Immunochemical identity of peroxisomal enoyl-CoA hydratase with the peroxisome-proliferation -associated 80,000 mol wt polypeptide in rat liver

Peroxisome proliferators, which induce proliferation of hepatic peroxisomes, have been shown previously to cause a marked increase in an 80,000 mol wt polypeptide predominantly in the light mitochondrial and microsomal fractions of liver of rodents. We now present evidence to show that this hepatic peroxisome-proliferation-associated polypeptide, referred to as polypeptide PPA-80, is immunochemically identical with the multifunctional peroxisome protein displaying heat-labile enoyl-CoA hydratase activity. This conclusion is based on the following observations: (a) the purified polypeptide PPA-80 and the heat- labile enoyl-CoA hydratase from livers of rats treated with the peroxisome proliferators Wy-14,643 {[4-chloro-6(2,3-xylidino)-2-pyrimidinylthio]acetic acid} exhibit identical minimum molecular weights of approximately 80,000 on SDS polyacrylamide gel electrophoresis; (b) these two proteins are immunochemically identical on the basis of ouchterlony double diffusion, immunotitration, rocket immunoelectrophoresis, and crossed immunoelectrophoresis analysis; and (c) the immunoprecipitates formed by antibodies to polypeptide PPA-80 when dissociated on a sephadex G-200 column yield enoyl-CoA hydratase activity. Whether the polypeptide PPA-80 exhibits the activity of other enzyme(s) of the peroxisomal β-oxidation system such as fatty acyl-CoA oxidase activity or displays immunochemical identity with such enzymes remains to be determined. The availability of antibodies to polypeptide PPA-80 and enoyl-CoA hydratase facilitated immunofluorescent and immunocytochemical localization of the polypeptide PPA- 80 and enoyl-CoA hydratase in the rat liver. The indirect immunofluorescent studies with these antibodies provided direct visual evidence for the marked induction of polypeptide PPA-80 and enoyl-CoA hydratase in the livers of rats treated with Wy-14,643. The present studies also provide immunocytochemical evidence for the localization of polypeptide PPA- 80 and the heat-labile enoyl-CoA hydratase in the peroxisome, but not in the mitochondria, of hepatic parenchymal cells. These studies, therefore, provide morphological evidence for the existence of fatty acyl-CoA oxidizing system in peroxisomes. An increase of polypeptide PPA-80 on SDS polyacrylamide gel electrophoretic analysis of the subcellular fractions of liver of rodents treated with lipid-lowering drugs should serve as a reliable and sensitive indicator of enhanced peroxisomal β- oxidation system.     

Water Flow in Wheat Seedlings after Small Water Deficits

Cultures of Scenedesmus obliquus when grown heterotrophically for 10 or 30 days without addition of fresh medium showed 85 and 98% loss of their photosynthetic capacity respectively. This loss in photosynthetic capacity was accompanied by an increase in quantum requirement. No major changes in the pigment amounts or types were detected which would explain the decay in photosynthetic capacity. Partial reactions mediated by photosystem II or I showed a more or less constant decay over a period of 30 days. Photosystem II reactions appeared less stable than those of photosystem I, decaying by 95% as compared with 70%, over this time period. The results of comparative studies on aged cells for their potential of cytochrome f photooxidation, fluorescence kinetics, 520 nm absorbance change and the variable influence of 3-(3,4-dichlorophenyl)-1,1-dimethylurea and 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone on the photosynthetic capacity of such cells, suggest that it is the inherent ability of the cells to photooxidize plastohydroquinone which is affected primarily. In addition, secondary changes were noted in the activity of reactions on the water-splitting side of photosystem II and in the P700 — plastocyanin — cytochrome f complex.     

Electrical and adaptive properties of rod photoreceptors in bufo marinus. I. Effects of altered extracellular Ca(2+) levels

The effects of altering extracellular Ca(2+) levels on the electrical and adaptive properties of toad rods have been examined. The retina was continually superfused in control (1.6 mM Ca(2+)) or test ringer’s solutions, and rod electrical activity was recorded intracellularly. Low-calcium ringer’s (10(-9)M Ca(2+)) superfused for up to 6 min caused a substantial depolarization of the resting membrane potential, an increase in light-evoked response amplitudes, and a change in the waveform of the light-evoked responses. High Ca(2+) ringer’s (3.2 mM) hyperpolarized the cell membrane and decreased response amplitudes. However, under conditions of either low or high Ca(2+) superfusion for up to 6 min, in both dark-adapted and partially light-adapted states, receptor sensitivity was virtually unaffected; i.e., the V-log I curve for the receptor potential was always located on the intensity scale at a position predicted by the prevailing light level, not by Ca(2+) concentration. Thus, we speculate that cytosol Ca(2+) concentration is capable of regulating membrane potential levels and light-evoked response amplitudes, but not the major component of rod sensitivity. Low Ca(2+) ringer’s also shortened the period of receptor response saturation after a bright but nonbleaching light flash, hence accelerating the onset of both membrane potential and sensitivity recovery during dark adaptation.

Exposure of the retina to low Ca(2+) (10(-9)M) ringer’s for long periods (7-15 min) caused dark-adapted rods to lose responsiveness. Response amplitudes gradually decreased, and the rods became desensitized. These severe conditions of low Ca(2+) caused changes in the dark-adapted rod that mimic those observed in rods during light adaptation. We suggest that loss of receptor sensitivity during prolonged exposure to low Ca(2+) ringer’s results from a decrease of intracellular (intradisk) stores of Ca(2+); i.e., less Ca(2+) is thereby released per quantum catch.

     

Zerumbone induced apoptosis in liver cancer cells via modulation of Bax/Bcl-2 ratio

Background  

Zerumbone is a cytotoxic component isolated from Zingiber zerumbet Smith, a herbal plant which is also known as lempoyang. This new anticancer bioactive compound from Z. zerumbet was investigated for its activity and mechanism in human liver cancer cell lines.     

耐甲氧西林金黄色葡萄球菌在动物流行病学中的研究进展

葡萄球菌是动物中重要的机会性病原体,耐甲氧西林金黄色葡萄球菌（MRSA）因其多药耐药的特征日益成为动物和公众健康的主要威胁。由于动物与动物及人畜间存在相互传染的风险,在控制MRSA感染的整个体系中,分析MRSA在动物中的流行显得尤为重要。     

中国岩黄芪属(豆科)植物资料增补

根据对标本的研究及文献资料的整理,证实了西伯利亚岩黄芪在中国的分布;山竹岩黄芪在新疆的分布新记录。另外,还报道了地中海岩黄芪在陕西的栽培记录。     

A Femtomol Range FRET Biosensor Reports Exceedingly Low Levels of Cell Surface Furin: Implications for the Processing of Anthrax Protective Antigen

Furin, a specialized endoproteinase, transforms proproteins into biologically active proteins. Furin function is important for normal cells and also in multiple pathologies including malignancy and anthrax. Furin is believed to cycle between the Golgi compartment and the cell surface. Processing of anthrax protective antigen-83 (PA83) by the cells is considered thus far as evidence for the presence of substantial levels of cell-surface furin. To monitor furin, we designed a cleavage-activated FRET biosensor in which the Enhanced Cyan and Yellow Fluorescent Proteins were linked by the peptide sequence SNSRKKR↓STSAGP derived from anthrax PA83. Both because of the sensitivity and selectivity of the anthrax sequence to furin proteolysis and the FRET-based detection, the biosensor recorded the femtomolar levels of furin in the in vitro reactions and cell-based assays. Using the biosensor that was cell-impermeable because of its size and also by other relevant methods, we determined that exceedingly low levels, if any, of cell-surface furin are present in the intact cells and in the cells with the enforced furin overexpression. This observation was in a sharp contrast with the existing concepts about the furin presentation on cell surfaces and anthrax disease mechanism. We next demonstrated using cell-based tests that PA83, in fact, was processed by furin in the extracellular milieu and that only then the resulting PA63 bound the anthrax toxin cell-surface receptors. We also determined that the biosensor, but not the conventional peptide substrates, allowed continuous monitoring of furin activity in cancer cell extracts. Our results suggest that there are no physiologically-relevant levels of cell-surface furin and, accordingly, that the mechanisms of anthrax should be re-investigated. In addition, the availability of the biosensor is a foundation for non-invasive monitoring of furin activity in cancer cells. Conceptually, the biosensor we developed may serve as a prototype for other proteinase-activated biosensors.     

Investigation of Electrode Erosion Parameters in Direct and Alternating Current Plasma Torches

Plasma Physics Reports - This paper deals with the study of the wear resistance (erosion) of the material of electrodes in direct and alternating current plasma torches. The life time of electrodes...     

内蒙古植被枯黄期变化及其与气候和植被生产力的关系

基于2001—2018年MODIS NDVI数据,采用累计归一化植被指数(NDVI)的Logistic曲线曲率极值法,识别内蒙古植被枯黄期及其时空变化特征,并在生态区尺度上分析枯黄期对气候因子和NDVI的响应特征。结果表明: 研究期间,内蒙古植被平均枯黄期主要集中在第260～280天。森林生态区枯黄期为第270～280天,从南向北推迟;草原生态区枯黄期最早,介于第257～273天,从东北向西南逐渐推迟;荒漠生态区枯黄期为第270～283天,东北向西南呈推迟态势。2001—2018年间,3个生态区植被枯黄期均呈不显著推迟趋势。植被生产力从东北向西南逐渐降低,在时间上呈增加趋势的面积大于呈减小趋势的面积。全内蒙古和各生态区植被枯黄期受季前2～3个月降水量的正面影响较大,与季前平均温度、最高温度和最低温度均呈正相关关系。全内蒙古和各生态区,8和9月植被生产力的增加(或减少)将推迟(或提前)植被枯黄期,而6和7月植被生产力的增加(或减少)将提前(或推迟)草原和荒漠生态区植被枯黄期。