Objective To evaluate the feasibi1ity and efficacy of transcatheter closure of perimembranous and muscular ventricular septal defects (VSD) using the new Amplatzer membranous and muscular VSD occluder and observe the effect of membranous VSD occluding procedure on atrioventricular(AV) conductive system.Methods Twelve patients (7 males,5 females) with perimembranous VSD and two patients (1 male,1 female) with muscular VSD underwent an catheter closure using the new Amplatzer membranous and muscular VSD occluder.All patients who were eligible for device closure by means of cardiac Doppler echocardiography were routinely measured the parameters of blood dynamics before catheter closure. Artery-venous track was set up under the X-ray fluoroscopy,transesophageal (TEE) or transthoracic echocardiography (TTE) guidance. Devices were released in the right ventricular side.Twelve patients with perimembranous VSD underwent the cardiac electrophysiologic examination,including atrioventricular conductive time (AV interval) and atrioventricular nodal refractory time,before and after catheter closure.A11 patients were followed up at 2 weeks,1 month,3 months and 6 months after the procedures.Results The devices were deployed successfully in 14 patients.There was complete closure in 12 patients immediately,and tiny (

Objective To compare the results of anti-cardiolipin (ACA)measuring by two commercial available kits.Methods ACA in total of 66 serum samples were both determined by kits from Euroimmun and YHLO simultaneously,then the re-sults were analyzed comparatively and correlatively.The Euroimmun kit was applied to determination the level of ACA-IgA/G/M,and the YHLO kit determined ACA-IgG/M and anti-β2-glycoprotein I antibody (β2GPI IgG).Results The positive rate by Euroimmun kit was 37.88% (25/66),while 31.82% (21/66)was positive (one positive among ACA-IgG,IgM andβ2GPI IgG)when determined by YHLO kit,and there was no significant difference between the two kits.The accordance rate of the two kits was 87.88% (58/66).The ACA-IgA/G/M value by Euroimmun kit and the summation of ACA-IgG, IgM andβ2GPI IgG by YHLO kit showed well linear correlation (r 2 =0.892,P <0.01).Conclusion Results from the two kits were consistent and correlated well,and they are suitable for the clinical application;these two kits have their own char-acteristics,which could be used by individual or combination accordingly.

OBJECTIVE: To explore the factors related to the length of hospital stay for cerebrovascular accident and to provide the basis for health administrative department to formulate measures, and for clinical department to develop treatment guidelines. METHODS: We collected the medical record of the hospitalized cerebrovascular accident patients from 2008 to 2013 in the Third Xiangya Hospital, Central South University. The collected data included demographic information, disease characteristics, treatment information and health economics information. Then we analyzed the factors related to the length of hospital stay for cerebrovascular accident. SPSS 13.0 was used for statistical analysis and logistic regression and nonparametric rank sum test was performed. RESULTS: The length of stay in hospital was from one day to 513 days, with a median of 10 days. The length of stay for women was shorter than that of men (OR=0.869). The length of stay for the older patients was longer than that of younger patients (OR=1.158). The length of stay for patients who implemented a surgery was 1.686 times longer than those who were not implemented a surgery (OR=1.686). The length of stay for ischemic cerebrovascular patients was shorter than that of the hemorrhagic cerebrovascular patients (OR=0.275). The patients with new rural cooperative medical insurance or without health insurance usually stayed a short time in hospital. CONCLUSION Sex, age, surgery, type of cerebrovascular accident and medicare type are the factors that affect the length of hospital stay for cerebrovascular accident.
Female ; Humans ; Length of Stay ; Logistic Models ; Male ; Stroke

Objective: To investigate the mechanism of vascular endothelial growth factor(VEGF) inducing tolerogenic dendritic cells(DCs) in oral squamous cell carcinoma (OSCC). Methods: The DCs were divided into four groups: Control group (DC), VEGF group (VEGF added into DC), Co-culture group (DC co-cultured with SCC7) and Anti-VEGF group (anti-VEGF antibody added into DC co-cultured with SCC7). Flow cytometry (FCM) was used to detect DC surface markers. To detect the effect of DC on proliferation activity of T lymphocyte, the experiment included five groups: Nc group (T lymphocyte), Control group (T lymphocyte added into DC), VEGF group (T lymphocyte + DC + VEGF), Co-culture group (T lymphocyte + DC + supernatant of SCC7) and Anti-VEGF group (T lymphocyte + DC + supernatant of SCC7 + anti-VEGF antibody). Subsequently, the mixed lymphocyte reaction(MLR) was conducted. The expression levels of indole-2, 3-doxygenase(IDO)and programmed cell death 1 ligand 1(PD-L1)in DC were detected by western blot, real time PCR and FCM respectively. For the cytotoxic lymphocyte (CTL) assay, SCC7 cells and CTLs were mixed and CTL-mediated SCC7 cells cytotoxicity was tested. The experiment included four groups: Control group (T lymphocyte + DC), IDO inhibition group (T lymphocyte + DC + IDO inhibitor), Anti-PD-L1 antibody group (T lymphocyte + DC + anti-PD-L1 antibody) and Combination group (T lymphocyte + DC + IDO inhibitor + anti-PD-L1 antibody). The SCC7 tumor-bearing mice treated with IDO inhibitor and the anti-PD-L1 antibody were sacrificed and the tumor inhibition rate and the spleen index were determined. Results: Compared with Control group, exogenous VEGF or SCC7 co-culture inhibited the relative number of DC expressing CD11C, CD80, CD86, CD40 and MHC Ⅱ. The positive DCs were increased in the Anti-VEGF group compared with VEGF or Co-culture group. In VEGF or Co-culture group, the number of T cells stimulated by SCC7-pulsed DCs was decreased compared with Control group. However, the ability of Anti-VEGF group to induce T cell proliferation was significantly increased compared with VEGF or Co-culture group. Significantly increased expression of IDO and PD-L1 were observed in VEGF and Co-culture group. However, this was partially reversed by addition of anti-VEGF antibody into the co-culture system. Compared with Control group, the expressions of CD11C and CD86 in DC in both the IDO inhibition group and Anti-PD-L1 antibody group were increased, and were significantly higher in the Combination group compared with the single drug groups. The similar results were exhibited in MLR and CTL assay. In vivo, the results revealed that the tumors obtained from the mice in three experimental groups were smaller than those in the control group. Furthermore, the tumor volume of the Combination group was the smallest. The spleen index of each group was calculated and the results showed the spleen index of the three experimental groups was significantly higher than that of Control group. Conclusion VEGF in OSCC micro-environment inhibits the maturation and function of DC that are transformed into tolerogenic DC by high expression of IDO and PD-L1.

OBJECTIVETo explore the characteristics and therapies of patients with acute myocardial infarction (AMI) in Wuxi city, China.

METHODSA network was established to obtain information of patients with AMI who were admitted to 9 designated hospitals between 2011 and 2012. A total of 1 714 patients were enrolled (1 334 males, 754 smokers, 1 076 hypertension, 270 hyperlipidemia and 398 diabetes) including 1 410 patients with acute ST-segment elevation myocardial infarction (STEMI) and 304 patients with acute non ST-segment elevation myocardial infarction (NSTEMI). Patients' characteristics, therapies, the incidence of major adverse cardiovascular events (MACEs) and all-cause mortality were analyzed.

RESULTS(1) Medication therapy was as follows: antiplatelet therapy 98.3% (1 685 cases) , beta-blockers 59.1% (1 013 cases) , ACEI or ARB 67.6% (1 159 cases) , statins 98.1% (1 682 cases) , and nitrates 71.1% (1 218 cases) . Of the patients, 7.1% (132 cases) received temporary pacemakers, 34.0% (480 cases) with acute STEMI underwent reperfusion [direct PCI 18.4% (260 cases) and thrombolysis 15.6% (220 cases)]. (2) According to the hospital admission data, patients were divided into three groups: group A, transported to the hospital by ambulance (n = 361); group B, transported to the hospital by private vehicles (n = 1 318); and group C, AMI occurred in the hospital (n = 35). The median time of AMI onset to physician contact of the 3 groups was 178 min, 368 min, and 9 min, respectively. The median time from AMI onset to the first ECG was 181 min, 379 min, and 10 min, respectively. The median time from AMI onset to cardiology specialist consultation was 187 min, 431 min, and 69 min, respectively. AMI onset-to-physician contact, AMI onset-to-first ECG, and AMI onset-to-specialized treatment time was the shortest in group C, followed by group A and group B. For patients with STEMI underwent reperfusion therapy, the median AMI onset-to-reperfusion therapy time was significantly shorter in group A patients than group B patients [thrombolysis group: 224(171, 514) min vs. 378 (158, 785) min, PCI group: 318 (154, 674) min vs. 489 (143, 816) min, all P < 0.05]. (3) The total incidence of MACEs was 16.3% (279/1 714), the all-cause in-hospital mortality rate was 13.1% (224/1 714). According to the AMI onset-to-physician contact, patients were divided into 4 groups: <3 h, 3-6 h, 6-12 h, and >12 h. The incidence of MACEs [4.4% (23/517), 13.3% (60/451), 19.1% (77/404) and 34.8% (119/342),χ(2) = 114.36, P < 0.01] and all-cause in-hospital mortality rate [4.1% (21/517) , 10.4% (47/451), 18.6% (75/404), 23.7% (81/342), χ(2) = 84.36, P < 0.01] increased in proportion to the time of AMI onset-to-physician contact. Among STEMI patients, the incidence of MACEs [5.8% (15/260) , 12.3% (27/220) , 20.9% (194/930) ,χ(2) = 39.93, P < 0.01] and all-cause in-hospital mortality [1.5% (4/260) , 10.0% (22/220) , 18.2% (170/930) ,χ(2) = 50.90, P < 0.01] was the lowest in the primary PCI group, followed by thrombolysis group and was the highest in the early conservative treatment group.

CONCLUSIONSGuideline is well followed in terms of drug treatments of AMI in this cohort, but only a small proportion of AMI patients in Wuxi received reperfusion therapy. There is a considerable out-of-hospital time delay for AMI patients in this cohort which is shorter in group A than in group B. All-cause in-hospital mortality and MACEs is the lowest in AMI patients underwent primary PCI.

Adult ; Aged ; Aged, 80 and over ; China ; Cross-Sectional Studies ; Female ; Humans ; Male ; Middle Aged ; Myocardial Infarction ; therapy

To explore the immunomodulatory effects of interleukin-17 (IL-17) on acute lung injury (ALI) induced by lipopolysaccharide (LPS). Methods Thirty-six SPF-class C57BL/6 mice were divided into normal saline control group (NS group) and LPS-induced ALI model group (LPS group, LPS 5 mg/kg intratracheal drip) according to random number table method, with 18 mice in each group. Six mice were sacrificed at 2, 6 and 24 hours after model reproduction, and peripheral blood, lung and spleen tissues were harvested. After staining with hematoxylin-eosin (HE), the pathological changes of lung tissue were observed under microscope and the infiltration level of lymphocytes, neutrophils and macrophages in the alveolar wall and tracheal wall were detected. Immunohistochemistry was used to detect the protein expression of IL-17 in alveolar wall and tracheal wall, and the correlation between IL-17 expression and lymphocytes, neutrophils and macrophages infiltration in alveolar wall and tracheal wall were analyzed. The level of IL-17 in lung tissue homogenate was determined by enzyme linked immunosorbent assay (ELISA). Flow cytometry was used to detect the proportion of CD4+IL-17+ helper T cells (Th17 cells) in CD4+ T cells in peripheral blood, lung tissue and spleen tissue. Results ① Microscopy showed that the lung tissue structure of NS group was basically normal at each time after model reproduction, and there was no obvious inflammatory cell infiltration, while the lung tissue edema and inflammatory reaction were gradually aggravated in the LPS group, and the lung injury score was significantly higher than that in NS group at each time (2 hours: 4.47±1.42 vs. 1.10±0.55, 6 hours: 7.93±2.14 vs. 1.23±0.50, 24 hours:12.67±2.67 vs. 1.20±0.61, all P < 0.01). ② Immunohistochemistry showed that the protein expression of IL-17 in alveolar wall and tracheal wall of LPS group increased gradually with time, while that in NS group was negative or weak positive. Quantitative analysis showed that the immunohistochemical staining score of IL-17 protein in alveolar wall and tracheal wall of LPS group were higher than those of NS group (alveolar wall: 2.70±1.40 vs. 0.90±0.37 at 2 hours, 5.10±1.76 vs. 1.17±0.59 at 6 hours, 9.67±1.32 vs. 1.10±0.45 at 24 hours; tracheal wall: 2.87±0.89 vs. 0.90±0.39 at 2 hours, 4.97±1.48 vs. 1.10±0.41 at 6 hours, 8.67±1.54 vs. 1.03±0.29 at 24 hours; all P < 0.05). ③ Correlation analysis showed that the protein expression of IL-17 in alveolar wall and tracheal wall were positively correlated with the degree of lymphocyte, neutrophil and macrophage infiltration (alveolar wall: r value was 0.632, 0.550, 0.466; tracheal wall: r value was 0.695, 0.662, 0.575, respectively; all P < 0.01). ④ IL-17 content (μg/L) in lung tissue homogenate was significantly higher than that in NS group at each time after model reproduction (2 hours: 1.37±0.14 vs. 1.01±0.18, 6 hours: 1.65±0.19 vs. 1.11±0.18, 24 hours: 1.92±0.36 vs. 1.17±0.24, all P < 0.01). ⑤ The proportion of Th17 cells in the peripheral blood, lung tissue and spleen tissue of the LPS group were higher than those of the NS group at each time after model reproduction [peripheral blood: (2.62±0.62)% vs. (1.42±0.40)% at 2 hours, (3.74±0.43)% vs. (1.27±0.32)% at 6 hours, (4.44±0.65)% vs. (1.59±0.45)% at 24 hours; lung tissue: (2.32±0.44)% vs. (1.50±0.25)% at 2 hours, (3.66±0.36)% vs. (1.33±0.24)% at 6 hours, (4.60±0.54)% vs. (1.60±0.27)% at 24 hours; spleen tissue: (1.49±0.36)% vs. (0.69±0.21)% at 2 hours, (2.58±0.55)% vs. (0.59±0.18)% at 6 hours, (3.76±0.57)% vs. (0.65±0.26)% at 24 hours; all P < 0.01]. Conclusion IL-17 is involved in the inflammatory immune regulation of ALI mice.

Topical anesthesia are being widely used in clinical diagnostic or therapeutic fields such as ophthalmology, ENT, dermatology, urology. It is defined as superficial loss of sensation in mucous membranes or skin, produced by direct application of penetrating local anesthetics. Topical anesthesia has the advantages of simple performance, high safety, quick recovery, which can effectively improve patient's satisfaction. In recent years, more and more attention has been paid to the concept of comfortable diagnosis and treatment. The new drugs and application methods of topical anesthesia are emerging constantly, special attention must be paid to their pharmacological characteristics and possible adverse reactions when using them. This article reviews the research progress of topical anesthesia in clinical application in order to provide reference for clinical practice.

Modulating Tankyrases (TNKS), interactions with USP25 to promote TNKS degradation, rather than inhibiting their enzymatic activities, is emerging as an alternative/specific approach to inhibit the Wnt/β-catenin pathway. Here, we identified UAT-B, a novel neoantimycin analog isolated from Streptomyces conglobatus, as a small-molecule inhibitor of TNKS-USP25 protein-protein interaction (PPI) to overcome multi-drug resistance in colorectal cancer (CRC). The disruption of TNKS-USP25 complex formation by UAT-B led to a significant decrease in TNKS levels, triggering cell apoptosis through modulation of the Wnt/β-catenin pathway. Importantly, UAT-B successfully inhibited the CRC cells growth that harbored high TNKS levels, as demonstrated in various in vitro and in vivo studies utilizing cell line-based and patient-derived xenografts, as well as APC^min/+ spontaneous CRC models. Collectively, these findings suggest that targeting the TNKS-USP25 PPI using a small-molecule inhibitor represents a compelling therapeutic strategy for CRC treatment, and UAT-B emerges as a promising candidate for further preclinical and clinical investigations.