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| http://dx.doi.org/10.1016/j.ajpath.2024.02.002 | DOI Listing |
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Loss of mucin 2 and MHC II molecules causes rare resistance to murine RV infection.
J Virol
December 2024
Department of Molecular Virology and Microbiology, Baylor College of Medicine, Houston, Texas, USA.
Enteric pathogen rotavirus (RV) primarily infects mature enterocytes at the tips of the intestinal villi; however, the role of secretory Paneth and goblet cells in RV pathogenesis remains unappreciated. Atoh1 knockout mice (Atoh1cKO) were used to conditionally delete Paneth, goblet, and enteroendocrine cells in the epithelium to investigate the role of secretory cells in RV infection. Unexpectedly, the number of infected enterocytes and the amount of RV shedding in the stool were greatly decreased following secretory cell deletion.
View Article and Find Full Text PDFSubchondral bone marrow adipose tissue lipolysis regulates bone formation in hand osteoarthritis.
Osteoarthritis Cartilage
December 2024
Rheumatology, Department of Musculoskeletal Medicine, University Hospital Lausanne and University of Lausanne (CHUV-UNIL), Lausanne,Switzerland. Electronic address:
Objective: Bone marrow adipose tissue (BMAT) is emerging as an important regulator of bone formation and energy metabolism. Lipolysis of BMAT releases glycerol and fatty acid substrates that are catabolized by osteoblasts. Here, we investigated whether BMAT lipolysis is involved in subchondral bone formation in hand osteoarthritis (OA).
View Article and Find Full Text PDFHyperaminoacidemia from interrupted glucagon signaling increases pancreatic acinar cell proliferation and size via mTORC1 and YAP pathways.
iScience
December 2024
Department of Molecular Physiology & Biophysics, Vanderbilt University, Nashville, TN, USA.
Increased blood amino acid levels (hyperaminoacidemia) stimulate pancreas expansion by unclear mechanisms. Here, by genetic and pharmacological disruption of glucagon receptor (GCGR) in mice and zebrafish, we found that the ensuing hyperaminoacidemia promotes pancreatic acinar cell proliferation and cell hypertrophy, which can be mitigated by a low protein diet in mice. In addition to mammalian target of rapamycin complex 1 (mTORC1) signaling, acinar cell proliferation required , the most highly expressed amino acid transporter gene in both species.
View Article and Find Full Text PDFMacrophage Notch1 signaling modulates regulatory T cells via the TGFB axis in early MASLD.
JHEP Rep
January 2025
Department of Pharmacology, Wuhan University TaiKang Medical School (School of Basic Medical Sciences), Wuhan 430071, China.
Background & Aims: Hepatic immune imbalance is crucial for driving metabolic dysfunction-associated steatotic liver disease (MASLD) progression. However, the role of hepatic regulatory T cells (Tregs) in MASLD initiation and the mechanisms responsible for their change are not completely understood.
Methods: A mouse model subjected to a short-term high-fat diet (HFD) to mimic early steatosis, along with liver biopsy samples from patients with simple steatosis, and macrophage-specific Notch1-knockout mice (Notch1), were used to investigate the role of Tregs in early MASLD and the effect of hepatic macrophage Notch1 signaling on Treg frequency.
Role of primary care for individuals with childhood-onset neurologic conditions.
Health Care Transit
December 2023
Department of Global Health Promotion, Tokyo Medical and Dental University, 1-5-45, Yushima, Bunkyo-ku, Tokyo 113-8519, Japan.
Background: Individuals with childhood-onset neurologic conditions often face challenges in the pediatric-to-adult health care transition (HCT). Furthermore, the importance of implementing primary care is unrecognized. We investigated the situation of adults with childhood-onset neurologic conditions from the perspective of health care professionals (HCPs) in community- and hospital-based primary care practice.
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