ObjectiveTo investigate the mechanism of protective effect of Xuebijing injection on vascular endothelial cells in rats with heat stress.Methods Ninety Sprague-Dawley(SD) rats were randomly divided into control, model and Xuebijing injection treatment groups, 30 rats in each group. Heat stress model was reproduced by placing rats in constant temperature box at 40℃, 60% relative humidity for 1 hour, Xuebijing injection group was treated by intraperitoneal injection of Xuebijing 2.5 g/kg, while the control and model groups were treated by intraperitoneal injection of normal saline 2 mL/kg, once a day only in 1 day for both groups. After model establishment, the rectum temperature, heart rate and the mean arterial pressure(MAP) were recorded at 2, 6, 12 hours in each group. At the same time, the rat abdominal aortic blood was collected and serum was separated, the enzyme-linked immunosorbent assay(ELISA) was used to determine the aortic serum levels of lipopolysaccharide(LPS), nuclear factor-κB(NF-κB) and p53, and the prothrombin time(PT), activated partial thromboplastin time(APTT) and D-dimer of venous blood were detected by automatic blood coagulation analyzer(ACLTOP).Results Compared with those in control group, the rectum temperature, heart rate, LPS, NF-κB, p53, PT, APTT, D-dimer were significantly increased, and MAP was obviously decreased in model group(P<0.05 orP<0.01). Compared with model group, the above indexes were improved significantly in Xuebijing injection treatment group at 2 hours〔rectum temperature(℃): 38.02±0.22 vs. 39.32±0.33, heart rate(bpm): 507±14 vs. 562±35, MAP(mmHg, 1 mmHg=0.133 kPa): 98±6 vs. 87±13, LPS(ng/L): 0.65±0.03 vs. 0.82±0.05, NF-κB(ng/L): 1.10±0.04 vs. 1.33±0.05, p53(ng/L): 1.33±0.03 vs. 1.73±0.02, PT(s):15.47±1.03 vs. 20.28±2.01, APTT(s): 40.26±2.46 vs. 47.46±3.51, D-dimer(μg/L): 238.54±8.32 vs. 323.12±8.14,P<0.05 orP<0.01〕.Conclusion Xuebijing injection can correct the disorders of blood PT, APTT, D-dimer via decreasing the secretion of the levels of NF-κB, p53 from vascular endothelial cells in rats with heat stress, thus the integrity of the vascular endothelium can be protected, and LPS entering into the blood stream can be inhibited.

Objective To explore the effectiveness of ω-3 fatty acids in intervening rat models of chronic obstructive pulmonery disease (COPD).Methods The rat COPD models were established by cigarette smoking and intratracheal lipopolysaccharide instillation.Totally 90 rats were randomly divided into 3 groups:normal control group (treated with normal saline),COPD group,and intervention group (the COPD rat models treated with ω-3 fatty acids).Lung tissues were obtained on the 7th,21st,and 28th day.The left lower lobes were analyzed to determine the expressions of nuclear factor-kappa beta (NF-κB) and interferon-γ (IFN-γ)and the right lung lobes were sliced for detecting the cell apoptosis.Double antibody sandwich enzyme-linked immunosorbent assay (DAS-ELISA) was used to detect the serum IFN-γ and interleukin-6 (IL-6).Results (1) The pathological changes of lung tissue:there were a large number of inflammatory exudation,alveolar wall thickening,hyperplasia of vascular smooth muscle and the alveolar structure destruction in the COPD model group,but the lung tissue were part of alveolar cavity and a little inflammatory exudate in ω-3 fatty fish acids treatment group,control rats were almost no alveolar inflammation on the 28th days.(2) On the 28th day,NF-κB protein expression of the lung tissue (18.91 ± 3.07) in rats of COPD model group was significantly higher than the control group and the intervention group (5.47 ±4.86 and 7.23 ±2.21) (P ＜0.01).On the 28th day,IFN-γ protein expression in lung tissue of the rats in the model group was 7.12 ±3.37,significantly lower than the intervention group (18.74 ± 2.65),the difference was statistically significant (P ＜ 0.01).(3) The IL-6 levels of the blood-serum of model group rats were (13.43 ± 2.47) ng/L,significantly higher than the control group and the intervention group [(4.78 ± 1.93) and (4.98 ± 1.89) ng/L],the differences were statistically significant (P ＜ 0.01) on the 28th day,,but the IFN-γ level [(2.23 ± 0.63) ng/L] in COPD group was more poorer than ω-3 fatty acids group and the intervention group [(4.51 ± 0.71) and (7.05 ± 0.52) ng/L] (P ＜ 0.01).Conclusions The ω-3 fatty acids can lower NF-κB protein expressions in lung tissues and serum and IL-6 levels in COPD rats; aslo,it can increase the IFN-γ protein expression in lung tissue and serum.Thus,it can prevent the lung inflammation in COPD rats.

Objective To investigate the clinical efficacy of acupoint application plus Simo decoction oral liquid in treating functional dyspepsia (FD).Method Ninety-five FD patients were randomized to a treatment group (48 cases) and a control group (47 cases).The treatment group received acupoint application plus Simo decoction oral liquid and the control group,oral administration of omeprazole enteric-coated capsules and mosapride citrate tablets.The clinical therapeutic effects were compared between the groups after four weeks of treatment.Result After one week of treatment,the cure and marked efficacy rate and the total efficacy rate were 20.8％ and 54.2％,respectively,in the treatment group and 40.4％ and 66.0％,respectively,in the control group (P＜0.05).There was a statistically significant difference in the cure and marked efficacy rate between the two groups (P＜0.05).After four weeks of treatment,the cure and marked efficacy rate and the total efficacy rate were 81.3％ and 89.6％,respectively,in the treatment group and 61.7％ and 72.3％,respectively,in the control group.There were statistically significant differences in both the cure and marked efficacy rate and the total efficacy rate between the two groups (P＜0.05).Conclusion Acupoint application plus Simo decoction oral liquid is an effective way to treat FD.

Volatile organic compounds (VOCs) in ambient air can participate in photochemical reactions, which lead to the generation of secondary pollutants such as ozone and aerosol. So real-time and accurate monitoring of atmospheric VOCs plays an important role in the study of the causes of air pollution. On the basis of proton transfer reaction mass spectrometry (PTR-MS) research, a novel dipolar proton transfer reaction mass spectrometer (DP-PTR-MS) for real-time and on-line monitoring atmospheric VOCs was developed. Compared with the conventional PTR-MS with one kind of reagent ion H3O+, DP-PTR-MS had three kinds of reagent ions H3O+, OH-, (CH)2COH+, which could be switched according to the actual detection need. So DP-PTR-MS can improve the qualitative ability and expand the detection range effectively. The reagent ion H3O+can be used for detecting VOCs whose proton affinities are greater than that of H2O. The reagent ion OH-can be used to identify VOCs cooperating with the reagent ion H3O+,and can also be used for detecting some inorganic substances such as CO2. The reagent ion (CH3)2COH+can be used for accurately detecting NH3under interference elimination circumstances. The limit of detection (LOD) and sensitivity of DP-PTR-MS were measured by using six kinds of standard gases. The results showed that the LOD for detecting toluene was 7×10-12(V/V) and the sensitivity for detecting ammonia has reached 126 cps/10-9 (V/V). The ambient air in Hefei city was on-line and real-time monitored for continuous 78 hours with DP-PTR-MS. The results showed that the newly developed DP-PTR-MS could be used for long-term and real-time monitoring atmospheric VOCs with the concentration of 10-12(V/V) level. DP-PTR-MS is an important tool for the study of the causes of atmospheric pollution and the monitoring of trace VOCs emissions.

OBJECTIVETo investigate the influence of heat shock factor1 (HSF1) on gene expression of inflammatory mediators in RAW264.7 murine macrophage cells induced by burn serum.

METHODSSera were separated from blood of normal rats and rats with severe burns, and the recombinant vector pcDNA3. 1/HSF1 was constructed. RAW264.7 macrophages were divided into non-transfection group, vacant vector group (with burn and normal sera stimulation, respectively after vacant vector transfection) and recombinant vector group (with burn and normal sera stimulation, respectively after recombinant vector transfection). Some recombinant vector transfected macrophages without serum stimulation were prepared for the determination of HSF 1 expression with Western blotting. The mRNA expressions of TNF-alpha, HMGB 1 and IL-10 were determined with RT-PCR.

RESULTSThe cell line attained after recombinant vector transfection was comparatively stable,with partial activation of HSF 1. Burn sera markedly upregulated TNF-alpha, HMGB1 mRNA expression (0.910 +/- 0.100, 0.860 +/- 0.020, respectively), but downregulated IL-10 expression (0.430 +/- 0.010, respectively) in normal macrophages, while these genes maintained in a very low level in normal macrophages with normal serum stimulation . macrophages with recombinant vector transfection and burn serum stimulation could obviously inhibit the expression of TNF-alpha and HMGB 1, but enhance the IL-10 gene expression (0.130 +/- 0.100, 0.450 +/- 0.020 , 0.450 +/- 0.020, respectively )when compared with that with vacant vector transfection and burn serum stimulation (0.800 +/- 0.050, 0.880 +/- 0.030, 0.420 +/- 0.010, respectively).

CONCLUSIONHSF1 can inhibit the expression of some pro-inflammatory mediators in macrophages after a severe burns, indicating that appropriate upregulation of anti-inflammatory mediators might exert protective effects on the organism.

Animals ; Burns ; metabolism ; Cell Line ; DNA-Binding Proteins ; genetics ; Female ; Gene Expression ; HMGB1 Protein ; metabolism ; Heat Shock Transcription Factors ; Heat-Shock Response ; genetics ; Inflammation Mediators ; metabolism ; Interleukin-10 ; metabolism ; Macrophages ; metabolism ; Male ; Rats ; Rats, Sprague-Dawley ; Serum ; Transcription Factors ; genetics ; Transfection ; Tumor Necrosis Factor-alpha ; metabolism

OBJECTIVESThe purpose of this study is to define and clarify the causes of differences in physique between urban students and rural students in China.

METHODSSubjects are 2,524 students (male, 838; female, 1686) who entered K University in Shanghai in September, 2001. The data used in this study is based upon K university's Yearly Health Check Record and Students' Family Condition Record. Correlation analysis, analysis of variance (ANOVA) and analysis of covariance (ANCOVA) were applied to analyze the relationships between physique and gross family income, family income per capita, latitude, air temperature, precipitation or altitude.

RESULTSUrban students' height and weight are significantly greater than rural students' in both males and females. Both male students and female students are significantly taller and heavier in accordance with per capita increases in students' family income. The height and weight of male and female students whose parents are peasant farmers are least. With regard to the relationship between physique and urban-rural factors, the F value decreases clearly when family income per capita is taken as a covariate, while the F values slightly decrease also when factors of latitude etc. are taken as covariates. The main cause of differing family income is occupational difference between urban areas and rural ones.

CONCLUSIONStudents born in urban areas are taller and heavier than those born in rural areas. The main cause of these differences is family income per capita. The main cause of variations in family income is the income difference in occupations.

OBJECTIVETo understand the relationships between CDH13 (T-cadherin) genetic polymorphisms, adiponectin levels and ischemic stroke, and possible interactions between CDH13 polymorphisms and other risk factors.

METHODSWe recruited 342 Chinese ischemic stroke sib pairs. We genotyped rs4783244 and rs7193788 on CDH13 using time-of-flight mass spectrometry genotyping technology and measured total and high-molecular weight (HMW) adiponectin levels. We investigated associations between SNPs and ischemic stroke, and interactions between SNPs and other risk factors using multi-level mixed-effects regression model.

RESULTSIn individuals without ischemic stroke, CDH13 rs4783244 was associated with total adiponectin levels (per T: Coef = -0.257, P = 0.001). CDH13 rs7193788 was associated with total adiponectin levels (per A: Coef = -0.221, P = 0.001) and HMW adiponectin levels (per A: Coef = -0.163, P = 0.003). rs7193788 was significantly associated with ischemic stroke (GA/AA vs. GG: OR = 1.55, 95% CI: 1.07 to 2.24, P = 0.020) after Bonferroni correction (α = 0.025). There was an interaction between rs7193788 and diabetes (P = 0.036). Compared to diabetes-free individuals with rs7193788 GG genotype, diabetes patients with rs7193788 GA/AA genotypes had higher risks for ischemic stroke (OR = 2.64, 95% CI: 1.58-4.40, P < 0.001).

CONCLUSIONCDH13 genetic polymorphisms are associated with adiponectin levels and ischemic stroke. An interaction is found between CDH13 SNP and diabetes for ischemic stroke.

Adiponectin ; blood ; Aged ; Brain Ischemia ; blood ; genetics ; Cadherins ; genetics ; China ; Female ; Humans ; Male ; Middle Aged ; Polymorphism, Genetic ; Risk Factors ; Stroke ; blood ; genetics

The present study investigated the effect of extract of Poria cocos polysaccharides(PCP) on cytochrome P450 2 E1(CYP2 E1) and nuclear factor κB(NF-κB) inflammatory signaling pathways in alcoholic liver disease(ALD) mice and explored its protective effect and mechanism. Sixty male C57 BL/6 N mice of SPF grade were randomly divided into a control group, a model group, a positive drug group(bifendate, 200 mg·kg~(-1)), and high-(200 mg·kg~(-1)) and low-dose(50 mg·kg~(-1)) PCP groups. Gao-binge mo-del was induced and the mice in each group were treated correspondingly. Liver morphological and pathological changes were observed and organ index was calculated. Serum levels of alanine aminotransferase(ALT) and aspartate aminotransferase(AST) were detected. Malondialdehyde(MDA) and superoxide dismutase(SOD) in liver tissues were detected by assay kits. The levels of interleukin-6(IL-6) and tumor necrosis factor-α(TNF-α) were detected by ELISA. The activation of macrophages was observed by immunofluorescence staining and protein expression of CYP2 E1, Toll-like receptor 4(TLR4), NF-κB p65, and phosphorylated NF-κB p65(p-NF-κB p65) were analyzed by Western blot. The ALD model was properly induced. Compared with the model group, the PCP groups significantly improved the pathological injury of liver tissues. Immunofluorescence staining revealed that compared with the model group, the groups with drug intervention showed decreased macrophages in liver tissues. Additionally, the PCP groups showed reduced ALT, AST, MDA, IL-6, and TNF-α(P<0.05), and potentiated activity of SOD(P<0.01). PCP extract has the protective effect against alcoholic liver injury in mice, and the underlying mechanism may be related to the regulation of the expression of CYP2 E1 and inhibition of TLR4/NF-κB inflammatory signaling pathway to reduce oxidative stress and inflammatory injury, thereby inhibiting the development of ALD.
Animals ; Cytochrome P-450 CYP2E1/pharmacology* ; Liver ; Liver Diseases, Alcoholic/pathology* ; Male ; Mice ; NF-kappa B/metabolism* ; Plant Extracts/pharmacology* ; Polysaccharides/pharmacology* ; Wolfiporia

OBJECTIVE: To investigate the cytotoxic effect and its mechanism of the micromolecule compound on the leukemia cells. METHODS: The cytotoxic effects of 28 Nilotinib derivatives on K562, KA, KG, HA and 32D cell lines were detected by MTT assays, and the compound Nilo 22 was screen out. Cell apoptosis and cell cycle on leukemia cells were detected by flow cytometry. The effect of compound screened out on leukemogenesis potential of MLL-AF9 leukemia mice GFP RESULTS: Nilo 22 serves as the most outstanding candidate out of 28 Nilotinib derivatives, which impairs leukemia cell lines, but spares normal hematopoietic cell line. Comparing with Nilotinib, Nilo 22 could induce the apoptosis of GFP CONCLUSION Nilo 22 shows a significant cytotoxic effect on mice and human leukemia cells, especially for drug resistance cells. Nilo 22 is a promising anti-leukemia agent to solve the common clinical problems of drug resistance and relapse of leukemia.
Animals ; Apoptosis/drug effects* ; Cell Cycle/drug effects* ; Cell Line, Tumor ; Humans ; Leukemia ; Mice ; Myeloid-Lymphoid Leukemia Protein/genetics* ; Telomerase/metabolism* ; Telomere/metabolism*