The Snell dwarf mouse (dw/dw) is the result of a single recessive gene that is not sex-linked. The dwarfism is caused by the congenital deficiency of growth hormone, thyrotropin, and prolactin. This unique genetic model was selected to study compensatory renal hypertrophy. Compensatory renal hypertrophy occurred to a significant degree (P less than 0.01) in the unilaterally nephrectomized dwarf mutant (dw/dw), normal heterozygous (dw/DW), and normal homozygous (DW/DW) male littermates. There was no significant difference in the amount of compensatory renal hypertrophy between the groups (P greater than 0.5). These results suggest that three of the anterior pituitary hormones are not necessary for the compensatory hypertrophy response to unilateral nephrectomy.
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Pharmaceutics
January 2025
Department of Clinical Biochemistry and Pharmacology, Faculty of Health Sciences, Ben-Gurion University of the Negev, Beer-Sheva 84105, Israel.
Background/objectives: Leukocytes play a significant role in both acute kidney injury (AKI) and chronic kidney disease (CKD), contributing to pathogenesis and tissue damage. The process of leukocyte infiltration into the inflamed tissues is mediated by the interactions between the leukocytes and cell adhesion molecules (CAMs, i.e.
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January 2025
Department of Surgery and Leiden Transplant Center, Leiden University Medical Center, Leiden, the Netherlands. Electronic address:
Ischemia-reperfusion (IR) injury remains a major contributor to organ dysfunction following transient ischemic insults. Although numerous interventions have been found effective to reduce IR injury in preclinical models, none of these therapies have been successfully translated to the clinical setting. In the context of the persistent translational gap, we systematically investigated the mechanisms implicated in IR injury using kidney donation and transplantation as a clinical model of IR.
View Article and Find Full Text PDFIntern Med
January 2025
Department of Internal Medicine 1, Shimane University Faculty of Medicine, Japan.
We herein report a 56-year-old man with severe hypocalcemia during ruxolitinib therapy for myelofibrosis transitioning from JAK2 mutation-positive polycythemia vera. Blood transfusions were administered every one to two weeks for ruxolitinib-induced anemia. Blood tests revealed hypocalcemia with low TRACP-5b, 25-hydroxyvitamin D (25 (OH) D), and 1,25-dihydroxyvitamin D (1,25 (OH) D) levels within the lower reference range.
View Article and Find Full Text PDFProc Natl Acad Sci U S A
January 2025
Department of Biology, Faculty of Science and Technology, Mount Royal University, Calgary, AB T3E 6K6, Canada.
With over 14 million people living above 3,500 m, the study of acclimatization and adaptation to high altitude in human populations is of increasing importance, where exposure to high altitude (HA) imposes a blood oxygenation and acid-base challenge. A sustained and augmented hypoxic ventilatory response protects oxygenation through ventilatory acclimatization, but elicits hypocapnia and respiratory alkalosis. A subsequent renally mediated compensatory metabolic acidosis corrects pH toward baseline values, with a high degree of interindividual variability.
View Article and Find Full Text PDFSci Rep
January 2025
Department of Nephrology, Fujian Medical University Union Hospital, Fuzhou, 350001, China.
Glomerular endothelial cells (GECs) are pivotal in developing glomerular sclerosis disorders. The advancement of focal segmental glomerulosclerosis (FSGS) is intimately tied to disruptions in lipid metabolism. Sphingosine-1-phosphate (S1P), a molecule transported by high-density lipoproteins (HDL), exhibits protective effects on vascular endothelial cells by upregulating phosphorylated endothelial nitric oxide synthase (p-eNOS) and enhancing nitric oxide (NO) production.
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