Plasma and erythrocyte alpha-tocopherol and plasma retinol concentrations in term infants fed formula enriched with long-chain polyunsaturated fatty acids

OBJECTIVE: To assess the effect of long-chain polyunsaturated fatty acids (LCPUFA)- and vitamin E-supplemented formula feeding on erythrocyte and plasma alpha-tocopherol (VE), and plasma retinol (VA) concentrations in neonates and to compare these values with those found in infants feeding on infant formula without LCPUFA or breast milk SETTING: University Hospital of Granada, Spain. SUBJECTS: 49 full-term infants. DESIGN AND INTERVENTION: Subjects who chose not to breast feed were fed either (i) unsupplemented infant formula (F) or (ii) infant formula supplemented with LCPUFA and vitamin E (FL). Alpha-tocopherol and retinol were measured at 7 days, 1 month and 3 months. RESULTS: Plasma and erythrocyte VE concentrations and plasma VE/total lipids ratio increased significantly in all groups at 1 month of life (P < 0.05), but did not change significantly between 1 month and 3 months in any group (P > 0.05). Erythrocyte VE and VA retinol concentrations were higher in infants fed an infant formula than in breast milk-fed infants at 1 month of life (P < 0.05). Finally, there were no significant differences in plasma or erythrocyte VE levels, plasma VA or plasma VE/total lipid ratio between any groups at 3 months of life (P > 0.05). CONCLUSION: Infants fed on LCPUFA- and vitamin E-supplemented infant formula for 3 months have similar vitamin E and A status to infants fed on breast milk or infant formula without LCPUFA supplementation.     

Radiolabeled nucleoside analogs in cancer diagnosis and therapy

Radiolabeled nucleosides, specifically 5-iodo-2'-deoxyuridine (IUdR) radioiodinated with the Auger-electronemitting 123I or 125I, have been shown to produce extensive DNA damage in mammalian cell systems in vitro. Such nucleosides are cycle-dependent agents that are taken up by mitotically dividing cells in the S phase of the cell cycle. The degree of damage that occurs is related to the fact that these nucleosides bind covalently to DNA bringing the decaying Augerelectron-emitting radionuclide in close proximity to the genome. The use of these radiohalogenated nucleosides in vivo is associated with several problems. The first relates to their extremely short biologic half-life in blood (T1/2 of minutes in humans). The second involves achieving therapeutic ratios in tumor cells in the face of efficient hepatic dehalogenation. The third concerns the uptake of these radiopharmaceuticals by actively proliferating normal cell renewal systems, thus potentially causing toxic side effects. The fourth, one shared with other cycle-dependent drugs, relates to the matter of labeling the whole tumor cell population. To facilitate targeting to tumors, investigators have been examining the direct introduction of these agents into the targeted area or into an arterial blood supply that immediately precedes the target. For example, radiopharmaceutical administration could be intracavitary (bladder, spinal fluid, peritoneum), intralesional (brain tumor, breast mass) or intra-arterial (liver, pancreas). In all these situations, the following conditions must be met: (a) once within the vicinity of the tumor the agent can freely diffuse through the tissues and is selectively taken up by cancerous cells; (b) once the agent has left the target area it is converted quickly into a nontoxic form and/or excreted from the body; and finally, (c) the biologic behavior of the agent is not altered by repeated injections. We report herein our experience and that of others with [123I/125I/131I]IUdR in cultured cells, animal tumor-model systems, and patients. In vitro, DNA incorporation of 123I- and 125I-labeled IUdR leads to an exponential decrease in cell survival (no shoulder on the survival curve). However, the total number of decays needed to produce a given lethal effect with [123I]IUdR is approximately twice that required with [125I]IUdR. In vivo, the scintigraphic and antineoplastic capabilities of radioiodinated IUdR have been demonstrated in an intraperitoneal murine ovarian tumor model following intraperitoneal injection; in an intracerebral rat gliosarcoma model after intracranial administration; in an intrathecal rat gliosarcoma model after intrathecal infusion; and in a rat transitional cell bladder cancer model following intravesicular infusion. [123I]IUdR, [125I]IUdR, and/or [131I]IUdR have been administered to patients with brain, breast, colorectal, or gastrointestinal cancers (intratumorally); ovarian cancer (intraperitoneally); bladder cancer (intravesically); liver metastases from colorectal cancer (through the hepatic artery, permanent intra-arterial catheter). These studies have confirmed the observations made in animal models. The data indicate that 5-iodo-2'-deoxyuridine radiolabeled with an Auger electron emitter (123I or 125I) may be a useful agent for the scintigraphic diagnosis and/or therapy of neoplastic diseases that are accessible to direct radiopharmaceutical administration. This radiopharmaceutical should serve as a prototype for, and facilitate the development of, other radiolabeled nucleoside analogs. Further investigations are certainly warranted.     

Reduced skin tumor development in cyclin D1-deficient mice highlights the oncogenic ras pathway in vivo

Cyclin D1 is part of a cell cycle control node consistently deregulated in most human cancers. However, studies with cyclin D1-null mice indicate that it is dispensable for normal mouse development as well as cell growth in culture. Here, we provide evidence that ras-mediated tumorigenesis depends on signaling pathways that act preferentially through cyclin D1. Cyclin D1 expression and the activity of its associated kinase are up-regulated in keratinocytes in response to oncogenic ras. Furthermore, cyclin D1 deficiency results in up to an 80% decrease in the development of squamous tumors generated through either grafting of retroviral ras-transduced keratinocytes, phorbol ester treatment of ras transgenic mice, or two-stage carcinogenesis.     

发电机推力轴承温度量异常的处理方法

分析湖北黄龙滩水力发电厂3、4号水轮发电机自投运以来推力轴承瓦温度计引线频繁断线及温度量不能正常显示上传的原因,介绍相关改进优化处理方法。     

1957-2017年泾河流域降雨量及降雨侵蚀力时空变化分析

泾河流域受土壤侵蚀的影响,水土流失较为严重,为对流域水土流失风险评估和防治等提供参考依据,根据1957-2017年泾河流域5个气象站点的日降水资料,运用ArcGIS空间插值、小波分析、R/S分析等方法,分析了该时段降雨量及降雨侵蚀力时空变化规律。结果表明:泾河流域及各气象站点的降雨量与降雨侵蚀力均呈显著正相关关系;泾河流域降雨量与降雨侵蚀力年内分布不均,主要集中在夏季,分别占全年的67.80%和52.86%;泾河流域年均降雨量和降雨侵蚀力分别为496.83 mm和1 481.24 (MJ·mm)/(hm~2·h),年际总体呈波动上升趋势且未来降雨侵蚀力将延续增加趋势,两者均在1996和2009年出现突变点且第一主周期分别为27和17 a;泾河流域降雨量和降雨侵蚀力在空间上均呈从西北到东南递增的趋势。     

高强紫外光强化降解消毒副产物氯乙酸的效能及作用机制

氯乙酸是一种化学性质稳定的氯化消毒副产物,传统高级氧化技术对氯乙酸的降解效率低、矿化不彻底,拟采用强度高达3.13×10-6 Einstein/(cm2·s)(强度约合1000 mW/cm2,比传统高级氧化工艺中使用的紫外光强度高两个数量级以上)的紫外光作为光源,考察其对3种氯乙酸(一氯乙酸、二氯乙酸和三氯乙酸)的降解效果、影响因素和矿化过程.研究结果表明,与传统紫外光降解技术相比,高强紫外光可高效降解氯乙酸,前者在360 min内对氯乙酸的去除率不足5％,后者可在50 min内实现99％以上的降解,且3者的降解速率关系为:三氯乙酸>二氯乙酸>一氯乙酸.高强紫外光对氯乙酸的降解过程遵循伪一级动力学,光强、pH和DO这3个光解反应影响因素中,pH对氯乙酸光解过程影响不大,但光强和DO对光解速率影响显著,光解的反应速率随紫外光子通量的提高呈一次线性增加,随着DO由1 mg/L增加至9 mg/L,光解速率提高1倍.此外,高强紫外光对氯乙酸的矿化过程彻底,几乎不产生中间产物,氯乙酸的矿化过程可能主要是通过脱卤和脱羧基两个反应路径实现,DO和pH对光解过程的影响从侧面佐证了氯乙酸高强紫外光光解路径.该结果表明,高强紫外光可有效降解光稳定物质氯乙酸,可为氯化消毒副产物的高效去除提供技术借鉴.     

城市污水处理新型生物脱氮除磷技术研究进展

当下,我国城市污水处理厂的主要矛盾已由有机物的去除转向氮、磷等营养物的去除.而城市污水处理厂目前普遍采用的传统生物脱氮除磷工艺因其自身的特点及城市污水特征,导致氮、磷污染物去除效率无法满足愈发严格的国家标准.针对这种问题,通过对同步硝化反硝化、厌氧氨氧化、反硝化除磷、短程硝化反硝化这些新型技术及其研究现状进行介绍,探究新型生物脱氮除磷技术在城市污水处理领域中应用的优越性与合理性.并基于多菌群协同除污机理,结合我国城市污水处理可持续发展现状,探索未来的技术发展方向.     

冲压-刚度的耦合仿真分析技术

提出冲压——刚度的耦合仿真方法，即用动力显式算法计算冲压，静力隐式算法计算回弹，用动力显式算法计算最终的刚度，给出耦合仿真过程中3个环节的实施过程及其关键技术点。应用本方法对双曲率的盒形件进行了刚度仿真分析，并和试验结果进行了比较，取得了令人满意的计算精度。     

丙烯酸酯三元共聚物酸掺杂改性聚苯胺的研究

选择丙烯酸 (AA)、丙烯酸丁酯 (BA)和甲基丙烯酸甲酯 (MMA)三元共聚物对聚苯胺 (PAn)进行改性 ,研究了BA的用量和引发剂浓度对PAn导电率的影响 ,对样品进行DSC、FTIR和SEM测试。结果表明 ,丙烯酸酯三元共聚物酸对PAn有良好的掺杂改性作用 ,当共聚单体 (AA -BA -MMA)组成为 10∶45∶45 (质量比 ) ,引发剂浓度为0 0 5 48mol·L-1时 ,可制得电导率达 1 42 1S·cm-1的导电PAn。     

常温精脱硫新工艺在合成氨联醇中的应用

介绍了如何提高甲醇触媒的活性及寿命,进一步降低电耗。文中对“精脱硫新工艺”的研发及设备的选取作了详细的论述。