广西九万山藓类植物区系分析及其对划分热带,亚热带分界线的意义

九万山位于广西北部的中央(25°10’～25°25’N,108°27’E),界于泛北极植物区和古热带植物区的交汇处。其主要植被为亚热带常绿阔叶林。最高海拔为1693m,最低处仅170m。经对1850号标本的鉴定,共计有藓类植物35科、101属和189种。本文分析了九万山的藓类植物区系成分,将其划分为 10种类型。其中东亚成分最为丰富(39.33％),热带、亚热带成分次之(38.20％),而温带成分居第三位(18.54％)。本文选择了九万山临近的五个地区加以比较。其中,金佛山与九万山藓类植物的属和种的相似性系数分别为60.68％和36.87％,神农架为57.29％和33.13％。尖峰岭为48.83％和22.29％,西双版纳为57.29％和29.63％。而我国东部的武夷山则为69.86％和39.57％,其相似性系数在相比较的五个山区中为最高。九万山区有4个特有属并明显受喜马拉雅的影响。特别值得注意的是,在九万山区藓类区系中约有7％的种类是典型的热带成分。根据定量和定性的分析,笔者认为九万山的藓类区系表现出由热带向亚热带过渡的特性,其分界线可能位于九万山的南侧。     

Demonstration of retinal afferents in the RCS rat,with reference to the retinohypothalamic projection and suprachiasmatic nucleus

In the Royal College of Surgeons (RCS) rat, characterized by inherited retinal dystrophy, retinal projections to the brain were studied using anterograde neuronal transport of cholera toxin B subunit upon injection into one eye. The respective immunoreactivity was found predominantly contralateral to the injection site in the lateral geniculate nucleus, superior colliculus, nucleus of the optic tract, medial terminal nucleus of the accessory optic tract, and bilateral hypothalamic suprachiasmatic nuclei. Although terminal density was somewhat reduced in dystrophic rats, the projection patterns in these animals appeared similar to those seen in their congenic controls and were comparable to the visual pathways described for the rat previously. In dystrophic rats, the number of cell bodies exhibiting immunoreactivity to vasoactive intestinal polypeptide, viz. a population of suprachiasmatic neurons receiving major retinohypothalamic input, was reduced by one-third, and some differences were observed in the termination pattern of the geniculohypothalamic tract, as revealed by immunoreactivity to neuropeptide Y in the suprachiasmatic nucleus.This study was supported by grants from the DFG (Re 644/2-1) and the NMFZ, Mainz (to S.R.).     

鳗鲡爱德华氏菌病的组织病理学研究

鳗鲡爱德华氏菌病病变性质为化脓性炎症。症理分型主要有两种：化脓性肝炎型、混合型。较早发生病变部位主要在肝脏,其化脓性病杜按病程分为初、中、晚期。肾脏、脾脏、胃粘膜、体表出现散在的脓肿、脓性溃疡、炎性血栓及血斑。此外,肝脏、肾脏实质细胞均出现变性和坏列、血管充血、出血等。本文详细报告了肝脏、脾脏、肾脏的超微结构变化并初步讨论了细胞、组织损伤的过程及细胞病理学、超微病理学意义。     

脑干内的混沌

对脑干听觉诱发电位进行了非线性动力学分析,计算了关联维数Ｄ２和最大Ｌｙａｐｕｎｏｖ特征指数,确认ＢＡＥＰ是一个来源于低维混沌动力系统的时间序列,从而证明人类脑干存在着混沌现象,利用满足最小互信息标准的最佳延迟重构了二维混沌吸引子。     

Variations in the levels of asterone and asterogenol, two steroids from the saponins of the starfish, Asterias vulgaris (Verrill)

The levels of two steroids, asterone 1 and asterogenol 4, obtained by hydrolysis of the crude asterosaponin mixture from the starfish Asterias vulgaris, were highest in winter and spring, then the steroid levels fell to their annual minima in July, after the spawning period. Levels also varied geographically, but the ratio of these steroids remained approximately constant.     

Inhibition of surfactant release from isolated type II cells by compound 4880

Release of [³H]phosphatidylcholine from pulmonary Type II epithelial cells was stimulated by terbutaline, forskolin and cytochalasin D. Compound $\text{48}\text{80}$ inhibited both basal and agonist-stimulated release of [³H]PC. The IC₅₀ for inhibition by compound $\text{48}\text{80}$ was 1–2 μg/ml, and was similar for inhibition of both basal and stimulated release of [³H]phosphatidylcholine. Inhibitory effects of $\text{48}\text{80}$ were noted following a 1 h exposure to compound $\text{48}\text{80}$ and persisted up to 3 h. The inhibitory effect of compound $\text{48}\text{80}$ was entirely reversed by removing compound $\text{48}\text{80}$ from the external milieu. Compound $\text{48}\text{80}$ had no effect on cytosolic cyclic AMP levels or lactate dehydrogenase release. Inhibition of surfactant release produced by compound $\text{48}\text{80}$ was unaffected by changes in extracellular calcium concentrations. Compound $\text{48}\text{80}$ is a non-toxic inhibitor of phosphatidylcholine release from Type II epithelial cells.     

Energy metabolism in the cyanobacterium Plectonema boryanum. Participation of the thylakoid photosynthetic electron transfer chain in the dark respiration of NADPH and NADH

The oxidation of NADPH and NADH was studied in the light and in the dark using sonically derived membrane vesicles and osmotically shocked spheroplasts. These two types of cell-free membrane preparations mostly differ in that the cell and thylakoid membranes are scrambled in the former type and that they are more or less separated in the latter type of preparations. In the light, using both kinds of preparations, each of NADPH and NADH donates electrons via the plastoquinone-cytochrome $\text{b}\text{c}$ redox complex (Qbc redox complex) to the thylakoid membrane-bound cytochrome c-553 preoxidized by a light flash and to methylviologen via Photosystem I. NADPH donates electrons to the thylakoid membrane via a weakly rotenone-sensitive dehydrogenase to a site that is situated beyond the 3(3′,4′-dichlorophenyl)-1,1-dimethylurea sensitive site and before plastoquinone. Ferredoxin and easily soluble cytoplasmic proteins are presumably not involved in light-mediated NADPH oxidation. Inhibitors of electron transfer at the Qbc redox complex as the dinitrophenylether of 2-iodo-4-nitrothymol, 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone and 2-n-heptyl-4-hydroxy-quinone-N-oxide are effective, but antimycin A and KCN are not. The oxidation of NADH showed comparable sensitivity to these inhibitors. However, the oxidation of NADH is antimycin-A-sensitive regardless of the kind of membrane preparation used, indicating that in this case electrons are donated to a different site on the thylakoid membrane. In the dark, NADPH and NADH donate electrons at sites that behave similar to those of light-mediated oxidation, indicating that the initial steps of electron transfer are situated at the thylakoid membranes. However, NADPH oxidation is in some cases not sensitive to inhibitors active at the Qbc redox complex. It is concluded that O₂ reduction takes place at two different sites, one partly developed in vitro, situated near the rotenone-sensitive NADPH dehydrogenase, and another, highly KCN-sensitive one, situated beyond the Qbc redox complex and used in vivo. The terminal oxygen-reducing step of NADPH and NADH oxidation in the dark showed a preparation-dependent sensitivity for KCN, more than 80% inhibition in sonically derived membrane vesicles and less than 30% inhibition in osmotically shocked spheroplasts. From this result we tentatively conclude that the highly KCN-sensitive oxidase is not necessarily located at the thylakoid membrane and could be located at the cytoplasmic membrane.     

An analysis of proton fluxes coupled to electron transport and ATP synthesis in chloroplast thylakoids

Electron transport, phosphorylation and internal proton concentration were measured in illuminated spinach chloroplast thylakoid membranes under a number of conditions. Regardless of the procedure used to vary these parameters, the data fit a simple chemiosmotic model. Protons from Photosystem II did not appear to be utilized differently from those derived from Photosystem I. The maximal phosphorylation efficiency ($\text{P}\text{e}{}_2$) for photophosphorylation in washed thylakoids under oxidizing conditions is likely to be $\text{4}\text{3}$. This value is consistent with a proton-to-electron-pair ratio of 4 for electron flow through both photosystems and a proton-to-ATP ratio of 3 for the chloroplast proton-ATPase.     

The chloride requirement for photosynthetic oxygen evolution. Analysis of the effects of chloride and other anions on amine inhibition of the oxygen-evolving complex

In the presence of Cl^?, the severity of ammonia-induced inhibition of photosynthetic oxygen evolution is attenuated in spinach thylakoid membranes (Sandusky, P.O. and Yocum, C.F. (1983) FEBS Lett. 162, 339–343). A further examination of this phenomenon using steady-state kinetic analysis suggests that there are two sites of ammonia attack, only one of which is protected by the presence of Cl^?. In the case of Tris-induced inhibition of oxygen evolution only the Cl^? protected site is evident. In both cases the mechanism of Cl^? protection involves the binding of Cl^? in competition with the inhibitory amine. Anions (Br^? and NO^?₃) known to reactive oxygen evolution in Cl^?-depleted membranes also protect against Tris-induced inhibition, and reactivation of Cl^?-depleted membranes by Cl^? is competitively inhibited by ammonia. Inactivation of the oxygen-evolving complex by NH₂OH is impeded by Cl^?, whereas Cl^? does not affect the inhibition induced by so-called ADRY reagents. We propose that Cl^? functions in the oxygen-evolving complex as a ligand bridging manganese atoms to mediate electron transfer. This model accounts both for the well known Cl^? requirement of oxygen evolution, and for the inhibitory effects of amines on this reaction.