The aim of the study is to expand information on the histological aspect, presence, and distribution of cytoskeletal proteins: smooth muscle alpha-actin (α-SMA), desmin and vimentin in ovaries of three lizards Leiosauridae. In all analysed species, the ovaries were paired organs, located inside the coelomic cavity, covered in a simple cubic epithelium. Below the surface was the tunica albuginea. The organs can be divided into two regions: the cortex and the medulla. The pre-vitellogenic follicles consist of an oocyte surrounded by the pellucid zone periodic acid schiff positive, the granulosa layer consisting of three cell types: small, intermediate, and large and the theca layer. The vitellogenic follicles presented only a single layer of cubic granulosa cells. In the three lizards, α-SMA microfilaments (MFs) were verified along the theca layer and in endothelial cells of the blood vessels of the analysed follicles. Researchers have observed desmin intermediate filaments immunostaining exclusively muscle fibers of the albuginea and the ovarian stroma of Enyalius perditus. There was no immunostaining for vimentin in the ovaries of all the lizards studied. Results obtained revealed that the MFs of α-SMA could be responsible for a contractile activity present in the lizards assessed.
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http://dx.doi.org/10.1016/j.tice.2020.101477 | DOI Listing |
Arch Dermatol Res
January 2025
Department of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
We have recently shown that fluoxetine (FX) suppressed polyinosinic-polycytidylic acid-induced inflammatory response and endothelin release in human epidermal keratinocytes, via the indirect inhibition of the phosphoinositide 3-kinase (PI3K)-pathway. Because PI3K-signaling is a positive regulator of the proliferation, in the current, highly focused follow-up study, we assessed the effects of FX (14 µM) on the proliferation and differentiation of human epidermal keratinocytes. We found that FX exerted anti-proliferative actions in 2D cultures (HaCaT and primary human epidermal keratinocytes [NHEKs]; 48- and 72-h; CyQUANT-assay) as well as in 3D reconstructed epidermal equivalents (48-h; Ki-67 immunohistochemistry).
View Article and Find Full Text PDFSci Rep
January 2025
INSERM, Bergonié Institute, BPH, U1219, CIC-P 1401, University of Bordeaux, Bordeaux, France.
In vitro and animal studies have suggested that inoculation with herpes simplex virus 1 (HSV-1) can lead to amyloid deposits, hyperphosphorylation of tau, and/or neuronal loss. Here, we studied the association between HSV-1 and Alzheimer's disease biomarkers in humans. Our sample included 182 participants at risk of cognitive decline from the Multidomain Alzheimer Preventive Trial who had HSV-1 plasma serology and an amyloid PET scan.
View Article and Find Full Text PDFLearn Mem
January 2025
Psychology Department, Hunter College, City University of New York, New York, New York 10065, USA
Social isolation is a risk factor for cognitive impairment. Adolescents may be particularly vulnerable to these effects, because they are in a critical period of development marked by significant physical, hormonal, and social changes. However, it is unclear if the effects of social isolation on learning and memory are similar in both sexes or if they persist into adulthood after a period of recovery.
View Article and Find Full Text PDFNeurology
February 2025
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN.
Background And Objectives: Chronic kidney disease (CKD) is known to be associated with increased plasma phosphorylated tau217 (p-tau217) concentrations, potentially confounding the utility of plasma p-tau217 measurements as a marker of amyloid pathology in individuals with suspected Alzheimer disease (AD). In this study, we quantitatively investigate the relationship of plasma p-tau217 concentrations vs estimated glomerular filtration rate (eGFR) in individuals with CKD with and without amyloid pathology.
Methods: This was a retrospective examination of data from 2 observational cohorts from either the Mayo Clinic Study of Aging or the Alzheimer's Disease Research Center cohorts.
PLoS Genet
January 2025
Department of Pediatric and Adolescent Medicine, Mayo Clinic, 200 1st St. SW, Rochester, Minnesota 55905, United States of America.
Motor neuron diseases, such as amyotrophic lateral sclerosis (ALS) and progressive bulbar palsy, involve loss of muscle control resulting from death of motor neurons. Although the exact pathogenesis of these syndromes remains elusive, many are caused by genetically inherited mutations. Thus, it is valuable to identify additional genes that can impact motor neuron survival and function.
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