Objective To investigate whether intrauterine hypoxia and ischemia can produce long-time effects or NOSI can prevent these damages. Methods Fetal rat intrauterine distress model was constructed. The rats were divided into the normal group, hypoxia and ischemia reperfnsion group and treatment group. Pupa were given to surrogate mothers and the ability of learning and memory at 40 day of age after delivery were examined. Then the water maze test was performed to detect the space learning ability and memory function of rats, and the changing of synaptophysin levels in hippocampns were detected by immunohistochemical staining. Result Behavioral results show that fetal distress produces cognitive impairment demonstrated by Morris water maze performance including a higher escape latency score and a de-creased cross platform time. The COD of Syp positive immunoreactive product in hippocampus were less decreased than that in the normal group or NOSI group. But the behavioral results and the COD of synaptophysin had no difference between normal group and NOSI group. Conclusions Fetal distress produced cognitive impairment and led to the decreasing of synaptophysin in hippocampns. Effective measure can relieve these damages.

Objective To investigate the risk factors for clopidogrel resistance (CR) in patients with ischemic stroke.Methods Turbidimatry was used to measure the platelet aggregation rate changes after the patients with acute ischemic stroke taking 75 mg of clopidogrel per day for 10-14 days.The patients were divided into either a CR or a clopidogrel sensitivity (CS) group according to the platelet aggregation rate changes.The demographic and clinical data of both groups were compared.Multivariate logistic regression analysis was used to identify the independent risk factors for CR.Results A total of 147 patients with acute ischemic stroke were included,42 of them (28.57％ ) were in the RC group and 105 (71.43％) were in the CS group.The proportion of patients in diabetes (54.76％ vs.11.43％ ;x2 =31.054,P =0.000),the history of transient ischemic attack (TIA) (80.95％ vs.26.67％ ;x2 =36.251,P=0.000) or percutaneous coronary intervention (PCI) (26.19％ vs.3.81％;x2 =16.400,P=0.000),taking calcium channel blocker (CCB) (83.33％ vs.54.29％ ;x2 =10.810,P =0.001 ),angiotensin converting enzyme inhibitor (ACEI)/angiotensin receptor blocker (ARB) (66.67％ vs.42.86％;x2 =6.803,P=0.009),and proton pump inhibitor (47.62％ vs. 14.29％;x2 =18.375,P =0.000) in the CR group,as well as the levels of plasma total cholesterol (TC),glucose,and glycated hemoglobin were significantly higher than those in the CS group.Multivariate logistic regression analysis showed that diabetes (odds ratio [ OR] 13.711,95％ confidence interval [ CI] 1.667 - 112.784; P =0.015),increased TC level (OR 2.828,95％CI 1.574 - 5.080; P =0.001),previous history of TIA (OR16.627,95％ CI 4.691 - 58.934; P =0.000),and long-term taking CCB (OR 4.147,95％ CI 1.053 - 16.332;P =0.042),and ACEI/ARB (OR 4.841,95％ CI 1.539 - 15.231; P =0.007) were the independent risk factors for CR.Conclusions CR in patients with ischemic stroke is associated with a variety of factors,in which diabetes,increased TC,as well as long-term taking CCB and ACEI/ARB are the independent risk factors for CR.

OBJECTIVE:To explore clinical efficacy and safety of Ulinastatin injection combined with Xingnaojing injec-tion in the treament of severe craniocerebral injury(CCI). METHODS:A total of 120 severe CCI patients selected from our hospital during Sept. 2014-Nov. 2015 were divided into ulinastatin group,Xingnaojing group and combination group according to therapy plan,with 40 cases in each group. Three groups were given routine treatment timely after admission. On the basis of routine treatment,Ulinastatin group additionally received Ulinastatin injection 200 000 U,ivgtt,bid;Xingnaojing group addi-tionally received Xingnaojing injection 20 mL,ivgtt,qd;combination group additionally received Ulinastatin injection com-bined with Xingnaojing injection,same usage as above(with 1 h intervals). Three groups received therapy for consecutive 14 d. Serum inflammatory factors(CRP,IL-1,IL-6,TNF-α),serologic indexes of craniocerebral injury [neuron specific enolase (NSE),myelin basic protein(MBP),S100B protein(S100B)] and GCS scores before and after treatment as well as GOS scores after treatment were all observed in 3 groups. The occurrence of ADR was recorded during treatment. RESULTS:Before treatment,there was no statistical significance in serum inflammatory factors,serologic indexes of craniocerebral injury or GCS scores among 3 groups(P>0.05). Compared to before treatment,inflammatory factors of 3 groups were decreased signifi-cantly after treatment,the ulinastatin group was significantly lower than the Xingnaojing group,combination group was signifi-cantly lower than two single drug groups,with statistical significance(P<0.05). Levels of serologic indexes of craniocerebral injury and GCS scores of 3 groups were improved significantly,and the combination group was significantly better than the two single drug groups,with statistical significance(P<0.05). There was no statistical significance between ulinastatin group and Xingnaojing group(P>0.05). Six months after treatment,GOS score of combination group(4.17±0.81)was significantly better than those of ulinastatin group(3.05±0.97)and Xing-naojing group(2.97 ± 0.89),with statistical significance (P<0.05);there was no statistical significance between ulinastatin group and Xingnaojing group(P>0.05). During treatment,the incidence of ADR in combination group(27.50%)was significantly lower than ulinastatin group(50.00%)and Xingnaojing group(42.50%),with statistical significance(P<0.05);there was no statistical significance between ulinastatin group and Xingnaojing group(P>0.05). CONCLUSIONS:Ulinastatin injection combined with Xingnaojing injection can sig-nificantly decrease serum inflammatory factor levels,relieve craniocerebral injury,protect cerebral tissue and improve short-term prognosis with good safety.

Objective:To assess plasma microfibrillar associated protein 5(MFAP5) level in patients with polycystic ovary syndrome(PCOS), and to explore its relationship with glucose and lipid metabolism as well as sex hormones.Methods:Fifty PCOS patients and 65 healthy female subjects were selected as PCOS group and control group, respectively. Clinical data and plasma MFAP5 levels between the two groups were compared.Results:The plasma MFAP5 level in PCOS group was significantly higher than that in control group( P<0.01), and the plasma MFAP5 level in PCOS overweight subgroup was higher than that in control subgroup( P<0.01). No difference was observed in plasma MFAP5 level between the two non-overweight subgroups( P>0.05). Correlation analysis showed that plasma MFAP5 level was positively correlated with waist circumference, low density lipoprotein-cholesterol, fasting insulin, homoeostasis model assessment of insulin resistance index(HOMA-IR), HbA 1C, testosterone, LH/FSH ratio, and leukocyte( P<0.05 or P<0.01). There was no significant correlation of MFAP5 with body weight, body mass index(BMI), hip circumference, waist hip ratio, high density lipoprotein-cholesterol(HDL-C), triglyceride, total cholesterol, and blood glucose( P>0.05). In PCOS group, plasma MFAP5 level was positively correlated with body weight, BMI, waist circumference, hip circumference, total cholesterol, and leukocyte( P<0.05 or P<0.01). There was no significant correlation of MFAP5 with waist hip ratio, HDL-C, triglyceride, blood glucose, fasting insulin, HOMA-IR, leukocyte, and sex hormones( P>0.05). Multivariate logistic regression analysis showed that MFAP5 was an independent risk factor for PCOS( P<0.05). Conclusion:Plasma MFAP5 level is increased in PCOS patients and is closely related to BMI, waist circumference, hip circumference, and total cholesterol. Plasma MFAP5 is an independent risk factor for PCOS, which may be involved in the pathogenesis of PCOS.

Tumor cells have unique metabolic programming that is biologically distinct from that of corresponding normal cells. Resetting tumor metabolic programming is a promising strategy to ameliorate drug resistance and improve the tumor microenvironment. Here, we show that carboxyamidotriazole (CAI), an anticancer drug, can function as a metabolic modulator that decreases glucose and lipid metabolism and increases the dependency of colon cancer cells on glutamine metabolism. CAI suppressed glucose and lipid metabolism utilization, causing inhibition of mitochondrial respiratory chain complex I, thus producing reactive oxygen species (ROS). In parallel, activation of the aryl hydrocarbon receptor (AhR) increased glutamine uptake via the transporter SLC1A5, which could activate the ROS-scavenging enzyme glutathione peroxidase. As a result, combined use of inhibitors of GLS/GDH1, CAI could effectively restrict colorectal cancer (CRC) energy metabolism. These data illuminate a new antitumor mechanism of CAI, suggesting a new strategy for CRC metabolic reprogramming treatment.