硒的抗癌作用及其作用机理

硒(Se)主要以硒半胱氨酸形式存在于蛋白质中,是红细胞谷胱甘肽过氧化物酶(GSH—Px)的组成成份,是人体生命活动所必需的微量元素。一、硒与癌症发生的关系缺硒可能会使癌症发病率升高。施劳泽等计算了28个国家和地区居民微量元素饮食摄入量与癌症的相关性,发现各类癌症与硒呈负相关。低硒地区及血硒低的人群中以消化道癌(食道癌、肝癌、结肠癌)及乳腺癌发病率为高。于树玉等发现肝癌的地区分布与肝癌高发     

舌头的作用

"最近,纪录片《舌尖上的中国》很火。主创人员之所以取这么个名字,显然是因为他们认为人们品尝美食主要是通过舌头,尤其是舌尖,可这个想法大错特错。一种食物的滋味,是由气味、味道、口感、温度等多方面综合而成的,其中最重要的不是味道,而是气味。被我们说成"味道"的东西其实百分之八九十来自香味。这些香味是挥发性的气体,它们从鼻孔或嘴巴飘     

童便的作用

治病用药,不一定要贵药、补药,价贱之药亦能救急。童便自古即列入药物,《本草纲目》记载“咸寒无毒”,“主久嗽,上气失音,及症积满腹,明日益声,润肌肤补大肠,推陈致新……止吐血衄血滋阴降火甚速”。童便采用方便,余临床用之确有卓效,追忆既往治验,曾用以治李××,男性,四十余岁,因劳动负重,突然吐血,顷刻之间,吐血数碗,面唇皆白,家人惊恐万分,左右邻居亦慌张失措,延余急诊。是时农村离药铺二十余里,往返需花四小时,奈病重,远水难救近火,是以急中生计,用回龙汤急治。即取其小儿之小便,去头尾,约大半碗饮之,服后约半小时能安睡,随之血即止,次日举止如常人,其功之捷实可贵也。尿可以治病,亦可加工炮制中药,使中药发挥其效果,如童便制香附,可以理气行瘀;童便调入生化汤,可以消瘀活血;童便配苏木、降香、牛膝、丹皮、蒲黄,可治跌打损伤;童便加入白通汤可治少阴下利;童便加入四逆汤可回阳救逆。是渭古之有鉴,今日有验,不可忽视也。     

药酒的作用

药酒是指以酒溶药所得到的澄明液体制剂。 　　药酒在祖国医学上的应用最早载于《史记·扁鹊列传》。《史记》还收载了西汉名医淳于意用药酒治疗内、妇科病的两个病案，一个是济北王患病，诏淳于意诊治，淳按了脉诊为“风厥胸满”病，配了三种药酒让其服用，病就痊愈了。     

蚯蚓的作用

在这个地球上,蚯蚓可谓是大自然赐予人类的神奇礼物,浑身是宅。蚯蚓俗称曲蟮,中药称地龙,其经济价值很高。蚯蚓是耕耘土壤的“大力士”,通过它的活动,使土壤疏松,团粒结构增强,从而促进农作物的生长;蚯蚓食性广,许多污染环境的有机物质部可成为它的食料;蚯蚓体内富含很多营养成分,含有丰富的蛋白质、维生素、各种矿物质、微量元素和18种氨基酸;此外,     

活性炭的作用

从二十世纪九十年代中期开始，活性炭一直用于医药和化工市场。由于活性炭的短缺，以活性炭为原料生产的药品还停留在实验室内，没有将产品推向市场或大量用于临床。     

多糖的免疫调节作用及其作用机制研究进展

多糖具有肯定的调节机体免疫功能的作用,其作用是多途径、多环节、多靶点的,如促进免疫细胞增殖与分化,分泌各种淋巴因子,调节神经－内分泌－免疫调节网络（ＮＩＭ）的平衡等。在世界药物研究趋势由化学合成药物转向天然药物的今天,人们对中药多糖类药物的研究也正如火如荼。本文对近年来多糖的免疫调节作用及其作用机制的研究进展作一概述。     

苦参的抗溃疡作用及作用成分

为了对用于胃肠疾患的生药作药理学评价,常用与胃粘膜防御因子有关的盐酸乙醇溃疡作用模型进行研究。作者对苦味健胃药苦参进行了研究,认为50％甲醇浸膏有强抑制作用,进而对其作用成分进行了研究,搞清了黄烷酮类结构的kurarinone并加以报道。取雄性大白鼠禁食24h后,用盐酸乙醇(60％乙醇+ISOmmol/L盐酸)1.5ml经口给药,1h后测定损伤系数,被检药物在盐酸乙醇投与1h前经口或腹腔给药,其结果是Kurarinone按50,25mg/kg经口给药抑制了盐酸乙醇溃疡,但100,50mg/kg的腹腔给药却完全没有抑制作用,而且经口给药时,Kurarinone的抑制作用在事先用消炎痛制剂     

丙泊酚的作用机制及非麻醉作用

丙泊酚是一种静脉全身麻醉药,起效迅速、作用时间短、清醒快而完全、不良反应少。近几年研究发现,其除了麻醉效应外,还存在一些其他效应,包括机体器官保护作用,对血小板的抑制作用,免疫调节作用,减少术后呕吐,控     

Electroencephalographic characteristics of lithium hydroxybutyrate

Lithium hydroxybutyrate influence on excitability, functional mobility and frequency range power of the cortex electrograms, midbrain reticular formation, posterior hypothalamus caudate nucleus, dorsal hippocampus, basolateral amygdala and medial thalamus in rabbits has been investigated. It has been shown that the drug suppresses the non-specific activating systems of the midbrain and posterior hypothalamus, intensifies work of the caudatocortical inhibitory mechanisms and the forebrain limbic formations (the hippocampus and amygdala).     

A neurophysiological analysis of the serotoninergic effects of lithium oxybutyrate

Single intravenous injections of lithium hydroxybutyrate (10 mg/kg) to rabbits prevented the effects of stimulation of the dorsal nucleus of the raphe on the electrogenesis of the cortex and subcortical structures. At long-term administration (7 days, 10 mg/kg daily intramuscularly) lithium hydroxybutyrate prevented the influence of stimulation on the electrogram (EG) of this structure and the motor cortex but enhanced it with respect to EG of the amygdala, hippocampus, thalamus and caudate nucleus.     

Effect of lithium chloride on bioelectric activity of the cortex and various subcortical structures of rabbit brain]

In a dose of 100 mg/kg and with intravenous administration to rabbits lithium chloride produces a depressing influence on the spontaneous bioelectric activity of the cerebral cortex and its subcortical formations, which extends from the cortex to subcortical structures. The compound brings down the electric excitability of the hippocampus, caudate nucleus, tonsils, reticular formation of the mesensephalic segment and of the thalamus, while in a dose of 300 mg/kg it increases the excitability of the motor cortex. No correlation between the lithium chloride induced electroencephalographic changes in the cerebral structures, on the one hand, and the content therein of biogenic amines and accumulation of lithium ions, on the other, was revealed.     

Influence of chlordiazepoxide on paroxysmal EEG activity induced by hippocampal and/or thalamic cobalt foci

The influence of chlordiazepoxide (Librium) on the paroxysmal 7–9/sec spike and wave and polyspike EEG discharges induced by chronic cobaltgelatine implantation into the dorsal hippocampus and/or nonspecific thalamus has been studied in rats with electrodes in the frontal cortices, dorsal hippocampi and the mesencephalic reticular formation.Both low (1.5–9 mg/kg i.p.) and high (9–15 mg/kg i.p.) doses of chlordiazepoxide reduced the incidence of paroxysmal EEG manifestations and shortened their duration (when present). Both effects were more pronounced after higher doses. The frequency of spike-wave complexes or spikes within the paroxysmal EEG discharges did not change systematically after chlordiazepoxide.The influence of the drug on the paroxysmal discharges is independent of whether the EEG after chlordiazepoxide is desynchronized or synchronized. In the latter case desynchronization of the EEG by reticular stimulation does not facilitate the occurrence of paroxysmal EEG dischartes.IBRO/UNESCO fellow on leave from the Department of Physiology, Faculty of Medicine, University of Mexico (present address) and Direction General de Acción Social Educativa S.E.P. México.     

Direct action of amphetamine and its furane derivatives on the excitability of neurone populations in various cerebral structures

The direct effect of β-phenylisopropylamine and its furane derivatives upon the excitability of the midbrain reticular formation, the dorsal hippocampus, the medial thalamus, the caudate nucleus, several phylogenetically different paleo- and neocerebellum structures, and the brain cortex was investigated in acute experiments using rabbits. The experiments were carried out on the basis of local microinjections and recordings of spontaneous EEG and EEG-reactions, evoked by stimulation of the above brain structures. It was ascertained that the direct action of amphetamine is characterized by a rise in the excitability of the neurone populations of the brainstem reticular formation and the paleocerebellar cortex, as well as by a stimulating effect upon the neurones of the hippocampus and medial thalamus. At the same time a microinjection of amphetamine inhibits the induced activity of cortical neurones, but does not affect the excitability of the caudate nuclei or the neocerebellar cortex. The N-furfuryl-substiuted derivatives of amphetamine exert a pronounced depressant effect upon the neurone populations of the medial thalamus, the hippocampus and the caudate nucleus. It was also shown that the substitution of the amphetamine molecule by certain furfuryl radicals diminished its stimulating action upon the reticular formation of the midbrain and the paleocerebellum, as well as its inhibiting effect upon the excitability of the neurone populations in the brain cortex.     

Hippocampal seizure discharge produced by systemic digitoxigenin is antagonized by reserpine or p-chlorophenylalanine

EEG was recorded from several brain regions during the i.v. infusion of digitoxigenin to conscious, freely-moving rats. Two seizure episodes were recorded from the ventral hippocampus with the second, more severe seizure characterized by low-frequency (3-6/sec), high-amplitude (0.9-1.5 mV) discharges. Secondary activity was recorded from the mesencephalic and reticular formations. Pretreatment of rats with p-chlorophenylalanine or reserpine prevented the first seizure and markedly delayed the second seizure to appear after 1.85 mg or 4.66 mg digitoxigenin/kg, respectively, compared to 0.79 mg/kg in untreated rats. The pretreatments did not alter the frequency of the discharges but reduced their amplitude to 0.4 -0.75 mV. The results suggest a role for monoamines, and in particular serotonin, in the effect of digitoxigenin to cause hippocampal seizure discharge.     

Attenuation of cerebral glucose use in kainic acid-treated rats by diazepam

Diazepam's impact on kainic acid seizure-induced local cerebral glucose utilization (LCGU) was assessed by a quantitative [14C]2-deoxyglucose method. Male rats were injected i.p. with either kainic acid (12 mg/kg) or its vehicle, 3 or 48 h before LCGU determination. Diazepam (3.2 mg/kg) or its vehicle were injected i.m. 15 min before, 1 and 2.5 h after kainic acid. Diazepam blocked kainic acid-induced overt convulsions, attenuated LCGU increases at 3 h and prevented 48 h LCGU decreases in piriform cortex and amygdala. LCGU in (% of vehicle): CA3 (438%), CA4 (537%) and CA1-ventral (340%) of hippocampus, interpeduncular nucleus (200%) and lateral lemniscus (213%) were still significantly above vehicle levels in the 3 h diazepam-kainic acid group. These results suggest that diazepam suppresses the spread of kainic acid-induced seizure activity from the proposed CA3 epileptogenic focus. In addition, diazepam reduces, but does not abolish, hypermetabolic activity at the foci itself.     

Electroencephalographic analysis of the central action of halonal

The experiments on rabbits revealed the depressant effect of anticonvulsant drug halonal on spontaneous bioelectrical activity and electroexcitability of the motor area of the cerebral cortex, caudate nucleus, intralaminar nuclei of the thalamus and midbrain reticular formation. The drug exerts no effect on the amygdala and hippocamp. The mechanism of the anticonvulsant effect of halonal involves inhibition of the caudo-thalamo-cortical synchronizing system that presumably disorders the occurrence of the hypersynchronous charge in the cortical neurons and prevents the development of a convulsive fit.     

Effects of some antiepileptic and proconvulsant drugs on kainic acid-induced limbic epilepsy in cats

The effects of parenteral administration of diazepam (3 mg/kg), DL-C-allylglycine (60–80 mg/kg), and ketamine (20 mg/kg) on kainic acid (KA)-induced limbic seizures were investigated in cats. Single microinjections of KA (1–4 μg) into the amygdaloid complex were followed by local sustained paroxysmal discharges in the limbic system. Seizures consisted of tonic clonic EEG discharges accompanied by orienting reaction to the ipsilateral side of injection and masticatory movements, facial jerks, and aggressive behaviour. Ictal discharges occurred every 5–10 min during the first hours after KA injection and then progressively disappeared within 1 wk. Interictal discharges remained for longer periods, but after 3 or 4 wk they were abolished. Diazepam completely blocked limbic seizures but not high-frequency discharges in the site of injection and the ipsilateral hippocampus. The animals were protected for 30 to 60 min. At the same time, diazepam decreased multiple-unit activity in the pontine reticular formation and the lateral geniculate nucleus and produced a general hypotonia state. DL-C-allylglycine activated KA amygdaloid focus during the remission state and ketamine produced independent epileptiformlike activity which interfered with that produced by KA injection.