Stimulation of pituitary-adrenocortical system by ginseng saponin.

Effects of preparations of saponin mixture and isolated ginsenosides, extracted from the root of Panax ginseng, on plasma corticotropin (ACTH) and corticosterone concentrations in rats were determined by the radioimmunoassay and competitive protein binding method. When ginseng saponin mixture was administered to rats intraperitoneally, plasma ACTH and corticosterone increased significantly 30, 60 and 90 min after the treatment. The kinetic pattern of the increase in plasma ACTH was almost parallel to that in plasma corticosterone. Isolated ginsenoside, protopanaxadiol or protopanaxatriol glycoside, also increased plasma corticosterone. The ginseng-induced increase in plasma corticosterone was suppressed by pretreatment with dexamethasone. Thus the ginseng saponin was found to act on the hypothalamus and/or hypophysis primarily, and stimulated ACTH secretion which resulted in increased synthesis of corticosterone in the adrenal cortex.     

The rate of allelism of lethal genes in a geographically structured population

The expected rate of allelism, E[I(x)], of lethal genes between two colonies with distance x in a structured population is studied by using one- and two-dimensional stepping-stone models. It is shown that E[I(x)] depends on the magnitude of selection in heterozygous condition (h), the rate of migration among adjacent colonies (m), the number of loci which produce lethal mutations (n) and the effective population size of each colony (N).——E[I(x)] always decreases with distance x. The rate of decrease is affected strongly by the magnitude of m. The rate of decrease is faster when m is small. E[I(x)] also decreases with increasing N and n. The effect of h on E[I(x)] is somewhat complicated. However, E[I(0)] is always smaller when h is small than when it is large.——For large x, the following approximate formulae may be obtained: (see PDF) where q and Var (q) are the mean and the variance of gene frequencies in each colony, t is approximated as t=h, (see PDF), -h for the partially recessive, completely recessive, and overdominant lethals, respectively, and C₀ is a function of m and t. It is clear that E[I(x)] declines exponentially with x in a one-dimensional habitat. The decrease E[I(x)] is faster in a two-dimensional habitat than in a one-dimensional habitat. The present result is applied to some of the existing data and the estimation of population parameters is also discussed.     

Binding of bacterial lipopolysaccharide to histocompatibility-2-complex proteins of mouse lymphocytes.

The membrane binding sites for lipopolysaccharide (LPS) were isolated by affinity chromatography of the solubilized membranes prepared from 125I-labeled mouse B-cells and T-cells on an affinity adsorbent prepared by coupling Salmonella minnesota R595 LPS to activated Sepharose 4B. The membrane proteins bound to the affinity adsorbent and eluted with 1.0% Triton X-100 were analyzed according to their mobility on polyacrylamide gel electrophoresis in sodium dodecylsulphate. These membrane proteins were further identified by immunoprecipitation with specific antisera. Immunoglobulins, possibly immunoglobulins M and D, were identified in the eluate from the B-cell membranes. The histocompatibility-2-complex proteins (H-2D, H-2K and Ia antigens) were also found to be binding sites for LPS on both B-cells and T-cells.     

Cell expansion and microfibril deposition inClosterium ehrenbergii

Cells ofClosterium ehrenbergii expanded for about 4.5 hr after vegetative cell division and about 3 hr after sexual cell division. Short cells were produced by the sexual expansion. At the early stage of the vegetative and the sexual expansion, most microfibrils were deposited transversely to the cell axis on the inner surface of the new wall. Then, bundles of microfibrils, running in various directions, overlaid the transverse microfibrils already deposited, at the late stage of the both types of expansion. The pattern of microfibril deposition changed from the transverse to the bundled pattern about 4 hr after the vegetative and about 2 hr after the sexual cell division, respectively. The change of pattern of microfibril deposition seemed to be highly correlated with cessation of cell expansion.     

The interaction of apolipoproteins with lecithin:cholesterol acyltransferase

The rate of lecithin:cholesterole acyltransferase reaction was measured in a cholesterol-containing single bilayer lecithin vesicle system. ApolipoproteinA-I (apoA-I) activated the enzyme by itself; the other components of apolipoproteins of high density lipoproteins (HDL) (rho = 1.08--1.2 g/cm3), or rabbit serum gamma globulin inhibited the reaction. The reaction which was activated by pure apoA-I was strongly inhibited by anti-apoA-I antibody. Quantitative analysis of the results showed that the lecithin:cholesterol acyltransferase reaction was activated by the binding of apoA-I to the surface of lipid substrates. The rate of the lecithin:cholesterol acyltransferase-catalyzed reaction was strictly proportional to the surface density of apoA-I. The inhibition was due to the decrease of the amount of apoA-I on the lipid surface, either through competitive exclusion by apoA-II or by other proteins, or through specific extraction with antibody. The presence of components of apoHDL, other than apoA-I, prevented the inhibitory action of anti-apoA-I antibody.     

Preparation and chemical properties of the outer membrane of a moderately halophilic gram-negative bacterium.

Outer membranes, almost free from peptidoglycan components, were prepared from a moderately halophilic gram-negative bacterium grown in a medium containing 2 M NaCl. The outer membrane was easily released, leaving mureinoplasts, by mild desalting in a 20% sucrose solution containing 50 mM tris(hydroxymethyl)aminomethane-HCl buffer, pH 7.8. The membrane was recovered by treatment with DNase I and CsCl buoyant density centrifugation. Chemical analyses revealed that the outer membrane was mainly composed of 31% protein, about 20% extractable lipids (mainly phospholipids), and lipopolysaccharides. The proteins had about 18 mol % excess of acidic over basic amino acids. The phospholipids comprised phosphatidyl ethanolamine, phosphatidyl glycerol, cardiolipin, and an unidentified phospholipid containing glucose, which seemed mainly associated with the outer membrane. The content of lipopolysaccharides in the outer membrane was calculated arbitrarily as 30% from the heptose content. A unique feature of these lipopolysaccharides seemed to be higher lipid content than found in lipopolysaccharides of other gram-negative bacteria. The major fatty acids of bound lipids of the outer membrane resembled those of the lipopolysaccharides obtained from cell envelope preparation and contained high concentrations of 3-hydroxy lauric acid.     

Hypothalamic and hormonal control of the photoperiodically induced vernal functions in the White-crowned Sparrow,Zonotrichia leucophrys gambelii

To assess the role of the hypothalamo-hypophysial complex in the control of photoperiodically induced vernal premigratory responses in the White-crowned Sparrow, the effects of hypothalamic lesions and systemic administration of several hormones on these responses were investigated. Lesions that destroyed the posterior median eminence (PME) or the entire median eminence (ME) inhibited photoperiodically induced testicular growth, premigratory fattening and Zugunruhe. Lesions in the basal infundibular nucleus (IN) that resulted in complete inhibition of testicular growth abolished Zugunruhe, but allowed varying degrees of fattening. The systemic administration of prolactin, testosterone propionate (TP) or the combination thereof in the PME-lesioned birds induced fattening similar to that observed in photostimulated controls but did not induce Zugunruhe. It is concluded that testosterone and prolactin are the most important hormones involved in the control of vernal premigratory fattening. The role of these hormones in the induction of vernal Zugunruhe is not positively proven.     

The Evolutionary Advantage of Recombination. II. Individual Selection for Recombination

Based on the Fisher-Muller theory of the evolution of recombination, an argument can be constructed predicting that a recessive allele favoring recombination will be favored, if there are either favorable or deleterious mutants occurring at other loci. In this case there is no clear distinction between individual and group selection. Computer simulation of populations segregating for recessive or dominant recombination alleles showed selection favoring recombination, except in the case of a dominant recombination allele with deleterious background mutants. The relationship of this work to parallel investigations by Williams and by Strobeck, Maynard Smith, and Charlesworth is explored. All seem to rely on the same phenomenon. There seems no reason to assume that the evolution of recombination must have occurred by group selection.     

Effects of 4-[beta-(diethylamino)-ethoxy]-benzophenone upon carotenogenesis in Rhodospirillum rubrum.

Carotenoid production was determined in illuminated anaerobically maintained cultures of Rhodospirillum rubrum in media with and without 4-[beta-(diethylamino)-ethoxy]-benzophenone. In treated cultures, lycopene--which normally is not produced by R. rubrum--accumulated as the predominant pigment, and total carotenoids increased five- to sixfold.     

Structure--activity relationships of chemical inducers of carotenoid biosynthesis

Fifteen amines having a profound effect on carotenogenesis in Marsh seedless grapefruit are reported. The compounds fall into three series: Et₂N(CH₂)_nMe (n = 4–8), Et₂N(CH₂)_nPh (n = 1–5), and Et₂NCH₂CH₂OC₆H₄R (R=H, p-Me, p-Et, p-iso-Pr, p-tert-Bu), There was up to an 11-fold increase in the total carotene content. Lycopene, not normally accumulated, became a major pigment. The inducing ability of the amines on carotenoid biosynthesis is correlated with the octanol-water partition coefficient. The mode of action appears to be similar to that of 2-(4-chlorophenylthio)triethylamine hydrochloride.