Resultados de investigación

dataset del artículo Mitochondrial function of peripheral lymphocytes: role on multiple sclerosis clinical subtypes y archivo Readme.txt. asociado, AIMS: Multiple sclerosis (MS) is an immune-mediated neurodegenerative disease of unknown etiology, resulting in unmet therapeutic needs. Symptoms heterogeneity and incomplete mechanistic understanding hinder effective patient stratification. We aimed to evaluate the integrated peripheral immune response in established MS clinical subtypes, focusing on differences in mitochondrial function that might validate this stratification and further clarify MS etiology. MATERIALS AND METHODS: Mitochondrial activity of peripheral blood mononuclear cells (PBMCs) upon PHA-stimulation was analysed in MS patients (58 relapsing-remitting (RRMS), 21 secondary progressive (SPMS), and 35 primary progressive (PPMS)) and 35 healthy controls (HC). KEY FINDINGS: In unstimulated conditions, MS patients presented higher mitochondrial ROS (reactive oxygen species) and decreased coupling than HC. Compared with other progressive MS (PMS) subtypes, PBMCs from RRMS presented significantly higher early/late activation and proliferation after PHA stimulation (P = 0.013/P = 0.002, and P = 0.04, respectively), with increased mitochondrial depolarization (P = 0.017). Compared to HC, PHA-stimulated PBMCs from PMS exhibited marked decreases in basal (P = 0.017), maximal, and ATP-linked respiration, increased coupling (P = 0.009), and lower spare respiratory and glycolytic capacities (basal: P = 0.015, maximal: P = 0.064), with parallel decreased GLUT1 expression (P = 0.025). These changes appeared independent of some treatments. SIGNIFICANCE: Upon PHA-stimulation, PMS patients displayed decreased basal, maximal, ATP-linked respiration, and reduced spare respiratory and glycolytic capacities, compared to RRMS and HC, mirroring opposed trends in unstimulated conditions. These findings suggest a severity gradient across MS clinical forms, supporting a disease continuum rather than strictly defined subtypes. The central role of unresolved mitochondrial dysfunction in MS warrants further investigation and may guide novel therapeutic strategies.

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Relative concentrations of 74 inflammation-related serum proteins obtained by proximity extension assay (PEA, Olink) in patients with celiac disease and in non-celiac controls. Measurements were obtained while participants were on a gluten-free diet (≥1 month) at two time points: baseline (on GFD) and 4 hours after a single gluten challenge (10 g). NA indicates values below the limit of quantification., Background Diagnosis of celiac disease (CD) remains challenging in individuals already on a gluten-free diet (GFD). Although several alternative methods have been proposed, they have limitations. Identifying inflammation-related proteins that rapidly respond to gluten exposure in blood may offer diagnostic alternatives. Objective To characterize the inflammatory protein response to gluten in patients with CD on a GFD, and to assess the diagnostic potential of candidate biomarkers and their association with clinical symptoms. Methods Seventeen patients with CD and 15 non-CD individuals on a GFD (≥ 1 month) consumed 10 g of gluten. Serum, plasma and clinical symptoms were collected at baseline and 4 h post-gluten ingestion to assess changes in 92 inflammation-related proteins. Results Following gluten consumption, 18 proteins changed significantly only in patients with CD. Six showed an AUC ≥80%, and CCL20 achieved 85.7% sensitivity and 92.7% specificity for CD diagnosis. CCL20 level increases post-gluten challenge were higher in patients with vomiting but were also observed in those with absent or mild symptoms. Conclusion Gluten reintroduction triggers alterations in the inflammation-related protein profile of patients with CD. CCL20 emerges as a promising diagnostic candidate, its increase in plasma or serum, with low dependence on symptom presentation, may complement existing diagnostic approaches., Base de datos

Esta tabla corresponde a los datos utilizados para el artículo "Genetic variation in UGT1A1 is not associated with altered liver biochemical parameters in healthy volunteers participating in bioequivalence trials", Sí

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Background: Helping people recover from aphasia is among the top 10 research priorities relating to life after stroke. Objective: We aimed to evaluate the feasibility of dubbing techniques (using newly developed software) for post-stroke aphasia therapy and explore its potential efficacy. Methods: Randomised, crossover, interventional, feasibility trial that included patients with chronic post-stroke non-fluent aphasia. The intervention consisted of an individualised programme (16 sessions; 8 weeks) based on dubbing words and sentences progressively adapted to the severity of the aphasia. Patients were allocated to groups that underwent therapy within the first 3 months, or between 3 and 6 months from inclusion, each group serving as the control during the non therapy periods. Outcomes were the pre-post differences in the Communicative Activity Log, the Boston Diagnostic Aphasia Examination, the General Health Questionnaire-12, the Stroke Aphasia Quality of Life Scale, and the Western Aphasia Battery Revised, administered by psychologists blinded to the patients’ allocation. Results: Recruitment was limited due to COVID-19 and prematurely stopped because of funding coming to an end. A total of 23 patients were randomised, 20 of whom completed the study (1 withdrew consent, and 2 dropped out). The adherence rate to the allocated group was 95.3%. No statistically significant differences were found in any of the outcomes; however, 17 (85%) patients reported subjective improvements in communication skills. Conclusions: This trial shows the feasibility of dubbing therapy (using dedicated software) for patients with post-stroke non-fluent aphasia. Although it lacks statistical power, certain effects on language and communication cannot be ignored.