陶瓷化骨对人牙囊细胞分化的影响

目的:培养人牙囊细胞(DFCs),观察陶瓷化骨(CBB)对人牙囊细胞生长和分化的影响.方法:体外分离胚胎期人DFCs,将第三代细胞以CBB为载体立体培养,以平面接种为对照组,用矿化液持续诱导,利用光镜观察细胞生长状态、免疫组织化学观察细胞矿化基质牙骨质附着蛋白(CAP,)及骨涎蛋白抗体(BSP)分泌、Vokassa染色观察矿化情况,了解CBB对DFCs生物学行为的影响.结果:体外连续诱导28 d,实验组光镜下可见DFCs与CBB相容性好,材料周边细胞生长密集,并有向BBC趋化迁移现象,附近细胞聚集,形成Vokassa染色阳性的矿化结节,免疫组织化学染色BSP,CAP阳性着色,部分细胞强阳性着色.对照组细胞复层生长,未形成矿化结节,免疫组织化学染色BSP,CAP阴性着色.结论:体外培养条件下,CBB可诱导人DFCs向成骨和成牙骨质细胞分化.     

Association of Empirically Derived Food-Based Inflammatory Potential of the Diet and Breast Cancer: A Hospital-Based Case-Control Study

BackgroundDiet may be a modifiable factor in the prevention of breast cancer (BC) by modulating inflammation. We used a food-based empirical dietary inflammatory index (FDII) to evaluate the association between FDII and odds of breast cancer in Iranian women.MethodsThe present case-control study carried out on 150 age-matched women with newly diagnosed breast cancer and controls. Data for dietary intake and anthropometric measures were collected. FDII score was developed according to participants dietary intakes of 27 pre-defined food groups. Multivariate odds ratios (OR) with 95% confidence intervals (CI) were used to investigate the association of empirically derived food-based inflammatory potential of the diet and breast cancer.ResultsThe odds ratios of BC according to quartiles of FDII score by multivariate logistic regression models indicated the FDII score was significantly associated with BC risk (OR: 2.38; 95% CI: 1.23-4.59, P _trend = .04). After controlling confounders, multivariate logistic regressions remained significant which revealed in participants at the fourth quartile of FDII score chance of breast cancer was 2.8 times higher than participants in the first quartile.ConclusionsThe results of our study suggested that more pro-inflammatory diet (higher FDII scores) was associated with increased BC risk. These findings suggest that developing an effective dietary modification based on FDII may reduce risk of BC.     

Safety and efficacy of oral nemonoxacin versus levofloxacin in treatment of community-acquired pneumonia: A phase 3, multicenter,randomized, double-blind,double-dummy,active-controlled,non-inferiority trial

Background/Purpose

Nemonoxacin is a novel nonfluorinated quinolone with excellent in vitro activity against most pathogens in community-acquired pneumonia (CAP), especially Gram-positive isolates. The purpose of this study was to assess the efficacy and safety of nemonoxacin compared with levofloxacin in patients with CAP.

Carvedilol attenuates CPB-induced apoptosis in dog heart: regulation

Objective To evaluate the effects of Carvedilol on cardiopulmonary bypass (CPB)-induced myocardiocyte apoptosis and its effect on regulation of Fas, FasL expression, caspase-3 activity and oxidative stress in the left ventricle (LV) in this setting.Methods Ten adult dogs undergoing conventional hypothermic CPB were randomly divided into control and Carvedilol treated groups (n=5, respectively). Dogs in Carvedilol treated group 3 μg·min-1·kg-1 received a bolus of Carvedilol (1 mg/kg) intravenously and a maintenance dosage of Carvedilol for 3 hours after the reperfusion of the heart. Dogs in control group received no carvediolol. LV samples were obtained before, during and 3 hours after CPB. In situ nick end-labeling (TUNEL) technique was used to detect the apoptotic cells. The expressions of Fas and FasL were detected immunohistochemically and quantified by fluorescence activated cell sorting (FACS). The activity of caspase-3 enzyme and malondialdehyde (MDA) level were measured by cleavage of Z-DEVD-AMC substrate and thiobarbituric acid reactive substances (TBARS) method, respectively. Results Before and during CPB, all the parameters were not significantly different between groups (P>0.05). After CPB, these parameters in both groups were significantly elevated compared with those of before and during CPB (P<0.028, respectively). However, the number of apoptotic cells in Carvedilol treated group was significantly decreased compared with that of the control group (P<0.021). The expressions of Fas and FasL were significantly downregulated by Carvedilol (P<0.001 and 0.003, respectively). The caspase-3 activity and the content of MDA in the Carvedilol treated group was also significantly reduced (P<0.026 and 0.005, respectively). Conclusions Carvedilol significantly reduces CPB-induced cardiomyocyte apoptosis in dog hearts and the reduction of cardiomyocyte apoptosis is associated with downregulation of Fas and FasL expression, inhibition of caspase-3 activity and oxidative stress in LV.     

脂联素对巨噬细胞源性泡沫细胞内胆固醇含量的影响

目的 通过研究脂联素对细胞内胆固醇的影响,探讨其抗动脉粥样硬化作用的可能机制.方法 以人急性单核细胞白血病细胞株(THP-1细胞株)来源的泡沫细胞模型为研究对象,用不同浓度的脂联素(1 mg/L,5 mg/L和10 mg/L)进行体外干预.采用油红O观察泡沫细胞形成,用胆固醇氧化酶法检测细胞内胆固醇含量的变化,用荧光显微镜观察巨噬细胞对Dil标记的氧化低密度脂蛋白(Dil-Ox-LDL)的摄取率.结果 脂联素(1 mg/L,5 mg/L和10 mg/L)干预对巨噬细胞内总胆固醇(TC)无显著影响,却能促进胆固醇酯(CE)转化为游离胆固醇(FC),CE/TC比值明显降低(P<0.05);同时观察到脂联素(10 mg/L)干预后可抑制巨噬细胞对Dil-Ox-LDL的摄取.结论 脂联素能减少巨噬细胞对Ox-LDL的摄取和促进巨噬细胞内胆固醇酯的水解,这可能是脂联素抑制胆固醇沉着从而发挥抗动脉粥样硬化作用的机制之一.     

Experimental study of acute lung injury induced by different tidal volume ventilation in rats

Mechanical ventilation (MV) is a dual blade sward which if misused could lead to lung injury, called ventilator induced lung injury (VILI). Pathogenesis of VILI is very complex with various manifestations, which is the focus in MV field in recent years.^1 In our research, the rats were ventilated with different tidal volume,     

Aprepitant exerts anti-fibrotic effect via inhibition of TGF-β/Smad3 pathway in bleomycin-induced pulmonary fibrosis in rats

Bleomycin is a well-recognized antineoplastic drug. However, pulmonary fibrosis (PF) is considered to be the principal drawback that greatly limits its use. Here, we sought to investigate ability of the neurokinin receptor 1 blocker, aprepitant, to prevent PF caused by bleomycin. Male adult Wistar rat groups were given a single intratracheal injection of bleomycin, either alone or in combination with aprepitant therapy for 3 or 14 days. Collagen deposition and a rise in transforming growth factor beta (TGF-β) immunoreactivity in lung tissue serve as evidence of bleomycin-induced PF. The serum levels of lactate dehydrogenase, alkaline phosphatase, and total antioxidant improved after aprepitant therapy.Additionally, it reduced the protein expressions of interferon alpha, tumor necrosis factor alpha, and lung lipid peroxidation. Moreover, aprepitant treatment led to an increase in the antioxidant indices glutathione, glutathione peroxidase, and catalase. Aprepitant is postulated to protect against bleomycin-induced PF by decreasing TGF-β, phosphorylating Smad3, and increasing interleukin 37, an anti-fibrotic cytokine, and G Protein-coupled Receptor Kinase 2. Aprepitant for 14 days considerably exceeded aprepitant for 3 days in terms of improving lung damage and having an anti-fibrotic impact. In conclusion, aprepitant treatment for 14 days may be used as an adjuvant to bleomycin therapy to prevent PF, mostly through inhibiting the TGF-/p-Smad3 fibrotic pathway.     

Ochratoxin A induced differentiation nephrotoxicity in renal tubule and glomeruli via autophagy differential regulation

Ochratoxin A (OTA) is a mycotoxin that mainly causes nephrotoxicity. The single nephrotoxicity of OTA exposure on glomeruli or renal tubule had been well documented, however, the comparison toxicity between it is still unclear. Here, C57BL/6 mice and two types of nephrocyte were treated with concentration-gradient OTA to explore its differentiation nephrotoxicity. Results showed that OTA induced nephrotoxicity in vivo and in vitro, manifested as the deteriorative kidney function in mice and the cut-down cell viability in nephrocyte. Besides, results of murine kidney pathological section and IC₅₀ of two types nephrocyte indicated that OTA-induced toxicity in renal tubule was higher than its in glomeruli. In addition, OTA exposure induced autophagy signaling differentiation expression. It revealed that autophagy was implicated in OTA-induced differential nephrotoxicity in glomeruli and renal tubule. Altogether, we proved that OTA induces a differentiation nephrotoxicity in glomeruli and renal tubule, and it is related to autophagy differential regulation.