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Oral Biomimetic Nanotherapeutics for Ulcerative Colitis Targeted Treatment by Repairing Intestinal Epithelial Barrier and Restoring Redox Homeostasis.
ACS Appl Mater Interfaces
January 2025
Department of Pharmaceutics, School of Pharmacy, Ningxia Medical University, No. 1160 Shengli South Street, Yinchuan 750004, PR China.
The structural disruption of intestinal barrier and excessive reactive oxygen/nitrogen species (RONS) generation are two intertwined factors that drive the occurrence and development of ulcerative colitis (UC). Synchronously restoring the intestinal barrier and mitigating excess RONS is a promising strategy for UC management, but its treatment outcomes are still hindered by low drug accumulation and retention in colonic lesions. Inspired by intestine colonizing bacterium, we developed a mucoadhesive probiotic -mimic entinostat-loaded hollow mesopores prussian blue (HMPB) nanotherapeutic (AM@HMPB@E) for UC-targeted therapy via repairing intestinal barrier and scavenging RONS.
View Article and Find Full Text PDFAdrenomedullin 2/Intermedin Exerts Cardioprotective Effects by Regulating Cardiomyocyte Mitochondrial Function.
Hypertension
January 2025
Department of Cardiovascular Research, Shinshu University School of Medicine, Matsumoto, Nagano, Japan. (Y. Zhao, T. Sakurai, A.K., M.T., Y.I.-S., H.K., Y.M., Y. Zhang, Q.G., P.L., K.H., M.H., J.L., T. Shindo).
Background: Adrenomedullin 2 (AM2) plays critical roles in regulating blood pressure and fluid balance. However, the specific involvement of AM2 in cardiac hypertrophy has not been comprehensively elucidated, warranting further investigation into its molecular mechanisms and therapeutic implications.
Methods: Cardiac hypertrophy was induced in adult mice lacking AM2 (AM2-/-) using transverse aortic constriction surgery.
V-ATPase Disassembly at the Yeast Lysosome-Like Vacuole Is a Phenotypic Driver of Lysosome Dysfunction in Replicative Aging.
Aging Cell
January 2025
Department of Biochemistry and Molecular Biology, SUNY Upstate Medical University, Syracuse, New York, USA.
Declines in lysosomal acidification and function with aging are observed in organisms ranging from yeast to humans. V-ATPases play a central role in organelle acidification, and V-ATPase activity is regulated by reversible disassembly in many different settings. Using the yeast Saccharomyces cerevisiae as a replicative aging model, we demonstrate that V-ATPases disassemble into their V and V subcomplexes in aging cells, with release of V subunit C (Vma5) from the lysosome-like vacuole into the cytosol.
View Article and Find Full Text PDFNational Medical Commission's new rule on capping the number of undergraduate medical seats in high performing States: pragmatic or quixotic?
Indian J Med Ethics
January 2025
Professor & Head, Dept of Pediatrics, All India Institute of Medical Sciences, Mangalagiri, Andhra Pradesh, INDIA.
The article analyses the recent amendment by the National Medical Commission (NMC) in India, capping the number of undergraduate medical seats in high-performing states, which has sparked a debate. With a healthcare system catering to the diverse needs of 1.4 billion people, regional disparities in healthcare personnel distribution have emerged, especially among doctors.
View Article and Find Full Text PDFCell type-specific upregulation of NKG2D ligand MICA in response to APTO253.
Ann Transl Med
December 2024
Institute for Tumor Immunology, Center for Tumor Biology and Immunology, Philipps-University Marburg, Marburg, Germany.
One of the most important targets for natural killer (NK) cell-mediated therapy is the induction of natural killer group 2D ligand (NKG2D-L) expression. APTO253 is a small molecule that selectively kills acute myeloid leukemia (AML) cells, and it has been reported that APTO253 can induce Krüppel-like factor 4 (KLF4) expression and downregulate c-MYC expression. Recently, we discovered a novel role of APTO253 in modulating the NK cell response by inducing surface expression of NKG2D-Ls, especially MHC class I polypeptide-related sequence A (MICA), in AML cells.
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