Objective To investigate the influence of recombinant human parathyroid hormone [rhPTH (1-34)]on the proliferation of HaCaT cells induced by tumor necrosis factor-α (TNF-α) in vitro.Methods Cultured HaCaT cells were treated with various concentrations of rhPTH (1-34) for different durations after incubation with recombinant human TNF-α of 10 g/L for 24 hours.MTT assay and flow cytometry were performed to detect the proliferation and cell cycle of HaCaT cells,respectively.Results As contrast phase microscopy showed,the growth of HaCaT cells was inhibited by rhPTH (1-34) along with a decrease in the growth speed.MTT assay showed a suppressed proliferation of HaCaT cells after being treated with rhPTH (1-34) of 0.05,0.2,0.8,3.2 and 12.8 pmol/L for 36 and 48 hours (P＜ 0.01 or 0.05).The percentage of cells at G1 phase in HaCaT cells markedly increased (all P ＜ 0.01 ),while that at S phase declined (all P ＜ 0.01 )after 48-hour treatment with rhPTH(1-34) of 0.2,0.8,3.2 and 12.8 μ mol/L.Conclusions rhPTH(1-34) has an obvious inhibitive effect on the proliferation of HaCaT cells induced by TNF-α in vitro,and the effect is in a dose-dependent manner.

Sleep quality is closely related to human health. It is very important to correctly discriminate the sleep stages for evaluating sleep quality, diagnosing and analyzing the sleep-related disorders. Polysomnography (PSG) signals are commonly used to record and analyze sleep stages. Effective feature extraction and representation is one of the most important steps to improve the performance of sleep stage classification. In this work, a collaborative representation (CR) algorithm was adopted to re-represent the original extracted features from electroencephalogram sig- nal, and then the kernel entropy component analysis (KECA) algorithm was further used to reduce the feature dimension of CR-feature. To evaluate the performance of CR-KECA, we compared the original feature, CR feature and readied CR feature (CR-PCA) after principal component analysis (PCA). The experimental results of sleep stage classification indicated that the CR-KECA method achieved the best performance compared with the original feature, CR feature, and CR-PCA feature with the classification accuracy of 68.74 +/- 0.46%, sensitivity of 68.76 +/- 0.43% and specificity of 92.19 +/- 0.11%. Moreover, CR algorithm had low computational complexity, and the feature dimension after KECA was much smaller, which made CR-KECA algorithm suitable for the analysis of large-scale sleep data.
Algorithms ; Electroencephalography ; Entropy ; Humans ; Polysomnography ; Principal Component Analysis ; Sleep Stages ; Sleep Wake Disorders ; diagnosis ; Software

Objective To observe insulin resistance in first-degree relatives of patients with Graves disease. Methods All subjects in control group and experiment group including first-degree relatives of GD patients underwent oral glucose tolerance tests (OGTT) and insulin releasing tests then the degree of insulin resistance was analyzed. Results Blood glucose at each point of OGTT, insulin level and insulin resistance index 1 (HOMA-IR) of experiment group were higher than those in control group, while insulin activity index (IAI) and HOMA-βwere significantly lower than those in control group. Conclusion Patients insulin resistance could be found among first-degree relatives of GD patients.

Objectives: To observe the effects and the mechanisms of exogenous fatty acids on colorectal cancer cells(LoVo). Methods:The effect of exogenous fatty acids on LoVo cells was determined by 5 diphenyl tetrazolium bromide(MTT) assay.The content of MDA was examined to evaluate the extent of lipid peroxidation. Results:The growth of LoVo cells was inhibited by polyunsaturated fatty acids(PUFAs).The inhibitory effect of saturated fatty acids and monounsaturated fatty acids on LoVo cells was not showed.None of the fatty acids was found to fibroblast cells(HLF).PUFAs caused the significant rising of intracellular MDA content. Conclusions:PUFAs could inhibit the growth of colorectal cancer cells.The strengthening of lipid peroxidation may be one of the mechanisms.

Objectives:To observe the changes in metabolism of fatty acids in breast cancer cells and the effects of inhibiting fatty acid synthase(FAS) on the growth of breast cancer cells. Methods:By RT PCR,the expression of FAS mRNA in breast cancer cell line was examined.The growth inhibition of breast cancer cells by specific FAS inhibitor, cerulenin, was determined by MTT assay.Flow cytometric analysis was used to study the changes of cell cycle. Results:FAS mRNA expression in MCF 7 cells was high.We found that cerulenin caused dose and time dependent inhibition of growth of MCF 7 cells.The growth inhibition of MCF 7 after 48 hours exposure of cerulenin at 2.5,5,10 and 20 mg/L was ( 43.47 ?4.58)%,(62.92?2.68)%,(81.93?0.91)% and (67.7?12.27)%( P

Objective: To develop a headspace gas chromatography ( HS-GC ) assay for simultaneous determination of dichloroacetic acid ( DCA ) and trichloroacetic acid ( TCA ) in urine. Methods: Urine samples (5 mL) were transferred to a 22 mL headspace bottle, added with 0.5 mL 10% sodium acetate solution , immediately sealed, and shaken evenly. The bottle was placed in the HS-GC system, and equilibrated at 90 ℃ for 60 minutes. The mixture was separated with the HP-INNOWAX chromatographic column, and the DCA and TCA concentrations were detected with the hydrogen flame detector. Results: Under the optimal experimental conditions, the correlation coefficient of DCA and TAC was both > 0.999 0 within the range of 10-500.0 μg/L, and the lowest detection limits of DCA and TAC were 2.0 and 3.5 μg/L, with the spike recovery rate of 87.40% to 101.44%, and relative standard deviations of 1.89% to 3.25%. Of the 35 urine samples sampled from occupational populations, DCA and TCA were not detected. Conclusions The establishment of the HS-GAS assay through addition of sodium acetate and optimization of the headspace conditions, has high recovery and precision, which is effective to meet the requirements for daily determination of DCA and TCA in urine samples.

Objective To evaluate the curative effect and safety of emergency therapeutic endoscopic retrograde cholangiopancreatography (ERCP) and treatment strategy of mobidity and combined diseases for patients aged over 90.Methods The clinical and follow-up data of 116 cases treated by ERCP from January 2002 to December 2006 were analyzed retrospectively.Results The success rate was 97.41% for biliary drainage.The occurrence rate of mobidity was 21.24%(24/113),of which 6 cases of acute pancreatitis (25.00%),2 cases of upper gastrointestinal bleeding (8.33%),12 cases of electrolyte disorders (50.00%),acid-base balance disorders in 4 cases (16.67%).Except the higher incidence of hypokalemia disorders of emergency group than out-patient group (P=0.003),the rest of the mobidity rates were similar in the two groups.The mortality rate and deterioration rate of combined disease between the two groups were also similar.Conclusion Simplify operations,rapid drainage,positive preoperative preparation can effectively reduce the incidence of mobidity and avoid the aggravation of combined diseases.Emergency ERCP for treatment of patients aged over 90 is safe and effective.

Objective To evaluate the success rate, safety and efficacy of endoscopic retrograde cholangiopancreatography (ERCP) after Billroth Ⅱ gastrectomy. Methods Data of 75 patients with biliary disease after Billroth Ⅱ gastrectomy, who underwent ERCP from January 2007 to November 2009, were retrospectively analyzed. Results In 75 patients, afferent loop intubation was achieved in 69 (92%) and selective cannulation of bile duct were successful in 68 (68/69, 98. 5%). Diagnostic procedures were carried out in 3 patients, and therapeutic in 65 others, which included EST plus stone removal and ENBD in 16, ERBD in 19, EMBE in 18 and EBD plus stone removal and ENBD in 12. Afferent loop perforation occurred in 1 patient (1.3%) and was treated surgically, and 2 acute pancreatitis (2. 6%) were treated conservatively.There was no complication of bleeding. Conclusion ERCP after Billroth Ⅱ gastrectomy is safe and efficiency for biliary disease.

Objective To explore the mechanism by which the anti-human P185erbB2 scFv-Fc-IL-2(HFI)modulates tumor surface molecules and activates immune effector cells in vitro. MethodsMTT assay was used to test the proliferation and the LAK-like cytotoxicity. Flow cytometry assay was used to test the expression of ICAM-1, Fas and erbB2 receptors in tumor cells and the expression levels of CD molecules FasL and LFA-1 in human PBMC. Antibody-dependent cell-mediated cytotoxicity(ADCC)mediated by HFI against SKOV3, MCF-7 and SGC-7901 tumor cells was explored hv LDH release assay. Results The expression levels of ICAM-1 and Fas on SKOV3 cell treated with HFI were upregulated, from 24.85％ and 0.53％ to 85.36％ and 59.19％ respectively, while the expression levels of erbB2 on SKOV3, MCF-7 and SGC-7901 tumor cells treated with HFI were downregulated, from 98.48％, 42.60％ and 36.66％ to 94.01％,30.95％ and 12.36％ respectively. HFI could significantly enhance the proliferation activity of human PBMC, and CD3+ CD8+ T cells and CD3- CD16+ CD56+ NK cells were elevated, from 24.37％ and 6.90％ to 38.80％ and 13.45％ respectively. The expression levels of CD25, LFA-1 and FasL were significantly enhanced from 3.99％, 86.52％ and 5.02％ to 12.96％, 99.06％ and 16.19％. The LAK-like cytotoxicity of human PBMC treated with HFI against SKOV3, MCF-7,SGC-7901 tumor cells was significantly improved:HFI was effective in mediating ADCC against SKOV3,MCF-7 and SGC-7901 tumor cells which expressed high,medium and low levels of erbB2,respectively,and HFI-induced ADCC was correlated with the degrees of erbB2 expression on the tumor cells. Conclusion The expression levels of ICAM-1 and Fas on SKOV3 cell treated with HFI are significantly upregulated. The expression levels of erbB2 on SKOV3, MCF-7 and SGC-7901 tumor cells treated with HFI are downregulated. HFI can significantly enhance the proliferation activity of human PBMC. The LAK-like eytotoxicity of human PBMC treated with HFI against tumor cells is significantly enhanced. HFI iS effective in mediating ADCC and the activity of HFI-induced ADCC is correlated with the degrees of erbB2 expression on the tumor cells.

Objective To study the regulation of microRNA 199a (miR-199a) on adhesion,migration and invasion ability of human eutopic endometrial stromal cells (ESC) from patients with endometriosis.Methods ESC were transfected with miR-199a mimics or negative control (NC) RNA by lipofectamine 2000.The adhesion,migration and invasion ability of ESC were detected by cell adhesion assay,scratch assay,cell migration assay and matrigel invasion assay,respectively.Luciferase reporter assay was used to evaluate whether IKKβ was the target gene of miR-199a.The expression of ikappa B kinase beta (IKKβ),inhibitory kappa B alpha (IκB-α),phospho-IκB-α (p-IκB-α) and nuclear factor-kappa B (NF κB) protein were measured by western blot.Results ( 1 ) Adhesion potential:the adhesion inhibitory rates were ( 14 ± 4 )％ in miR-199a group and 0 in control group,which showed significant difference (P＜0.01 ).(2) Migration and invasion:in the scratch assay,ESC transfected with miR-199a exhibited a lower scratch closure rate than that of controls.In migration and invasion assays,the migration and invasion ability of miR-199a group were significantly decreased compared with those of NC group [ 130 ± 31 vs.247±36 (P＜0.01); 63 ± 15 vs.133 ± 17 (P＜0.01),respectively].(3) The luciferase activity of miR-199a group was significantly lowered than that of control group [ 0.160 ± 0.006 vs.0.383 ± 0.083 ( P ＜0.01 ) ].The protein levels of IKKβ,p-IκB-α,IκB-α and NF-κB of 0.350 ±0.195,0.443 ±0.076,1.970 ±0.486 and 0.454 ± 0.147 in miR-199a group were significantly different compared with the NC group in which the protein levels were set at 1.000 ( P ＜ 0.01 ).Conclusions miR-199a can inhibit the adhesion,migration and invasion of the ESC.IKKβ is the target gene of miR-199a in ESC.One of the mechanisms of the inhibition effect is probably that miR-199a inhibits the activation of NF-κB signaling pathway by targeting IKKβ gene.