Objective To verify if there are differences in Chronic Obstructive Pulmonary Disease (COPD) patient exacerbator and non-exacerbator phenotypes undergoing a Pulmonary Rehabilitation Program (PRP). Methods A real life retrospective study included outpatients with COPD from public primary care who completed a 12-weeks PRP, three times a week. All were assessed before and after PRP using the six-minute walk test (6MWT), the modified Medical Research Council (mMRC) dyspnea index, quality of life and Body-mass Index, airflow Obstruction, Dyspnea and Exercise (BODE index). Results A total of 151 patients were analyzed and mean age was 65.0 ± 8.1 years and mean Forced Expiratory Volume (FEV) 1% of predicted was 39.8 ± 15.9. The predominant gender was male (66.9%). Of these patients 31 (20.5%) were exacerbator phenotype There was a significant improvement in the mean distance in the 6MWT in both groups, with the largest change observed in the exacerbator group [mΔ (95% CI): 84.9 (57.1-112.6) vs. 48.6 (37-60.2) p= 0.018]. Significant reduction in dyspnea on the mMRC scale occurred in both groups, with the highest intensity in the exacerbator group [mΔ (95% CI): - 0.8 (-1.11 to 0.51) vs. -1.6 (-2.20 to -1.13) p = 0.006]. Improvement in the BODE index occurred in both groups, but the mean variation was also significantly greater in the exacerbator group [mΔ (95% CI): -1.44 (-2.17 to -0.70) p= 0.045]. Conclusion Patients with COPD exacerbator phenotype had a greater magnitude of response to PRP (36 meters) when compared to non-exacerbator phenotype regardless the severity of airflow obstruction, also showing improvement in prognosis measured by the BODE index.
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This paper is based on a presentation made at the 9th London-Innsbruck Colloquium on Status Epilepticus and Acute Seizures in April 2024. Status Epilepticus (SE) is a neurological emergency involving prolonged seizures that disrupt brain function and may cause severe, long-term neurological damage. Developmental and Epileptic Encephalopathies (DEEs), a group of severe genetic disorders with early-onset epilepsy, often exhibit SE episodes that compound their inherent cognitive and developmental challenges.
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January 2025
Department of Developmental Genetics and Behavioral Neuroscience, Gunma University Graduate School of Medicine, Maebashi, Gunma, Japan.
Autism spectrum disorder (ASD) is characterized by social deficits and restricted behaviors, with developmental defects in GABAergic circuits proposed as a key underlying etiology. Here, we introduce the V-Y assay, a novel space preference test in which one arm of the Y-maze is initially hidden and later revealed as a novel space. Using an ASD mouse model with haploinsufficiency, which exhibits ASD-like social impairments that can be either exacerbated or ameliorated by GABAergic circuit manipulations, we observed impaired novel space preference and exploratory behavior in the V-Y assay.
View Article and Find Full Text PDFJOR Spine
March 2025
Department of Clinical Sciences, Faculty of Veterinary Medicine Utrecht University Utrecht Netherlands.
Background: Cell-free regenerative strategies, such as notochordal cell (NC)-derived extracellular vesicles (EVs), are an attractive alternative in developing new therapies for intervertebral disc (IVD) degeneration. NC-EVs have been reported to elicit matrix anabolic effects on nucleus pulposus cells from degenerated IVDs cultured under basal conditions. However, the degenerative process is exacerbated by pro-inflammatory cytokines contributing to the vicious degenerative cycle.
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Department of Cardiology, Beijing Anzhen Hospital, Capital Medical University, No.2 Anzhen Road, Chaoyang District, 100029, Beijing, China.
Introduction: Bone marrow-derived mesenchymal stem cell-derived extracellular vesicles (BMSC-EVs) are widely used for therapeutic purposes in preclinical studies. However, their utility in treating diabetes-associated atherosclerosis remains largely unexplored. Here, we aimed to characterize BMSC-EV-mediated regulation of autophagy and macrophage polarization.
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January 2025
Department of Cell Biology, Emory University, 615 Michael St, Atlanta, GA, USA, 30322.
Rare inherited diseases caused by mutations in the copper transporters (CTR1) or induce copper deficiency in the brain, causing seizures and neurodegeneration in infancy through poorly understood mechanisms. Here, we used multiple model systems to characterize the molecular mechanisms by which neuronal cells respond to copper deficiency. Targeted deletion of CTR1 in neuroblastoma cells produced copper deficiency that produced a metabolic shift favoring glycolysis over oxidative phosphorylation.
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