Effects of secretin and gastric inhibitory polypeptide on human pancreatic growth hormone-releasing factor(1-40)-stimulated growth hormone levels in the rat

Synthetic human pancreatic growth hormone-releasing factor containing 40 amino acids ([hpGRF (1-40)]-OH) significantly stimulated plasma growth hormone (GH) levels in both sodium pentobarbital and urethane anesthetized rats. Synthetic secretin, gastric inhibitory polypeptide (GIP), and glucagon significantly decreased plasma GH levels while synthetic vasoactive intestinal peptide (VIP) had no effect. Secretin and GIP also altered the in vivo plasma GH response to [hpGRF(1-40)]-OH. Whether this effect is the result of an interaction at the pituitary level or is due to an extra-pituitary effect of secretin and GIP awaits further study.     

Dose-response comparisons of canine plasma gastroenteropancreatic hormone responses to bombesin and the porcine gastrin-releasing peptide (GRP)

This study compares the potencies of the porcine gastrin-releasing peptide (pGRP) and bombesin, in causing elevations of canine plasma gastroenteropancreatic (GEP) levels. In the dose range 0-600 pmol . kg-1 . h-1, infusion of both peptides resulted in obvious dose-related elevations of plasma levels of gastrin, pancreatic polypeptide, enteroglucagon, immunoreactive pancreatic glucagon, and insulin. In this dose range, no significant difference in potency between the two peptides in elevating plasma levels of the above hormones was observed. The results of this study, demonstrating equimolar potency of pGRP and bombesin, are in contrast to previous studies reporting that pGRP was less potent than bombesin in causing certain bioactivities in the rat following intracranial administration of the two peptides.     

Development and specificity of inhibitory terminal arborizations in the central nervous system

This study examined the morphological development of single inhibitory arborizations in the gerbil central auditory brain stem. Using a brain slice preparation, neurons of the medial nucleus of the trapezoid body (MNTB) were filled with horseradish peroxidase (HRP), and their complete arborizations were analyzed along the tonotopic axis of the lateral superior olive (LSO). The projections in neonatal animals displayed well-defined arbors that were ordered appropriately within the LSO. It was evident from the axonal pathways that the MNTB afferents could correct for projection errors after reaching the postsynaptic population. As development progressed, a number of arbors established diffuse or inappropriate projections within the LSO. These immature arborizations were no longer apparent by 18–25 days postnatal. The anatomical specificity of arbors at 12–13 and 18–25 days was quantified by measuring the distance that terminal boutons spread across the frequency axis. There was a significant reduction of this distance in older animals. In addition, there was a significant reduction in the mean number of boutons per arbor between 12–13 days and 18–25 days. The maximum nucleus cross-sectional area continued to increase through 15–16 days, indicating that the refined arbors occupied an even smaller fraction of the postsynaptic structure. Taken together, these observations suggest that central inhibitory arbors form exuberant contacts that must be eliminated during development.     

兔下丘脑室旁核刺激引起的肾交感神经传出活动的抑制

本实验用家兔,氯醛糖及尿酯混合静脉麻醉,制动,人工呼吸,颈部分离出三对神经——迷走、窦及主动脉神经,以备实验中切断。记录股动脉压、肾交感神经传出性放电活动(RSED)及其频率幅度直方图。借助脑立体定向仪刺激下丘脑室旁核,当刺激较强时,在交感神经放电短暂增加之后,可引起血压升高及RSED抑制。这一抑制过程可分为两个时相:血压不变期间的初期抑制时相及与血压升高同时并存的后期抑制时相。实验发现RSED总抑制时程及后期抑制时程均与血压变动具有正相关关系,而初期抑制时程与血压变动无相关关系。切断压力感受性神经前后,虽初期抑制时程的均值无显著差异,但在切断压力感受性神经后,总抑制时程及后期抑制时程的均值大大缩短。当用较弱刺激施于室旁核时,可不引起血压变化,但仍能引起RSED抑制。这个抑制亦可因切断压力感受神经而显著缩短。上述实验结果表明:(1) 在中枢内存在着一个室旁核-肾交感传出系统的抑制机制;(2) 初期抑制来源于中枢性抑制机制,而后期抑制时相主要来源于压力感受性反射,但亦有中枢抑制机制的参与;(3) RSED的中枢抑制可能并不是兴奋后压抑,而是自室旁核至脊髓交感节前神经元的主动性抑制。     

Rhizoplane colonization of pea seedlings by Rhizobium leguminosarum and a deleterious root colonizing Pseudomonas sp. and effects on plant growth

Some pseudomonads produce a toxin that specifically inhibits winter wheat (Triticum aestivum L.) root growth and the growth of several microorganisms. The toxin does not inhibit pea (Pisum sativum) root growth, but the organisms are aggressive root colonizers and their effect on Rhizobium leguminosarum growth, colonization, and nodulation of peas was not known. Peas were grown in Leonard jars in the greenhouse. Pea roots were inoculated with R. leguminosarum, a toxin-producing Pseudomonas sp., both, or neither (control). The Pseudomonas sp. colonized pea roots more rapidly and in greater number than R. leguminosarum after ten days. In the presence of the Pseudomonas sp., the R. leguminosarum population on the rhizoplane was less at ten days. When the roots were inoculated with both R. leguminosarum and Pseudomonas sp., the number of nodules were greater than when R. leguminosarum was inoculated alone, but nodule dry weight and pea shoot biomass were similar to plants inoculated with only R. leguminosarum. Although these results need confirmation with non-sterile soil and field studies, these preliminary results indicate that peas will not be affected by wheat root-inhibitory rhizobacteria.     

Temperature-dependent changes in Photosystem II heterogeneity support a cycle of Photosystem II during photoinhibition

High light treatments were given to attached leaves of pumpkin (Cucurbita pepo L.) at room temperature and at 1°C where the diffusion- and enzyme-dependent repair processes of Photosystem II are at a minimum. After treatments, electron transfer activities and fluorescence induction were measured from thylakoids isolated from the treated leaves. When the photoinhibition treatment was given at 1°C, the Photosystem II electron transfer assays that were designed to require electron transfer to the plastoquinone pool showed greater inhibition than electron transfer from H₂O to paraphenyl-benzoquinone, which measures all PS II centers. When the light treatment was given at room temperature, electron transfer from H₂O to paraphenyl-benzoquinone was inhibited more than whole-chain electron transfer. Variable fluorescence measured in the presence of ferricyanide decreased only during room-temperature treatments. These results suggest that reaction centers of one pool of Photosystem II, non-Q_B-PS II, replace photoinhibited reaction centers at room temperature, while no replacement occurs at 1°C. A simulation of photoinhibition at 1°C supports this conclusion.Abbreviations BSA bovine serum albumin - Chl chlorophyll - DCMU 3-(3,4,-dichlorophenyl)-1,1,-dimethylurea - DCPIP dichlorophenol-indophenol (2,6-dichloro-4((4-hydroxyphenyl)imino)-2,5-cyclohexadien-1-one) - DPC diphenyl carbazide (2,2-diphenylcarbonic dihydrazide) - FeCN ferricyanide (hexacyanoferrate(III)) - _app apparent quantum yield of photosynthetic oxygen evolution - MV methyl viologen (1,1-dimethyl-4,4-bipyridinium dichloride) - PPBQ phenyl-p-benzoquinone - PPFD photosynthetic photon flux density - PQ pool plastoquinone - Q_B secondary quinone acceptor of PS II - RT room temperature - WC whole chain electron transfer     

A possible mechanism of high temperature dormancy regulation in seeds of Avena sativa L. (cv. Moyencourt)

Embryos of Avena sativa L. (cv. Moyencourt) show no high temperature dormancy. The dormancy is induced by the presence of endosperm-aleurone part of the seed. Germination of isolated embryos at 30°C can be prevented by ABA and the inhibition is reversed by GA. Inhibitors of GA synthesis also inhibit embryo germination. The embryos of dormant and non-dormant seeds vary greatly in their sensitivity to exogenous ABA. High temperature dormancy of the entire seeds can be relieved by low concentrations of ethanol. On the basis of these facts a hypothetic model is proposed showing how interaction between endogenous GA and ABA-like inhibitory substance, may regulate the high temperature dormancy of the seeds.     

Stopped-flow mechanistic study of bromide substitution by an organonitrile at an iron(II) phosphinic centre; a π-electron driven process

The kinetics of the displacement reactions of the bromide ligands of trans-[FeBr₂(depe)₂] (depe = Et₂PCH₂CH₂PEt₂) by the organonitrile NCCH₂C₆H₄OMe-4, in tetrahydrofuran (either in the absence or in the presence of added Br⁻), to give the corresponding mono- and dinitrile complexes trans-[FeBr(NCCH₂C₆H₄OMe-4)(depe)₂]⁺ and trans-[Fe(NCCH₂C₆H₄OMe-4)₂(depe)₂]²⁺, have been investigated by stopped-flow spectrophotometry. The substitution reaction occurs by a mechanism involving rate-limiting dissociation of bromo ligands to form the unsaturated intermediates [FeBr(depe)₂]⁺ (k₁ = 1.52 ± 0.02 s⁻¹) and [Fe(NCR)(depe)₂]²⁺ (k₃ = 0.063 ± 0.008 s⁻¹) which add the nitrile ligand to form those nitrile complexes. The competition between the nitrile and Br⁻ for such metal centres has also been investigated and a stronger inhibiting effect of added Br⁻ is observed for the substitution of the second bromo ligand relative to the first one. The kinetic data are rationalized in terms of π-electronic effects of these unsaturated metal centres and of the bromide and nitrile ligands.