A series of 286 cases with gastric cancer identified by endoscopy and surgery was subjected to the study to probe the correlation of endoscopic findings in morphology,size and cell differentiation with cancerous in- vasion and metastasis of the tumor by means of TNM staging.Results showed that the superficial size of the lesion 3cm increased in T_2,up to 44.9% in T_4;lymphatic involvement was found in 12.5% of T_1a;remote metastasis occurred in 4.7% of T_2,being statistically higher(P

This study evaluated the effects of early treatment with β-adrenergic blocker metoprolol on ventricular remodeling and function after acute myocardial infarction (AMI) by using high frequency ultrasound. The relationship between the efficacy and the expression level of cardiac myocardial inflammatory cytokine was examined in rats. The rat model of AMI was induced by ligating the left anterior descending artery. The surviving rats were randomly assigned to two experimental groups: MI control (MI) group and MI metoprolol (MI-B) group, with the rats undergoing sham operation serving as normal control (Sham). MI-B group was given metoprolol for 4 weeks (refer to the CCS-2 protocol) and the other two groups received equal volume of saline via intragastric (i.g.) administration. The ventricular remodeling and function were evaluated by high frequency ultrasound 4 weeks after the treatment. Then all rats were sacrificed for pathological examination and immunohistochemistrical detection of inflammatory cytokines, including IL-1β, IL-6, IL-10 and TNF-α. Compared with the MI group, the left ventricular end-systolic dimension, end-diastolic dimension, end-systolic volume and end-diastolic volume of the MI-B group were significantly decreased (P<0.01), while the left ventricular anterior wall end-diastolic thickness, ejection fraction and fractional shortening were obviously increased (P<0.01). The conspicuous improvement in the left ventricular morphology and function was coincident with the markedly reduced TNF-α and IL-1β expression and the increased IL-10 expression. We are led to conclude that early metoprolol treatment for AMI can regulate myocardial inflammatory cytokine expression to improve cardiac function and the underlying mechanism might be that it decreases the level of pro-inflammatory cytokines and increases the level of its anti-inflammatory counterparts in cardiac myocytes. Our study also showed that echocardiography is a useful technique for the structural and functional assessment of left ventricle after acute myocardial infarction.

Objective:To investigate the effects of exenatide on podocyte in diabetic nephropathy mice.Methods:Diabetic nephropathy mice models were induced by using streptozocin-treated C57BL/6J mice on high fat diets, which were randomized by random number table to diabetic nephropathy control group (DN group, n=8) and exenatide treatment diabetic nephropathy group (DN+ Ex group, n=8). The C57BL/6J mice on normal chow diet were used as normal control group (NC group, n=8). After the intervention, blood glucose, renal function, and urine albumin/creatinine ratio were measured. Pathological glomerular changes were observed by pexiodic acid-Schiff stain (PAS) staining. The mRNA expression of profibrotic molecules Collagen Ⅳ, transforming growth factor-β (TGF-β), and Fibronectin in glomerular lysates were measured by realtime quantitative PCR (RT-PCR). Podocyte injury and apoptosis were evaluated by immunofluorescent staining and transmission electron microscopy. The expression of Nephrin, Cleaved caspase-3, protein kinase B (Akt), and phosphorylated Akt (p-Akt) in glomerular lysates were examined by western blotting. Results:Compared with the DN group, urine albumin/creatinine ratio was significantly decreased in the DN+ Ex group ( P<0.01). PAS staining and analysis found that exenatide administration ameliorated mesangial matrix expansion and glomerular hypertrophyin in DN group ( P<0.05). RT-PCR analyses showed that the glomerular expression for Fibronectin, TGF-β, and Collagen Ⅳ were significantly decreased in the DN+ Ex group compared with the DN group ( P<0.01). Immunofluorescent staining and transmission electron microscopy revealed that exenatide treatment improved podocyte injury and apoptosis in DN group. Western blotting analyses showed that exenatide increased the Nephrin expression, decreased the Cleaved caspase-3 expression, increased the p-Akt expression in glomerular lysatesin diabetic nephropathy mice ( P<0.01). Conclusion:Exenatide attenuates podocyte injury and apoptosis and proteinuria, and prevents the progression of diabetic nephropathy mice. Phosphatidylinositol 3-kinase (PI3K)/Akt pathway in glomerular lysates may be related to the protective effects of exenatide.

Objective To investigate the status and rehabilitation needs of stroke patients. Methods 127 patients with stroke in communitywere investigated with questionnaire designed ourselves. Results 127 questionnaires responded. The most patients needed the educationof rehabilitation, the training of limbs function and psychological rehabilitation. Conclusion The needs of stroke patients in the communitywere obtained.

In view of the evaluation of fundus image segmentation, a new evaluation method was proposed to make up insufficiency of the traditional evaluation method which only considers the overlap of pixels and neglects topology structure of the retinal vessel. Mathematical morphology and thinning algorithm were used to obtain the retinal vascular topology structure. Then three features of retinal vessel, including mutual information, correlation coefficient and ratio of nodes, were calculated. The features of the thinned images taken as topology structure of blood vessel were used to evaluate retinal image segmentation. The manually-labeled images and their eroded ones of STARE database were used in the experiment. The result showed that these features, including mutual information, correlation coefficient and ratio of nodes, could be used to evaluate the segmentation quality of retinal vessel on fundus image through topology structure, and the algorithm was simple. The method is of significance to the supplement of traditional segmentation evaluation of retinal vessel on fundus image.
Algorithms ; Databases, Factual ; Diagnostic Imaging ; methods ; Diagnostic Techniques, Ophthalmological ; Fundus Oculi ; Humans ; Image Processing, Computer-Assisted ; Retina ; Retinal Vessels ; anatomy & histology

0.05).However,phosphor-ERK and phosphor-STAT3,NF-?B were higher in CVB_3 group than those in control groups(P

Objective To study the protective effect of GYY4137 on rat myocardial cells infected by Coxsackie virus B3 (CVB3) and its signal transduction mechanism.Methods Cardiomyocytes were treated with different concentrations of GYY4137(10,50,100 μmol/L) for 24 hours before addition of 100 TCID50 CVB3 for 2 hours before serum-free conditions.After treatment,the cell viability was ascertained with Cell Counting Kit-8 (CCK-8) assay.At the same time,the levels of tumor necrosis factor-α (TNF-α),interleukin-1β (IL-1β),interleukin-6 (IL-6) in the supernatants were analyzed by enzyme-linked immunosorbent assay (ELISA).Western blot was used to study the expression of nuclear factor kappa-B (NF-κB) protein and the inhibitory subunit of (IκBα) in myocardial cells.Results After exposure of cardiomyocytes to GYY4137 with different concentration (10,50,100 μmol/L)for 24 hours cell viability had no change.The NF-κB expression and the levels of TNF-α,IL-1β,IL-6 [(175.80 ± 5.05) ng/L,(25.80 ± 1.97) ng/L,(65.33 ± 3.51) ng/L] in the GYY4137-treated CVB3 infection group were significantly reduced when compared with untreated CVB3 infection group (P ＜ 0.01),respectively.Compared with the normal group,the GYY4137 concentration-dependently restrained the CVB3-mediated IκBα degradation(P ＜ 0.01).Conclusions GYY4137 exerts anti-inflammatory effects in CVB3-infected cardiomyocytes.This anti-inflammatory mechanism may be associated with suppression of the activation of the NF-κB.

Asian Continental Ancestry Group ; genetics ; Carcinoma, Hepatocellular ; genetics ; China ; Gene Frequency ; Genetic Predisposition to Disease ; Humans ; Liver Neoplasms ; genetics ; Mongolia ; Polymorphism, Single Nucleotide

Objective To investigate the effects of c?myc promoter binding protein 1(MBP?1)gene on the proliferation of human Saos?2 osteo?sarcoma cells in vitro. Methods Saos?2 cells were divided into three groups:blank control group(untransfected cells),negative group(cells transfected with missense sequence)and experimental group(cells transfected with MBP?1 shRNA). Two MBP?1 shRNA sequences and one neg?ative control shRNA sequence were designed ,synthesized and cloned into pSIREN?retroQ plasma. Then the recombinant plasmids were construct?ed and transfected into human Saos?2 osteosarcoma cells by Lipofectamine 2000. The expressions of MBP?1 mRNA and protein in Saos?2 cells were detected by real?time PCR and Western blot ,respectively. The effects of altered expression of MBP?1 on cell proliferation were measured by CCK?8 cell proliferation assay. The expressions of cyclin D1 and cyclin E in Saos?2 were determined by Western blot. Results PCR and sequenc?ing results indicated that the recombinant plasmids pSIREN?retroQ was constructed. The relative expression level of MBP?1 mRNA in the MBP?1 siRNA transfection group was significantly decreased than that in blank control group(P<0.05). Compared with the blank control group,the ex?pression levels of MBP?1 protein in the experimental group also significantly decreased. The proliferation abilities of Saos?2 cells at 48,72,and 96 hours after MBP?1 siRNA transfection were significantly increased than those in the blank control group(P<0.05). Compared with the blank con?trol group,the expression levels of cyclin D1 and cyclin E protein in the experimental group also significantly increased(P<0.05). Conclusion Knockdown of the expression of MBP?1 gene promotes the proliferation of human Saos?2 osteosarcoma cells. MBP?1 gene may become the new tar?get of gene therapy for osteosarcoma.

Objective To study whether the human bone marrow mesenchymal stem cells (HBMSCs) can repair damaged neural cells induced by okadaic acid (OA).Methods Neuroblastoma cell line SH-SY5Y cells were used to incubate with 20nmol/L okadaic acid for 24h,establishing Alzheimer's Disease cell model;Three groups were set up:normal group,okadaic acid-damaged (OA-damaged) group,hBMSCs-treatment group.The cells were injured for 24h with 20nmol/L OA in OA-damaged group,and treated with conditioned medium obtaining hBMSCs for 24h after 24h OA injury in the treatment group.Then CCK-8 was used for detecting cell vitality,immune fluorescence dyed microtubules and micro filaments for determining the dendritic cell length and fluorescence intensity,in addition,Western blotting for analyzing the protein level of phosphorylated tau and total tau proteins.Results Okadaic acid damaged SH-SY5Y cells,contributed to shrinkage,collapse,cavitation of the SH-SY5Y cell body,dendritic shortening and fracture,and irregular arrangement of microtubule microfilaments;while BMSCs conditioned medium made SHSYSY cell body become round and longer,dendrites restored,and microtubules and microfilaments arranged regularly,fluorescence intensity enhanced.Meanwhile,it also down-regulated the level of OA-induced tau phosphorylation.Conclusion hBMSCs have repair effects on the neural cell damage induced by okadaic acid.