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Biomedical subjects

E Solcia

Publications and source records attributed to E Solcia.

At least 109 records · Page 6Linked to original sources
PubMed1988

The morphology and neuroendocrine profile of pancreatic epithelial VIPomas and extrapancreatic, VIP-producing, neurogenic tumors.

The histology, histochemistry, and ultrastructure of 43 VIP-producing tumors (34 from the pancreas, one jejunal, six retroperitoneal and two mediastinic), 37 of which were associated with the WDHA syndrome, have been investigated on paraffin sections of primary or metastatic tumor tissue. The pancreatic and jejunal tumors showed all structural and secretory patterns of epithelial endocrine tumors, including expression of cytokeratin, neuroendocrine markers like neuron-specific enolase, chromogranins and synaptophysin, peptides like VIP, PHM, GRH, PP, insulin, neurotensin, glucagon, somatostatin and enkephalin, secretory granules, small clear vesicles, peculiar osmiophilic bodies, and occasional formation of tubules or microacini with specialized luminal surfaces. All the remaining tumors were neurogenic, showing either neurons and nerve fibers together with Schwann cells (ganglioneuromas and ganglioneuroblastomas) or endocrine cells (pheochromocytomas) reacting with VIP, PHM, NPY, enkephalin, somatostatin, neuron-specific enolase, synaptophysin, and MAP2 (but not cytokeratin, PP, or GRH) antibodies. A possible origin of pancreatic VIPomas from transformed pancreatic PP cells or ductular stem cells partially committed to differentiation along the PP cell line is suggested.

Adenoma, Islet Cell↗
PubMed1988

Widespread expression of intestinal markers in gastric carcinoma: a light and electron microscopic study using BD-5 monoclonal antibody.

BD-5 monoclonal antibody reacted with tumour cells in 262 of 316 cases of gastric cancers, including 121 of 134 early, 141 of 182 advanced tumours (p less than 0.01), and 113 of 146 glandular, 72 of 83 diffuse, 22 of 25 mucoid, and 55 of 59 mixed tumours. No difference in reactivity was observed between metastatic and non-metastatic advanced tumours. Immunocytochemical techniques applied to light and electron microscopical specimens of colorectal mucosa and gastric cancer showed that BD-5 immunoreactive material occurred in the Golgi complex, in small clear, to dense cored, cytoplasmic vesicles, and in the glycocalix of the luminal and lateral membranes of normal and neoplastic cells in the glands, as well as in the peripheral membrane of dispersed neoplastic cells. Mucin granules stored in the cytoplasm of goblet cells were unreactive or poorly reactive. Ultrastructural features consistent with colorectal type differentiation were observed in many reactive tumours. Unreactive tumours showing ultrastructural patterns consistent with intestinal differentiation, especially of small bowel type, were also observed. Signs of intestinal differentiation, including BD-5 immunoreactivity, often occur in gastric cancer, irrespective of histological type and stage of disease.

Adult↗
PubMed1988

Histopathological classification of nonantral gastric endocrine growths in man.

Recently, the gastric endocrine system has been recognized as the origin of benign and malignant tumors in pernicious anemia. It has also been found that the gastric endocrine cells respond to permanent elevation of serum gastrin levels induced by changes in acid secretion in response to surgical procedures, drug therapy and age. Therefore, a definition of nonantral gastric endocrine hyperplasia (simple or diffuse, linear or chain-forming, micronodular, adenomatoid), dysplasia (enlarging or fusing micronodules, microinvasion, nodular growth) and neoplasia (intramucosal carcinoid, invasive carcinoid) is presented. The individual entities are illustrated, together with the literature discussed and the techniques for their identification presented.

Endocrine System Diseases↗
PubMed1987

Endocrine cells producing regulatory peptides.

Recent data on the immunolocalization of regulatory peptides and related propeptide sequences in endocrine cells and tumors of the gastrointestinal tract, pancreas, lung, thyroid, pituitary (ACTH and opioids), adrenals and paraganglia have been revised and discussed. Gastrin, xenopsin, cholecystokinin (CCK), somatostatin, motilin, secretin, GIP (gastric inhibitory polypeptide), neurotensin, glicentin/glucagon-37 and PYY (peptide tyrosine tyrosine) are the main products of gastrointestinal endocrine cells; glucagon, CRF (corticotropin releasing factor), somatostatin, PP (pancreatic polypeptide) and GRF (growth hormone releasing factor), in addition to insulin, are produced in pancreatic islet cells; bombesin-related peptides are the main markers of pulmonary endocrine cells; calcitonin and CGRP (calcitonin gene-related peptide) occur in thyroid and extrathyroid C cells; ACTH and endorphins in anterior and intermediate lobe pituitary cells, alpha-MSH and CLIP (corticotropin-like intermediate lobe peptide) in intermediate lobe cells; met- and leu-enkephalins and related peptides in adrenal medullary and paraganglionic cells as well as in some gut (enterochromaffin) cells; NPY (neuropeptide Y) in adrenaline-type adrenal medullary cells, etc.. Both tissue-appropriate and tissue-inappropriate regulatory peptides are produced by endocrine tumours, with inappropriate peptides mostly produced by malignant tumours.

Animals↗
PubMed1987

Subcellular localization of pepsinogen II in stomach and duodenum by the immunogold technique.

We have determined the ultrastructural localization of pepsinogen II (PG II) in aldehyde-osmium fixed, resin-embedded ultrathin sections of human gastric fundic and pyloric gland mucosa and duodenum using the protein A immunogold technique and antiserum specific for PG II. Chief cells contained homogeneous, finely granular secretory granules that were uniformly PG II-positive. In contrast, mucous neck, pyloric gland, and Brunner's gland cells contained secretory granules consisting of an eccentrically placed dense core surrounded by a clear matrix; PG II immunoreactivity was concentrated over the dense core of these biphasic granules. Pyloric gland cells also contained monophasic secretory granules having the same electron density, texture, and PG II immunoreactivity as the nucleoids of biphasic granules and clear vesicular granules that were PG II-negative. Vesicular granules also were found in Brunner's gland cells. The Golgi region of pyloric gland cells contained small PG II-positive monophasic granules adjacent to small PG II-negative vesicular granules. This observation suggests that biphasic granules may form in the Golgi region of pyloric gland cells by fusion of PG II-containing monophasic granules and PG II-unreactive vesicular granules.

Brunner Glands↗
PubMed1987

Glucagon, glicentin, proglucagon, PYY, PP and proPP-icosapeptide immunoreactivities of rectal carcinoid tumors and related non-tumor cells.

Glucagon/PP-related peptides were detected immunohistochemically in 18 out of 22 cases of rectal tumors investigated. The reactive tumors showed prevalence of trabecular or mixed trabecular-acinar structure and moderate staining with Grimelius' silver and lead-hematoxylin. Three of the remaining 4 cases were characterized by reactivity for 5-hydroxytryptamine only, prevalence of a solid nest structural component and intense staining with Grimelius' silver technique and lead-hematoxylin. Fifteen of the 18 glucagon/PP-reactive cases were investigated immunohistochemically with a series of 6 sera directed against different sequences of glucagon, glicentin and proglucagon, and of 7 sera directed against PP, PYY and proPP-icosapeptide. A large spectrum of glucagon-related immunoreactivities, including C-terminus and mid-portion glucagon-immunoreactivity, N- and C-terminus glicentin-immunoreactivity, GLP1- and GLP2-immunoreactivity, were detected in human rectal L cells and most rectal carcinoids. With the exception of a few scattered cells in the rectal mucosa and in 3 tumors, C-terminus glucagon-immunoreactivity was obtained only after trypsin or subtilisin treatment of tissue sections. Both PYY and PP/proPP-like peptide(s) were detected in rectal L cells and carcinoids, with prevalence of PYY in normal cells and PP/proPP-like peptides in tumor cells. It is concluded that the same or closely related hormone/prohormone sequences are synthesized and stored in rectal endocrine cells and carcinoid tumors although differences of quantitative expression, post-translational cleavage or reactivity to antibodies may occur. The usefulness of protease treatments of tissue sections to unmask immunoreactivities of uncleaved propeptides or fixative-denatured peptides is outlined.

Animals↗
PubMed1987

Synaptophysin immunoreactivity and small clear vesicles in neuroendocrine cells and related tumours.

Synaptophysin (protein p38) immunoreactivity has been detected immunohistochemically in neuroendocrine cells of the human adrenal medulla, carotid body, skin, pituitary, thyroid, lung, pancreas and gastrointestinal mucosa as well as in 87 out of 93 neuroendocrine tumours investigated, including pheochromocytomas, chromaffin and non-chromaffin paragangliomas, ganglioneuromas, pituitary adenomas, thyroid medullary carcinomas, parathyroid adenomas, lung carcinoids and neuroendocrine carcinomas, pancreatic and gut endocrine tumours and cutaneous merkelomas. Parallel ultrastructural investigation of synaptophysin-reactive cells and tumours revealed the presence, in addition to dense-cored, secretory granules, of a population of pleomorphic, small, clear vesicles resembling synaptic vesicles of nerve terminals as well as the synaptophysin immunoreactive vesicles already described in rat adrenal medullary and pituitary cells. Synaptophysin immunoreactivity showed several differences in its distribution among tumour and non-tumour endocrine cells when compared to chromogranin A immunoreactivity, a well known marker of the core of endocrine granules. Synaptophysin represents a reliable general marker of neuroendocrine cells and tumours, which may be useful in diagnostic histopathology.

Chromogranin A↗
PubMed1987

Characterization of four main cell types in gastric cancer: foveolar, mucopeptic, intestinal columnar and goblet cells. An histopathologic, histochemical and ultrastructural study of "early" and "advanced" tumours.

Gastrectomy specimens of 148 gastric cancers, 40 of them being intramucosal or microinvasive, 27 penetrating the submucosa and 81 invading the muscularis propria, with or without involvement of the serosa and perigastric tissues, have been investigated with conventional histopathologic techniques, mucin histochemistry and electron microscopy to characterize the various lines of tumour cell differentiation and to correlate these with the histologic patterns of tumour growth. More or less differentiated intestinal columnar, intestinal goblet, gastric foveolar or mucopeptic cells were recognized in most tumours, of glandular, diffuse or mucoid type. Although simultaneous expression of more than one cell type into the same tumour occurred very frequently, intestinal columnar cells were more prominent in tubular adenocarcinomas, goblet cells (especially of colorectal type) in mucoid cancers, mucopeptic cells in diffuse cancers of invasive desmoplastic type and foveolar cells in diffuse cancers of intramucosal signet-ring cell type. In general, an increased tendency to foveolar cell differentiation and a reduced tendency to mucopeptic differentiation has been found in intramucosal cancers as compared to invasive cancers. It is concluded that the type of tumour cell differentiation, which might have some influence on the natural history of gastric cancer, is better related with more defined tumour subtypes than with the usually recognized glandular or diffuse patterns.

Gastric Mucosa↗
PubMed1987

High incidence of Campylobacter-like organisms in endoscopic biopsies from patients with gastritis, with or without peptic ulcer.

Campylobacter-like organisms (CLOs) were histologically detected in 230 (74.5%) of 310 patients undergoing endoscopy with multiple gastric biopsies for symptoms suggestive of upper digestive disease. CLOs were found in 78.6% of nonulcerous dyspeptic patients, 82.2% of healed ulcers, 88.2% of duodenal or pyloric ulcers and 90.0% of gastric ulcers but only in 46.9% of gastric stumps and 47.6% of nonulcerous patients without dyspepsia. Among 274 subjects with gastritis, CLOs were found in 83.9%, while none of the 36 gastritis-free stomachs harbored CLOs. Severe atrophic gastritis was less frequently infected with CLO (55.5%) as compared with superficial, interstitial or preatrophic gastritis (84.4%). CLOs were only slightly more frequent in the presence of intraepithelial granulocytes and were never found in areas of complete intestinal metaplasia. Foveolar and superficial epithelia heavily infected with CLOs showed peculiar ultrastructural changes (micropapillary hyperplasia with luminal bulging of mucous cells, cytoplasmic vacuolization and edema, etc.) suggesting a direct link between CLO infection and epithelial damage, which in turn may have a role in the genesis of mucosal inflammation.

Adolescent↗
PubMed1986

Electron immunocytochemical localization of pepsinogen I (PgI) in chief cells, mucous-neck cells and transitional mucous-neck/chief cells of the human fundic mucosa.

Specific PgI antibodies devoid of PgII cross reactivity have been applied to aldehyde-osmium fixed human, fundic-type, gastric mucosa investigated with the protein A-immunogold technique. PgI immunoreactivity has been detected in the homogeneous secretory granules of glandular chief cells, in bipartite granules of mucous-neck cells, in the granules of cells showing intermediate patterns and topography in between chief and mucous-neck cells (transitional cells), as well as in the granules of a few cells in the foveolar/mucous-neck boundary zone showing mixed foveolar/mucous-neck granule populations. The findings support progressive transformation of mucous-neck cells into chief cells.

Gastric Fundus↗
PubMed1986

Chromogranin A, B and C immunoreactivities of mammalian endocrine cells. Distribution, distinction from costored hormones/prohormones and relationship with the argyrophil component of secretory granules.

Antibodies specific for chromogranin A, B or C have been used to detect immunohistochemically these three anionic proteins. Pancreatic A, B and PP cells, gut argentaffin EC, argyrophil ECL and gastrin G cells, thyroid C cells, parathyroid cells, adrenal medullary cells, pituitary TSH, FSH and LH cells as well as some axons of visceral nerves have been found to react with chromogranin A antibodies. Pancreatic A, gut EC and G, adrenal medullary and pituitary cells as well as some gut nerve fibers showed chromogranin B immunoreactivity. Chromogranin C immunoreactivity has been detected in pancreatic A, pyloric D1, intestinal L, thyroid C, adrenal medullary and pituitary cells, as well as in some gut neurons and nerve fibers. No crossreactivity has been found in immunohistochemical tests between chromogranins A, B or C and costored monoamines or peptide hormones/prohormones, from which chromogranins can be separated by selective extraction during fixation. On both morphological and chemical grounds a relationship seems to exist between chromogranin A and Grimelius' argyrophilia. Sialooligosaccharide chains of chromogranin A and, possibly, chromogranins' phosphoserine/phosphothreonine groups, seem to interact with guanidyl, amino, and/or imidazole groups of non-chromogranin components to form silver complexing sites accounting for granules' argyrophilia, which can be removed or blocked without affecting chromogranin immunoreactivities. The abundant anionic groups of the three proteins should contribute substantially to granules' basophilia, the partly "masked" pattern of which supports the existence of a close interaction of such groups with other components of secretory granules, including monoamines and peptide hormones or prohormones. Chromogranins could play a rôle in hormone postranslational biosynthesis and intragranular packaging.

Adrenal Medulla↗
PubMed1986

Gastric carcinoids and related endocrine growths.

A series of 30 gastric endocrine tumours has been revised in the light of available available cytologic and clinicopathologic information. Among 24 well differentiated endocrine tumours-16 with and 8 without chronic atrophic gastritis (CAG)-3 gastrin cell tumours have been distinguished from 21 argyrophil carcinoids, 15 of which showed light- and/or electronmicroscopy patterns of enterochromaffin-like (ECL) cell tumours, 2 of EC cell tumours and 1 of D1/P cell tumour. One case of mixed carcinoid/adenocarcinoma and 5 cases of endocrine carcinomas, 4 poorly and 1 moderately differentiated, were also identified. Achlorhydria, due to type A CAG or HCl-suppressing drugs, and bombesin hyperstimulation are among possible factors inducing G cell hyperfunction and/or hyperplasia. Hypergastrinaemia is among causative agents of argyrophil ECL cell hyperplasias and, possibly, of tumours of the oxynticopeptic mucosa, while chronic inflammation and gland atrophy with or without concomitant hypergastrinaemia are important factors in inducing both hyperplastic and tumour argyrophil growths in CAG mucosa.

Carcinoid Tumor↗
PubMed1985

Amphicrine cells, dysplasias, and neoplasias.

The existence of epithelial cells displaying synchronous features of exocrine and endocrine differentiation has been well established. Sporadic descriptions of neoplasms comprising or including such cells have also been recorded. The authors investigated eight carcinomas (lung, two; stomach, two; colon, one; appendix, one; esophagus, one; and pancreas, one). By conventional light microscopy, all eight neoplasms appeared as moderately to well-differentiated adenocarcinomas. Mucosubstance stains showed positive material within well-defined lumina and as intracytoplasmic droplets. Argyrophil stains were positive in seven of the eight neoplasms. The esophageal tumor was a predominantly solid carcinoma; it compromised small to intermediate cells with focal mucosubstance positivity and squamous pearls. By electron microscopy, all these carcinomas including cells displaying variable complements of neurosecretory granules, which were concentrated in the basal pole or in cytoplasmic processes. The granule population was often heterogeneous. The pancreatic carcinoma also showed typical zymogen granules. In all cases, many of the neoplastic cells had true lumina or intracytoplasmic lumina, as well as arrays of filaments; secretory granules were also observed in cells with true or intracytoplasmic lumina. Immunohistochemical studies revealed in all cases either serotonin or one of a spectrum of neuropeptides. Five tumors contained more than one immunoreactive material. The authors conclude that synchronous exocrine and endocrine differentiation may be comparatively frequent in a spectrum of tumors that may be properly termed "amphicrine" carcinomas. This demonstrable heterogeneity of malignant cell populations, however variably expressed, may prove to have considerable significance in the diagnosis and management of these neoplasms.

Adenocarcinoma↗
PubMed1985

Ultrastructural localization of cholecystokinin in endocrine cells of the dog duodenum by the immunogold technique.

Cholecystokinin (CCK) has been localized by the immunogold technique in a type of endocrine cell of the dog duodenum characterized by small (166 +/- 38 nm) secretory granules with fairly dense, homogeneous core separated from its enveloping membrane by a thin clear space. The CCK cell is immunocytochemically distinct and cytologically different from other types of endocrine cells, as the secretin, GIP and motilin cells, already identified in the dog duodenum.

Animals↗
PubMed1985

Early and late sarcoplasmic reticulum changes in doxorubicin cardiomyopathy. An ultrastructural investigation with the zinc iodide-osmium tetroxide (ZIO) technique.

The sequence of myocardial changes in the mouse induced by doxorubicin (Dx) treatment (10 mg/kg i.v.) has been investigated by electron microscopy with the help of the zinc iodide-osmium tetroxide (ZIO) technique. Accumulation of ZIO-reactive material, possibly oxidized glutathione and other disulfides, in the sarcoplasmic reticulum (S.R.) is among the earliest (1 h after Dx injection), more prominent and persistent findings (up to 100 days). It may have a pathogenic relationship with a number of functional and morphologic changes occurring in myocardial cells, including impairment of calcium transport and contractility, S.R. dilation up to extensive vacuolization, as well as inhibition of DNA, RNA and protein synthesis leading to atrophy and disruption of sarcomeres. The latter finding, first appearing in a few cells 4 to 7 days after Dx and progressively increasing in severity and extension during the next 3 months, may represent a key factor in the evolution of chronic cardiomyopathy to cardiac insufficiency. In most cells, only a minority of mitochondria showed obvious ultrastructural lesions, which were first observed 24 h after treatment and disappeared by the end of the first month, when no more mitochondrial damage was found outside degenerating cells. The myocardium of mice receiving multiple Dx injections (4 mg/Kg, 10 times, or 9 mg/Kg, 5 times) showed the same changes observed in animals treated with a single dose, though they were more severe and extensive.

Animals↗
PubMed1985

Glucagon- and PP-related peptides of intestinal L cells and pancreatic/gastric A or PP cells. Possible interrelationships of peptides and cells during evolution, fetal development and tumor growth.

The immunohistochemical detection of six distinct sequences of proglucagon and its derivatives (GRPP, glicentin, glucagon-37, glucagon-29, GLP1, GLP2 and MPGF) in both intestinal L cells and pancreatic or gastric A cells of some mammals (dog, man, guinea pig) confirms that the two cell types produce the same proglucagon molecule, although the final step of its post-translational processing differs in the two cells. Immunohistochemical and ultrastructural patterns of glucagon/glicentin cells in the pancreas of lower vertebrates and early human fetuses, as well as tumor cell studies, suggest an evolution of gastropancreatic A cells from L cells. On the contrary, the PP-related peptide PYY of intestinal L cells, and PP with its C-terminal icosapeptide extension of pancreatic PP cells, likely originate from different prohormones. Although intermediate patterns of peptide expression can be observed, including some F-type PP cells of the dog pancreas (uncinate process) and pyloric mucosa showing PYY immunoreactivity or rare PYY and/or HPP immunoreactive cells of the human rectum lacking glicentin reactivity, no obvious relationship can be established between L cells and pancreatic (F-type) PP cells. However, some evolutionary, embryogenetic and oncogenetic link may exist between L cells and human D1-type PP cells, a minor population of PP cells scattered in the pancreatic tissue of dorsal pouch origin and a major fraction of tumor PP cells.

Animals↗