Little information on the structural norm of the aging detrusor is currently available. To gain insight into the pathophysiology of geriatric voiding dysfunction, detrusor biopsies were examined by electron microscopy to identify structural correlates of specific, urodynamically defined abnormalities of vesical function in 35 elderly subjects. Prospective urodynamic grouping of the subjects and segregation of the detrusor specimens by ultrastructural features were done independently and blindly. One structural pattern so identified, the dense band pattern, matched the urodynamic group with neither detrusor overactivity nor bladder outlet obstruction. This neither group included 11 women and 2 men 65 to 91 years old (mean age 76 years). Except for 2 patients with minimal stress incontinence, all were symptom-free. None of the patients had diabetes or a neurological deficit. Urodynamically, 10 patients had impaired and 3 had normal detrusor contractility. The dense band structural pattern was characterized by overall normal configuration of muscle cells and cell junctions, sarcolemma (muscle cell membrane) dominated by dense bands with depleted caveolae in interposed zones and slight widening of spaces between muscle cells with little-collagen content. Specimens from the 10 subjects with impaired contractility displayed, in addition, widespread degeneration of muscle cells and axons. The remaining 3 specimens, without degeneration, matched the subjects with normal contractility, who were continent and symptom-free. It is proposed that the dense band pattern represents the structural norm of aging detrusor, heralds a process of muscle cell de-differentiation in the detrusor accompanying natural aging, and may affect exchange and storage of ions involved in the excitation-contraction coupling mechanism of muscle cells through depletion of caveolae. Widespread degeneration of muscle cells and axons, superimposed on the dense band pattern, is proposed as the structural correlate of impaired detrusor contractility in the aging detrusor.
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http://dx.doi.org/10.1016/s0022-5347(17)35867-6 | DOI Listing |
Pulmonology
December 2025
Laboratory of Experimental Therapeutics, LIM-20, Department of Clinical Medicine, School of Medicine, University of Sao Paulo, Sao Paulo, Brazil.
Background: Chronic obstructive pulmonary disease (COPD) induces an imbalance in T helper (Th) 17/regulatory T (Treg) cells that contributes to of the dysregulation of inflammation. Exercise training can modulate the immune response in healthy subjects.
Objective: We aimed to evaluate the effects of exercise training on Th17/Treg responses and the differentiation of Treg phenotypes in individuals with COPD.
Front Pharmacol
December 2024
College of Pharmacy, Jinan University, Guangzhou, China.
Bone homeostasis encompasses two interrelated aspects: bone remodeling and cartilage metabolism. Disruption of bone homeostasis can lead to the development of metabolic bone diseases such as osteoporosis and osteoarthritis. The maintenance of bone homeostasis is a complex process that does not solely rely on the functions of the bone tissue itself.
View Article and Find Full Text PDFFront Physiol
December 2024
Raw Materials and Optimalization, Nofima AS, Ås, Norway.
Introduction: Skeletal muscle satellite cells (MuSCs or stem cells) play a crucial role in muscle development, maintenance, and regeneration, supporting both hypertrophy and regenerative myogenesis. Syndecans (SDCs) act as communication bridges within the muscle microenvironment, regulating interactions with extracellular matrix components and contributing significantly to tissue repair and inflammation. Specifically, syndecan-4 (SDC4) is involved in muscle regeneration at multiple stages.
View Article and Find Full Text PDFThis study aimed to elucidate the impact of advanced glycation end products (AGEs) and glucose shock on cardiomyocyte viability, gene expression, cardiac biomarkers, and cardiac contractility. Firstly, AGEs were generated in-house, and their concentration was confirmed using absorbance measurements. AC16 cardiomyocytes were then exposed to varying doses of AGEs, resulting in dose-dependent decreases in cell viability.
View Article and Find Full Text PDFThe activation of progenitor cells near wound sites is a common feature of regeneration across species, but the conserved signaling mechanisms responsible for this step in whole-body regeneration are still incompletely understood. The acoel undergoes whole-body regeneration using Piwi+ pluripotent adult stem cells (neoblasts) that accumulate at amputation sites early in the regeneration process. The EGFR signaling pathway has broad roles in controlling proliferation, migration, differentiation, and cell survival across metazoans.
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