0.05). As compared with Qingkailing group, the body temperature at the 5th day of treatment and WBC at the 3rd day of treatment were significantly decreased (P

Objective To investigate the effects of propofol on lipopolysaccharide (LPS)-induced brain injury in rats.Methods Fifty-four pathogen-free SD rats of both sexes, aged 6 weeks, weighing 200-250 g, were randomly divided into 3 groups: control group (group C, n = 6) ; LPS group (group L, n = 24) ; propofol group (group P, n = 24) . Brain injury was produced by injection of LPS 1 mg/kg via the left internal carotid artery in L and P groups. Propofol 100 mg/kg was injected intraperitonealry immediately after the LPS administration in group P, while the equal volume of normal saline was given instead of propofol in group L. The equal volume of normal saline was given instead of LPS and propofol in group C. Six rats in each group were sacrificed and the brain tissues were immediately removed at 24 h after intraperitoneal administration in group C, and at 6, 24, 48 and 72 h after intraperitoneal administration in L and P groups for determination of brain water content, high-mobility group box 1 ( HMGB1) expression and NF-κB activity, and microscopic examination. Results The brain water content and NF-kB activity were significantly increased, and HMGB1 expression was up-regulated in group L as compared to group C (P ＜ 0.05) . The brain water content, expression of HMGB1 and NF-kB activity were significantly lower in group P than in group L ( P ＜ 0.05) . The microscopic examination showed that brain injury was attenuated in group P compared with group L. The brain water content was positively correlated with the HMGB1 expression and NF- κB activity (r = 0.692 and 0.769 respectively, P ＜ 0.05). Conclusion Propofol can reduce the LPS- induced brain injury by reducing inflammatory response of the brain tissues.

Aim To observe the effects of Xiatianwu tota l alkaloids ( XA ) on learning and memory impairment and the central cholinergic f unction in rats with quinolinic acid microinjected into bilateral hippocampus. Methods Alzheimers disease (AD) rat models were made by damagin g bilateral hippocampus with quinolinic acid (150 nmol in 2 ?l for each hippoca mpus). XA 0.25, 0.5, 1 mg?kg -1 was administrated ig from 1 week before model established to 3 weeks after model established. Y-maze was used to measur e the learning and memory ability. The activity of the acetylcholinesterase ( AC hE ) in hippocampus and the contents of acetylcholine ( ACh ) was determined by spectrophotometry. Results Microinjection of quinolinic acid in to the rats hippocampus induced learning and memory dysfunction (P

Objective To study the expression and significance of CEA in occult micrometastasis ofcolorectal carcinoma. Methods 287 cases without metastatic lymph nodes were observed in 54 cases ofcolorectal carcinoma by immunohistochemical (LSAB) method. Results 15 cases of lymph nodes werefound with occult micrometastasis in 8 patients. All micrometastasis was positive in detection of CEA.Conclusion Detection of CEA was conducive to detect micrometastasis of lymphnode. It is significant forDukes staging,prognostic determination and treatment.

Objective To explore the changes of serum leptin level in patients with diabetic microangiopathy.Methods A total of 90 subjects were assigned to three groups which included 30 healthy controls,30 diabetic patients without microangiopathy and 30 patients with diabetic microangiopathy.The studing groups were matched for sex and BMI.The level of serum leptin ,ⅣC,insulin and glucose of these patients were measured,and the correlation between serum leptin level and other indexes was analyzed.Results The level of serum leptin in controls,diabetic patients without microangiopathy and patients with diabetic microangiopathy were (7.20?2.11) ?g/L, (7.95?3.78)?g/L and (10.26?4.37)?g/L respectively .The patients with diabetic microangiopathy had higher serum leptin levels than in the diabetic patients without microangiopathy( t =2.18, P

Aim To study the role and mechanism of opioid receptor on IL-1?-induced fever.Methods Rats were dealed with intracerebreventricular administration of naloxone and/or IL-1?.Changes in body temperature were measured.The content of cAMP and HSP70 expression in hypothalamus were detected.Results Naloxone can limit IL-1?-induced fever and decrease the content of cAMP and HSP70 expression in hypothalamus(P

Objective To explore the effect of Eight-Section Brocadeon improving extrapulmonary performance and lung function in elderly stable chronic obstructive pulmonary disease (COPD) patients. Methods A total of 120 elderly stable COPD patients were divided into experimental group and control group by random digits table method with 60 cases each. The experimental group received Eight-Section Brocade and the control group took a walk both based on the routine health education. The World Health Organization Quality of Life (WHOQOL)-BREF, 6 min walking test and lung function were conducted before and after intervention 12, 24 and 36 weeks. Results After intervention, the score of each field of WHOQOL-BREF were higher than those before intervention, comparison of two groups of physiological fields Ftime=57.112, Fgroup=10.510, Finteractive=13.653, all P<0.01; psychological field Ftime=240.209, Fgroup=6.201, Finteractive=6.902, all P<0.05;field of social relations Ftime=34.957, Fgroup=7.265, Finteractive=11.554, all P<0.01; environmentfield Ftime=66.431, Fgroup=8.197, Finteractive=18.413, all P<0.01, and there were significant differences in time, groups and interactive. Comparison of two groups of the result of 6 min walking test after intervention, Ftime=327.697, Fgroup=37.181, Finteractive=61.420, all P<0.01. Comparison of two groups of the result of lung function indexforced expiratory volume in one second, Fgroup=5.083, P<0.05, there was significant difference;after intervention the index of Forced expiratory volume in 1 second take up of the expected value, Fgroup=4.141, P<0.05, there was significant difference. Conclusions Eight-Section Brocade can effectively improve the elderly stable COPD patients with exercise endurance and quality of life, improve the extrapulmonary performance, delay the progressive decline of lung function.

Objective To investigate the effects of 2.45 GHz microwave on the apoptosis of HeLa cells and explore the underlying mechanism.Methods HeLa cells were divided into five groups randomly:control group,sham-irradiation group,and three irradiation groups exposed with 10,15 and 20 mW/cm2 2.45 GHz microwave for 10 min.Cell survival was tested by MTT assay,cell nucleus fashion was observed by a laser scanning confocal microscope,cell cycle distribution was measured by flow cytometry,and cell protein expressions were detected by Western blot.Results The cell survival in control group,shamirradiation group and low dose irradiation group had no difference but it became lower in the middle and high dose irradiated group(t =-16.47,-14.23,P ＜ 0.05).The abnormal rates of nuclear fashion in the low,middle and high dose irradiation groups were obviously higher compared with control group (t =9.37,11.25,8.47,P ＜ 0.05),while high dose irradiation group was higher than the low and middle dose group (t =15.32,10.25,P ＜0.05).The rate of HeLa cells in sub-G1 in the irradiation groups were higher than that in control group (t =15.24,22.31,10.69,P ＜ 0.05).The results of immunohistochemistry showed that the expression of Bax and Caspase-3 in irradiation groups was significantly increased,and the expression of Bcl-2 was decreased.Conclusions 2.45 GHz microwave can induce HeLa cells apoptosis with a positive correlation with microwave dose.