Objective To investigate the role of astrocytes activation in post herpetic neuralgia (PHN). Methods The kunming mice (20-25 g) were used in this study. Resiniferatoxin was injected into the peritoneal cavity.Immunofuorescence was used to detect the activation of astrocytes , mechanical paw withdrawal threshold (MWT)and thermal withdrawal latency (TWL) were used to assay the mechanical allodynia and thermal hyperalgesia, respectively. Fluorocitrate, an inhibitor of astrocytes was intrathecally (i.t.) or intraperitonealy (i. p.) injected into the mice. Results Compared with the vehicle group, MWT was decreased, and TWL was increased significantly in the RTX group. Pre-treatments of fluorocitrate (Fc, i.t.,or i.p.) inhibited the decrease of MWT. Conclusion The activation of astrocytes mediates the post herpetic neuralgia.

Objective To evaluate the relationship between sevoflurane-induced cognitive decline and α1A norepinephrine receptor (ADRA1A) in the cerebral cortex of rats.Methods Forty-eight cleangrade healthy adult Sprague-Dawley rats (24 male,24 female),weighing 220-260 g,aged 3-4 months old,were divided into 2 groups (n =24 each) using a random number table method:control group (group C) and sevoflurane group (S group).Group S inhaled 3％ sevoflurane for 5 h.Rats underwent the Barnes maze test on days 1 and 7 after anesthesia.Rats were sacrificed immediately after anesthesia and on days 1 and 7 after anesthesia,and the cerebral cortex was removed for determination of the expression of ADRA1A protein and mRNA (by Western blot or fluorescent quantitative real-time polymerase chain reaction).Results Compared with group C,the number of entering incorrect holes was significantly increased,and the latency of entering the target hole and the distance were prolonged,and the expression of ADRA1A protein and mRNA in cerebral cortex was down-regulated at each time point in group S (P＜0.05).Conclusion The mechanism of sevoflurane-induced cognitive decline is related to down-regulated expression of ADRA1A in the cerebral cortex of rats.

Objective To evaluate the relationship between sevoflurane-induced cognitive impairment and α1B adrenoceptors (ADRA1B) and ADRA1D in the cerebral cortex of rats.Methods Forty-eight SPF adult Sprague-Dawley rats (half male,half female),weighing 220-260 g,were divided into control group (C group,n =24) and sevoflurane group (S group,n =24) using a random number table method.Group C and group S inhaled air and 3％ sevoflurane,respectively,for 5 h.Eight rats in each group were sacrificed immediately after anesthesia,and the cerebral cortex was removed.Eight rats in each group were selected on days 1 and 7 after anesthesia and underwent Barnes maze test.The rats were then sacrificed,and the cerebral cortex was removed.The expression of ADRA1B and ADRA1D protein and mRNA in cerebral cortex tissues was detected by Western blot and fluorescent quantitative real-time polymerase chain reaction,respectively.Results Compared with group C,the number of entering incorrect holes was significantly increased at 1 and 7 days after anesthesia,the latency and total distance to enter the target hole were prolonged,and the expression of ADRA1B and ADRA1D protein and mRNA in cerebral cortex was down-regulated immediately after anesthesia and at 1 and 7 days after anesthesia in group S (P＜0.05).Conclusion The mechanism underlying sevoflurane-induced cognitive impairment may be related to the down-regulated expression of ADRA1B and ADRA1D in cerebral cortex of rats.

Objective:To investigate the effects of exogenous nitric oxide (NO) on radiation response of nasopharyngeal carcinoma 5-8F radiotherapy resistant cell line (5-8FRs) and to provide experimental basis for finding suitable radiosensitizer on nasopharyngeal carcinoma.Methods:5-8FRs cells were cultured in vivo and treated with sodium nitroprusside (SNP) of different concentrations. The inhibition rate of cell proliferation was detected by cell counting kit-8 (CCK8) method. A concentration of IC 01 SNP (1% SNP) which had no obvious effect on the proliferation of 5-8FRs cells was screened out. The 5-8FRs cells were intervened with 1, 2, 4, 6 Gy and 8 Gy radiation to determine the radiation dose of IC 15 (15% radiation dose). 5-8FRs cells were treated with IC 01 SNP concentration, IC 15 radiation dose and radiotherapy alone or in combination. The morphological changes of 5-8FRs cells were observed under microscope. The proliferation inhibition rate of each group was detected by CCK-8 method, the apoptosis was detected by flow cytometry, and the concentration of NO in cell supernatant was detected by nitrate reduction method. Results:⑴ The proliferation of 5-8FRs had been inhibited in a concentration-dependent manner by SNP and a dose-dependent manner by radiation. The SNP concentration of IC 01 was (513.89±14.69)μmol/L (SNP group). The radiation dose of IC 15 was (3.96±0.33)Gy (radiotherapy group); ⑵ Compared with single SNP group and radiotherapy group, the morphology of 5-8FRs cells in combination group (SNP+ radiotherapy) was significantly different, floating cells increased significantly, the number of adherent cells gradually decreased and lost their original morphology; ⑶ SNP concentration of IC 01 had no significant effect on the proliferation of 5-8FRs cells, but the inhibition rate of combined group was significantly higher than that of radiotherapy group ( t=7.708, P<0.01); The concentration of NO in the combined group was significantly higher than that in the single radiotherapy group [(310.03±5.76)μmol/L vs (77.34±2.60)μmol/L, P<0.05]; ⑷ The spontaneous apoptosis rate of 5-8FRs was (1.35±0.06)%, while the apoptosis rate in the group of IC 01SNP was (2.22±0.37)%, with no significant difference. The apoptosis rate of 5-8FRs in the combined group (50.27±2.24)% was significantly higher than that of the group of IC 15 radiation dose(15.37±0.65)%. Conclusions:Under no obvious toxicity to cells themselves circumstances, exogenous nitric oxide with appropriate concentration could significantly enhance the radiosensitivity on 5-8FRs.

Objective To investigate the clinical features of aortic dissection (AD) and emergency treatments. Methods Data from 784 patients with aortic dissection were collected in the Department of Emergency from January 2000 through December 2009. A retrospective analysis was carried out to determine the survival rate, mortality rate and treatment efficiency. Results Pain was the most common onset symptom (77.7% , 609/784). The majority of patients (86.5%) had essential hypertension (678/784). All the patients with preoperative diagnosis of aortic dissection underwent emergency medical intervention by internists resulting in 81.5% survival rate (639/784) and 18.5% mortality rate (145/784). There were 157 patients without improvement (20.0% ) and the total efficiency rate was (83. 1% ). The efficiency rate of conventional treatment was 76.4% , while the efficiency rate of triple four-procedure treatment was 89. 8% (P<0.05). Of them, 139 patients (17. 7% ) died in the hospital. Among them,. 26 patients died within 24 hours (18.4% ) and 47 cases died within 48 hours (33. 8% ) and 66 patients died within 72 hours (47.2% ). There were 92 patients who refused treatments after diagnosis, and among them, 81 patients died within 72 hours (88.04% ). The difference in mortality rate between two groups was significant (P<0.05). Conclusions The diagnosis of aortic dissection depends on detailed history, physical examination and CT or MRI imaging. Analgesia, sedation and control of blood pressure are essential for emergency treatments. Early diagnosis and effective emergency treatments are the critical strategy for the early surgical intervention and time window for further treatment to improve the survival rate of AD.

Objective    To explore the effects of PKD1 gene on mouse aortic smooth muscle (MOVAS) cells autophagy. Methods    The shRNA and over-expression lentiviral vectors for the target gene of PKD1 were constructed. MOVAS cells were infected by a number of successful packaging shRNA (PKD1 knockdown) or ETS-1 (PKD1 over-expressing) lentiviral vectors, and qPCR was used to test interference and over-expressing effects. Then qPCR and Western blotting were used to detect the expression levels of autophagy markers including Atg5, Beclin1 and LC3 in control group, shPKD1 group and ETS-1 group. Results    Compared with the control group, PKD1 mRNA level was decreased in the shPKD1 group (P<0.05); ETS-1 and PKD1 mRNA levels were increased in the ETS-1 group (P<0.05). In contrast with the control group, the mRNA levels of autophagy markers including Atg5 (P<0.05) and Beclin1 (P<0.01) were obviously decreased in the shPKD1 group, but they were obviously increased in the ETS-1 group (P<0.001). Protein levels of Atg5, Beclin1 and LC3 were significantly decreased in the shPKD1 group (P<0.05), but they were increased obviously in the ETS-1 group (P<0.05) in contrast with the control group. Conclusion    PKD1 gene is involved in MOVAS cells autophagy, low expression of PKD1 gene can inhibit autophagy and high expression of PKD1 promotes autophagy in vascular smooth muscle cells.

To explore the pharmacogenomic markers that affect the platinum-based chemotherapy response in non-small-cell lung carcinoma (NSCLC), we performed a two-cohort of genome-wide association studies (GWAS), including 34 for WES-based and 433 for microarray-based analyses, as well as two independent validation cohorts. After integrating the results of two studies, the genetic variations related to the platinum-based chemotherapy response were further determined by fine-mapping in 838 samples, and their potential functional impact were investigated by eQTL analysis and in vitro cell experiments. We found that a total of 68 variations were significant at P < 1 × 10^-3 in cohort 1 discovery stage, of which 3 SNPs were verified in 262 independent samples. A total of 541 SNPs were significant at P < 1 × 10^-4 in cohort 2 discovery stage, of which 8 SNPs were verified in 347 independent samples. Comparing the validated SNPs in two GWAS, ADCY1 gene was verified in both independent studies. The results of fine-mapping showed that the G allele carriers of ADCY1 rs2280496 and C allele carriers of rs189178649 were more likely to be resistant to platinum-based chemotherapy. In conclusion, our study found that rs2280496 and rs189178649 in ADCY1 gene were associated the sensitivity of platinum-based chemotherapy in NSCLC patients.