Objective To investigate the common etiologies,sports and learning situation of children in Nantong with short stature,and discuss the relationship between the two. Methods Did a retrospective analysis of 108 cases of children with short stature in Nantong University′s affiliated hospital since January 2012. Through detailed past illnesses, physical examination, laboratory tests, diagnose short stature and clarify the cause. Did a questionnaire to these children with short stature about sports and learning situation. Use statistical methods like multivariate Logis-tic regression analysis and link analysis to analyze sports and learning situation of children in Nantong with short sta-ture and find the relation with the etiology. According to the principle of group matching,the control group elected representative of 108 children. Results In 108 cases, 61 cases were because of growth hormone deficiency (GHD), accounting for 56. 5% ; 47 cases were because of non-growth hormone deficiency (NGHD), accounting for 43. 5% . Logistic regression analysis showed that participation in physical exercise was a protective factor. Rest-less anxiety and inattention were as risk factors,and these make a lot(P < 0. 001, OR = 7. 483, 95% CI = 2. 620 ~21. 374). There was no significant relation between common cause and sports, learning situation ( P > 0. 05). Conclusion Various types of sports (basketball, badminton, running, cycling) are protective factors for children of short stature. Restless anxiety and inattention are risk factors for children with short stature. Whether there is growth hormone deficiency or not, children with short stature should increase the right exercise as much as possible and avoid or reduce exposure to these risk factors.

Objective The epidemiology of Acinetobacter baumannii isolates from bloodstream infections,their antibiotic resistance profiles and virulence-associated factors were studied.Methods A total of 90 isolates from 17 hospitals were collected from the patients with bloodstream infections during July 2013 and July 2014.Vitek-2 Compact system was used for identification of the strains and antibiotic susceptibility testing.The epidemiology was studied by pulsed-field gelectrophoresis(PFGE).Drug-resistant genes and associated virulence genes were amplified by PCR.Results According to antimicrobial susceptibility testing,75 isolates are multi-drug resistant Acinetobacter baumannii.PFGE results showed that 75 multi-drug resistant Acinetobacter baumannii isolates belonged to eight clone types(A to H),with the A (n=51)and B (n=14)clone being the dominant PFGE clone types.Different clone isolates spread in different hospitals.Most of the hospitals were given priority to with clone A.Clone A only maintaining high sensitive rate to cefoperazone/sulbactam、amikacin and tigecycline.Virulence gene abaI,cusE,ompA,bap,bfms detection rates are 93.3% (84/90),92.2% (83/90),100.0% (90/90),84.4% (76/90),92.2% (83/90),respectively.There were 7 mucoid isolates,which are all multi-drug resistant Acinetobacter baumannii,all belong to clone B and all associated virulence genes can be detected.Conclusions The dominant clone type of multi-drug resistant Acinetobacter baumannii from bloodstream infections is clone A.The abaI-,bap-and bfms-positive strains are associated with a higher incidence of antibiotic resistance in most types of antimicrobials.The acquisition of mucous type may indicate the emergence of virulent strains,which should be paid attention to during clinical treatment.

AIM: To make evaluation on fluid resuscitation with either hypertonic saline(HS) or dextran 40(Dx) on pancreatic microthrombi and dysfunction of microcirculation in rats with severe acute pancreatitis(SAP).METHODS: SD rats were allocated into 4 groups randomly,ie.SAP group,HS group,Dx group,which respectively received normal saline(NS,4 mL/kg),HS(4 mL/kg),Dx(4 mL/kg) for 2 h by the tail intravenous injection consecutively after being made as SAP animal models,and operate sham group(OS).12 h after the operation,all animals were blooded to assess the serum amylase levels,plasma D-dimer,von Willebrand factor and GMP-140 levels.The amount of ascites was measured and the samples of the pancreas were collected for pathologic examination under light microscopy as well as transmission electron microscope.The numbers of pancreatic microthrombi were also counted with microscopy.RESULTS:(1) 12 h later when the rats were sacrificed,the survival rate in SAP group was the lowest,significantly lower than that in the 2 fluid resuscitation groups(P

AIM:To observe the effect of captopril on the genesis and development of gastric cancer , and to explore its clinical treatment feasibility for gastric cancer .METHODS:The human gastric cancer cell line AGS was used to establish a tumor model in nude mice , and the model mice were randomly divided into 3 groups: positive control ( 5-fluorouracil) group, normal control (saline) group and experimental (captopril) group.After intraperitoneal injection or intragastric administration of the drugs , the tumor growth curve was determined , and the tumor tissues were also sampled to detect the expression of Ki-67, STAT3, Bax and Bcl-2 by real-time quantitative PCR and immunohistochemistry .The apop-tosis was detected by TUNEL +DAPI staining .RESULTS: The tumor growth curve showed that the tumor model in the nude mice was successfully established .The tumor volumes among groups showed significantly different after 14 d growth. The increase in the tumor volume in normal control group was significantly faster than that in the other two groups , and that in positive control group was the slowest .The expression of Bax in captopril group increased , and the expression of STAT3, Ki-67 and Bcl-2 was reduced as compared with normal control group and positive control group .Compared with normal con-trol group, the apoptotic rate increased significantly , and the protein expression of p-STAT3 and STAT3 decreased obviously in positive control group and captopril group .CONCLUSION:With better feasibility , angiotensin-converting enzyme in-hibitor captopril has a significant effect on treating gastric cancer in the AGS nude mouse model by regulating the expression of STAT3, Bax, Bcl-2 and Ki-67 to accelerate the apoptosis of cancer cells , thus inhibiting tumor growth .

Objective To evaluate the diagnostic accuracy of ultrasound miniature probe(UMP)examination in tumor invasion(T staging) and local lymphatic node metastasis(N staging) for colorectal carcinoma. Methods Preoperative UMP examinations(12 MHz) were performed on 53 patients with colorectal carcinoma undergoing surgeries.The diagnosis accuracy of UMP examination in T and N staging was determined by comparison of the results of operation exploration and histopathologic findings. Results The accuracy in T staging for colorectal carcinoma was 86% with UMP examination,and that for early stage colorectal carcinoma was 100%.The accuracy,sensitivity and specificity in N staging for colorectal carcinoma were 81%,77%,and 84%,respectively with UMP examination. Conclusion UMP examination works well in determining T stage of colorectal carcinoma,especially for early stage colorectal carcinoma and those with tumor stenosis.

ObjectiveTo observe the effect of Shenxiong-Huayu Capsule preconditioning on cell apoptosis and the expression of c-fos、c-jun in the hippocampal CA1 area of rats with acute cerebral ischemia reperfusion injury.Methods SD rats were divided into 3 groups by completely randomized method:sham operation group(n=6),ischemia reperfusion group (model group),and Shenxiong-Huayu Capsule preconditioning group (preconditioning group).The last two groups were divided randomly into 6 h,24 h,48 h and 72 h reperfusion subgroups (each n=6).Intragastric administration for 7 days,once a day.Middle cerebral artery occlusion and reperfushion model was made by an intraluminal filament method.Cell apoptosis was detected by TUNEL method,the expression of c-fos、c-jun was observed by immunohistochemistry.Results ① The number of apoptosic cells at 6、24、48、72hin the hippocampal CA1 area ofrats was respectively (11.17±3.71、39.83 ± 5.67、48.33± 5.32 and 22.17± 3.7 1) single/High power field in the model group,and was respectively (7.83±2.04、15.00±3.58、29.50±6.89 and 10.17±2.32) single/High power field in Shenxiong-Huayu Capsule preconditioning group.Compared with the model group,the number of apoptosic cells at each time point in the hippocampal CA1 area of rats was decreased in Shenxiong-Huayu Capsule preconditioning group(P＜0.05 or P＜0.01 ).② The number ofc-fos at 6、24、48、72 h in the hippocampal CA1 area of rats was respectively (14.50± 3.45、33.67± 1.63、42.33±3.32 and 32.00 ±2.90) single/High power field in the model group,and was respectively (10.17 ± 2.93、21.50 ± 2.43、30.83 ± 3.76 and 25.17 ± 5.27) single/High power field in Shenxiong-Huayu Capsule preconditioning group.The number of c-jun at 6、24、48、72 h in the hippocampal CA1 area of rats was respectively (15.50±4.19、22.83±5.64、33.10±4.19 and 14.67±3.08) single/High power field in the model group,and was respectively (9.67± 3.63、15.67±2.73、21.26±3.63 and 9.33 ±3.61)single/High power field in Shenxiong-Huayu Capsule preconditioning group.Compared with the model group,the expression of c-fos、c-jun at each time point in the hippocampal CA1 area of rats was decreased in Shenxiong-Huayu Capsule preconditioning group (P＜0.05 or P＜0.01).ConclusionShenxiong-Huayu capsule can inhibit apoptosis by restraining the expression of c-fos、c-jun and relive cerebral ischemia reperfusion injury in rats.

Objective To investigate the role of miR-126 (micro RNA-126) in rat endothelial progenitor cells (EPCs) proliferation and migration and the starget gene of miR-126 by bioinformatics and experimental survey.Method EPCs were transfected with control oligoes and miR-126 mimics or inhibitor by electroporation.MTT was performed to evaluate the growth of EPCs subjecting to miR-126 overexpression.Cell migration analysis was done by wound healing and transwell assay.The target genes of miR-126 were predicted by TargetScan and validated by Western blot.Result (1) miR-126 mimics promoted EPCs growth at 24 h post cell transfection (P ＜ 0.01).In contrast,the EPCs growth was immue from miR-126 application at 48 and 72 h.(2) Both the wound healing and transwell assay show that miR-126 promotes EPCs migration (P ＜ 0.01) and miR-126 inhibitor inhibits EPCs migration (P ＜ 0.01).(3)It is predicted that KANK2 is the potential target gene of miR-126 by TargetScan online software.(4) The results of Western blot indicated that miR-126 mimics repress the expression of KANK2 compared with NC but miR-126 inhibitor enhances KANK2 expression.Conclusions miR-126 has a transient effect on the promotion of EPCc growth.miR-126 promotes EPCs migration and targets KANK2 protein.

Intrahepatic bile duct stones located at the upper part of the hepatic duct.The percentage of intrahepatic biliary cholesterol calculus is increasing in recent years,and the incidence of this type of bile duct stones is free from infection or obstruction.The formation of intrahepatic bile duct stones might not only related to the micro-environment changes in the biliary tract,but also related to the changes of metabolic function of hepatocytes or cholangiocytes.In this article,the mechanism of biliary hydrodynamics on the formation of intrahepatic bile duct stones was reviewed.

Surgical resection remains the only curative option of treatment for hepatocellular carcinoma,but centrally located tumors remain problematic.Extended right or left hepatectomy removes 60％ to 85％ of the hepatic parenchyma and is associated with more hepatic failure.Mesohepatectomy,resection of central hepatic segments (Couinaud's segments Ⅳ,Ⅴ,Ⅷ) and leaving the right and left segments in situ,preserves more functional hepatic tissues than extended hepatectomy.Despite its technical demands,mesohepatectomy should be considered as an alternative treatment for central huge hepatic tumors.

Objective To investigate whether baicalein inhibits the proliferation, cell cycle of and pseudopod formation in A431, a skin squamous cell carcinoma cell line, by suppressing the expression of ezrin protein. Methods A431 cells were grouped to be transfected with ezrin-targeting siRNA (siRNA group), treated with baicalein of 5, 10, 20, 40 μmol/L, respectively (baicalein group), or remain untreated (control group). After additional culture, wound healing assay and Transwell assay were performed to observe the migration and invasion of A431 cells, RT-PCR to detect the mRNA expression of ezrin in A431 cells, Western blot and immunoflu-orescence to measure the expression of ezrin protein and its phosphorylation. The pseudopod formation in A431 cells was observed by using scanning electron microscopy. Results After 24-hour culture, wound healing assay displayed that the percent wound closure was 13.3 ± 1.7, 7.6 ±1.6 and 5.9 ± 1.3, respectively, in A431 cells treated with baicalein of 5, 10, 20μmol/L, significantly lower than that in untreated A431 cells (16.3 ± 2.3, all P < 0.01), and the inhibition of baicalein on the migration of A431 cells was concentration-dependent. In the Transwell assay, a significant decrease was observed in the number of A431 cells per high power field permeating through the artificial basement membrane in the groups treated with baicalein of 5, 10, 20 μmol/L for 48 hours compared with the control group (46.5 ± 3.8, 34.3 ± 3.4, 25.3 ± 2.3 vs 56.3 ± 3.8, all P < 0.01), whereas no significant difference was noted between these baicalein-treated groups and siRNA-transfected group (28.3 ± 2.1, all P > 0.05). RT-PCR analysis showed that the mRNA expression of ezrin in baicalein-treated A431 cells significantly decreased compared with that in untreated cells (all P< 0.01), but showed no difference from that in siRNA group (P > 0.05). A statistical difference was also observed in the expression of ezrin and phosphorylated ezrin protein between baicalein-treated A431 cells and untreated cells (all P< 0.05), but not between 40 μmol/L baicalein-treated A431 cells and siRNA-transfected cells (P> 0.05). Furthermore, the suppression of baicalein on ezrin protein and mRNA expression was concentration dependent. The number of pseudopod per cell was significantly lower in 20 μmol/L baicalein-treated A431 cells and siRNA-transfected cells than that in untreated A431 cells (5.3 ± 1.9, 4.5 ± 2.8 vs 22.6 ± 2.8, both P < 0.01), while no significant difference was observed between the former two groups of cells (P > 0.05); the length of pseudopodia also reduced in baicalein-treated cells. Conclusions Baicalein may inhibit the proliferation and invasion of A431 cells by directly or indirectly suppressing the expression of ezrin and phosphorylated ezrin, which in turn contributes to the effect of baicalein against tumor proliferation and metastasis.