Objective:To investigate whether the AP-PCR fingerprint of mutans streptococci(MS) can be displayed by PAGE-AgNO 3 staining. Methods: Amplification products of 200 MS clinical isolates by AP-PCR was separated and stained by ?=3.5%PAGE-AgNO 3 and agarose-EB respectively. Results were compared and the agreement value of Kappa between two methods was calculated. Results: ?=3.5%PAGE-AgNO 3 discerned both homogeneity and heterogeneity of MS genotypes, just as agarose-EB,Kappa value for agreement was 1.00 . Moreover, more bands was showed by PAGE-AgNO 3 staining than by agarose-EB, so PAGE-AgNO 3 gave a clearer pattern than agarose-EB. Conclusion: AP-PCR fingerprint of MS can be displayed by ?=3.5%PAGE-AgNO 3 staining.

This paper reports the methods of inducing animal model of abdominal aortic aneurysm(AAA) and the research on etiology.The formation of AAA is the result of cooperation of multifactors such as genetic and biochemistric facfors.Different animal models of AAA can provide a possibility in researching the etiology and pathogenesis of AAA etc, and useful in judging the therapy and prognosis .

Objective We tried to design a Instructor Rating Scale Identified by Nursing Students,and then evaluate its rehability and validity.Methods The original item pool was formulated by investigating 351 nursing students with convenience samphng method to develop a prehminary scale.Then it was used to investigate 273 nursing students to test its rehability and validity.Results The formal scale consisted of six dimensions,which contained 19 items.The cumative contribution rate of these dimensions was 62.30％.The Cronbach's α coefficient was 0.54,test and re-test reliability was 0.48.Conclusions The Instructor Rating Scale Identified by Nursing Students can be applied to evaluate the instructors by nursing students.

Objective To establish brain hypoxic-ischemic (HI) model using postnatal day 3(P3) SD rats and evaluate the apoptotic neuronal cells in cerebral cortex and neurofunctional development.Methods The P3 rats were randomly divided into HI group (n=35) and control group(n=18).HI was induced in P3 rats with right carotid artery ligation followed by 2.5 h hypoxia in 60 mL?L-1 oxygen at 37 ℃.The injury of neural cells in the cerebral cortex was evaluated by tumor necrosis factor receptor-1(TNF-R1),Caspase-3 immunostaining and Hematoxylin-Eosin (HE) staining in 24 h and 7 d after HI,respectively.Furthermore,the neurofunctional development was evaluated by negative geotaxis reflex and eye opening time.The data were analyzed by SPSS 12.0 software.Results Caspase-3 and TNF-R1 positive cells were abundant in the ipsilateral cortex at 24 h after HI,compared with contralateral part and control group(P

Objective To explore the characteristics and treatment of pain after inflammatory spinal demyelination. Methods 271 patientssuffered from inflammatory spinal demyelination with pain were analyzed retrospectively. Results Acute radicular pain and Lhermitte'ssign were common in the acute pain syndromes. Individual therapy showed a benefit of decreased pain. Conclusion Pain is a commonclinical symptom of inflammatory spinal demyelination. Individualized therapeutic decisions could relieve symptom and improve outcome.

Adult ; Dust ; Humans ; Middle Aged ; Noise, Occupational ; Occupational Diseases ; epidemiology ; Risk Factors ; Welding ; Workplace ; Young Adult

Objective To evaluate the effects of alpha-lipoic acid (α-LA)on autophagy in human skin fibroblasts (HSFs). Methods HSFs at passage 3 - 5 were divided into several groups to be cultured with α-LA at final concentrations of 0, 0.01, 0.05, 0.10, 0.15, 0.20 and 0.50 mmol/L for 4, 12 and 24 hours, respectively. Methyl thiazolyl tetrazolium(MTT)assay was performed to evaluate cellular proliferative activity, monodansylcadaverin(MDC)staining to determine autophagy levels, and Western blot to measure the expression of the microtubule-associated protein 1 light chain-3B(LC3-B). Results After incubation for 24 hours, there was a significant difference in the proliferative activity of HSFs among all the groups (F = 10.41, P < 0.05), while no significant differences were observed after incubation for either 4 or 12 hours (F = 2.85, 1.34, respectively, both P > 0.05). MDC staining also showed a significant difference in the percentage of autophagosome-positive cells among all the groups after 24-hour incubation (F = 8.03, P < 0.05), but no significant difference after either 4- or 12-hour incubation (F = 0.11, 0.10, respectively, both P > 0.05). Western blot revealed that the degree of conversion from LC3-Ⅰ to LC3-Ⅱ(LC3-Ⅱ/LC3-Ⅰratio)was significantly different among all the groups after 24-hour incubation (F = 37.49, P < 0.05), but similar after 4- and 12-hour incubation (F = 3.38, 2.13, respectively, both P > 0.05). Conclusion α-LA may inhibit basal autophagy in HSFs.

Objective To evaluate the effects of ultraviolet A (UVA) on autophagy in human skin fibroblasts (HSFs).Methods Cultured HSFs were randomly divided into chronic and acute UVA radiation groups.HSFs in the chronic UVA radiation groups were irradiated with UVA at 5,10 and 20 J/cm2 separately once a day for 4 consecutive days,with HSFs receiving no radiation serving as the chronic radiation control group;HSFs in the acute UVA radiation groups received a single session of radiation with 5,10,30 and 60 J/cm2 UVA separately,with HSFs receiving no radiation serving as the acute radiation control group.After additional culture for different durations,methyl thiazolyl tetrazolium (MTT) assay was performed to evaluate the proliferative activity of HSFs,monodansylcadaverin (MDC) staining to determine autophagy levels,and Western blot analysis to track the conversion of the microtubule-associated protein 1 light chain-3 (LC3)-Ⅰ to LC3-Ⅱ.Statistical analysis was carried out by using one-way analysis of variance followed by Students-Newman-Keuls (SNK) test for multiple-group comparisons and by the independent sample t test for two-group comparisons.Results The cellular proliferative activity significantly decreased in the 3 chronic radiation groups at 1 hour after the final UVA radiation compared with the chronic radiation control group (F =155.5,P ＜ 0.05),and in the 4 acute radiation groups at 1,6 and 12 hours after UVA radiation compared with the acute radiation control group (F =1 335,1 649,2 774,all P ＜ 0.05).MDC staining showed that the autophagy levels in HSFs significantly increased in the 3 chronic radiation groups after UVA radiation compared with the chronic radiation control group (F =748.62,P ＞ 0.05),but showed no significant changes in any of the acute radiation groups at 1,6 or 12 hours after UVA radiation compared with the acute radiation control group (F =0.014,0.004,0.002,all P ＞ 0.05).The ratio of LC3-Ⅱ to LC3-Ⅰ was significantly elevated in all the 3 chronic radiation groups at 1 hour after UVA radiation compared with the chronic radiation control group (t =9.002,21.772,18.33,all P ＜ 0.05),but experienced no obvious changes in any of the acute radiation groups at 1,6 or 12 hours after UVA radiation compared with the acute radiation control group (F =0.13,0.27,0.06,all P ＞ 0.05).Conclusion Chronic UVA radiation can upregulate autophagy levels in HSFs,but acute UVA radiation has no evident effects on it.

5-(4-Hydroxyphenyl)-3H-1,2-dithiole-3-thione (ADT-OH) is a slowly releasing H2S donor with some neuroprotective effect.In order to study the structure-activity relationships,seventeen compounds (Y1-Y17) were synthesized by modification of ADT-OH at the aromatic ring position,and their structures were confirmed by 1H NMR,13C NMR and HR-MS.Among them,6 compounds (Y4,Y13-Y17) were novel compounds.Their effects had been evaluated on HT-22 hippocampal neuron cells damaged by glutamate with MTF method.The pharmacological results demonstrated that all the Y compounds had potent neuroprotection at most of the tested concentrations (1-100 μmol/L).Compounds Y1-Y9 and Y11 significantly improved the survival rates of the damaged cells at 1-100 μmol/L (P ＜0.01).Specially,compounds Y1,Y4,Y6-Y9,Yu are more potent than their parent compound ADT-OH at concentration of 1-10 μmol/L,which is worthy of further study.

Objective To investigate the effects of BMI-1 expression inhibition by RNA interference on the radiosensitivity of esophageal cancer TE-13 cells and its mechanism.Methods The siRNA based on the sequence of BMI-1 mRNA was synthesized to transfect cultured TE-13 cells as BMI-1 siRNA group,a negative one was synthesized to transfect cultured TE-13 cells as negative control group (NC group),and untransfected TE-13 cells were named as control group.The expression of the BMI-1 mRNA and protein in TE-13 cells was measured by quantitative real-time PCR and Western blot,respectively.The cell proliferation and the radiosensitivity of TE-13 cells were measured by MTS and colony-forming assay,respectively.Flow cytometry was used to analyze cell cycle and apoptosis.The expression of BCL-2 and BAX in TE-13 cells was measured by Western blot.Comparison between groups was made by analysis of variance.Results The BMI-1 siRNA group had significantly lower expression of BMI-1 mRNA and protein than the control group and the NC group (P=0.000,0.000).The proliferation of TE-13 cells in the BMI-1 siRNA group decreased significantly after irradiation (P=0.031).The colony-forming assay showed that the BMI-1 siRNA group had a significantly higher radiosensitivity than the control group and the NC group (P=0.000).After irradiation,the BMI-1 siRNA group had a significantly lower percentage of cells in G2/M phase than the control group and the NC group (P=0.000,0.000).The BMI-1 siRNA group had a significantly increased apoptosis rate (P=0.000,0.000),significantly reduced expression of BCL-2(P=0.000,0.000),and significantly increased expression of BAX after irradiation (P=0.000,0.000).Conclusions BMI-1 siRNA can inhibit the expression of BMI-1 gene in esophageal cancer TE-13 cells,eliminate the cell cycle arrest in G2/M phase,induce cell apoptosis after ionizing irradiation in vitro,and increase the radiosensitivity,which may be related to the regulation of the expression of BCL-2 and BAX.