Objective To investigate the relationship between hypoxia-inducible factor-1α(HIF-1α) and construction of collateral circulation in patients with coronary artery disease. Methods Collateral vessels were determined in 96 patients with≥70% narrowing of at least one coronary artery without prior revascularization,42 patients with coronary artery collaterals and 54 patients with no coronary artery collaterals.Another 50 cases with normal coronary arteries were selected as control.The levels of HIF-lα expression in monocytes and lymphocytes were tested by immunohistochemistry (IHC) and Western blot.Results Compared to the controls,the patients had higher expression of HIF-1α(P<0.01).Higher HIF-1α expression was found in patients with collaterals than in those without collaterals (P<0.01).Positive correlation was observed between the expression of HIF-1α protein and collateral score (r1=0.78,r2=0.84,P<0.01).Conclusion HIF-1α expression in circulating monocytes and lymphocytes are associated with collateral circulation.Detection HIF-1α might be helpful in the prognosis of patients with coronary artery disease.

ObjectiveThis study is designed to investigate the relationship between STR polymorphism in HO-1 gene promoter and susceptibility of CAD,in order to provide a new strategy for prevention and treatment of CAD by using HO-1.Methods200 patients who were diagnosed as CAD by coronary angiography were selected in this study.100 subjects without evidence of CAD under coronary angiography with their sex and age similar to CAD patients were selected as controls.Genotyping was performed using polymerase chain reaction followed by capillary electrophoresis automated DNA sequencer.Each size of the (GT) n repeat was calculated using the GeneMapper Analysis software.ResultsA (GT)n polymorphism was found in the HO-1 gene promoter with n =16 ～39.Subjects with n≤29 expressed much more HO-1 protein than those with n ＞29( P ＜0.01 ).The alleles were then classified into two subgroups,S'allele (n 29 ) and L'allele (n ＞29),the subjects were then classified as having an S/S,S/L,or L/L genotype.Subjects with the L allele ( L/L + L/S genotypes) had more chance to get CAD than those with S/S genotype ( adjusted OR =1.83,95 ％ CI =1.04 - 3.24).Stratified analysis further showed that L allele ( L/L + L/S genotypes) was susceptive to CAD in patients who smoke (adjusted OR =2.59,95％ CI =1.16 -5.80).ConclusionsThe (GT)n polymorphism in HO-1 gene promoter is related to susceptibility to CAD,especially in those patients who smoke.

Objective To observe the clinical characteristics, risk factors, and sensitivity to antibiotics of nosocomial infections caused by acinetobacter baumannii. Methods Data were retrospectively collected from all isolated 37 strains acinetobacter. The clinical features, results of suptum culture and test of drug sensitivity were reviewed. Results The 37 acinetobacter baumannii strains mainly distributed in intensive care unit (ICU), most of them had the risk factors of receiving invasive treatment, mechanical ventilation, ect. The antibiotics imipenem, amikacin, pipercillin/tazobactam showed good efficacy for patients with acinetobacter infection, but other antibiotics had highly drug resistant rate. 5 were dead. The mortality of nosocomial infections caused by multi-drug resistant acinetobacter was 41.7%, which was much higher than the non-multi-drug resistant's (2 dead, the mortality was 8%). Conclusion Acinetobacter is one of the most important multi-drug resistant pathogen in nosocomial infections. Antimicrobial agents should be chosen according to antimicrobial susceptibility teat results. Patients who have the risk factors of nosocomial infections caused by acinetobacter should have suptum culture and antibiotic susceptibility studies as soon as possible.

Objective To summarize the clinical characteristics and laboratory test results of children with Henoch - Schonlein purpura(HSP),and further to analyze the risk factors for HSP combined with cardiac damage. Methods The clinical and laboratory tests findings from 707 children diagnosed as HSP at Nanjing Children's Hospi-tal were retrospectively analyzed,who were recruited from November 2011 to December 2012. The possible risk factors for HSP with cardiac damage in children were recorded,including gender,age,predisposing causes,gastrointestinal symptoms,joint pain,kidney disorders,serum electrolytes,anti - streptolysin 〝O〝 test,erythrocyte sedimentation rate, and complement level were summarized. Chi - square test and Logistic regression were performed to analyze the risk fac-tors of cardiac damage in children with HSP. Results Among 707 cases,192(27. 2% )patients were combined with car-diac damage,115 male and 77 female,and the proportion of men to women was 1. 00: 0. 67;age ranged from 11 months to 15 years and 4 months(6 years and 5 months for median age),6 patients ﹤ 3 years old occupying 3. 1% ,103 patients≥3 - 7 years old occupying 53. 7% ,82 patients≥7 - 14 years old occupying 42. 7% ,1 patient≥14 years old occupying 0. 5% ,and the age of onset in preschool and school age. Electrocardiogram(ECG)abnormalities were found in 190 patients,the main manifestations including long Q - T interval,ST - T segment falling down and sinus bradycar-dia,and one or more items of abnormal myocardial enzymes existed in 24 cases;echocardiography was performed in 35 cases of children,but no abnormality was detected,no obvious symptoms such as flustered or chest tightness or precor-dial distress. Statistical analysis showed that gender,predisposing causes,mixed HSP,complement level were related to the incidence of cardiac damage in children with HSP(P ﹤ 0. 05). Furthermore binary Logistic regression identified that in male patients,the ratio of X1 vs OR ratio was 0. 654(95% CI 0. 462 - 0. 926,P ﹤ 0. 05),for predisposing causes,the ratio of X2 vs OR ratio was 2. 63(95% CI 1. 838 - 3. 765,P ﹤ 0. 001),for mixed HSP,the ratio of X3 vs OR ratio was 2. 452(95% CI 1. 301 - 4. 621,P ﹤ 0. 01),which were independent factors for cardiac damage in chil-dren with HSP. Conclusions ECG and/ or myocardial enzyme spectrum abnormalities are the main clinical ma-nifestations of cardiac damage in children with HSP. Male patients,predisposing causes of the respiratory tract infec-tion,mixed HSP and hypocomplementemia were high risk factors in the development of cardiac damage,which require special consideration clinically,and earlier ECG and myocardial enzymes examination,early diagnosis and treatment are necessary to avoid the occurrence of severe cases.

Vascular endothelial growth factor (VEGF) is a powerful angiogeuetic factor. In recent years, it has been found that it has a powerful capacity to promote nerve regeneration, and has potential value in the treatment of ischemic cerebrovascular disease. Newborn endothelial celts can form "vascular niche", and promote neurogenesis by releasing an array of neurotrophic factors. Also, newborn neuronal cells can enhance angiogenesis. There is a "cross-talk" between angiogenesis and neurogenesis, and VEGF plays a very important intermediary role in it. This article reviews the studies of VEGF in promoting angiogenesis and neurogenesis after cerebral ischemia.

Objective To explore the protection of early autophagy activation on podocyte injury induced by aldosterone.Methods In vitro cultured mouse podocyte clones (MPC5) were treated with aldosterone for 6,12,24,48 h respectively.Apoptosis of podocytes was detected by Annexin V combined with flow cytometry.After 24 h treatment with aldosterone,the existence of apoptotic body and autophagosome was observed by electron microscopy.The protein expressions of LC3,caspase-3 and nephrin were examined by Western blotting.The mRNA expression of Beclin-l was detected by real-time PCR.Results The induction of apoptosis and autophagy by aldosterone in podocytes was in timedependent mannner.After 24 h treatment with aldosterone,the apoptosis was increased by 26.5％ (P ＜ 0.05)and the expression of nephrin was decreased by 28.0％ (P ＜ 0.05) compared to control group.Aldosterone remarkably induced the expression of Beclin-1 at 6 h and promoted the transformation of LC3-Ⅰ to LC3-Ⅱat 12 h (P ＜ 0.05).Compared to simple aldosterone treatment,the apoptosis rate of podocyte was increased by 39.0％ (P ＜ 0.05) and the expression of nephrin was declined by 19.5％ (P ＜ 0.05) after 3-methyladenine (3-MA) pre-treatment.Conclusions Aldosterone can induce autophagy and apoptosis in podocytes.Autophagy occurs earlier (12 h) than apoptosis (24 h).The occurrence of autophagy can inhibit the apoptosis,so the autophagy pathway may be a new research topic of glomerular disease treatment.

Objective To explore the clinical value of GLCCI1 gene detection in guiding administration of inhaled corticosteroids in patients with asthma.Methods Eighty asthma patients were divided into wild type allele group (n =64) and mutant type allele group (n =16) according to GLCCI1 gene detection.Both groups were treated with budesonide aerosol,and the clinical effect was compared between two groups.Results In wild type allele group,the total effective rate was 92.2％ and the incidence rate of adverse reaction was 7.8％,which were significantly better than 75.0％ and 25.0％ in mutant type allele group (P ＜ 0.05).There were significant differences in FEV1,FEV/FVC ratio,FVC and PEF between two groups (P ＜ 0.05).Conclusion The GLCCI1 gene detectiou can significantly improve the effect of inhaled corticosteroids and reduce the incidence rate of adverse reactions.

Objective To explore the clinical value of GLCCI1 gene detection in guiding administration of inhaled corticosteroids in patients with asthma.Methods Eighty asthma patients were divided into wild type allele group (n =64) and mutant type allele group (n =16) according to GLCCI1 gene detection.Both groups were treated with budesonide aerosol,and the clinical effect was compared between two groups.Results In wild type allele group,the total effective rate was 92.2％ and the incidence rate of adverse reaction was 7.8％,which were significantly better than 75.0％ and 25.0％ in mutant type allele group (P ＜ 0.05).There were significant differences in FEV1,FEV/FVC ratio,FVC and PEF between two groups (P ＜ 0.05).Conclusion The GLCCI1 gene detectiou can significantly improve the effect of inhaled corticosteroids and reduce the incidence rate of adverse reactions.

Objective To detect the α1-antitrypsin (AAT) concentration in urine samples of children with primary nephrotic syndrome (PNS) before initiation of glucocorticoid treatment,in order to verify whether it could predict the response to glucocorticoid-based therapy.Methods Forty-three children diagnosed as PNS initially were chosen as subjects,namely steroid-sensitive nephrotic syndrome (SSNS) and steroid-resistant nephrotic syndrome (SRNS) depending on reaction to glucocorticoid therapy four weeks later,and 15 healthy children serving as normal control.The mid stream of the first morning urine samples were collected from children before taking glucocorticoid.ELISA kit was used to quantify the urinary AAT concentration which was revised by urine creatinine further.The data of urine AAT/Cr were expressed as median with interquartile range.Data analysis was performed using the SPSS 17.0.Results AAT was absent in urine samples of normal healthy children,and there were no statistic differences of the AAT concentrations in urine between children with SSNS and SRNS [(30.4+4.5) mg/L vs (31.8+4.6) mg/L,t=-1.0,P=0.33].The level of urine AAT/Cr in children with SRNS was higher than that in children with SSNS [0.049(0.028-0.073) vs 0.028(0.022-0.036),Z=2.4,P=0.02].Among the laboratory parameters of the two subgroups before taking glucocortiod,the levels of platelet,blood white cell count,serum globulin,urine white cell count,urine red cell count,urine IgG and urine α1-microglobulin were significantly different (P＜0.05).Three parameters that included urine AAT/Cr (OR=6.81 × 1028,P=0.O05),serum globulin (OR=1.69,P=0.01) and urine α1-microglobulin (OR=1.05,P=0.009) further entered the logistic regression model to predict the SRNS independently.The ROC curve based on the level of the urine AAT/Cr was constructed,and the area under the curve (AUC) was 0.72.When the cutoff value of urine AAT/Cr was 0.035,the sensitivity and specificity of the urine AAT/Cr prediction were 68％ and 75％ respectively (Youden' s index 0.43).The AUC that based on the logistic regression model which included urine AAT/Cr,serum globulin and urine α1-mieroglobulin was improved to 0.94,and the sensitivity and specificity of the model prediction were 95％ and 83％ respectively (Youden' s index 0.78).There was no significant difference of the urine AAT/Cr level among the different pathological types of the children undergoing renal biopsy.Conclusions There are no statistic differences of the AAT concentrations in urine between children with SSNS and SRNS.The level of urine AAT/Cr is significantly higher in the SRNS than that in the SSNS which can be as a candidate biomarker to predict the response to glucocorticoid-based therapy.It has a better prediction efficacy based on the model which includes urine AAT/Cr,serum globulin and urine α1-microglobulin.

Objective To explore the effects and mechanism of hydrogen sulfide on myocardial ischemia reperfusion in rats. Methods With sodium hydrogen sulfide (NaHS) as a donor of hydrogen sulfide ( H2S), we established myocardial ischemia-reperfusion injury model in rats. The SD rats were randomly divided into control group,myocardial ischemia reperfusion group (I/R group), H2S group,and H2S and glibenclamide (H2S + GLI)group. We monitored the hemodynamics index of rats, including heart rate, arterial pressure, left ventricular pressure. The rate of ventrical arrhythmia was also observed in each group. Results H2 S significantly reduced the ventricular arrhythmia (VA) occurrence (H2S group 66.5% vs I/R group 33.5% (P ＜0.05) and score in myocardial ischemia reperfusion rats (H2S group 2. 6 ±0. 7 vs I/R group 4. 5 ±0. 8(P＜0.05). The KATP channel blocker,glibenclamide,could weaken the antiarrhythmic effects of H2S ( H2S group 2. 6 ±0. 7 vs. H2S + GLI group 4. 0 ± 0. 6, P ＜ 0.05 ). Conclusions H2S has the protective effect against myocardial ischemia reperfusion damage. This function may be associated with the KATP signal transduction pathway in cells.