Objective:To evaluate the reliability and validity of the Chinese version of Interpersonal Stress-Coping Inventory for Undergraduates(ISI).Methods:Totally 421 college students of 1～3 grades in two colleges of Anhui province were selected.They were asked to complete the ISI and Simplified Coping Style Questionnaire(SCSQ)at the same time to test the reliability and validity of ISI.Two weeks later,52 of them were retested to test the re-test reliability.Results:Cronbach α of the Chinese version of ISI was 0.79,re-test reliability was 0.87.ISI Scores were correlated with SCSQ scores(r=0.69).Exploratory factor analysis was applied to the data,and three subscales were derived:positive coping,negative coping,and dilution coping.The factor loadinps were 0.41～0.68.The explained variances were 14.82,14.10,and 7.06 respectively.Conclusion:The Chinese version of Interpersonal Stress-Coping Inventory has good psychometric quality and can be used in Chinese undergraduates of interpersonal stress coping research.

Objective To detect the percentage of cultured neuron apoptosis after the neurons were treated with anoxia and specific inhibitors of protein kinase A (PKA) and protein kinase C (PKC). Methods After establishment of the model of neurons cultured under hypoxic condition, the neurons were cocultured with different concentrations of Rp-cAMP and Calphostin C, specific inhibitors of protein kinase A and C, respectively. Then neurons were cultured under an ischemic condition until the number of survived neurons, the activity of mPKA,and mPKC, and the apoptotic neurons stained by TUNEL in each group were observed. Results The activity of mPKA and mPKC significantly increased after the onset of hypoxia. With the increases in concentrations of Rp-cAMP or Calphostin C, the percentage of apoptotic neurons obviously decreased or increased, respectively. Conclusion The pathways of PKA and PKC signal transduction may participate in the hypoxic neuron injury. The functions of these two kinases are opposite for apoptotic regulation. It suggests that the signal transduction of PKA and PKC in hypoxic neurons belongs to a monophasic controlling system and the ratio of PKA to PKC in cells may determine the survival of hypoxic neurons.

Objective To evaluate the effects of dexmedetomidine-propofol-fentanyl combined anesthesia on somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) in patients undergoing cervical spine surgery. Methods Thirty-six patients undergoing cervical spine surgery were randomly divided into 2 groups (n = 18 each): propofol-fentanyl combined anesthesia group (group C) and dexmedetomidine-propofol-fentanyl combined anesthesia group (group D). Anesthesia was induced with TCI of propofol and iv injection of fentanyl.After the consciousness disappeared, a laryngeal mask airway was placed and the patients were ventilated. In group D, dexmedetomidine 0.5 μg/kg was injected over 10 min after the consciousness disappeared, followed by an infusion at a rate of 0.5 μg·kg-1 ·h-1 until the end of surgery. In group C, the equal volume of normal saline was administered instead of dexmedetomidine. SEPs (P15-N20) amplitudes and latency were measured and recorded before dexmedetomidine administration and at 10 min of dexmedetomidine infusion. The no-elicitation of MEPs was recorded. Results Compared with group C, there was no significant difference in P15-N20 amplitudes and latency in group D. The no-elicitation rate of MEPs in two groups was 0. Conclusion Dexmedetomidine-propofol-fentanyl combined anesthesia does not affect SEPs and MEPs in patients undergoing cervical spine surgery.

Objective To investigate the relationship between the protein kinase A (PKA) and apoptosis of cultured neurons after hypoxia Methods Model of cultured rat neuron under hypoxia condition was established. Rp cAMP, a specific inhibitor for PKC, at 4 different concentrations were separately cocultured for 2 h with the neurons having been cultivated under hypoxic condition for different times The activity of PKA, the expression of caspase 3 and the situation of neuron apoptosis were studied Results With the prolonging of hypoxic time the activity of PKA was increased significantly And the expression of activated caspase 3 and apoptotic DNA were increased as well The positive rate of fluorescence staining and the average fluorescent intensity of caspase 3 and TUNEL were significantly decreased along with the increasing concentration of Rp cAMP Conclusion ① PKA and caspase 3 are involved in the neuronal apoptosis after hypoxia ② Rp cAMP can attenuate the hypoxic neuronal apoptosis through the signal transduction of caspase 3 ③ The activating of PKA can aggravate hypoxic neuron apoptosis

Objective To explore the effect and possible mechanism of protein kinase C (PKC) on the apoptosis of cultured neurons after hypoxia Methods Model of cultured rat neurons under hypoxia condition was established. Calphostin C, an inhibitor for the catalytic subunit of PKC, at 4 different concentrations were separately cocultured for 2 h with the neurons having been cultivated under hypoxic condition for different times The activity of membrane PKC (mPKC), the expression of Bcl 2 and the situation of neuron apoptosis were studied Results With the prolonging of hypoxic time the activity of mPKC was increased significantly And the expression of Bcl 2 was decreased obviously and positive rate of TUNEL were significantly increased in a calphostin C concentration dependent manner Conclusion ① The activation of mPKC and Bcl 2 are involved in the apoptosis of neurons after hypoxia ② Hypoxia and calphostin C can aggravate the hypoxic neuronal apoptosis through the signal transduction of Bcl 2 ③ The activation of PKC can protect neuron against hypoxia

Objective To establish a cerebral hemorrhage model in rats by local injection of type Ⅳcollagenase, and explore the factors affecting the speed and volume of hematoma formation Methods A total of 150 healthy male Wistar rats weighing from 200 to 250 g were randomly divided into 3 groups, control, collagenase, and collagenase/heparin groups Animals in those groups received injection of saline, collagenase (0 2 U/?l), and collagenase (same dose) and heparin (2 U/?l) with different volume respectively at the caudate nucleus The volume of the hematoma in the rats ( n =6 at each time point) was observed 6, 12, and 24 h, and 3, 7d after the injection Results Permeation of blood was found in 12 h after injection in control group Hematoma about 3 mm in diameter was found in 3 d after injection in collagenase group, while in collagenase/heparin group, it was found in 24 h Conclusion Cerebral hemorrhage model established by local injection of collagenase/heparin in saline solution is ideal and reliable, and the size of hematoma is in correlation with the volume of solutions injected into the brain

Objective To study the inhibitory effect of antigliomatin on the expression of vascular endothelial growth factor(VEGF) in rat C6 brain glioma cells.Methods The rat brain glioma cells was cultivated with the stationary culture technique.The different rat C6 brain glioma cells groups were treated with 2,4,8,and 16 ng?L-1 antigliomatin for 72 h in vitro and then the inhibitory effect of antiglioma on the expression of VEGF was observed with immunohistochemical method.Results The cytoplasm and(or) nucleus of most VEGF positive cells were stained to yellow brown.VEGF expressed significantly in cytoplasm of the rat C6 glioma cells in control group.The density of the VEGF positive cells was decreased in glioma compared with control group after treated with antigliomatin for 72 h(P

Objective To investigate the influence of the purging fire and removing toxin method on chemokines and adhesion factors related to vascular endothelialitis injury induced by toxin of trimeresurus stejnegeri bite.Methods ① Animal experiment:50 healthy New Zealand white rabbits were chosen.According to random numbers generated by statistical software,they were divided into normal control group,model group,low,middle and high dose Sheshang capsule groups,10 in each group.Trimeresurus stejnegeri bite model was replicated by injecting 0.75 mL/kg snake venom into subcutaneous tissues of rabbits' right hind legs.And the same volume of normal saline was injected into the rabbit in the normal control group.After the model was established for 6 hours,the rabbits in low,middle and high dose Sheshang capsule groups received 174,348 and 522 mg· kg-1 · d-1 of Sheshang capsule solution respectively (the content of capsules was dissolved in normal saline to make liquid with 17.4,34.8 and 52.2 g/L Sheshang solution respectively,so the volume of gavage of each group was 10 mL· kg-1 · d-1);in the model and normal control groups,the same amount of normal saline was given by gavage,once daily for consecutive one week.24 hours after the last gavage,the blood of the rabbits was collected through an auricular border vein and the serum was separated by centrifuge ready for use.Meanwhile,the whole abdominal aorta segment of the rabbit was harvested and kept them in liquid nitrogen ready for use.② Cell experiment:human umbilical vascular endothelial cell (HUVEC) was cultured with MEM for 24 hours.The solution was replaced and according to the random number generated by statistical software,the cells were divided into blank control group,model group and low,middle,high dose Sheshang capsule medicinal serum groups,10 wells in each group.Trimeresurus stejnegeri toxin cell model was reproduced by addition of 5 mg/L snake venom into the cell culture medium.After 6-hour culture,the cells of model group and blank control group received 10％ normal rabbit serum,and the cells of low,middle and high dose Sheshang medicinal serum capsule groups received serum containing 5％,10％ and 15％ drug,respectively.After culture for 72 hours,the cells were collected and the total RNA was extracted.The real-time fluorescent quantitative polymerase chain reaction (qPCR) was used to detect the levels of mRNA of interleukin-8 (IL-8),monocyte chemoattractant protein-1 (MCP-1),intercellular adhesion molecule-1 (ICAM-1) and vascular endothelial cell adhesion molecule-1 (VCAM-1) in the vascular endothelial cells of rabbit aorta abdominalis and human umbilical vein,and the content of serum E-select element (CD62E) was measured by enzyme linked immunosorbent assay (ELISA).Results In model group,the expression levels of mRNA in IL-8,MCP-1,ICAM-1,VCAM-1 and the content of CD62E were all increased significantly in the endothelial cells of rabbit aorta abdominalis and HUVEC compared with those in control group [when the mRNA expression levels of IL-8,MCP-1,ICAM-1 and VCAM-1 in normal and blank control group were all being 1,the mRNA expression levels (2-△ △Ct) of the above mentioned inflammatory factors and adhesion molecule in animal model group were 3.96 ± 0.39,3.07 ± 0.27,3.71 ± 0.26,3.94 ± 0.26,and the mRNA expression levels (2-△ △Ct) of the above mentioned inflammatory factors and adhesion molecule in HUVEC model group were 3.53±0.70,2.24±0.48,3.13±0.44,2.80±0.13,respectively,all P ＜ 0.01].The content of CD62E in serum was increased significantly in model group compared with that in normal control group (μg/L:1.31 ± 0.22 vs.0.82 ± 0.13,P ＜ 0.01),the mRNA expression levels of IL-8,MCP-1,ICAM-1 and VCAM-1 were decreased significantly in low,middle,high dose Sheshang capsule groups compared with those in model group in endothelial cells of aorta abdominalis of rabbits and HUVEC [abdominal aorta:IL-8 mRNA (2-△ △Ct) were 1.13 ± 0.19,1.26 ± 0.16,1.27 ± 0.17 vs.3.96 ± 0.39,MCP-1 mRNA (2-△ △ Ct) were 1.79 ± 0.24,2.22 ± 0.38,1.76±0.19 vs.3.07±0.27,ICAM-1 mRNA (2 △△Ct) were 2.05±0.11,1.68±0.09,2.37±0.48 vs.3.71±0.26,VCAM-1 mRNA (2-△△Ct) were 1.59±0.08,1.40±0.11,1.84±0.11 vs.3.94±0.26;HUVEC:IL-8 mRNA (2-△△Ct) were 2.33±0.59,2.82±0.82,2.51±0.77 vs.3.53±0.70,MCP-1 mRNA (2-△△Ct) were 1.59±0.35,1.48±0.36,1.54±0.29 vs.2.24±0.48,ICAM-1 mRNA (2-△△Ct) were 1.46±0.38,1.77±0.65,1.73±0.50 vs.3.13±0.44,VCAM-1 mRNA (2-△△Ct) were 2.49±0.24,2.18±0.19,2.45±0.24 vs.2.80±0.13,all P ＜ 0.05].The contents of CD62E were decreased significantly in middle,high dose Sheshang capsule groups compared with the content in model group (μg/L:1.01 ±0.14,1.04±0.13 vs.1.31 ±0.22,all P ＜ 0.01),but there were no statistical significant differences among the three drug group (all P ＞ 0.05).Conclusion The therapy of purging fire and removing toxin can treat vascular endothelial injury by inhibiting the inflammatory response induced by Trimeresurus stejnegeri bites.

Objective:To investigate the association of plasma EBV-DNA copy number, serum cytokines and B symptoms in patients with extranodal natural killer/T-cell lymphoma, nasal type (ENKTL), unravel the mechanism and assess the prognostic value of clinical indicators.Methods:Clinical data of 173 newly-diagnosed ENKTL patients (116 male, 57 female; median age: 43, 4 to 71 years)were retrospectively analyzed. According to Ann Arbor stage, 126 cases were classified as stage I-II and 47 cases of stage Ⅲ-IV. The primary sites of tumors included nasal cavity (n=100), extranasal upper aerodigestive tract (extranasal UADT, n=34), and extra-upper aerodigestive tract (extra-UADT, n=39). Prior to treatment, 91 patients had B symptoms and 82 cases of without B symptoms. According to plasma EBV-DNA copy levels, all patients were divided into the negative group (n=36), low load group (<10 4 copies/ml, n=73) and high load group (≥10 4 copies/ml, n=64). Serum cytokines including IFN-γ, IL-2, IL-4, IL-6, IL-10 and TNF-α were detected. Correlation analysis was performed by Cochran-Armitage trend test and Spearman correlation analysis. Survival analysis was conducted using univariate and multivariate Cox regression hazard analysis and survival curves were derived from Kaplan-Meier survival analysis. Results:The incidence of B symptoms and fever showed a significant upward trend with the increasing plasma EBV-DNA copy levels. In addition, serum levels of IFN-γ, IL-6 and IL-10 cytokines were higher in patients with B symptoms than those without B symptoms (all P<0.05). Serum IFN-γ, IL-6, and IL-10 levels were also positively correlated with plasma EBV-DNA copy number. The occurrence of B symptoms was associated with high-risk clinical features including advanced stage, primary tumor invasion, regional lymph node involvement, and elevated pre-treatment LDH. Survival analysis showed that stage, B symptoms, plasma EBV-DNA, and the above serum cytokines affected the prognosis of overall survival (OS) and progression-free survival (PFS) (all P<0.05). However, multivariate analysis showed that the occurrence of B symptoms was not an independent prognostic factor of ENKTL patients. Conclusion:This exploratory study suggests that the incidence of B symptoms is associated with increasing levels of EBV-DNA copies and cytokines, and these indicators are also important factors influencing the prognosis of ENKTL patients.