氟中毒抑制大鼠泌鼠的实验研究

The effect of fluorosis on lactation, lactotroph function and ultrastructure were studied in lactating rats. The results were as follows: 1) Inhibition of lactation in lactating rats with chronic fluorosis was assessed by stunting growth of pups and decrease in the amount of milk suckled by pups in 30 min. Metoclopramide, a blocker of dopamine receptor, could improve lactation in these rats. 2) During chronic fluorosis serum PRL level was decreased, however, PRL content in pituitary was increased. Electronmicroscopic examination showed accumulation of large mature secretory granules and appearance of extremely large abnormal secretory granules in lactotroph cytoplasma. These findings indicate that hormone release of pituitary lactotrophs is obstructed in lactating rats with fluorosis, and the toxic effect of fluoride is mediated by an enhanced function of dopaminergic system in hypothalamus.     

Oxidation-induced increase in activity of angiotensin converting enzyme in the rat kidney

The activity of angiotensin converting enzyme(ACE) in crude extracts of the rat renal cortex was increased when the oxidizing agent diamide was added to the extract. The maximal activity was obtained at concentrations over 1 mM, and the value was twice or more the activity in the absence of the pretreatment. The activity of ACE was also increased by the diamide-pretreatment of the isolated membrane fraction of the renal cortex, thereby indicating that the increase in activity was not due to oxidation of endogenous glutathione (GSH) that may lower the ACE activity, but rather that ACE itself was oxidized. When O2 was included in the extract for 2 h, the ACE activity also increased to about twice the original activity. Lineweaver-Burk plots analysis demonstrated that, after oxidation with diamide and O2, the Vmax was increased but the Km remained unchanged. We conclude that the action of ACE in the kidney functions may differ in relation to oxidation of the tissue.     

A photoreversible conformational change in 124 kDa Avena phytochrome

Tryptophan (Trp) fluorescence quenching of phytochrome has been studied using anionic, cationic and neutral quenchers, I-, Cs+ and acrylamide, respectively, in an effort to understand the molecular differences between the Pr and Pfr forms. The data have been analyzed using both Stern-Volmer and modified Stern-Volmer kinetic treatments. The anionic quencher, I-, was proven to be an ineffective quencher with Stern-Volmer constants, Ksv, of 0.60 and 0.63 M-1, respectively, for the Pr and Pfr forms of phytochrome. The cationic quencher, Cs+, showed about a 2-fold difference in the Ksv of Pr and Pfr, indicating a significant change in the fluorescent Trp environments during the Pr to Pfr phototransformation. However, only 25-37% of the fluorescent Trp residues were accessible to the cationic quencher. Most of the fluorescent Trp residues were accessible to acrylamide, but the quenching by acrylamide was indistinguishable for the Pr and Pfr forms. An additional quenching by acrylamide after a saturated quenching with Cs+ showed more than 40% increase in the Ksv of Pfr over Pr. These observations, along with the finding of two distinct components in the Trp fluorescence lifetime, indicate the existence of Trp residues in at least two different sets of environments in the phytochrome protein. The two components of the fluorescence had lifetimes of 1.1 ns (major) and 4.7 ns (minor) for Pr and 0.9 ns (major) and 4.6 ns (minor) for Pfr. Fluorescence quenching was found to be both static and dynamic as the Stern-Volmer constants for the steady-state fluorescence quenching were higher than for the dynamic fluorescence quenching. Based on the quenching results, in combination with the location of Trp residues in the primary structure, we conclude that the Pr to Pfr phototransformation involves a significant conformation change in the phytochrome molecule, preferentially in the 74 kDa chromophore-bearing domain.     

Kinetics of adsorption of proteins at interfaces: role of protein conformation in diffusional adsorption

To elucidate the role of protein conformation in the kinetics of adsorption at interfaces, seven structural intermediates of bovine serum albumin were prepared and their adsorption at the air/water interface was studied. Molecular area calculations indicated two distinct molecular processes, the first being the creation of an area, delta A1, for anchoring the molecule during the initial phase of adsorption and the second being the delta A2 cleared during subsequent reorientation and rearrangement of adsorbed molecules at the interface. The delta A1 values for all the albumin intermediates were the same, indicating that the initial work pi delta A1 needed to anchor the molecule at the interface was independent of solution conformation of the protein. Unlike delta A1, delta A2 exhibited a bell-shaped relationship with the extent of refolded state of the intermediates. Calculation of diffusion coefficients indicated that greater the unfolded state of the albumin intermediate, the greater was the diffusion coefficient. It is shown that the simple diffusion theory is inadequate to explain quantitatively the kinetics of protein adsorption. Specific, conformation-dependent, solute-solvent and solute-interface interactions also seem to influence the kinetics of adsorption of proteins.     

横断山齿突蟾属一新种(两栖纲:锄足蟾科)

1982年在横断山区考察期间,发现四川木里截族自治县的齿突蟾Scutiger标本在第二性征、趾蹼等特征与已知的各种齿突蟾均不相同,描述为新种木里齿突蟾Scutiger muliensis。     

齿突蟾属某些种的多态现象

本文报道某些锄足蟾科Pelobatidae动物的多态现象。讨论了同域或不同域的四种齿突蟾Scuti-ger,即刺胸齿突蟾S. mammatus(Guenther)、胸腺齿突蟾S. glandulatus(Liu)、木里齿突蟾S. mulicnsis Fei et Ye和皱纹齿突蟾S. ruginosus Zhao et jiang的皮肤瘰疣、第二性征等性状;用薄层等电聚焦电泳方法分析了同域三种齿突蟾的晶体蛋白。结果表明:前三种是有效种;后一种,即皱纹齿突蟾分别是前三种的多态性变体;这些变体以相同性状(即皮肤多瘭疣)同时表现在三个种中的现象,属于平行多态现象。     

The effects of a known family-size distribution on the estimation of genetic parameters.

We consider the question: In a segregation analysis, can knowledge of the family-size distribution (FSD) in the population from which a sample is drawn improve the estimators of genetic parameters? In other words, should one incorporate the population FSD into a segregation analysis if one knows it? If so, then under what circumstances? And how much improvement may result? We examine the variance and bias of the maximum likelihood estimators both asymptotically and in finite samples. We consider Poisson and geometric FSDs, as well as a simple two-valued FSD in which all families in the population have either one or two children. We limit our study to a simple genetic model with truncate selection. We find that if the FSD is completely specified, then the asymptotic variance of the estimator may be reduced by as much as 5%-10%, especially when the FSD is heavily skewed toward small families. Results in small samples are less clear-cut. For some of the simple two-valued FSDs, the variance of the estimator in small samples of one- and two-child families may actually be increased slightly when the FSD is included in the analysis. If one knows only the statistical form of the FSD, but not its parameter, then the estimator is improved only minutely. Our study also underlines the fact that results derived from asymptotic maximum likelihood theory do not necessarily hold in small samples. We conclude that in most practical applications it is not worth incorporating the FSD into a segregation analysis. However, this practice may be justified under special circumstances where the FSD is completely specified, without error, and the population consists overwhelmingly of small families.     

Molecular cloning of the gene of a penicillin-binding protein supposed to cause high resistance to beta-lactam antibiotics in Staphylococcus aureus.

A novel penicillin-binding protein, PBP-2' (Mr about 75,000), is known to be induced in excessively large amount by most beta-lactam compounds in cells of a clinically isolated strain of Staphylococcus aureus, TK784, that is highly resistant to beta-lactams and also most other antibiotics. This protein has very low affinities to most beta-lactam compounds and has been supposed to be the cause of the resistance of the cells to beta-lactams. A 14-kilobase DNA fragment was isolated from the cells that carried the gene encoding this penicillin-binding protein and also a genetically linked marker that is responsible for the resistance to tobramycin. This DNA was cloned on plasmid pACYC184 and was shown to cause both production of PBP-2' and resistance to tobramycin in Escherichia coli cells. However, the formation of PBP-2' in E. coli was only moderate and was independent of normal inducer beta-lactams. The PBP-2' formed in the E. coli cells showed slow kinetics of binding to beta-lactams similar to that of PBP-2' formed in the original S. aureus cells and gave a similar pattern of peptides to the latter when digested with the proteolytic V8 enzyme of S. aureus.