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T J Nevalainen

Publications and source records attributed to T J Nevalainen.

At least 163 records · Page 9Linked to original sources
PubMed1977

Ultrastructural and functional changes in pancreatic acinar cells during autolysis.

Effects of anoxemic cell injury on rat pancreatic acinar cells were studied in a preparation where tissue samples were incubated at temperature between 18-20 degrees C in a moist atmosphere for 0, 0.5, 1, 3, 6, 12, and 24 h in vitro. Electron microscopy revealed that disintegration of acinar cells began by swelling of various cell compartments and gradual breakdown of cell membranes. Zymogen granules remained morphologically intact for at least 3 h. There were no signs of increased autophagic activity during the period of observation. Myelin figures and other membranous remnants of disintegrated cells, together with individual cells and cell organelles whose morphology was relatively well preserved were seen even after w4 h incubation. The secretory response of acinar cells to pancreozymin stimulation, as measured by amylase release into the incubation medium in vitro, decreased progressively closer to zero during 12 h autolysis. No active trypsin could be detected in the tissue samples during the 24 h observation time. It was concluded that during hypoxic autolysis at room temperature between 18-20 degrees C in vitro: 1. Acinar cell disintegration results from breakdown of cellular membranes, 2. autophagocytosis is not involved, 3. most of zymogen granules remain morphologically intact even at the time when cell membranes show evidence of damage, 4. there is no trypsin activation taking place in the tissue, and 5. the acinar cells are capable of responding to secretory stimulation for 3 to 6 h after removal of the tissue from the experimental animal.

Amylases↗
PubMed1977

Ultrastructure of intestinal and diffuse type gastric carcinoma.

Samples from 56 resected stomachs, including 28 cases of intestinal and 14 of diffuse type gastric carcinoma, were studied by electron microscopy. The main ultrastructural features of intestinal and diffuse type gastric carcinomas were described and compared to the ultrastructure of normal gastric mucosal cells and cells occurring in intestinal metaplasia of the gastric mucosa. Many similarities were demonstrated between intestinal metaplasia and intestinal type carcinomas. The cells of diffuse type carcinomas closely resembled the goblet cells of intestinal metaplasia. Microvilli, similar to those in the brush border of the intestinal columnar cells, could be demonstrated in the carcinomatous surface epithelium and occasionally also in individually spreading cells of the diffuse type carcinoma. Intracellular cysts with microvilli on the cyst wall were occasionally found in both types of carcinoma. The histogenetic origin of gastric carcinoma was discussed.

Adenocarcinoma↗
PubMed1977

Ultrastructure of the benign and borderline Brenner tumours.

One benign Brenner tumour and one Brenner tumour of borderline malignancy were investigated by electron microscopy. The cells of the benign Brenner tumour nests and the cells in the borderline tumour were similar in ultrastructure. The intercellular spaces were large and reinforced by a moderate number of desmosomes. The nuclei were round or oval. The nuclear membrane was irregular in shape with deep infoldings corresponding to the characteristic nuclear groovings seen by light microscopy. Only few secreting cells could be found in the benign of Brenner tumour. The cystic cavities of the borderline Brenner tumour were lined by nonciliated secreting and ciliated nonsecreting cells. The secretory granules were PAS-positive and diastaseresistant. The granules stained homogeneously and strongly with the PASM-method at the electron microscopical level indicating the presence of 1.2-hydroxyl groups. The Brenner tumours have many similarities to the transitional epithelium and to the Muellerian-derived tubular structures. The findings support the theory that Brenner tumours are of coelomic origin and develop by direct metaplasia from the ovarian surface epithelium.

Brenner Tumor↗
PubMed1977

Ultrastructural characteristics of tuft cells in mouse gallbladder epithelium.

Mouse gallbladder was fixed by perfusion or immersion in glutaraldehyde and/or osmium tetroxide for electron microscopy. Besides usual columnar epithelial cells there were infrequent tuft cells in the epithelium. The cells rested on the basal lamina and extended to the gallbladder lumen. The microvilli on the apical cell surface were tall and thick and there was a rich network of microfilaments radiating from the core of the microvilli to the apical and juxta-nuclear cytoplasm. Among the bundles of microfilaments there were vertically oriented microtubules in the apical cytoplasm. Although the function of the tuft cells in the gallbladder epithelium remains unknown, it is proposed that their unique morphology may reflect a specialized resorptive function involving motility of microvilli and other cell organelles.

Animals↗
PubMed1977

Foreign serum-induced pancreatitis in mice. II. Secretory disturbances of acinar cells.

As previously reported, pancreatic acinar cell necrosis and inflammation develop in mice a few hours after one intraperitoneal injection of foreign serum. However, sublethally injured acinar cells exhibited notable increases in both zymogen granule numbers and amylase activity, observed within 3 hours and increasing with time. These two changes were coupled with a progressive decrease in the secretory response to pilocarpine and were preceded by significant disturbances in pancreatic tissue concentrations of sodium and potassium. We conclude that (1) the granule increase results from an induced disturbance of the granule exocytosis mechanism while granule formation continues and, therefore, (2) the granule secretory process is more sensitive to the serum injury mechanism than is the zymogen synthesis process. Although the granule increases developed in acinar cells throughout most of the nonnecrotic gland and persisted for at least 24 hours, acinar cell necrosis was maximal in extent--approximately 25% of the gland in severest form--by 12 to 15 hours. We conclude, therefore, that the increase in granules is neither the primary determinant nor initiator of acinar cell death. The latter is likely caused by disturbed plasma membrane functions, sufficient in some cells to result in lethal changes in ion and fluid composition. The injury mechanism, which permits granule formation to go on in the face of impaired granule exocytosis, is yet to be worked out. The possibilities are discussed in relationship to the reactivity of foreign sera for target cell plasma membranes.

Amylases↗
PubMed1976

Improved periodic acid-silver methenamine staining procedure for electron microscopy.

Mucosubstances can be stained for electron micrsocopy with silver methenamine after periodic acid oxidation in ultrathin Epon sections mounted on nickel grids. The grids are transferred from a solution to another during the staining procedure conveniently in a container made of polyvinyl chloride plastic. This staining procedure is easy to perform and gives reproducible results. It is especially suitable for simultaneous handling of a large number of grids.

Glycosaminoglycans↗
PubMed1976

Intracellular cysts in gastric carcinoma.

Intracellular cysts were often found in the tumour cells in gastric carcinomas of intestinal as well as diffuse type in specimens from stomachs resected for gastric cancer. In the light microscope, the cysts appeared usually as solitary cytoplasmic vacuoles. In the electron microscope, the intracellular cysts were seen as round cavities, often containing homogenous or granular mucous material which stained with the periodic acid-silver methenamine (PASM)-method. Relatively long microvilli were lining the cysts and, not infrequently, abundant cytoplasmic microfilaments would surround the cyst wall. Similar cysts have been observed in a number of other tumours and, accordingly, their diagnostic significance must be considered in connection with other methods such as differential staining of cellular mucosubstances.

Cell Membrane↗
PubMed1976

Lamellated osmiophilic bodies in mouse gallbladder epithelium.

Mouse gallbladder epithelium was studied in the electron microscope after glutaraldehyde and osmium tetroxide fixation and Epon embedding. Special attention was paid to dense cytoplasmic bodies. Heterogeneous dense bodies with osmiophilic and loose granular components were identified. Many of these bodies consisted of lamellated osmiophilic structures, similar to the phospholipid bodies of the large alveolar (type II) cells of the mammalian lung. The dense bodies containing the lamellar structures were membrane-limited and 0.5-1.0 mum in diameter. They were located in the supranuclear cytoplasma and were often closely associated with the Golgi apparatus. Acid phosphatase activity was demonstrated within these bodies and in some of the Golgi vacuoles. The contents were disposed in concentric lamellar osmiophilic structures, sometimes appearing as scroll-like configurations. These morphological findings were interpreted as indication of these presence of phosphlipid absorbed from the gallbladder lumen and stored in phagosomes in the central cytoplasm of the gallbladder epithelial cells.

Acid Phosphatase↗
PubMed1975

Ultrastructure of primary lymphosarcoma of testis.

A case of primary lymphosarcoma of testis was studied by light and electron microscopy. The fine structure of the lymphosarcoma cells was simple and monotonous. The cytoplasm was scanty and contained normal-looking organelles. Free ribosomes were abundant and the Golgi apparatus was well developed. The nuclei were large and irregular in shape with prominent nucleoli. "Nuclear pockets" enclosing material similar to the cytoplasmic ground substance were found infrequently. Remnants of disintegrating cells were also encountered.

Aged↗
PubMed1975

Inhibition of pancreatic exocrine secretion by vinblastine.

Inbred BALB/c mice were given vinblastine sulfate (VelbeR) and/or pilocarpine hydrochloride (30 mg/kg) intraperitoneally and amylase activity was determined in the pancreas homogenate. When vinblastine was given 5 hours before measuring the pancreatic amylase content it inhibited the pilocarpine stimulated (2 hours) pancreatic secretion in a dosis-dependent fashion at doses 4, 40 and 400 mg/kg. Vinblastine (200 mg/kg) also delayed amylase accumulation during 3 hours in mice given vinblastine 2 hours after pilocarpine stimulation. The results support the hypothesis that faultless function and integrity of microtubules might be a prerequisite of pancreatic acinar cell secretion in vivo. Other effects of vinblastine, such as interference with amino acid metabolism, anticholinergic action, and cell injury must also be considered when interpreting the present findings form the point of view of the secretory mechanism of the pancreatic acinar cells.

Amylases↗
PubMed1975

Cytotoxicity of vinblastine and vincristine to pancreatic acinar cells.

BALB/c mice were given vinblastine (Velbe), 40 and 200 mg/kg, or vincristine (Oncovin), 20 mg/kg, dissolved in saline as single intraperitoneal injections. Nontreated mice served as controls. Animals were killed 1, 2, 5, and 24 hours and 4 days after the drug administration and small pieces from the pancreas were processed for electron microscopy. Autophagocytotic activity increased 3 hours after the injection and at 5 and 24 hours there were large amounts of autophagic vacuoles containing altered cell organelles and membranous or amorphous debris in the acinar cells. Cell death and acinar atrophy were evident at later time intervals. It was concluded that the vinca alkaloids caused autophagy and degeneration in pancreatic acinar cells and that their inhibitory effect on pancreatic enzyme secretion might depend partly or solely on their cytotoxic action.

Animals↗
PubMed1975

Use of phast contrast microscopy of semithin epoxy sections in histochemistry.

A number of histochemical staining methods can be applied to semithin (1-2 mum) Epon sections either unmodified or after slight modification of the original method. While only the histochemically stained specific component is visible in bright field illumination, phase contrast microscopical study of the same field of view shows also the histological and cytological details of the specimen and thus allows exact localization of the specific component in the tissue. Applications will be found in several areas in histochemistry. Practical examples are given for demonstration of periodic acid-SCHIFF-reactive mucosubstances, exogenous perioxidase, and acid phosphatase activity.

Acid Phosphatase↗
PubMed1975

Acute pancreatitis caused by closed duodenal loop in the rat.

Closed duodenal loop was created in the rat by obstructing the duodenum on both sides of the common bile duct. Acute haemorrhagic pancreatitis developed in these animals within 24 hours. Increased serum amylase activity, pancreatic acinar cell necrosis, pancreatic oedema and haemorrhages, and intra-abdominal fat necroses, together with formation of ascites fluid containing high levels of amylase, were observed in the experimental animals. The findings support the view that reflux of the duodenal contents into the pancreatic duct is an important early pathogenetic mechanism in the development of acute pancreatitis. The closed-loop technique in the rat offers a simple and reliable experimental model for studies on acute pancreatitis.

Acute Disease↗
PubMed1975

Foreign serum-induced pancreatitis in mice. I. A new model of acute pancreatitis.

Within a few hours after one injection of fresh human serum by the intraperitoneal route only, mice developed pancreatic acinar cell necrosis and inflammation, fat necrosis, elevated serum amylase and a shocklike state. The extent of these lesions and mortalities were roughly dose dependent and were not noticeably modified by either different fasting cycles or pilocarpine. Acinar cell changes and necrosis usually developed first in subserosal acini. The earliest ultrastructural change detected was nonspecific swelling of cytoplasmic compartments which was reversible but also preceded the cytoplasmic degradation that developed in cells undergoing necrosis. Notably, zymogen granule dissolution neither preceded nor accompanied this swelling, but developed pari passu with cell degradation. Occasionally, intact granules were found in necrotic cells. Serum was cytotoxic for isolated acinar cells in vitro, even in the presence of soybean trypsin inhibitor. These results (1) indicate that the injury mechanism in vivo is directly initiated through contact of serum with acinar cell surfaces and is independent of zymogen secretions and trypsin activation, and (2) suggest that a rapid disturbance in cell membrane permeability results, the magnitude of which being the primary determinant of cell death. Pancreatic toxicity of human serum was abolished by aging, heating, ethylenediaminetetraacetic acid, heparin, zymosan, cobra venom factor, and absorptions with mouse red blood cells, against which fresh, unabsorbed serum was hemolytic. Pancreatic toxicity in vitro and, to a much lesser extent, in vivo was reconstituted by combining the red blood cell-absorbed serum with either heated serum, or with IgM-enriched, but not IgG serum fractions. Fresh cord serum was virtually nontoxic and could substitute for absorbed serum in such reconstitutions. These results indicate that the injury mechanism involves at least two serum components. By both circumstance and analogy, other results and a review of other examples of foreign sera toxicity suggest that they are components of a complement-dependent, cytotoxic heterophile antibody system. The relevance of this odd phenomenon is that it offers a simple model of acute pancreatitis, contributes to the debunking of traditional notions of the pivotal role of zymogens in the initiation of acute pancreatitis, and hints at a potential pathogenetic connection between pancreatitis and products of immune or related reactions.

Acute Disease↗