Objective To explore the effect of bionic urine bags on dysuria in stroke patients and improve the effect of bladder function training. Methods Forty patients with urinary incontinence were selected and randomly divided into control group (n=46) and observation group (n=44) by random number table. The patients in the control group were treated with Kangwei anti-reflux urine bags and the urine was discharged every 3 hours at daytime, once every 4 hours at night. The patients in the experimental group were treated with OT-U bionic urine bags for drainage urine, the threshold of urine bag pressure set:when the bladder pressure reached more than 35cm H2O, the bladder urine flowed into the urine bag. The two groups were compared in view of catheter catheterization time, urination after urination time, self-urination, re-intubation rate, urine overflow, urinary tract infection. Results The duration of indwelling catheters in the observation group was significantly higher than that of the control group (P <0.05). The rates of re-intubation and urinary tract infection were significantly lower as well (P<0.05). Conclusion Biomimetic urine bag can effectively promote the training of bladder function, shorten the time of indwelling catheter and reduce the occurrence of urinary tract infection after extubation.

Objective To evaluate the effectiveness of ultrafiltration in acute heart failure syndrome(AHFS).Methods Da-tabases including PubMed,WanFang and CBM were searched to collect RCTs on ultrafiltration in AHFS.Two reviewers independ-ently screened literature according to the inclusion and exclusion criteria,extracted data,and evaluated the methodological quality of the included studies.Then the Meta-analysis was conducted using RevMan5.3.Results A total of 14 trials involving 755 patients were included.The results of Meta-analyses showed that ultrafiltration was not associated with significantly decreased risk of all-cause mortality(RR=0.95,95%CI :0.65 to 1.38,P =0.77),rehospitalization(RR =0.78,95%CI :0.49 to 1.24,P =0.29)and change in serum creatinine(WMD = 0.02 mg/dL,95%CI :- 0.18 to 0.21,P = 0.87 ).However,there was significantly more weight loss(WMD =1.32 kg,95%CI :0.29 to 2.35,P =0.01)and net fluid removal(WMD =1.27 kg,95%CI :0.43 to 2.12,P =0.003)in the ultrafiltration group.Conclusion For patients with AHFS,ultrafiltration is effective in reducing fluid retention,with no significant benefits in renal function preservation,mortality and rehospitalization.

Nerve injury as a kind of tissue damage, inevitably stimulates nerve tissue inflammatory reaction, mediates neural tissue repair and regeneration, and participates in the occurrence of chronic pain. The high mobility group protein B1 (HMGB1) and Toll-like receptor 4 (TLR4) in neurological pain plays an important role, HMGB1-TLR4 pathway is involved in the initiation and progression of neuropathy pain. If the mechanism of HMGB1-TLR4 pathway in the neurological pain is identified, it can provide an effective pain-relieving methods and new target for drugs.

Objective To observe changes in mean platelet volume ( MPV) and investigate its possibility as a predictor and influence in patients with pulmonary artery hypertension associated with secundum atrial septal defect (ASD-PAH) . Methods 627 patients who suffered from secundum ASD were included in the study from the First Affiliated Hospital of Xinjiang Medical University Heart Center between January 2010 and March 2014. Patients were divided into two groups based on whether they had PAH or not (PAH group, n = 420 and non-PAH group, n = 207) . We also included 690 healthy people as a control group who received routine body check up at the same time. Examinations including complete blood count, serum biochemistry and ECG were done. Right heart catheterization examination was performed in patients who suffered from secundum ASD. Results The MPV was significantly higher in secundum ASD patients than in the control group [ (9. 4 ± 1. 6) fl vs. (8. 9 ± 1. 5) fl, P ﹤ 0. 001] . No significant difference was observed in MPV between PAH group and non-PAH group (P = 0. 268) . In univariate and multivariate logistic regression analysis, age ( OR 1. 401, 95% CI 1. 087 to 1. 806, P = 0. 009), RV diameter (OR 1. 101, 95% CI 1. 026 - 1. 181, P = 0. 008) and ASD defect diameter (OR 1. 064, 95% CI 1. 013 - 1. 118, P = 0. 013) were associated with ASD-PAH. Conclusions Our study demonstrated that age, RV diameter and ASD defect diameter were associated with ASD-PAH. Platelet activation exists in ASD-PAH, but this may not be the precipitating cause that contribute to the pathogenesis of ASD-PAH. MPV at admission does not predict the risk of PAH in patients with secundum ASD.

Objective To observe changes of cognitive function and the expression of tumor necrosis factor alpha(TNF-α),interleukin 10(IL-10) in hippocampus of diabetic rats,and assess the role of inflammation in the possible pathogenesis of diabetic encephalopathy (DE).Methods 30 male SD rats were randomly divided into control group and diabetes mellitus group.After 4 weeks of feeding high fat diet,diabetes mellitus group according to 30mg/kg injected with streptozotocin to establish type 2 diabetic rat model.At the end of the experiment,cognition were evaluated using water maze test.The concentration of beta-amyloid(Aβ) in hippocampus of diabetic rats were detected through enzyme linked immunosorbent assay,and the expression of TNF-α,IL-10 were detected by Western blotting.The expression of Aβ,TNF-α,IL-10 were observed through immunohistochemistry.Results Time spent in the target quadrant in diabetes mellitus group was shorter than that in control group ((38.21± 3.68)s vs (42.10±2.62)s,t=3.105,P＜0.01).The frequency of crossing original platform site was less than that in control group((2.62±0.77) vs(3.69±0.95),t=3.184,P＜0.01).Compared with control group the expression of Aβ,TNF-α were higher(BothP＜0.01),and IL-10 were lower(P＜0.01)in diabetes mellitus group.The positive expression of Aβ,TNF-α were obviously and IL-10 were less obviously observed in diabetes mellitus group according to immunohistochemistry.Conclusion The cognitive decline in diabetic rats is possibly related to inflammatory cytokines expressing out of balance.

Objective To explore the effects of aging on ventricular remodeling and cardiac rupture after acute myocardial infarction in mice. Methods　Male C57BL/6 mice of 3 months and 12 months old were randomly divided into sham operation group and myocardial infarction(MI)group.Following acute myocardial infarction(AMI)modeling induced by open-chest surgery,the events of cardiac rupture were monitored and the echocardiography and hemodynamics were performed on the 7th day after surgery.Zymography,immunohistochemical method and pathological staining were used to measure the activity of matrix metalloproteinases(MMPs),the content of collagen and the degree of inflammatory cell infiltration on the 3rd and 7th days after surgery,respectively. Results　The incidence of cardiac rupture was higher in elderly group than that in young group(38.0% vs.16.0%,X2=6.139,P＜0.05).Compared with young group,significant infarct expansion,left ventricular (LV)remodeling and hemodynamic deterioration were showed in elderly group on the 7th day after surgery(t=5.754,P＜0.05).The degree of inflammatory cell infiltration and the expression of MMP-9 were significantly increased in elderly group on the 3rd day following AMI modeling(P＜0.05),and the collagen content and the expression of type Ⅲ collagen were significantly increased (P＜0.05)compared with young group. Conclusions　Aging is a risk factor for post-infarct cardiac rupture in the mice model.The mechanisms which are responsible for this age-related difference of cardiac rupture are related to increasing degree of inflammatory cell infiltration, overexpression of MMP-9 and type Ⅲ collagen and aggravated early LV remodeling.

Objective To investigate the association between matrix metalloproteinase-9 (MMP-9) gene polymorphism (-1562C ＞ T/R279Q) and acute coronary syndrome (ACS) in Uygur nationality of Xinjiang Autonomous Region of China. Methods A total of 352 patients with ACS including 213 patients with unstable angina pectoris and 139 patients with acute myocardial infarction evidenced by using coronary arteriography and 421 control subjects were recruited in this study. The MMP-9-1562C ＞ T and R279Q genotypes were detemined by using PCR-RFLP method. The relationship between the polymorphism in the MMP-9 gene and the severity of coronary arterial stenosis was analyzed. All polymorphisms were determined for confimation with Hardy-Weinberg expectations in both groups separately. Differences in distributions of genotypes and alleles between two groups were analyzed with x2 test. The association between the MMP-9 polymorphisms and the risk of ACS was estimated by odds ratio(Ors) and their 95% confidence intervals (CIs), and the comprehensive evaluation of the factors associated with ACS was determined by using multifactor logistic regression. P ＜ 0. 05 was considered to be statistically significant. Results The genotype frequencies for CT + TT genotypes and T allele were 25.9 and14.5 percent in ACS subjects and 15.7 and 8.4 percent in control subjects, respectively. The genotype frequencies were different significantly between the two groups (x2 = 12.26,P ＜ 0.01;x2 = 14.15,P ＜ 0.01, respectively). No relationship between R279Q polymorphism and ACS was found in this study ( P ＞ 0.05). The multifactor logistic regression analysis showed that the T allele carrier (CT + TT) significantly increased the risk of ACS compared with the CC genotype ( OR = 1.791,95 % CI: 1. 088 - 2.951, P = 0.022) after adjustment for tradition risk factors. The frequencies for CT + TT and CC genotypes of the -1562C ＞ T polymorphism were not statistically different among ACS patients with one, two and three or more significantly diseased vessels ( x2 = 1.15, P = 0.56). Conclusions The findings suggest that the polymorphism in MMP-9 gene promoter (-1562C ＞ T) is associated with the susceptibility to the ACS. The T allele might be an independent risk factor for the ACS. But the -1562C ＞ T polymorphism may not be useful as a predictor of the severity of coronary arterial stenosis. The R279Q polymorphism of MMP-9 gene was not significantly associated with ACS in this studied population.

AIM: To explore the changes in extracellular regulated protein kinase (ERK1/2) in the hypertrophic myocardium induced by pressure overload at the different time courses and to determine the molecular mechanism in the myocardium from hypertrophy to heart failure. METHODS: C57/BL mice, aged 12 week old, were subjected to sham-operation (SH) or transversing aortic constriction (TAC) to establish left ventricular hypertrophy. Echocardiographic assessments, hemodynamic determination, organ weight measurement, morphological and histological examination were performed at 1, 4, 8, 12 and 16 weeks after surgery. Meanwhile mRNA levels of atrial natriuretic peptide (ANP), α-myosin heavy chain (α-MHC), bcl-2 and bax were measured by RT-PCR, and ERK1/2 levels were detected by Western blotting. The animals in SH group were performed the same tests then sacrificed at 16 weeks. RESULTS: (1) Compared to SH group, LVESd, LVEDd, Awsth, Awdth, Pwsth and Pwdth progressively increased after TAC. Meanwhile, ejection fraction (EF%) significantly decreased at 16th week (P<0.05). LVSP, dp/dt_(max) and dp/dt_(min) in TAC group were progressively increased after 4 weeks. From 8-12 weeks these parameters maintained stable and then sharply decreased at 16th week (all P<0.05). However, LVEDP was statistically increased at 8th week. These echocardiographic and hemodynamic changes indicated a development of LVH and eventually progressing towards to heart failure. (2) Histologically, cardiac collagen measured by percentage of Sirius red positive stained area and apoptosis index showed progressive increases from 4 to 16 weeks. (3) Compared to SH group, mRNA levels of ANP was time-dependently increased while α-MHC and Bcl-2 were time-dependently decreased. The ratio of Bcl-2 /Bax was decreased. Phosphorylation of ERK1/2 was increased at 4th week, then decreased with age of TAC (all P<0.05). CONCLUSION: Pressure-overload induced by TAC results in a development of LVH from early concentric hypertrophy to late eccentric hypertrophy, and eventually toward cardiac dysfunction or heart failure. Those changes are associated with increase in cell size and cardiac fibrosis. ERK1/2 signaling pathway may involve in the regulation of myocardial cell apoptosis in hypertrophic and failure heart.

Objective To investigate the effect of β3-adrenoreceptor (β3-AR)overexpression on cardiac hypertrophy. Method Sprague-Dawley rat neonatal ventricular cardiomyocytes (NRVMs) were isolated and cul-tured in vitro.The infection of lentiviruswas examined after cardiomyocytes were infected with lentivirus at differ-ent multiplicity of infection (MOI) of 20、50、80 and 100. Fluorescence microscopy was used to observe the ex-pression of GFP and to confirm the best MOI for lentivirus infection. Following the enforced expression of β3-AR by lentivirus, 2uM norepinephrine (NE) was used to treatment the infected cardiomyocytes for 48h. Expressions of β3-AR、c-myc and c-fos protein in cardiomyocytes were detected by Western Blot. Results The results of fluorescence microscopy indicated that the best MOI was 50. The protein level of β3-AR was significantly in-creased in β3-AR overexpression group compared with the control group and the NE treatment group (P < 0.05). Following the treatment of NE , the expressions of c-myc and c-fos were also significantly increased in β3-AR overexpression group compared with the control group (P < 0.05). Conclusion Over-expression of β3-AR can aggravate cardiomyocyte hypertrophy.

BACKGROUND:Recombinant adeno-associated virus serotype 9 has a high affinity in myocardial tissue, and the expression of recombinant adeno-associated virus serotype 9-enhanced green fluorescent protein (rAAV9-eGFP) in the aorta of atherosclerosis mice is not clear. OBJECTIVE:To explore the optimal time point of rAAV9-eGFP expression in the aorta of atherosclerosis mice. METHODS:Atherosclerosis model was established with high-fat diet in 30 ApoE-/-mice for 16 weeks. Among them, 25 mice were injected with 5.0×1011 vg (virus genomes) rAAV9-eGFP through the tail vein, while the remaining 5 mice were injected with saline, serving as the control group. The virus-transfected mice were kil ed at 14, 21, 28, 35 and 60 days after transfection, and aortic tissue was harvested. The expression of enhanced green fluorescent protein was detected with laser scanning confocal microscope. Western blot assays were used to detect the expression of enhanced green fluorescent protein in aorta. The expression of enhanced green fluorescent protein in vivo was observed and the optimal expression time point was determined. RESULTS AND CONCLUSION:rAAV9-eGFP effectively transfected the aorta of atherosclerosis mice, enhanced green fluorescent protein was expressed in aortic tissue, and the expression intensity increased gradual y with the increasing transfection time. The highest expression level was found at 35 days after transfection and then maintained stable at 60 days. There were significant differences at different time points after transfection (P<0.001). These data indicate that rAAV9-eGFP can be effectively expressed in the aorta of atherosclerosis ApoE-/-mice and rAAV9-eGFP can be regarded as the optimal vector in the treatment of atherosclerosis.