Protection performance evaluation of the respirators and personal exposure measurement in a Belgian viscose rayon factory

This paper presents the evaluation results of protective performance of the respirators (full face supplied-fresh air respirators and half-mask active charcoal filter) and personal exposure measurement (Infacepiece sampling) in a Belgian viscose rayon factory. With in-facepiece sampling technique and personal sampling method, we measured the CS₂ concentrations inside and outside of the different respirators. We found two kinds of the respirators have significant effect on decreasing the CS₂ exposure level for the subject, especially for the spinners. Full face supplied-fresh air respirator have good protective effect for the spinners and have limit protection for the high exposure job although the PF value is more than 10. It still need to improve more. In-facepiece sampling for all the subjects exposed to CS₂ in the factory found most subjects have exposed to low CS₂ concentration, most exposure levels were under the control range, but sulfuror are high exposure, the exposure level is higher than ACGIH TLV value. Supported by the Belgian Science Research Office, (DWTC, Belgium) under contact number ST/02/034 Tan Xiaodong: born in 1963, Associate professor, Medical doctor and Master of Public Health     

高产1,3-丙二醇的海洋克雷伯氏菌株的分离鉴定（英文）

从海洋环境中分离并鉴定用于发酵生产1,3-丙二醇的海洋微生物菌株.1,3-丙二醇是一种重要的工业原料,主要用于生产新型聚酯材料——聚对苯二甲酸丙二醇脂.通过富集与选择培养、摇瓶发酵测试,筛选得到一株高产1,3-丙二醇菌株;通过API20E试剂条反应、16S r RNA基因序列比对分析、电镜形态观察及相关基因簇分析,鉴定命名该菌株为Klebsiella pneumonia HSL4.进一步分析表明该菌株具有耐盐、耐有机酸的特征.补料发酵实验表明,该菌株合成1,3-丙二醇浓度、生产强度、转化率分别达到80.08 g L-1,2.22 g L-1 h-1和0.53 mol mol-1.     

Targeted mutation of Cyln2 in the Williams syndrome critical region links CLIP-115 haploinsufficiency to neurodevelopmental abnormalities in mice

Williams syndrome is a neurodevelopmental disorder caused by the hemizygous deletion of 1.6 Mb on human chromosome 7q11.23. This region comprises the gene CYLN2, encoding CLIP-115, a microtubule-binding protein of 115 kD. Using a gene-targeting approach, we provide evidence that mice with haploinsufficiency for Cyln2 have features reminiscent of Williams syndrome, including mild growth deficiency, brain abnormalities, hippocampal dysfunction and particular deficits in motor coordination. Absence of CLIP-115 also leads to increased levels of CLIP-170 (a closely related cytoplasmic linker protein) and dynactin at the tips of growing microtubules. This protein redistribution may affect dynein motor regulation and, together with the loss of CLIP-115-specific functions, underlie neurological alterations in Williams syndrome.