely on for survival. Unexpectedly, potency of 249C varies with the identity of the Ras driver mutation, with the highest potency for KRASG13D and G12V both in vitro and in vivo, highlighting a mutant-specific dependence on macropinocytosis and lysosomal pH. Indeed, 249C potently inhibits tumor growth without adverse side effects in mouse xenografts of KRAS-driven lung and colon cancers. A comparison of isogenic SW48 xenografts with different KRAS mutations confirmed that KRASG13D/+ (followed by G12V/+) mutations are especially sensitive to 249C treatment. These data establish proof-of-concept for targeting V-ATPase in cancers driven by specific KRAS mutations such as KRASG13D and G12V.
وصف الملف: application/pdf
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::39a71129bb71ed4aab46b2badda735d5Test
https://pubmed.ncbi.nlm.nih.gov/35879364Test -
7
المؤلفون: Matthew Wortham, Eric R. Griffis, Susan Ferro-Novick, Smriti Parashar, Ravi Chidambaram, Shuliang Chen, Christina R Liem, Gerard G. Lambert, Nathan C. Shaner, Jesse C. Hay
المصدر: eLife, Vol 10 (2021)
مصطلحات موضوعية: Protein Folding, ER-phagy, endocrine system diseases, Mutant, Endoplasmic Reticulum, Mice, 0302 clinical medicine, cell biology, Biology (General), SEC24C, Receptor, COPII, Proinsulin, 0303 health sciences, Tumor, Chemistry, General Neuroscience, General Medicine, Cell biology, Medicine, Protein folding, hormones, hormone substitutes, and hormone antagonists, endocrine system, Cell signaling, QH301-705.5, Science, Knockout, Protein subunit, ER structure, Lunapark, General Biochemistry, Genetics and Molecular Biology, Cell Line, Protein Aggregates, 03 medical and health sciences, Autophagy, Animals, Humans, protein quality control, 030304 developmental biology, General Immunology and Microbiology, Endoplasmic reticulum, Membrane Proteins, misfolded neuropeptides, HEK293 Cells, nervous system, Other, Biochemistry and Cell Biology, Lysosomes, Carrier Proteins, misfolded prohormones, 030217 neurology & neurosurgery
الوصف: The endoplasmic reticulum (ER) is composed of sheets and tubules. Here we report that the COPII coat subunit, SEC24C, works with the long form of the tubular ER-phagy receptor, RTN3, to target dominant-interfering mutant proinsulin Akita puncta to lysosomes. When the delivery of Akita puncta to lysosomes was disrupted, large puncta accumulated in the ER. Unexpectedly, photobleach analysis indicated that Akita puncta behaved as condensates and not aggregates, as previously suggested. Akita puncta enlarged when either RTN3 or SEC24C were depleted, or when ER sheets were proliferated by either knocking out Lunapark or overexpressing CLIMP63. Other ER-phagy substrates that are segregated into tubules behaved like Akita, while a substrate (type I procollagen) that is degraded by the ER-phagy sheets receptor, FAM134B, did not. Conversely, when ER tubules were augmented in Lunapark knock-out cells by overexpressing reticulons, ER-phagy increased and the number of large Akita puncta was reduced. Our findings imply that segregating cargoes into tubules has two beneficial roles. First, it localizes mutant misfolded proteins, the receptor, and SEC24C to the same ER domain. Second, physically restraining condensates within tubules, before they undergo ER-phagy, prevents them from enlarging and impacting cell health.
وصف الملف: application/pdf
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::f2bf632d40ec35678367dc11ba4f9ac4Test
https://doi.org/10.7554/elife.71642Test -
8
المؤلفون: Nathan C. Shaner, Gerard G. Lambert, Shuliang Chen, Eric R. Griffis, Matthew Wortham, Jesse C. Hay, Ravi Chidambaram, Smriti Parashar, Susan Ferro-Novick, Christina R Liem
مصطلحات موضوعية: Chemistry, Endoplasmic reticulum, Biophysics, Limit (mathematics)
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_________::041a945121b006d5cd3aec582a62f707Test
https://doi.org/10.7554/elife.71642.sa2Test -
9
المؤلفون: Susana A. Ribeiro, Xiaowei Yan, Max A. Horlbeck, Marvin E. Tanenbaum, Ronald D. Vale, Marco Jost, Jonathan S. Weissman, Christina R. Liem, Nico Stuurman
المساهمون: Hubrecht Institute for Developmental Biology and Stem Cell Research
المصدر: The Journal of cell biology, vol 220, iss 2
The Journal of Cell Biology
Journal of Cell Biology, 220(2). Rockefeller University Pressمصطلحات موضوعية: Technology, Optics and Photonics, Cell Nucleus/genetics, Green Fluorescent Proteins, Computational biology, Biology, Medical and Health Sciences, Flow cytometry, Cell Line, Imaging, Tools, 03 medical and health sciences, Imaging, Three-Dimensional, 0302 clinical medicine, medicine, Genetics, CRISPR, Humans, Guide RNA, Genetic Testing, Gene, High content imaging, 030304 developmental biology, Green Fluorescent Proteins/metabolism, Cell Nucleus, 0303 health sciences, medicine.diagnostic_test, Cell Nucleus Size/genetics, CRISPR-Cas Systems/genetics, Cell Biology, Cell sorting, Biological Sciences, Flow Cytometry, Phenotype, Cell culture, Cell Nucleus Size, Three-Dimensional, Generic health relevance, CRISPR-Cas Systems, 030217 neurology & neurosurgery, Cell Cycle and Division, Developmental Biology
الوصف: Yan et al. demonstrate high-throughput screening of pooled CRISPR libraries for phenotypes detectable by microscopy. Their approach uses photoactivation of cells displaying the phenotype of interest and FACS sorting of marked cells, followed by sequencing, and facilitates discovery of genes involved in cell biological processes.
CRISPR (clustered regularly interspaced short palindromic repeats)-based gene inactivation provides a powerful means for linking genes to particular cellular phenotypes. CRISPR-based screening typically uses large genomic pools of single guide RNAs (sgRNAs). However, this approach is limited to phenotypes that can be enriched by chemical selection or FACS sorting. Here, we developed a microscopy-based approach, which we name optical enrichment, to select cells displaying a particular CRISPR-induced phenotype by automated imaging-based computation, mark them by photoactivation of an expressed photoactivatable fluorescent protein, and then isolate the fluorescent cells using fluorescence-activated cell sorting (FACS). A plugin was developed for the open source software μManager to automate the phenotypic identification and photoactivation of cells, allowing ∼1.5 million individual cells to be screened in 8 h. We used this approach to screen 6,092 sgRNAs targeting 544 genes for their effects on nuclear size regulation and identified 14 bona fide hits. These results present a scalable approach to facilitate imaging-based pooled CRISPR screens.وصف الملف: application/pdf
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::8f769ae2b6532434e14d43455145a3bbTest
https://hdl.handle.net/20.500.11755/ab13b382-4bd8-4a36-ab6b-f591f1d6c8cfTest -
10
المؤلفون: Rishi Singhal, Abd A Tahrani, Christian Ludwig, Kamal Mahawar, A Abou-Mrad-Fricquegnon, A Alasfur, A Alexandrou, A Barbosa, A Bashir, A Bosco, A Charalabopoulos, A Curell, A Davarpanah Jazi, A Diego, A Elghandour, A Ergin, A Garcia, A Ghazal, A Haddad, A Ibarzábal, A Khazraji, A Lale, A Lázaro, A Leyva-Alvizo, A Liagre, A Maleckas, A Osman, A Pantelis, A Pazouki, A Plamper, A Raziel, A Rizzi, A Sanchez, A Sharma, A Spaventa, A Sumer, A Torres, A Türkçapar, A Ugale, A Velikorechin, A Vitiello, B Alkhaffaf, B Bomans, BJ Ammori, B Pares, B Smeu, B Zilberstein, C Boeker, C Brodén, C Copaescu, C Guevara, C Güldoğan, C Kirkil, C Matthys, C Nagliati, C Parmar, C Trindade, C Vaz, C Wietzycoski, C Zerrweck, D Bedi, D de Marchi, D Faraj, D Foschi, D Goitein, D Hazzan, D Lapatsanis, D Mazza, D Mohammed, D Padilla-Armendariz, D Pennisi, D Pham, D Pournaras, D Swank, D Thakkar, E Baena, E Baili, E Bastos, E Dilektasli, E Hazebroek, E Kaplan, E Lopes, E Manno, E Pinotti, E Sdralis, F Barrera-Rodriguez, F Cantu, F Frattini, F Martini, G Berardi, G Cesana, G Dapri, G Dinescu, G Juglard, G Martinez de Aragon, G Menaldi, G Ören, G Pavone, G Rana, G Vrakopoulou, H Aboshanab, H Al-Momani, H Balamoun, H Çiyiltepe, H de Vasconcelos Cunha, H Elghadban, H Gislason, H Hamed, H Heneghan, H Ibrahim, H Melali, H Reyes, H Sebbag, I Hakami, I Hutopila, J Balibrea, J Bernardo, J Campos, J Chevallier, J Dargent, J Estrada, J Gonzalez, J Hewes, J Himpens, J Mall, J Monterrubio, J Pasquier, K Albanopoulos, K Bartosiak, K Kaseja, K Kumar, K Rheinwalt, K Shah, K. van de Pas, L Angrisani, L Benuzzi, L Chong, L Layani, L Lee, L Level, L Taylor, L Zinai, M Akbaba, M Alejandro, M Altarawni, M Beisani, M Bertrand, M Cantu, M Dincer, M Elbanna, M Elfawal, M Focquet, M Forero, M Hadad, M Hii, M Iovino, M Islam, M Josa, M Kaplan, M Kermansaravi, M Khaitan, M Kizilkaya, M Kotowski, M Montouri, M Musella, M Narwaria, M Navarro, M Niazi, M Özmen, M Qassem, M Romeijn, M Said, M Salman, M Solovyeva, M Takieddine, M Uccelli, M Ustun, M Valeti, M Walędziak, N Arora, N Dukkipati, N Fearon, N Kiran, N Paleari, N Sakran, N Silva, N Tartaglia, O Savas, O Şen, O Viveiros, P Fabbri, P García, P Major, P Martinez, P Martinez Duartez, P Salminen, P Shah, R Gadani, R Gokay, R Gudaityte, R Kassir, R Liem, R Mohan, R Palma, R Quinino, R Ribeiro, R Vilallonga, S Arana-Garza, S Chiappetta, S Davakis, S Ghareeb, S Gregorio, S Khaldi, S Martinez, S Okkema, S Olmi, S Ortiz, S Pinango, S Shah, S Shahabi, S Taha, S Ugale, T Barreiro, T Beck, T Poghosyan, T Samarkandy, T Yigit, V Borrelli, V Bottino, V Marco, V Ormando, V Pol, V Sierra Esteban, V Valentí, W Leclercq, W Souza, W Vening, W Vleeschouwers, Y van der Burgh
المساهمون: Singhal, R., Tahrani, A. A., Ludwig, C., Mahawar, K., Abou-Mrad-Fricquegnon, A., Alasfur, A., Alexandrou, A., Barbosa, A., Bashir, A., Bosco, A., Charalabopoulos, A., Curell, A., Davarpanah Jazi, A., Diego, A., Elghandour, A., Ergin, A., Garcia, A., Ghazal, A., Haddad, A., Ibarzabal, A., Khazraji, A., Lale, A., Lazaro, A., Leyva-Alvizo, A., Liagre, A., Maleckas, A., Osman, A., Pantelis, A., Pazouki, A., Plamper, A., Raziel, A., Rizzi, A., Sanchez, A., Sharma, A., Spaventa, A., Sumer, A., Torres, A., Turkcapar, A., Ugale, A., Velikorechin, A., Vitiello, A., Alkhaffaf, B., Bomans, B., Ammori, B. J., Pares, B., Smeu, B., Zilberstein, B., Boeker, C., Broden, C., Copaescu, C., Guevara, C., Guldogan, C., Kirkil, C., Matthys, C., Nagliati, C., Parmar, C., Trindade, C., Vaz, C., Wietzycoski, C., Zerrweck, C., Bedi, D., de Marchi, D., Faraj, D., Foschi, D., Goitein, D., Hazzan, D., Lapatsanis, D., Mazza, D., Mohammed, D., Padilla-Armendariz, D., Pennisi, D., Pham, D., Pournaras, D., Swank, D., Thakkar, D., Baena, E., Baili, E., Bastos, E., Dilektasli, E., Hazebroek, E., Kaplan, E., Lopes, E., Manno, E., Pinotti, E., Sdralis, E., Barrera-Rodriguez, F., Cantu, F., Frattini, F., Martini, F., Berardi, G., Cesana, G., Dapri, G., Dinescu, G., Juglard, G., Martinez de Aragon, G., Menaldi, G., Oren, G., Pavone, G., Rana, G., Vrakopoulou, G., Aboshanab, H., Al-Momani, H., Balamoun, H., Ciyiltepe, H., de Vasconcelos Cunha, H., Elghadban, H., Gislason, H., Hamed, H., Heneghan, H., Ibrahim, H., Melali, H., Reyes, H., Sebbag, H., Hakami, I., Hutopila, I., Balibrea, J., Bernardo, J., Campos, J., Chevallier, J., Dargent, J., Estrada, J., Gonzalez, J., Hewes, J., Himpens, J., Mall, J., Monterrubio, J., Pasquier, J., Albanopoulos, K., Bartosiak, K., Kaseja, K., Kumar, K., Rheinwalt, K., Shah, K., van de Pas, K., Angrisani, L., Benuzzi, L., Chong, L., Layani, L., Lee, L., Level, L., Taylor, L., Zinai, L., Akbaba, M., Alejandro, M., Altarawni, M., Beisani, M., Bertrand, M., Cantu, M., Dincer, M., Elbanna, M., Elfawal, M., Focquet, M., Forero, M., Hadad, M., Hii, M., Iovino, M., Islam, M., Josa, M., Kaplan, M., Kermansaravi, M., Khaitan, M., Kizilkaya, M., Kotowski, M., Montouri, M., Musella, M., Narwaria, M., Navarro, M., Niazi, M., Ozmen, M., Qassem, M., Romeijn, M., Said, M., Salman, M., Solovyeva, M., Takieddine, M., Uccelli, M., Ustun, M., Valeti, M., Waledziak, M., Arora, N., Dukkipati, N., Fearon, N., Kiran, N., Paleari, N., Sakran, N., Silva, N., Tartaglia, N., Savas, O., Sen, O., Viveiros, O., Fabbri, P., Garcia, P., Major, P., Martinez, P., Martinez Duartez, P., Salminen, P., Shah, P., Gadani, R., Gokay, R., Gudaityte, R., Kassir, R., Liem, R., Mohan, R., Palma, R., Quinino, R., Ribeiro, R., Vilallonga, R., Arana-Garza, S., Chiappetta, S., Davakis, S., Ghareeb, S., Gregorio, S., Khaldi, S., Martinez, S., Okkema, S., Olmi, S., Ortiz, S., Pinango, S., Shah, S., Shahabi, S., Taha, S., Ugale, S., Barreiro, T., Beck, T., Poghosyan, T., Samarkandy, T., Yigit, T., Borrelli, V., Bottino, V., Marco, V., Ormando, V., Pol, V., Sierra Esteban, V., Valenti, V., Leclercq, W., Souza, W., Vening, W., Vleeschouwers, W., van der Burgh, Y.
المصدر: The Lancet Diabetes & Endocrinology
GENEVA Collaborators 2021, ' Global 30-day outcomes after bariatric surgery during the COVID-19 pandemic (GENEVA) : an international cohort study ', The Lancet Diabetes and Endocrinology, vol. 9, no. 1, pp. 7-9 . https://doi.org/10.1016/S2213-8587Test(20)30375-2
The Lancet. Diabetes & Endocrinologyمصطلحات موضوعية: 2019-20 coronavirus outbreak, medicine.medical_specialty, Internationality, Time Factors, Coronavirus disease 2019 (COVID-19), Time Factor, Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), Endocrinology, Diabetes and Metabolism, MEDLINE, Bariatric Surgery, Global Health, Cohort Studies, Endocrinology, Pandemic, Correspondence, medicine, Global health, Internal Medicine, Humans, Mortality, Mortality trends, Pandemics, Manchester Cancer Research Centre, business.industry, ResearchInstitutes_Networks_Beacons/mcrc, COVID-19, Treatment Outcome, Emergency medicine, Cohort Studie, business, Cohort study, Human
الوصول الحر: https://explore.openaire.eu/search/publication?articleId=doi_dedup___::7913225665062f9e25020ba90a7bf98aTest
النص الكامل