慢性阻塞性肺疾病患者呼出气NO含量的变化及吸入NO对其肺功能的影响

为探讨一氧化氮 (NO)在慢性阻塞性肺疾病 (COPD)发病中的作用及吸入NO对COPD肺功能的影响 ,本研究检测了COPD患者鼻、口呼出气中NO的含量及吸入不同浓度 (10～ 80ppm)NO时肺功能和血气指标。结果表明 :COPD患者鼻、口呼出气NO含量均明显低于对照组 (P <0 .0 1) ,且COPD和对照组口呼出气NO含量低于鼻呼出气 (P <0 .0 1) ;吸入 2 0～ 80ppmNO能明显改善COPD患者部分肺通气功能指标(FEV1、FEV1/FVC、FEV1%、PEF) ,且呈效量依赖关系 ,但对肺容量和肺弥散功能指标无明显影响 ;吸入NO后COPD患者PaCO2 增加 ,但对PaCO2 和高铁血红蛋白无明显影响。提示NO合成减少可能介导了COPD的发病 ,吸入一定浓度的NO可改善COPD患者肺通气功能和PaO2     

Hard tissue laser ablation mechanisms

The aim of this work is the experimental and theoretical investigation of the influence of variable laser parameters (wavelength, fluence, pulse repetition rate) and of the optical and thermophysical properties of bone tissue (absorption coefficient, tissue inhomogeneity) as well as of the sample thickness on ablation thresholds and ablation rate. Ablation and perforation experiments were conducted using a semiconductively pre-ionized transverse excitation atmospheric pressure (TEA) carbon dioxide (CO₂) laser (10.6m and a sliding discharge TEA [hydrogen fluoride (HF)] laser (2.9m). The experimental data are discussed with respect to the following ablation mechanisms: thermal melting and vaporization process, pressure oscillation of gases released by the thermal decomposition of collagen and/or apatite, stresses due to the expansion of superheated water.     

飞行员不成熟防御机制与心理健康、 个性、生活事件、社会支持的相关性研究

目的　探讨飞行员心理防御机制与心理社会因素的相关性。方法　对312 例飞行员进行防御方式问卷,卡特尔16 种个性因素问卷,症状自评量表,紧张性生活事件量表,社会支持评定量表测评。结果　揭示飞行员不成熟防御机制与心理健康水平,生活事件,社会支持显著相关,个性因素明显的影响不成熟防御机制;患病飞行员采用不成熟防御机制明显的多。结论　在飞行员心理卫生保健工作中,揭示并修正飞行员不成熟防御机制是十分必要的。     

波特竞争战略与现代医院战略管理

通过对现代企业战略界所所推崇的波特竞争战略的探讨,简单波特的三种竞争战略,分析了随着我国市场经济的建立,开放改革的不断深入,医院战略管理所面临的困惑,根据我国现代医院管理的实际,提供了波特竞争战略对医院战略的一些启示。     

Endothelin receptors and calcium translocation pathways in human airways

Tension and phosphatidyl inositol (PI) turnover experiments were conducted to investigate the receptors and signal transduction pathways responsible for contractions elicited by endothelin (ET) ligands in human bronchus. Nicardipine (1 μM), the L-type calcium channel inhibitor, or incubation in Ca²⁺-free medium, produced marked inhibition of contractions to the ET_B receptor-selective agonist, sarafotoxin S6c, and especially those induced by KCl. In contrast, Ca²⁺-free medium was without appreciable effect against contraction produced by endothelin-1 (ET-1), the non-selective ET_A and ET_B receptor agonist. In Ca²⁺-free medium, ryanodine (10 μM), which inhibits intracellular calcium mobilization, reduced sarafotoxin S6c- and ET-1-induced responses, but was without effect on responses to KCl. Similarly, nickel chloride (Ni²⁺; 1 mM) caused marked inhibition of contractions induced by sarafotoxin S6c or ET-1, but had no significant effect on KCl concentration-response curves. The mixed ET_A/ET_B receptor antagonist SB 209670 (3 μM) inhibited responses to sarafotoxin S6c and ET-1 such that concentration-response curves were shifted rightward, at the 30% maximum response level, by 10.0- and 3.8-fold, respectively, whereas BQ-123 (3 μM), the ET_A receptor antagonist, was without effect on responses induced by either agonist. ET-1 (1 nM–0.3 μM) caused a concentration-dependent stimulation of PI turnover, whereas sarafotoxin S6c (0.3 nM–0.1 μM) induced only small and variable increases, except at the highest concentration. The increase in PI turnover evoked by ET-1 was inhibited by SB 209670 (3 μM), and also by BQ-123 (3 μM). This is consistent with linkage of ET_A receptors to activation of inositol phosphate generation in human bronchial smooth muscle cells. Collectively, the data suggest that differences exist in the relative contributions of intracellular and extracellular Ca²⁺ mobilization mechanisms elicited by ET_A and ET_B receptor activation. Thus, sarafotoxin S6c-induced, ET_B receptor-mediated contraction in human bronchial smooth muscle appears to be dependent, in part, upon extracellular Ca²⁺, although a significant component of the response was also mediated by intracellular Ca²⁺ release, including from ryanodine-sensitive stores. ET_A receptor-mediated contraction of human airway smooth muscle was activated largely via the release of intracellular Ca²⁺. Received: 21 July 1998 / Accepted: 26 January 1999     

Locomotor activity and catecholamine receptor binding in adult normotensive and spontaneously hypertensive rats

Summary The binding of³H-WB 4101, an ₁-adrenoceptor antagonist, to membranes of the cerebral cortex, the hypothalamus, and the lower brainstem was examined in adult spontaneously hypertensive (SH) rats and in normotensive Wistar Kyoto (WK) controls. The specific binding of³H-WB 4101 (0.33 nM) was significantly higher in homogenates from the cerebral cortex of SH rats as compared to WK rats. No differences were detected between SH and WK rats in the specific binding of³H-spiroperidol (0.25 nM), a dopamine receptor antagonist, to membranes from the corpus striatum and the limbic forebrain. The locomotor activity was significantly higher in SH rats as compared to WK controls, in all probability due to a lack of habituation to environmental change. It is suggested that the high reactivity of SH rats is related to a dysfunction in the noradrenergic neurons in the central nervous system.     

Vegetables,fruit, and cancer. II. Mechanisms

The epidemiologic literature on the relationship between vegetable and fruit consumption and human cancer at a variety of sites was reviewed systematically in Part I.¹ It was concluded that consumption of higher levels of vegetables and fruit is associated consistently, although not universally, with a reduced risk of cancer at most sites, and particularly with epithelial cancers of the alimentary and respiratory tracts. Possible mechanisms by which vegetable and fruit intake might alter risk of cancer are addressed here. A large number of potentially anticarcinogenic agents are found in these food sources, including carotenoids, vitamins C and E, selenium, dietary fiber, dithiolthiones, glucosinolates and indoles, isothiocyanates, flavonoids, phenols, protease inhibitors, plant sterols, allium compounds, and limonene. These agents have both complementary and overlapping mechanisms of action, including the induction of detoxification enzymes, inhibition of nitrosamine formation, provision of substrate for formation of antineoplastic agents, dilution and binding of carcinogens in the digestive tract, alteration of hormone metabolism, antioxidant effects, and others. It appears extremely unlikely that any one substance is responsible for all the associations seen. Possible adverse effects of vegetable and fruit consumption are also examined. One way to consider the relationships reviewed here is to hypothesize that humans are adapted to a high intake of plant foods that supply substances crucial to the maintenance of the organism, but only some of which are currently called essential nutrients. Cancer may be the result of reducing the level of intake of foods that are metabolically necessary—it may be a disease of maladaptation.Authors are with the Division of Epidemiology, School of Public Health, University of Minnesota, 1-210 Moos Tower, 515 Delaware Street SE, Minneapolis, MN 55455, USA. Address correspondence to Dr Potter. This work was supported by NIH Grants CA 50305, CA 46618, and CA 09607.     

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.     

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