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Obesity is a rapidly growing health problem worldwide, affecting both adults and children and increasing the risk of chronic diseases such as type 2 diabetes, hypertension and cardiovascular disease (CVD). In addition, obesity is closely linked to chronic kidney disease (CKD) by either exacerbating diabetic complications or directly causing kidney damage. Obesity-related CKD is characterized by proteinuria, lipid accumulation, fibrosis and glomerulosclerosis, which can gradually impair kidney function.

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Background: Lipid Accumulation Product (LAP), which is derived from measurements of waist circumference and triglyceride (TG) levels, serves as a comprehensive indicator of lipid accumulation. Emerging research indicates that lipid accumulation dysfunction might significantly contribute to the pathogenesis of Chronic Obstructive Pulmonary Disease (COPD). Nevertheless, the investigation into the association between LAP and COPD risk is still insufficient, particularly in population-based research.

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Elucidating the genetic contributions to Parkinson's disease (PD) etiology across diverse ancestries is a critical priority for the development of targeted therapies in a global context. We conducted the largest sequencing characterization of potentially disease-causing, protein-altering and splicing mutations in 710 cases and 11,827 controls from genetically predicted African or African admixed ancestries. We explored copy number variants (CNVs) and runs of homozygosity (ROHs) in prioritized early onset and familial cases.

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Systemic lupus erythematosus (SLE) is a chronic autoimmune disorder characterized by widespread immune dysregulation that affects multiple organ systems, including the skin and cardiovascular system. The crosstalk between different cell death pathways-such as apoptosis, necroptosis, and neutrophil extracellular trap (NETosis), plays a pivotal role in the pathogenesis of SLE, influencing both cutaneous and cardiac manifestations. Cutaneous lupus erythematosus (CLE) is one of the most common early signs of SLE, affecting up to 80% of patients.

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Pulmonary fibrosis significantly contributes to the pathogenesis of acute respiratory distress syndrome (ARDS), markedly increasing patient mortality. Despite the established anti-fibrotic effects of mesenchymal stem cells (MSCs), numerous challenges hinder their clinical application. A recent study demonstrated that microvesicles (MVs) from MSCs (MSC-MVs) could attenuate ARDS-related pulmonary fibrosis and enhance lung function hepatocyte growth factor mRNA transcription.

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