Reduced dosage of genes encoding ribosomal protein S18 suppresses a mitochondrial initiation codon mutation in Saccharomyces cerevisiae

A yeast mitochondrial translation initiation codon mutation affecting the gene for cytochrome oxidase subunit III (COX3) was partially suppressed by a spontaneous nuclear mutation. The suppressor mutation also caused cold-sensitive fermentative growth on glucose medium. Suppression and cold sensitivity resulted from inactivation of the gene product of RPS18A, one of two unlinked genes that code the essential cytoplasmic small subunit ribosomal protein termed S18 in yeast. The two S18 genes differ only by 21 silent substitutions in their exons; both are interrupted by a single intron after the 15th codon. Yeast S18 is homologous to the human S11 (70% identical) and the Escherichia coli S17 (35% identical) ribosomal proteins. This highly conserved family of ribosomal proteins has been implicated in maintenance of translational accuracy and is essential for assembly of the small ribosomal subunit. Characterization of the original rps18a-1 missense mutant and rps18a delta and rps18b delta null mutants revealed that levels of suppression, cold sensitivity and paromomycin sensitivity all varied directly with a limitation of small ribosomal subunits. The rps18a-1 mutant was most affected, followed by rps18a delta then rps18b delta. Mitochondrial mutations that decreased COX3 expression without altering the initiation codon were not suppressed. This allele specificity implicates mitochondrial translation in the mechanism of suppression. We could not detect an epitope-tagged variant of S18 in mitochondria. Thus, it appears that suppression of the mitochondrial translation initiation defect is caused indirectly by reduced levels of cytoplasmic small ribosomal subunits, leading to changes in either cytoplasmic translational accuracy or the relative levels of cytoplasmic translation products.     

Reexpansion pulmonary edema

Reexpansion pulmonary edema is a rare complication attending the rapid reexpansion of a chronically collapsed lung, such as occurs after evacuation of a large amount of air or fluid from the pleural space. The condition usually appears unexpectedly and dramatically-immediately or within 1 h in 64% of patients and within 24 h in the remainder. The clinical manifestations are varied; they range from roentgenographic findings alone in asymptomatic patients to severe cardiorespiratory insufficiency. The radiographic evidence of reexpansion pulmonary edema is a unilateral alveolar filling pattern, seen within a few hours of reexpansion of the lung. The edema may progress for 24-48 h and persist for 4-5 days. Human data on the pathophysiology of reexpansion pulmonary edema derive from small series of patients, case reports, and reviews of the literature. On the other hand, a larger body of data exists on experimental reexpansion pulmonary edema in cats, monkeys, rabbits, sheep, and goats. This review examines the clinical and experimental evidence for reexpansion pulmonary edema. In addition, we detail the historical background, clinical setting, treatment, and outcome of reexpansion pulmonary edema.     

Lysophosphatidylcholine is involved in the antigenicity of oxidized LDL

Lysophosphatidylcholine (LPC) is formed by hydrolysis of PC in low density lipoprotein (LDL) and cell membranes by phospholipase A2 or by oxidation. Oxidized (ox) LDL activates endothelial cells, an effect mimicked by LPC. oxLDL also has the capacity to activate T and B cells, and antibody titers to oxLDL are related to the degree of atherosclerosis. The antigen in oxLDL responsible for its immune-stimulatory capacity is not well characterized, and we hypothesized that LPC was involved. We demonstrate herein the presence of antibodies against LPC, both of the IgG and IgM isotype, in 210 healthy individuals. This antibody reactivity was not specifically related to oxidation of the fatty acid moiety in LPC, since LPC containing only palmitic acid showed antibody titers equivalent to those of LPC containing unsaturated fatty acids. Antibody titers to PC were low compared with LPC, and hydrolysis of PC at the sn-2 position is thus essential for immune reactivity. There was a close correlation between anti-oxLDL and anti-LPC antibodies. Furthermore, LPC competitively inhibited anti-oxLDL reactivity, which indicates that LPC may explain a significant part of the immune-stimulatory properties of oxLDL. LPC, being a lipid, is not likely to be an antigen itself. Instead, LPC could form immunogenic complexes with peptides, which may induce and potentiate immune reactions in the vessel wall. This study adds to the evidence that LPC is an important component of oxLDL and emphasizes the potential role of phospholipase A2 in atherosclerosis.     

Cytoplasmic mRNA for human triosephosphate isomerase is immune to nonsense-mediated decay despite forming polysomes

Nonsense codons between position 14 within the first exon and position 193 within the penultimate exon of the human gene for triosephosphate isomerase reduce mRNA abundance to 25% of normal. The reduction in abundance is due to the decay of newly synthesized mRNA that copurifies with nuclei. TPI mRNA that copurifies with cytoplasm is immune to decay. We show here that immunity is not due to the failure of nonsense-containing mRNA to form polysomes. This finding indicates that cytoplasmic mRNA, in contrast to nucleus-associated mRNA, may have lost one or more factors that are required for nonsense-mediated decay or gained one or more factors that confer immunity to nonsense-mediated decay.     

A new class of tobacco chitinases homologous to bacterial exo-chitinases displays antifungal activity

A novel chitinase gene of tobacco was isolated and characterized by DNA sequence analysis of a genomic clone and a cDNA clone. Comparative sequence analysis of both clones showed an identity of 94%. The proteins encoded by these sequences do not correspond to any of the previously characterized plant chitinases of classes I-IV and are designated as class V chitinases. Comparison of the chitinase class V peptide sequence with sequences in the Swiss Protein databank revealed significant sequence similarity with bacterial exo-chitinases from Bacillus circulans, Serratia marcescens and Streptomyces plicatus. It was demonstrated that class V chitinase gene expression is induced after treatment of tobacco with different forms of stress, like TMV-infection, ethylene treatment, wounding or ultraviolet irradiation. Two related chitinase class V proteins of 41 and 43 kDa were purified from Samsun NN tobacco leaves inoculated with tobacco mosaic virus. The proteins were purified by Chelating Superose chromatography and gel filtration. In vitro assays demonstrated that class V chitinases have endo-chitinase activity and exhibit antifungal activity toward Trichoderma viride and Alternaria radicina. In addition, it was shown that class V chitinase acts synergistically with tobacco class I beta-1,3-glucanase against Fusarium solani germlings.     

在超便携应用中模拟开关的关键设计参数

近年来，开关产品纷纷进入PC、服务器、笔记本电脑和底座应用等领域，令许多芯片供应商推出各式总线开关产品。总线开关能够在板卡或器件插拔期间方便地隔离总线电容，通过隔离对数据(高速缓存和内存)进行多路复用，分解操作或进行电压变换。典型的总线开关设计为一个单独的NMOS器件，其缺点是：随着源电压接近Vcc，栅极的源-漏区被夹断，会限制电流的驱动能力和输出电压。     

Health economics and cost implications of anxiety and other mental disorders in the United States

BACKGROUND: Mental disorders impose a multi-billion dollar burden on the economy each year; translating the burden into economic terms is important to facilitate formulating policies about the use of resources. METHODS: For direct costs, data were obtained from national household interview and provider surveys; for morbidity costs, a timing model was used that measures the lifetime effect on current income of individuals with mental disorders, taking into account the timing of onset and the duration of these disorders, based on regression analysis of Epidemiologic Catchment Area study data. RESULTS: The total economic costs of mental disorders amounted to US$147.8 billion in 1990. Anxiety disorders are the most costly, amounting to $46.6 billion, or 31.5% of the total; schizophrenic disorders accounted for $32.5 billion, affective disorders for $30.4 billion, and other mental disorders for $38.4 billion. CONCLUSIONS: Mental illnesses, especially anxiety disorders, are costly to society. Although anxiety disorders have a higher prevalence than affective disorders and schizophrenia, use of medical care services is lowest for anxiety disorders. Anxiety disorders appear to be under-recognised and untreated even though treatment interventions have been shown to be effective and can be delivered in a cost-efficient manner.