Objective To analyze the molecular epidemiological characteristics of E. coli O 157∶H 7 of Xuzhou, Jiangsu. Methods The virulence gene spectrum of E. coli O 157∶H 7 strains were analyzed by PCR and the homology of E. coli O 157∶H 7 strains were detected by PFGE and RAPD. Results In all E. coli O 157∶H 7 strains isolated from epidemic area, 100% possess Hly and eaeA gene, 95.35% possess SLT 2 gene, and 11.63% possess SLT 1 gene. The PFGE spectrum showed that the strains isolated from epidemic area were distinctively different from the strains isolated from Japan, and similar to but not identical with the standard strain 882364. The PFGE spectrum of strains isolated from epidemic area patients were identical with those of strains isolated from excrements of poultries, domestic animals and insect intestine.Conclusions Poultries and domestic animals which carry E.coli O 157∶H 7 could be the source of infection. PFGE could be used to analyze E.coli O 157∶H 7 and played an important role in epidemiology study. The results showed that the method of analysis of E. coli O 157∶H 7 by RAPD was convenient and time saving.

Objective To explore the effect of pre-hospital nursing intervention in the new regional cooperative rescue model on treatment delay and the therapeutic effect in patients with myocardial infarction.Methods From January 2012 to May 2014,158 patients with acute myocardial infraction (AMI) were selected.Patients were divided into two groups,intervention group and control group,The first medical contact to balloon(FMC-to-B) time,referral time,cardiac function were analysed.Results Mean FMC-to-B time [(94±21)min vs.(102±23) min],referral time in nursing intervention [(5±3) min vs.(9±4) min)] were significantly shorter than those in control group (t=2.14,6.67,P＜0.05).After a month compared with control group,LVEF was increased [(54.8±6.9)％ vs.(48.8±6.9)％],and LVED was deceased [(50.1±8.2) mm vs.(50.5±5.6)mm] in intervention group.Conclusions Pre-hospital nursing intervention can decrease the FMC-to-B time,which could improve the cardiac function.

Objective To investigate the feasibility and effects of whole-procedure seamless nursing intervention during regional collaborative treatment of patients with acute coronary syndrome.Methods Nursing intervention was performed on pre-hospital collaboration,transfer collaboration and catheter room collaboration during regional collaborative treatment of patients with ACS.Treatment time point,therapeutic effects and major hospitalization indicators were compared before(the control group) and after(the experimental group) implementation of nursing intervention.Results There were significant differences in mean FMC-to-B time,D-to-B time,referral time,obtaining informed consent time,mortality,LVEF and LVED between two groups(P＜0.05).There were significant differences in days of hospitalization,expenditures,percentage of consumables,percentage of medication,and in-hospital mortality between two groups (P＜0.05).Conclusion Whole-procedure nursing intervention can reduce time of regional collaborative treatment of patients with acute coronary syndrome,improve prognosis,decrease financial burden and increase efficiency of ACS treatment.

Objective:To retrieve and analyze the relevant literatures on vancomycin added into bone cement to provide the evi-dence for the treatment of osteomyelitis and other orthopedic infections. Methods:Search strategy and criteria of inclusion and exclu-sion for literatures were designed. PubMed, SCI, Embase, CNKI, VIP and the other databases were searched, and the articles from the establishment date to February 2014 were statistically analyzed using bibliometric methods. The final included documents were sta-tistically analyzed in respect of the article type, year, contents, citation frequency and the maln contents of the study. Results:A total of 1 941 articles were searched, and 430 of them were in the final inclusion. The total number of the articles in every year was in an es-calating trend. The paper focused on the research and analysis of clinical studies, and there were 74 clinical studies among the includ-ed literatures, which accounted for 17. 2% of all the included literatures. The highest citation frequency was 97 for one literature. The research included the overall situation, year distribution, publishing country, research type analysis, corresponding author and their in-stitutions, journals, citation frequency, and the maln content of work and clinical studies on vancomycin added into bone cement. The analysis could provide reference for the clinical treatment of orthopedic diseases. Conclusion: The results of the analysis show that vancomycin added into bone cement in the treatment of chronic osteomyelitis is effective with high security, and the technology is ma-ture.

A 54-year-old female patient with congenital heart disease had a persistent complete left bundle branch block three months after closure by an Amplatzer ventricular septal defect occluder. Nine months later, the patient suffered from chest distress, palpitation, and sweating at daily activities, and her 6-min walk distance decreased significantly (155 m). Her echocardiography showed increased left ventricular end-diastolic diameter with left ventricular ejection fraction of 37%. Her symptoms reduced significantly one week after received cardiac resynchronization therapy. She had no symptoms at daily activities, and her echo showed left ventricular ejection fraction of 46%and 53%. Moreover, left ventricular end-diastolic diameter decreased 6 and 10 months after cardiac resynchronization therapy, and 6-min walk dis-tance remarkably increased. This case demonstrated that persistent complete left bundle branch block for nine months after transcatheter closure with ventricular septal defect Amplatzer occluder could lead to left ventricular enlargement and a significant decrease in left ventricular systolic function. Cardiac resynchronization therapy decreased left ventricular end-diastolic diameter and increased left ventricular ejection fraction, thereby improving the patient’s heart functions.

).The complication rate in RIVVH was lower than that in the control group (P<0.05).Conclusions Early RIVVH was effective in the treatment of SAP,and may be an option as adjuvant treatment measure.

OBJECTIVETo investigate the proportion of hemorrhagic colitis (HC) caused by Escherichia coli O157:H7 in bacterial diarrhea in Xuzhou city, Jiangsu province.

METHODSAll stool samples from patients with diarrhea were screened for O157 antigen, using Immuno-gold kits. Positive samples were cultured to detect the existence of pathogens. All of the HC patients confirmed by bacterial isolation and identification were investigated for clinical symptoms and laboratory tests.

RESULTSOf the diarrhea patients identified in Feng county in May, and in Tongshan county of Xuzhou city in June 2000, Jiangsu province 0.98% and 5.89% were caused by Escherichia coli O157:H7 respectively, confirmed by bacteriological isolation and identification of stool samples. At the early phase of hemorrhagic colitis, 18.5% patients had at least one abnormal clinical laboratory test results including protein in urea and increased BUN or creatinine that indicating the possibility of kidney damage. In 27 strains of E. coli O157:H7 isolated from those patients, 13 and 14 were identified as Shiga toxin producing and Shiga-toxin negative E. coli O157:H7 (Stx-positive or Stx-negative) respectively. By analysis of the two groups of patients divided by according to the nature of Shiga toxin, four of 13 patients of Stx-positive group showed positive urea protein. However only 1 of the 13 patients of Stx-negative group was urea protein positive. The decreased Platelets counts were observed in 6 of 13 patients with Stx-positive group, but only in 1 of 14 patients with stx-negative group. These differences were statistically significant.

CONCLUSIONHC patients caused by E. coli O157:H7 were commonly seen (up to 5.89%) in Xuzhou city, Jiangsu province. Early laboratory tests should be conducted for HC patients as early as possible in order to find early indictor of kidney failure which was critical for prevention of hemolytic uremic syndrome.

Adolescent ; Adult ; Aged ; Child ; Child, Preschool ; Diarrhea ; etiology ; Escherichia coli Infections ; etiology ; Escherichia coli O157 ; isolation & purification ; Female ; Humans ; Infant ; Male ; Middle Aged

Objective: To investigate the feasibility and efficacy of the establishment of regional cooperative acute ST-segment elevation myocardial infarction (STEMI) rescue network among the prefectural-level city hospitals in China. Methods: Based on real-time remote electrocardiogram transmission and "120" emergency systems, we established a regional collaborative STEMI treatment network with our hospital as the network unclears including 8 second-class affiliated hospitals of Jiangsu University in 2013. STEMI treatment time, therapeutic effects and economic indexes were compared before (from January 2010 to December 2012, 180 cases, pre-network) and after (From January 2013 to December 2015, 374 cases, post-network) the establishment of the regional collaborative STEMI treatment network. Results: Post establishment of the rescue network, mean first medical contact (FMC) to balloon (FMC-to-B) time, referral time and obtaining informed consent time were all significantly decreased from (191±41), (94±18), (25±9) minutes to (93±19), (53±18), (7±5) minutes, respectively, in comparison with the pre-network era(all P<0.05). There was a trend of prolonged FMC-to-B time in proportion to aging of STEMI patients(trend P<0.05). Three months post discharge, LVEF was higher (55.3%±10.7% vs. 48.8%±12.1%, P<0.05) and LVEDd was lower ((49.1±10.8)mm vs.(51.8±9.2)mm, P<0.05) in the post-network group compared to pre-network group.In-hospital mortality was also significantly reduced post the establishment of the rescue network (2.14%(8/374) vs. 3.89%(7/180), P<0.05). The results also showed that the total costs (42 017(25 069, 75 148)yuan vs.51 030(28 137, 105 861)yuan), days of hospitalization ((9.1±4.5) days vs. (15.3±4.8)days) and percentage of medicine and consumables were all significantly decreased in the post-network group compared to pre-network group(all P<0.05). Conclusion Establishment of the regional cooperative rescue network is feasible among the prefectural-level city hospitals in China. Establishment of such network can improve the prognosis and decrease the FMC-to-B time, the rate of in-hospital mortality and financial burden of patients with STEMI, and serves as an effective strategy to improve the rescue ability for STEMI patients.

Objective: To investigate whether CD137-CD137L signaling can affect the autophagy of mouse vascular smooth muscle cells(VSMCs) through JNK signal pathway. Methods: Primary culture of C57BL/6J mouse thoracic aorta VSMCs was performed by tissue block adherence method. VSMCs between the third to fifth passages were isolated and cultured. VSMCs were divided into 4 groups: control group, CD137 agonist group, JNK inhibition group, and DMSO group. VSMCs in CD137 agonist group were treated with recombinant protein of CD137L (10 μg/ml), VSMCs in JNK inhibition group were treated with JNK inhibitor SP600125 (10 μmol/L) for 30 minutes followed by recombinant protein of CD137L (10 μg/ml) and DMSO group was treated with the same amount of DMSO in JNK inhibition group for 30 minutes, then added recombinant protein of CD137L (10 μg/ml). Western blot was used to detect the protein expression of p-JNK, LCⅡ and p62 in each group. Fluorescence microscopy was used to track the changes of autophagy in cells which was infected with adenovirus expressing tandem mRFP-GFP-LC3. Transmission electron microscope (TEM) was used to observe intracellular autophagosomes and autolysosomes. Results: (1) Compared with the control group, stimulating CD137-CD137L axis by recombinant protein of CD137L significantly upregulated the expression of p-JNK, LCⅡ and p62 (1.15±0.19 vs. 0.72±0.21, P<0.05;1.03±0.13 vs. 0.59±0.15, P<0.05, and 1.10±0.19 vs. 0.76±0.15, P<0.05). These effects could be reduced by JNK inhibitor (0.61±0.21 vs. 1.15±0.19, P<0.05;0.74±0.11 vs. 1.03±0.13, P<0.05, and 0.21±0.12 vs. 1.10±0.19, P<0.05). The expression of these proteins in DMSO group remained unchanged compared with CD137 agonist group (P>0.05). (2) Changes of autophagy in cells of various group: the number of total fluorescent spots and yellow fluorescent spots in CD137 agonist group was significantly increased compared to control group (total fluorescent spots:(93.00±14.11)/cell vs. (52.33±9.61)/cell, P<0.05, and (64.33±6.81)/cell vs. (25.67±3.51)/cell, P<0.05), moreover, the number of yellow fluorescent spots was higher than the red fluorescent spots fluorescent spots in CD137 agonist group. Compared with CD137 agonist group, pretreatment with JNK inhibitor significantly reduced the number of total fluorescent spots and yellow fluorescent spots ((53.00±3.17)/cell vs. (93.00±14.11)/cell, P<0.05,and (15.33±4.51)/cell vs. (64.33±6.81)/cell, P<0.05). The red fluorescent spots were higher than the yellow fluorescent spots in JNK inhibition group. The number of total fluorescent spots and yellow fluorescent spots in CD137 agonist group was not affected by pretreatment with DMSO (P>0.05). (3) The number of intracellular autophagosomes and autolysosomes was significantly higher in CD137 agonist group than in control group((17.67±6.03)/cell vs. (5.67±2.52)/cell, P<0.05), and the number of autophagosomes was higher than that of autolysosomes in CD137 agonist group((14.00±4.00)/cell vs. (3.67±2.08)/cell, P<0.05). The number of intracellular autophagosomes and autolysosomes was significantly lower in JNK inhibition group compared to CD137 agonist group((5.67±4.04)/cell vs. (17.67±6.03)/cell, P<0.05) and the number of autophagosomes was lower than that of autolysosomes in JNK inhibition group((1.33±1.53)/cell vs. (4.33±2.52)/cell, P<0.05). The number of intracellular autophagosomes and autolysosomes was similar between DMSO group and CD137 agonist group (P>0.05). Conclusion CD137-CD137L signal may influence autophagy of mouse VSMCs via JNK pathway.

Objective: To explore whether CD137-CD137L interaction could induce mouse vascular smooth muscle cells(VSMCs) calcification via P38 MAPK signaling. Methods: (1) Mouse VSMCs obtained from 8-week old male C57 mice were cultured by using method of tissue piece inoculation.The cells from 3 to 8 passage were divided into 4 groups: control group, agonist-CD137 group(recombinant CD137L protein), anti-P38 group(agonist-CD137 group+P38 inhibitor), single anti-P38 group(P38 inhibitor). The calcification was induced by adding a mixture of 10 mmol/L β-glycerophosphate+10^-8 mol/L dexamethasone+10^-7 mol/L insulin in the culture medium.Immunofluorescence was used to observe the changes of VSMCs markers(α-SMA and OPN).Real time-PCR was used to observe the mRNA expression of OPN and RUNX-2. Western blot was used to observe the protein expression of p-P38, OPN and RUNX-2. The level of cell calcification was observed by detecting alkaline phosphatase activity and calcium concentration. (2) The degeree of local calcium deposition was also tested on Von Kossa staining and Alizarin red staining methods in following 5 mouse VSMCs groups: control group, agonist-CD137 group(recombinant CD137L protein), anti-P38 group (agonist-CD137 group+P38 inhibitor), anti-CD137 group (agonist-CD137 group+CD137 inhibitor),agonist-P38 group(anti-CD137 group+P38 agonist). Results: (1) Compared with the control group, the fluorescence intensity of α-SMA was lower in the agonist-CD137 group(2.79±0.25 vs. 5.42±0.47,P<0.05), while the fluorescence intensity of OPN was higher(4.91±0.23 vs. 1.63±0.26, P<0.05). The fluorescence intensity of α-SMA was partly recovered after adding P38 inhibitor(4.48±0.27 vs. 2.79±0.25,P<0.05),but it was still lower than the control group (4.48±0.27 vs. 5.42±0.47, P<0.05),the fluorescence intensity of OPN decreased(2.66±0.15 vs. 4.91±0.23,P<0.05),but it was still higher than that in the control group (2.66±0.15 vs. 1.63±0.26,P<0.05).The fluorescence intensity of α-SMA and OPN(5.32±0.67 vs. 5.42±0.47,1.82±0.30 vs.1.63±0.26,both P>0.05) was similar between the control group and single anti-P38 group.(2) Compared with the control group, the protein level of p-P38(4.15±0.24 vs. 3.48±0.26, P<0.05), OPN(2.43±0.21 vs. 1.53±0.08, P<0.05), RUNX-2(3.20±0.23 vs. 1.13±0.10, P<0.05) was significantly increased in agonist-CD137 group,the above effects were blocked by adding specific P38 inhibitor SB203580(1.16±0.12 vs. 4.15±0.24, 0.50±0.02 vs. 2.43±0.21,and 1.74±0.14 vs. 3.20±0.23,all P<0.05);the protein level of p-P38(2.93±0.60 vs. 3.48±0.26,P>0.05),OPN (1.4±0.64 vs. 1.53±0.08,P>0.05),RUNX-2(1.26±0.26 vs.1.13±0.10, P>0.05) was similar between single anti-P38 group and the control group. (3) Compared with the control group, the mRNA level of OPN (1.51±0.34 vs. 1, P<0.05) and RUNX-2(2.67±0.19 vs. 1, P<0.05) was significantly upregulated in agonist-CD137 group, and these effects were blocked by adding specific P38 inhibitor SB203580(0.33±0.14 vs. 1 and 0.45±0.03 vs. 1,P<0.05);the mRNA level of OPN (1.05±0.09 vs. 1, P>0.05) and RUNX-2(1.18±0.10 vs. 1, P>0.05) was similar between the single anti-P38 group and the control group.(4) Compared with the control group,the ALP activity and calcium concentration(2.40±0.25 vs. 1.40±0.21,5.51±0.33 vs. 3.15±0.31,both P<0.05) were significantly increased in agonist-CD137 group,while the effects could be blocked by adding specific P38 inhibitor SB203580((1.99±0.07) king unit/gprot vs. (2.40±0.25) king unit/gprot, (3.74±0.20) mmol/gprot vs. (5.51±0.33) mmol/gprot, both P<0.05).The ALP activity and calcium concentration was similar between single anti-P38 group and the control group((1.60±0.25) king unit/gprot vs. (1.40±0.21)king unit/gprot, (2.66±0.28) mmol/gprot vs. (3.15±0.31) mmol/gprot, both P>0.05). (5) Compared with the control group,the calcification of VSMCs in the agonist-CD137 group was significantly increased,while the calcification in the anti-P38 group was significantly reduced.Compared with the agonist-CD137 group,the level of calcification in the anti-CD137 group was obviously increased,and the calcification in the agonist-P38 group was significantly higher than that in the anti-CD137 group and the control group. Conclusion These findings suggest that CD137-CD137L signaling may regulate VSMCs calcification via modulating P38 pathway.