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Basic Science and Pathogenesis.
Alzheimers Dement
December 2024
University of Virginia, Charlottesville, VA, USA.
Background: The microvasculature of the central nervous system (CNS), which delivers oxygen and nutrients and forms a critical barrier protecting the CNS, is deleteriously affected by both Alzheimer's Disease (AD) and Type 2 Diabetes (T2D). Previous studies have shown pericyte dropout and vessel constriction in brain capillaries in AD, while other studies have shown pericyte bridging and dropout in retinal capillaries in T2D. T2D patients have increased risk of AD, suggesting potentially related microvascular pathological mechanisms.
View Article and Find Full Text PDFBone marrow niches orchestrate stem-cell hierarchy and immune tolerance.
Nature
January 2025
Columbia Center for Translational Immunology, Department of Medicine, Columbia University Vagelos College of Physicians and Surgeons, New York, NY, USA.
Stem cells reside in specialized microenvironments, termed niches, at several different locations in tissues. The differential functions of heterogeneous stem cells and niches are important given the increasing clinical applications of stem-cell transplantation and immunotherapy. Whether hierarchical structures among stem cells at distinct niches exist and further control aspects of immune tolerance is unknown.
View Article and Find Full Text PDFDevelopment and growth of cavernosal sinusoidal endothelia in the external genitalia of human fetuses.
Ann Anat
December 2024
Department of Urology, Graduate School of Medicine and Dentistry, Hiroshima University School of Medicine, Hiroshima, Japan.
Background: There is little information about when and how cavernosal sinusoidal endothelia develop in the external genitalia of fetuses.
Methods: We examined histological sections of erectile tissue in 37 human fetuses (25 males and 12 females) whose gestational age (GA) ranged from 8 to 40 weeks.
Results: The sinusoidal lumen was filled with blood in the glans of the penis and clitoris at a GA of 10 to 11 weeks, and in the corpus spongiosum at a GA of 15 to 16 weeks.
Lupus nephritis and related renal disease: review from case series.
Clin Exp Nephrol
December 2024
Department of Pathology, Toranomon Hospital, Tokyo, Japan.
Renal lesions due to systemic lupus erythematosus (SLE) are defined as lupus nephritis (LN), a renal disease characterized by the deposition of immunoglobulin (Ig)G-based immune complexes in the kidney and the appearance of double-stranded DNA and Smith antibodies. In particular, deposition of IgG3, which has strong complement binding properties, under the endothelium or in the mesangium activates the classical complement pathway of C1q, C4, and C3, leading to renal damage. This step is followed by migration of inflammatory cells, including neutrophils and monocytes, which induce inflammation in the glomerular capillaries and cause mesangiolysis and endothelial cell damage, resulting in endocapillary proliferative nephritis.
View Article and Find Full Text PDFEndothelial Dysfunction and Liver Cirrhosis: Unraveling of a Complex Relationship.
Int J Mol Sci
November 2024
Liver Unit, CEMAD-Centro Malattie dell'Apparato Digerente, Medicina Interna e Gastroenterologia, Fondazione Policlinico Universitario Gemelli IRCCS, 00168 Rome, Italy.
Endothelial dysfunction (ED) is the in the background of multiple metabolic diseases and a key process in liver disease progression and cirrhosis decompensation. ED affects liver sinusoidal endothelial cells (LSECs) in response to different damaging agents, causing their progressive dedifferentiation, unavoidably associated with an increase in intrahepatic resistance that leads to portal hypertension and hyperdynamic circulation with increased cardiac output and low peripheral artery resistance. These changes are driven by a continuous interplay between different hepatic cell types, invariably leading to increased reactive oxygen species (ROS) formation, increased release of pro-inflammatory cytokines and chemokines, and reduced nitric oxide (NO) bioavailability, with a subsequent loss of proper vascular tone regulation and fibrosis development.
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