This study was aimed to observe the acute toxicity and long-term toxicity of Meng-Gen-Wu-Su-18 (MGWS-18) Pills, in order to provide references for safety application of this medicine in the clinical practice. MGWS-18 Pills suspension was intragastric administered to mice twice (0.2 mL/10 g) in 6 hours with maximal con-centration (0.4 g·mL-1). And the acute toxicity reaction was observed for 14 days. The dose of maximum, middle and minimum (3.67 g·kg-1, 1.84 g·kg-1, 0.92 g·kg-1) of MGWS-18 Pills were intragastric administered continuously to rats once a day for 180 days. The rats were observed 60 days after drug withdrawal. The results showed that the maximal tolerated dose (MTD) of MGWS-18 Pills was bigger than the dose of 16 g·kg-1 (which was equivalent to 436.36 times in clinical doses). There were significant differences on ALB, UREA, AST, TBIL, and CHOL between the control group and the maximum dose group of MGWS-18 Pills (P<0.05, or P<0.01) after 180 days of medica-tion. There were significant differences on ALB and UREA between the control group and the middle dose group (P< 0.05). There was no significant difference between the control group and the minimum dose group. Protein cast and degeneration necrosis at different levels of the epithelial cells of the proximal tubules were appeared in the maximum dose group after medication for 180 days. After 60 days of drug withdrawal, there were no significant dif-ferences on the general condition, body weight, hematological indexes, serum biochemical indexes, organ coefficient and etc. between the control group and each animal group. There was recovery tendency on the kidney damage of the maximum dose group. It was concluded that the basic safety intragastric administration dosage of MGWS-18 Pills in rats was 0.92 g·kg-1 (which was equivalent to 25 times in clinical doses).

[Objective]To investigate the methord of nursing care of patients with cervical fracture-dislocation and spinal cord injuries during the perioperative period.[Method]Fifty-six patients with cervical fracture-dislocation and spinal cord injuries experienced preoperative training,psychology nursing and posture exercise,and postoperative position nursing and founctional exercising.The improvement of spinal cord founction was observed.[Result]All patients were followed up from 6 to 31 months,with an average of 17.6 months.According to JOA scores,the preoperative scores was from 0 to 13,with an average of 7.76 points.The postoperative score was 6-17 with an average of 10.3.The relief rate was 68.5%.Satisfaction rate was 74.1%.[Conclusion]The perioperative nursing is important for preventing and lessening complications,achieving good operative effect and promoting rehabilitation.

Objective To investigate the effect and mechanism of low-dose remifentanil(RF)on systemic artery tension of baby rabbit with septic shock.Methods Thirty-six systemic artery strips were prepared from 12 baby rabbits and randomly divided into 6 groups:control group,lipopoly-saccharide(LPS)group,RF group,LPS + RF group,NG-nitro-L-arginine(L-NNA)pretreated group,LPS + L-NNA pretreated group.Each group had six rings(n =6).The effect of low-dose RF on the systemic artery tension of baby rabbit with septic shock was observed with isolated vascular ring technique.The change was also obversed after L-NNA pretreatment.Results In control group:the relaxant rates after low-dose RF at the time point of 5 min,10 min,20 min were(18.48±3.96)％,(23.63±4.42)％,(28.33±3.73)％(P＜0.05),compared with NS group.After pretreatment with L-NNA,RF-related relaxant rates of systemic arteries decreased significantly to(8.15 ± 1.01)％,(13.08 ± 1.46)％,(18.54 ±2.94)％(P ＜ 0.05).In LPS group,low dose RF(4 μg/L)did not bring out any response to systemic arteries(P ＞0.05).The tension was not affected with pretreatment of L-NNA(P ＞ 0.05).Conclusion These results suggest that low dose RF has relaxant effect on systemic arteries of baby rabbits,and NO may be involved.Low dose RF has no relaxant effect on LPS-pretreated systemic arteries of baby rabbits,and it has no association with NO.

Objective To investigate the risk factors of gallstone disease in Inner Mongolia populations.Methods A case-control study was conducted in 180 consecutive patients who had undergone cholecytectomy for gallstones in the hospital of Inner Mongolia during December 2010 to December 2011.Another 200 patients (age 19 to 81 years old) with no gallstone disease were enrolled as controls.All the participants completed a questionnaire and took physical or ultrasonographic examinations.Univariate analysis and Multivariate logistic regression analysis were used for data analysis.Results Mean age of the study group and the control group was (51.7 ± 13.2) and (54.6 ± 12.1) years old,respectively.More female patients were found in the study group (130:50,x2 =9.552,P ＜ 0.05).After adjusting age and gender,multivariate logistic regression showed that gallstone disease was significantly associated with higher educational level (OR =7.05; 95％ confidence internal (CI):1.28-38.85),animal viscera intake (OR =12.75,95 ％ CI:4.67-34.82),fried food intake (once and twice a week:OR =9.04,95％ CI:4.67-17.51; twice a week:OR=5.39,95％ CI:1.60-18.21) and dyslipidaemia (OR=2.81,95％ CI:1.49-5.30).Vegetables intake (2-3 times a week:OR =0.28,95％ CI:0.03-2.65 ; 4-5 times a week:OR =0.09,95 ％ CI:0.01-0.80 ; once a day:OR =0.02,95％ CI:0.002-0.19) was inversely associated with gallstone disease.Risk factors of gallstone disease were different by genders.Conclusions Animal viscera or fried food intake and dyslipidaemia may increase the risk of gallstone disease.However,vegetables intake may prevent the development of gallstone disease.

Objective To explore the regulatory roles of butorphanol on isolated rabbit pulmonary arteries by lipopolysaccharide(LPS)pre-incubation and assay the protective effect of ketamine on clinic sep tic shock patients.Methods Vascular ring tension detection technique was applied to observe the effect of butorphanol on the normal or lipopolysaccharide incubated pulmonaryvascular.Results In normal group, the final concentration of butorphanol(0.1 μmol,1μmol,10μmol,100μmol)were used to make pretreat ment- phenylephrine(PE)pulmonary artery relaxation.In LPS group,the effect of vasodilation of butor phanol was enhanced.Conclusions LPS can enhance the effect of butorphanol on pulmonary artery relaxa tion reaction.And the direct effect of butorphanol on pulmonary arteries was vasodilation.

Objective To observe the effect of different temperatures on endoplasmic reticulum stress, calcium overload, mitochondria and cell damage in pulmonary microvascular endothelial cells (PMVEC) induced by heat stress, and clarify the mechanism of endothelial cell injury in the process of heat stress to provide experimental basis for clinical prevention and treatment of heat stree. Methods Heat stress model of PMVEC cell was set up. Control group cells were incubated at 37℃, 5%CO2, while heat stress group cells were incubated at 39℃, 41℃, 43℃ for 2h, respectively, then further incubated at 37℃, 5%CO2 for 6h. Pretreatment of cells with 20μmol/L BAPTA-AM or 50μmol/L CsA before heat stress at 43℃. The protein levels of p-PERK, PERK p-eIF2a, eIF2a, ATF4 and GRP78 were analyzed by Western blotting. Intracellular Ca2+, mitochondrial membrane potential and the changes in mitochondrial permeability transition pore were investigated by flow cytometry. The change of caspase-3 was detected by Caspase Assay Kit. Millicell-ERS Volt-Ohm Meter and Accessories was used for determining the changes of transepithelium electrical resistance (TER). Results Compared with the control group, with the increase of heat stress temperature (41-43℃), the phosphorylation of p-PERK and p-eIF2a protein and the expressions of ATF4 and GRP78 proteins were gradually activated, intracellular Ca2+ increased, MPTP pore was opened, mitochondrial membrane potential decreased, cell permeability increased and apoptosis occurred, and it was the most obvious in the 43℃ heat stress group, and the difference was statistically significant (P<0.05). Pretreatment with Ca2+ inhibitors promoted the recovery of the MPTP hole, mitochondrial membrane potential and cell permeability, and reduced the occurrence of apoptosis. While pretreatment with the mitochondrial protective agent did not reduce the release of Ca2+, but it could promote the recovery of cell permeability and reduce the occurrence of apoptosis. Conclusion Heat stress activates endoplasmic reticulum stress response, induces intracellular Ca2+ overload mediated cell and mitochondrial damages in PMVEC cells, which may be one of the important mechanisms of endothelial cell injury induced by heat stress.

Objective To study the effects of epigallocatechin-3-gallate(EGCG) on noise-induced cochlear injuries.Methods A total of 45 guinea pigs were divided into three groups: the EGCG+noise exposure group, the normal saline+noise exposure group, and the control group.15 Guinea pigs in each group.For EGCG administration, the guinea pigs were given abdominal injection (25 mg/1 000 g) 1 day before and 1 hour before noise exposure (120 dB SPL, 4 h),where for the control group, the guinea pigs received nothing.The hearing function was detected by the auditory brainstem response (ABR) recording after noise exposure immediately, and at 1,3,7, and 14 days after noise exposure.On the 14th day, the cochlea were isolated, and the cells morphology of basal membrane and vascular stria, the outer hair cell movement protein (Prestin), and the 3-nitrotyrosine (3-NT) were examined by immunohistochemistry staminy.Results After noise exposure, ABR thresholds in the EGCG group were higher than that of in the control group(P<0.05), but lower than the normal saline group(P<0.05),though the differences between the other two groups became smaller from day 3.Immunohistochemistry (IHC) staining showed that the three rows of outer hair cells of the control group with Prestin protein stained were arranged neatlyand lack of cell absent, and 3-NT was mainly distributed in the cytoplasm and epidermis.Compared with the normal saline + noise group, after noise exposure, the outer hair cells of EGCG + noise group were in better shape, and prestin staining was clear.Besides, the basal membrane and vascular stria were slightly damaged, the cells arranged neatly and the 3-NT distribution was decreased.Conclusion Preventive intraperitoneal injection of EGCG may reduce cochlea damage caused by noise.

ING1 family is a candidate for tumor suppressor,which has three splicing isoforms named p47ING1a,p33ING1b,and p24ING1c. Study of the effect of different isoforms of ING1 on HeLa cells proliferation and its molecular mechanism would help further identifying the functional relationship of ING1 isoforms,and finding important genes regulated by ING1. Cell growth curve and cell cycle analysis were used to observe the effect of ING1a,ING1b,and ING1c on HeLa cells growth,and the result indicated that they could all inhibit HeLa cells growth by arresting cell cycle at G0/G1 phase. PCR method was used to construct the PHD domain deletions of ING1a and ING1b. ING1a,ING1b,ING1c and the PHD domain deletions 1a?C and 1b?C were then overexpressed in HeLa cells. p16INK4a,PTEN/p27Kip1 and p53/p21Waf1 protein levels were detected by Western blot. The result showed that ING1a,ING1b,ING1c,and 1a?C except for 1b?C induced p16INK4a protein expression,in which ING1c had the most powerful effect. Luciferase assay identified that overexpression of pcDNA3.1(+)-1a?C facilitated p16INK4a transcription through enhancing p16INK4a promoter activity,while pcDNA3.1(+)-1b?C repressed the p16INK4a promoter activity . In a word,it was found for the first time that except for the p53/p21Waf1 pathway,three splicing isoforms of ING1 family could also inhibit HeLa cells proliferation though upregulation of p16INK4a and PTEN,and the PHD domain deletion of ING1a enhanced p16INK4a transcription. These findings provide new clews to further study on the mechanisms of ING1 family suppressing cancer cells growth.

Objective To observe the effects of capsaicin on PGE2 concentration of IL-1β-induced human large cell carcinoma NCI-H460 cells,and further observe its effect on COX-2 and mPGES-1 so as to explore the possible mechanisms against non-small cell lung cancer.Methods NCI-H460 cells were cultured in vitro ;the effect of capsaicin in inhibiting NCI-H460 cells proliferation was observed.The 50% inhibitory concentration (IC50 ) was measured by MTT assay.IL-1βstimulation method was used to construct inflammation model,and the effects of capsaicin on COX-2 activity and PGE2 concentration in NCI-H460 cells were measured by ELISA.The effects of capsaicin on COX-2 and mPGES-1 protein level in NCI-H460 cells were analyzed by Western blot;the effects of capsaicin on COX-2 mRNA and mPGES-1 mRNA expressions in NCI-H460 cells were analyzed by Real-time PCR. Results MTT assay results showed that the growth of NCI-H460 cells treated with capsaicin was significantly inhibited compared with the control group (P <0.05 or P <0.01 ).Capsaicin could significantly decrease COX-2 activity and PGE2 concentration in NCI-H460 cells,and significantly decrease COX-2,mPGES-1 protein levels as well as COX-2,mPGES-1 mRNA expressions in NCI-H460 cells in a dose-dependent manner compared with the control group (P < 0.05 ).Conclusion Capsaicin inhibits the release of PGE2 by downregulating COX-2 and mPGES-1 mRNA expressions in NCI-H460 cells,which may be one mechanism of its effect against non-small cell lung cancer.

Adenocarcinoma ; metabolism ; pathology ; surgery ; Adult ; Choriocarcinoma ; metabolism ; pathology ; surgery ; Diagnosis, Differential ; Endometrial Neoplasms ; metabolism ; pathology ; surgery ; Female ; Humans ; Keratin-7 ; metabolism ; Mucin-1 ; metabolism ; Ovarian Neoplasms ; metabolism ; pathology ; surgery