Effect of sodium bicarbonate on aspirin-induced damage and potential difference changes in human gastric mucosa

Two aspirin tablets in 100 ml fluid will produce microscopical damage to the human stomach. A study was performed to determine whether a small amount of sodium bicarbonate (equivalent to one-third of a teaspoonful of baking soda) could protect against this damage. Sequential gastric biopsy specimens were taken from 15 healthy subjects before, during, and after intragastric instillation of one of the following isotonic solutions: saline; sodium bicarbonate; 600 mg aspirin suspended in sodium bicarbonate; and aspirin suspended in saline. On a separate day the same solutions were instilled, but gastric transmucosal potential differences were monitored. Light microscopy and scanning electron microscopy of the biopsy specimens showed occasional mucous degranulation of mucosal surface cells, but no cell damage during instillation of sodium bicarbonate. Light microscopy studies 10 minutes after aspirin in saline showed damage in 20% of surface cells, with focal areas of cellular disruption and microscopic erosions, but only 3·4% of cells were damaged after aspirin in bicarbonate and there were no erosions. Electron microscopy showed a damaged honeycombed appearance of surface epithelium after aspirin in saline and a normal cobblestone appearance after aspirin in bicarbonate. Aspirin dissolved in bicarbonate failed to induce the usual fall in potential difference.These findings indicate that sodium bicarbonate in amounts equivalent to one-third of a teaspoonful of baking soda protects the gastric mucosa against aspirin-induced damage and prevents the usual fall in potential difference after aspirin.     

Influence of triiodothyronine and growth hormone on growth of dwarf and normal chickens: interactions of hormones and genotype

The effects of dietary triiodothyronine (T3), injections of a preparation of growth hormone (GH) (purified from chicken pituitary tissue) and their combination on growth were investigated in three lines of chickens. The three lines were the Cornell K strain (K) (a single Comb White Leghorn strain), the Cornell K strain hemizygous for the sex-linked dwarfing gene (SLD), and the Cornell K strain homozygous recessive for the autosomal dwarfing gene (ADW). A dietary T3 treatment by genotype interaction was observed. Dietary T3 (0.1 ppm) decreased growth in the K line, tended to decrease growth in the ADW line while it tended to increase growth in the SLD line. Chicken growth hormone (100 micrograms/kg body wt) alone did not affect growth in any of the lines studied. There was, however, a GH treatment by T3 treatment interaction. Chicken GH overcame the growth-depressing effects of T3 in the K and ADW lines while it tended to promote growth in T3 treated SLD birds. Dwarf (SLD) chickens had higher basal circulating GH concentrations, lower circulating immunoreactive somatomedin C concentrations, and lower circulating T3 concentrations than the K or ADW chickens.     

蛙虹彩病毒一个序列保守基因(RGV-12L)的克隆表达及定位分析

从蛙虹彩病毒(Rana grylio virus,RGV)中克隆出一个虹彩病毒科的序列保守基因RGV-12L, 序列分析表明该基因全长894 bp, 编码一个含297个氨基酸的多肽,分子量为33 kD。构建包含该基因全长的原核表达载体, 进行原核表达,获得了分子量约53 kD的融合蛋白。将融合蛋白经腹腔注射免疫小鼠,制备出鼠抗RGV-12L血清。通过RT-PCR和Western blotting分析RGV感染细胞后RGV-12L的转录时序, 感染4h可以在RNA水平检测到RGV-12L的转录, 感染8h可以在蛋白水平检测到RGV-12L的表达。用DNA复制抑制剂阿糖胞苷(Arac)进行药物抑制实验,鉴定出RGV-12L是一个晚期基因。免疫荧光分析显示RGV-12L分布于感染细胞的细胞核和细胞质中, 在病毒加工厂中也有该蛋白的分布, 提示该基因可能与病毒的装配、释放有关。       

低温胁迫对建兰叶片内源多胺含量的影响

以素心建兰为材料,研究低温胁迫(5℃)对建兰内源多胺含量的影响。结果表明,在低温胁迫下建兰生长期的叶片多胺(PAs)总量和亚精胺(Spd)、腐胺(Put)含量都表现为先升后降的变化,精胺(Spm)含量则是下降然后上升最后稳定在比原来含量更高的水平上,说明有可能在低温胁迫下建兰通过调节内源多胺的总量和不同多胺种类的比例来抵御低温对生理的破坏作用;开花期的建兰叶片因受低温胁迫的影响未能合成足够的亚精胺(Spd),从而抑制了建兰的开花。     

一个玉米CMS-C恢复基因的精细定位

为挖掘玉米C型细胞质雄性不育(CMS-C,C-type cytoplasmic male sterility)的育性恢复基因并解析基因功能,用恢复系K932R与2个CMS-C同质异核不育系K169S和K932S分别构建2个F2定位群体,结合SSR分子标记和分离群体分析法全基因组重测序(BSA-reseq)技术定位育性恢...     

Deconvoluting the Cu2+ binding modes of full-length prion protein

The prion protein (PrP) is a cell-surface Cu(2+)-binding glycoprotein that when misfolded is responsible for a number of transmissible spongiform encephalopathies. Full-length PrP-(23-231) and constructs in which the octarepeat region has been removed, or His(95) and His(110) is replaced by alanine residues, have been used to elucidate the order and mode of Cu(2+) coordination to PrP-(23-231). We have built on our understanding of the appearance of visible CD spectra and EPR for various PrP fragments to characterize Cu(2+) coordination to full-length PrP. At physiological pH, Cu(2+) initially binds to full-length PrP in the amyloidogenic region between the octarepeats and the structured domain at His(95) and His(110). Only subsequent Cu(2+) ions bind to single histidine residues within the octarepeat region. Ni(2+) ions are used to further probe metal binding and, like Cu(2+), Ni(2+) will bind individually to His(95) and His(110), involving preceding main chain amides. Competitive chelators are used to determine the affinity of the first mole equivalent of Cu(2+) bound to full-length PrP; this approach places the affinity in the nanomolar range. The affinity and number of Cu(2+) binding sites support the suggestion that PrP could act as a sacrificial quencher of free radicals generated by copper redox cycling.     

Role of sigma-1 receptor C-terminal segment in inositol 1,4,5-trisphosphate receptor activation: constitutive enhancement of calcium signaling in MCF-7 tumor cells

Sigma-1 receptor (sigma-1R) agonists enhance inositol 1,4,5-trisphosphate (IP3)-dependent calcium release from endoplasmic reticulum by inducing dissociation of ankyrin B 220 (ANK 220) from the IP3 receptor (IP3R-3), releasing it from inhibition. MCF-7 breast tumor cells express little or no sigma-1R and were used here to investigate the effect of receptor overexpression and the role of its N- and C-terminal segments in function. We stably expressed intact sigma-1R (amino acids (aa) 1-223; lines 11 and 41), N-fragment (aa 1-100; line K3), or C-fragment (aa 102-223; line sg101). C-fragment expressed as a peripheral membrane-bound protein that was removable from the endoplasmic reticulum membrane by chaotropic salt wash, consistent with lack of a putative transmembrane domain. The expressed sigma-1R, N-fragment, and C-fragment exhibited normal, low affinity, and no [3H](+)-pentazocine binding activity, respectively. All transfected lines showed constitutive enhancement of bradykinin (BDK)-induced calcium release, because of a decrease in BDK ED50 values. Interestingly, sigma-1R and C-fragment had high activities, whereas the N-fragment was much less active. The antagonist BD1063 behaved as an inverse agonist in sigma-1R cells, whereas C-fragment was insensitive to ligand regulation. Like BDK, vasopressin- and ATP-induced calcium release was enhanced with the same pattern in cell lines. Anti-IP3R-3 immunoprecipitates from cells expressing sigma-1R or C-fragment contained significantly less ANK 220 compared with untransfected or N-fragment cells, indicating a higher amount of ankyrin-free IP3R-3. Anti-ankyrin B immunoprecipitates contained sigma-1R or C-fragment, with markedly lower levels of N-fragment present. These results suggest that sigma-1R overexpression drives sigma agonist-independent dissociation of ANK 220 from IP3R-3, resulting in activation. The C-terminal segment plays a key role in the interaction.