The histone H1°/H5 variant and terminal differentiation of cells during development of Xenopus laevis

The maintenance of the differentiated condition is supposed to be associated with the presence of a histone of the H1(0)/H5 subclass. If the H1(0)/H5 variant has an important role in differentiation distinct from that of H1, it should display differential expression in time and position during development. Here we report that this prediction is verified during Xenopus laevis development, in which tadpoles exhibit a very characteristic, developmentally regulated pattern of histone H1(0)/H5 expression that is different for the derivatives of each embryonic germ layer. However, the pattern of appearance of this variant during development does not reflect a simple correlation between its presence and the state of differentiation. Therefore, these results are pertinent to current ideas on differentiation and the involvement of lysine-rich histones in the repression of eukaryotic genes.     

下丘脑外侧区注射TRH对大鼠胃酸分泌的影响

本文采用连续收集胃腔灌流法,观察下丘脑外侧区(LHA)注射促甲状腺激素释放激素(TRH)对大鼠胃酸分泌的影响,并分析TRH在LHA促进胃酸分泌的作用机制。结果表明:(1)LHA注射TRH(1μg)明显地刺激胃酸分泌;(2)预先向LHA注射酚妥拉明(10μg)、美多心安(5μg)及胃泌素抗体1μl(1:640)并不影响TRH的泌酸作用,如预先向LHA注射阿托品(5μg)则可消除TRH的泌酸效应;(3)垂体摘除及肾上腺切除均不影响TRH的泌酸作用;(4)隔下迷走神经切断后,LHA注入TRH的泌酸效应仍然出现,但持续时间显著缩短;腹腔交感神经节摘除后,TRH仍能促进胃酸分泌,但分泌量少而平稳。以上结果提示:LHA是TRH中枢泌酸效应的有关结构之一,其中枢机制是通过胆碱能M受体中介的,腹腔交感神经节和膈下迷走神经是TRH泌酸效应的传出途径。前者引起的泌酸反应出现较早且引起泌酸高峰,但持续时间短;后者则引起低平的持续分泌。     

Localization of c-ERB A proteins in rat liver using monoclonal antibodies

Monoclonal antibodies were raised against the nuclear thyroid hormone receptors encoded by c-ERB A genes and against a purified nuclear receptor fraction. These antibodies recognize the c-ERB A protein in nuclear extracts from rat liver and are able to compete with thyroid hormone in Scatchard analyses. In sections of rat liver they react with all the hepatocyte nuclei as well as with the cells of the hepatic bile ducts. Comparison with another putative T3 receptor antibody, described previously, showed that distinct 57 kD proteins with a different cellular distribution were recognized.     

立枯丝核菌蛋白质电泳图谱研究 Ⅰ.融合群与图谱的相关性

用来自日本和美国的立枯丝核菌8个融合群11个类群代表菌株进行可溶性蛋白质电泳,其结果表明,各融合群及亚群之间电泳图谱有显著差异,而同一类群菌株的电泳图谱则相似。分析来源于华东等地已鉴定的融合类群117个菌株的电泳图谱显示,同一融合群内菌株,虽然采集地区、寄主植物或致病力不同,其蛋白质图谱仍十分相似;而不同融合类群的菌株,即使在同一田块中同一种寄主植物上引起相似病害,其图谱也显示出明显差异。本文就上述可溶性蛋白质图谱显示的结果与其它研究者在血清学、DNA同源性.酯酶等生化水平上对融合群的研究结果进行了比较和探讨。     

Early indicators of exocrine pancreas carcinogenesis produced by non-genotoxic agents

In the past 40 years the incidence of pancreatic cancer in many Western countries had increased. Since no single factor responsible for the development of pancreatic cancer has been identified, it is believed that non-genotoxic factors may play an important role in the pathogenesis of this highly fatal form of cancer. Focal abnormalities of acinar cells, referred to as atypical acinar cell foci or nodules, occur spontaneously in rats and some other species. Their incidence increases with age from zero at birth to about 75% in 2-year-old rats. These spontaneous lesions have a phenotype that cannot be distinguished from the putative, atypical preneoplastic, acinar cell foci induced in rat pancreas by the carcinogen azaserine. Unsaturated fat (corn oil) has been found to increase the incidence of atypical acinar cell nodules and adenomas in the pancreas of non-carcinogen-treated rats without influencing the weight of the pancreas. Furthermore, unsaturated fat has a specific promoting effect on the growth potential of atypical acinar cell foci and nodules induced in rat pancreas by azaserine, resulting in an increase in the number and size of these lesions. Rats fed raw soya flour or trypsin inhibitors develop an enlarged pancreas as a result of hypertrophy and hyperplasia. They also develop acidophilic atypical acinar cell foci and nodules, adenomas and adenocarcinomas after being fed full-fat raw soya flour for 2 years. It may be concluded from the observations in rat pancreas that non-genotoxic compounds or conditions that enhance pancreatic growth may be classified as non-genotoxic pancreatic tumour promoters. The observations with corn oil, however, indicate that there may be non-genotoxic compounds that specifically enhance growth of spontaneous initiated atypical acinar cell foci without causing hyperplasia of the pancreas. The possible mechanisms whereby unsaturated fat and trypsin inhibitors exert their effects on exocrine pancreatic carcinogenesis are discussed.     

Effect of the specific cholecystokinin-receptor antagonist loxiglumide on bombesin stimulated pancreatic enzyme secretion in man.

We have investigated the effects of the specific cholecystokinin (CCK) receptor antagonist loxiglumide on basal and bombesin stimulated pancreatic enzyme secretion, bilirubin output and plasma CCK release in six healthy subjects. The data were compared with those obtained in control experiments where saline was infused instead of loxiglumide. Basal amylase output (4.7 +/- 0.8 kU/45 min), trypsin output (2.9 +/- 0.8 kU/45 min) and bilirubin output (7.7 +/- 2.8 mmol/45 min) gradually declined during infusion of loxiglumide to values of 1.3 +/- 0.3 kU/45 min, 0.5 +/- 0.1 kU/45 min and 0.4 +/- 0.0 mmol/45 min, respectively, reaching statistical significance (P less than 0.05) in the 30 to 45-min period after the start of the loxiglumide infusion. In the control experiments saline infusion failed to influence basal amylase, trypsin and bilirubin output, while bombesin stimulated amylase output from 4.7 +/- 0.8 kU/45 min to 25.1 +/- 5.1 kU/45 min (P less than 0.05), trypsin output from 2.9 +/- 0.8 kU/45 min to 11.6 +/- 2.0 kU/45 min (P less than 0.05) and bilirubin output from 7.7 +/- 2.8 mmol/45 min to 68.0 +/- 16.0 mmol/45 min (P less than 0.05). Loxiglumide failed to significantly influence bombesin stimulated amylase output (36.7 +/- 9.0 kU/45 min) and trypsin output (8.3 +/- 2.9 kU/45 min), but almost abolished bilirubin output (9.7 +/- 3.6 mmol/45 min) (P less than 0.05). Basal plasma CCK (2.4 +/- 0.1 pM) was not significantly influenced by loxiglumide (2.4 +/- 0.2 pM).(ABSTRACT TRUNCATED AT 250 WORDS)     

Accumulation of carbamoylphosphate-synthetase and phosphoenolpyruvate-carboxykinase mRNA in embryonic rat hepatocytes. Evidence for translational control during the initial phases of hepatocyte-specific gene expression in vitro

The aim of this study was to establish whether the initial accumulation of hepatocyte-specific proteins after hormone induction is regulated at the pretranslational and/or the translational level. To this end, mRNA molar concentrations were determined and compared with rates of protein synthesis from previous studies [van Roon, M.A., Charles, R. & Lamers, W.H. (1987) Eur. J. Biochem. 165, 229-234]. In vivo, carbamoylphosphate-synthetase mRNA starts to accumulate at day 17 of pregnancy. Phosphoenolpyruvate-carboxykinase mRNA starts to accumulate only just prior to birth. Embryonic day 14 (i.e. 8 days before the expected day of birth), livers were chosen to study the regulation of the initiation of hepatocyte-specific mRNA accumulation in vitro. Accumulation of carbamoylphosphate-synthetase and phosphoenolpyruvate-carboxykinase mRNA is regulated by the same hormones as accumulation of the respective proteins. The rate at which carbamoylphosphate-synthetase and phosphoenolpyruvate-carboxykinase mRNA molecules accumulate in cultured embryonic hepatocytes is relatively low, compared to that of postnatal hepatocytes. However, the increase of the rate of synthesis of carbamoylphosphate-synthetase and phosphoenolpyruvate-carboxykinase protein is even 3-6-fold slower than that of mRNA. This shows that initially mRNAs accumulate intracellularly to a relatively high concentration without being efficiently translated or translatable. Only after the mRNA concentration reaches a plateau of 72 h and 48 h respectively, the cellular capacity to synthesize the respective proteins increases. Therefore, the translational efficiency is certainly one of the major rate-limiting factors of the initial phases of expression of the hepatocyte-specific genes for carbamoylphosphate synthetase and phosphoenolpyruvate carboxykinase.     

Developmental and hormonal regulation of carbamoyl-phosphate synthase gene expression in rat liver: evidence for control mechanisms at different levels in the perinatal period

Carbamoyl-phosphate synthase gene expression is found to be primarily regulated by conditions that enhance hepatic glucocorticosteroid levels (hormone injections) and cyclic AMP levels (induction of diabetes). After birth, changes in the level of carbamoyl-phosphate synthase protein follow changes in the level of carbamoylphosphate synthase mRNA, suggesting a pretranslational control mechanism. In fetal rats, carbamoyl-phosphate synthase gene expression is regulated by the same factors as in adults. However, both the level to which carbamoyl-phosphate synthase mRNA can accumulate and the extent to which mRNA can be translated appear to be limited, indicating control mechanisms at the pretranslational and translational level. Finally, in the immediate postnatal period, a transient but pronounced decrease in the rate of degradation of carbamoyl-phosphate synthase protein may play a role in the accumulation of the enzyme.