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Twelve-hour ultradian rhythmic reprogramming of gene expression in the human ovary during aging.

J Assist Reprod Genet

January 2025

Center of Reproductive Medicine, The Sixth Affiliated Hospital, Sun Yat-Sen University, Guangzhou, 510655, China.

Background: The 12-h ultradian rhythm plays a crucial role in metabolic homeostasis, but its role in ovarian aging has not been explored. This study investigates age-related changes in 12-h rhythmic gene expression across various human tissues, with a particular focus on the ovary.

Methods: We analyzed transcriptomic data from the GTEx project to examine 12-h ultradian rhythmic gene expression across multiple peripheral human tissues, exploring sex-specific patterns and age-related reprogramming of both 12-h and 24-h rhythmic gene expression.

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Osteoporosis and vascular calcification are chronic metabolic diseases threatening the health of aging people. The incidence of osteoporosis and vascular calcification increases year by year, and has drawn much attention from the scientific and clinical area. Many studies have found that osteoporosis and vascular calcification are not completely independent, but there are close correlations between them in the pathogenesis and underlying mechanisms.

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Natural variations of adolescent neurogenesis and anxiety predict the hierarchical status of adult inbred mice.

EMBO Rep

January 2025

Center for Psychiatric Neuroscience, Department of Psychiatry, Lausanne University Hospital, University of Lausanne, Prilly, Switzerland.

Hierarchy provides a survival advantage to social animals in challenging circumstances. In mice, social dominance is associated with trait anxiety which is regulated by adult hippocampal neurogenesis. Here, we test whether adolescent hippocampal neurogenesis may regulate social dominance behavior in adulthood.

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Background: Cyanobacteria, particularly Synechocystis sp. PCC 6803, serve as model organisms for studying acclimation strategies that enable adaptation to various environmental stresses. Understanding the molecular mechanisms underlying these adaptations provides insight into how cells adjust gene expression in response to challenging conditions.

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The pathogenesis of Lewy body diseases (LBDs), including Parkinson's disease (PD), involves α-synuclein (α-Syn) aggregation that originates in peripheral organs and spreads to the brain. PD incidence is increased in individuals with chronic renal failure, but the underlying mechanisms remain unknown. Here we observed α-Syn deposits in the kidneys of patients with LBDs and in the kidney and central nervous system of individuals with end-stage renal disease without documented LBDs.

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