The Effects of Ethanol on the Germination of Seeds of Japonica and Indica Rice (Oryza sativa L.) under Anaerobic and Aerobic Conditions

An examination was made of the effects of ethanol at 0.2–6.0%(v/v) on the germination, under aerobic conditions, of intactand dehusked seeds of indica rice (cv. Assam IV), which hadbeen harvested 14, 21 and 28 d after anthesis, and of the japonicarice (cv. Sasanishiki), which had been harvested 30 and 60 dafter anthesis. The inhibition of germination caused by dehuskingjaponica rice was overcome by 0.5–5% ethanol, with maximumgermination (frequently 100%) achieved at 3–5% (30 d afteranthesis) or 1–4.5% (60 d after anthesis) ethanol. Furtherincreases in the ethanol concentration reduced germination.The germination of dehusked indica rice was slightly inhibitedat 0.5 and 1% ethanol, whilst the promotion of germination by2% ethanol increased as the seeds matured. At all harvests germinationwas greatest at 3% ethanol, and at 5–6% ethanol germinationfell to 0%. Inhibition, no effect, or minimal stimulation ofthe germination of intact seeds of both japonica and indicarice by ethanol was observed at the concentrations examined.The absence of oxygen stimulated germination of dehusked japonicarice, but this germination was inhibited by ethanol. In contrastethanol had little or no effect on the failure of dehusked indicaseeds to germinate in anaerobic conditions. Thus ethanol treatmentmay help break the strong dormancy of dehusked seeds of indicaand japonica rice. The possible role of ethanol in stimulatinggermination in rice is discussed. Rice; Oryza sativa L.; seed germination; dehusking treatment; ethanol; indica; japonica; oxygen; dormancy; germination inhibition; seed formation     

INDUCTION OF CELLULAR PROCESSES CONTAINING COLLAGENASE AND RETINOID BY INTEGRIN-BINDING TO INTERSTITIAL COLLAGEN IN HEPATIC STELLATE CELL CULTURE

Cultered hepatic stellate cells were induced to elongate long, multipolar cellular processes by interstitial collagen gel used as a substratum, as compared to flattened or round cell shapes on polystyrene surface or on Matrigel containing the basement membrane components, respectively. The process induction was inhibited by several reagents as follows: (1) anti-integrin α2 antibody; (2) an oligopeptide, DGEA, an integrin-binding sequence in type I collagen molecule; (3) wortmannin, a phosphatidylinositol 3-kinase inhibitor. Protein tyrosine phosphorylation was enhanced throughout cells including cellular processes by culturing on type I collagen gel. Dual fluorescence staining showed that the core of the processes contained microtubules, whereas the periphery of the processes comprised fibrillar actin. Thus, the process extension was found to depend on integrin-binding to type I collagen fibres, followed by signal transduction and cytoskeleton assembly. The cellular processes included interstitial collagenase and vitamin A-containing lipid droplets. The lipid droplets and vitamin A-autofluorescence were increased by retinyl acetate addition to the culture medium, suggesting an important role of processes in hepatic stellate cell function.     

低剂量率下高线性能量转移碳离子束辐照人类唾液腺细胞的存活效应

利用日本千叶重离子医用加速器 HIMAC 提供的碳离子束,对人类唾液腺细胞 (HSG) 在剂量率为 0.5 Gy/h 的低剂量率条件下进行了辐照,运用标准的克隆形成法得到了 3 种不同剂量平均线性能量转移 (LET) 碳离子束辐照 HSG 细胞的剂量存活效应 . 与先前 HSG 细胞在治癌剂量率 (1~5 Gy/min) 下对相近剂量平均 LET 碳离子束辐照的剂量存活效应数据相比, HSG 细胞对高 LET 碳离子束辐射表现出明显的剂量率效应 . 为在相同条件下得到碳离子束对 HSG 细胞的相对生物学效应 (RBE) ,利用 60Co-γ射线在剂量率为 0.5 Gy/h 的条件下辐照了 HSG 细胞,得到该细胞系对低 LET 射线响应的剂量存活效应 . 与先前在治癌剂量率下得到的 RBE 值相比,低剂量率条件下得到的 RBE 值总体减小 . 由实验发现的剂量率效应及低剂量率条件下 RBE 值的减小,表明由高 LET 碳离子束造成的辐射损伤在低剂量率条件下也存在着显著的修复效应 . 据此,对辐射造成细胞致死的原因进行了探讨 .     

ATTEMPTS TO CULTURE ISOLATED URODELAN BLASTOMERES THAT CONTINUE TO DIVIDE WITHOUT AGGREGATING*

The blastomeres isolated from urodelan blastulae continued to divide without aggregating of daughter cells when inoculated with Ca²⁺-free neutral Holtfreter solution into glass culture dishes coated with agar. When standard Holtfreter solution with pH 8.2 was used as a culture medium, Ca²⁺ content from 1/40 to 1/20 of the original strength was essential for the purpose of the present observations; other divalent cations such as Mg²⁺, Ba²⁺ or Mn²⁺ replaced Ca²⁺. Under these experimental conditions, cell pedigrees were obtained during the incubation period. The greatest number of cell divisions so far observed in vitro was 8 for Hynobius lichenatus, and 9 for Cynops pyrrhogaster. Some related observations on the behavior of isolated blastomeres are also presented.     

Histopathological Analysis of Acinetobacter baumannii Lung Infection in a Mouse Model

Acinetobacter baumannii is the main causative pathogen of nosocomial infections that causes severe infections in the lungs. In this study, we analyzed the histopathological characteristics of lung infection with two strains of A. baumannii (ATCC 19606 and the clinical isolate TK1090) and Pseudomonas aeruginosa PAO-1 in C3H/HeN mice to evaluate the virulence of A. baumannii. Survival was evaluated over 14 days. At 1, 2, 5, or 14 days postinfection, mice of C3H/HeN were sacrificed, and histopathological analysis of lung specimens was also performed. Histopathological changes and accumulation of neutrophils and macrophages in the lungs after infection with A. baumannii and P. aeruginosa were analyzed. Following intratracheal inoculation, the lethality of ATCC 19606- and TK1090-infected mice was lower than that of PAO-1-infected mice. However, when mice were inoculated with a sub-lethal dose of A. baumannii, the lung bacterial burden remained in the mice until 14 days post-infection. Additionally, histopathological analysis revealed that macrophages infiltrated the lung foci of ATCC 19606-, TK1090-, and PAO-1-infected mice. Although neutrophils infiltrated the lung foci of ATCC 19606- and TK1090-infected mice, they poorly infiltrated the lung foci of PAO-1-infected mice. Accumulation of these cells in the lung foci of ATCC 19606- and TK1090-infected mice, but not PAO-1-infected mice, was observed for 14 days post-infection. These results suggest that A. baumannii is not completely eliminated despite the infiltration of immune cells in the lungs and that inflammation lasts for prolonged periods in the lungs. Further studies are required to understand the mechanism of A. baumannii infection, and novel drugs and vaccines should be developed to prevent A. baumannii infection.