Objective: To study the long-term effect of Tangshan earthquake on psychosomatic health of paraplegic suffers. Method: 64 paraplegic suffers of Tangshan earthquake and 64 normal controls were interviewed and assessed with self made questionnaire for psychosomatic health, SCL-90, SAS, SDS, CMI (Cornell Medical Index) and SSRS (Social Support Rating Scale). Results: 6 patients (9%) were diagnosed as PTSD according to CCMD-2-R, this rate was higher than that of normal citizen experienced the earthquake. 32 patients had Acute Stress Reaction. At present, patients' group had poorer mental health than control reflected by SCL-90, SAS, SDS and CMI. Conclusion: The severity of trauma both mentally and physically has great influence on mental health of suffers even after 25 years.

Objective To explore whether the inhibited expression of fibrocystin by RNA interference can increase epidermal growth factor (EGF)-induced cell proliferation and its possible mechanism . Methods A stable PKHD1-silenced HEK 293 cell line was established . Cell proliferation rate, intracellular Ca2+ concentration and extracellular signal-reguhted kinase 1/2(ERK1/2) activity were assessed after treatment with EGF, verapamil and Bay K8644 . Results The proliferation rate of PKHD1-silenced HEK-293 cells was found to be significantly higher after EGF stimulation compared to the control HEK 293 cell (231 .5% vs 152 .8%, P＜0 .01) . PKHD1-silencing lowered the intracellular Ca2+ concentration and caused EGF-induced ERK1/2 overactivation in the cells(P＜0 .01 ) . When cells were treated with verapamil for 4 hours to lower the intracellular Ca2+ concentration, the cell proliferation rate was significantly increased after 20 ng EGF for 24 hours . The verapamil treatment increased the level of activated ERK1/2 in EGF-treated cells . An increase of intracellular Ca2 + in PKHD1-silenced ceils repressed the EGF-dependent ERK1/2 activation and the hyperproliferative response to EGF stimulation . Conclusions Inhibition of fibrocystin can cause EGF-induced excessive proliferation through decreasing intracellular Ca2+ resulting in EGF-induced ERK1/2 activation . The loss of fibrocystin may lead to abnormal proliferation in kidney epithelial cells and cyst formation in ARPKD through modulation of intracellular Ca2+ concentration .

Objective:To investigate if a plant-derived polysaccharide sulfate(M33A) binding to HIV1 gp120 may induce the exposure of neutralization epitopes of gp120,and if M33A-bound HIV-1ⅢB antigens may be used as a AIDS vaccine for inducing neutralizing antibodies against HIV-1.Methods:Whole-inactivated M33A-bound HIV-1ⅢB antigens were prepared and used to immunize mice after mixing with FCA or FIA.The titers of anti-HIV-1 IgG antibodies in immunized mouse plasma were detected by ELISA,and the HIV-1 neutralization by those plasma was detected by the improved microtiter neutralization assay.Results:M33A-bound HIV-1 antigens induced higher titers of anti-HIV-1 IgG antibodies(group C:1.5?10~6;group D:1.5?10~6) than HIV-1 antigens alone(4.9?10~5),and female mice produced 3 times higher titers of anti-HIV-1 IgG antibodies than male mice after immunized with various HIV-1 antigens.All three immunization schemes did not induce the production of anti-HIV-1 neutralizing antibodies.Conclusion:M33A binding does not induce gp120 to expose neutralization epitopes.However,M33A may improve the level of mice immune responses to HIV-1 antigens,suggesting M33A may enhance immune response to HIV-1 antigens.

Objective To observe the polysomnographic manifestation of sleep disorder and the characteristics of sleep architecture in patients with PD.Methods 42 patients with PD and 40 normal controls underwent night polysomnography.The parameters of sleep architecture and progress in two groups and video-monitoring features were analyzed.Results According to PSG recordings,the incidence of difficulties in the initiation of sleep(73.8%),fragmented sleep(59.5%),excessive daytime sleepiness (46.1%)were respectively increased in PD patients group than that in controls(all P5)、 ESS were increased(P=0.022,0.000,0.007, 0.001,0.000,respectively).SOREMPs occurred in 6 patients(14.3%)in PD group,but didn't oecure in controls.In PD group REM without atonia(RWA)was demonstrated in 36 patients(85.7%),RBD in 19 patients;in control group,however,REM in 6 and RBD in 2 separately.The statistics analysis showed the incidence of RWA(85.7%)and RBD(45.2%)in PD group was significantly higher than that in control group(P

Objective To detect the relationship between CAG repeat in IT15 gene and clinical manifestations of Huntington's disease (HD).Methods Non-denaturing polyacrylamide gel electro- phoresis method was used to detect CAG repeat.Clinical manifestations were scored by UHDRS and MMSE. Results Genotypes of IT15 were heterozygous in all 29 HD patients.CAG repeat in the HD chromosome, being 42—62,13—28 in normal chromosome,was inversely correlated with age of onset (r=-0.539,P

Silent information regulator 1 (SIRT1) is a NAD+-dependent histone deacetylase,which plays an important role in cerebral ischemia.It mainly stabilizes cerebral vascular endothelium,prevents vascular stenosis and the anti-inflammatory and anti-oxidative stress effects after cerebral ischemia.This article reviews the protective effects of STRT1 and its related mechanisms in cerebral ischemia.

Objective:To explore the relative factors of hospitalized schizophrenics with metabolic syndrome. Methods: Patients data were collected by the way of face-to-face questionnaire to patients or their guardians, consulting patients medical record, checking physical or laboratory examination. Information include age, duration of the disease, the classification of antipsychotics and dosage, fast plasma glucose, plasma lipids, blood pressure, etc of hospitalized schizophrenics. The relative factors of metabolic syndrome were analyzed. Results; Among 797 schizophrenics, there were 153 cases (19. 2% ) suffered from metabolic syndrome. Single-factor analysis showed that the patients with longer duration of the disease, taking clozapine, etc, were at high risk of metabolic syndrome, and sex didnt relate to metabolic syndrome; Logistic regression analysis appeared that metabolic syndrome correlated with age, clozapine, CRP concentration, etc. Conclusion: The possible risk factors causing metabolic syndrome in schizophrenia include, duration of the disease, etc.

Conopeptides (Conotoxin) derived from tropical marine gastropod, cone snail ( Conus ) venoms have been an useful tool agent in neuro investigation and new drug source. Recently, new method of Conotoxin genes cloning from Conus genomic DNA has been established. So to get Conus genomic DNAs rapidly is the basis for diverse Conotoxin gene isolation, gene bank construction and the medical source exploitation. In this report, different DNA extractions from different tissue and organs of six cone snail species were performed in order to optimize the DNA isolation methods. The optimized brief phenol SDS method was established which fit for cone snails genomic DNA extraction.

AIM: Although the evidence indicates that extracellular matrix metalloproteinase inducer (EMMPRIN) is closely associated with matrix metalloproteinase (MMP) expression in tumor cells, tumor invasion and metastasis, no direct proof that EMMPRIN regulates MMPs in monocytes, especially in the atherogenic milieu is observed. Here we tested this hypothesis by examining MMP-9 expression in macrophages/foam cells and monocyte migration through EMMPRIN knockdown by siRNA. METHODS: The methods of qPCR and Western blotting were used to detect the suppressions of EMMPRIN mRNA and protein expression in macrophages and foam cells transfected with EMMPRIN-specific siRNA. The protein expression of MMP-9 in macrophages and foam cells was also determined. Monocyte migration after EMMPRIN knockdown was observed by a Transwell assay. RESULTS: EMMPRIN knockdown by siRNA markedly abolished the MMP-9 expression by 50% and 40% in macrophages and foam cells, respectively. Migration induced by chemotactic factor MCP-1 and VEGF was significantly attenuated (P<0.05) in monocytes treated with EMMPRIN-siRNA. CONCLUSION: The protein expression and secretion of MMP-9 are down-regulated by EMMPRIN knockdown during monocyte differentiation into macrophages and foam cells. Moreover, EMMPRIN siRNA treatment also prevents monocyte migration. Thus, EMMPRIN plays a key regulatory role for MMP activity and monocyte migration, making it a potential target for pharmacological intervention of atherosclerosis.

g this model, trainees could improve their basic techniques, such as resection and vaporization technique.