红细胞同工酶ADA－EAP一AK_1同步电泳分型方法的建立

综合、改良了分别分型的方法，建立了红细胞同工酶ＡＤＡ一ＥＡＰ一ＡＫ１同步电泳分型方法，为ＡＤＡ，ＥＡＰ和ＡＫ１３种红细胞同工酶在法医学鉴定中更广泛的应用，提供了一种可靠、经济、实用的方法。     

丙帕锗的制备及分析

目的 探索合成条件，制备体内活性和稳定性好的高聚物丙帕锗．并分析其结构确定目的物的正确性。方法 以GeO2为起始原料，磷酸二氢钠为还原剂,制备3-氧锗丙烯酸低分子量聚合物和高分子量3-氧锗丙烯酸(丙帕锗)，并进行元素、红外光谱、核磁共振和X-射线的分析。结果 高分子量聚合物生成，在320℃以下不分解，终产率为72．9％。结论 所采用的方法可行，合成的产品结构正确。     

Impact of early dietary gamma-linolenic acid supplementation on atopic eczema in infancy

Polyunsaturated fatty acids (PUFAs) are components of cell membranes and may play an immunomodulating role in the pathogenesis of atopic dermatitis (AD). The goal was to determine the impact of PUFAs on AD by dietary supplementation of infants. Based on the parents' decision on their babies' primary feeding, mothers and newborns were randomized to the supplementation with gamma-linolenic acid (GLA) or placebo for up to 6 months. Breastfed infants received GLA by supplementing their mothers. Formula diet was commercial whey hydrolysate unsupplemented with PUFAs. Of 131 eligible infants, 24 developed AD within the first year of life. Of these, nine belonged to the exclusively breastfed group (n = 58), 14 to the combined-fed group (n = 53), and one to the never breastfed group (n = 20). We could not find an influence of GLA on the development of AD. In subjects with AD, at 1 yr of age the serum-immunoglobulin E (IgE) was the lowest in the GLA-supplemented group A-subjects. In the GLA-supplemented group, GLA-levels in breast milk were similar in atopic and non-atopic infants. In the non-supplemented group the GLA-content of breast milk was 0.07% of total fatty acids in atopic infants vs. 0.17% in non-atopic infants (p < 0.01). Dietary GLA-supplementation could not prevent AD. Interestingly, the number of infants developing AD was the lowest in never breastfed children. In infants suffering from AD, GLA-supplementation seemed to reduce total IgE in the first year of life.     

Toluene vapor exposure and urinary excretion of hippuric acid among workers in China.

A factory survey was conducted in three provinces in China from 1985 to 1989. The time-weighted average toluene concentrations in breathing zone air were monitored by diffusive sampling, whereas hippuric acid (HA) concentrations in shift-end urine samples were measured by high performance liquid chromatography (HPLC). Exposed workers (456 men and women) were those for whom toluene (up to 548 ppm toluene) accounted for greater than or equal to 90% of total exposure (by vapor concentration in ppm), whereas 517 nonexposed controls were recruited from the same factories or from factories of the same region. There was a linear correlation between the intensity of toluene exposure and HA concentration in the shift-end urine. Comparison of the results with findings in the literature shows that the toluene-induced increase in urinary HA concentration among workers in China is significantly smaller than the published values, whereas HA concentrations in urine samples from nonexposed controls are comparable to the levels previously reported.     

格林—巴利综合症血清唾液酸、磷脂、胆固醇的测定及其临床意义

本文应用硫代巴比妥酸(TBA)法对34例格林—巴利综合征(GBS)患者51次血清唾液酸(SA)测定。结果显示:患者血清SA含量显著高于50例对照组,血清SA阳性率亦显著高于对照组;GBS患者四肢肌力与血清SA呈负相关;以重型GBS血清SA含量显著高于轻型,病程初期高于患病后期;血清磷脂含量GBS明显高于对照组,而血清胆固醇两组变化无显著性意义。本文提示GBS血清SA含量变化能够反映周围神经损伤的程度。     

Inhibition of glutamate release in rat hippocampus by kynurenic acid does not protect CA1 cells from forebrain ischemia

We assessed the effect of a broad spectrum glutamatergic receptor antagonist, kynurenic acid (500 mg/kg) on ischemia-induced hippocampal glutamate release and neuronal damage. Kynurenic acid significantly decreased glutamate release during ischemia but had no effect on the hippocampal lesion. Some protection was observed in the cortex and in the striatum. These data suggested that the extracellular accumulation of glutamate during forebrain ischemia does not play a major role in the hippocampus.     

Developmental changes of glutamate acid decarboxylase 67 in mouse brain after hypoxia ischemia

Objective To study the developmental changes of glutamic acid decarboxylase-67 (GAD-67, a GABA synthetic enzyme) in normal and hypoxic ischemic (HI) brain. Methods C57/BL6 mice on postnatal day (P) 5, 9, 21 and 60, corresponding developmentally to premature, term, juvenile and adult human brain were investigated by using both Western blot and immunohistochemistry methods either in normal condition or after hypoxic ischemic insult. Results The immunoreactivity of GAD67 was up regulated with brain development and significant difference was seen between mature (P21, P60) and immature (P5, P9) brain. GAD67 immunoreactivity decreased in the ipsilateral hemisphere in all the ages after hypoxia ischemia (HI) insult, but, significant decrease was only seen in the immature brain. Double labeling of GAD67 and cell death marker, TUNEL, in the cortex at 8h post-HI in the P9 mice showed that (15.6±7.0)% TUNEL positive cells were GAD67 positive which was higher than that of P60 mice. Conclusion These data suggest that GABAergic neurons in immature brain were more vulnerable to HI insult than that of mature brain.     

Effects of immobilization stress on hippocampal monoamine release: Modification by mivazerol, a new α2-adrenoceptor agonist

Mivazerol is a new and selective α₂-adrenoceptor agonist which has demonstrated anti-ischemic effects, both in animals and in patients with myocardial ischemia. In the present study, mivazerol was evaluated for its ability to inhibit the release of catecholamines and serotonin (5-HT) in the hippocampus of freely moving rats, and also was compared to clonidine. In vivo microdialysis in combination with high-performance liquid chromatography (HPLC) was employed. Intravenous administration of mivazerol (8.0 μg/kg) had no effect on basal outflow of norepinephrine (NE), dopamine (DA) and 3,4-dihydroxyphenylacetic acid (DOPAC). In contrast, clonidine (8.5 μg/kg, i.v.) attenuated the basal release of DOPAC, which has been proposed to reflect NE biosynthesis, suggesting that clonidine has an inhibitory effect on NE synthesis. In addition, both mivazerol and clonidine decreased the spontaneous release of 5-HT, which provided further evidence that α₂-adrenoceptors in the hippocampus modulate 5-HT. Sixty-min immobilization stress significantly increased the release of NE (177 ± 28%), DA (209 ± 46%) and DOPAC (337 ± 72%). Mivazerol (2.5, 8.0 and 25 μg/kg, i.v.) completely prevented the immobilization stress-induced enhancement of NE, DA and DOPAC, which was equi-effective to clonidine at a dose of 8.5 gmg/kg, i.v. These findings demonstrate that mivazerol has a profound modulatory effect on stress-induced neurotransmitter release in the hippocampus, at dose levels reported to protect against myocardial ischemia.     

茶碱和双丁酰-cAMP对巨噬细胞水解酶影响的细胞化学观察

本文通过细胞体外培养,细胞化学定量分析等方法,观察了茶碱和双丁酰-cAMP对C_(57)BL/6J小鼠腹腔巨噬细胞酸性磷酸酶、α-醋酸萘酚酯酶的作用和影响.卡介苗活化的巨噬细胞与固有巨噬细胞相比,其酸性磷酸酶、α-醋酸萘酚酯酶活性明显升高.卡介苗活化的巨噬细胞在茶碱或双丁酰-cAMP作用下。酸性磷酸酶、α-醋酸萘酚酯酶活性明显受到抑制.茶碱或双丁酰-cAMP对固有巨噬细胞的酸性磷酸酶、α-醋酸萘酚酯酶无抑制作用.     

Ascorbic acid (vitamin C) modulates the mutagenic effects produced by an alkylating agent in vivo

Recent reports suggest that ascorbic acid (vitamin C) inhibits tumorigenesis as well as exerts a protective effect against mutagenesis in vitro; however, there is no information on its ability to affect gene mutations induced in vivo. In this study, we have investigated the antimutagenic effects of ascorbic acid on the frequency of 6-thioguanine-resistant (6-TGr) T-lymphocytes produced in Fischer 344 rats dosed with the direct-acting alkylating agent, N-ethyl-N-nitrosourea (ENU). The freqeuncy of 6-TG^r T-lymphocytes from the spleen measured five weeks after ENU treatment indicated that ENU produced a substantial mutagenic response. Pretreatment and/or post-treatment of rats with ascorbic acid administered in the drinking water appeared to inhibit the response, but the inhibition was statistically significant only when data from the various dosing schedules were pooled. In addition, there was no clear dose-dependency to the inhibitory effect of ascorbic acid. To further evaluate the time effects of the vitamin supplement on ENU mutagenicity, rats were exposed to the mutagen together with ascorbic acid, which was given continuously for the entire duration of the experiment. At specific times after ENU treatment, the frequency of 6-TG^r T-cells was determined in lymphocytes isolated from the spleen and the thymus. Time-dependent increases in the frequency of 6-TG^r T-cells were observed with ENU treatment; ascorbic acid significantly reduced the ENU-mediated mutagenic responses, most dramatically in the spleen at weeks 6 and 8 (P < 0.0001), and to a lesser extent in the thymus (P < 0.01 at week 6 and P < 0.006 at week 8). Our data suggest that ascorbic acid intake affects the in vivo mutagenicity of ENU, a direct-acting mutagen/carcinogen, and that the reported inhibitory effects of the antioxidant on carcinogenesis may be partially mediated by its effects on mutagenesis. Although it is difficult to extrapolate from rodent studies to humans, the results presented suggest an explanation for epidemiological data that link vitamin C ingestion with decreased cancer risk. © 1994 Wiley-Liss, Inc.