The damage to skeletal muscle capillaries in advanced Chagas' disease (stages II and III) was investigated in the vastus lateralis muscle of six patients and compared to that of six normal subjects. Capillaries were visualized by the PAS-amylase reaction and muscle fibres were classified by the ATPase histochemical method. Transmission electron microscopy was used to look for capillary alterations. The capillary-to-fibre ratio and number of capillaries adjacent to type I and type IIa fibres were decreased in the patient group. At the ultrastructural level, all patients showed capillary abnormalities, mainly basement membrane thickening and reduplication, capillary occlusion, proliferative endothelial cell cytoplasm with dense bodies, large vacuoles, altered mitochondria and prominent rough endoplasmic reticulum, as well as pericyte abnormalities. Capillary alterations are similar to those in patients affected by autoimmune diseases, suggesting an autoimmune component in the chronic phase of this disease. The reduction in capillarity may contribute to altered muscle performance in these patients.
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http://dx.doi.org/10.1007/s00436-004-1107-7 | DOI Listing |
Physiol Rep
December 2024
School of Molecular Sciences, The University of Western Australia, Crawley, Western Australia, Australia.
Exercise-induced muscle damage (EIMD) can affect athlete performance and is a risk factor for major muscle injury. The temporal profile of thiol-oxidized albumin, a marker of oxidative stress, has shown potential in assessing recovery from EIMD in non-athletically trained participants but not yet in trained participants. Our primary aim was to assess whether there are changes in the level of thiol-oxidized albumin after a marathon in athletically trained participants.
View Article and Find Full Text PDFCell Metab
December 2024
State Key Laboratory of Analytical Chemistry for Life Science, Medical School, Nanjing University, Nanjing 210093, China; Center for Translational Medicine and Jiangsu Key Laboratory of Molecular Medicine, Medical School, Nanjing University, Nanjing 210093, China. Electronic address:
The essential amino acid methionine plays a pivotal role in one-carbon metabolism, facilitating the production of S-adenosylmethionine (SAM), a critical supplier for DNA methylation and thereby a modulator of gene expression. Here, we report that the methionine cycle is disrupted in skeletal muscle during cancer cachexia, leading to endoplasmic reticulum stress and DNA hypomethylation-induced expression of the DNA damage inducible transcript 4 (Ddit4) gene, encoding the regulated in development and DNA damage response 1 (REDD1) protein. Targeting DNA methylation by depletion or pharmacological inhibition of DNA methyltransferase 3A (DNMT3A) exacerbates cachexia, while restoring DNMT3A expression or REDD1 knockout alleviates cancer cachexia-induced skeletal muscle atrophy in mice.
View Article and Find Full Text PDFDent J (Basel)
December 2024
Department of Morphological Disciplines, Faculty of Medicine and Pharmacy, University of Oradea, 410087 Oradea, Romania.
Dental malocclusions are highly prevalent worldwide, negatively impacting patients' quality of life and leading to complex, often costly, orthodontic treatments. In Romania, the economic status of patients and the limited public funding for orthodontic care significantly influence treatment accessibility and choices. Advanced technologies, such as mini-implants (MIs), offer improved anchorage and treatment efficiency but are often underutilized due to financial constraints and variability in clinical training.
View Article and Find Full Text PDFJ Cachexia Sarcopenia Muscle
February 2025
Mitodicure GmbH, Kriftel, Germany.
Background: Recent studies provide strong evidence for a key role of skeletal muscle pathophysiology in myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In a 2021 review article on the pathophysiology of ME/CFS, we postulated that hypoperfusion and ischemia can result in excessive sodium and calcium overload in skeletal muscles of ME/CFS patients to cause mitochondrial damage. Since then, experimental evidence has been provided that supports this concept.
View Article and Find Full Text PDFAm J Physiol Cell Physiol
December 2024
Exercise Metabolism Research Group, Department of Kinesiology, McMaster University, Hamilton, Ontario, Canada.
Cellular senescence has been implicated in the aging-related dysfunction of satellite cells, the resident muscle stem cell population primarily responsible for the repair of muscle fibres. Despite being in a state of permanent cell cycle arrest, these cells remain metabolically active and release an abundance of factors that can have detrimental effects on the cellular microenvironment. This phenomenon is known as the senescence-associated secretory phenotype (SASP), and its metabolic profile is poorly characterized in senescent muscle.
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