The case of a 29-year-old white female with a 7-year history of typical scleroderma is presented who developed excessive fibrosis of the supraclavicular lymph nodes. After 3 years of disease, firm right supraclavicular lymphadenopathy appeared, accompanied by a high fever. Biopsy revealed non-caseating granulomas and short-term antituberculous therapy was ineffective. The symptoms finally responded to steroids, but adenopathy persisted. A second biopsy, 40 days after the first, disclosed a similar picture with some degree of fibrosis of the granulomas. Four years later, with stony hard right supraclavicular adenopathy persisting, a third biopsy showed excessive fibrosis of the granulomas within the node and destruction of its architecture. It is postulated that the primary disease of this patient might be responsible for this clinical picture. The present seems to be the first report of such a case in the literature.
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http://dx.doi.org/10.1007/BF00301013 | DOI Listing |
Although current treatments for Duchenne Muscular Dystrophy (DMD) have proven to be effective in delaying myopathy, there remains a strong need to identify novel targets to develop additional therapies. Mitochondrial dysfunction is an early pathological feature of DMD. A fine balance of mitochondrial dynamics (fission and fusion) is crucial to maintain mitochondrial function and skeletal muscle health.
View Article and Find Full Text PDFJHEP Rep
January 2025
Vrije Universiteit Brussel, Liver Cell Biology research group, Laarbeeklaan 103, 1090 Brussel, Belgium.
Background & Aims: The progression of chronic liver disease (CLD) is characterized by excessive extracellular matrix deposition, disrupting hepatic architecture and function. Upon liver injury, hepatic stellate cells (HSCs) differentiate towards myofibroblasts and become inflammatory, proliferative and fibrogenic. To date, it is still unclear whether HSC activation is driven by similar mechanisms in different aetiologies.
View Article and Find Full Text PDFBMB Rep
January 2025
Department of Physiology, School of Medicine, Kyungpook National University, Daegu 41944, Korea; Cell & Matrix Research Institute, Kyungpook National University, Daegu 41944, Korea.
Metabolic Dysfunction Associated Steatotic Liver Disease (MASLD) and its progressive form, Metabolic Dysfunction Associated Steatohepatitis (MASH), represent significant health concerns associated with the metabolic syndrome. These conditions are characterized by excessive hepatic fat accumulation, inflammation, and potential progression to cirrhosis and hepatocellular carcinoma. Neutrophils are innate immune cells that play a pivotal role in the development of MASLD and MASH.
View Article and Find Full Text PDFTransl Res
January 2025
Department of Medicine, Université de Montréal, Centre de recherche du Centre hospitalier de l'Université de Montréal (CRCHUM), 900 Saint Denis Street, Montréal, QC, Canada H2 X 0A9. Electronic address:
Renal hedgehog interacting protein (Hhip) activates sodium-glucose cotransporter 2 (Sglt2) expression and promotes tubular senescence in murine diabetic kidney disease (DKD), yet its underlying mechanism(s) are poorly understood. Here we study the effect of the SGLT2 inhibitor, canagliflozin on tubulopathy (fibrosis and apoptosis) in Akia/Hhip-transgenic (Tg) mice with overexpression of Hhip in their renal proximal tubular cells (RPTCs) and its relevant mechanisms. The DKD-tubulopathy with pronounced Sglt2 expression was aggravated in the kidney of Akita/Hhip-Tg cf.
View Article and Find Full Text PDFLife Sci
January 2025
Department of Biological Sciences (Regulatory Toxicology), National Institute of Pharmaceutical Education and Research (NIPER), Balanagar, Hyderabad, TS 500037, India. Electronic address:
Pulmonary fibrosis (PF) arises from dysregulated wound healing, leading to excessive extracellular matrix (ECM) deposition and impaired lung function. Macrophages exhibit high plasticity, polarizing to pro-inflammatory M1 during early inflammation and anti-inflammatory, fibrosis-inducing M2 during later stages of PF. Additionally, neutrophils and neutrophil extracellular traps (NETs) release mediated by peptidyl arginine deiminase (PAD-4), also play a key role in PF progression.
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