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1.
Journal of Medical Postgraduates ; (12): 186-189, 2017.
Article in Chinese | WPRIM | ID: wpr-514623

ABSTRACT

Objective Diabetes is a common chronic disease in the elderly and needs long-term treatment. This study aims to determine the effect of extended nursing service in rehabilitation of army retired officers with diabetes. Methods We selected 78 ca-ses of military retired officers with diabetes from September 2010 to September 2012 in Nanjing General Hospital of Nanjing Military Region. According to the different intervention methods, patients were divided into experimental group and control group( n=39 cases) . The control group used conventional nursing service, and the experimental group added extended nursing service on the basis of the control group . After one year follow-up, the fasting blood glucose level, glycosylated hemoglobin ( HbAlc) , self-rating depression scale (SDS) evaluation and self-rating anxiety scale (SAS) and the changes of patients′ satisfaction of the two groups were observed. Results The fasting blood glucose levels and HbAlc of experimental group were significantly better than control group, with statisticalsignificance (P<0.05);The SAS scores (34.9±5.9)and SDS scores (36.9±4.5) of experimental group were significantly lower than the control group(52.3±4.2 and 55.9±3.9), with statistical significance ( t=5.489, t=5.226, P<0.05);The satisfaction degree of the exper-imental group was significantly higher than the control group (99.8%vs 79.9%, χ2=4.898, P<0.05). Conclusion the extension ofnursing service in health rehabilitation in the retired veteran cadres in the army with diabetes can effectively improve the patient′s fast-ing blood glucose levels, reduce depression, as well as improving the nursing service satisfaction.

2.
Chinese Journal of Primary Medicine and Pharmacy ; (12): 536-539, 2017.
Article in Chinese | WPRIM | ID: wpr-507886

ABSTRACT

Objective To analyze the expression and clinical significance of tumor suppressor phosphatase -tension protein gene(PTEN)in differentiated thyroid carcinoma and the relationship with the V600E gene site muta-tion of murine sarcoma viral oncogene homolog B1(BRAF).Methods The expression of PTEN was assayed by im-munohistochemical staining in differentiated thyroid carcinoma and adjacent tissues.The differences were compared between clinical pathological features.The BRAF V600E gene mutation was detected by fluorescence quantitative pol-ymerase chain reaction(PCR)and to investigate the correlation between the expression of PTEN and BRAF V600E mutation.Results The negative rate of PTEN was 78.75%(63 /80)in differentiated thyroid carcinoma,13.75%(11 /80)in adjacent tissues(χ2 =27.236,P =0.000).There were significant differences in the expression of PTEN between I -II and III -IV in TNMstage,grade I and II,and lymph node metastasis(χ2 =10.395,6.948,9.263,P =0.000,0.006,0.000).The differences were not significant in the expression of PTEN between different gender,≤45 years and >45 years different pathological types and tumor diameter <2cm and ≥2cm(χ2 =1.113,0.941, 2.301,1.567,P =0.185,0.213,0.087,0.181).There was correlation between the expression of PTEN and BRAF V600E mutations(r =0.301,P =0.004).Conclusion The expression of PTEN is involved in the occurrence and development of differentiated thyroid cancer and is associated with BRAF V600E.The PTEN has the predictive value of prognosis in tumors.

3.
Journal of Biomedical Engineering ; (6): 618-623, 2015.
Article in Chinese | WPRIM | ID: wpr-359597

ABSTRACT

The aim of this study was to observe whether necroptosis is involved in the process of cardiac hypertrophy induced by pressure overload. SD rats underwent transverse abdominal aortic constriction (TAC) operation for establishing cardiac hypertrophy model. The structure and function of the left ventricle of rats were evaluated via echocardiography, left ventricular mass index, the expression of markers of cardiac hypertrophy and histological detection. Real-time PCR and Western blot were used to measure the gene and protein expression of receptor interacting protein kinase 1 and 3 (RIPK1 and RIPK3, the necroptosis markers) respectively. Four weeks after TAC operation, rat model for cardiac hypertrophy was established. The experimental data showed that the gene and protein expressions of RIPK1 and RIPK3 in the rat heart hypertrophic tissues after TAC for 4 weeks were increased significantly compared with those in the sham group. HE staining showed cardiomyocytes injury and hypertrophy in the hearts of TAC rat models. By transmission electron microscope, we observed that mitochondria of cardiomyocytes were damaged seriously in the TAC models. Treatment with losartan used, the selective antagonist of angiotensin II type I receptor could improve the cardiac function of TAC rats. Moreover, losartan treatment decreased the expression of RIPK1 and RIPK3 in heart tissues of TAC rats. The results suggest that necroptosis occurrs in the process of cardiac hypertrophy with pressure overload, and losartan could alleviate the cardiac hypertrophy and inhibit necroptosis.


Subject(s)
Animals , Rats , Apoptosis , Cardiomegaly , Pathology , Disease Models, Animal , Echocardiography , Heart , Losartan , Pharmacology , Myocytes, Cardiac , Pressure , Protein Serine-Threonine Kinases , Metabolism , Rats, Sprague-Dawley , Real-Time Polymerase Chain Reaction , Receptor-Interacting Protein Serine-Threonine Kinases , Metabolism
4.
Journal of Biomedical Engineering ; (6): 393-399, 2015.
Article in Chinese | WPRIM | ID: wpr-266666

ABSTRACT

The aim of this study is to construct specific shRNA expressing plasmids, and to observe their effects on H9c2 cardiomyocytes injury induced by hypoxia/reoxygenation (H/R). RIPK1 and RIPK3 are the key kinases mediating the process of necroptosis. Using recombinant DNA technology, we inserted the synthetic shRNA into pSUPER vector to construct RIPK1-shRNA or RIPK3-shRNA plasmid respectively. We transfected H9c2 cardiomyocytes with the two shRNA plasmids respectively, before we treated them with H/R stimulation. Then, we measured the relevant genes and proteins by real-time PCR and Western blot. Meanwhile,we detected the markers of necroptosis and cardiomyocytes injury. The results showed that inhibition of ripk1 or ripk3 gene expression by its specific shRNA might protect the cardiomyocytes injury induced by H/R stimulation.


Subject(s)
Animals , Rats , Apoptosis , Cell Hypoxia , Cell Line , Gene Expression , Myocytes, Cardiac , Pathology , Protein Serine-Threonine Kinases , Genetics , Metabolism , RNA, Small Interfering , Real-Time Polymerase Chain Reaction , Receptor-Interacting Protein Serine-Threonine Kinases , Genetics , Metabolism , Transfection
5.
Journal of Biomedical Engineering ; (6): 379-384, 2014.
Article in Chinese | WPRIM | ID: wpr-290749

ABSTRACT

The aim of the current study is to investigate the effect of visfatin on cardiomyocyte hypertrophy. Cultured H9c2 cardiomyocytes were exposed to visfatin at different concentrations for different periods of time, and the markers of cardiomyocyte hypertrophy were detected. Moreover, pravastatin, the inhibitor of endoplasmic reticulum stress (ERS) or thapsigargin, an ERS agonist was used respectively to pre-treat the cells before visfatin stimulation. F-actin staining was performed to measure the cell surface change. The mRNA expressions of atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and ERS markers including glucose-regulated protein 78(GRP78), C/EPB homologous protein (CHOP) and activating transcription factor 6 (ATF6) were assessed by real time RT-PCR. The change of protein level of GRP78 and CHOP was detected by Western blot. The experimental data demonstrated that exposure to 100 or 150 ng/mL concentrations of visfatin for 24 h, or 100 ng/mL of visfatin for 24 or 48 h, significantly increased the expression of markers for cardiomyocyte hypertrophy. Visfatin stimulation provoked ERS in H9c2 cells. Furthermore, pre-treatment with pravastatin partially inhibited the visfatin-induced mRNA expression of ANP and BNP in H9c2 cells, whereas thapsigargin promoted the visfatin-induced expression of cardiomyocyte hypertrophy markers. The results suggest that visfatin might induce cardiomyocyte hypertrophy via ERS -dependent pathways.


Subject(s)
Animals , Rats , Actins , Activating Transcription Factor 6 , Metabolism , Cell Line , Heat-Shock Proteins , Metabolism , Hypertrophy , Myocytes, Cardiac , Cell Biology , Natriuretic Peptide, Brain , Metabolism , Nicotinamide Phosphoribosyltransferase , Pharmacology , Transcription Factor CHOP , Metabolism
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