Synthesis of 2‐[18F]fluoroadenosine (2‐[18F]FAD) as potential radiotracer for studying malignancies by PET

2‐[¹⁸F]fluoroadenosine (2‐[¹⁸F]FAD), a potential radioligand for assessment of adenylate metabolism, was synthesized by carrier‐added and no‐carrier‐added procedures via nucleophilic radiofluorination of 2‐fluoroadenosine and 2‐iodoadenosine. The radiochemical yield, specific radioactivity and radiochemical purity of carrier‐added and no‐carrier‐added 2‐[¹⁸F]FAD were 5%, 22–30 mCi/µmol and 99%, and 0.5%, 1200–1700 mCi/µmol and 99%, respectively. Copyright © 2006 John Wiley & Sons, Ltd.     

回肠Ｎａ+/胆汁酸转运体抑制剂SC-435对豚鼠胃肠移行性复合波的作用

目的：研究回肠Na+/胆酸转运体( IBAT)抑制剂SC-435喂养后，豚鼠胃肠移行性复合波(MMC)与胆酸池大小的变化。方法：60只豚鼠分别给予正常饮食和IBAT抑制剂SC-435饮食2周、4周、8周。喂养结束后，评估胆囊动力并将4对电极植入胃窦、12指肠、空肠、回肠。7d后，记录MMC并测量胆酸池大小。结果：IBAT抑制剂喂养后，胆囊动力在4周与8周组下降。胆酸池在4周组减小17.11% (P<0.05)，8周组减小48.35%(P<0.05)。MMC起源部位发生改变：胃窦起源(37%)和十二指肠起源(46%)减少而空肠起源(17%)增多。与对照组相比，MMC周期延长(4周组1.16倍,P<0.05; 8周组1.38倍,P<0.05)而波幅降低 (4周组降低10.58%,P<0.05; 8周组降低49.17 %,P<0.05)。在对照组与2周组之间，所有MMC参数无统计学意义差异。结论：IBAT抑制剂 SC-435减小胆酸池并抑制MMC运动； MMC与胆酸肠肝循环有关，与胆酸池大小改变一致。     

巩膜潜池式小梁切除术

目的探讨巩膜潜池式小梁切除术的疗效。方法手术显微镜下作以穹隆部为底的结膜瓣和5mm×5mm、1/3巩膜厚度的浅层巩膜瓣。再作边长各3mm的等边三角形,厚1/3的中层巩膜切除。作小梁切除。虹膜根切。巩膜瓣固定。球结膜瓣缝合。术毕枣核形棉球加压包扎。结果76例(92眼)近期眼压均≤21mmHg。远期随访35例(38眼),眼压≤21mmHg36眼,>21mmHg2眼。结论巩膜潜池式小梁切除术降眼压效果确切,并发症少。     

催化-臭氧在游泳池水质处理的应用

目的:建立一种用催化-臭氧方法氧化游泳池水中尿素,以使得游泳池水中的尿素、细菌总数、大肠菌群指标符合国家标准。方法:用不同的方法,如改性沸石过滤试验;加氯试验;臭氧氧化试验;臭氧加入催化剂(催化剂为硫酸铜或五氧化二矾)等试验观察尿素的去除效果。结果:催化-臭氧方法去除尿素效果最好,臭氧加入以硫酸铜为催化剂的催化方法尿素去除率为76.3%,臭氧加入以五氧化二矾为催化剂的催化方法尿素去除率为76.8%,高浓度氯(有效氯含量5.0 mg/L)消毒剂效果次之,去除率为46.1%。结论:理想的去除游泳池水尿素及杀灭细菌的有效方法为臭氧发生器连接游泳池本身的循环水处理系统。     

硒的化学形式对人血中含硒组分的影响

在低膳食硒地区的农村,对健康男性受试者进行了为期一年的补硒干预试验。所有受试者每天服硒200μg,以硒酸钠或硒蛋氨酸形式供给。血样分析结果表明,这两种形式的硒均能有效地提高低硒人体的谷胱甘肽过氧化物酶(GPx)活力,因而在预防克山病工作中可采用较为经济的硒酸钠;但补硒蛋氨酸后可见“富裕”硒进入了红细胞的Hb和血浆的白蛋白中,而补硒酸钠后未见“富裕”硒,因而为提高人体硒营养水平,以补充硒蛋氨酸形式的硒为宜。     

In vitro interactions of agonists and antagonists with beta-adrenergic receptors

Neurotransmitters and hormones mediate their effects through interaction with specific receptors. A complete understanding of the effects of these chemical signals requires detailed knowledge, at the molecular level, of agonist/receptor interactions. It is likely that agonists and antagonists interact with the same site on a receptor. Agonists, however, are by definition different from antagonists in that agonists are responsible for transducing information across the cell membrane, ultimately resulting in a biological response, while antagonists appear to act through passive occupancy of receptors. Implicit in this concept is the idea that these fundamental differences between agonists and antagonists arise from the sequelae induced by agonist-specific interactions with receptors.     

The source of origin of PACAP- and VIP-immunoreactive fibers in the laterodorsal division of the bed nucleus of the stria terminalis in the rat

The bed nucleus of the stria terminalis (BSTL), which is known to be involved in the modulation of stress responses, exhibits a dense network of pituitary adenylate cyclase activating polypeptide (PACAP) and vasoactive intestinal polypeptide (VIP) immunoreactive (ir) fibers. The origin of the PACAP-ir fibers is unknown, and the origin of the VIP-ir fibers remains uncertain. The most important brain regions connected to the BSTL are the amygdaloid nuclei, the paraventricular and ventromedial hypothalamic nuclei, mesencephalic periaqueductal grey, the dorsal and linear raphe nuclei, the parabrachial nucleus, and the dorsal vagal complex. After microinjecting cholera toxin B subunit (CTB) in the BSTL as a retrograde tracer, neurons were double labeled for CTB and PACAP or VIP immunohistochemistry and the cells from which the PACAP- and VIP-ir fiber networks in the BSTL originated were identified. Cholera toxin B subunit labeled and VIP-ir cells were found in the mesencephalic periaqueductal grey and the dorsal and linear raphe nuclei, but no double labeled cells were seen in the amygdaloid nuclei or the hypothalamic region. CTB- and PACAP-ir neurons were observed in the paraventricular nucleus and the dorsal vagal complex. No double labeled perikarya were seen in the parabrachial nucleus or in the amygdaloid nuclei.     

Circadian changes in PACAP type 1 (PAC1) receptor mRNA in the rat suprachiasmatic and supraoptic nuclei

A receptor for pituitary adenylate cyclase activating polypeptide (PACAP), denoted as PAC₁, is expressed in the suprachiasmatic nuclei (SCN). Since the circadian clock demonstrates phase-dependent sensitivity to PACAP, we have used in situ hybridization histochemistry to examine whether PAC₁ mRNA is differentially expressed in the rat SCN across the 24-h cycle. There was a significant variation in PAC₁ mRNA within the SCN and supraoptic nuclei during the light–dark cycle and in constant darkness, with peaks at the middle of both the real and subjective day and night; no significant variation was observed in the cingulate cortex. The results suggest that the phase-dependent actions of PACAP on the clock may involve phase-specific changes in the availability of PAC₁ receptors within the SCN.     

The relative role of dopamine and norepinephrine receptor blockade in the action of antipsychotic drugs: Metoclopramide,thiethylperazine, and molindone as pharmacological tools

The aim of the present studies was to further delineate the role of striatal and limbic dopaminergic versus limbic noradrenergic blockade in the pharmacologic and perhaps therapeutic action of antipsychotic drugs. Metoclopramide shares many properties of antipsychotic neuroleptic drugs, including the production of extrapyramidal side effects, but is not an efficacious antipsychotic agent. This drug was a potent blocker of dopamine (DA) receptors in both striatum and limbic forebrain (comparable in potency to that of chlorpromazine) as evidenced from the increase in homovanillic acid in both brain structures. In contrast, metoclopramide was a weak inhibitor of the norepinephrine (NE) receptor-coupled adenylate cyclase system in the limbic forebrain. Molindone, which is reported not to block DA-sensitive adenylate cyclase, was a potent in vivo blocker of DA receptors in both striatum and limbic forebrain and also inhibited markedly the cyclic AMP response to NE in the limbic forebrain. The phenothiazine derivative, thiethylperazine, was also a potent blocker of DA receptors in both brain areas and displayed an IC₅₀ for NE blockade in the limbic forebrain comparable to that of chlorpromazine. The present results support the view that the ability and potency of drugs to block DA receptors parallels their ability and potency to cause extrapyramidal symptoms in man. Moreover, these results suggest that the blockade of NE receptor-coupled adenylate cyclase systems in brain may be relevant to both the pharmacologic and therapeutic activity of antipsychotic drugs.