Impairment of schedule-controlled behavior by pre- and postnatal exposure to hexachlorobenzene in rats

 Hexachlorobenzene (HCB) is still frequently found at elevated levels in human adipose tissue and breast milk. As intoxication with HCB causes neurological disturbance in human beings, the purpose of the present study was to examine neurobehavioral functions in rats after pre- and postnatal exposure. Female rats were fed diets with 0, 4, 8, or 16 mg HCB/kg diet. Exposure started 90 days prior to mating and was continued throughout mating, gestation, and lactation. Thereafter, the offspring were given the same diets as their respective mothers. HCB levels were determined in the brain, the liver, and in the adipose tissue from virgin rats, dams, and the offspring. Concentrations on a lipid basis were found to decline in the order adipose>liver>brain. The exposure levels chosen did not cause gross toxic effects in dams or offspring. There were dose-related increases in liver-to-body-weight ratios in exposed dams, but not in unmated females treated alike. Behavioral testing was conducted in the offspring. Examination of open-field activity on PND 21, and of active avoidance learning on PND 90 failed to reveal significant differences between groups. Training of operant behavior started at the age of 150 days in the offspring from the control, the 8-mg group, and the 16-mg group. Animals were trained on a fixed interval schedule of 1 min (FI-1). On this schedule, responses were reinforced by a food pellet every time 1 min had elapsed after the preceding reinforcement. There were dose-dependent reductions in the post-reinforcement pause, e.g. the time between each reinforcement and the first reaction emitted after it. In addition, the index of curvature, which describes the efficiency of performance on the FI-1 schedule, was decreased in a dose-dependent fashion. Received: 12 April 1994 / Accepted: 26 June 1995     

Embolization of nonvariceal portosystemic collaterals in transjugular intrahepatic portosystemic shunts

Percutaneous embolization of large portosystemic collaterals was performed in three patients following placement of a transjugular intrahepatic portosystemic shunt in order to improve hepatopetal portal flow. Improved hepatic portal perfusion was achieved in these cases, thereby theoretically reducing the risk of chronic hepatic encephalopathy.     

Induction of HSP72 in Rat Liver by Chronic Ethanol Consumption Combined with Exercise: Association with the Prevention of Ethanol-Induced Fatty Liver by Exercise

Ethanol-induced fatty liver in rats was attenuated by repeated running exercise, and the protective effect of exercise was associated with the synergistic expression of heat shock proteins (HSP72). Rats were placed in four groups of six. The two ethanol-fed groups of rats received a liquid diet (Lieber-DeCarli formulation) in which 36% of the calories were derived from ethanol. One group remained sedentary (S/E), whereas the other was trained to run on a rodent treadmill at a speed of 27 m/min, 1 hr/day, 5 days/week, for 7 weeks (R/E). Two other groups–one exercised as previously mentioned (R/C) and one sedentary (S/C)–received control-liquid diets in which the ethanol was isocalorically substituted with a dextran/maltose mixture. The degree of fatty infiltration in liver sections stained with hematoxylin and eosin was graded on a 0–4 scale and the data analyzed by ANOVA on ranks. Ethanol significantly induced fatty infiltration in the S/E group, whereas fatty infiltration in the livers of the R/E group was not different from the S/C group. Electrophoresis and Western blotting of liver homogenates demonstrated that HSP72 was not expressed in either the S/C or S/E groups and was only slightly expressed in the R/C group. The combination of exercise and ethanol, however, resulted in an elevated expression of HSP72 in the R/E group. The content of HSP73 was unaffected by any treatment.     

Chemical traumatization of adult mouse olfactory epithelium in situ stimulates growth and differentiation of olfactory neurons in vitro

This study demonstrates that ZnSO₄ induced chemical trauma results in an in situ regeneration of the olfactory epithelium which, when maintained in vitro, provides an enriched population of olfactory neurons. Therefore, the ability of the olfactory epithelium to respond to chemical trauma with increased mitotic activity can be used to increase growth of neurons in culture. Tissue obtained from normal or vehicle-treated adult mice produced few olfactory neurons, when maintained in culture, compared to cultures established from tissue following an in situ ZnSO₄ trauma. Maximal neuronal yields were obtained in cultures established from tissue that was removed 4–6 days following chemical trauma. The morphological appearance and the presence of cell specific intermediate filament proteins were used to classify the cell types in these olfactory epithelial cultures. Single cells and aggregates of cells which were immunopositive for keratin, but immunonegative for neurofilament protein and GFAP, were identified as epithelioid. Flattened polygonal cells immunopositive for GFAP were identified as glia. A small population of flattened cells was immunonegative for all of the antibodies used in this study. Cells that had processes were immunonegative for GFAP and keratin. Some were immunopositive for 200 kDa and 160 kDa neurofilament proteins but immunonegative for the 68 kDa neurofilament protein. A few of these cells showed positive immunoreactivity with the olfactory marker protein (OMP) antibody and most likely represented the most mature olfactory neurons in the cultures. This trauma-induced culture model using olfactory tissue from adult mice can serve as a source of CNS neurons for comparison with cultured embryonic neurons.     

血清Ⅲ型原胶原含量与肝纤维化的关系（附102例肝活检分析）

为进一步研究血清Ⅲ型原胶原（ＰＣⅢ）含量与肝纤维化的关系，对肝炎患者血清ＰＣⅢ含量与肝炎组织学变化进行对比分析．方法：用ＲＩＡ法测定６１６例急、慢性肝炎及肝硬化患者的血清ＰＣⅢ含量，其中１０２例同时做肝活检，按照Ｋｎｏｄｅｌｌ肝组织炎症活动性指数标准记分．结果：急、慢性肝炎及肝硬化患者血清ＰＣⅢ含量明显高于正常人，差异有显著性（Ｐ＜ｏ．０５～０．０１）．其升高的血清ＰＣⅢ含量与肝细胞坏死范围及门管区炎症程度无相关性（ｒ＝０．４９４，Ｐ＞０．０５），而与肝纤维化程度呈正相关（ｒ＝０．６６８，Ｐ＜０．０１）．结论：血清ＰＣⅢ测定是判断慢性肝炎及肝硬化时肝纤维化程度的有用指标．     

肝阳上亢证甲皱微循环观察与分析

以我所统一标准,确诊为“肝阳上亢证”者,进行微循环观察,肝阳上亢证者90例;阴虚阳上亢证者88例,健康对照组48例。观察发现肝阳上亢组与健康对照组及阴虚阳亢组与健康对照组均有显著性差异。通过卡方证明本检测数据可靠,微循环观测可作为“肝阳上亢证”的客观检测指标之一。     

成人斯蒂尔病的肝损害

目的；探讨成人斯蒂尔病（adult-onset Stil's disease,AOSD))合并肝损害的发生、表现、治疗和预后。方法；对27例成人斯蒂尔病患者中出现肝损害的13例，根据病情轻重采用中药水剂茵陈蒿汤中味或益肝灵片加服联苯双酯滴丸、强力宁注射液进行治疗。结果：11例（84.6%）肝功能恢复正常，1例好转，1例因急性肝功能衰竭死亡。结论：成人斯蒂尔病患者合并肝损害甚为常见。经中药和西药联合应用合理治疗后多数患者可恢复或好转。应重视和警惕发生危及生命和急性肝功能衰竭。     

金丹肝泰1号对大鼠急性肝损伤防治作用的实验研究

用D-氨基半乳糖（D-GaIN）制备大鼠急性肝损伤模型。方法：检测血清丙氨酸氨基转氨酶（ALT）和血清天门冬氨酸氨基转氨酶（AST）的活性，观察光镜下肝组织的病理学改变，探讨对急性肝损伤的保护作用。结果：口服浸膏可显降低急性肝损伤大鼠血清ALT和AST水平，减轻肝细胞的变性坏死，其作用强度与肝炎宁相当，但弱于联苯双酯。     

Research review: DNA polymerases as molecular markers of the regenerating capacity of hepatocytes

Hepatocyte regeneration has been widely investigated, with the mitotic index and the incorporation of [³H]thymidine being used as regeneration markers. We focused on the induction of DNA replication enzymes, particularly DNA polymerases (pol) α, δ, and ε. Using rat models, we have shown that the activity of pol α in crude liver extract well represents the regenerating capacity of hepatocytes. Using pol α as an indicator, we analyzed liver regeneration in rat models under various conditions: obstructive jaundice, external or internal biliary drainage, and the obstruction of portal vein branches. It has been revealed that the ligation of the common bile duct alone induces a certain amount of hepatocyte proliferation. It was striking that external biliary drainage suppressed regeneration capacity in cholestatic rat liver after partial hepatectomy. The strong regeneration in nonligated lobes induced by portal branch ligation was similar to the liver regeneration seen after partial hepatectomy with respect to the induction of DNA polymerases. Taken together, the aspects of DNA replication, particularly the induction of DNA polymerases, may contribute to shedding new light on the regeneration of human liver. This work was supported in part by a Grant-in-Aid for General Scientific Research and for Cancer Research from the Ministry of Education, Science and Culture, Japan, and by grants from the Uehara Memorial Foundation