Monoaminergic-cholinergic relationships and the chemical communication matrix of the substantia nigra and neostriatum

The historical development of histochemical methods for monoamines and chemicals involved with cholinergic function is reviewed. The use of these methods to elucidate neurochemical interactions in the substantia nigra and caudate-putamen complex is then discussed. Three hypotheses accounting for the localization of acetylcholinesterase within and/or on substantia nigra, pars compacta neurons are presented and evaluated:

1. (a) to catabolize acetylcholine released from afferent cholinergic fibers,

2. (b) to catabolize substance P released from some neostriato-nigral axon terminals, and/or

3. (c) to serve as a communication link with nigral vasculature.

Despite experimental evidence in favor of each of these possibilities, none have met with unqualified acceptance. Possible mechanisms and morphologic substrates accounting for dopaminergic-cholinergic, serotonergic-cholinergic, GABAergic-cholinergic, enkephalinergic-cholinergic, and cholinergic-cholinergic interactions in the caudate-putamen complex are discussed. These include synaptic and non-synaptic relationships, dendroaxonic information flow, and mutual regulatory processes.

The pharmacology of aggressive behavioural phenomena elicited by muscarine injected into the cerebral ventricles of conscious cats

Atropine and scopolamine, injected intraventricularly, abolished typical emotional behaviour with aggression and autonomic and motor phenomena, as well as with clonic-tonic convulsions of intraventricularly injected muscarine. On the other hand, adrenergic and dopaminergic blocking agents, antihistamines, 5-hydroxytryptamine antagonists, antiepileptic drugs, and 5-hydroxytryptamine, administered intraventricularly, failed to antagonize the gross behavioural effects of intraventricular muscarine. However, ganglionic and sometimes neuromuscular blocking agents, as well as catecholamines and histamine injected intraventricularly, antagonized the emotional behaviour with aggression and depressed the autonomic and motor phenomena of small doses of intraventricular muscarine. In addition, emotional behaviour with aggression and autonomic and motor phenomena evoked by high doses of intraventricular muscarine were resistant to these antagonists administered intraventricularly. From these experiments it is concluded that the sites activated by muscarine in the CNS producing aggressive behaviour have the following characteristics: in high doses muscarine acted on muscarinic cholinoceptive sites, while in small doses it activated the cholinoceptive sites having muscarinic and nicotinic characteristics. Finally, the ability of single intraventricular injections of muscarine to trigger and to maintain the long-lasting gross behavioural effects cannot be ascribed to a rapid detonator transmission, but rather to an action that differs from a conventional transmitter function.     

Genetic basis of neonatal methicillin-resistant Staphylococcus aureus in Japan

Methicillin-resistant Staphylococcus aureus (MRSA) is still one of major problems of drug-resistant microorganisms and healthcare-acquired infections. Methicillin-resistant Staphylococcus aureus is highly prevalent in patients in neonatal intensive care units (NICU) in Japan. The most predominant MRSA in NICU is multidrug resistant and produces superantigenic exotoxin, toxic shock syndrome toxin-1 (TSST-1) and staphylococcal enterotoxin C (SEC). These predominant MRSA strains belong to coagulase type II, SCCmec type II, mecA-Tn554 polymorph type I-A and show closely related pulse field gel electrophoresis types. The dissemination of MRSA is wide, and there is a pandemic distribution of a single MRSA clone in the NICU of Japan. Since 1992, the nationwide spread of this clone has also led to the development of a new neonatal disease known as neonatal toxic shock-like exanthematous disease (NTED), which is caused by overactivation of vbeta2+ T cells induced by TSST-1. The spread of MRSA in NICU in Japan has been attributed to overcrowding, high rates of extremely low birthweight babies, understaffing, low control measures of infection and overuse of antibiotics. The environment of NICU and infection control intervention should be improved and a new strategy for control like vaccination or probiotics is required.     

α_1受体对不同状态心肌细胞的作用

目的　通过激活和阻断不同状态心肌的α1 受体 ,探讨α1 受体的活化状态与不同状态心肌的关系。方法　采用Langedorff灌流技术复制动物模型。第 1个实验检验不同浓度的α1 受体激动剂 phenylephrine和阻断剂 prazosin(0 0 1、0 1、1、1 0、1 0 0 μmol·L- 1 )在缺血前 1 0min、缺血期和再灌注时的效应。第 2个实验研究 phenylephrine和 prazosin的时间依赖性。每组实验的末期 ,测量磷酸肌酸激酶、细胞凋亡和坏死情况。结果　 0 1、1 μmol·L- 1 的 phenylephrine可发挥最大效益 ,但prazosin浓度超过 1 0 μmol·L- 1 可产生有害作用。缺血前激活、缺血期间阻断α1 受体可保护心肌。再灌注时激活α1 受体效应不明确 ,但阻断α1 受体有害。结论　激动或阻断α1 受体所产生的效应与心肌的状态有关     

肺癌胸水中肿瘤浸润淋巴细胞的生物学活性研究

目的 :探讨肺癌胸水中肿瘤浸润淋巴细胞 (TIL)的生物学活性 ,便于更好地应用于临床。方法 :用白细胞介素2 (IL 2 )诱导培养肺癌胸水TIL ,按常规法计数TIL细胞增殖量 ,采用流式细胞仪分析TIL细胞表型及MTT法检测其杀瘤活性。结果 :经IL 2诱导培养TIL 2 1天后 :TIL增殖大于 10 0 0倍的患者有 17例占 77%。CD3差异无显著性 (P >0 0 5 ) ,CD4、CD8差异有显著性 (P <0 0 1) ,而CD4 /CD8比值高达 3 5 3± 0 82 ,并且在 2 1天时TIL具有较高的细胞毒性。结论 :肺癌胸水中的TIL体外诱导培养 2 1天时TIL具有较强的生物活性 ,此时用于胸水治疗可取得可靠的疗效     

碳酸锂对环磷酰胺的抑瘤及毒副作用的影响

观察碳酸锂（Ｌｉ２ＣＯ３）对环磷酰胺（ＣＰ）的抑瘤作用和毒副作用的影响。按标准方法对每只小鼠进行肿瘤（肝癌Ｈ２２、肉瘤Ｓ１８０）接种。Ｌｉ２ＣＯ３［２０、４０ｍｇ／ｋｇ．ｄｉｇ，连续１０天。ＣＰ（９０、１８０ｍｇ／ｋｇ）一次ｉＰ。结果显示：Ｌｉ２ＣＯ３与ＣＰ联合应用可显著提高抑瘤率，增加荷瘤鼠的外周血白细胞（ＷＢＣ）数和降低骨磷嗜多染红细胞（ＰＣＥ）的微核率（ＭＮＦ）。提示Ｌｉ２ＣＯ３能明显增强Ｃ     

2005年上海市霍乱弧菌菌株表型及ctxA毒力基因分析

目的：分析本市2005年不同来源01群和0139群霍乱弧菌菌株表型和ctxA毒力基因特征。方法：以PCR方法，对所有菌株进行ctxA毒力基因检测。采用WHO推荐的改良K—B纸片法，对所有菌株均进行了12种抗菌药物的药敏试验。结果：从病人和外环境中分离出的0139群霍乱弧菌均为产毒株；从病人中分离出的01群霍乱弧菌流行株均产毒，外环境中分离出的非流行株少数也产毒。0139群霍乱弧菌菌株耐药谱较01群霍乱弧菌菌株广；两者对氨苄青霉素、强力霉素、庆大霉素、复方新诺明、利福平耐药率有显著差异。结论：本市2005年霍乱的流行株都是产毒株，但产毒株不一定是流行株。药敏结果显示，对01群和0139群霍乱弧菌应采取不同抗菌治疗，0139群霍乱弧菌多重耐药应引起重视。     

在美欧非洲用中医治疗HIV、AIDS的体会

中医药具有纯天然、很少毒副作用和抗药性,并价廉适应面广特点,据笔者近10多年在美欧非洲几十个国家和地区的千余例HIV、AIDS病人的临床实践证实,中医中药、针灸对治疗HIV、AIDS疗效显著。     

克仑特罗的急性毒性作用

目的:观察克仑特罗 (瘦肉精) 的急性毒性作用.方法:新西兰兔灌胃(ig)中毒剂量的盐酸克仑特罗溶液(150 μg·kg-1),记录心电图(ECG)II导联及V5导联;测定肌钙蛋白I (cTnI)及其他血液生化指标;对心、肝、肾进行病理组织学检查. 结果:克仑特罗能使心电图(ECG)II导联及V5导联T波显著降低,药后6 h肌钙蛋白I(cTnI)升高,对其他生化指标也有明显影响.可引起心、肝、肾发生病理学改变. 结论:克仑特罗(单剂量150 μg·kg-1,ig)能明显改变兔血清某些生化指标,对心、肝、肾功能均有一定程度的损伤.本试验为临床提供实验依据.     

干扰素诱导肿瘤凋亡的分子机制

干扰素(interferons,IFNs)是一类重要的抗病毒、抗肿瘤和免疫调节细胞因子。IFNs广泛用于造血系统恶性肿瘤、淋巴瘤及多种实体瘤的临床治疗。IFNs与细胞表面受体结合后,主要通过JAK/STAT信号途径,调节一系列干扰素刺激基因(IFN-sti mulated genes,ISGs)表达,这些功能性基因包括凋亡相关分子Fas/FasL、TRAIL/APO-2、抑癌基因bax、bak及p53等,这些ISGs与细胞凋亡及抑制细胞周期密切相关。此外,IFN还可放大由caspase诱导的线粒体功能紊乱效应,诱导细胞经线粒体途径凋亡。因而,IFNs主要通过抑制细胞周期、诱导抑癌基因的表达及增强肿瘤细胞对凋亡信号敏感性,诱导肿瘤细胞凋亡,而发挥其抗肿瘤生物学活性。