species are the 4 leading cause of nosocomial infections in the US affecting both men and women. Since males of many species can be more susceptible to infections than females, we investigated whether male mice were more susceptible to systemic () infection and if sex hormones were responsible for sex-dependent susceptibility to this infection. Non-gonadectomized or gonadectomized mice were supplemented with sustained release 5α-dihydrotestosterone (5αDHT) or 17-β-estradiol (E2) using subcutaneous pellet implantation. Mice were challenged intravenously with 5 × 10 /mouse seven days after pellet implantation and monitored for survival and weight change. We observed that male mice were more susceptible to systemic infection than female mice while gonadectomized male mice were as resistant to the infection as female mice. 5αDHT supplementation of gonadectomized female or male mice increased their susceptibility to the yeast infection while E2 supplementation of gonadectomized male mice did not increase their resistance to the infection. Overall, our results strongly suggest that testosterone plays an important role in decreasing resistance to systemic infection.
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http://dx.doi.org/10.1016/j.heliyon.2020.e04437 | DOI Listing |
Adv Sci (Weinh)
January 2025
Department of Molecular Biology, Cellular Biology, and Biochemistry, Brown University, Providence, RI, 02912, USA.
Pulmonary hypertension (PH) increases the mortality of preterm infants with bronchopulmonary dysplasia (BPD). There are no curative therapies for this disease. Lung endothelial carnitine palmitoyltransferase 1a (Cpt1a), the rate-limiting enzyme of the carnitine shuttle system, is reduced in a rodent model of BPD.
View Article and Find Full Text PDFImmun Inflamm Dis
January 2025
Department of Clinical Laboratory, the Second Affiliated Hospital of Anhui Medical University, Hefei, China.
Backgrounds And Aims: CD8+T cells are crucially associated with the fight against hepatitis B virus (HBV) infection. CD161 has been shown to express remarkably on HCV-specific CD8+T cells. However, the accurate function of CD161+CD8+T cells in HBV immunity or pathogenesis remains undetermined.
View Article and Find Full Text PDFJ Biochem Mol Toxicol
January 2025
Laboratory of Translational Medicine in Microvascular Regulation, Medical Research Center, The First Affiliated Hospital of Shandong First Medical University and Shandong Provincial Qianfoshan Hospital; Shandong Provincial Key Laboratory of Medicine in Microvascular Ageing; Laboratory of Future Industry of Gene Editing in Vascular Endothelial Cells of Universities in Shandong Province, Jinan, China.
Cadmium (Cd) is a toxic heavy metal which induces vascular disorders. Previous studies suggest that Cd in the bloodstream affects vascular endothelial cells (ECs), potentially contributing to vascular-related diseases. However, the molecular mechanisms of effects of Cd on ECs remain poorly understood.
View Article and Find Full Text PDFJ Bone Miner Res
January 2025
Human Genetics Program, Sanford Burnham Prebys Medical Discovery Institute, La Jolla, CA, United States.
We previously documented successful resolution of skeletal and dental disease in the infantile and late-onset murine models of hypophosphatasia (HPP), with a single injection of an adeno-associated serotype 8 vector encoding mineral-targeted TNAP (AAV8-TNAP-D10). Here, we conducted dosing studies in both HPP mouse models. A single escalating dose from 4x108 up to 4x1010 (vg/b) was intramuscularly injected into 4-day-old Alpl-/- mice (an infantile HPP model) and a single dose from 4x106 up to 4x109 (vg/b) was administered to 8-week-old AlplPrx1/Prx1 mice (a late-onset HPP model).
View Article and Find Full Text PDFJ Biochem Mol Toxicol
January 2025
Department of Cardiothoracic Surgery, Jingzhou Hospital Affiliated to Yangtze University, Jingzhou City, Hubei Province, China.
Abdominal aortic aneurysm (AAA) is a severe cardiovascular disease (CVD) that is partly attributable to endothelial dysfunction, inflammatory response, and angiogenesis. G protein-coupled receptor 4 (GPR4), a proton-sensitive G protein-coupled receptor that is abundantly expressed in vascular endothelial cells, has been associated with numerous physiological functions. Nevertheless, its potential involvement in the development of AAA remains unexplored.
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