乳酸杆菌发酵滤液中核酸抗肿瘤效应及对荷瘤鼠免疫功能的影响

目的探讨乳酸杆菌DM9811培养基滤液中核酸在体外对肿瘤细胞生长及对荷瘤鼠免疫功能的影响。方法抽提乳酸杆菌DM9811对数生长期培养基滤液中核酸,进行琼脂糖电泳分析;MTT法体外观察其对于结肠癌HT-29细胞系生长的影响;动物实验观察不同组别小鼠生存期、瘤重体重比、NK细胞活性、T细胞亚群指标。结果乳酸杆菌DM9811滤液中核酸组分为RNA;在细胞浓度为1×106时,每孔加入RNA 100μg能够明显抑制结肠癌HT-29细胞系的生长;预防组荷瘤鼠除CD8＋T细胞比例之外各项指标与阴性对照组相比差异都有统计学意义（P〈0.05）,其中NK细胞杀伤活性（58.97±3.62）、CD4＋T细胞比例（27.77±5.40）和生存期（15.1±4.48）均高于阴性对照组（43.87±3.92）、（19.68±3.00）、（10.2±3.08）,瘤重体重比（0.029±0.017）低于阴性对照组（0.066±0.024）;治疗组生存期（11.8±3.12）与阴性对照组（10.2±3.08）相比差异有统计学意义（P〈0.05）,治疗组生存期长于阴性对照组。结论乳酸杆菌DM9811培养基滤液中存在核酸组分,为100200 bp的RNA片段。100μg/mL乳酸杆菌DM9811培养基滤液中RNA组分对结肠癌HT-29细胞系生长有明显抑制作用。RNA组分可以上调荷瘤鼠的细胞免疫水平,延长荷瘤鼠的生存期。     

棉株上烟粉虱若虫种群的垂直分布与统计方法研究

对烟粉虱Bemisiatabaci在棉花植株上的垂直分布调查发现 ,烟粉虱在棉株各部位均有分布 ,且分布极不均匀 ,统计分析表明棉株各部位间烟粉虱的种群数量存在显著的差异。棉花顶部烟粉虱的若虫数量约占全棉株若虫总量的 1 6%,通过对棉株各部位烟粉虱的若虫数量与整株若虫总量的回归分析 ,建立了相应的回归方程式     

Evaluation of the cytoprotective effects of bovine lactoferrin against intestinal toxins using cellular model systems

This study investigated the effects of bovine lactoferrin (BLf) on the growth of different groups of bacteria in vitro. BLf showed a significant inhibitory effect on the growth of selected pathogens but not probiotics. BLf, in combination with probiotics, has the potential to influence the composition of the gut microflora via inhibition of intestinal pathogens with no significant effect on probiotic bacteria.     

An alternative excited-state proton transfer pathway in green fluorescent protein variant S205V

Wild-type green fluorescent protein (wt-GFP) has a prominent absorbance band centered at approximately 395 nm, attributed to the neutral chromophore form. The green emission arising upon excitation of this band results from excited-state proton transfer (ESPT) from the chromophore hydroxyl, through a hydrogen-bond network proposed to consist of a water molecule and Ser205, to Glu222. Although evidence for Glu222 as a terminal proton acceptor has already been obtained, no evidence for the participation of Ser205 in the proton transfer process exists. To examine the role of Ser205 in the proton transfer, we mutated Ser205 to valine. However, the derived GFP variant S205V, upon excitation at 400 nm, still produces green fluorescence. Time-resolved emission spectroscopy suggests that ESPT contributes to the green fluorescence, and that the proton transfer takes place approximately 30 times more slowly than in wt-GFP. The crystal structure of S205V reveals rearrangement of Glu222 and Thr203, forming a new hydrogen-bonding network. We propose this network to be an alternative ESPT pathway with distinctive features that explain the significantly slowed rate of proton transfer. In support of this proposal, the double mutant S205V/T203V is shown to be a novel blue fluorescent protein containing a tyrosine-based chromophore, yet is incapable of ESPT. The results have implications for the detailed mechanism of ESPT and the photocycle of wt-GFP, in particular for the structures of spectroscopically identified intermediates in the cycle.     

糖尿病大鼠肋间肌酶组织化学研究

目的探讨糖尿病早期肋间肌酶组织化学变化。方法应用酶组织化学方法观察糖尿病2周和4周大鼠肋间肌组织脱氢酶、水解酶和氧化酶活性变化。结果糖尿病2周大鼠肋间肌组织琥珀酸脱氢酶、谷氨酸脱氢酶和辅酶Ⅰ黄递酶活性较对照组增强,乳酸脱氢酶活性较对照组减弱,苹果酸脱氢酶、异柠檬酸脱氢酶、葡萄糖-6-磷酸脱氢酶、酸性磷酸酶、酸性-α-萘酸性酯酶和细胞色素氧化酶无变化。糖尿病4周大鼠肋间肌组织琥珀酸脱氢酶、苹果酸脱氢酶、谷氨酸脱氢酶、辅酶Ⅰ黄递酶、酸性磷酸酶和酸性-α-萘酸性酯酶活性较对照组增强,乳酸脱氢酶和细胞色素氧化酶活性较对照组减弱,异柠檬酸脱氢酶、葡萄糖-6-磷酸脱氢酶无变化。结论糖尿病2周大鼠肋间肌组织有氧氧化代谢能力增强,糖酵解能力减弱。糖尿病4周大鼠肋间肌组织有氧氧化能力增强、糖酵解能力减弱及能量代谢紊乱。在糖尿病早期呼吸肌存在代谢异常。     

Blockade of L-type voltage-gated Ca channel inhibits ischemia-induced neurogenesis by down-regulating iNOS expression in adult mouse

Neurogenesis in the adult mammalian hippocampus may contribute to repairing the brain after injury. The signals that regulate neurogenesis in the dentate gyrus following ischemic stroke insult are not well known. We have previously reported that inducible nitric oxide synthase (iNOS) expression is necessary for ischemia-stimulated neurogenesis in the adult dentate gyrus. Here, we show that mice subjected to 90 min of middle cerebral artery occlusion (MCAO) significantly increased the number of new neurons and up-regulated iNOS expression in the dentate gyrus. Blockade of the L-type voltage-gated Ca(2+) channel (L-VGCC) prevented neurogenesis in the dentate gyrus and subventricular zone (SVZ), and down-regulated iNOS expression in the dentate gyrus after cerebral ischemia. This study suggests that Ca(2+) influx through L-VGCC is involved in ischemia-induced neurogenesis by up-regulating iNOS expression.     

Clinorotation upregulates inducible nitric oxide synthase by inhibiting AP‐1 activation in human umbilical vein endothelial cells

Alterations of nitric oxide contribute to post‐flight orthostatic intolerance. The aim of this study was to investigate the changes of inducible nitric oxide synthase (iNOS) and the mechanisms underlying regulation of iNOS by simulated microgravity in human umbilical vein endothelial cells (HUVECs). Clinorotation, a simulated‐model of microgravity, increased iNOS expression and promoter activity in HUVECs. The transactivations of NF‐κB and AP‐1 were suppressed by 24 h clinorotation. A key role for AP‐1, but not NF‐κB in the regulation of iNOS was shown. (1) PDTC, a NF‐κB inhibitor, had no effect on clinorotation upregulation of iNOS. (2) SP600125, a JNK‐specific inhibitor, which resulted in inhibition of AP‐1 activity, enhanced the iNOS expression and promoter activity in clinorotation. (3) Overexpression of AP‐1 remarkably attenuated the upregulation effect of clinorotation. These findings indicate that clinorotation upregulates iNOS in HUVECs by a mechanism dependent on suppression of AP‐1, but not NF‐κB. These results support a key role for AP‐1 in the signaling of postflight orthostatic intolerance. J. Cell. Biochem. 107: 357–363, 2009. © 2009 Wiley‐Liss, Inc.