浅谈功率因数的补偿及其应用

根据我国当前电力系统运行情况，对电网无功功率补偿的必要性及通用补偿方法及其装置进行了具体阐述。     

西文期刊回溯建库中几个重要项目的著录

在实践的基础上，从期刊的出版日期、出版周期、卷、期、年、月及其他标识、ISSN、增刊、出版者以及期刊的历史发展等方面对西文期刊机读目录的标准化著录问题进行了探讨。     

顶凌覆盖节水增产技术研究

通过1998年、2000年的试验研究，系统分析了顶凌覆盖技术在高寒区节水增温保温、增产增收的机理及其应用效果。提出该技术可以缓解低温干旱特别是春旱对农业生产的困扰，是一项可以抗旱保春播增产增收的实用技术，在高寒地区具有较高的推广价值。     

The Shwachman-Bodian-Diamond syndrome protein mediates translational activation of ribosomes in yeast

The autosomal recessive disorder Shwachman-Diamond syndrome, characterized by bone marrow failure and leukemia predisposition, is caused by deficiency of the highly conserved Shwachman-Bodian-Diamond syndrome (SBDS) protein. Here, we identify the function of the yeast SBDS ortholog Sdo1, showing that it is critical for the release and recycling of the nucleolar shuttling factor Tif6 from pre-60S ribosomes, a key step in 60S maturation and translational activation of ribosomes. Using genome-wide synthetic genetic array mapping, we identified multiple TIF6 gain-of-function alleles that suppressed the pre-60S nuclear export defects and cytoplasmic mislocalization of Tif6 observed in sdo1Delta cells. Sdo1 appears to function within a pathway containing elongation factor-like 1, and together they control translational activation of ribosomes. Thus, our data link defective late 60S ribosomal subunit maturation to an inherited bone marrow failure syndrome associated with leukemia predisposition.     

Sul meccanismo di azione della streptomicina

Summary A study was undertaken on the variations of the redox potential level produced by streptomycinin vitro andin vivo. We have been able to show that, owing to an oxidative effect, streptomycin produces an increase of the redox potential level. This oxidative effect varies in degree according to the condition of the patient.We also found that in the blood and in the spinal fluid of patients suffering from tubercular meningitis factors are present which inhibit the action of streptomycin.The results of our findings lead to the conclusion that the dose of streptomycin must be varied according to the condition of the patient if the constant level required for an efficient therapy is to be maintained in the blood and in the spinal fluid.     

Kondensationsprodukte von Oxyketonen und Aminoketonen mit 2,4,5-Triamino-6-oxy-pyrimidin

Summary By condensing 2:4:5-triamino-6-hydroxy-pyrimidine with dihydroxyacetone (diacetate), diaminoacetone or acetone-1,3-di (p-formylaminobenzoic acid) not the expected 8- or 9-oxymethyl resp. -aminomethyl-pteridines but 8-or 9-methyl-pteridines were obtained. With p-tolyl-d-isoglucosamine not a tetrahydroxybutyl-pteridine but a trihydroxybutyl-pteridine was formed. For an explanation of these results it is supposed that from the dihydro-pteridines formed at first by intramolecular splitting off of H₂O or R·NH₂ aromatization takes place.     

Phytanic acid impairs mitochondrial respiration through protonophoric action

Refsum disease is a rare, inherited neurodegenerative disorder characterized by accumulation of the dietary branched-chain fatty acid phytanic acid in plasma and tissues caused by a defect in the alphaoxidation pathway. The accumulation of phytanic acid is believed to be the main pathophysiological cause of the disease. However, the exact mechanism(s) by which phytanic acid exerts its toxicity have not been resolved. In this study, the effect of phytanic acid on mitochondrial respiration was investigated. The results show that in digitonin-permeabilized fibroblasts, phytanic acid decreases ATP synthesis, whereas substrate oxidation per se is not affected. Importantly, studies in intact fibroblasts revealed that phytanic acid decreases both the mitochondrial membrane potential and NAD(P)H autofluorescence. Taken together, the results described here show that unesterified phytanic acid exerts its toxic effect mainly through its protonophoric action, at least in human skin fibroblasts. Received 4 August 2007; received after revision 26 September 2007; accepted 10 October 2007 J. C. Komen, F. Distelmaier: These authors contributed equally to this work.     

Regulation of insulin receptor function

Resistance to the biological actions of insulin contributes to the development of type 2 diabetes and risk of cardiovascular disease. A reduced biological response to insulin by tissues results from an impairment in the cascade of phosphorylation events within cells that regulate the activity of enzymes comprising the insulin signaling pathway. In most models of insulin resistance, there is evidence that this decrement in insulin signaling begins with either the activation or substrate kinase activity of the insulin receptor (IR), which is the only component of the pathway that is unique to insulin action. Activation of the IR can be impaired by post-translational modifications of the protein involving serine phosphorylation, or by binding to inhibiting proteins such as PC-1 or members of the SOCS or Grb protein families. The impact of these processes on the conformational changes and phosphorylation events required for full signaling activity, as well as the role of these mechanisms in human disease, is reviewed in this article. Received 3 August 2006; received after revision 1 December 2006; accepted 8 January 2007