Objective To study the anti-proliferative effects of Okam extract on bleomycin induced pulmonary fibrosis in rats and its underlying mechanisms.Methods Pulmonary fibrosis was induced in Wistar rats by intratracheal instillation of bleomycin.Then test groups received daily Okam at doses of 25 and 50 mg?kg~(-1) orally and control group received normal saline.The expressions of collagen-Ⅲ.tumor necrosis factor(TNF-?) and vascular endothelial growth factor(VEGF) proteins were determined by immunohistochemistry.Results Pulmonary fibrosis of test groups was improved as compared with that of model group.Protein expressions of collagen-ll,VEGF and TNF-?in 50mg?kg~(-1)group were markedly lower than those in model group.Protein expressions of collagen-Ⅲand VEGF in 25 mg?kg~(-1)group were lower than those in model group,while protein expression of TNF-?showed no difference with that in model group.Conclusion Okam extract alleviates bleomycin induced pulmonary fibrosis in rats by inhibiting the expressions of collagen-Ⅲ,TNF-?and VEGF.

Objective To observe the expression of epidermal growth factor receptor(EGFR) and vascular endothelial growth factor(VEGF) in non-small cell lung cancer(NSCLC) and the reletionship with clinic-pathologic parameters.Methods Immunohistochemistry of tissue sections was used to study the expression of EGFR and VEGF in 124 NSCLC tissues and 15 normal lung tissues adjacent to cancer tissues.Results The positive rates of EGFR and VEGF in 124 NSCLC samples were 52.4％,66.1％,while no expressed in the 15 normal lung tissues adjacent to cancer tissues.The positive rate of VEGF with stage Ⅲ was higher than that with stage Ⅰ - Ⅱ ( 80.4％ vs 56.2％,P ＜0.05).The positive rate of VEGF with lymph node metastasis was higher than that without lymph node metastasis (78,2％ vs 53.3％,P ＜ 0.05 ).The expression of VEGF and EGFR had no relationship with clinic pathological factors including histological type of lung cancer,sex,age.EGFR and VEGF expression was statistically correlated with each other( r =0.93,P ＜0.05 ).Conclusion EGFR and VEGF were overexpressed in NSCLC tissues.The expression of VEGF was correlated with TNM stages and lymph node metastasis.The expression of EGFR was correlated with VEGF expression in NSCLC tissues,which indicates they might act synergistically in angiogenesis of NSCLC.

OBJECTIVE To explore production of ?-lactamase induced by antibiotics in Pseudomonas aeruginosa biofilm and planktonic bacteria.METHODS In vitro models of P.aeruginosa biofilm were built up.The planktonic bacteria and P.aeruginosa biofilms were exposed to different concentrations of imipenem and ceftazidime.The quantitative analysis of ?-lactamase was undertaken.The class of ?-lactamase was verified by modified cefoxitin three-dimensional test.RESULTS Both P.aeruginosa biofilm and planktonic bacteria showed significant ?-lactamase activity in the presence of antibiotics.The maximal ?-lactamase activities of both were significantly different with the statistic method of test(P

Objective To explore the application of bumetanide to inhibition of tumor cell proliferation.Methods In different cell lines, the expression of natrium,kalium, chloride cotransporter 1 ( NKCC1) was detected by Western blotting while the proliferation of different tumor cells was examined by CCK-8 kit.Results The target protein NKCC1 expression in lung cancer cell line ( A549 ) and colorectal cancer cell line ( HCT116 ) was significantly higher than that in chronic myelogenous leukemia cell line (K562), esophageal cancer cell line (Eca109), cervical carcinoma cell line (HeLa), T lymphocytic leukemia cell line (Jurkat) and breast cancer cell line (MCF7).IC50 Values of bumetanide were significantly lower in A549 and HCT116 than in K562, Eca109,HeLa,Jurkat and MCF7.Furthermore, the inhibiory rate and the target protein expression level were positively correlated.Conclusion Bumetanide can inhibit tumor cell proliferation and NKCC1 can serve as a potential target of anticancer drugs.

OBJECTIVE To study the existence of the ?-lactamase gene produced by multidrug-resistant Pseudomonas aeruginosa isolated from respiratory tract. METHODS Antimicrobial susceptibility was tested by K-B method. A modified three-dimensional test was used to detect the ?-lactamase phenotypes. The genotypes were analyzed by PCR amplification and product sequencing. RESULTS ?-Lactamases were detected in 29 out of the 46 isolates. Twenty-one isolates produced AmpC ?-lactamase,two of them harboring CARB-3 gene. Two isolates produced ESBLs harbored TEM gene. Six isolates produced other type of ?-lactamases. Four out of 6 harbored CARB-3 gene and three IMP gene. The oprD2 gene was deleted in 34 isolates. CONCLUSIONS Chromosomal-mediated AmpC ?-lactamase is the major ?-lactamases produced by multidrug-resistant P. aeruginosa and CARB-3 is second. Lack oprD2 gene is popular.

It is purposed to analyze therapeutic effectiveness at community and designated hospitals for extensive influenza A H1N1 outbreaks at five universities in Qingdao,Shandong,east China during September 1 to 30,2009,including 28 confirmed cases,182 suspected cases and 136 close contacts treated at community health-care facilities,and 56 confirmed cases treated at designated hospitals.There was no significant difference in therapeutic effectiveness between community health-care facilities and designated hospitals (P ＞ 0.05).No new cases occurred seven days after their isolation was lifted for suspected cases and close contacts at community,indicating influenza A H1N1 could be prevented,controlled and cured and its mild cases could be treated at community health-care facilities.

OBJECTIVETo study the correlation of vascular endothelial growth factor-C (VEGF- C) expression and lymphatic microvessel density (LMVD) with clinicopathological features and prognosis in colon cancer.

METHODSThe expression of VEGF-C and VEGFR-3 was detected by immunohistochemical staining with monoclonal antibodies against VEGF-C and VEGFR-3 in 44 cases with primary colon cancer. LMVD was calculated.

RESULTSVEGF-C positive rate was 43.2% (19/44). VEGF-C expression was associated with tumor (P=0.003), lymph node metastasis (P=0.002), Dukes stage (P=0.001). The mean LMVD was 10.14+/- 4.19. LMVD was associated with lymph node metastasis (P=0.002), Dukes stage (P=0.001). LMVD in VEGF-C(+) group was (11.34+/- 4.83) higher than (9.24+/- 3.48) in VEGF-C(-) group, but there was no statistically significance between the two groups (P=0.105). The survival rate of the patients with positive VEGF-C was lower than that with negative VEGF-C (P=0.0225). The median survival time of the patients with LMVD(+) group was shorter than that with LMVD(-) (P=0.0036). Distant metastasis (P=0.0004), lymphatic metastasis (P=0.021) and LMVD (P=0.0469) were independent prognostic factors.

CONCLUSIONSVEGF-C and LMVD appear to be new prognostic factors for colon cancer. Furthermore, LMVD may be a new independent prognostic factor.

Adult ; Aged ; Aged, 80 and over ; Colonic Neoplasms ; metabolism ; pathology ; Female ; Humans ; Lymphangiogenesis ; Lymphatic Metastasis ; Lymphatic Vessels ; Male ; Middle Aged ; Prognosis ; Vascular Endothelial Growth Factor C ; metabolism ; Vascular Endothelial Growth Factor Receptor-3 ; metabolism

OBJECTIVESTo assess the changes of the levels of plasma endothelin (ET-1), nitric oxide (NO) and atrial natriuretic peptide (ANP) after cardiopulmonary bypass (CPB) and the influence of inhaled nitric oxide in patients with ventricular septal defect (VSD) and pulmonary hypertension (PH).

METHODSSixty patients with VSD were enrolled in this study. They were divided into 2 groups: group A [no-PH group, mean pulmonary artery pressure (mPAP) < 20 mm Hg (1 mm Hg = 0.133 kPa) n = 20] and group B (PH group, mPAP > 20 mm Hg, n = 40). Group B was subdivided into two groups by randomized block, group B(1) (inhaled NO group, n = 20) and group B(2) (contrast group, n = 20). The plasma ET-1, NO, ANP concentrations were assayed at 24 h pre-operation and 0 h, 1 h, 5 h, 12 h, 24 h, 48 h after CPB.

RESULTSThe preoperative plasma ET-1, NO and ANP concentrations in group B were significantly higher than those in group A. In three groups, the plasma ET-1 concentration at 0 h after CPB was significantly higher than that at 24 h pre-operation, and the plasma NO concentration at 0 h after CPB was significantly lower than that at 24 h pre-operation. In group B, the plasma ANP concentration at 0 h after CPB was significantly higher than that at 24 h pre-operation. After CPB, the plasma ET-1 concentration in group B(1) decreased faster than that in group B(2), and the plasma NO concentration in group B(1) increased faster than that in group B(2). In group B, the preoperative plasma ET-1 concentration negatively correlated with the preoperative plasma NO concentration and positively correlated with the preoperative ANP concentration.

CONCLUSIONSThe broken dynamic balance of ET-1/NO may take part in generation and development of pulmonary hypertension. ANP acts as a favorable physiological regulating factor in the pathogenesis of pulmonary hypertension. CPB can regulate the level of ET-1 up and NO and ANP down while inhaled NO can cause the level of ET-1 down and the level of NO up.

Administration, Inhalation ; Atrial Natriuretic Factor ; blood ; Cardiopulmonary Bypass ; Child, Preschool ; Endothelin-1 ; blood ; Female ; Heart Septal Defects ; blood ; surgery ; Humans ; Hypertension, Pulmonary ; blood ; surgery ; Male ; Nitric Oxide ; blood ; pharmacology

The bile acid-responsive G-protein-coupled receptor TGR5 is expressed in monocytes and macrophages, and plays a critical role in regulating inflammatory response. Our previous work has shown its role in promoting the progression of non-small cell lung cancer (NSCLC), yet the mechanism remains unclear. Here, using Tgr5-knockout mice, we show that TGR5 is required for M2 polarization of tumor-associated macrophages (TAMs) and suppresses antitumor immunity in NSCLC via involving TAMs-mediated CD8⁺ T cell suppression. Mechanistically, we demonstrate that TGR5 promotes TAMs into protumorigenic M2-like phenotypes via activating cAMP-STAT3/STAT6 signaling. Induction of cAMP production restores M2-like phenotypes in TGR5-deficient macrophages. In NSCLC tissues from human patients, the expression of TGR5 is associated with the infiltration of TAMs. The co-expression of TGR5 and high TAMs infiltration are associated with the prognosis and overall survival of NSCLC patients. Together, this study provides molecular mechanisms for the protumor function of TGR5 in NSCLC, highlighting its potential as a target for TAMs-centric immunotherapy in NSCLC.