Objective To compare the T cell receptor recombination excision cycle (TREC) levels in peripheral blood mononuclear cells (PBMC) of systemic lupus erythematosus (SLE) patients with normal age- and gender- matched controls. To investigate the correlations between TREC levels of SLE patients and their clinical features. Methods We studied TREC levels in peripheral blood mononuclear cells (PBMC) of 21 SLE patients and 22 normal age- and sex- matched controls. TREC concentration was determined by real-time quantitative polymerase chain reaction (real-time qPCR) as the number of TREC copies/1000 PBMCs. The clinical features of the SLE patients such as systemic lupus erythematosus disease activity index (SLEDAI) , ESR, C reaction protein (CRP) , ANA, anti-dsDNA and complement levels and organ involvement were recorded and assessed. Results SLE patients had lower TREC levels [ (9.6 ± 7.5 )copies/1000 PBMC] than controls[ (16.1 ±11.1) copies/1000 PBMC,P = 0.033]. There was an inverse correlation between age and TREC levels in controls (r =- 0. 614, P = 0. 002) but not in SLE patients.There was an inverse correlation between SLEDAI and TREC levels in SLE patients(r =-0. 656, P =0. 001) and TREC levels seemed to have relations to skin lesions ( r = - 0. 620, P = 0. 003 ). No other clinical association was observed between TREC levels and clinical and laboratory SLE manifestations.Conclusion SLE patients had lower TREC levels than normal controls and there is a tendency that TREC level is reversely correlated with disease activity. The decrease PBMC TREC level is indicative of a low proportion of recent thymic emigrant (RTE) in SLE and could be caused by decreased RTE output and/or by increased peripheral T cell proliferation in this disease. The under-representation of RTE in the peripheral T cell pool may play a role in the immune tolerance abnormalities observed in SLE.

AIM:To set up a glutamate-induced cell damage model in cultured hippocampal neurons, and to determine whether glutamate-induced neuronal apoptosis changes and whether this process is mediated by mitochondrial signal transduction pathways involving the release of cytochrome C. METHODS: Hippocampal neurons, isolated and cultured from new born Wistar rats, were exposed to various concentrations of glutamate. Extent of cell death was assessed by measuring the release of lactate dehydrogenase (LDH) in the culture media. Based on these data, an appropriate concentration of glutamate was selected, and all subsequent experiments were carried out under the concentration. Kinetics of glutamate-induced both apoptotic and necrotic cell death after exposure to glutamate for various times(3-24 h) were determined by flow cytometry and LDH release. The caspase-3 protein levels and cytochrome C release from mitochondria into cytosol in hippocampal neurons were determined by Western blotting. RESULTS: Glutamate treatment induced hippocampal neurons death in dose-dependent and time-dependent manners. A significant increase in LDH release (18.4%) was induced in the cells treated with 50 ?mol/L glutamate, compared to control untreated cells(P

Objective To investigate the satisfaction degree with nursing for discharged patients by telephone interview,and understand the nursing quality improvement during hospitalization of patients.Methods In January and December 2011,24 clinical departments were selected as the research object,10 patients were selected from each department.The questionnaires of satisfaction degree with nursing were adopted to investigate the satisfaction degree of patients by telephone interview.The difference of satisfaction degree with nursing were compared between January and December 2011.Results Compared with the results of January,there were statistical differences in overall mean score of satisfaction degree and the dimensions of service attitude,knowledge information,ward management and working ability.While the means of dimensions of basic nursing care and care-taking patient were in high levels.Conclusions The method of telephone interview to investigate the satisfaction degree of discharged patients is direct,real and objective.It is convenient for the hospital to understand the nursing quality and existing problems during hospitalization of patients,and offers scientific way for continuous improvement of nursing service.

Objective To observe the survival,migration and differentiation of grafted neural stem cells(NSCs)transfected with cardiotrophin-1(CT1)in hippocampus in status epilepticus(SE)rats,and investigate its effect on neuron loss and mossy fiber sprouting(MFS)in hippocampus of SE rats.Methods (1)Lithium-pilocarpine induced SE model rats were divided into 3 groups randomly:CT1-NSCs transplantation group(n=18);NScs transplantation group(n=18)and SE model group(n=18).Another 18 rats served as normal control group.Each group was further divided into 3 time points testing groups(n=6 at each point)corresponding to 1,4 and 8 weeks after transplantation respectively.(2)Under the confocal microscopy,the survival,migration and differentiation of the grafted cells were observed by immunofluorescenee.(3)Morphological changes and neuron loss in the hippocampal CA1 region were examined by Nissl staining.(4)MFS in hippocampal dentate gyrus in rats was obserred by Timm histochemistry.Results(1)At 4 and 8 weeks post-tmusplantation,the numbers of double-labeled NF-200 and EGFP pesitive cells in the CT1-NSCs group were significantly hisher than those in NSCs group.In the former group most of the grafted NSCs migrated away from the needle tract,but in the latter group,grafted ceHs remained at the transplantation site.(2)The numbers of neuron in the hippocampal CA1 region reduced gradually after SE.The numbers of neuron in the CA1 region in CT1-NSCs transplantation rats (68.85±11.49,60.89±12.17 and 51.51±13.34 in 1,4,8 weeks after transplantation respectivelv)were greater than that in NSCs transplantation rats(67.92±10.78,42.56±11.47 and 30.49±10.12).tvalue were 4.650 and 5.334 in 4 and 8 weeks after transplantation(P<0.05).(3)Aberrant MFS in the inner molecular layer of dentate gyrus was observed,and the scores of MFS gradually increased with timelapse.The scores of MFS in CT1-NSCs transplantation rats(0.77±0.04,2.48±0.89 and 2.39±0.82 in 1,4,8 weeks after transplantation respectively)were significant lower than that in NSCs transplantation rats (1.12±0.62,3.17±0.64 and 3.88±0.51,t=6.059,9.511 and 9.728,P<0.05).Conclusions CT1 could promote the survival,migration and differentiation of engrafted NSCs in hippocampud in SE rats.Engrafted NSCs transfected with CT1 have effect on repair of the injured hippocampus,and could inhibit hippocampus MFS in SE rats.

ObjectiveTo explore the factors associated with activity of daily living (ADL) in patients injured from earthquake and to observe the rehabilitation nursing of fractures for them. Methods367 patients were reported and analyzed with Logistic regression. Results and ConclusionThe age (OR=1.016), renal failure (OR=4.648), lower limb fractures (OR=2.404), spine fracture (OR=3.558), right hand fractures (OR=1.190), right foot fractures (OR=4.389) and the complex fractures (OR=2.600) were associated with the poor ADL (<60). The rehabilitation nursing for fracture were reported and discussed.

potential use in clinical therapy and prognosis estimation of the tumor.

Objective To investigate whether the activation of secretory prophospholipase A2 (sPLA2) plays the role in the pathophysiological mechanism of acute aristolochic acid nephropathy (AAN) in rats. Methods Wistar rats were randomly divided into two groups. Model group received decocted Aristolochia Manshuriensis Kom 30 g·kg-1d-1 by gavage for 7 days following tap water in same way for additional 7 days. Control group received only tap water by garage at parallel time. The renal pathological changes were observed at the 4th, 8th and 14th day. The injury of renal tubules and interstitium was observed under light microscope following a semi-quantity grade. The level of Scr was measured to evaluate glomerular function. Urinary N-acetyl-beta-glucosaminidase (NAG) was tested as renal tubular injury marker. The activity of sPLA2 in serum was detected by manifesting the color of thiols in the substrate. The protein expression of renal cortex and medulla COX-2 was analyzed by Western blot. The metabolic products of pretaglandins (PC, s) including 6-kcto-PGF1α and TXB2 in the plasma and urine were assayed by radioimmunoassay. The ratio of 6-keto-PGF1α/TXB2 was calculated. Results After Aristolochia administration, the tubulointerstitial injury and Scr increased in AA rats and reached the peak at the 8th day, the tubulointerstitial injury index(8.14±2.55 vs 1.50±0.71, P<0.05) and Scr[(0.24±0.10) vs (0.19±0.02) μmol/g, P<0.05] increased significantly in AA rats compared with control group. The activity of sPLA2 (μmol ·min-1·mg-1) in AA group elevated by 1.3-fold compared to control group at 8th day (133.15±17.05 vs 101.3±16.07, P<0.05), while theexpression of COX-2 in renal cortex increased (1.16±0.36 vs 0.69±0.28, P<0.05) with no change in renal medulla. Even though the levels of serum 6-keto-PGF1α and TXB2 did not change obviously in both AA and control group, but urinary levels of 6-keto-PGF1α and TXB2 increased by 2-fold and 3-fold in AA group compared to control group, respectively (all P<0.05), while the ratio of 6-keto-PGF1α/TXB2 decreased significantly (207.53±17.52 vs 296.64±51.31, P<0.05). All of above changes recovered to the control level at the 14th day except the tubulointerstitial injury index. Conclusion Serum sPLA2 is activated in the rots with acute kidney injury induced by aristolochic acid, which accompanied by up-regulated expression of COX-2 in renal cotex and increased the metabolic products of vasoconstrictive PG s in urine. These changes may participate the mechanism of renal peritubular ischemia in AAN.

Objective To evaluate the influence of tissue factor pathway inhibitor 2(TFPI-2)gene on the proliferation and invasion of K562.Methods The expression vector pcDNA3.0/TFPI-2 was transfected into human leukemia line K562 cells(K562-T)by using liposome,then the mRNA and protein TFPI-2 were detected by real-time RT-PCR and western blot separately.The growth curve and the colony-forming unit assay were used to measure the ability of cells growth and transwell chamber model was employed to test the ability of cell invasion in vitro.Results Expression of mRNA and protein of TFPI-2 was detected in transfected cells.The growth rate and self-replication ability of K562-T cells were lower than those of the two control groups obviously.The number of K562-T cells to traverse a Matrigel-coated membrane was dramatically decreased compared with that of non-expressing cells.Conclusion The gene of TFPI-2 can inhibit the growth,proliferation and invasion of the K562 cells.

Objective To observe the curative effect of imatinib mesylate combined with myeloablative allogeneic hematopoietic stem cell transplantation for treatment of chronic myeloid leukemia advanced phase. Methods To retrospectively analyze clinical effect of 6 patients with chronic myeloid leukemia advanced phase were treated with imatinib mesylate combined with myeloablative allogeneic hematopoietic stem cell transplantation from July 2005 to April 2009, and literature review. Results The disease-free survival and the survival rate of 4 patients were 66.67 %. 2 patients died (one case die for Chemotherapy pretreatment in the third transplantation after two years, the other case die for Chemotherapy pretreatment in the second transplantation after six months ). Conclusion The clinical cure rate of chronic myeloid leukemia advanced phase may be improved with the treatment of imatinib mesylate combined with myeloablative allogeneic hematopoietic stem cell transplantation.

Objective To investigate the reversal effect of Topo Ⅱα-shRNA and Topo Ⅱβ-shRNA on Topo Ⅱ gene in K562/AS2 cells. Methods Three pieces of Topo Ⅱα-shRNA and three pieces of Topo Ⅱβ-shRNA were designed,synthesized and transfected into K562/AS2 cells by liposome. Expression level of Topo Ⅱα and Topo Ⅱβ mRNA were determined by real time fluorescence quantitative PCR. The expressions of Topo Ⅱα and Topo Ⅱβ protein were assayed with flow cytometer. Results After treated with Topo Ⅱα-shRNA or Topo Ⅱβ-shRN A for 24 hours,the expression level of Topo Ⅱα mRNA and Topo Ⅱβ mRNA protein in K562/AS2 cells decreased at most (78.22±0.01) %,(31.17±1.27) % (P <0.05),and (57.36±0.01)%,(23.98±1.22) % (P <0.05) respectively. Conclusion The expression of Topo Ⅱ gene can be down-regulated after infected with Topo Ⅱ-shRNA in K562/ AS2 cell line.