地砷病患者部分生化指标的测定

对病区地砷病、非地砷病患者及对照组居民体内的部分生化指标进行了检测。结果表明,地砷病患者血清中的ＧＰＴ活性、ＵＮ和ＳＡ含量明显高于对照组,ＬＤＨ及ＧＳＨＰｘ活性明显降低;病区非地砷病患者ＬＤＨ活性、ＳＡ含量明显升高,ＧＳＨＰｘ活性明显降低,其它各组及各指标与对照组相比无显著差异。相关分析显示,病区病人组及非病人组血中ＳＡ含量与各自尿砷水平呈正相关（ｒ＝０５０,ｒ＝０４６）,ＧＳＨＰｘ与尿砷呈负相关（ｒ＝－０５１,ｒ＝－０４８）。提示,ＳＡ和ＧＳＨＰｘ可作为砷中毒的早期诊断指标。砷可能对接砷居民肝功、肾功产生一定影响。     

Luteolytic effects of DL111-IT in pregnant rats

The present studies were conducted to evaluate the effects of DL111-IT [3-(2-ethyl phenyl)-5-(3-methoxy phenyl)-1H-1,2,4 triazol] on ovaries of pregnant rats. Pregnant rats were i.m. treated with DL111-IT 2.5 mg kg(-1) day(-1) or camellia oleum (vehicle control) 0.2 ml/day from day 6 of pregnancy for 1, 3 or 5 days. Blood and ovaries were collected 24 h after the last injection. Ovarian fresh weight and protein contents, activities of the 3beta-hydroxysteroid dehydrogenase (3beta-HSD) and 20alpha-hydroxysteroid dehydrogenase (20alpha-HSD) in ovaries, and cell apoptosis of corpus luteum (including hematoxylin-eosine stain, in situ 3'-end labeling and nucleosomal banding) were estimated. Compared with that in the control group, ovarian fresh weight declined 11% and 22% after DL111-IT-3 days and -5 days; protein content dropped 29% after 5-day administration. DL111-IT for 3 days provoked a marked decrease of serum progesterone, by 31% of the control; the activity of 3beta-HSD decreased 34.4% after i.m. DL111-IT for 5 days, while that of 20alpha-HSD increased dramatically after only one injection of DL111-IT (P < 0.01). Histological analysis and in situ 3'-end DNA labeling indicated that DL111-IT induced the pyknosis of cells and the formations of apoptotic bodies and intense oligonucleosomes in luteal cells of pregnant rats. The cell apoptosis induced by DL111-IT was further confirmed by evaluation of nucleosomal DNA fragmentation by agarose gel electrophoresis in cultured luteal cells exposed to DL111-IT for 24 h. In conclusion, all results, including shrunken luteal cells, decreased concentration of protein content and serum progesterone, changed activities of 3beta-HSD and 20alpha-HSD and formation of DNA fragments in luteal cells, showed the luteolytic effect of DL111-IT in pregnant rats.     

Long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency—diagnosis,plasma carnitine fractions and management in a further patient

Long-chain 3-hydroxyacyl-coenzyme A dehydrogenase (LCHAD), the third enzyme of the mitochondrial -oxidation pathway, carries out the dehydrogenation of 3-hydroxyacyl-CoA compounds of 12–18 carbon length. To date only nine cases of LCHAD deficiency have been documented. We report a further patient who as a neonate developed non-specific gastro-intestinal symptoms and at 5 months of age cardiomyopathy, recurrent hypoketotic hypoglycaemia and gross alterations of plasma carnitine fractions. Dietary management with medium chain triglycerides led rapidly to clinical improvement. There was a close correlation between the clinical condition, plasma carnitine fractions and cardiac function. At 2 years of age she is developing normally.     

Breast tumor-derived factors stimulate reduction of estrone to estradiol in nonmalignant breast tissue

Summary This study examines the paracrine influence by human breast carcinoma cells (UISO-BCA-1) on nonmalignant breast tissuein vitro. The 17-OH-SDH-mediated reductive pathway (estroneestradiol) was significantly increased in nonmalignant breast tissue coincubated with human breast carcinoma cells, compared to control tissues incubated in the media alone. No influence on the enzyme activity was noticed in coincubated breast cancer cells. Preincubation of breast cancer cells with estradiol (10^–8 M) significantly decreased the enzyme activity in coincubated nonmalignant breast tissue, which was restored to control levels by addition of R5020 (10^–8 M), tamoxifen (10^–6 M), or a combination of both. In nonmalignant tissues incubated in the presence of growth factor TGF, enzyme activity was reduced to between 46% and 76%. No other growth factors (IGF I, IGF II, PDGF) influenced enzyme activity. In nonmalignant tissues incubated with malignant tumor cytosol, enzyme activity was increased in 16% cases, inhibited in 21%, and not significantly changed in 63%.The data from the present study suggest that factors produced by breast carcinoma cells may influence interconversion of estradiol in nonmalignant tissue. In patients, factors produced by malignant tumor mass may have paracrine influence on surrounding nonmalignant breast tissue and, thereby, may influence the estrogen availability to tumor mass.     

3-Hydroxydicarboxylic aciduria due to long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency associated with sudden neonatal death: protective effect of medium-chain triglyceride treatment

Two siblings were found to be affected by longchain 3-hydroxyacyl-CoA dehydrogenase deficiency, one of which died suddenly and unexpectedly on the 3rd day of life suffering from extreme hypoketotic hypoglycaemia. The younger sibling started to have feeding problems, lowered consciousness, and liver dysfunction at the age of 5 months. Her urine contained large amounts of C₆–C₁₄ 3-hydroxydicarboxylic acids and conjugated 3-hydroxyoctanoic acid, as verified by gas chromatography/mass spectrometry. Plasma long-chain acylcarnitine was increased. A clue to the diagnosis was given by the results of a phenylpropionic acid loading test. This revealed small, but significant amounts of conjugated 3-hydroxyphenylpropionic acid (phenylhydracrylic acid) in the patient's urine. Subsequently, the activity of long-chain 3-hydroxyacyl-CoA dehydrogenase was found to be deficient in cultured skin fibroblasts. Based on the findings obtained by a medium-chain triglyceride load, a diet enriched in this type of fat was prescribed. On this regimen the patient started to thrive, signs of cardiomyopathy disappeared, and her liver function normalized.     

Immunocytochemical localization of 11 Beta-hydroxysteroid dehydrogenase in hippocampus and other brain regions of the rat

The dehydrogenase form of 11 β-hydroxysteroid dehydrogenase (11-DH) which catalyzes the oxidation of the biologically active steroid, corticosterone, to its inactive metabolite, 11-dehydrocorticosterone, is found in rat brain. The distribution and localization of 11-DH-like labeling in the rat brain was examined by immunocytochemistry. 11-DH-like immunostaining was found in all subfields of the hippocampus and in many other parts of the brain, including the preoptic area (POA), central nucleus of the amygdala, bed nucleus of the stria terminalis (NIST) and the cerebral cortex. Percentages of 11-DH-positive cells ranged from 10% in the POA and NIST to 50% to 60% in the hippocampus. When combined with neuronal or glial markers, 11-DH-like immunostaining was found to be predominantly localized within neurons, ranging from 10% or less glial labeling in hippocampus, amgydala and cortex to 22% glial labeling in the POA and NIST. Immunostaining was present in both the cytoplasmic and nuclear components of some cells in addition to their projections. In the kidney, 11-DH has been postulated to be a key component in a mechanism by which aldosterone gains access to renal Type I receptors despite the presence of much higher concentrations of glucocorticoids. The present data is consistent with a similar mechanism occurring in at least some parts of the brain, although the hippocampus appears to be an important exception because it does not appear to be differentially responsive to aldosterone in spite of its high 11-DH activity and immunoreactivity. However, the hippocampus is not implicated in neural control of salt appetite and fluid balance, whereas some of the other brain regions like the POA, NIST and amygdala are believed to be involved. Other aspects of 11-DH localization must therefore be examined in future studies, including the co-presence of mineraiocorticoid receptors and 11-DH in the same or adjacent cells and the possible significance of the relatively high glial localization of 11-DH immunoreactivity in the POA and NIST.     

乳酸脱氢酶同工酶“非脱氢酶”效应的鉴定

一组体外循环下行心脏直视手术的患者,在开胸前后的不同时间,分别取静脉血测定乳酸脱氢酶LDH总活性及其同工酶,观察到LDH同工酶电泳谱带的LDH阳极端有一快速移动的新区带,随着手术的进行逐渐消失。经过稳定性试验、改变基质成份试验、双氧水氧化试验、异常带的定位试验及红细胞的溶血试验等,最终证实此异常带为静脉注射大剂量还原性物质VitC(200mg/kg体重)所致的“非脱氢酶”效应。并且进一步做了VitC的体内、外试验以及还原NAD和NBT反应的荧光扫描,认为用荧光扫描方法可在一定程度上防止LDH同工酶测定过程中异常的干扰作用,并为LDH同工酶“非脱氢酶”效应的鉴定提供了一套较完整的试验方法。     

Effects of lead,copper, and zinc on the rat's lactate dehydrogenase in vivo and in vitro

Following subacute intoxication of rats with Pb-, Cu-, and Zn-salts (separately or in mixture) for 5 weeks, the chelating agent D-penicillamine was administered for 3 weeks. In the course of the 3-month experiment, lactate dehydrogenase (LDH) was estimated in serum and in cytoplasmic fraction of the kidney. Pb²⁺ treatment resulted in an increase of LDH activity, Cu²⁺ in a slight decrease, whereas Zn²⁺ had no effect, respectively. Mixture of these metals caused a significant rise in the enzymatic activity. Seven weeks after the stoppage of the administration of toxic substances, altered LDH activity, both in serum and in kidney returned to normal. D-penicillamine treatment was found to accelerate a restoration of the enzyme activity.In the experiments in vitro, Cu²⁺ inhibited significantly the kidney LDH activity, Pb²⁺ and Zn²⁺ being 100- and 400-times less efficient, respectively. Cu²⁺ inhibition was reversed by D-penicillamine, whereas inhibition of LDH by Zn²⁺ or Pb²⁺ was irreversible.     

Comparative patterns of i-antigen expression, F-cell frequency and Hb A2 level in acute myeloid leukemia and in acute lymphoid leukemia

Hb F, Hb A₂ and i-antigen expression were investigated in adulthood acute leukemias. The study of i-antigen expression by immuno-agglutination and immunofluorescence showed that it is preferentially increased among AML patients. A similar result was obtained for F-cell frequency which was often increased in AML, while it was normal in ALL. Hb A₂ level was significantly lower in AML than in ALL. These differences between AML and ALL red cell patterns further suggest that the leukemic clone involves the erythroid lineage in AML but not in ALL.     

HPLC测定心可宁胶囊中原儿茶醛的含量

目的　采用高效液相色谱法测定心可宁胶囊中原儿茶醛的含量。方法　InertsilC1 8柱 (5 μm ,1 5 0mm× 4 .6mm) ;流动相为甲醇 - 0 .0 5mol·L-1 磷酸二氢钾缓冲液 (磷酸调pH 3.0 ) (2 0∶80 ) ;检测波长为 2 80nm。结果　原儿茶醛进样量在 0 .0 5 5 3～2 .2 1 30 μg范围内线性关系良好 (r=0 .9999) ;平均加样回收率为 99.7% (n =9) ;方法精密度RSD =0 .5 0 % (n =6 )。 结论　本方法操作简便、准确、重复性好 ,可作为该制剂中原儿茶醛的含量测定方法