المؤلفون: Kulkarni, Subhash, Ganz, Julia, Bayrer, James, Becker, Laren, Bogunovic, Milena, Rao, Meenakshi

المصدر: Journal of Neuroscience. 38(44)

مصطلحات موضوعية: Biomedical and Clinical Sciences, Neurosciences, Digestive Diseases, Underpinning research, 1.1 Normal biological development and functioning, Neurological, Animals, Brain, Enteric Nervous System, Gastrointestinal Diseases, Gastrointestinal Tract, Humans, Neurobiology, Medical and Health Sciences, Psychology and Cognitive Sciences, Neurology & Neurosurgery

الوصف: The enteric nervous system (ENS) is a large, complex division of the peripheral nervous system that regulates many digestive, immune, hormonal, and metabolic functions. Recent advances have elucidated the dynamic nature of the mature ENS, as well as the complex, bidirectional interactions among enteric neurons, glia, and the many other cell types that are important for mediating gut behaviors. Here, we provide an overview of ENS development and maintenance, and focus on the latest insights gained from the use of novel model systems and live-imaging techniques. We discuss major advances in the understanding of enteric glia, and the functional interactions among enteric neurons, glia, and enteroendocrine cells, a large class of sensory epithelial cells. We conclude by highlighting recent work on muscularis macrophages, a group of immune cells that closely interact with the ENS in the gut wall, and the importance of neurological-immune system communication in digestive health and disease.

وصف الملف: application/pdf

الوصول الحر: https://escholarship.org/uc/item/7313q39mTest

المؤلفون: Kulkarni, Subhash, Saha, Monalee, Slosberg, Jared, Singh, Alpana, Nagaraj, Sushma, Becker, Laren, Zhang, Chengxiu, Bukowski, Alicia, Wang, Zhuolun, Liu, Guosheng, Leser, Jenna M, Kumar, Mithra, Bakhshi, Shriya, Anderson, Matthew J, Lewandoski, Mark, Vincent, Elizabeth, Goff, Loyal A, Pasricha, Pankaj Jay

المساهمون: National Institutes of Health, Ludwig Family Foundation, Augusta University, Burroughs Wellcome Fund, Johns Hopkins University, Maryland Stem Cell Research Fund

المصدر: eLife ; volume 12 ; ISSN 2050-084X

الوصف: The enteric nervous system (ENS), a collection of neural cells contained in the wall of the gut, is of fundamental importance to gastrointestinal and systemic health. According to the prevailing paradigm, the ENS arises from progenitor cells migrating from the neural crest and remains largely unchanged thereafter. Here, we show that the lineage composition of maturing ENS changes with time, with a decline in the canonical lineage of neural-crest derived neurons and their replacement by a newly identified lineage of mesoderm-derived neurons. Single cell transcriptomics and immunochemical approaches establish a distinct expression profile of mesoderm-derived neurons. The dynamic balance between the proportions of neurons from these two different lineages in the post-natal gut is dependent on the availability of their respective trophic signals, GDNF-RET and HGF-MET. With increasing age, the mesoderm-derived neurons become the dominant form of neurons in the ENS, a change associated with significant functional effects on intestinal motility which can be reversed by GDNF supplementation. Transcriptomic analyses of human gut tissues show reduced GDNF-RET signaling in patients with intestinal dysmotility which is associated with reduction in neural crest-derived neuronal markers and concomitant increase in transcriptional patterns specific to mesoderm-derived neurons. Normal intestinal function in the adult gastrointestinal tract therefore appears to require an optimal balance between these two distinct lineages within the ENS.

الإتاحة: https://doi.org/10.7554/elife.88051Test
https://cdn.elifesciences.org/articles/88051/elife-88051-v1.pdfTest
https://cdn.elifesciences.org/articles/88051/elife-88051-v1.xmlTest
https://elifesciences.org/articles/88051Test

المؤلفون: Namkoong, Hong, Lee, Bomi, Swaminathan, Gayathri, Koh, Seong-Joon, Rogalla, Stephan, Paraskevopoulou, Maria D., Tang, Jay, Mikhail, David, Becker, Laren S., Habtezion, Aida

المصدر: Frontiers in Oncology ; volume 13 ; ISSN 2234-943X

الوصف: Introduction The chemoattractant receptor, G protein-coupled receptor 15 (GPR15), promotes colon homing of T cells in health and colitis. GPR15 function in colon cancer is largely unexplored, motivating our current studies. Methods In human study, immune cells were isolated from tumor tissues and healthy surgical tumor margins (STM), and their proportions as well as expression of GPR15 was analyzed by flow cytometry. In mouse studies, colon cancer was induced in GPR15-deficient (KO) and GPR15-suficient (Het) mice using azoxymethane (AOM) and dextran sulfate sodium (DSS) solution in drinking water. Serial endoscopy was performed in mice to monitor and visualize the distal region of colon. Mice were euthanized 10 weeks after the initial DSS administration, and the colon length and the number of polyps were recorded. Next, we identified the effects of GPR15L on established tumors in the MC38-colorectal cancer (CRC) mouse model. Immune cells were isolated from the mice colons or tumors and assessed by flow cytometry. Results Our analysis of human CRC tissue revealed a significant reduction in GPR15 + immune cell frequencies in tumors compared to ‘tumor-free’ surgical margins. Similarly, our data analysis using The Cancer Genome Atlas (TCGA) indicated that lower GPR15 expression is associated with poor survival in human colon cancer. In the AOM/DSS colitis-associated colon cancer model, we observed increased colonic polyps and lower survival in Gpr15 + -KO compared to Gpr15 -Het mice. Analysis of immune cell infiltrates in the colonic polyps showed significantly decreased CD8 + T cells and increased IL-17 + CD4 + and IL-17 + CD8 + T cells in Gpr15-KO than in Het mice. Consistent with a protective role of GPR15, administration of GPR15L to established tumors in the MC38-CRC model increased CD45 + cell infiltration, enhanced TNFa expression on CD4+ and CD8+ T cells at the tumor site and dramatically reduced tumor burden. Discussion Our findings highlight an important, unidentified role of the GPR15-GPR15L axis in ...

الإتاحة: https://doi.org/10.3389/fonc.2023.1254307Test

المؤلفون: Bishop, Estelle Spear, Namkoong, Hong, Aurelian, Laure, McCarthy, Madison, Nallagatla, Pratima, Zhou, Wenyu, Neshatian, Leila, Gurland, Brooke, Habtezion, Aida, Becker, Laren

المساهمون: National Institutes of Health

المصدر: Gastro Hep Advances ; volume 2, issue 2, page 261-276 ; ISSN 2772-5723

الإتاحة: https://doi.org/10.1016/j.gastha.2022.09.006Test
https://api.elsevier.com/content/article/PII:S2772572322001583?httpAccept=text/xmlTest
https://api.elsevier.com/content/article/PII:S2772572322001583?httpAccept=text/plainTest

المؤلفون: Ulsh, Lauren, Halawi, Houssam, Triadafilopoulos, George, Gurland, Brooke, Nguyen, Linda, Garcia, Patricia, Sonu, Irene, Fernandez‐Becker, Nielsen, Becker, Laren, Sheth, Vipul, Neshatian, Leila

المصدر: Neurogastroenterology & Motility; Jul2024, Vol. 36 Issue 7, p1-9, 9p

مصطلحات موضوعية: OTTOMANS (Furniture), DEFECATION

مستخلص: Background: Whether patients with defecatory disorders (DDs) with favorable response to a footstool have distinctive anorectal pressure characteristics is unknown. We aimed to identify the clinical phenotype and anorectal pressure profile of patients with DDs who benefit from a footstool. Methods: This is a retrospective review of patients with high resolution anorectal manometry (HR‐ARM) and balloon expulsion test (BET) from a tertiary referral center. BET was repeated with a 7‐inch‐high footstool in those who failed it after 120 s. Data were compared among groups with respect to BET results. Key Results: Of the 667 patients with DDs, a total of 251 (38%) had failed BET. A footstool corrected BET in 41 (16%) of those with failed BET. Gender‐specific differences were noted in anorectal pressures, among patients with and without normal BET, revealing gender‐based nuances in pathophysiology of DDs. Comparing patients who passed BET with footstool with those who did not, the presence of optimal stool consistency, with reduced instances of loose stools and decreased reliance on laxatives were significant. Additionally, in women who benefited from a footstool, lower anal pressures at rest and simulated defecation were observed. Independent factors associated with a successful BET with a footstool in women included age <50, Bristol 3 or 4 stool consistency, lower anal resting pressure and higher rectoanal pressure gradient. Conclusion & Inferences: Identification of distinctive clinical and anorectal phenotype of patients who benefited from a footstool could provide insight into the factors influencing the efficacy of footstool utilization and allow for an individualized treatment approach in patients with DDs. [ABSTRACT FROM AUTHOR]

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المؤلفون: Kulkarni, Subhash, Micci, Maria-Adelaide, Leser, Jenna, Shin, Changsik, Tang, Shiue-Cheng, Fu, Ya-Yuan, Liu, Liansheng, Li, Qian, Saha, Monalee, Li, Cuiping, Enikolopov, Grigori, Becker, Laren, Rakhilin, Nikolai, Anderson, Michael, Shen, Xiling, Dong, Xinzhong, Butte, Manish J, Song, Hongjun, Southard-Smith, E Michelle, Kapur, Raj P, Bogunovic, Milena, Pasricha, Pankaj J

المصدر: Proceedings of the National Academy of Sciences of the United States of America. 114(18)

مصطلحات موضوعية: Digestive Diseases, Neurosciences, Stem Cell Research - Nonembryonic - Non-Human, Stem Cell Research, Underpinning research, 1.1 Normal biological development and functioning, Neurological, Animals, Apoptosis, Enteric Nervous System, Humans, Mice, Mice, Transgenic, Nestin, Neurogenesis, Receptors, Nerve Growth Factor, SOXE Transcription Factors, enteric neurons, adult neurogenesis, enteric neural precursor cells, neuronal apoptosis

الوصف: According to current dogma, there is little or no ongoing neurogenesis in the fully developed adult enteric nervous system. This lack of neurogenesis leaves unanswered the question of how enteric neuronal populations are maintained in adult guts, given previous reports of ongoing neuronal death. Here, we confirm that despite ongoing neuronal cell loss because of apoptosis in the myenteric ganglia of the adult small intestine, total myenteric neuronal numbers remain constant. This observed neuronal homeostasis is maintained by new neurons formed in vivo from dividing precursor cells that are located within myenteric ganglia and express both Nestin and p75NTR, but not the pan-glial marker Sox10. Mutation of the phosphatase and tensin homolog gene in this pool of adult precursors leads to an increase in enteric neuronal number, resulting in ganglioneuromatosis, modeling the corresponding disorder in humans. Taken together, our results show significant turnover and neurogenesis of adult enteric neurons and provide a paradigm for understanding the enteric nervous system in health and disease.

وصف الملف: application/pdf

الوصول الحر: https://escholarship.org/uc/item/1fz0k4cnTest

المؤلفون: Neshatian, Leila, Grant, Gabrielle, Fernandez‐Becker, Nielsen, Yuan, Ye, Garcia, Patricia, Becker, Laren, Gurland, Brooke, Triadafilopoulos, George

المصدر: Neurogastroenterology & Motility ; volume 36, issue 4 ; ISSN 1350-1925 1365-2982

الوصف: Background Vitamin‐D is essential for musculoskeletal health. We aimed to determine whether patients with fecal incontinence (FI): (1) are more likely to have vitamin‐D deficiency and, (2) have higher rates of comorbid medical conditions. Methods We examined 18‐ to 90‐year‐old subjects who had 25‐hydroxy vitamin‐D levels, and no vitamin‐D supplementation within 3 months of testing, in a large, single‐institutional electronic health records dataset, between 2017 and 2022. Cox proportional hazards survival analysis was used to assess association of vitamin‐D deficiency on FI. Key Results Of 100,111 unique individuals tested for serum 25‐hydroxy vitamin‐D, 1205 (1.2%) had an established diagnosis of FI. Most patients with FI were female (75.9% vs. 68.7%, p = 0.0255), Caucasian (66.3% vs. 52%, p = 0.0001), and older (64.2 vs. 53.8, p < 0.0001). Smoking (6.56% vs. 2.64%, p = 0.0001) and GI comorbidities, including constipation (44.9% vs. 9.17%, p = 0.0001), irritable bowel syndrome (20.91% vs. 3.72%, p = 0.0001), and diarrhea (28.55% vs. 5.2%, p = 0.0001) were more common among FI patients. Charlson Comorbidity Index score was significantly higher in patients with FI (5.5 vs. 2.7, p < 0.0001). Significantly higher proportions of patients with FI had vitamin‐D deficiency (7.14% vs. 4.45%, p < 0.0001). Moreover, after propensity‐score matching, rate of new FI diagnosis was higher in patients with vitamin‐D deficiency; HR 1.9 (95% CI [1.14–3.15]), p = 0.0131. Conclusion & Inferences Patients with FI had higher rates of vitamin‐D deficiency along with increased overall morbidity. Future research is needed to determine whether increased rate of FI in patients with vitamin‐D deficiency is related to frailty associated with increased medical morbidities.

الإتاحة: https://doi.org/10.1111/nmo.14753Test

المؤلفون: Jain, Sanjay, Pei, Liming, Spraggins, Jeffrey M., Angelo, Michael, Carson, James P., Gehlenborg, Nils, Ginty, Fiona, Gonçalves, Joana P., Hagood, James S., Hickey, John W., Kelleher, Neil L., Laurent, Louise C., Lin, Shin, Lin, Yiing, Liu, Huiping, Naba, Alexandra, Nakayasu, Ernesto S., Qian, Wei-Jun, Radtke, Andrea, Robson, Paul, Stockwell, Brent R., Van de Plas, Raf, Vlachos, Ioannis S., Zhou, Mowei, Ahn, Kyung Jin, Allen, Jamie, Anderson, David M., Anderton, Christopher R., Curcio, Christine, Angelin, Alessia, Arvanitis, Constadina, Atta, Lyla, Awosika-Olumo, Demi, Bahmani, Amir, Bai, Huajun, Balderrama, Karol, Balzano, Leandro, Bandyopadhyay, Gautam, Bandyopadhyay, Shovik, Bar-Joseph, Ziv, Barnhart, Kurt, Barwinska, Daria, Becich, Michael, Becker, Laren, Becker, Winston, Bedi, Kenneth, Bendall, Sean, Benninger, Kathy, Betancur, David, Bettinger, Keith, Billings, Sunteasja, Blood, Philip, Bolin, Daniel, Border, Samuel, Bosse, Marc, Bramer, Lisa, Brewer, Maya, Brusko, Maigan, Bueckle, Andreas, Burke, Karl, Burnum-Johnson, Kristin, Butcher, Eugene, Butterworth, Elizabeth, Cai, Long, Calandrelli, Riccardo, Caldwell, Michael, Campbell-Thompson, Martha, Cao, Dongfeng, Cao-Berg, Ivan, Caprioli, Richard, Caraccio, Chiara, Caron, Anita, Carroll, Megan, Chadwick, Chrystal, Chen, Angela, Chen, Derek, Chen, Fei, Chen, Haoran, Chen, Jing, Chen, Li, Chen, Lu, Chiacchia, Kenneth, Cho, Sanghee, Chou, Peter, Choy, Lisa, Cisar, Cecilia, Clair, Geremy, Clarke, Laura, Clouthier, Kelly A., Colley, Madeline E., Conlon, Kristin, Conroy, John, Contrepois, Kevin, Corbett, Anthony, Corwin, Alex, Cotter, Daniel, Courtois, Elise, Cruz, Aaron, Csonka, Christopher, Czupil, Kimberley, Daiya, Vicky, Dale, Kali, Davanagere, Shakeel Ahamed, Dayao, Monica, de Caestecker, Mark P., Decker, Aubrianna, Deems, Stephen, Degnan, David, Desai, Tushar, Deshpande, Vikrant, Deutsch, Gail, Devlin, Michelle, Diep, Dinh, Dodd, Carla, Donahue, Sean, Dong, Weixiu, dos Santos Peixoto, Rafael, Duffy, Michael, Dufresne, Martin, Duong, Thu Elizabeth, Dutra, Jennifer, Eadon, Michael T., El-Achkar, Tarek M., Enninful, Archibald, Eraslan, Gokcen, Eshelman, Diane, Espin-Perez, Almudena, Esplin, Edward D., Esselman, Allison, Falo, Louis D., Falo, Louis, Fan, Jean, Fan, Rong, Farrow, Melissa A., Farzad, Negin, Favaro, Patricia, Fermin, Jamie, Filiz, Ferda, Filus, Shane, Fisch, Kathleen, Fisher, Eyal, Fisher, Stephen, Flowers, Katelyn, Flynn, William F., Fogo, Agnes B., Fu, Dongtao, Fulcher, James, Fung, Anthony, Furst, Derek, Gallant, Michael, Gao, Fu, Gao, Yu, Gaulton, Kyle, Gaut, Joseph P., Gee, James, Ghag, Reetika R., Ghazanfar, Shila, Ghose, Soumya, Gisch, Debora, Gold, Ilan, Gondalia, Aashay, Gorman, Brittney, Greenleaf, William, Greenwald, Noah, Gregory, Brian, Guo, Rong, Gupta, Rajat, Hakimian, Hunter, Haltom, Jeff, Halushka, Marc, Han, Kyu Sang, Hanson, Casey, Harbury, Pehr, Hardi, Josef, Harlan, Linda, Harris, Raymond C., Hartman, Austin, Heidari, Elyas, Helfer, Jesse, Helminiak, David, Hemberg, Martin, Henning, Nathaniel, Herr, Bruce W., Ho, Jonhan, Holden-Wiltse, Jeanne, Hong, Seung-Hyun, Hong, Young-Kwon, Honick, Brendan, Hood, Greg, Hu, Po, Hu, Qiwen, Huang, Molly, Huyck, Heidie, Imtiaz, Tamjid, Isberg, Olof Gerdur, Itkin, Maxim, Jackson, Dana, Jacobs, Marni, Jain, Yashvardhan, Jewell, David, Jiang, Lihua, Jiang, Zhenghui G., Johnston, Sarah, Joshi, Pujan, Ju, Yingnan, Judd, Audra, Kagel, Adam, Kahn, Ari, Kalavros, Nikolaos, Kalhor, Kian, Karagkouni, Dimitra, Karathanos, Thomas, Karunamurthy, Arivarasan, Katari, Suhas, Kates, Heather, Kaushal, Madhurima, Keener, Nicholas, Keller, Mark, Kenney, Mariah, Kern, Colin, Kharchenko, Peter, Kim, Junhyong, Kingsford, Carl, Kirwan, Jessica, Kiselev, Vladimir, Kishi, Jocelyn, Kitata, Reta Birhanu, Knoten, Amanda, Kollar, Charles, Krishnamoorthy, Praveen, Kruse, Angela R. S., Kuang, Da, Kundaje, Anshul, Kutschera, Eric, Kwon, Yumi, Lake, Blue B., Lancaster, Samuel, Langlieb, Jonah, Lardenoije, Roy, Laronda, Monica, Laskin, Julia, Lau, Ken, Lee, Hayan, Lee, Maria, Lee, Mejeong, Levites Strekalova, Yulia, Li, Dongshunyi, Li, Jennifer, Li, Jilong, Li, Xiangtang, Li, Zhi, Liao, Yen-Chen, Liaw, Tiffany, Lin, Pei, Lin, Yulieh, Lindsay, Scott, Liu, Chunjie, Liu, Yang, Liu, Yuan, Lott, Marie, Lotz, Martin, Lowery, Lisa, Lu, Peiran, Lu, Xinyue, Lucarelli, Nicholas, Lun, Xiaokang, Luo, Zhifei, Ma, Jian, Macosko, Evan, Mahajan, Mayank, Maier, Libby, Makowski, Danika, Malek, Morad, Manthey, David, Manz, Trevor, Margulies, Kenneth, Marioni, John, Martindale, Matthew, Mason, Cayla, Mathews, Clayton, Maye, Peter, McCallum, Chuck, McDonough, Elizabeth, McDonough, Liz, Mcdowell, Hannah, Meads, Morgan, Medina-Serpas, Miguel, Melo Ferreira, Ricardo, Messinger, Jeffrey, Metis, Kay, Migas, Lukasz G., Miller, Brendan, Mimar, Sayat, Minor, Brittany, Misra, Ravi, Missarova, Alsu, Mistretta, Christopher, Moens, Roger, Moerth, Eric, Moffitt, Jeffrey, Molla, Gesmira, Monroe, Matthew, Monte, Emma, Morgan, Mike, Muraro, Daniele, Murphy, Bob, Murray, Evan, Musen, Mark A., Naglah, Ahmed, Nasamran, Chanond, Neelakantan, Taruna, Nevins, Stephanie, Nguyen, Hieu, Nguyen, Nam, Nguyen, Tram, Nguyen, Tri, Nigra, Deb, Nofal, Michel, Nolan, Garry, Nwanne, Gerald, O'Connor, Martin, Okuda, Kenichi, Olmer, Merissa, O'Neill, Kathleen, Otaluka, Nancy, Pang, Minxing, Parast, Mana, Pasa-Tolic, Ljiljana, Paten, Benedict, Patterson, Nathan Heath, Peng, Ting, Phillips, Gesina, Pichavant, Mina, Piehowski, Paul, Pilner, Hannah, Pingry, Ellie, Pita-Juarez, Yered, Plevritis, Sylvia, Ploumakis, Athanasios, Pouch, Alison, Pryhuber, Gloria, Puerto, Juan, Qaurooni, Danial, Qin, Ling, Quardokus, Ellen M., Rajbhandari, Presha, Rakow-Penner, Rebecca, Ramasamy, Ramalakshmi, Read, David, Record, Elizabeth G., Reeves, David, Ricarte, Allyson, Rodríguez-Soto, Ana, Ropelewski, Alexander, Rosario, Jean, Roselkis, Morla-Adames, Rowe, David, Roy, Tarun Kanti, Ruffalo, Matt, Ruschman, Nancy, Sabo, Angela, Sachdev, Nina, Saka, Sinem, Salamon, Diane, Sarder, Pinaki, Sasaki, Hiroshi, Satija, Rahul, Saunders, Diane, Sawka, Riley, Schey, Kevin, Schlehlein, Heidi, Scholten, David, Schultz, Sarah, Schwartz, Lauren, Schwenk, Melissa, Scibek, Robin, Segre, Ayellet, Serrata, Matthew, Shands, Walter, Shen, Xiaotao, Shendure, Jay, Shephard, Holly, Shi, Lingyan, Shi, Tujin, Shin, Dong-Guk, Shirey, Bill, Sibilla, Max, Silber, Michal, Silverstein, Jonathan, Simmel, Derek, Simmons, Alan, Singhal, Dhruv, Sivajothi, Santhosh, Smits, Thomas, Soncin, Francesca, Song, Qi, Stanley, Valentina, Stuart, Tim, Su, Hanquan, Su, Pei, Sun, Xin, Surrette, Christine, Swahn, Hannah, Tan, Kai, Teichmann, Sarah, Tejomay, Abhiroop, Tellides, George, Thomas, Kathleen, Thomas, Tracey, Thompson, Marissa, Tian, Hua, Tideman, Leonoor, Trapnell, Cole, Tsai, Albert G., Tsai, Chia-Feng, Tsai, Leo, Tsui, Elizabeth, Tsui, Tina, Tung, Jason, Turner, Morgan, Uranic, Jackie, Vaishnav, Eeshit Dhaval, Varra, Sricharan Reddy, Vaskivskyi, Vasyl, Velickovic, Dusan, Velickovic, Marija, Verheyden, Jamie, Waldrip, Jessica, Wallace, Douglas, Wan, Xueyi, Wang, Allen, Wang, Fusheng, Wang, Meng, Wang, Shuoshuo, Wang, Xuefei, Wasserfall, Clive, Wayne, Leonard, Webber, James, Weber, Griffin M., Wei, Bei, Wei, Jian-Jun, Weimer, Annika, Welling, Joel, Wen, Xingzhao, Wen, Zishen, Williams, MacKenzie, Winfree, Seth, Winograd, Nicholas, Woodard, Abashai, Wright, Devin, Wu, Fan, Wu, Pei-Hsun, Wu, Qiuyang, Wu, Xiaodong, Xing, Yi, Xu, Tiangyang, Yang, Manxi, Yang, Mingyu, Yap, Joseph, Ye, Dong Hye, Yin, Peng, Yuan, Zhou, Yun, Chi (Jina), Zahraei, Ali, Zemaitis, Kevin, Zhang, Bo, Zhang, Caibin, Zhang, Chenyu, Zhang, Chi, Zhang, Kun, Zhang, Shiping, Zhang, Ted, Zhang, Yida, Zhao, Bingqing, Zhao, Wenxin, Zheng, Jia Wen, Zhong, Sheng, Zhu, Bokai, Zhu, Chenchen, Zhu, Diming, Zhu, Quan, Zhu, Ying, Börner, Katy, Snyder, Michael P., HuBMAP Consortium

المصدر: Nature Cell Biology, 26, (2024-03-01)

مصطلحات موضوعية: Cell Biology

الوصف: The Human BioMolecular Atlas Program (HuBMAP) aims to create a multi-scale spatial atlas of the healthy human body at single-cell resolution by applying advanced technologies and disseminating resources to the community. As the HuBMAP moves past its first phase, creating ontologies, protocols and pipelines, this Perspective introduces the production phase: the generation of reference spatial maps of functional tissue units across many organs from diverse populations and the creation of mapping tools and infrastructure to advance biomedical research. ; © Springer Nature Limited 2023. ; Correction to: Nature Cell Biology https://doi.org/10.1038/s41556-023-01194-wTest. Published online 19 July 2023. In the version of this article originally published, the name of Tianyang Xu was misspelled as Tiangyang Xu. The name has been corrected in the HTML and PDF versions of the article. ; The HuBMAP Consortium GitHub athttps://github.com/hubmapconsortiumhas 120 repositories that support data ingest, analysis, visualization and search plus HRA construction and usage. Documentation is available athttps://software.docs.hubmapconsortium.org/apis.html. ; We thank L. M. McGuire, SciStories, F. Goncalves, H. Schlehlein and V. A. Deshpande for their efforts in designing and creating graphics. We thank A. Honkala for assistance with manuscript formatting. We thank Z. Galis from the National Heart, Lung, and Blood Institute for many useful comments. Support for title page creation and format was provided by AuthorArranger, a tool developed at the National Cancer Institute. The authors gratefully acknowledge NIH HuBMAP grants U54HL165442 and U01HL166058 (L.P.); U54DK134301 and OT2OD033753 (S.J.); U54EY032442, U54DK120058 and U54DK134302 (J.M.S.); OT2OD033756 and OT2OD026671 (K.B.); UH3CA246635 (N.L.K.); UG3CA256967 (H.L.); U54HG010426 (M.P.S.); UH3CA246633 (M.A.); U54HD104393 (L.C.L. and P.R.); U54DK127823 (E.S.N., J.P.C. and W.-J.Q.); OT2OD033758 (N.G.); UH3CA246594 (F.G.); U54EY032442 and U54DK134302 (J.P.G.); U54HL145611 (S.L. and ...

العلاقة: https://authors.library.caltech.edu/records/44139-r9855Test; https://doi.org/10.1038/s41556-024-01384-0Test; oai:authors.library.caltech.edu:r1dag-ysc77

الإتاحة: https://doi.org/10.1038/s41556-024-01384-0Test

المؤلفون: Gubatan, John, Zikos, Thomas, Spear Bishop, Estelle, Wu, John, Gottfried, Andrés, Becker, Laren, Habtezion, Aida, Neshatian, Leila

المصدر: Neurogastroenterology & Motility ; volume 34, issue 4 ; ISSN 1350-1925 1365-2982

الوصف: Background The coronavirus disease 2019 (COVID‐19) pandemic has led to unprecedented disruptions in healthcare. Functional gastrointestinal and motility disorders (FGIMD) are associated with significant healthcare utilization. The clinical implications of these healthcare disruptions due to the COVID‐19 pandemic on clinical outcomes in patients with FGIMD are unclear. Methods We performed a retrospective study of patients with three common FGIMD (irritable bowel syndrome [IBS], gastroparesis, functional dyspepsia [FD]) tested for SARS‐CoV‐2 to describe alterations in gastrointestinal symptoms, medication use, and healthcare utilization during and before the pandemic and factors associated with COVID‐19. Key Results The prevalence of COVID‐19 during the pandemic (03/2020–09/2020) was 3.20% (83/2592) among patients with FGIMD, 3.62% in IBS (57/1574), 3.07% in gastroparesis (23/749), and 2.44% in FD (29/1187) at our institution. Patients with FGIMD had increased abdominal pain, nausea/vomiting, diarrhea, constipation, and weight loss ( p < 0.001) along with increased proton pump inhibitor, H2 blocker, and opioid use ( p < 0.0001). Both inpatient hospitalizations and outpatient visits ( p < 0.0001) and number of diagnostic tests including cross‐sectional imaging ( p = 0.002), and upper and lower endoscopies ( p < 0.0001) were significantly higher during the pandemic as compared to 6 months prior. Diarrhea‐predominant IBS was positively (OR 2.37, 95% CI 1.34–4.19, p = 0.003) associated with COVID‐19, whereas functional dyspepsia was negatively (OR 0.46, 95% CI 0.27–0.79, p = 0.004) associated. Conclusions & Inferences Patients with common functional gastrointestinal and motility disorders have reported more gastrointestinal symptoms during the COVID‐19 pandemic with concurrent increased medication use and healthcare utilization.

الإتاحة: https://doi.org/10.1111/nmo.14243Test

المؤلفون: Sheth, Vipul, Becker, Laren, Liang, Tie, Gurland, Brooke, Neshatian, Lelia

المصدر: American Journal of Gastroenterology ; volume 116, issue 1, page S243-S243 ; ISSN 0002-9270 1572-0241

الإتاحة: https://doi.org/10.14309/01.ajg.0000774612.73970.95Test