Effect of taurine on arterial, uterine and cardiac PGI2 and TXA2 synthesis in the rat

The influence of taurine (in drinking water for 6 weeks) on PGI₂ and TXA₂ synthesis by some female rat organs was investigated using radioimmunoassay and platelet antiaggregatory bioassay. Taurine 100 and 200 mg/kg/day increased aortic PGI₂ release from 0.59 ± 0.04 (control) to 0.85 ± 0.05 and 1.01 ± 0.06 ng/mg, respectively and that by the myometrium from 0.24 ± 0.02 (control) to 0.38 ± 0.01 and 0.50 ± 0.04 ng/mg wet tissue, respectively (P < 0.05, n = 6). It did not affect PGI₂ and TXA₂ production in the heart or TXA₂ in the aorta. Taurine 200 mg/kg depressed uterine TXA₂ synthesis from 148.6 ± 9.8 (control) to 85.4 ± 6.8 pg/mg (P < 0.05, n = 6). Furthermore taurine 0.4 and 0.8 mM in vitro stimulated PGI₂ released by the myometrial and aortic tissues from pregnant rats. The stimulant effect of taurine on PGI₂ may be related to its antioxidant effect whereas its inhibitory effect on uterine TXA₂ may result from direction of synthesis towards PGI₂. It is concluded that endogenous taurine may participate in regulation of PGs synthesis and that prostanoids may contribute to its known actions. On broad basis, taurine-induced release of PGI₂ may prove of potential value in those ailments characterised by deficiency in PGI₂ release.     

Regulation of insulin mRNA abundance and adenylation: dependence on hormones and matrix substrata.

The insulin mRNA levels of rat insulinoma cell lines increased six- to eightfold, and the cells entered a transient state of growth arrest when they were cultured in serum-free, hormonally defined medium and on an extract of extracellular matrix derived from a basement membrane-secreting tumor line, EHS. Insulinoma cultures in growth arrest responded to glucose with a two- to threefold increase in insulin secretion associated with an insulin mRNA that contained a poly(A) tail that was 120 to 140 bases longer than normal.     

Effect of the polysaccharide ofAgrobacterium radiobacter on the growth of plants and occurrence of damping-off in sugar beet

Agrobacterium radiobacter, strain B6 (a strain isolated in this laboratory, which limited the occurrence of damping-off of sugar beet and influenced growth of plants in hot-house and field experiments) was found to produce an acidic exopolysaccharide in a mineral medium with various carbon sources. Hydrolyzates of the polysaccharide contained glucose, galactose, glycerol, succinic acid and pyruvic acid, whose quantitative content varied according to the carbon source used. The polysaccharide isolated from the medium containing glucose exhibited the highest physiological activity. Seeds germinated best and sugar beet roots were found to grow most rapidly in a medium containing 0.2 % (W/W) of the polysaccharide. The roots exposed for 3 d in this medium grew 2.7-fold as compared with non-treated plants. Higher sumbers of microorganisms were detected on the surface of roots treated with the polysaccharide. Growth of roots was also stimulated when immersing the seeds (30 min) in a 0.2 –0.4 % solution of this polysaccharide. After a two-fold treatment the roots were less damaged by the fungusPythium ultimum. Plants from seeds treated with the polysaccharide grew in the field soil more rapidly than the non-treated plants but worse than after bacterization of the seeds byA. radiobacter B6 and were only partially protected against the damping-off of sugar beet.     

Preliminary Observations on the Pathogenesis of a Virulent Strain of Newcastle Disease Virus in Chickens

Development of Newcastle disease, after experimental and natural infection with the virulent strain VLT of Newcastle disease virus, and its growth and distribution in some selected tissues as assayed by the enumeration of plaques are reported.     

QUANTITATIVE MEASUREMENTS OF INTERACTIONS BETWEEN CROWN-GALL TUMORS AND THE PINTO BEAN HOST

Interactions between crown-gall tumors on the primary pinto bean leaf and the pinto bean seedling (Phaseolus vulgaris L. ‘Pinto‘) were estimated by quantitative measurements of tumor initiation and growth as affected by certain modifications of the host. Effects of the tumors on the host were estimated by measurements of host growth and correlation responses. The presence of crown-gall tumors was found to reduce the growth of the leaf in area but to nearly double the weight of the leaf 9 days after inoculation with Agrobacterium tumefaciens (Smith and Town.) Conn, strain B6. The presence of tumors on only one of the two primary leaves resulted in a decrease in the weight of the leaf without tumors, showing the tumors to be effective mobilization centers. Tumors also delayed the abscission of petiole explants and delayed the growth of the epicotyl bud, both reminiscent of auxin effects. The excision of the cotyledons, the epicotyl bud, or one of the pair of primary leaves at the time of inoculation increased the number of tumors initiated per leaf. Removing the epicotyl bud or one of the primary leaves, or placing a cytokinin on one of the leaves, altered leaf growth but failed to alter tumor growth, indicating that tumor growth is not affected by the changes responsible for the compensatory growth effects induced by these treatments. Tumor growth was shown to be generally correlated with leaf growth from day 2 through 8 after inoculation, suggesting that the factors normally limiting leaf growth in a determinate type leaf are also active in limiting tumor growth. The changes in the plant cell responsible for the enhanced rate of growth seen in crown-gall tumor cells, therefore, appear to occur in regulatory systems other than those normally limiting leaf growth. The regulatory systems that are affected may be identical with those activated in compensatory host growth effects.     

Influence of acetic and butyric acid addition on polysaccharide formation byClostridium acetobutylicum

Summary The production of granulose (an intracellular reserve polygranule), capsule and exopolysaccharide was investigated in a synthetic medium in which the oxido-reduction level was modified by the addition of acetic or butyric acid. After addition of the acids, granulose synthesis increased from 150 to 300 mg glucose equivalents ·1^–1 and capsular synthesis decreased by 25%. Exopolysaccharide production was unchanged under these conditions. A hypothesis that attributes a role to the polymer in the oxido-reduction sequences is discussed.     

Mivazerol, a Novel α2-Agonist and Potential Anti-Ischemic Drug, Inhibits KCl-Stimulated Neurotransmitter Release in Rat Nervous Tissue Preparations

Abstract: In this study, we have investigated the effect of mivazerol, [3-(1H-imidazol-4-yl)methyl-1]-2-hydroxy-benzamide hydrochloride, a new α₂-agonist lacking hypotensive properties and a potential anti-ischemic drug, on the evoked release of norepinephrine, aspartate, and glutamate in tissue preparations from hippocampus, spinal cord T1–T5 section, rostrolateral ventricular medulla, and nucleus tractus solitarii of the brainstem of rat. A simple and efficient in vitro procedure to study pharmacologically the release of norepinephrine and glutamate is described. Tissues were chopped into (0.3 × 0.2 × 0.2 mm³) sections and the resulting minces were used for this study. Exposure to KCl (10–75 mM) for 5 min served as a stimulus for the release response. One, S (for aspartate and for glutamate release), or two such stimuli, S₁ and S₂ (for norepinephrine release) were conducted. The release of norepinephrine (+150% above baseline) was inhibited in a dose-dependent manner by mivazerol in hippocampus (IC₅₀ = 1.5 × 10^?8M), spinal cord (IC₅₀ = 5 × 10^?8M), rostrolateral ventricular medulla (IC₅₀ = 10^?7M), and nucleus tractus solitarii (IC₅₀ = 7.5 × 10^?8M), and by clonidine in hippocampus (IC₅₀ = 5 × 10^?8M), spinal cord (IC₅₀ = 4.5 × 10^?8M), rostrolateral ventricular medulla (IC₅₀ = 2.5 × 10^?7M), and nucleus tractus solitarii (IC₅₀ = 10^?7M). This effect was counteracted by the selective α₂-antagonists yohimbine and rauwolscine. A significant glutamate and aspartate release response was also induced by KCl (35 mmol/L) in hippocampus (+250 and +135%, respectively) and spinal cord (+120 and +55%, respectively), in vitro. However, neither mivazerol nor clonidine, at doses up to 10 µM, had any significant effect on KCl-induced glutamate release in spinal cord, whereas mivazerol blocked completely the release of both amino acids in hippocampus and only the release of aspartate in spinal cord. On the other hand, clonidine (1 µM) was only effective in reducing by 40% the release of aspartate in hippocampus. These data indicate that (1) inhibition of KCl-induced norepinephrine release by mivazerol is mediated by its action on α₂-adrenergic receptors; (2) at concentrations selective for α₂-adrenergic receptors, only mivazerol was effective in blocking the KCl-induced glutamate release in hippocampal tissue; and (3) at the same concentrations, both mivazerol and clonidine were unable to inhibit glutamate release in the spinal cord. These data suggest that prevention of hyperadrenergic activity by mivazerol in perioperative patients may be mediated through its effect on the release of norepinephrine and/or the release of glutamate and aspartate in regions of the CNS that are involved in the control of cardiovascular homeostasis.