0.05).Histological type,gross type,tumor site,lymph node metastasis and depth infiltration were related to the prognosis of gastric cancer(P

Objective To observe the change of sinus heart rate turbulence (HRT) and its relation to left ventricular systolic function (LVSF) in patients with acute coronary syndrome (ACS). Methods The 103 ACS patients and 62 healthy subjects were enrolled in this study, all of them received 24-hour Holter monitor. And the values of turbulence onset (TO), turbulence slope (TS)and heart rate variability (HRV) SDNN were calculated according the Holter records. The clinical information, left ventricular ejection fraction (LVEF) and left ventricular end diastolic diameter (LVEDD) were recorded. Then the ACS patients were divided into acute myocardial infarction (AMI)group and unable angina pectoris (UAP) group according to the cardiac enzymes and electrocardiogram. Results The value of TO was significantly higher in ACS group than in control group [(0.17±1.40)％ vs. (- 0.26±0.99)％, P＜0.05], and TS was significantly lower in ACS group than in control group [R-R interval:(0.88±2.51) ms vs. (2.60±2.76) ms, P＜0.01].There were significant differences in TS, LVEF and LVEDD between AMI group and UAP group (all P＜0.01), but there were no differences in HRV and TO between the two groups. TS was positively correlated with LVEF (r=0.21, P＜0.05), while TO was negatively correlated with LVEF (r=-0.26, P＜0.05) by Spearman correlation analysis. Conclusions HRT is significantly blunted in ACS patients and can evaluate cardiac autonomic function. It may be as a predictor of LVSF in ACS patients.

The incidence of adenocarcinoma of esophagogastric junction is increasing worldwide during recent decades.The therapeutic strategies have been transformed from surgery alone to multimodal treatments involing also perioperative chemoradiotherapy.Although there are still many problems on preoperative staging,surgical approach,excisional extent and perioperative chemoradiotherapy regimen,multidisciplinary team collaboration can provide an optimal diagnosis and treatment to achieve the principles of standardization and individualization in malignant tumor,which will prolong the survival and improve the quality of life for every patient.

Objective To investigate the therapeutic effect of fluvastatin in bleomycin-induced pulmonary fibrosis in rats. Methods Pulmonary fibrosis was induced in SD rats by intratracheal instillation of bleomycin A_ 5 . The rats were than divided randomly into three groups: the rats in the first group received daily fluvastatin 20mg/kg (group Flu),those of the second group received normal saline (group BLM) orally only,and those of controls (group N) received normal saline both intratracheally and orally. Five rats in each group were sacrificed 1,3,7,14 and 28 days after intratracheal instillation of bleomycin. Pathological changes in the lungs were evaluated by HE stain and Masson′s trichrome stain. Collagen content of the lung tissue was assessed by hydroxyproline concentration. Alveolar macrophages,polymorphonuclear leukocytes and lymphocytes in bronchoalveolar lavage fluid (BALF) were counted. Hyaluronic acid (HA) and laminin (LN) in BALF were determined by radioimmunoassay. Results The degree of alveolitis and pulmonary fibrosis in group Flu was improved as compared with that of group BLM. Hydroxyproline concentrations of group Flu were significantly lower than that of group BLM 7 days after bleomycin A_ 5 instillation. Total cell counts and percentage of polymorphonuclear leukocytes and lymphocytes in BALF were significantly reduced in group Flu. HA and LN levels in BALF were also lower in group Flu compared with group BLM. Conclusion Fluvastatin could alleviate bleomycin-induced pulmonary fibrosis in rats.

Objective:To observe the inhibitory effect of fluvastatin (Flu) on the proliferation of the rat lung fibroblasts cultured in vitro . Methods: Normal rat lung derived fibroblasts were cultured in media containing Flu. The influences of Flu on the growth curve of the fibroblasts were observed by cell count and MTT colorimetry. The inhibition effect of Flu serial dilutions on the fibroblasts proliferation was investigated. Influence of Flu on division index of the fibroblasts was analyzed by direct cell count. Chemical colorimetry was used to detect the hydroxyproline in the media. Results: Flu inhibited the proliferation of the normal rat lung fibroblasts in the manner of dose dependence( P

Objective To observe the effects of cystamine, a tissue transglutaminase (tTG) inhibitor, on the development of rat liver fibrosis induced by carbon tetrachloride. Methods One hundred male SD rats were randomly divided into control group (n=20), hepatic fibrosis group (n=40) and cystamine group (n=40) . Liver fibrosis model was induced by intraperitoneal injection of carbon tetrachloride. Cystamine (112 mg·kg-1·d-1) was administered by intraperitoneal injection 2 days before injection of carbon tetrachloride. The rats were sacrificed at weeks 4 and 8, and the liver tissues and serum specimens were obtained. The mRNA expression of tTG, smooth muscle-alpha (α-SMA), collagen-Ⅰ and tissue inhibitors of metalloproteinase-1 (TIMP-1) were detected by real time PCR. The protein expression of tTG and α-SMA, liver function and content of hydroxyproline in liver tissues were determined by Western blot. Histological changes of the liver was observed under microscope. The fibrosis conditions of rat liver in each group were evaluated according to the semi-quantita-tive scoring system. All the data were analyzed by one-way ANOVA. Results Eight weeks after the injection of carbon tetrachloride, obvious injury of the liver in liver fibrosis group was observed. The levels of alanine trans-aminase (ALT), total bile acid, total bilirubin, hydroxyproline, tTG, α-SMA, collagen-Ⅰ and TIMP-1 were (1313±157)U/L, (99.9±18.5)μmol/L, (10.9±1.6)μmoL/L, (55±12)μg/g, 145.6±51.2, 130.3±44.6, 211.3±75.1 and 162.4±53.5. After administration of cystamine, the levels of ALT, total bile acid, total bilirubin, hydroxyproline, tTG, α-SMA, collagen-Ⅰ and TIMP-1 were (378±87) U/L, (61.0±12.7) μmol/L, (9.8±1.7) μmol/L, (70±14 ) μg/g, 48.6±12.3, 40.7±12.3, 63.9±16.0, 59.2μ23.4. Conclusion Cystamine can alleviate the carbon tetrachloride-induced rat liver fibrosis by inhibiting the tTG pathway.

Objective To investigate the anti-fibrosis effect of a 5-lipoxygenase (5-LO)specific inhibitor AA-861 on liver fibrosis. Methods Liver fibrosis was induced in male Sprague Dawley rats by intraperitoneal injection of carbon tetrachloride(CCI4).AA-861(0.2 mg/100 g/d)was administrated by intraperitoneal injection starting 2 days before the first dosage of CCI4 and rats were killed at weeks 2,4,and 6.Liver specimens were obtained from each animal and fixed with 4%formaldehyde for histological analysis. The Mrna expression of 5-LO,smooth muscle-alpha(α-SMA),Collagen-1,matrix metalloproteinase-2(MMP-2)and tissue inhibitors of metalloproteinase-1(TIMP-1),the protein expression of 5-LO were evaluated by real time PCR and Western blot respectively. Histological analysis was performed by microscopy observation. Fibrosis conditions in rat liver in each group were evaluated according to the semi-quantitative scoring system (SSS), Hyp in rat livers and the hepatic functional biochemistry were also detected. Results Along with the aggravation of liver fibrosis, the gene expression of 5-Lo,α-SMA,Collagen-1,MMP-2 and TIMP-1 increased gradually, and the level of ALT, TBA, Hyp and SSS score also increased gradually. With the administration of AA-861,the Mrna expression of 5-LO,α-SMA,Collagen-1,MMP-2,TIMP-1 and the protein expression of 5-LO decreased remarkably, and the reduction in TIMP-1 Mrna expression was more significant than that in MMP-2.Six weeks after AA-861 treatment, the level of ALT, TBA, Hyp and SSS score were also decreased significantly. Conclusion AA-861 ameliorates CCI4 induced rat liver fibrosis by inhibiting the 5-LO pathway and decreasing the expression of 5-LO,α-SMA,Collagen-1,MMP-2 and TIMP-1.

Supernumerary teeth is one kind of teeth dysplasia.2 cases with more than 3 supernumerary teeth located in premolar region are re-ported.

Objective To investigate the short-term efficacy and safety of gefitinib combined with dendritic cells-cytokine induced killer (DC-CIK) cells in the treatment of advanced lung adenocarcinoma.Methods Fifty patients with lung adenocarcinoma who in previous had underwent radiotherapy and first-line chemotherapy failure received DC-CIK in combination with gefitinib treatment,blood count changes,imaging data,carcinoembryonic antigen and changes in the quality of life before and after treatment were compared and evaluated.Results DC-CIK could improve effectively and relieve bone marrow suppression response after chemotherapy and significantly increase the WBC content of blood (P ＜ 0.01).After treatment,the tumor carcinoembryonic antigen (CEA) was significantly lower in patients (P ＜ 0.01).Fifty cases of patients in complete remission (CR) were 0 cases,partial remission (PR) were 24 cases,stable disease (SD) were 17 cases and progression (PD) were 9 cases,and the response rates (RR) were 48％;The quality of life of patients was significantly improved (P ＜ 0.05).Common adverse reactions were rash,diarrhea,chill and fever,but mild symptoms could be relieved after symptomatic treatment.Conclusions Gefitinib with autologous DC-CIK cell infusion second-line treatment of advanced lung cancer have a certain short-term efficacy,without significant adverse reactions.Gefitinib with autologous DC-CIK cell therapy can mitigate the response of bone marrow suppression in patients with advanced lung cancer and improve the quality of life of patients.Long-term effect remains to be investigated.

Objective To investigate autoantibody against endothelin receptor type A (ENRA-Ab) in patients with systemic lupus erythematosus associated pulmonary arterial hypertension (SLE-PAH).The possibility of autoantibody-mediated pathogenesis in the development of SLE-PAH has also been explored.Methods ENRA-Ab in the serum of SLE-PAH and controls were detected by using a human ETRA epitope peptide-based ELISA.The clinical relevance of ENRA-Ab in SLE-PAH was analyzed.Proliferation of vascular smooth muscle cells (SMCs) and permeability of endothelial cells in vitro under the stimulation of polyclonal ENRA-Ab IgG were assessed.The expressions of PAH-related markers, i.e., 5-HTT, PDGFR-b, VEGF-A and PDGF-B were measured by qPCR.The effect of ENRA-Ab in vivo was also determined in a suboptimaldose monocrotaline-induced model with the assessment of right ventricle hypertrophy index and pathology parameters.Independent t-test, Tukey-Kramer test of variance analysis and Pearson' s correlation analysis were used for statistical analysis.Results ENRA-Abs was presented in a higher occurrence in SLE-PAH (35/85,41％) compared with controls (0/60;0, 13/80, 16％).There was a significant correlation between ENRA-Ab and echocardiograph estimated pulmonary arterial systolic pressure (r=0.392, P=0.002) in SLE-PAH.ENRA-Ab could promote SMCs proliferation, disrupt endothelial barrier and up-regulate PAH-related markers expression,which could be blocked in the presence of ETR antagonist.ENRA-Ab aggravated right ventricle hypertrophy and vascular remodeling in vivo.Conclusion ENRA-Ab is a new biomarker, in SLE-PAH, which may mediate PAH development in SLE.