BACKGROUND: At present, more and more people pay attention to the protection of sub-hypothermia on cerebral ischemic tissue and the effect of sub-hypothermia treatment on inflammatory reaction after cerebral ischemia-reperfusion.OBJECTIVE: To investigate the effect of sub-hypothermia on inflammatory cytokine in cerebral ischemic area of rats and protection on cerebral reperfusion injury.DESIGN: Randomized controlled study on the basis of animals.SETTLNG: People's Hospital of Hubei Province.MATERIALS: The experiment was completed at Laboratory Center of Renmin Hospital of Wuhan University from October 2004 to February 2005. Totally 50 healthy SD rats of clean grade were selected in this study.METHODS: Ten SD rats were divided randomly into normal group and sham operation group with 5 in each group. Other 40 rats were divided randomly into normal temperature cerebral ischemia group and sub-hypothermia cerebral ischemia group with 20 in each group. Rats except 5 in normal group were used to establish reversible ligation model of left middle cerebral artery (MCA) with Longa ligation method. Rats in sham operation group and normal temperature group were put in 20 ℃ room, and anus temperature was maintained at 37 ℃; rats in sub-hypothermia group were put in 4 ℃ room and anus temperature was maintained at (33.0±1.0) ℃.Rats in sub-hypothermia group were treated with sub-hypothermia on whole body, after ischemia, temperature was changed normally, and reperfusion was started 3 hours after cerebral ischemia. All modeling rats were scored with neurological defect: 0 point: none of neurological defect; 1 point: unable to unfold bilateral anterior claws; 2 points: cycling to hemiplegia side during walking; 3 points: falling to hemiplegia side; 4 points: unable to self-walk and with unconsciousness.MAIN OUTCOME MEASURES: Expression of tumor necrosis factor (TNF) andinterleukin-1 in cerebral tissue of ischemic rats, percentage of volume of cerebral infarction,and neurological functional scores.RESULTS: Fifteen rats were excluded because of intracranial hemorrhage,anesthetic accident and unqualified neurological functional scores. Other 15 rats with successful modeling were supplied randomly, and totally 50rats entered the final analysis. ① Number of TNF positive cell in immunohistochemical staining: There were no significant differences between normal group and sham operation group [(3.54±1.24, 3.71±1.50) /sight]; but numbers in sub-hypothermia group were lower than those in normal temperature group [(31.94±7.23, 69.20±9.43)/sight, F=179.16, P ＜ 0.001]. ②Numbers of interleukin-1 positive cells in immunohistochemical staining:There were not significant differences between normal group and sham operation group [(3.20±1.34, 3.89±2.08) /sight]; but numbers in sub-hypothermia group were lower than those in normal temperature group [(28.95±4.97, 55.79±7.93)/sight, F=174.95, P ＜ 0.001]. ③ Volume percentage of infarct focus: Percentage in sub-hypothermia group was lower than that in normal temperature group [(21.06±2.42)%, 30.32±2.71], F =374.87, P ＜ 0.001]. ④ Neurological functional scores: Percentage in subhypothermia group was lower than that in normal temperature group [(1.35±0.27)%, (2.04±0.34)%, F=117.17, P ＜ 0.001].CONCLUSION: ① Volume of cerebral infarction focus is lower in subhypothermia group than that in normal temperature group, this suggests that sub-hypothermia can protect ischemic neurons. ② Positive expressions of TNF and interleukin-1 are observed rarely in normal group and sham operation group, but more expression of positive cells are observed in cerebral ischemic area with 24-hour reperfusion after ischemia, this suggests that cerebral ischemia starts expression of inflammatory cytokine, evoke inflammatory cascade reaction, deteriorate cerebral ischemia-reperfusion injury. Therefore, inhibition of inflammatory cascade reaction is one of important mechanisms of protecting brain.

Objective To investigate the protective effect of mild hypothermia during cerebral ischemia and reperfusion. Methods After 3 hours of middle cerebral artery occlusion (MCAO) in rats, the myeloperoxi-dase (MPO) activity, the positive expression of intercellular adhesion molecule-1 (ICAM-1) , and the leukocyte integrin Mac-1 (CD11b/CD18) level in the ischemic regions were determined at different times (6 h,12 h,24 h, 48 h and 72 h) during and after 24 h of reperfusion. Cerebral infarction volume and neurological function were also evaluated in a control group, in addition to the above variables, at 24 hours of reperfusion. Results The MPO activity and the expression of ICAM-1 and Mac-1 were significantly elevated at 6 h after cerebral ischemia during reperfusion. These variables peaked at 48 h. There was a remarkable difference between the various groups and a sham-operated group ( P

Objective To evaluate the protective effect of mild hypothermia against inflammatory cascade reaction in rats during cerebral ischemia and reperfusion.Methods After middle cerebral artery occlusion(MCAO)for 3 h in rats,the expression levels of ICAM-1,TNF-? and IL-1 ? in the ischemic regions were determined at different reperfusion time (6 h,12 h,24 h,48 h and 72 h).At 24 h,the cerebral infarction volume and neurologic function were evaluated.In the control,these were assessed at 24 hours reperfusion.Results (1)Mild hypothermia could ameliorate neurological deficit score and decrease infarct volume induced by cerebral ischemia and reperfusion.(2)The expression of ICAM-1,TNF-? and IL-1? rose obviously at 6 h after cerebral ischemia-reperfusion,and peaked each at 48 h,24 h and 6 h.There was significant difference between the various groups and the sham-operative group(P

Objective:To observe the effect of combined Sanjin Tablets and antibiotic on women with urinary tract infection after sex life. Methods: 306 patients were randomly divided into two groups. The treatment group, taking oral SanJin Tablets and intravenous drip of ciprofloxacin, and the control group only ciprofloxacin given by intravenous drip, treatment course lasted for half a month. Results: In the treatment group, the total effective rate reached 96.77% and the rate of symptomatic improvement was 100.00%, and those indexes in the control group can only reached 80.00% and 82.35% respectively. There were obvious difference between the two groups in the rate of total effective rate and symptomatic improvement (P

BACKGROUND: With the deep investigations of pathophysiological mechanism of acute cerebral infarction, it is discovered that inflammation occupies an important stance in the ischemic injuries of central nervous system ( CNS ), in which tumor necrosis factor-αt (TNF-α), interleukin- 1β(IL-1β), and soluble intercellular adhesion molecule(sICAM-1) become hotspots in the researches.OBJECTIVE: To investigate the relationship between the levels of serous inflammatory cell factors and the course of the disease, the severity of the situation in patients with ischemic stroke.DESIGN: A case-control study based on patients and healthy individuals.SETTING: Department of neurology in a university hospital.PARTICIPANTS: Fifty ischemic stroke patients including 23 males and 27 females with an average age of(60.26 ± 8.77) years old were selected from the outpatient and inpatient Departments of Neurology of the Renmin Hospital of Wuhan University between January 2001 and December 2003. Forty healthy controls including 18 males and 22 females with an average age of (61.05 ± 8.09) years old were selected from the subjects who had physical check up at outpatient department during corresponding period.INTERVENTIONS: Serous TNF-α, IL-1 β and sICAM-1 levels were detected by double-antibody-ELISA.MAIN OUTCOME MEASURES: Serous levels of TNF-α, IL-1β and sICAM-1 in patients with ischemic stroke of different stage, with different infarction volume and different neural functional defects.RESULTS: Serous TNF-α, IL-1β and sICAM-1 levels of patients with cerebral infarction during acute phase and convalescence were significant higher than that of control group( P ＜ 0.01 ), and the levels was significantly higher in acute phase than convalescence ( P ＜ 0.05 ) . The elevation was closely correlated with the degree of neural functional defect and the size of infarction volume, and furthermore, the serous content of TNF-α was also correlated with IL-1β and sICAM-1 levels.CONCLUSION: TNF-α, IL-1β and sICAM-1 interact and participate in the inflammation and reperfusion injury of acute cerebral infarction. Surveillance on them can provide experimental indicators for early clinical therapy and rehabilitative intervention, which is good for the control of the development and recurrence of stroke.

Objective To investigate the effects of mobility training on mobility and the mRNA levels of both synaptophysin and growth associated protein 43 (GAP-43) in the region around an infarction in rats with acute cerebral infarction. Methods Models of cerebral infarction were created in 100 rats through middle cerebral artery occlusion. They were then randomly divided into training and control groups. The motor skill of the rats was examined using a beam walking test. The mRNA levels of both synaptophysin and GAP-43 in the region around the infarction were observed at the 1st, 3rd, 7th, 14th and 28th days after model-creation using a semi-quantitive reverse transcrip-tion polymerase chain reaction. Results The rats' mobility scores increased with training, and significant differ-ences were observed between the average scores of the two groups at the 3rd, 7th and 14th days. The scores were higher in the training group. The mRNA levels of both synaptophysin and GAP-43 in the region around the infarction increased significantly from the 1st to the 3rd and 7th days. Synaptophysin mRNA levels were significantly higher in the trained group at each time point, but the levels of GAP-43 mRNA were significantly higher in the trained group only on the 3rd and 7th days. Conclusions Motor skill and the mRNA levels of synaptophysin and GAP-43 in the region around an infarction can be increased by motor skill training, at least in rats with model acute cerebral infarc-tion.

Objective To investigate the changes and significance of plasma level of homocysteine (Hcy) in Parkinson disease (PD) patients with cognitive dysfunction. Methods Ninety-two PD patients were enrolled. Among them, 51 patients had mild cognitive impairment (CI), and the other 41 had not CI. Forty healthy subjects were enrolled as control group. The information including gender, age, illness duration, years of education and Hoehn and Yahr (H-Y) stage were recorded. Cognitive function of all the patients with PD and the controls were measured by using Montreal Cognitive Assessment (MoCA) scale. Plasma levels of Hcy, folic acid and vitamin B12 were measured by high performance liquid chromatography or radioimmunoassay. Results The plasma level of Hcy in PD group was significantly higher than that in control group: (16.72 ± 5.52) μmol/L vs. (13.65 ± 5.16) μmol/L, there was statistical difference (P<0.05). The plasma level of Hcy in patients with CI was (18.13 ± 4.67)μmol/L, and the patients without CI was (15.44 ± 3.71) μmol/L, the plasma levels of Hcy in patients with CI and without CI were significantly higher than that in control group, furthermore the plasma level of Hcy in patients with CI was significantly higher than that in patients without CI, there were statistical differences (P<0.05). The plasma level of folic acid in PD group was significantly lower than that in control group:(7.15 ± 3.54) μg/L vs. (8.73 ± 3.78) μg/L, there was statistical difference (P<0.05). The plasma level of folic acid in patients with CI was (7.11 ± 3.95) μg/L, and the patients without CI was (7.36 ± 3.84) μg/L, the plasma levels of folic acid in patients with CI and without CI were significantly lower than that in control group, there were statistical differences (P<0.05). But there was no statistical difference in the plasma of folic acid between patients with CI and patients without CI (P>0.05). There was no statistical difference in the plasma of vitamin B12 between the 2 groups (P>0.05). There was a negative relationship between plasma levels of Hcy and folic acid (r =-0.576, P<0.01). The plasma level of Hcy in early PD patients was significantly lower than that in middle-late patients:(15.14 ± 5.31)μmol/L vs. (17.75 ± 5.87) μmol/L, there was statistical difference (P<0.05), and there were no statistical differences in the plasma levels of folic acid and vitamin B12 between early PD patients and middle-late patients (P>0.05). The correlation analysis results showed that MoCA score was positive correlation with years of education (β = 0.541, P = 0.000), MoCA score was negative correlation with illness duration, H-Y stag and plasma level of Hcy (β=-0.417, -0.367 and-0.515;P=0.026, 0.037 and 0.000), but MoCA score was not correlation with age, plasma levels of folic acid and vitamin B12 (P>0.05). Conclusions The changes of plasma level of Hcy may be involved in the pathogenesis of patients with PD. The elevated plasma level of Hcy is significantly correlated with CI, it is an important risk factors of CI in patients with PD.

Objective:To explore the predictive value of systemic immune inflammation index (SII) for the risk of hospital death in critically ill patients.Methods:The basic information and clinical data of critically ill patients were extracted from the Medical Information Mart for Intensive Care database-Ⅳ (MIMIC-IV) database, including demographic data, vital signs, blood routine, Logistic organ dysfunction score (Lods), Oxford acute severity of illness score (Oasis), simplified acute physiology score (Saps-Ⅱ), acute physiology score Ⅲ (APS-Ⅲ), sequential organ failure score (SOFA) and outcome. The main outcome was hospital death, and the secondary outcomes were length of hospital stay, continuous renal replacement therapy (CRRT), invasive ventilation and 1-year mortality. Patients were divided into two groups according to in-hospital death, and the differences between the groups were compared. According to the SII tripartite for inter-group comparison, the patients were further divided into three groups for comparison, and Logistic regression model was used to analyze the odd ratio ( OR) of the three groups. Results:A total of 32 450 critically ill patients were included in the study, of which 3765 died in hospital, with a mortality rate of 11.6%. ① Compared with the survival group, the SII in the death group were significantly higher ( P < 0.05). ② The mortality for the SII tripartite grouping (<817; 817~2 151; >2 151) were 8.4%, 10.2% and 16.3%, respectively, and the differences between groups were statistically significant. ③ Further, Logistic regression model analysis showed that the risk of death increased gradually with the increase of groups (the first group was the reference group, OR of the second group was 1.38, 95% CI 1.24-1.54, and OR of the third group was 2.03, 95% CI 1.83-2.24 ( P < 0.05). Conclusions:SII has a certain value in predicting hospital death in critically ill patients. It is easy to obtain and can be used for risk stratification of critically ill patients.