OBJECTIVE:To establish the method for the residues determination of 5 organic solvents in teicoplanin raw materi-al and injection. METHODS:Headspace GC was performed on the column with 6% cyanopropylphenyl-94% dimethyl polysiloxane (DB-624)as the stationary phase capillary column,the carrier gas was nitrogen,using the temperature program. The temperature of inlet was 200 ℃,detector was hydrogen flame ionization detector with the flow rate of 1 ml/min,split ratio was 40 ∶ 1 and the vol-ume was 1 ml. RESULTS:Good linearity of ethanol,acetone,ethyl acetate,tetrahydrofuran and triethylamine were obtained(r were 0.999 0-0.999 3);the average recoveries were respectively 95.6%,97.0%,103.2%,94.3%and 98.2%(RSD were 2.1%-4.9%, n=9);RSDs of precision and repeatability tests ≤2.6%;and the minimum detectable concentration were respectively 2,2,2,0.7 and 0.3 μg/ml. CONCLUSIONS:The established method is rapid,sensitive and accurate,and can be used for the residues determi-nation of organic solvents in teicoplanin raw materials and injection.

Objective To evaluate reliability and validity the Chinese-version of chronic pain acceptance questionnaire-8(CPAQ-8).Methods The reliability and validity of CPAQ-8 was tested in 223 old patients with chronic pain.Result The Chinese-version of CPAQ-8 was (23.79±-5.23),AE was (12.84±4.96),PW was(10.97 ±2.90).Cronbach' s of CPAQ-8 was 0.853,and Guttmann Split-Half Coefficient was 0.843.Two factors were extracted by factor analysis through exploratory factor analysis,whose cumulative contribution was 58.217％.While confirmatory factor analysis showed probability level of the modified model was P=0.322,with indexes as follows: x2/df =1.124,GFI =0.979,AGFI =0,956,TLI =0.069,RMSEA =0.024,NFI =0.960,TLI =0.992,CFI =0.995.Conclusion Reliability and validity of CPAQ-8 were both well.

Objective:To explore the correlation between Traditional Chinese Medicine (TCM) excessive patterns and clinical characteristics of acute exacerbation of chronic obstructive pulmonary disease (COPD) complicated with chronic pulmonary heart disease (CPHD) in high altitude environment.Methods:Patients with acute exacerbation of COPD complicated with CPHD admitted to the Pulmonology Department of Qinghai Provincial Hospital of Traditional Chinese Medicine from December 2016 to November 2017 were selected. Demographic data and clinical medical characteristics data of the patients were collected, and TCM patterns differentiation was conducted. The correlation between each pattern type and clinical characteristics and all collected laboratory indexes were analyzed by multivariate logistic regression.Results:Phlegm obstructing lung pattern showed a negative correlation relationship with mMRC score [ OR=0.419, 95% CI (0.219-0.802), P=0.009], PCT [ OR=8.132×10 -11, 95% CI (1.632×10 -16-4.1×10 -5), P<0.001], Hb [ OR=0.971, 95% CI (0.952-0.989), P=0.002] and PaCO 2[ OR=0.914, 95% CI (0.853-0.980), P=0.011]; turbid phlegm obstructing lung pattern showed a negative correlation relationship with gender(0 male, 1 female) [ OR=0.427, 95% CI (0.204-0.892), P=0.024], Hb [ OR=0.960, 95% CI (0.945-0.975), P<0.001], and there was a positive correlation relationship with LVEF [ OR=1.061, 95% CI (1.006-1.118), P=0.028]; phlegm-heat obstructing lung pattern showed a negative correlation relationship with Hb [ OR=0.950, 95% CI (0.927-0.974), P<0.001]and cardiac function grade [ OR=0.468, 95% CI (0.248,0.881), P=0.019], and there was a positive correlation relationship with PCT [ OR=1.118×10 8, 95% CI (1.466×10 4-8.523×10 11), P<0.001] and D-D [ OR=2.283, 95% CI (1.300-4.010), P=0.004]; there was a negative correlation between phlegm and stasis blocking lung pattern with cardiac function grade[ OR=0.309, 95% CI (0.167-0.570), P<0.001], and there was a positive correlation relationship with Hb[ OR=1.060, 95% CI (1.042-1.078), P<0.001]; there was a negative correlation between wet phlegm and blood stasis heat pattern with PCT [ OR=1.266×10 -13, 95% CI (1.658×10 -21-0.1×10 -4), P<0.001], SaO 2 [ OR=0.934, 95% CI (0.892-0.979), P=0.004], LVEF [ OR=0.896, 95% CI (0.826-0.971), P=0.008], D-D [ OR=0.030, 95% CI (0.002-0.508), P=0.015], and there was a positive correlation relationship with CRP [ OR=1.042, 95% CI (1.018-1.067), P<0.001], RBC [ OR=3.411, 95% CI (1.684-6.910), P<0.001], cardiac function grade [ OR=8.573, 95% CI (2.410-30.504), P<0.001], pulmonary arterial pressure difference [ OR=2.091, 95% CI (1.243-3.516), P=0.005]. Conclusions:Male patients are more prone to phlegm and turbidities than female patients. PCT and D-D were the main risk factors of phlegm-heat obstruction syndrome. Elevated hemoglobin is a risk factor for patients with phlegm stasis and lung syndrome. Heart function classification is the main risk factor of phlegm-dampness-stasis heat syndrome.

Objective:To explore the expression of long non-coding RNA (lncRNA) CDK5RAP3 in gastric cancer tissue and its regulatory effect on gastric cancer cell proliferation and invasion.Methods:The expression differences of CDK5RAP3 in gastric cancer tissues and adjacent tissues were analyzed by TCGA database. By transfecting the pcDNA3.1-CDK5RAP3 plasmid into Hs-746T cells, a gastric cancer cell line overexpressing CDK5RAP3 (CDK5RAP3 group) was constructed, and the pcDNA3.1 plasmid was transfected into Hs-746T cells as a control group. The changes of CDK5RAP3 expression in the two groups of cells were detected by real-time quantitative PCR (qRT-PCR). The effects of overexpression of CDK5RAP3 on the proliferation and invasion of Hs-746T cells were detected by CCK-8 assay and Transwell assay, respectively. The binding sites of CDK5RAP3 and miR-223-3p were predicted by the starBase v2.0 database. The direct binding of CDK5RAP3 and miR-223-3p was verified by dual-luciferase reporter gene experiment. The expression levels of miR-223-3p in Hs-746T cells in each group were detected by qRT-PCR. Western blot was used to detect the expression levels of proliferation proteins and invasion proteins in Hs-746T cells in each group. The experimental data were analyzed by SPSS 17.0 software, and the measurement data conforming to the normal distribution were expressed as Mean±SD. The t-test was used to compare between two groups, and the one-way analysis of variance was used to compare the means of multiple groups. Results:Compared with adjacent tissues, the expression level of CDK5RAP3 in gastric cancer tissues was significantly lower ( P<0.01). The expressions of CDK5RAP3 in Hs-746T cells in the control group and CDK5RAP3 group were (1.08±0.77) and (10.63±2.14), respectively, and the difference was statistically significant ( P<0.01). Up-regulation of CDK5RAP3 significantly decreased the proliferation activity of Hs-746T cells ( P<0.05). The number of invasive cells in the control group and CDK5RAP3 group were (137.80±28.72) and (57.76±24.95), respectively, and the difference was statistically significant ( P<0.01). CDK5RAP3 could directly bind miR-223-3p ( P<0.01). The expression of miR-223-3p in Hs-746T cells in control group and CDK5RAP3 group were (6.22±1.20) and (1.01±0.98), respectively, and the difference was statistically significant ( P<0.01). Compared with the control group, up-regulation of CDK5RAP3 significantly reduced the expression levels of proliferation and invasive proteins. Conclusion:The expression of CDK5RAP3 is low in gastric cancer tissue, and CDK5RAP3 inhibits the proliferation and invasion of gastric cancer Hs-746T cells by targeting miR-223-3p.

Many efforts have been made to understand excitotoxicity and develop neuroprotectants for the therapy of ischemic stroke. The narrow treatment time window is still to be solved. Given that the ischemic core expanded over days, treatment with an extended time window is anticipated. Bestrophin 1 (BEST1) belongs to a bestrophin family of calcium-activated chloride channels. We revealed an increase in neuronal BEST1 expression and function within the peri-infarct from 8 to 48 h after ischemic stroke in mice. Interfering the protein expression or inhibiting the channel function of BEST1 by genetic manipulation displayed neuroprotective effects and improved motor functional deficits. Using electrophysiological recordings, we demonstrated that extrasynaptic glutamate release through BEST1 channel resulted in delayed excitotoxicity. Finally, we confirmed the therapeutic efficacy of pharmacological inhibition of BEST1 during 6-72 h post-ischemia in rodents. This delayed treatment prevented the expansion of infarct volume and the exacerbation of neurological functions. Our study identifies the glutamate-releasing BEST1 channel as a potential therapeutic target against ischemic stroke with a wide time window.