RÉSUMÉ
<p><b>OBJECTIVE</b>This study aimed to investigate the genetic background of mitochondrial genes in young patients with Coronary heart disease (CHD) to provide a foundation for the early prevention of young patients with CHD.</p><p><b>METHODS</b>115 cases of young (⋜ 45 years) CHD Chinese Han patients (case group), 100 cases of older (> 45 years) Chinese Han CHD patients (experimental group) hospitalized and 100 cases of healthy people through physical examination (control group) at the General Hospital of PLA between January 2014 and December 2015 were selected. General information, clinical assessment, pedigree analysis, and mitochondrial full sequence scanning were performed. The pedigrees of one patient harbouring the C5263T mutation were recruited. Mitochondrial functional analysis including cellular reactive oxygen species (ROS) levels and mitochondrial membrane potential (MMP) were performed on pedigrees with the C5263T mutation (mutation group) and without the mutation (non-mutation group).</p><p><b>RESULTS</b>The differences in biochemical tests (P > 0.05) between the case group and experimental group were not significant. The C5263T single-nucleotide mutation of the mitochondrial ND2 gene was observed in 2 young CHD patients in the case group. The premature CHD of these 2 patients followed a pattern of maternal inheritance. The mutation group (I1, II2) had higher ROS levels (4750.82 ± 1045.55 vs. 3888.58 ± 487.60, P = 0.022) and lower MMP levels (P = 0.045) than the non-mutation group (II1, III1, III2).</p><p><b>CONCLUSION</b>We speculated that the mitochondrial C5263T mutation might be associated with the occurrence CHD in Chinese Han young people.</p>
Sujet(s)
Adulte , Sujet âgé , Sujet âgé de 80 ans ou plus , Femelle , Humains , Mâle , Adulte d'âge moyen , Séquence nucléotidique , Chine , Épidémiologie , Maladie coronarienne , Épidémiologie , Génétique , Gènes de mitochondrie , Protéines mitochondriales , Génétique , Métabolisme , Mutation , NADH dehydrogenase , Génétique , MétabolismeRÉSUMÉ
<p><b>OBJECTIVE</b>To investigate the effect of tumor necrosis factor-α-induced protein 8 like-2 (TIPE2) on apoptosis of CD4T lymphocytes in a murine model of severe burn injury.</p><p><b>METHODS</b>A total of 140 male mice were randomly allocated into 6 groups. Small RNA interference technique was used to construct a siTIPE2-overexpressing lentivirus, and severe burn injury models were established in the mice. CD4T cells were purified from spleen of the mice, and the expressions of TIPE2, Smad2/Smad3, P-Smad2/P-Smad3 and Bcl-2/Bimprotein in CD4Tregs were detected. The changes in mitochondrial membrane potential and cytochrome C in CD4T cells were detected, and the activities of caspase-3, caspase-8, and caspase-9 were analyzed.</p><p><b>RESULTS</b>Down-regulation of TIPE2 promoted the apoptosis of CD4T lymphocytes in siTIPE2-burn group, in which the protein expressions of P-smad2/P-Smad3 decreased, Bcl-2 expression increased and Bim expression decreased significantly as compared with the other groups (P<0.01 or 0.05). The mitochondrial membrane potential and cytochrome C expression in CD4T cells were down-regulated in siTIPE2-burn group (P<0.05) with a lowered caspase-3 activity compared with TIPE2-burn group (P<0.01) and decreased caspase-8 and caspase-9 compared with the other groups (P<0.05). The apoptosis rate was the highest in TIPE2-burn group, whose Smad2/Smad3 was higher than that in the sham group (P<0.05) and the expression of P-smad2/P-Smad3 significantly increased compared with the other groups (P<0.05). In TIPE2-burn group, the mitochondrial membrane potential in CD4T cells was decreased (P<0.01), the expression of cytochrome C increased markedly (P<0.01), and the activities of caspase-3, caspase-8, and caspase-9 were all obviously higher than those in the other groups (P<0.05).</p><p><b>CONCLUSION</b>As an important immunoregulatory molecule, TIPE2 can promote the apoptosis of CD4T lymphocyte in mice with sever burn injury.</p>
Sujet(s)
Animaux , Mâle , Souris , Apoptose , Brûlures , Allergie et immunologie , Lymphocytes T CD4+ , Biologie cellulaire , Caspase-3 , Métabolisme , Caspase 8 , Métabolisme , Caspase-9 , Métabolisme , Régulation négative , Protéines et peptides de signalisation intracellulaire , Métabolisme , Protéine Smad2 , Métabolisme , Protéine Smad-3 , Métabolisme , RateRÉSUMÉ
<p><b>OBJECTIVE</b>To explore the association between serum homocysteine (Hcy) level and in-hospital death in patients with acute pulmonary embolism.</p><p><b>METHODS</b>A total of 186 acute pulmonary embolism patients [ (66.8 ± 12.7) years, 89 male] hospitalized in our department between June 2008 and June 2011 were included in this prospective study. Patients were divided into high Hcy group (Hcy ≥ 15.2 µmol/L, n = 95) and low Hcy group (Hcy < 15.2 µmol/L, n = 91). Patients were followed-up for 1 year for the incidence rate of early death associated with acute pulmonary embolism. The Cox proportional hazard model was used to analyze the relationship between serum Hcy level and early death in acute pulmonary embolism patients.</p><p><b>RESULTS</b>Patients were hospitalized for 1-37 days [(10 ± 6) days]. In-hospital death rate was 14.5% (27/186) and was significantly higher in high Hcy group than in low Hcy group [25.3% (24/95) vs. 3.3% (3/91) , P = 0.001]. Univariate Cox regression analysis indicated that admission heart rate, oxygen saturation, enlargement of right ventricle, Hcy ≥ 15.2 µmol/L, serum creatinine level, peak TnT level and deep venous thrombosis (P < 0.05) were independent risk factors for in-hospital death. Multivariate Cox regression analysis showed that Hcy ≥ 15.2 µmol/L (HR = 4.10, 95%CI:3.00-4.98, P = 0.017), admission heart rate (HR = 1.10, 95%CI:1.01-1.20, P = 0.031) , deep venous thrombosis (HR = 1.65, 95%CI:1.45-1.76, P = 0.034) and age (HR = 1.10, 95%CI:1.02-1.19, P = 0.010) were independent predictors of in-hospital death for acute pulmonary embolism patients. One-year follow up was finished in 142 patients (89.3%). There were 19 deaths ( 5 due to repeat pulmonary embolism, 4 due to decompensated respiratory and /or cardiac diseases, 6 due to malignant tumors, 2 due to fatal bleeding and 2 due to pneumonia) . Death rate was similar between the two groups during follow up.</p><p><b>CONCLUSION</b>Higher serum homocysteine is an independent for in-hospital death for patients with acute pulmonary embolism.</p>
Sujet(s)
Sujet âgé , Femelle , Humains , Mâle , Adulte d'âge moyen , Homocystéine , Sang , Mortalité hospitalière , Modèles des risques proportionnels , Études prospectives , Embolie pulmonaire , Sang , Mortalité , Facteurs de risqueRÉSUMÉ
<p><b>OBJECTIVE</b>To study the effect of hsa-miR-654-5p in repressing bone morphogenetic protein 2 (BMP2) mRNA and protein in human bone marrow mesenchymal stem cells (hBMSCs), and explore its regulatory role in osteogenic differentiation of hBMSCs.</p><p><b>METHODS</b>hBMSCs in the 4th passage were cultured for 16 h and transfected with hsa-miR-654-5p followed by further culture for 48 h. qRT-PCR and Western blotting were performed to detect the expressions of BMP2 mRNA and protein. Dual-luciferase?reporter gene assay was employed to examine the repression of the BMP2 gene.</p><p><b>RESULTS</b>BMP2 mRNA and protein expressions were significantly down-regulated in hBMSCs with hsa-miR-654-5p overexpression. Dualluci-ferase reporter gene assay indicated that the predicted target site of BMP2 was repressed directly by hsa-miR-654-5p, but this repression did not occur at the mutant predicted target site of BMP2.</p><p><b>CONCLUSION</b>hsa-miR-654-5p can directly repress the mRNA and protein expressions of BMP2 by binding to a specific target site. The changes in hsa-miR-654-5p can play an important role in osteogenic differentiation regulation of hBMSCs.</p>
Sujet(s)
Humains , Cellules de la moelle osseuse , Biologie cellulaire , Protéine morphogénétique osseuse de type 2 , Génétique , Métabolisme , Différenciation cellulaire , Cellules cultivées , Régulation de l'expression des gènes , Cellules souches mésenchymateuses , Biologie cellulaire , microARN , Génétique , Métabolisme , Ostéoblastes , Biologie cellulaire , Ostéogenèse , Génétique , ARN messager , Génétique , Métabolisme , TransfectionRÉSUMÉ
<p><b>OBJECTIVE</b>To study the role of contrast-enhanced ultrasound (CEUS) in the management of splenic trauma</p><p><b>METHODS</b>Forty patients with splenic trauma underwent CEUS examination and then different management were provided according to the examination results and the general status of patients: conservative treatment (group I, n = 19); CEUS-guided injective therapy (group II, n = 6); and surgery (group III, n = 15).</p><p><b>RESULTS</b>Eighteen patients were cured in group I and one patient experienced rehaemorrhagia. The haemostatic effect of CEUS-guided injective therapy was obvious in all six patients in group II. Among them, one patient experienced arteriovenous fistula, which was resolved after one week of injective therapy. Fifteen patients in Group III underwent surgery and were cured.</p><p><b>CONCLUSION</b>CEUS can provide reliable information for therapy mode selection in patients with splenic trauma and can be used to guide injective therapy.</p>