Inhibition of 5-lipoxygenase promotes the regeneration of the liver after partial hepatectomy in normal and icteric rats

The role of leukotriene (LT) on liver regeneration after hepatectomy is still unknown. LTB4 stagnates in the liver with obstructive jaundice, because LTB4 is excreted in the bile; therefore, LTB4 may have an effect on liver regeneration after hepatectomy with obstructive jaundice. Release of obstructive jaundice and simultaneous 70% hepatectomy was performed in rats to study the effect of 5-lipoxygenase inhibitor (AA-861) on liver regeneration. Group 1 underwent hepatectomy with administration of 0.1 mL dimethyl sulfoxide (DMSO), group 2 underwent hepatectomy with administration of AA-861 (20 mg/kg/d) dissolved in 0.1 mL DMSO, group 3 underwent hepatectomy with administration of AA-861 (40 mg/kg/d) dissolved in 0.1 mL DMSO, group 4 underwent release of obstructive jaundice and hepatectomy with administration of 0.1 mL DMSO, and group 5 underwent relief of obstructive jaundice and hepatectomy with administration of AA-861 (20 mg/kg/d). DMSO or AA-861 was administered 24 hours before, during, and 24 hours after hepatectomy in each group. Whole blood LTB4 and serum alanine aminotransferase (ALT), total bilirubin, and bromodeoxyuridine labeling index (LI) were measured before and after hepatectomy. The LTB4 level increased during obstructive jaundice and after hepatectomy. LTB4 and serum ALT levels were significantly lower after hepatectomy in the rats that were administered AA-861, and a significantly higher LI was observed at 24 hours after hepatectomy in rats receiving AA-861. Inhibition of 5-lipoxygenase promotes liver regeneration and decreases hepatocyte injury after hepatectomy associated with obstructive jaundice. (Hepatology 1996 Mar;23(3):544-8)     

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.     

Bcl-2 and Bcl-x: regulatory switches for lymphoid death and survival

The survival and death of lymphoid cells is under the control of a genetic program. Cell death is activated at different stages of development and serves to remove unnecessary and autoreactive lymphocytes, as well as to limit the immune response. The survival of cells is regulated by a set of genes that act as repressors of the cell death mechanism. Of these, bcl-2 and bcl-x exhibit a striking pattern of regulation during lymphoid maturation and can inhibit several forms of apoptotic cell death. Here, Gabriel Núñez and colleagues review recent developments in the field, particularly focusing on the role of the Bcl-2 and Bcl-x proteins in regulating lymphoid death and survival.     

儿童固定正畸治疗与疼痛的相关分析

目的：分析固定正畸治疗后患儿的疼痛情况,以期指导正畸的I临床工作和术后护理。方法：随机选取335例进行固定矫治器治疗的儿童患者,采用视觉模拟评分法（VAS）在治疗后2h、6h、夜间、24h、2d、3d及7d分别测量其术后疼痛情况,进行评分及统计分析。结果：正畸治疗2h后疼痛开始加重,其后24h内疼痛程度于夜间达到最高水平,第2d开始疼痛减轻,第7d基本恢复正常状态。咀嚼与否及前后牙的疼痛情况基本相似。结论：VAS法可有效分析儿童接受正畸治疗后的疼痛情况,为医生临床工作和治疗后护理提供有益的指导。     

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.