Depolarization and muscarinic excitation induced in a sympathetic ganglion by vasoactive intestinal polypeptide

The effects of vasoactive intestinal polypeptide (VIP) in the superior cervical ganglion of the cat were studied in vitro and in vivo with sucrose gap and multiunit recording, respectively. At a dose of 0.03 to 0.12 nanomole, VIP produced a dose-dependent, prolonged (3 to 15 minutes) depolarization of the ganglion and enhanced the ganglionic depolarization elicited by the muscarinic agonist acetyl-beta-methylcholine. At a dose of 1.8 to 10 nanomoles, the peptide enhanced and prolonged the postganglionic discharge elicited by acetyl-beta-methylcholine, enhanced muscarinic transmission in ganglia treated with an anticholinesterase agent, and enhanced the late muscarinic discharge elicited by acetylcholine. VIP did not affect the early nicotinic discharge elicited by acetylcholine or by electrical stimulation of the preganglionic nerve. It is concluded that VIP has a selective facilitatory action on muscarinic excitatory mechanisms in the superior cervical ganglion of the cat.     

Vasoactive intestinal polypeptide-like substance: the potential transmitter for cerebral vasodilation

In vitro pharmacological studies demonstrated that exogenously applied vasoactive intestinal polypeptide (VIP) relaxes the smooth muscle cells of cat cerebral arteries, whereas substance P constricts them. Ultrastructural-immunocytochemical techniques show that a VIP-like substance is present in the large granular vesicles of nonsympathetic nerve axons and terminals in the cerebral arterial walls. These results provide strong evidence in favor of the hypothesis that a VIP-like substance is the transmitter for vasodilation in cerebral blood vessels.     

Targeting of diacylglycerol degradation to M1 muscarinic receptors by beta-arrestins

Seven-transmembrane receptor (7TMR) signaling is transduced by second messengers such as diacylglycerol (DAG) generated in response to the heterotrimeric guanine nucleotide-binding protein Gq and is terminated by receptor desensitization and degradation of the second messengers. We show that beta-arrestins coordinate both processes for the Gq-coupled M1 muscarinic receptor. beta-Arrestins physically interact with diacylglycerol kinases (DGKs), enzymes that degrade DAG. Moreover, beta-arrestins are essential for conversion of DAG to phosphatidic acid after agonist stimulation, and this activity requires recruitment of the beta-arrestin-DGK complex to activated 7TMRs. The dual function of beta-arrestins, limiting production of diacylglycerol (by receptor desensitization) while enhancing its rate of degradation, is analogous to their ability to recruit adenosine 3',5'-monophosphate phosphodiesterases to Gs-coupled beta2-adrenergic receptors. Thus, beta-arrestins can serve similar regulatory functions for disparate classes of 7TMRs through structurally dissimilar enzymes that degrade chemically distinct second messengers.     

Vasoactive intestinal peptide: a possible transmitter of nonadrenergic relaxation of guinea pig airways

Vasoactive intestinal peptide, a smooth-muscle relaxant neuropeptide with neurotransmitter properties, was relaxed during electrical field stimulation of guinea pig trachea. The amount released correlated with the degree of relaxation, and the release was blocked by tetrodotoxin. Prior incubation of the trachea with antiserum to vasoactive intestinal peptide reduced the relaxation. Thus vasoactive intestinal peptide may mediate the nonadrenergic relaxation of tracheal smooth muscle.     

Neuroleptic drug-induced dopamine receptor supersensitivity: antagonism by L-prolyl-L-leucyl-glycinamide

An animal model of tardive dyskinesia was used to evaluate the potential antidyskinetic properties of the neuropeptide L-prolyl-L-leucyl-glycinamide (PLG). In rats, PLG administered concurrently with the neuroleptic drug haloperidol or chlorpromazine antagonized the enhancement of specific [3H]spiroperidol binding in the striatum that is associated with long-term neuroleptic treatment. The results are discussed in relation to a possible functional coupling of the putative PLG receptor with neuroleptic-dopamine receptor complex and clinical implications for tardive dyskinesia.     

Vasoactive intestinal peptide alters membrane potential and cyclic nucleotide levels in retinal horizontal cells

Vasoactive intestinal peptide stimulated the synthesis of adenosine 3',5'-monophosphate in fractions of isolated carp horizontal cells. When applied extracellularly to isolated and cultured horizontal cells, the peptide also induced a slow depolarization (30 to 40 millivolts) accompanied by a decrease in membrane resistance. However, analogs of adenosine 3',5'-monophosphate applied extracellularly or intracellularly, and forscolin applied extracellularly, had no effect on the membrane potential of cultured horizontal cells, indicating that the induced depolarization was not related to the accumulation of adenosine 3',5'-monophosphate in these cells.     

Corticotropin release: inhibition by intrahypothalamic implantation of atropine

Anterior hypothalamic implantations of crystalline atropine markedly inhibit the adrenocortical responses evoked by surgical stress, ether anesthesia, or intravenolus injection of arginine vasopressin. Similar implants in nearby regions of the brain or sham implantations in the same region were ineffective. The data suggest that the hypothalamic control of pituitary corticotropin may have a cholinergic component.     

Chemically induced porphyria: prevention by prior treatment with phenobarbital

The excessive induction of hepatic delta-aminolevulinic acid synthetase in rats after the administration of porphyria-inducing compounds is prevented by prior treatment with phenobarbital. Studies in vivo and in vitro indicate that phenobarbital prevents the induction of chemical porphyria by increasing the rate of detoxification of inducers by way of drug-metabolizing enzymes of the hepatic endoplasmic reticulum.     

Adrenergic excitation of cutaneous pain receptors induced by peripheral nerve injury

The mechanisms by which peripheral nerve injuries sometimes lead to causalgia, aberrant burning pain peripheral to the site of nerve damage, are uncertain, although the sympathetic nervous system is known to be involved. Whether such syndromes could be the result of the development of responsiveness by some cutaneous pain receptors (C-fiber nociceptors) to sympathetic efferent activity as a consequence of the nerve injury was tested in an animal model. After nerve damage but not in its absence, sympathetic stimulation and norepinephrine were excitatory for a subset of skin C-fiber nociceptors and enhanced the responsiveness of these nociceptors to tissue-damaging stimulation. These effects were demonstratable within days after nerve lesions, occurred at the cutaneous receptive terminal region, were manifest in sensory fibers that had not degenerated after the injury, and were mediated by alpha 2-adrenergic-like receptors.     

新生儿颅内出血患者血浆、脑脊液中生长抑素和血管活性肠肽的测定及意义

目的观察新生儿颅内出血患者血浆、脑脊液(CSF)中生长抑素(SS)和血管活性肠肽(VIP)的水平变化与临床意义。方法应用放射免疫法对19例新生儿颅内出血患儿的血浆、脑脊液SS和VIP的含量作了测定,并与以无神经系统疾病的入院新生儿12例作为对照。结果颅内出血新生儿CSF的SS和VIP含量高于其在血浆中的含量(P<0.01);颅内出血急性期患儿血浆和CSF的SS和VIP含量均显著高于恢复期和对照组,恢复期又显著高于对照组,差异均有统计学意义(P<0.01)。结论血浆、CSF中SS和VIP含量的变化可反映脑组织损伤的分期,推测病情和预后。     

Ultrastructural evidence for nephropathy induced by long-term exposure tosmall amounts of methyl mercury

A low dose of methyl mercuric chloride fed to female rats for 12 weeks caused extrusion of numerous cytoplasmic masses from kidney proximal tubule cells of the pars recta segment. These masses were characterized ultrastructurally by the presence of a smooth endoplasmic reticulum aggregate. The in vivo metabolism of methyl mercury to inorganic mercury may produce this effect and account for the proteinuria observed in persons occupationally exposed to organic mercury compounds.     

鸡小肠球虫病继发坏死性肠炎的诊治

随着肉杂鸡饲养量的不断增加,小肠球虫病在肉杂鸡的饲养过程中造成的损害越来越明显,其中主要以毒害艾美耳球虫的侵害为主。由于毒害艾美耳球虫的繁殖率低,发病日龄多在8周龄以后。发病鸡群表现出明显体重下降,死亡率升高,若继发魏氏梭菌感染,则死亡率明显升高,且病死鸡表现出明显肠毒血症症状。现对一养殖户饲养的1500只肉杂鸡暴发球虫病继发坏死性肠炎的诊疗过程报道如下。     

热处理提高采后果蔬抗冷性的机理分析

低温贮藏是采后果蔬最有效并且应用最广泛的一种保鲜技术,但是一些对低温敏感的水果和蔬菜,在低温贮藏中容易发生冷害现象,给采后果蔬造成重大的损失.热处理作为一种安全高效的物理处理措施,已被广泛应用于提高采后果蔬的抗冷性.目前多数研究集中在热处理对采后果蔬贮藏品质的影响以及对采后果蔬生理生化的影响,而热处理提高果蔬抗冷性的机理以及关键信号途径尚不太清楚.对热处理提高采后果蔬抗冷性可能存在的机理进行分析,表明热处理诱导的果蔬抗冷性与细胞膜完整性、活性氧信号、热激蛋白、精氨酸途径、糖代谢等因素相关.这些因素具有共同的特点:热处理最终均是通过诱导增强抗氧化酶体系的活性、维持细胞膜的完整性,从而提高了果蔬的抗冷性.     

超高压诱变小麦突变株系的光合特性及农艺性状

【目的】研究小麦超高压诱变突变体光合特性及农艺性状的变化,为小麦超高压诱变育种的可行性研究提供理论依据。【方法】以超高压诱变处理(120MPa,8h)获得的偃展4110突变株系高压2、高压3、高压5、高压9和高压11为试验材料,以未经高压处理的偃展4110纯系为对照,从抽穗期至成熟期测定其叶绿素相对含量(SPAD值)、净光合速率、气孔导度、蒸腾速率等光合生理及农艺性状指标,探讨超高压诱变小麦突变株系光合特性和农艺性状的变化规律。【结果】突变株系中,高压3、高压9和高压11在不同时期的叶绿素相对含量(SPAD值)均高于对照,且降幅小于对照。高压3和高压9的净光合速率从抽穗期到开花期增幅分别为29.7%和37.4%,而对照增幅仅为20.1%。从抽穗期至成熟期,高压3和高压5的气孔导度(Gs)均高于对照。从开花期到灌浆期,高压2和高压3的蒸腾速率(Tr)分别增加19.1%和16.0%,显著高于对照的增幅(11.3%)。从开花期到成熟期,高压2的胞间CO2浓度下降了0.6%,对照下降了4.7%,差异显著(P<0.05)。5个突变株系的气孔限制值(Ls)在抽穗期最大。高压2和高压3的叶片水分利用效率随抽穗期、开花期、灌浆期和成熟期的发育进程呈下降趋势。突变株系高压2和高压3的株高、穗粒数、有效穗数、千粒质量及产量均明显优于对照。【结论】超高压诱变小麦突变株系的光合特性及其农艺性状发生了变化,高压2和高压3的叶绿素含量、净光合速率、水分利用效率和产量均显著高于对照,是比较优异的突变株系,说明利用超高压诱变选育优质小麦品种是可行的。     

东北虎肠道阻塞的诊治

三门峡市人民公园东北虎郑郑,雌性,5岁,与商丘市动物园一东北虎交配,产下一雌性东北虎妞妞,2岁.妞妞3月龄时从商丘动物园拉回进行饲养,饲养到6月龄时,发现妞妞两后腿跛行,疑为缺钙造成.因而开始添加鸡肋、羊排骨以补充钙质.     

Antibody formation: initiation in "nonresponder" mice by macrophage synthetic polypeptide RNA

The RNA extracted from normal peritoneal macrophages exposed to a linear, random synthetic polypeptide, Glu(60)Ala(30)Tyr(10), initiated an immune response in C57B1/6J mice, although this strain responds very poorly to the antigen itself. From 10 to 150 micrograms of RNA obtained from mouse, rat, or rabbit macrophages was injected intraperitoneally into recipient mice, and specific antibody was detectable by passive hemagglutination 3 to 4 weeks later. Treatment of the RNA with ribonuclease destroyed its ability to initiate a specific immune response. The RNA contained by weight 0.02 percent of the (specific) antigen. The RNA obtained from cells incubated with a second polypeptide, Glu(36)Lys(24)Ala(40), initiated a response specific for this polymer. This RNA even when incubated in vitro with Glu(60)Ala(30)Tyr(10) failed to initiate antibody formation specific for Glu(60)Ala(30)Tyr(10).     

4-Leucine-oxytocin: natriuretic, diuretic, and antivasopressin polypeptide

During water diuresis in anesthetized rats, 4-leucine-oxytocin increased the urine output and the rates of sodium and chloride excretion. The potassium excretion rate was only slightly increased. During vasopressin-suppressed water diuresis, 4-leucine-oxytocin produced similar effects on urine and electrolyte excretions. In addition, it inhibited the vasopressin-induced free-water reabsorption, and it could reverse reabsorption to freewater clearance.     

维生素A对大豆7S球蛋白致仔猪肠上皮细胞屏障功能损伤的影响

以仔猪肠上皮细胞(IPEC-J2)为研究对象,用大豆7S球蛋白作为诱导因素,通过检测细胞活力、细胞跨膜电阻(TEER)、荧光素钠渗透率、细胞膜完整性相关指标与紧密连接蛋白的mRNA表达情况,探究维生素A(V_A)对大豆7S球蛋白致IPEC-J2细胞屏障功能损伤的影响。结果显示:5.0 mg·mL^-1大豆7S球蛋白导致IPEC-J2活力、TEER与ZO-1、Claudin-1、Occludin的mRNA表达量极显著(P<0.01)降低,而荧光素钠渗透率和细胞培养液中碱性磷酸酶(ALP)、乳酸脱氢酶(LDH)、二胺氧化酶(DAO)、肠型脂肪酸结合蛋白1(IFABP1)的含量极显著(P<0.01)升高;添加0.1和1 μmol·L^-1 V_A极显著提高了细胞活力(P<0.01),0.1~10 μmol·L^-1 V_A显著(P<0.05)缓解了大豆7S球蛋白导致的TEER、荧光素钠渗透率、细胞膜完整性相关指标与紧密连接蛋白mRNA表达的变化;10 000 μmol·L^-1 V_A反而加剧了这些影响。总体上,0.1~10 μmol·L^-1 V_A能通过保护细胞活力和细胞完整性、影响紧密连接蛋白的mRNA表达对大豆7S球蛋白导致的IPEC-J2细胞屏障功能损伤发挥保护作用,而10 000 μmol·L^-1 V_A反而加重了这种损伤。     

6-BA诱导黄瓜CsaIAAs基因的表达研究

Aux/IAA基因是一类典型的能被生长素诱导表达的基因家族,可以被生长素、细胞分裂素、盐及干旱胁迫等诱导表达。采用Trizol法提取黄瓜幼苗的根、茎、叶、花及卷须的总RNA,经反转录成cDNA,再利用CsaIAAs基因特异性引物进行半定量RT-PCR扩增,琼脂糖凝胶电泳检测CsaIAAs基因的表达情况。结果表明,黄瓜29个CsaIAAs基因中,除了CsaIAA25、CsaIAA26几乎在所有器官中都不表达外,CsaIAA07、CsaIAA09、CsaIAA16和CsaIAA20只在个别器官中表达,如CsaIAAs20只在茎中弱表达,CsaIAA29只在卷须中有弱的表达。而绝大部分的CsaIAAs基因（CsaIAA02、CsaIAA03、CsaIAA04、CsaIAA05、CsaIAA06、CsaIAA08、CsaIAA10、CsaIAA11、CsaIAA13、CsaIAA15、CsaIAA16和CsaIAA19等）在大多数器官中都可以被6-BA诱导表达,尤其是以根、茎、叶和卷须中表达量高。探讨CsaIAAs基因在黄瓜根、茎、叶、花及卷须中的表达情况,可为黄瓜CsaIAAs基因的功能研究提供重要的理论参考。