AIM To explore the protection effect of Blood-Replenishing Capsule (BRC) on hypoxic animals in order to lower the rate of altitude stress. METHODS Comparison of BRC on survival time of mice under ordinary pressure and chemical hypoxia were observed and the oxygen consumption was measured. RESULTS BRC-obviously prolonged the survival time of hypoxic mice, reduced the oxygen consumption and increased the hemoglobin (Hb) content in the bloods.Mouse brain's SOD was obviously higher and MDA concetration remarkable lower in BRC groups than those in control groups. CONCLUSION BRC shows remarkable effect on hypoxia tolerance in mice.

The target of offering medical literature novelty assessment course for medical postgraduates was analyzed with the problems in its teaching and the significance of its teaching reform pointed out.Its teaching contents, teaching methods, examination methods and its assessment system reform were described with suggestions proposed for its successful reform.

Objective To evaluate the effect and mechanism of IL‐6 induced Gefitinib resistance in non small cell lung cancer (NSCLC) .Methods The sensitivity of cells to Gefitinib ,the invasion ability of cells and the expression of phosphorylated p‐mTOR was assessed by MTT assay ,Transwell assay and Western blot ,respectively .PC‐9psb388 stable over expressing human recombi‐nant IL‐6(hrIL‐6) cell line was established by transfecting PC‐9 cells with a lentivirus psb388 expressing IL‐6 and stable transfecta‐nts over‐expressing IL‐6 in human lung cancer cell line PC‐9 .The sensitivity of cells to Gefitinib ,the invasion ability ,expression of p‐mTOR were then detected .PC‐9/PC‐9psb388 xenografts were established and the expression of p‐mTOR and IL‐6 in tumor sec‐tions were then detected .Results The sensitivity of PC‐9 cells to Gefitinib was reduced by IL‐6 ,the invasion ability of PC‐9 cells and the expression of p‐mTOR was significantly increased with IL‐6 treatment .The sensitivity of PC‐9 cells to Gefitinib was promi‐nent higher in PC‐9psb388 cells ,while the invasion ability of PC‐9psb388 cells and the expression of p‐mTOR was higher than PC‐9 cells .The sensitivity to Gefitinib was improved and expression of p‐mTOR reduced in rapamycin‐treated PC‐9psb388 cells and IL‐6 stimulated PC‐9 cells .Tumor volume of PC‐9psb388 xenografts was significantly higher than that of PC‐9 cells .The expression of p‐mTOR and IL‐6 in tumor sections of PC‐9psb388 group were higher than that of PC‐9 group .Conclusion IL‐6 could elevate the expression of p‐mTOR to induce Gefitinib resistance in non small cell lung cancer (NSCLC) .

The paper analyzes the effect ofInternet +on the purchase of periodical resources for libraries of medical colleges based on the discussion of the concept of Internet + ,points out the current situation and problems of purchase of periodicals for libraries of medical college,puts forward the periodical purchase modes and scheme proposals that conform to the current trend,and lays a foundation for the development of libraries of medical colleges.

In order to investigate the distribution of Yersinia enterocolitica in Citellus dauricus plague focuses in Inner Mongolia,three different ecological environ/ments were chosen as the sampling area.Feces,tongue roots throat swabs,and intestinal contents of rodent,livestock,and poultry were separately collected,and different Y.enterocolitica strains were isolated,and identified.PCR analysis was conducted to detect the toxicity genes of Y.enterocolitica.Statiscal analysis was performed by chisquare test.Of the 3 260 samples,65 Y.enterocolitica strains were isolated and the overall detection rate was 1.99％.To include O ∶ 3/3,O ∶ 5/1A,O ∶ 4/4 serum biological type,the pathogenic strain of serotype O ∶ 3 and biological typt 3 carryinq toxicity genes ail,ystA,VirF yadA and rfbc was isolated from pigs in Citellus dauricus plague focuses,Inner Mongolia are the major carrier of pathogenic Y.enterocolitica distributed in three different ecological environment,and distributed mainly in agricultural area.

Aim To investigate the protective effect and the underline mechanisms of total flavonoids from Sorbus Tianschanica L leaf (TFST) against myocardial ischemia/reperfusion (I/R) injury.Methods The I/R injury model of rat isolated heart was prepared by improved Langendorff retrograde perfusion method.Following the treatment,the coronary blood flow levels (CF),left ventricular developed pressure (LVDP) and maximal rise/fall rate of left ventricular pressure (±dp/dt_(max)) were monitored as the myocardial function.The superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in myocardial tissue were measured by the commercial kits. The in vitro anti-oxidative capacity of TFST was detected by the DPPH and lipid peroxidation reaction system.Results Compared with I/R injury group, pre-incubation with TFST (6.0 mg·L~(-1)) significantly improved the LVDP,±dp/dt_(max) and CF during reperfusion. TFST (6.0 mg·L~(-1)) treatment significantly increased the SOD activities and reduced the MDA levels in myocardium tissue.Moreover,TFST (from 6.25 to 100.0 mg·L~(-1)) scavenged the DPPH, hydroxyl radical and superoxide anion free radicals, and inhibited the lipid peroxidation reaction in a concentration-dependent way.Conclusions All the results demonstrate that TFST possesses the cardioprotective effect on ischemia/reperfusion injury.This efficacy may be due to its antioxidative activity.

Objective To study the effect of human G-coupled protein kinase 4(GRK4) A142V overexpression on angiotensin Ⅱ1 type(AT1 ) receptor and its-mediated proliferation of rat vascular smooth muscle cells .Methods We constructed a lentiviral vec-tor carrying human GRK4-EGFP gene and observed its expression in A10 cells .Expression of AT1 receptor were determined by im-munoblotting ,GRK4 activity were checked by spectrophotometry ;the linkage between GRK4 and AT1 receptor were determined by co-immunoprecipitation .[3 H] thymidine incorporation was used to detect changes of cell proliferation .Results As compared with the control cells ,A142V-transfected cells had higher GRK4 activity and higher AT1 receptor expression ;there was linkage between GRK4 and AT1 receptor ,the co-immunoprecipitation levels were lower in A142V cells .The basal levels of VSMC proliferation was higher in A142V cells ,Ang Ⅱ increased VSMC proliferation to a greater extent in A 142V cells .Conclusion GRK4 A142V ,via in-creasing GRK4 activity ,increases AT1 receptor expression and function in vascular smooth muscle cell proliferation .

Objective To investigate the effect of high-fat diet-induced obesity on oxidative stress and klotho promoter methylation in lung tissue of C57/BL6 mice. Methods Mice in the control group were feed with the normal diet,and mice in the obesity group were feed with high-fat diet. The lung tissue level of uperoxide dis-mutase(SOD)and malondialdehyde(MDA)were determined by using mice enzyme-linked immunosorbent assay (ELISA)kit. The klotho mRNA and protein expression was determined by qPCR and Western-blot ,respectively. The Klotho gene methylation status was determined by methylation specific PCR(MS-PCR). Results Compared with the control group,mice in the obesity group had high level of oxidative stress in lung tissue. Meanwhile,mice in the experimental group had lower levels of klotho mRNA and protein expression than those in the control group. The high-fat diet increased the degree of Klotho gene methylation. Conclusion High-fat diet could lead injure in lung tissue in C57/BL6 mice,klorho promoter methylation may play an important role involved in the process.

Objective: To explore the effects of oxidative stress on renal dopamine D₁ receptor dysfunction in offspring of diabetic rat dams. Methods: The pregnant Sprague Dawley (SD) rats (n=10) were randomly divided into the diabetic group (a single intraperitoneal injection of 35 mg/kg streptozotocin on day 0 of gestation) and control group (injected with the equal volume of 0.9% saline on day 0 of gestation) according to the random number table (n=5 each group). The offspring rats were divided into 4 groups including offspring of control dams treated with vehicle, offspring of control dams treated with antioxidant, offspring of diabetic dams treated with vehicle and offspring of diabetic dams treated with antioxidant (n=10 each group). After birth, the offspring rats were treated with normal drinking water or antioxidant (tempol, 1.0 mmol/L) from the age of 4 weeks until the end of the study (20 weeks). The blood pressure was monitored continuously by non-invasive tail-cuff method. The renal oxidative markers including superoxide dismutase (SOD) and malondialdehyde (MDA) activity and D₁ receptor agonist (fenoldopam)-mediated urinary and sodium excretion were detected. Furthermore, the protein expression of renal G protein-coupled receptor kinase 2 (GRK2), GRK4, dopamine D₁ receptor and the phosphorylation level of D₁ receptor were detected. Results: The mean arterial pressure of offspring from the diabetic dams treated with vehicle was significantly higher than that of offspring from control dams treated with vehicle (P=0.013), while the mean arterial pressure of offspring from diabetic dams treated with antioxidant was significantly lower than that of offspring from the diabetic dams treated with vehicle (P=0.038). The fenoldopam-mediated urinary flow and urinary sodium excretion rate were significantly lower in offspring of diabetic dams treated with vehicle than those in offspring of control dams treated with vehicle (P<0.01), which were significantly higher in offspring of diabetic dams treated with antioxidant as compared to offspring of diabetic dams treated with vehicle (both P<0.01). There was no significant difference in fenoldopam-mediated urinary flow and urinary sodium excretion rate in offspring of control dams treated with antioxidant or vehicle (urinary flow: P=0.772; urinary sodium excretion rate: P=0.716). Compared with offspring of control dams treated with vehicle, the renal MDA activity was significantly increased, while the SOD activity was significantly decreased in offspring of diabetic dams treated with vehicle (MDA: P<0.01; SOD: P=0.013). The renal MDA activity was significantly decreased, while the SOD activity was significantly increased in offspring of diabetic dams treated with antioxidant in comparison with offspring of diabetic dams treated with vehicle (MDA: P<0.01; SOD: P=0.035).The renal GRK2 and GRK4 protein expression in offspring of diabetic dams treated with vehicle were significantly higher than those in offspring of control dams treated with vehicle (P<0.01), while the expression levels of renal GRK2 and GRK4 in offspring of diabetic dams treated with antioxidant were significantly downregulated compared with offspring of diabetic dams treated with vehicle (P<0.01). There was no significant difference in the protein expression of dopamine D₁ receptor among 4 groups (P=0.735). The level of dopamine D₁ receptor phosphorylation in offspring of diabetic dams treated with vehicle was significantly higher than that in offspring of control dams treated with vehicle (P<0.01), while the dopamine D₁ receptor phosphorylation level was significantly lower in offspring of diabetic dams treated with antioxidant compared to that in offspring of diabetic dams treated with vehicle (P<0.01). Conclusion Oxidative stress is involved in the dopamine D₁ receptors dysfunction in the offspring of diabetic dams.

OBJECTIVE： To design and synthesize N-aroyl substituted indoline-3-acetic acid derivatives and evaluate their in vitro hypoglycemic activity. METHODS： Using indoline derivative 2-[5-（benzyloxy）-1-（4-chlorobenzoyl）-2-methyl-1H-inclol-3-yl]acetic acid （GY3） as leading compound， 4-（benzyloxy）phenyl hydrazine hydrochloride and methyl 4-oxopentanoate as raw material， 8 kinds of N-aroyl （3-hydroxybenzoyl， 3-cyanobenzoyl， 4-nitrobenzoyl， 4-methylsulfonylbenzoyl， 4-acetamidobenzoyl， 3-acetylaminobenzoyl， isoniacyl and pyridine-2-formyl） substituted indoline-3-acetic acid derivatives were synthesized via 4 steps reactions： Fischer indole cyclization， reduction， amidation and hydrolyzation. The human hepatoma HepG2 cell lines were used to investigate the glucose consumption activity of the target compounds. RESULTS： Totally 8 various N-aroyl substituted indoline-3-acetic acids were synthesized and their structures were confirmed by mass spectrum（MS）， nuclear magnetic resonance 1H-NMR and 13C spectrum. Under the condition of 1.0 μmol/L， the percentage of glucose- promoting consumption of the synthesized compounds on HepG2 cells was 5.4％-9.1％. 2-[（2R， 3S）-5-benzyloxy-2-methyl-1-（4-methylsulfonyl benzoyl）-2，3-dihydro-indole-3-yl] acetic acid showed the best hypoglycemic activity. The percentage of glucose- promoting consumption was （9.1±1.81）％， which was close to that of positive control metformin [（10.58±1.68）％]， but less potent than that of leading compound GY3[（12.15±0.78）％]. CONCLUSIONS： Different electron-withdrawing substituents are introduced into N-aroyl aromatic rings of dihydroindole compounds， such as cyano， nitro， methyl sulfonyl； hypoglycemic activity decreases in varying degrees and is weaker than halogen substituents.