镇痛“自助餐”

疼痛,一直被认为是预示疾病、创伤的不祥征兆。确实,很多表情痛苦的病人前来就诊,一坐到医生面前,第一句话并不是蜕“我有什么病”,而是“我哪里痛”。     

培训“自助餐”

通过对兼职内训师的培养、数据分析下的靶向培训、内训与外训相结合等手段,企业可以达到精确定位培训的目的。     

降压药不是“自助餐”

大多数高血压患者都是在家里自己服用降压药治疗。可目前各种各样的“降压药”铺天盖地，进了药店，就像进了“自助餐馆”，店员或药师会鼓励你“敞开肚皮”，尽情挑选。然而，降压药这个“自助餐”，可不能随便吃!     

吃自助餐：切莫贪食无度

<正>自助餐的真正起源是八至十一世纪北欧的斯堪的纳维亚半岛,那时的海盗们每有所猎获的时候,就要由海盗头头出面,大宴群盗,以示庆贺。但海盗们不熟悉也不习惯当时中西欧吃西餐的繁文缛节,于是便独出心裁,发明了这种自己到餐台上自选、自取食品及饮料的吃法。以后的西餐业者将其文明、规范化,并丰富了吃食的内容,就成了今日的自助餐。很多西方专业自助餐厅现在还冠以"海盗餐厅"的名字,缘由如此。今天我们——     

医院推出“自助餐”:选医选药自己来

我们在想起医院的时候,总会联想到“白衣天使”、“救死扶伤”这些神圣而充满温馨的名词。对于患者,医生就是希望,医院就是寻求健康的天堂。但事实并不尽然。我们有些医生,有些医院,对患者不负责任,开错方、配错药的事情屡屡发生。在医患矛盾越来越突出的情况下,为保护人民健康,维护人民的合法权益,国家卫生部和国     

警惕自助餐里的健康风险

从街边餐馆到高端酒店,自助餐这一饮食方式因菜品种类丰富、性价比高等优势而日益受宠,有的网红自助餐厅甚至一桌难求.由于按人收费,食物自取自选,很多人觉得弓着身子扶墙进,挺着肚皮扶墙出才是吃自助餐的正确姿态,否则就亏了.但实际上,自助餐除了会让人暴饮暴食,还有很多其他健康风险.     

精致的女人不会老

女人过了30岁。就过了如花的季节，漂亮就像是握在手里的沙。攥的越紧从指缝中流失的就越快。但是有了一把年纪，也有了底蕴和魅力，从内而外散发出来的成熟气息，是小女孩儿那种绢花似的漂亮所不及的。拴不住漂亮，就要力争做个精致的女人，精致而不老的女人自然会引来倾慕的目光!     

慢阻肺的康复"自助餐"(下)

上期我们着重介绍了慢性阻塞性肺病(简称慢阻肺)的诊疗常识和患者在生活上的一些注意事项。本期继续为您介绍慢阻肺的康复锻炼方法……     

慢阻肺的"康复自助餐"(上)

经过漫长冬春季的考验,慢性阻塞性肺病(简称慢阻肺)患者终于迎来了宝贵的夏季。在夏季,慢阻肺患者一般不容易着凉犯病,临床症状也有所缓解,是进行康复治疗的黄金季节。在这段远离医生、相对轻松的时间里,患者完全可以通过学习相关知识,自己完成慢阻肺的康复治疗。     

重庆：“国”“民”两极化

国有药品零售企业已取得压倒性胜利，而民营企业的市场占有率及品牌影响力都渐趋式微。     

治疗帕金森病新药:腺苷A_(2A)受体拮抗剂

腺苷A2A受体在基底神经节选择性表达并与运动行为有关。流行病学研究和实验室研究均表明阻断腺苷A2A受体能减轻多巴胺能神经元的退行性病变。腺苷A2A受体拮抗剂在改善PD症状的同时还能减缓疾病的进程。因此,腺苷A2A受体拮抗剂很可能成为治疗PD的新药物。     

SCH 58261: A selective A2A adenosine receptor antagonists

The recent discovery of selective antagonists for the A_2A adenosine receptors has been of great help to further research in this field. One compound, SCH 58261, 5- amino-7-(β-phenylethyl)-2-(8-furyl)pyrazolo[4,3-e]-1,2,4-triazolo[1,5-c]pyrimidine, is playing a key part in a variety of studies. This review describes its pharmacological characteristics as they are emerging in various laboratories. The compound has an affinity in the low nM range (Ki value of 1–2 nM) for A_2A receptors located on membranes from a variety of tissues and cell types, including rat and bovine brain striatum, human platelets, lymphocytes and neutrophils, porcine coronary arteries, and CHO cells transfected with the cloned human A_2A receptors. SCH 58261 has little or no affinity up to the μM range for adenosine A_2B, A₃, or other G protein-coupled receptors. Selectivity for A_2A vs. A₁ receptors varies from 53- to 750-fold, depending on membranes or type of assay. SCH 58261 blocks A_2A-receptor mediated increase of cyclic AMP formation with high potency (e.g., IC₅₀ values between 15 and 20 nM in human white blood cells). The tritiated form of SCH 58261 specifically labels A_2A receptors in discrete regions of the rat brain such as caudate-putamen, nucleus accumbens, and tuberculum olfactorium. In classic in vitro bioassays, such as A_2A-receptor-mediated vasodilation in coronary arteries, SCH 58261 displays competitive antagonistic properties (e.g., pA₂ value of 9.5 in porcine coronary arteries). In assays involving responses mediated by A₁ or A_2B receptors, SCH 58261 shows little or no activity up to concentrations about 100-fold higher than those affecting A_2A receptors (higher concentrations not being testable due to its poor water solubility). In the rat, SCH 58261 enhances locomotor activity (at 3.7 mg/kg ip), increases wakefulness (10 mg/kg ip) and slightly increases both blood pressure and heart rate (10 mg/kg ip). These activities appear to be specifically mediated by A_2A receptors since the drug counteracts the effect of A_2A receptor agonists in some experimental paradigms. In models mimicking CNS disorders, SCH 58261 potentiates the activity of L-DOPA or dopamine receptor agonists in the 6-hydroxydopamine-lesioned rat model. Moreover, the compound reduces brain infarct size in a rat model of cerebral ischemia. Altogether, SCH 58261 and its radiolabeled form have emerged as interesting tools for better understanding the function of A_2A receptors in physiological or altered conditions. Moreover, the neuroprotective properties of SCH 58261 indicate that drugs of this class have a potential for treatment of brain damage produced by Parkinson's disease or stroke. Drug Dev. Res. 42:63–70, 1997. © 1997 Wiley-Liss, Inc.     

Neurokinin A. A pharmacological study

Discovered in 1983, the decapeptide neurokinin A has been shown to occur in several peripheral organs and to exert a variety of biological effects. In this article, we review the most sensitive and selective in vivo and in vitro tests which have been used in various laboratories to evaluate naturally occurring or synthetic neurokinin A. A comparison of the effects of neurokinin A and those of its mammalian homologues, substance P and neurokinin B as well as those of tachykinins and related peptides is presented in the frame of a study directed toward characterization of neurokinin receptors. Indeed, neurokinin A has been shown to be particularly active on a neurokinin receptor subtype, the NK-2. Structure-activity studies performed with neurokinin A and its fragments as well as with several analogues of both the decapeptide and the heptapeptide NKA(4-10) have brought to the identification of the minimum structure required for activation of NK-2 receptors. Selective agonists for this receptor have been identified, in particular [Nle10]-NKA(4-10) and [beta-Ala8]-NKA(4-10).