可溶性细胞间粘附分子-1在妊娠期高血压疾病中的作用

目的:探讨可溶性细胞间粘附分子-1在妊娠期高血压疾病患者血浆中的变化,为临床诊治提供依据。方法:用ELISA法检测29例妊娠期高血压疾病患者血浆中可溶性细胞间粘附分子-1水平,并与正常妊娠组和正常对照组进行组间比较。结果:子痫前期组、妊娠期高血压组、正常妊娠组晚期及正常对照组的可溶性细胞间粘附分子-1水平分别为1129.82±399.16、794.35±255.57、661.51±301.79及549.23±139.98ng/ml。组间比较,子痫前期组与妊娠期高血压组之间P<0.05,与正常妊娠组晚期及正常对照组之间P<0.001;妊娠期高血压组与正常对照组之间P<0.001;妊娠期高血压组与正常妊娠组晚期相比P>0.05,正常妊娠组3个不同孕龄阶段P>0.05。结论:可溶性细胞间粘附分子-1在妊娠期高血压疾病时显著升高,并随病情的加重而增高,可作为该病诊断和监控的一项指标。     

Macrolide–lincosamide–streptogramin B resistance phenotypes and genotypes among Staphylococcus aureus clinical isolates in Japan

In total, 269 methicillin-resistant Staphylococcus aureus (MRSA) and 434 methicillin-susceptible S. aureus (MSSA) isolates were investigated to determine their macrolide-lincosamide-streptogramin B (MLS(B)) resistance phenotypes and genotypes. The constitutive phenotype (61.3% in MRSA, 1.3% in MSSA) and erm(A) gene predominated among the 261 erythromycin-resistant MRSA isolates, while the inducible phenotype (38.7% in MRSA, 94.0% in MSSA) and erm(C) gene were more prevalent among the 150 erythromycin-resistant MSSA isolates. There was a higher incidence of the MLS(B) inducible phenotype compared with other countries, perhaps because MLS(B) antibiotics are not recommended as first-line agents against S. aureus in Japan.     

丝烈霉素C诱发小白鼠骨髓细胞姐妹染色单体互换和染色体畸变

丝裂霉素C(MMc)诱导的姐妹染色单体互换(SCE)可反映出细胞DMA损伤修复的基本过程。有关MMC诱发活体的SCE研究不多。本实验目的,就是探讨MMC诱发小白鼠骨髓细胞SCE的剂量—效应关系,并对SCE指标与染色体畸变指标,在检测机体DNA损伤上的差异作一比较研究。结果证明,MMC诱发染色体畸变能办远低于诱发SCE的能力,MMC可诱发小白鼠骨髓细胞SCE产生,SCE值随MMC剂量的增加而增加。SCE即使在低剂量诱变剂的作用下也是敏感的。     

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。     

Pharmacological properties of the norepinephrine-induced depolarization of astrocytes in primary culture: evidence for the involvement of an α1-adrenergic receptor

The membrane potentials of astrocytes in primary cultures prepared from neonatal rat cerebral cortices were depolarized by (−)-norepinephrine. The average first response to 10⁻⁵ M (−)-norepinephrine was 24 mV from an average resting potential of −68 mV, and the average for the second response was 14 mV. Thus this process showed marked desensitization. The response was attributed to an activation of an α₁-receptor since it was about 1000 times more sensitive to inhibition by prazosin than to yohimbine or idazoxan. In addition, depolarization was seen to the application of 10⁻⁵ M phenylephrine.     

Axonal transport of dopamine D1 receptors in the rat brain

Binding of a specific dopamine D₁ receptor antagonist,¹²⁵I-SCH 23982, was measured in rat brain sections by quantitative autoradiography at various time intervals, following a knife cut through the striatonigral pathway. Twenty-four hours after lesioning, accumulations of D₁ receptor binding sites were found in sagittal sections both rostral and caudal to the lesion site. No other regions studied (caudate-putamen, nucleus accumbens, olfactory tubercle, and substantia nigra pars reticulata) showed any change in D₁ receptor binding 24h after the lesion. In brain sections obtained 10 days after lesioning, only the substantia nigra pars reticulata had a significant decrease in D₁ receptors ipsilateral to the lesion. These findings suggest the possibility of a presence of bidirectional axonal transport of D₁ receptors in rat striatonigral pathway.     

Influence of continuous infusion of interleukin-1 alpha on the core protein and the core protein fragments of the small proteoglycan decorin in cartilage.

Decorin, a collagen-binding small proteoglycan, is considered to have a specific function in the organization or stability of the collagen network. Therefore, alteration of its molecular properties may be of pathophysiological relevance during the development of cartilage damage. It is shown here that normal cartilage from rabbit knee-joint contains glycosaminoglycan chain-bearing core protein fragments of 39, 23, and 18 kDa, each one amounting to approximately 5-6% of the intact decorin core protein. Continuous infusion of human recombinant interleukin-1 alpha for 14 days (200 ng/day) into a knee-joint led in condylar cartilage to a reduction in the amount of intact core protein from 2 micrograms/mg wet tissue to about 1.1 micrograms/mg. The increase in its quantity found after infusion of heat-inactivated interleukin-1 was not statistically significant. The concentration of all three core protein fragments became reduced to a similar extent as the intact core protein under the influence of the cytokine, and additional fragments were not found. Surprisingly, there was a much smaller response to interleukin-1-treatment in patellar cartilage.     

The effects of A 5-HT1A receptor agonist and antagonist on the 5-hydroxytryptamine release in the central nucleus of the amygdala: a microdialysis study with flesinoxan and WAY 100635

The modulation of extracellular 5-hydroxytryptamine (5-HT) in the central nucleus of the amygdala (CeA) by 5-HT_1A receptors was studied by intracerebral microdialysis in awake and freely moving rats. Local administration of 1 μM tetrodotoxin (TTX), 60 mM K⁺ and perfusion with Ca²⁺-free Ringer containing EGTA confirmed that the major part of dialysate 5-HT levels from the CeA is of neuronal origin. Administration of 300 nM of RU 24969, a 5-HT_1B receptor agonist, through the probe into the CeA decreased dialysate 5-HT levels to 67.2% of the baseline value. Systemic administration of the 5-HT_1A receptor agonists 8-OH-DPAT and flesinoxan dose-dependently decreased 5-HT levels in the CeA. The effect of 0.3 mg/kg of flesinoxan could be completely antagonized by systemic administration of 0.05 mg/kg WAY 100635, a 5-HT_1A receptor antagonist. WAY 100635 alone had only minimal effects at this dose. These data show that a major part of the extracellular 5-HT in the CeA stems from 5-HT neurons and that the amount of 5-HT released into this brain region can be modulated by 5-HT_1A receptors. Received: 11 September 1996 / Accepted: 25 November 1996     

Cytoprotective effect of epidermal growth factor on acid- and pepsininduced damage to rat gastric epithelial cells: Roles of Na+/H+ exchangers

We have previously established a cell damage model, with damage induced by either acid or pepsin treatment for 30 min, involving a rat gastric epithelial cell line (RGM1). In the present study, pretreatment of cells with epidermal growth factor (EGF; 0.1–10ng/mL) or sucralfate (0.1–3 mg/mL) for 4 h prevented such cell damage in a concentration-dependent manner. Protection of cells by these drugs was not affected by pretreatment with indomethacin (10⁻⁵ mol/L) for 4 h. Removal of Na⁻, but not Ca²⁺, from the acidified medium totally abolished the inhibitory effect of EGF, but not that of sucralfate. Genistein (a tyrosine kinase inhibitor) apparently reduced the inhibitory effect of EGF. DNA synthesis by RGM1 cells did not increase when cells were incubated with EGF for 4 h. We conclude that both EGF and sucralfate protect RGM1 cells from acid- and pepsin-induced damage and that the mechanism of protection by EGF against acid-induced damage seems to be via activation of Na⁺/H⁺ exchangers.