磷脂酰肌醇激酶：肌醇磷脂代谢,肿瘤发生及其它

近年的研究已经表明,做为细胞膜结构成份的肌醇磷脂类化合物[包括磷脂酰肌醇(phosphatidylinositol,PI)、磷脂酰肌醇—4—磷酸(Phosphatidylinositol-4-Phosphate,PIP)和磷脂酰肌醇—4,5一二磷酸(Phosphatidylinositol-4,5-bisphosphate,PIP_2)]不仅代谢十分活跃,而且有许多重要的生理功能:PIP_2经肌醇磷脂特异性磷脂酶C(Phosphoinositide-specific     

磷脂酰肌醇特异性磷脂酶C活力的非同位素酶解测定法

作者以磷脂酰肌醇为底物,经特异性磷脂酶C水解后,分离产物二酰基甘油及肌醇一磷酸,再用碱性磷酸酶水解肌醇一磷酸的磷酸单酯键,用高灵敏度的磷测定法测定磷含量,建立了磷脂酰肌醇特异性磷脂酶C活力的非同位素酶解测定法。该法简便易行,C·V=5.8%。     

磷酸肌醇代谢与新的第二信使

<正> 磷酸肌醇是一类酸性磷脂,包括磷脂酰肌醇(Phosphatidylinositol,PI),磷脂酰肌醇-4-磷酸(Phosphatidy-linostol-4-phosphate,PIP)和磷脂酰肌醇-4,5-二磷酸(Phosphalitid-ynositol-4,5-bisphosphate,PIP_2)。它们约占细胞磷脂的8％。众所周知,当激动剂作用于受体后,可激活环化酶系统而产生cAMP作为第二信使。近来发现某些受体激活后,可代谢膜的磷酸肌醇,产生肌醇三磷酸(Inositol-1,4,5trisphosphate,IP_3)和二酰基甘油     

肌醇磷脂代谢与平滑肌收缩

<正> 细胞原生质膜的肌醇磷脂包括磷脂酰肌醇(Phosphatidylinositol,PI)、磷脂酰肌醇4—磷酸酯(phosphatidyi—nositol4-phosPhate,PIP)和磷酯酰肌醇4,5-二磷酸酯(phosphati-dyinositol4,5-bisphosphate,FIP_2)等三种。该三种磷脂约占原生质膜总磷脂的2%～10%左右。其量虽少,但作为第二信使的前体,它们在细胞的信息传递过程中起着极其重要的作用,因此,具有“机能脂质”之称。     

川芎嗪对血小板中肌醇磷脂和2OK蛋白质磷酸化的抑制作用

在Mg~(2+)存在下.用血小板膜与(γ—~(32)P)ATP保温,以观察川芎嗪对~(32)P掺入磷脂和蛋白质的影响,结果表明:血小板膜中存在磷脂酰肌醇(PI)激酶和磷脂酰肌醇—4—磷酸(PIP)激酶,而胞浆中缺乏或极少;ATP促进肌醇磷脂磷酸化;川芎嗪抑制血小板中PIP和20K蛋白质的磷酸化.半数抑制浓度分别为40μmol·L~(-1)和110μmol·L     

流式细胞术对再生障碍性贫血和阵发性睡眠性血红蛋白尿患者行CD55、CD59检测的临床意义

阵发性睡眠性血红蛋白尿(PNH)是一种造血干细胞基因突变的克隆性疾病糖化磷脂酰肌醇锚连蛋白(GPI-AP) 通过糖化磷脂酰肌醇(GPI)锚连到细胞表面,其中衰变加速因子(CD55,DAF)和反应性溶血的膜抑制物(CD59, MIRL)参与调节补体介导的溶膜反应。而CD55、CD59是细胞膜上糖化磷脂酰肌醇(GPI)锚定的细胞表面分子,故异     

大豆磷脂治疗高脂血症的有效剂量及其主要成分

为确定大豆磷脂治疗高脂血症的有效剂量及调血脂的主要成分，将183名高脂血症患者分成4组，每人每天口服：Ⅰ组10g大豆混合磷脂；Ⅱ组5g大豆混合磷脂；Ⅲ组5g磷脂酰胆碱为主要成分的大豆磷脂；Ⅳ组10g磷脂酰肌醇为主要成分的大豆磷脂；各组均服2个月。Ⅱ、Ⅳ组眼药前后血清总胆固醇（TC）、高密度脂蛋白胆固醇（HDL－C）水平无显著变化（P＞0．05），Ⅰ、Ⅲ组TC、甘油三酯（TG）非常显著下降（P＜0．01），HDL－C非常显著上升（P＜0．01）。大豆磷脂治疗高脂血症每天至少需要10g大豆混合磷脂，磷脂中磷脂酰胆碱是调血脂的主要有效成分。     

5′-氯-5′-脱氧腺苷对猪血小板中肌醇磷脂和蛋白质磷酸化的抑制作用(英文)

目的:研究腺苷对血小板中肌醇磷脂和蛋白质磷酸化的影响.方法:在Mg~(2 )和/或Ca~(2 )存在下,用猪血小板膜与[γ-~(32)P]ATP在30℃下保温3 min,测定~(32)P掺入磷脂或蛋白质.结果:5′-氯-5′-脱氧腺苷减少磷脂酰肌醇-4-磷酸和磷脂酰肌醇-4,5-二磷酸的生成[IC_(50)分别为71和75(95％可信限分别为60-85和62-90)μmol·L~(-1)],抑制与ATP呈竞争性,并抑制pleckstrin(C激酶主要底物)和肌球蛋白轻链的磷酸化[IC_(50)分别为75和82(95％可信限分别为62·90和66-102)μmol·L~(-1)].结论:腺苷影响血小板中肌醇磷脂信使通路,这有助于阐明腺苷对血小板活化的抑制作用.     

他视角

INPP4A,可抑制兴奋性神经元死亡 尽管磷酸酶调节3,4,5三磷酸磷脂酰肌醇[PtdIns（3,4,5）P3]的生物学功能已经阐述得较深入,但是其调节与PtdIns（3,4,5）P3密切相关的分子3，4二磷酸磷脂酰肌醇[PtdIns（3，4）P2]的功能却少有了解。     

系统性红斑狼疮的磷脂酶C-γ的致病机制及靶向治疗研究进展

磷脂酶C(PLC)是磷脂酰肌醇信号通路的关键酶。磷脂酰肌醇4,5二磷酸(PIP2)在活化的PLC作用下水解为二酯酰甘油(DAG)和肌醇三磷酸(IP3),这两种第二信使传递细胞外信息给下游效应分子,调节细胞的生命活动。PLC-γ是PLC的一种亚型,主要由蛋白酪氨酸激酶(PTK)激活,包括PLC-γ1与PLC-γ2两个亚型。系统性红斑狼疮(SLE)以对核抗原耐受性缺陷为特征,这与T、B细胞受体信号转导异常有关。SLE中PLC-γ1、γ2表达均增强。酪氨酸激酶在免疫细胞信号通路中起关键作用,现就PLC-γ的生物学功能、活化方式及其在红斑狼疮中的免疫机制以及SLE靶向治疗研究做一综述。     

Degraded and undegraded carrageenans and experimental gastric and duodenal ulceration

The prevention of histamine-induced gastric and duodenal ulceration in the guinea-pig has been examined using a series of undegraded and degraded carrageenans. Undegraded carrageenans were active at lower doses than degraded carrageenans. The high viscosity of the undegraded carrageenans in solution prevented their use in larger doses. Degradation of carrageenan without serious loss of sulphate, gives a product which allows the dose to be increased to an extent that its effect more than offsets the slight loss in activity caused by the degradation. No single feature of carrageenan structure can be related to anti-ulcer activity although degradation, and hence reduction of molecular size, generally reduces activity. Sulphate contents over 30% have little apparent effect on activity; κ-carrageenans were not consistently different in anti-ulcer activity from Λ-carrageenans. This contrasts with the antipeptic activity of carrageenans where κ-carrageenans are less active than their Λ-counter-parts. As with antipeptic activity, the degree of anti-ulcer activity is probably determined by a combination of structural features which includes molecular size and polyanionic properties.     

Affective and Anxiety Disorders and Alcohol and Drug Dependence:

Depression and anxiety frequently coexist in patients with substance use disorders. This clinically-oriented article examiens the relationship between these conditions and emphasizes data showing that substances of abuse can cause signs and symptoms of both depression and anxiety. These substance-related syndromes appear to have a different course and prognosis than uncomplicated, independent anxiety and major depressive disorders, and clinicians should consider the role of alcohol and other drugs in all patients presenting with these complaints. The authors will also outline an approach for diagnosing and managing patients with the combination of a substance use and depressive or anxiety disorder.     

Alcohol and Substance Use and Abuse in Women and Children

No abstract available for this article.     

Excretion and biotransformation of alfentanil and sufentanil in rats and dogs

The excretion and biotransformation of alfentanil (ALF) and sufentanil (SUF), two recent analogues of the synthetic opioid fentanyl, were studied after single iv administration of the tritium-labeled drugs in male rats and dogs. The drugs were almost completely metabolized in the two species, which resulted in a large number of metabolites. The excretion of the metabolites was rapid and exceeded 95% within 4 days, except for that of ALF metabolites in dogs (about 85%). For ALF, excretion of the radioactivity with the urine (73% in rats, about 76% in dogs) exceeded that with the feces. For SUF, excretion of the radioactivity with the urine amounted to 38 and 60% and that with the feces to 62 and 40%, in rats and dogs, respectively. Bile-cannulated rats excreted 68% with the bile within 24 hr after SUF dosing, and about 22% of this biliary radioactivity was subjected to enterohepatic circulation. After an ALF dose, the biliary excretion amounted to 24%, and the enterohepatic circulation was minimal. The main metabolic pathways of the two drugs were the oxidative N-dealkylation at the piperidine nitrogen and at the amide nitrogen, oxidative O-demethylation, aromatic hydroxylation, and the formation of ether glucuronides. N-[4-(Hydroxymethyl)-4-piperidinyl]-N-phenylpropanamide (M6) was the main metabolite of both ALF and SUF in rats. In dogs, the glucuronide of N-(4-hydroxyphenyl)propanamide (M5) was the main metabolite of ALF. After SUF dosing in dogs, N-[4-(methoxymethyl)-4-piperidinyl]-N-phenylpropanamide was more abundant than M5.