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النطاق السنوي
1.
Rev. chil. endocrinol. diabetes ; 14(4): 159-165, 2021. tab, ilus
مقالة ي الأسبانية | LILACS | ID: biblio-1344801

الملخص

La diabetes Tipo 1 (DT1) es una compleja enfermedad autoinmune con una etiología aún desconocida. La vitamina D ha sido ampliamente estudiada debido a su potencial terapéutico en los potenciales nuevos casos de DT1. Por otra parte, los microARNs (miRs) han sido propuestos como posibles biomarcadores en diversos procesos biológicos como en la apoptosis e inflamación. El objetivo de este estudio fue evaluar el efecto de la suplementación con vitamina D sobre el perfil de expresión del miR-21 y marcadores de apoptosis tales como: BCL2, STAT3, TIPE2 y DAXX, en células mononucleares periféricas provenientes de pacientes con DT1 y sujetos controles. RESULTADOS: El perfil de expresión de miR-21 se encontró disminuido en los pacientes con DT1 en comparación con los controles. La expresión relativa de BCL2 se encontró aumentada en controles al comparar con pacientes DT1 en todas las condiciones experimentales. La expresión relativa de DAXX mostró un perfil de expresión diferencial al comparar pacientes con DT1 versus controles (p=0.006). CONCLUSIÓN: El estímulo con vitamina D parece tener un posible efecto regulador sobre los genes BCL2 y DAXX.


Type 1 diabetes (T1D) is a complex chronic autoimmune disease. Vitamin D has been one of the most studied therapeutic potential outbreaks related to T1D. Specific miRNAs have been proposed as potential biomarkers in several biological processes as apoptosis and inflammation. The aim of this study was to evaluate the effect of vitamin D on the expression profiles of miR-21 and apoptotic markers BCL2, STAT3, TIPE2 and DAXX, in PBMCs from T1D patients and control subjects. RESULTS: miR-21 expression was increased in controls regarding T1D patients. BCL2 was increased in controls compared to T1D patients in all experimental conditions. DAXX showed different expression patterns between T1D patients and controls (p=0.006). CONCLUSION: Vitamin D showed a possible regulation effect on apoptosis markers mainly through the regulation of BCL2 and DAXX


الموضوعات
Humans , Child , Adolescent , Vitamin D/administration & dosage , Apoptosis , Diabetes Mellitus, Type 1/metabolism , Vitamin D/metabolism , Biomarkers , Molecular Chaperones/drug effects , Molecular Chaperones/genetics , Molecular Chaperones/metabolism , Proto-Oncogene Proteins c-bcl-2/drug effects , Proto-Oncogene Proteins c-bcl-2/genetics , Proto-Oncogene Proteins c-bcl-2/metabolism , MicroRNAs/drug effects , MicroRNAs/genetics , MicroRNAs/metabolism , STAT3 Transcription Factor/drug effects , STAT3 Transcription Factor/genetics , STAT3 Transcription Factor/metabolism , Co-Repressor Proteins/drug effects , Co-Repressor Proteins/genetics , Co-Repressor Proteins/metabolism , Glucose/administration & dosage
2.
Mem. Inst. Oswaldo Cruz ; 104(4): 531-548, July 2009. ilus, tab
مقالة ي الانجليزية | LILACS | ID: lil-523716

الملخص

Corticosteroids are widely used to treat a diversity of pathological conditions including allergic, autoimmune and some infectious diseases. These drugs have complex mechanisms of action involving both genomic and non-genomic mechanisms and interfere with different signal transduction pathways in the cell. The use of corticosteroids to treat critically ill patients with acute respiratory distress syndrome and severe infections, such as sepsis and pneumonia, is still a matter of intense debate in the scientific and medical community with evidence both for and against its use in these patients. Here, we review the basic molecular mechanisms important for corticosteroid action as well as current evidence for their use, or not, in septic patients. We also present an analysis of the reasons why this is still such a controversial point in the literature.


الموضوعات
Humans , Adrenal Cortex Hormones/therapeutic use , Receptors, Glucocorticoid/drug effects , Respiratory Distress Syndrome/drug therapy , Shock, Septic/drug therapy , Clinical Trials as Topic , Evidence-Based Medicine , Genomics , Immunity, Innate/drug effects , Immunity, Innate/genetics , Molecular Chaperones/drug effects , Molecular Chaperones/genetics , Receptors, Glucocorticoid/genetics , Transcriptional Activation/drug effects , Transcriptional Activation/genetics
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