Objective To investigate the clinical values of serum histidine decarboxylase(HDC),intestinal fatty acid binding protein(I-FABP),and diamine oxidase(DAO)for diagnosing intestinal mucosal injury (IMI)in patients with intestinal obstruction.Methods The expression levels of serum HDC,I-FABP,and DAO in 28 patients with strangulated intestinal obstruction,19 patients with simple intestinal obstruction,17 patients with acute simple appendicitis,and 20 healthy control were determined by enzyme-linked immunosorbent assay (ELISA)before clinical treatment,and then the areaa under receiver operating characteristic curves(AUC)of these diagnostic indicators were compared.In addition,the incidences of systemic inflammatory response syndrome (SIRS)and infectious complications were closely observed.The difference of the expressions of HDC,I-FABP,and DAO and their relationship with SIRS and infectious complications were compared among these patients and controls.Results The expression levels of serum HDC, I-FABP, and DAO were the highest in patients with strangulated intestinal obstruction (all P < 0.001), and the expression levels of these three indicators were significantly higher in patients with simple intestinal obstruction than in those with acute simple appendicitis or healthy controls (all P<0.05).The AUC of HDC (0.913) was significantly larger than that of I-FABP (0.877, P =0.000) and DAO (0.873, P = 0.000).When the cut-off value of HDC ≥31.00 ng/ml, the sensitivity, specificity, false negative rate, and false positive rate of HDC were 74.5% , 94.6% , 25.5% , and 5.4% , respectively,which were all better than those of I-FABP and DAO.There were significant differences of the incidence of SIRS ( P = 0.046) and abdominal infection (P = 0.027) among patients with strangulated intestinal obstruction, patients with simple intestinal obstruction, and patients with acute simple appendicitis, while lung infection showed no such significant difference (P = 0.728).The expression level of serum HDC was significantly higher in patients with strangulated intestinal obstruction who were also suffered from SIRS ( P = 0.000) or abdominal infection ( P =0.002) than that of uninfected patients.Meanwhile, the expression levels of serum I-FABP and DAO were significantly higher in the SIRS patients with strangulated intestinal obstruction than that of uninfected patients ( P = 0.027, P=0.017, respectively).The expression levels of HDC, I-FABP, and DAO were significantly correlated with the incideces of SIRS and abdominal infection ( all P < 0.05 ) , among which the level of HDC and the incidence of SIRS had the highest correlation (R = 0.608, P = 0.001).Conclusion HDC can be an effective indicator for diagnosing IMI in patients with intestinal obstruction.

Intestinal ischemia is a severe and life-threatening acute abdomen. Although its incidence is low,early diagnosis remains relatively difficult. The efficiencies of conventional laboratory biochemical tests are low. In recent years, many new markers for the early diagnosis of intestinal ischemia have been developed. In this article,we summarize their diagnostic efficiencies and relevant factors.

Intestinal immunologic barrier plays an important role in preventing the bacterium and endotoxin.Lymphocyte homing to the intestine is one of the normal intestinal immunologic functions,and has the theoretical significance and clinical value for the balance of intestinal immunologic barrier.The basic and clinical researches of lymphocyte homing to the intestine are reviewed.

Objective To evaluate and analyze the effect of treatment on fractures of the clavicle with reconstruction plate or with Kirschner wire.Methods Of 56 clavicular fracture cases for treatment with surgical procedures,22 cases were fixated with reconstruction plate.34 cases were fixated with Kirschner wire.Results All 56 cases were followed up for 10~48 months,on average 21 months.Reconstruction plate fixation group:2 cases concomitant with delayed fracture healing were multiple trauma patients.The mean union time in this group was 3.6 months(range from 3 to 5 months).Kirschner wire fixation group:3 cases with wires migration.The mean union time in this group was 2.3 months(range from 2 to 3 months).According to Kalarsson's shoulder function evaluating criteria,all cases were excellent.Conclusion Surgical technique with Kirschner wire is simple and credible treatment for clavicular uncomminuted fractures.,it complys with the conception of minimally invasive technique and is a recommendable way.

Objective To detect the effect of deep hypothermia on the function of mitochondria in hippocampus after global ischemia in rats and to explore the protection mechanism. Methods The animal model of cardiopulmonary bypass (CPB) was established in rats that were then randomly divided into three groups,ie,control group,normothermia ischemia group and hypothermia ischemia group,eight rats per group.The mitochondria was extracted from the hippocampus of each rats for observing the mitochondrial respiratory function,the activities of succinate dehydrogenase (SDH),the cytochrome oxidese(CCO),the lnembrane fluidity and the content of intramitochondria free calcium and MDA. Resuits The content of intramitochondria free calcium and MDA in the normothermia ischemia group was increased significantly compared to the control group and that in the hypothermia ischemia group wag decreased significantly compared with the normothermia ischemia group(P<0.05).Respiratory state Ⅲ (R3),respiratory state IV(R4),P/O ratio and oxidative phosphorylation (OPR) in the normothermia ischemia group were decreased significantly compared to the control group (P<0.05).R3,R4,P/O ratio and OPR in the hypothermia ischemia group were increased significantly compared with the normothermia ischemia group (P<0.05).Membrane fluidity in the normothermia ischemia group wag decreased significantly compared to the control group (P<0.01),while that in the hypothermia ischemia group was increased significantly compared with the normothermia ischemia group(P<0.05).The activities of SDH and CCO in the normothermia ischemia group were decreased significantly compared to the control group (P<0.01),while those in the hypothermia ischemia group were increased significantly compared with the normothermia ischemia group (P<0.05). Conclusion Profound hypothermia exerts a protective effect on the function of mitochondria in the hippocampus after global ischemia in rats.

Objectives To investigate the clinical significance of CYP2C19 genotype detection for antiplatelet therapy of elder cardiovascular and cerebrovascular diseases(CCVD).Methods We enrolled all elderly patients with either cardiovascular or cerebrovascular disorders who received clopidogrel as mono drug or in combination with another antiplatelet drug aspirin as secondary prevention for more than 12 months in our hospital from January to August 2015.Somatotypes of CYP2C19 genotypes of all participants were assessed to analyze the relapse of cardiac-cerebral vascular diseases in these patients.Results A total of 250 patients were enrolled,including 179 male and 71 female,with average age of (85.2 ± 7.9) years.Among these patients,there were 97 (38.8％) cases with EM CYP2C19 genotypes,110 cases(44.0 ％) with IM CYP2C19 genotypes,43 cases(17.2 ％) with PM CYP2C19 genotypes.When treated with clopidogrel for antiplatelet in secondary prevention process,the rate of the relapse in cardiovascular event was 34.9％ and higher in PM CYP2C19 genotype than in EM and IM CYP2C19 genotype (19.6 ％ and 15.5 ％,respectively) (x2 =7.251,P =0.027).This phenomenon was similar to patients who received stent implantation(x2=6.393,P =0.041).However,no statistically significant difference was observed in the recurrence rate of cerebral vascular disease between three different genotypes(EM 29.9 ％,IM 20.0 ％,PM 27.9％,x2 =2.880,P =0.237).Conclusions Our results highlight that CYP2C19 genotype might be a potential guidance for secondary prevention of cardiovascular and cercbrovascular disorders among elderly patients.Clopidogrel may be less effective in patients with SM CYP2C19 genotype than those with EM or PM CYP2C19 genotype for secondary prevention of cardiovascular disease.

AIM: To investigate the protective effect of fluvastatin and its influence on ICAM-1 mRNA expression in ischemia/reperfusion myocardium of normocholesterolemic rabbits. METHODS: 24 rabbits were divided into three groups randomly and myocardial ischemia/reperfusion model in the rabbit was made. Rabbits were subjected to 45 min of regional myocardial ischemia and 2 h of reperfusion. 10 mg?kg~ -1 ?d~ -1 fluvastatin were administered for one week. Dynamic index of blood flow was recorded and analyzed. Serum activity of CK, CKMB, LDH and LDH-1 were measured. The expression of ICAM-1 mRNA in ischemic myocardium was detected with semi-quantitative RT-PCR. RESULTS: In comparison with control group, pretreatment with fluvastatin decreased LVEDP at the whole observed duration, and spontaneously increased ?dp/dt_ max . Serum activities of CK, CKMB and LDH-1 in control group were significantly higher than those in sham group, but heavily reduced in fluvastatin group. Increased expression of ICAM-1 mRNA due to ischemia reperfusion was reduced significantly in fluvastatin group compare to control group. CONCLUSION: Pretreatment of fluvastatin may reduce inflammation reaction in reperfused myocardium, and this may contribute to its protective effect against experimental myocardial ischemia reperfusion injury.

Objective To investigate the effects and mechanism of different dosage of fluvastatin on the prevention of heart muscle ischemia reperfusion injury in rabbits.Method Thirty-five rabbits were randomly divided into 5 groups with 7 rabbits in each: sham group,myocardial ischemia reperfusion control group,low dosage of fluvastatin pretreatment group (2 mg/kg,Group F1),middle dosage of fluvastatin pretreatment group(5 mg/kg,Group F2) and large dosage of fluvastatin pretreatment group(20 mg/kg,Group F3).The left ventricular systolic pressure(LVSP),the max rate of rise of left ventricular pressure(?dp/dt_(-max)) and left ventricular end-diastolic pressure(LVEDP) were detected during the experiment.At the end of reperfusion,the infarct size and area at risk were defined by Evans blue and TTC staining,and the levels of myocardial nitrogen monoxidum(NO) and nitricoxide synthase(NOS) were measured.Result Compared with the ischemia reperfusion group,the indexes of heart function improved significantly,the level of myocardial NO was increased significantly and the myocardial infarct size was decreased significantly in the groups F2 and F3.There was no significant difference between the group F1 and ischemia reperfusion group.Conclusion Fluvastatin exerts a cardioprotective effect against myocardial ischemia reperfusion injury in rabbits.NO is likely involved in this protective mechanism.

Objective To detect the expression changes and location of the mouse developmental regulation brain protein(Dbn1)in the developmental mouse brain.Methods Monoclonal antibodies against drebrin protein were used to assess Dbn1 by immunohistochemistry and Western blot.The paternal expression of Dbn1 in developmental mouse brain(E14,P1,P7 and adult)was initially investigated by Western blot.Dbn1 was shown at various developmental stages(E14,P1 and P7)as well as in adult in different brain area of developmental mouse brain by immunohistochemical.Results Dbn1 protein was detected in developmental brain but a little in adult brain by Western blot,high at E14,decreased at P1,gradually increased at P7 and lowest in adult.Immunohistochemistry confirmed as follows:Dbn1 expressed mostly in cortex,hippocampus and ependyma areas at E14,and the positive signal was distributed at cells border;The expression of Dbn1 was decreased at P1,mainly distributed at the verge of cells or dendrites;The peak expression of Dbn1 appeared at P7,Dbn1 located at nucleus of hippocampus and cortex,and the positive signal located within cytoplasm and dendrites;Only a little positive Dbn1 cells were found in adult mouse brain.Conclusion Dnb1 may be involved in regulating the differentiation and migration of neurons during the development of mouse brain.