Mechanism of toxic action of fluoride in dental fluorosis: whether trimeric G proteins participate in the disturbance of intracellular transport of secretory ameloblast exposed to fluoride

In enamel fluorosis model rats treated with sodium fluoride, secretory ameloblasts of incisor tooth germs exhibited disruption of intracellular trafficking. We examined whether heterotrimeric G proteins participated in the disruption of vesicular trafficking of the secretory ameloblast exposed to fluoride, using immunoblotting and pertussis toxin (IAP)-induced adenosyl diphosphate (ADP)-ribosylation for membrane fractions of the cell. Immunoblotting of crude membranes, post supernatants of the ameloblast, with anti-G_i3/o and anti-G_s antibodies showed that G_i3 or G_o proteins existed in the secretory ameloblast, but G_s protein did not. Immunoblotting of the subcellular membrane fractions indicated that the G_i3 or G_o proteins were located in the Golgi membrane, but were not in the rough endoplasmic reticulum (rER) membrane. Autoradiograph of IAP-induced ADP-ribosylation, however, showed the existence of IAP-sensitive G proteins both in rER and Golgi membranes. Fluoride treatment decreased the G proteins bound to both membranes. These findings indicate that different G proteins, both of which are IAP-sensitive, are present in the rER and Golgi apparatus, and suggest that these G proteins participate in the disturbance of intracellular transport of the secretory ameloblast exposed to fluoride. Received: 24 June 1998 / Accepted: 8 September 1998     

Distribution of metabotropic glutamate receptor mGluR5 immunoreactivity in rat brain

The receptor mGluR5 is a metabotropic glutamate receptor with messenger RNA abundantly present throughout cortex, hippocampus, and caudate/putamen that is also coupled to phosphatidyl inositide hydrolysis and calcium mobilization. In this study, the distribution of mGluR5 was examined in rat brain by immunocytochemistry. The antibody utilized is highly specific and does not cross react with the most closely related other metabotropic glutamate receptor, as determined by Western blot analysis of nonneuronal cells transfected with metabotropic receptor coding sequences. The receptor mGluR5 is widely expressed with the highest density in olfactory bulb, caudate/putamen, lateral septum, cortex, and hippocampus, as confirmed with both immunocytochemistry and Western blot analysis. Electron microscopic studies in hippocampus and cortex indicate that the labeling is mostly on membranes of dendritic spines and shafts. Light and electron microscopic evidence indicates that some mGluR5 immunoreactivity is located in presynaptic axon terminals, suggesting that mGluR5 may function as a presynaptic receptor.     

见于湖南的一例血红蛋白G-台中家系

见于湖南江华县的一例慢泳血红蛋白α链变种,其先证者为汉族青年,属杂合子。家系调查发现其父、大姐和弟均携有同样的异常Hb。血液学常规检查一般正常。除先证者肝在肋缘下0.5cm扪及外,无任何临床症状。经一级结构分析,确证此例为HbG一台中[α74(EF3)Asp→His]。功能观测其氧平衡特征与HbA无差异。这是见于湖南的首例。     

高性能战斗机飞行员离心机高G训练方案

目的制定我国高性能战斗机飞行员离心机高Ｇ训练方案。方法拟定离心机高Ｇ训练方案，对４７名飞行员进行训练，训练后检验训练效果，提出训练方案。结果训练后受试者采用综合抗荷措施时的Ｇ耐力比基础Ｇ耐力高４．３Ｇ～４．７Ｇ，比训练前提高了１．９Ｇ～３．３Ｇ（Ｐ＜０．０１）。结论按本研究提出的高Ｇ训练方案进行训练，可显著提高飞行员的Ｇ耐力，该训练方案有效可行。     

壳聚糖辐射效应的研究（Ⅰ）──辐照剂量与分子量的关系及辐射裂解的G（S）值

通过粘度的测量，考察了壳聚糖在不同条件下经不同剂量γ射线辐照所引起的分子量的变化，并分别计算了真空和空气中壳聚糖辐射裂解的Ｇ（Ｓ）值。     

过氧化氢对白色念珠菌DNA破坏的研究

本文用热变性温度法研究一定浓度 H_2O_2对 C.albicans DNA 破坏作用。结果表明,经6%和10%H_2O_2处理后,C.albicans DNA G c Mol%(分别为28.1±0.82和14.4±1.51)显著低于对照 DNA G C Mol%(85.9±0.62),并推断 H_2O_2可能作用于 C.albicans DNA 碱基以及其间的氢键上;DNA 电泳图谱发现,经3%和6%H_2O_2处理的 C.albicans DNA 电泳带明显不同于对照,提示 H_2O_2更易造成 C.albicans DNA 核苷酸链的降解或断裂.H_2O_2对 C.albicans DNA 的破坏,增强了其杀菌作用。     

Prevalence and mechanism of streptokinase-induced platelet stimulation. Effect of acetylsalicylic acid.

It was recently shown that streptokinase may induce clot formation in vivo by immunoglobulin G mediated platelet stimulation. We evaluated the in vitro effect of streptokinase on platelet function in 103 subjects, of whom 52 were < or = 30 years and 51 were > or = 50 years old. Although streptokinase inhibited platelet aggregation in the majority of cases, in nine the threshold concentration of ADP required to induce irreversible aggregation decreased with streptokinase (1 million Units. l-1) by 30% or more. This observation was confirmed in five of the nine by repeated measurements indicating reproducible streptokinase-induced platelet stimulation. Among the five, two were < or = 30, and three were > or = 50 years old. In none of the five subjects did the radio allergo sorbent test detect type E immunoglobulins directed against streptokinase in the serum. In contrast, in four of the five subjects, streptokinase-induced platelet hyperaggregability was suppressed by addition of goat antibodies against human immunoglobulin G, or F(ab')2-fragments of such antibodies. Acetylsalicylic acid did not prevent streptokinase-induced platelet stimulation, but in three of five cases, led to an increase in the control threshold concentration for ADP, so that after the decrease induced by streptokinase the threshold concentration for ADP was in the same range as before acetylsalicylic acid and streptokinase administration. Thus, streptokinase led to an inhibition of platelet aggregation in the majority of subjects evaluated. In a minority of five out of 103, however, streptokinase reproducibly caused platelet stimulation, presumably mediated by immunoglobulin G.(ABSTRACT TRUNCATED AT 250 WORDS)     

Accentuated antagonism by angiotensin II on guinea-pig cardiac L-type Ca-currents enhanced by β-adrenergic stimulation

 To examine mechanism(s) underlying the accentuated antagonism by angiotensin II (A-II) on twitch tension, we recorded L-type Ca²⁺ currents (I _Ca,L) using conventional patch-clamp techniques in single, guinea-pig, ventricular myocytes. I _Ca,L was recorded by a step-pulse protocol after eliminating K⁺ conductances (internal Cs⁺ plus tetraethylammonium chloride and K⁺-free extracellular solution). A-II (100 nM) did not affect basal I _Ca,L, but inhibited I _Ca,L that had been enhanced (approximately 200% of control) by (ISO, isoproterenol 100 nM). The inhibitory action of A-II was concentration dependent (concentration eliciting 50% inhibition 88±9 pM, n=41) and the ISO-enhanced component of I _Ca,L was completely blocked by A-II at concentrations above 10 nM. CV-11974 (500 nM), an A-II type-1 receptor (AT₁) antagonist, prevented the inhibitory action of A-II. Pre-incubation with pertussis toxin (PTX) abolished the inhibitory effect of A-II. A-II also inhibited the I _Ca,L enhanced by histamine (500 nM) and forskolin (1 μM), but failed to affect I _Ca,L enhanced by intracellular cyclic adenosine monophosphate (1 mM). The inhibitory action of A-II may therefore involve AT₁ receptors/PTX-sensitive, guanine nucleotide-binding (G) proteins (Gi)/adenylate cyclase and partially explains the A-II-dependent accentuated antagonism of inotropy.     

中国汉族人VKORC1 G3673A基因多态性研究

目的检测汉族人VKORC1 G3673A基因的分布情况。方法应用PCR技术对正常人外周血VKO-RC1 G3673A基因进行扩增,以Msp I进行限制性酶切图谱分析。结果219名（男112人,女107人）中国汉族人VKORC1 G3673A基因中,表现型A/A的频率是81.3%（男90人,女88人）,表现型G/A是18.7%（男22人,女19人）,表现型G/G是0。VKORC1 G3673A基因A的频率是90.6%,基因G的频率是9.4%。结论中国汉族人VKORC1 G3673A基因的分布有自己的特点,为研究VKORC1 G3673A基因在华法林个体化给药方案的制定提供了可靠的理论资料。     

The Effects of Serum from Patients with Acute Liver Failure on the Growth and Metabolism of Hep G2 Cells

In many bioartificial liver systems currently being designed and evaluated for use in fulminant hepatic failure, direct contact is required between the patient's blood and the liver cells in the device. The efficacy of such devices will be influenced by the interaction of fulminant hepatic failure (FHF) patient serum with the cells. We have found that FHF serum inhibits the growth rate and the synthesis of DNA, RNA, and protein; disturbs glutathione homeostasis; and induces morphological changes in cultured human Hep G2 cells. These interactions should influence the design of bioartificial liver devices based on proliferating cell lines and indicate the requirement to pretreat FHF patient plasma to reduce the toxin load.