[The orthology of the endocrine cells of the distal part of the esophagus (author's transl)].
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The decrease in active kidney parenchyma amount causes disorders in hormone secretion processes and their inactivation failure. Experimental thyroparathyroidectomy is connected with an abrupt reduction in endocrine cells and hormones produced by them, which can be a stimulating factor as far as the increase and intensity of endocrine gastric cells activity is concerned. The aim of the study was the histomorphological and immunohistochemical evaluation of these cells in the gastric pylorus. Thyroparathyroidectomy was performed in rats 30 days after nephrectomy. Fragments of gastric pylorus were collected 14 days after the operation. Paraffin sections were stained with H+E and silver method. Immunohistochemical reactions were conducted using antibodies against calcitonin gene-related peptide (CGRP), somatostatin (ST), synaptophysin (SPh), neuron-specific enolase (NSE), and chromogranin (CgA). The results showed an increase in number of endocrine cells in stomachs of rats in experimental group as compared to controls. Endocrine cells were larger and contained more secretory granules.
Endocrine cells of the duodenal bulb producing adrenalin, noradrenalin, serotonin, histamine and beta-endorphine were assayed in 12 patients with preulcer and 39 patients with duodenal ulcer. It is shown that preulcer was mainly characterized by hyperplasia of endocrine cells in the duodenal bulb mucosa, secreting adrenalin and noradrenalin in the presence of the deficiency of beta-endorphine-producing cells. The recurrent duodenal ulcer was associated with a dramatic fall in the number of catecholamine-containing endocrine cells in the duodenal bulb.
The mitotic index in endometrial adenocarcinomas incorporating multiple endocrine cells was half that in tumors free from the said cells, this being independent of the degree of tumor parenchymal cell differentiation.
After 16 months, an established line of human small cell lung cancer (OH-1) underwent a subtle morphological change which was associated with a virtually complete loss of neuroendocrine differentiation as judged by electron microscopy studies and a 12-fold loss in L-dopa decarboxylase activity. In nude (athymic) mouse heterotransplants, the histology of the early-passage cells (oat or lymphocyte-like) differed only slightly from the late-passage cells (intermediate or polygonal type); cytology studies showed no diagnostic differences between the passages. However, the early-passage endocrine-like cells showed up to 100-fold less cell survival after irradiation than the late-passage cells. Thus, subtle changes in the morphology of OH-1 cells are accompanied by a profound loss of neuroendocrine differentiation and the emergence of radiation resistance. These changes could have important parallelisms for behavior of small-cell lung carcinoma in humans. The cell culture model described may be useful in investigating the interrelationships occurring between endocrine and nonendocrine cells in the spectrum of human lung cancer. The findings emphasize that neuroendocrine-related ultrastructure and biochemistry may help define important cell populations in lung cancer with respect to therapeutic sensitivity.
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To determine if gastrin in hyperparathyroid glands is true gastrin or artifact and to determine the frequency of gastrin in parathyroid glands, 20 parathyroid glands from 11 patients with hyperparathyroidism but without MEA were extracted and analyzed for gastrin. The parathyroid glands from 4 out of 11 patients had measurable gastrin immunoreactivity (10.7 + 6 pg/mg tissue). Column separation chromatography confirmed that this was true gastrin (40% G-34; 50% G-17). Immunohistochemistry with ABC (avidin biotin complex) immunoperoxidase confirmed the presence of gastrin in cytoplasmic vesicles in scattered parathyroid cells. True gastrin does exist in some cells in some patients with hyperparathyroidism.
We assessed the dynamics of neuroendocrine (NE) cell numbers, the intensity of specific 5-HT fluorescence, and the arterial medial thickness in the lungs of neonatal rabbits in normoxia and acute and chronic hypoxia. Hypoxic neonates had significantly higher NE cell numbers and medial thickness of the pulmonary arteries at 5 days of age than did normoxic controls; 1- and 3-day-old young that died in hypoxia also had significantly higher cell numbers and medial thickness than did hypoxic survivors. A decline in these cell numbers was noted between 1 and 5 days of age among normoxic young, whereas there was no significant change among hypoxic young. Medial thickness was unchanged among normoxic young but increased between 1 and 5 days of age among hypoxic survivors. A 1-day exposure to normoxia of hypoxic young four days postpartum caused a decrease in NE cell numbers and medial thickness to more normal values. Serotonin (5-HT) fluorescence intensity levels of groups of NE cells or neuroepithelial bodies (NEBs) in this group were equal to those of normal controls although these levels were decreased in early chronic hypoxia. Medial thickness and NE cell numbers were inversely correlated with serotonin levels, suggesting that serotonin may be associated with medial hypertrophy and presence of argyrophil material. Medial thickness was positively correlated with NE cell numbers. The above findings led to the following summary: pulmonary NE cells respond to changes in airway oxygen levels; hypoxia or decreased oxygen is associated with decreased cellular 5-HT content and an increase in NE cell numbers by argyrophil stain and medial thickness of pulmonary artery walls. The change to normoxia from hypoxia results in higher cellular 5-HT content and decreased NE argyrophil cell numbers along with reduced pulmonary artery wall medial thickness.
The amount of some endocrine cells in various forms of chronic gastritis with and without the presence of intestinal metaplasia of the stomach mucosa was studied immunohistochemically (PAP-reaction). The study was carried out on 18 samples of biopsied material for D-cells and on 31--for G cells. It was established that the amount of these cells as well as their ratio was changed in accordance with the form of chronic gastritis. Thus, for example++ , the number of D-cells was increased in mild forms of gastritis, but they were reduced in its grave form, while the number of G-cells gradually diminished from mild to grave forms. These changes give foundation to assume that hr hormonal disturbance of the stomach mucosa plays important role in pathogenesis of this disease. This suggestion is supported by the observed in dynamics quantitative changes of these cells, beginning even at the initial stages of this disease.
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The aim of the present study was to characterise immunohistochemically and ultrastructurally the neuroendocrine cells in the pulmonary systems of uraemic rats. Pieces of lung and trachea were collected 1, 2 and 4 weeks after nephrectomy. Paraffin-embedded sections were stained with H+E and by silver impregnation. For the identification of neuroendocrine cells immunohistochemical reactions were performed with the use of specific antibodies against calcitonin (CT), somatostatin (SOM), synaptophysin (SYN), neuron-specific enolase (NSE) and calcitonin gene-related peptide (CGRP). For electron microscopy, ultrathin sections were used. The analysis showed an increased number of both the solitary neuroendocrine cells and of neuroepithelial bodies in uraemic rats when compared to control animals.
Male F344 rats were given N-nitrosoheptamethyleneimine (NHMI) twice a week by gavage for 20 weeks. They developed peripheral squamous cell carcinomas of the lungs. Electron microscopy revealed the presence of mature keratin in the tumor centers and the formation of keratohyalin granules in the more peripheral tumor cells. Basal cells were identified as the actively growing component of the neoplasms. In contrast to NHMI-induced lung carcinomas in European hamsters, neither Clara, nor APUD-type, cells were found in the rat tumors. These data indicate that the mode of development of NHMI-induced lung tumors is different in these two species.
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A review of 955 patients with primary oesophageal carcinoma treated with this hospital revealed 23 cases of small cell anaplastic carcinoma of the oat cell type. Fifteen were females and eight were males. In each case the histological appearances were identical to those of the oat cell carcinoma which is much more commonly encountered in the lung. In none of these cases was there any evidence of a primary oat cell carcinoma outside the oesophagus. Argyrophilic granules were seen in three cases and granules of the neurosecretory type were present in five. We conclude that neither of these findings is a prerequisite for making a diagnosis of oesophageal oat cell carcinoma. The histogenesis of this tumour is reviewed and briefly discussed.
There was no significant variation in the numbers of bronchopulmonary endocrine cells immunoreactive for calcitonin in five pairs of adult human lungs either from case to case or between groups of anatomically equivalent lobes. This was the case whether their numbers were expressed in relation to epithelial length or to the total number of epithelial cells. The mean (SD) values for the frequency of occurrence of these cells in all 25 lobes studied were 4.3 (1.9) per 10 cm of epithelial length or 1.70 (0.78) per 10 000 epithelial cells. Most immunoreactive cells were single and situated in the airways; only three neuroepithelial bodies were observed, and no cells were present in the parenchyma examined. This study provides further evidence that the functional character of these cells may not be confined to early life.
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The regulation of the fluid balance of the mucus is important for a good function of the mucociliary system in the nose. The nasal glands and the goblet cells have been proposed to be the main source of fluid. Microvilli-equipped epithelial cells, ciliated and nonciliated, constituting 70% to 90% of the cells on the turbinates in the nose, are of importance for the regulation of the hydration of the mucus. These cells have the same characteristics as other fluid-secreting cells elsewhere in the body. They have microvilli, a terminal web, folding of the basolateral membrane, and numerous cell organelles. Blockage of the energy supply strongly reduces the fluid secretion.