After the connotation and application of Lib2.0 technology were described, how to construct the subject service platform in Library of Second Military Medical University using Lib2.0 technology was elaborated and the service-oriented subject service platform construction plan was proposed .

AIM:To study the effects of isoproterenol (Iso) on cardiac fibrosis and related cytokines in rats. METHODS:20 SD rats were divided into control and Iso group in random, with 10 rats each group. After injected Iso, cardiac histology was observed and cardiac function, collagen volume fraction (CVF), content of collagen protein and the concentrations of Angiotensin Ⅱ (Angll) and nitrogen monoxide (NO) were measured in the two groups. RESULTS:Compared with control group, microscopic examination showed that fibrosis increased in Iso group. Iso did decrease cardiac function and NO levels and increase CVF, content of collagen protein and AngII levels. Left ventricular pressure maximal rate of rise (+ dp/dt_(max)) and left ventricular systolic pressure (LVSP) were not significantly different from that of control group. CONCLUSIONS:Iso can induce myocardial fibrosis and change levels of related cytokines in rats.

The activity of erythrocyte membrane Na-pumping K~+-activated pera-nitro-phenylphosphatase (K~+-pNPPase) and red cell deformability (RCD) were stndied in 50adult patients with non-insulin-dependent diabetes mellitus (NIDDM). RCD was expressedas red blood cell filtration index (RBC-IF). In comparison with the healthy subject, theactivity of erythrocyte membrane Na-pumping K~+-pNPPase was significantly decreased,and RBC-IF was significantly increased. The above-mentioned changes were more severein NIDDM with retinopathy than those without. There was a very close negative corre-lation between Na-pumping K~+-pNPPase and RBC-IF. These results indicated that thedecrease of erythrocyte membrane Na-pumping K~+-pNPPase activity might be an importantfactor fot the decrease of RCD.

0.998. The detection limits were in the range of 16-40 ng/L(S/N=3). The quantitative detection limits were in the range of 45-105 ng/L(S/N=10) with recovery percentages ranging from 87.6% to 106% and the relative standard deviations was lower than 3%. Conclusion The method was proved to be satisfactory in precision,accuracy and sensitivity and applicable to the daily test of estrogens in water.

Aim To investigate whether Ca~(2+)/calmodulin-dependent kinase Ⅱ(CaMKⅡ)contribute to tumor necrosis factor α(TNF-α)-induced cardiomyocyte hypertrophy.Methods The protein content was assayed with Lowry's method.The cardiomyocytes volumes were measured by computer photograph analysis system.The protein synthesis was assayed with[~3H]-lencine incorporation method.[Ca~(2+)]_i transient was measured by Till image system by cell-loading Fura-2/AM.The expression of CaMKⅡδ_B was determined by Western blot.Results ① TNF-α significantly induced the increase of protein content, [~3H]-leucine incorporation and cell size;These responses were significantly suppressed by KN93, a selective CaMKⅡ inhibitor.② TNF-α increased the amplitude of the spontaneous Ca~(2+) transients in cultured ventricular myocytes from the neonatal rat;CaMKⅡ inhibitor KN93 can suppress the elevation induced by TNF-α.③ TNF-α significantly increased the expression of CaMKⅡδ_B.Concluslon CaMKⅡ signal pathway are involved in TNF-α-induced cardiomyocyte hypertrophy in rats.

Aim To investigate whether Ca2+/calmodulin-dependent kinase Ⅱ(CaMKⅡ)contribute to tumor necrosis factor ?(TNF-?)-induced cardiomyocyte hypertrophy.Methods The protein content was assayed with Lowry's method.The cardiomyocytes volumes were measured by computer photograph analysis system.The protein synthesis was assayed with[3H]-lencine incorporation method.[Ca2+]i transient was measured by Till image system by cell-loading Fura-2/AM.The expression of CaMKⅡ?B was determined by Western blot.Results ① TNF-? significantly induced the increase of protein content,[3H]-leucine incorporation and cell size;These responses were significantly suppressed by KN93,a selective CaMKⅡ inhibitor.② TNF-? increased the amplitude of the spontaneous Ca2+ transients in cultured ventricular myocytes from the neonatal rat;CaMKⅡ inhibitor KN93 can suppress the elevation induced by TNF-?.③ TNF-? significantly increased the expression of CaMKⅡ?B.Concluslon CaMKⅡ signal pathway are involved in TNF-?-induced cardiomyocyte hypertrophy in rats.

Objective To evaluate the diagnostic value of enlargement of the anterior space of the right branch of portal vein in early cirrhosis.Methods 37 cases with early cirrhosis and 42 cases with type B hepatitis proved by pathology as well as 40 health cases underwent MDCT examinations.The width of the anterior space of right branch of portal vein(RBPV)and the diameters of RBPV in each group were measured on CT imaging,then the results were analysed comparatively.Results The width of anterior space of RBPV and the diameters of RBPV were(5.5±2.4)mm and(11.84±1.91)mm in health group,(13.6±5.8)mm and(12.36±61.97)mm in early cirrhosis group,(5.7±3.1)mm and(12.13±1.89)mm in type B hepatitis group,respectively.There were significant differences in the width of the anterior space of RBPV between three groups(P＜0.0001).However,there were not significant differences in the width of RBPV among these three groups(P＞0.05).While,there were significant differences of the width of the anterior space of RBPV and the diameters of the RBPV between normal control and type B hepatitis(P＞0.05).Conclusion CT sign of the anterior space of RBPV increased is of important value in diagnosis of early cirrhosis.

Aim To demonstrate the effects and mechanism of adenosine A1 receptor agonist R(-)-N6-(2-phenylisopropyl) adenosine(R-PIA) on high glucose(HG)-induced myocardial hypertrophy by in vitro cultured myocardial cells from neonatal rats.Methods The protein content was assayed by the method of Lowry. The expression of p-ERK1/2 and ERK1/2 was determined by Western blot.The [Ca~(2+)]I transient changes of cell loaded Fura-2/AM were measured by Till image system.Results 1 μmol·L~(-1) R-PIA and U0126 inhibited similarly HG-induced increase of the protein content and [Ca~(2+)]I transient along with the relative expression of p-ERK1/2.These responses were completely abolished by adenosine A1 receptor antagonist 8-cyclopentyl-1,3-dipropylxanthine(CPDPX).Conclusion Adenosine A1 receptor stimulation significantly inhibits HG-induced myocardial hypertrophy by mediating ERK1/2 pathway and Ca~(2+).

After the importance to construct academic native resource repository platform was elaborated,the native resource repository platform designed and constructed by Library of Second Military Medical University according to the demands of Second Military Medical University was described, which improved the management efficiency of scientific research and academic achievements.

Aim To study the protective effects of SEP on the hypertrophic myocardial cells induced with high glucose and high insulin and the mechanism. Methods The protein content was assayed with Lowrys meth-od;the cardiomyocytes area was measured by computer photograph analysis system;the expression of ANF and PPAR-α was determined by RT-PCR;APS was select-ed as control drug. Results Compared with conctrol group,the protein content,cardiomyocytes area and the expression of ANF and PPAR-α of high glucose and high insulin group were significantly increased. Com-pared with conctrol group,the SEP of different dosages were able to decrease the protein content, area, the expression of ANF mRNA and PPAR-α mRNA of cul-tured hypertrophic myocadial cells induced with high glucose and high insulin. Conclusion SEP can pre-vent cardiomyocyte hypertrophy induced by high glu-cose and high insulin, which is related to its inhibition on PPAR-α signaling path.