麝鼠泌香期香囊腺形态及组织结构的研究

麝鼠香囊腺由腺细胞、支持细胞和排香管组成。其分泌腺属复管泡状腺。发育初期的腺泡胞质内含有大量的粗面内质同、光滑内质网、高尔基复合体、中心粒和线粒体、香腺细胞间连接发达,桥粒、半桥粒广为分布。胞质内含有电子致密度高和电子致密度低的两种分泌颗粒。其分泌方式为顶浆分泌。     

长江华溪蟹纳精囊超微结构的研究

利用电镜技术,对长江华溪蟹的纳精囊进行了研究。结果表明:在纳精囊上皮的顶分泌型腺细胞中,充满大量高尔基体和粗面内质网的潴泡和囊泡。泡中含有絮状或颗粒状分泌物。潴泡和囊泡先是单独存在,最后聚集在一起,形成大的分泌颗粒后排出囊腔。核糖体比比皆是。线粒体数量较大,作为一种载体参与了分泌物的形成。细胞化学显示,分泌物中含有蛋白质、脂肪和少量糖类。结论:纳精囊上皮的顶分泌型腺细胞具有积极的分泌活动。       

黄颡鱼仔稚鱼胃肠发育的显微和超微结构研究

利用光学显微技术和透射电镜技术,观察和研究了出膜后1-35日龄黄颡鱼(Pelteobagrus fulvidraco)仔稚鱼的胃肠发育.水温为23-25℃时,2日龄仔稚鱼的消化道分化出口咽腔、食道、胃、肠;3日龄肠道分化为前肠、中肠、后肠.3日龄黄颡鱼开口摄食时其胃贲门部黏膜层下出现胃腺,为已有鱼类研究报道中胃腺最早出现的日龄.超微结构显示3日龄胃腺细胞中可见胃蛋白酶原颗粒和丰富的管泡系统,为典型的泌酸胃酶细胞;随日龄增加,胃蛋白酶原颗粒越来越丰富而管泡系统越来越不明显.3日龄时前肠吸收细胞胞质中可见脂肪泡,后肠吸收细胞胞质中可见蛋白质胞饮体.直到25日龄后肠吸收细胞胞质中尚可见蛋白质胞饮体.以七结果表明黄颡鱼在3日龄开口摄食时消化道具备细胞外消化功能,但此功能不完善,期间继续通过胞饮作用等细胞内消化来弥补胞外消化的不足,直到25-30日龄后细胞外消化功能发育完善.采用符合其生理机能发育过程的投喂管理策略可以有效提高大规格苗种培育的成活率.     

分离的泌酸细胞的生理学研究

本文介绍近年来用分离的泌酸细胞,研究组织胺、乙酰胆碱和胃泌素以及组织胺、前列腺素(PG)和环一磷酸腺苷(cAMP)在盐酸分泌过程中的作用及其相互关系的一些设想。(1)组织胺、乙酰胆碱和胃泌素均可直接与泌酸细胞上各自的受体相结合而引起盐酸分泌,它们之间有着相互加强的作用;(2)组织胺通过增加泌酸细胞内的cAMP促进酸的分泌;(3)PG从两个方面对胃粘膜产生保护作用,即对抗依赖于组织胺的cAMP形成和促进另一细胞系统内依赖于PG的cAMP的形成。     

蓖麻蚕前胸腺细胞超微结构的变化与蜕皮激素分泌活动的关系

本研究叙述蓖麻蚕Philosamia cythia ricini四龄及五龄幼虫前胸腺蜕皮激素分泌活动各不同时期所显示的腺细胞超微结构变化。从幼虫蜕皮后至进入眠期之间的腺细胞结构可分为三个时期,(1)不活动期:细胞核呈圆形,核内密布染色质及核仁,细胞质内有结构完整的线粒体、粗面及滑面内质网、核糖体和高尔基氏体;细胞外围的细胞间区内有许多小囊泡及多泡囊。(2)活动期:细胞结构变化为细胞核膜出现内陷、外突,形成波浪形的核周膜;线粒体变形,出现内嵴稀疏的空心线粒体。(3)激素释放期:细胞核变形,形成若干长短不一向外伸出的指状突,有些伸达细胞边缘;其余细胞器退化,其后仅余残缺的高尔基氏体,稀疏的核糖体,线粒体的内崤逐渐消失,成为空腔扩大的及空腔内藏“膜轮”的线粒体,和一些溶解体及大形“膜轮”。     

蓖麻蚕前胸腺细胞超微结构的变化与蜕皮激素分泌活动的关系

本研究叙述蓖麻蚕Philosamia cythia ricini四龄及五龄幼虫前胸腺蜕皮激素分泌活动各不同时期所显示的腺细胞超微结构变化.从幼虫蜕皮后至进入眠期之间的腺细胞结构可分为三个时期,(1)不活动期:细胞核呈圆形,核内密布染色质及核仁,细胞质内有结构完整的线粒体、粗面及滑面内质网、核糖体和高尔基氏体;细胞外围的细胞间区内有许多小囊泡及多泡囊.(2)活动期:细胞结构变化为细胞核膜出现内陷、外突,形成波浪形的核周膜;线粒体变形,出现内嵴稀疏的空心线粒体.(3)激素释放期:细胞核变形,形成若干长短不一向外伸出的指状突,有些伸达细胞边缘;其余细胞器退化,其后仅余残缺的高尔基氏体,稀疏的核糖体,线粒体的内崤逐渐消失,成为空腔扩大的及空腔内藏“膜轮”的线粒体,和一些溶解体及大形“膜轮”.     

小地老虎雄蛾中胚层生殖道和附腺的细胞结构和分泌功能

通过光镜、电镜及组织化学等方法,研究了小地老虎生殖前期雄蛾中胚层生殖道和附腺的腺细胞结构和分泌功能,以及与精子形态和数量变化的关系,结果表明：(1)以缢缩位置、解剖形态、细胞结构、分泌方式、精子形态变化和数量变动为依据,将中胚层生殖道划分为修精囊、输精管、贮精囊、精包腺1～5段等8个区段;(2)中胚层生殖道和附腺具有相同的组织层次,自内向外分为单细胞上皮层、底膜、肌肉层和围膜等4层,但缺少表皮质内膜;(3)中胚层生殖道和附腺的腺细胞具有旺盛的合成和分泌蛋白质的能力,主要有内质网型和液泡型两种,前者有发达的粗面内质网和高尔基体,后者具有致密的核糖体和分泌泡;至少有4种分泌方式：即颗粒顶泌、液泡顶泌、胞质局泌和胞间分泌;修精囊、贮精囊、雄性附腺、精包腺1段的顶泌物为糖蛋白性质(PAS阳性)、局泌物为非糖蛋白性质(PAS阴性)。     

扬子鳄小胃黏膜的组织化学和细胞学

扬子鳄（Alligator sinensis）的小胃是在胃幽门部与十二指肠的交接处由胃幽门括约肌和十二指肠括约肌突入管腔形成的一个小腔,其生理功能一直不清楚。本文采用组织化学、电子显微镜和免疫组织化学技术对扬子鳄小胃黏膜的组织化学成分、细胞超微结构及细胞类型进行了较全面的研究。小胃黏膜上皮PAS反应呈强阳性,AB染色呈弱阳性,主要分泌中性糖蛋白和少量的含硫酸性糖蛋白。电子显微镜下,扬子鳄小胃黏膜上皮主要由表面黏液细胞组成,偶见内分泌细胞。小胃腺部则70％-90％为内分泌细胞,其余为少量的腺黏液细胞和泌酸胃酶细胞。应用7种胃肠激素的抗血清在小胃黏膜中检测出了5-羟色胺（5-HT）、胃泌素（Gas）、胰高血糖素（Glu）、生长抑素（SS）、P-物质（SP）和血管活性肠肽（VIP）细胞,以Glu细胞密度最高,VIP细胞密度最低。未检测到胰多肽（PP）细胞。本研究结果表明,从组织化学成分和细胞类型看,扬子鳄的小胃与胃同源;从细胞超微结构和内分泌细胞所占百分比例看,扬子鳄的小胃已出现了明显的特化,泌酸胃酶细胞中未见泌酸小管,可能没有泌酸功能。内分泌细胞含量丰富,可能在调节胃肠道功能中发挥重要作用[动物学报54（6）：1044—1050,2008]。     

鲤胚胎孵化腺细胞

鲤胚胎孵化腺为单细胞腺体,发生于外胚层,可特异地被PAS染色。最早可在眼色素期检验出孵化腺细胞(Hatching gland cell,HGC)它们主要分布在头部腹面及头部与卵黄囊连接处。开始,HGC位于表皮细胞下面,随发育迁移到胚胎表面。根据扫描和透射电镜观察,在分泌孵化酶的前后,HGC区表面细胞呈鸡冠花状和疣状两种突起。前者系HGC处于分泌孵化酶期间;后者系HGC业已完成分泌作用,由于相邻的表皮细胞活动而形成的。HGC内富有粗面内质网、线粒体、核糖体和高尔基体,并由后者合成酶原颗粒。HGC在完成分泌作用后,仍留在表皮中,以后逐渐退化,但在孵化后30h仍可见残留的HGC。     

中华蜜蜂工蜂蜡腺细胞的超微结构

本文描述了中华蜜蜂(Apis cerana)成体工蜂蜡腺细胞的超微结构.通过电镜观察发现蜡腺细胞具有许多质膜内陷形成的管腔,作为蜂蜡或其前体物的输送通道.细胞质中富含线粒体及粗面内质网,细胞核为不规则的形状,细胞质中还含有少量溶酶体,微管和微丝等结构.     

Histochemical investigations on the secretory cells in the oesophagogastric tract of the Eurasian green toad,Bufo viridis

The secretory cells of the oesophagogastric tract of the Eurasian toad, Bufo viridis, were examined using standard histochemical methods and lectin histochemistry. Two goblet cell types were found in the oesophageal epithelium, differing in their morphology and the histochemical features of the secretory granules. These contained mainly acidic glycoconjugates, both sulphated and carboxylated, and a small amount of pepsinogen. Type I goblet cells contained stable class-III mucosubstances, which were absent in Type II. No pluricellular oesophageal glands were found. The oesophagogastric junction had a superficial epithelium similar to that of the oesophageal epithelium, with alveolar pluricellular glands, secreting stable class-III mucins, and few oxynticopeptic cells. The gastric mucosa presented secretory cells both in the surface epithelium and in the gastric glands. Superficial and foveolar cells produced neutral mucins with Gal1,3GalNAc residues. Neck cells, oxynticopeptic cells and endocrine cells were found in the gastric glands. Neck cells produced stable class-III mucosubstances. A functional gradient was observed in the oxynticopeptic cells from the oral to the aboral fundus, with a decrease in pepsinogen secretion towards the aboral fundus and a possible increase in HCl secretion. In the pyloric mucosa, the oxynticopeptic cells disappeared and the glands produced only neutral mucins, without stable class-III mucosubstances.     

Electron microscopy of the oxynticopeptic cells of the gastric glands and the intestinal glands of the caecum of the guineapig.

Histomorphology of the gastric and intestinal glands was investigated in 19 sexually mature, adult guineapigs by light and transmission electron microscopy. Gastric glands exhibited the cytological characteristics of oxynticopeptic cells capable of both hydrochloric acid (HCl) and pepsinogen secretion. In the literature, occurrence of oxynticopeptic cells in the proventriculus of the domestic fowl (Toner, 1963; Bell & Freeman, 1971) and in the gastric glands of frogs has been reported (Sedar, 1961; Patt & Patt, 1969; Forte & Forte, 1970). It has been claimed by other investigators (Herriot et al., 1938; Long, 1967) that simultaneous secretion of HCl and pepsinogen by a single, not completely differentiated 'pure' cell type, was highly effective for rapid conversion of the zymogen to active enzyme. Under the light microscope with haematoxylin and eosin stain, the protein secreting activity of gastric glands in guineapigs was masked by the HCl secreting activity, thus morphologically resembling the oxyntic cells. Therefore, different cell types, for example protein-secreting peptic cells and the acid-secreting oxyntic cells, could not be distinguished on the basis of their morphology and staining affinity. For histochemical evaluation of the sections with stains-all method, most cells in the gastric glands responded by a positive reaction to protein. Further, protein containing cells were seen in the intestinal glands of the guineapig caecum. The function of this cell type was correlated with caecotrophic food habits of this species.     

Localization of pepsinogen and cellular differentiation in the human gastric mucosa using lowicryl K4M

The localization of pepsinogens (PG A and PG C) was studied intracellularly in human gastric biopsies embedded in Lowicryl K4M, using affinity purified antibodies and protein A-gold. The homogeneous secretory granules of the chief cells contained both PG A and PG C, as was proved in serial sections. Identical reaction was seen in the core of the biphasic mocous neck cell granules, whereas the mantle did not label. Even the rough endoplasmic reticulum (RER) and Golgi complex of the chief- and mucous neck cells contained label. Transitional cells identified by the presence of granules of both chief- and mucous neck cells were seen. This type of mucous neck cell is thought to transform into a chief cell. However an increase of RER that could explain an increase of the pepsinogen production was not observed. A mixture of these granules were also found in morphologically characterized young parietal cells, suggesting a common precursor for these three cell-types. These observations makes the transformation from mucous neck- into chief cells questionable. In conclusion Lowicryl K4M appeared to be a significant improvement compared to the Epon 812. Its shows a better preservation of both cytoplasmic antigens and cellular fine structure. This improvement adds information on the transformation hypothesis. Lowicryl K4M enables us, firstly to distinguish PG A and C synthesizing RER in different types of cell and secondly to recognize immature cells with the characteristics of chief-, mucous neck-, and parietal cells in the fundic gland. Very likely these three cell-types all arise from a common precursor. It is questionable that in normal human gastric mucosa the mucous neck cells transform into chief cells.     

Light and electron microscope observations on the gastric mucosa of the frog (Rana esculenta)

Summary The structure of the frog gastric and esophageal mucosa was studied in the course of a complete hibernation period and compared with that in summer frogs (see preceding article).It appeared that especially chief cells and parietal cells are liable to cytoplasmic remodelling. Thus, in chief cells the rough endoplasmic reticulum (RER) undergoes disorganization, the number of free ribosomes increases and the Golgi system becomes transformed into a compact vesicular structure. The number of pepsinogen granules in chief cells of late winter frogs is only 20% of that in frogs studied at the onset of hibernation. The loss of pepsinogen granules is at least partly due to autophagy. In addition, lysosomes are involved in focal degradation of the cytoplasm, which may ultimately result in complete degeneration of some chief cells. The presence of zymogen granules containing fibrocyte-like cells in the tunica propria proved heterophagocytosis by these cells.In parietal cells, the area occupied by smooth endoplasmic reticulum becomes reduced. The basal cytoplasm of both chief cells and parietal cells contains numerous lipid droplets, which, in contrast to those in summer frogs, are continuous with RER cisternae. The juxtaposition of lipid droplets and mitochondria seen in summer frogs is eventually lost in hibernating animals.Apart from the appearance of supra-nuclear lipid droplets, the mucous cells of the surface epithelium show no striking alterations. However, in the glandular pits both surface mucous cells and mucous neck cells contain less mucous granules than in summer frogs.The results are discussed in connection with parallel biochemical work and available literature, and in the light of our previous studies on the exocrine pancreas in hibernating frogs.     

Role of Na-K-2Cl cotransporter-1 in gastric secretion of nonacidic fluid and pepsinogen

Na-K-2Cl cotransporter-1 (NKCC) has been detected at exceptionally high levels in the gastric mucosa of several species, prompting speculation that it plays important roles in gastric secretion. To investigate this possibility, we 1) immunolocalized NKCC protein in the mouse gastric mucosa, 2) compared the volume and composition of gastric fluid from NKCC-deficient mice and their normal littermates, and 3) measured acid secretion and electrogenic ion transport by chambered mouse gastric mucosa. NKCC was localized to the basolateral margin of parietal cells, mucous neck cells, and antral base cells. In NKCC-deficient mice, gastric secretions of Na+, K+, Cl-, fluid, and pepsinogen were markedly impaired, whereas secretion of acid was normal. After stimulation with forskolin or 8-bromo-cAMP, chambered corpus mucosa vigorously secreted acid, and this was accompanied by an increase in transmucosal electrical current. Inhibition of NKCC with bumetanide reduced current to resting levels but had no effect on acid output. Although prominent pathways for basolateral Cl- uptake (NKCC) and apical Cl- exit [cystic fibrosis transmembrane conductance regulator (CFTR)] were found in antral base cells, no impairment in gastric secretion was detected in CFTR-deficient mice. Our results establish that NKCC contributes importantly to secretions of Na+, K+, Cl-, fluid, and pepsinogen by the gastric mucosa through a process that is electrogenic in character and independent of acid secretion. The probable source of the NKCC-dependent nonacidic electrogenic fluid secretion is the parietal cell. The observed dependence of pepsinogen secretion on NKCC supports the concept that a nonacidic secretory stream elaborated from parietal cells facilitates flushing of the proenzyme from the gastric gland lumen.     

Localization of pepsinogen (A and C) and cellular differentiation of pepsinogen-synthesizing cells in the human gastric mucosa

The localization of pepsinogens (PG A and PG C) was studied intracellularly in human gastric biopsies embedded in Lowicryl K4M, using affinity-purified antibodies and protein A-gold. The homogeneous secretory granules of the chief cells contained both PG A and PG C, as was proved by serial sections. Identical reaction was also seen in the core of the biphasic mucous neck cell granules, whereas the mantle did not label. The rough endoplasmic reticulum (RER) and Golgi complex of the chief cells and mucous neck cells contained ample label. Transitional cells identified by the presence of granules of both chief cells and mucous neck cells were recognized. This type of mucous neck cell is thought to transform into a chief cell. However, an increase of RER that could explain an increase of the pepsinogen production was not observed. A mixture of these granules was also found in cells morphologically characterized as young parietal cells, suggesting a common precursor for these three cell types. These observations make the transformation from mucous neck to chief cells questionable. Antral gland cells contained only PG C, as was shown in serial section, too.     

Effect of omeprazole on secretion,synthesis and the gene expression of pepsinogen in the guinea pig stomach mucosa

The effects of omeprazole, a proton pump inhibitor, on gene expression, protein synthesis, intracellular storage and secretion of pepsinogen in guinea pig stomach were investigated. After treatment with omeprazole for five days, acid and pepsinogen secretion into the gastric lumen was significantly reduced. Concomitant with this, there was an increase in intracellular pepsinogen as demonstrated by increased pepsin activity in the gastric mucosa, more intense immunohistochemical staining by antibodies specific of pepsinogen and accumulation of secretory granules in the cells producing pepsinogen. In these cells, the amount for pepsinogen mRNA was reduced as revealed by Northern blotting and in situ hybridization. Ultrastructurally the endoplasmic reticulum of these cells was poorly developed, the findings being consistent with a reduction in protein synthesis. It appears that omeprazole inhibits the secretion of pepsinogen, increasing the intracellular store and leading to the reduction in gene expression probably by a feedback mechanism and consequent reduction in pepsinogen synthesis. Since these changes were most evident in the acid-secreting fundic gland mucosa, as compared with other mucosae secreting only pepsinogen, namely pyloric and duodenal mucosa, it appears probable that these changes are linked with omeprazole-induced reduction in the acid secretion.     

Mice with a targeted disruption of the AE2 Cl-/HCO3- exchanger are achlorhydric

The AE2 Cl-/HCO3- exchanger is expressed in numerous cell types, including epithelial cells of the kidney, respiratory tract, and alimentary tract. In gastric epithelia, AE2 is particularly abundant in parietal cells, where it may be the predominant mechanism for HCO3- efflux and Cl- influx across the basolateral membrane that is needed for acid secretion. To investigate the hypothesis that AE2 is critical for parietal cell function and to assess its importance in other tissues, homozygous null mutant (AE2(-/-)) mice were prepared by targeted disruption of the AE2 (Slc4a2) gene. AE2(-/-) mice were emaciated, edentulous (toothless), and exhibited severe growth retardation, and most of them died around the time of weaning. AE2(-/-) mice exhibited achlorhydria, and histological studies revealed abnormalities of the gastric epithelium, including moderate dilation of the gastric gland lumens and a reduction in the number of parietal cells. There was little evidence, however, that parietal cell viability was impaired. Ultrastructural analysis of AE2(-/-) gastric mucosa revealed abnormal parietal cell structure, with severely impaired development of secretory canaliculi and few tubulovesicles but normal apical microvilli. These results demonstrate that AE2 is essential for gastric acid secretion and for normal development of secretory canalicular and tubulovesicular membranes in mouse parietal cells.