ABSTRACT
Objective Using Nutrition Risk Screening (NRS 2002),to assess the nutritional risk of inpatients with digestive diseases and evaluate its clinical significance.Methods The information of 274 patients med the inclusion criteria were collected in our department from August to October 2011.Nutrition status was assessed according to NRS 2002 by trained nurses.Results The prevalence of nutritional risk was 22.99 ％ (63/274).The rate of nutritional risk of the elderly inpatients (≥ 65y) with digestive diseases was significant higher the younger ones (＜ 65y)(32.95％ vs 18.28％,P ＜ 0.05).74.6％ inpatients with nutritional risk and 52.13％ with no risks were given enteral or parenteral nutritional support during the hospitalized period.Conclusion There was higher nutritional risk rate in inpatients with digestive diseases,especially the elderly ones.For deferent patients,the nutritional support should be on the basis of patient' s nutritional state.
ABSTRACT
Objective To explore the effect of cell apoptosis and oxidative stress on stressive liv-er injury after traumatic brain injury (TBI) in rats. Methods The model of TBI was duplicated by u-sing modified Allen's mehtods. Forty male Wistar rats were randomly divided into control group and groups at 6,12,24,48 hours after TBI. The serum levels of ALT and AST as well as the levels of superox-ide dismutase (SOD) and malandialdehyde in liver tissue were measured. The index of hepatocyte apopto-sis was detected through flow cytometer. Pathological changes of liver tissues were observed under light and electron microscopes. Results After TBI, the serum levels of ALT and AST were significantly in-creased, while malondialdehyde was increased and SOD decreased in liver tissues. The electron micro-scope showed that the index of hepatocyte apoptosis reached a peak at 6 hours after TBi. Aggressive inju-ries of the liver tissues were observed after TBI, showed by pathological observations. Conclusion Cell apoptosis and oxidative stress may be involved in the pathogenesis of stressive liver injury after TBI.
ABSTRACT
Objective To study the change of endothelial function during myocardial ischemia-reperfusion injury in rabbits and the effect of Rasuvastatin. Method Sixteen New Zealand rabbits were randomLy divided into two groups: ischemia/reporfusian injury group (control group) and Resuvastatin group(drug group). The myocar-dial ischemia-reperfusion model was established by occlusion of left anterior descending coronary artery for 40 min-utes evidenced by the elevation of the ST segment≥0.2 my on ECG waveform, and after release of ooclusion, the ST segment of ECG retttmed to 1/2 or more of the normal wavefonn, which was the evidence of successful reperfu-sion. The rabbit serum nitric oxide (NO) and plasma endothelia-1 (ET-1) content were assayed before occlusion, 40 minutes, 60 minutes and 180 minutes after reperfusion. SPSS11.5 software was used for ANOVA(Repested Measurement designs). P<0.05 was considered as statistically significant. Results There were no significant differences in serum NO and plasma ET-1 between two groups bsfore isehemia, but 40 minutes, 60 minutes and 180 minutes after reperfusion, the levels of serum NO in drug group were higher than those in control group [(82.000±13.825), (63.375±17.541), (50.250±18.987)μmol/L vs. (63.125±18.962), (43.500± 16.518), (29.625±14.162) μmol/L, P<0.05], and the levels of plasma ET-1 content in drug group were lower than those in the control group [(282.541±38.928), (315.152±55.263), (377.795±60.427) pg/mL vs. (331.785±35.341),(375.914±5.204),(459.829±70.110) pg/mL, P<0.05]. Conclusions By the means of increasing serum NO and decreasing plasma ET-1, rosuvastatin can improve the endothelial function in rabbits with isehemia-reperfusion injury.