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Biomedical subjects

D L Mainz

Publications and source records attributed to D L Mainz.

8 recordsLinked to original sources
PubMed1981

Gastric function in hypopituitarism: a biochemical study.

The specific trophic effects of gastrointestinal hormones on gastric function are now recognized. In addition, pituitary, thyroid and adrenal hormones play an important role in maintaining over all gastric function. The majority of studies regarding hormonal effects on the stomach, however, have been carried out only in experimental animals. This paper reports a patient with gastric atrophy and hypopituitarism. Following therapy of the hypopituitarism with cortisone acetate, sodium levothyroxine and testosterone, the following observations were made: serum gastrin increased 137%; mucosal DNA synthesis and content and gastric acid secretion all increased. These data indicate in this one patient the role of these hormones in gastric function.

Cortisone↗
PubMed1977

Eosinophilic ascites. A case report and review of the literature.

Hypereosinophilic syndrome is a multisystem disease with progressive valvular dysfunction as a prominent feature. Ascites has not been recognized as a part of this syndrome. This paper presents a patient with hypereosinophilic syndrome who initially developed ascites and was recognized to have cardiac disease. The differential diagnosis of eosinophilic ascites is discussed.

Adult↗
PubMed1977

Pancreatic acinar cell metabolism and function.

This review outlines progress made during the past 11 years in research related to pancreatic acinar cell metabolism and function. We have reviewed information gained at the cellular level concerning structural and functional relationships, and effects of fasting and feeding, as well as the action of gastrointestinal hormones and cholinergic agonists on acinar cells. In toto, this information outlines a significant role for gastrointestinal hormones as mediators of secretion, synthesis, and control of trophism. This information provides a basis for more sophisticated inquiries as to the mechanisms of injury of alcohol and drugs. The information may prove helpful in developing diagnostic modalities for pancreatic disease, as well as understanding the processes involved in neoplastic transformation.

Amino Acids↗
PubMed1976

Fine structure of pancreatic adenocarcinoma induced in rats by 7,12-dimethylbenz(a)anthracene.

We induced pancreatic adenocarcinomas in Long-Evans rats by placing crystals, 2-3 mg, of 7,12-dimethylbenz[a]anthracene (DMBA) in a 2- to 3-mm incision in the "head" of the pancreas approximately 1 cm from the duodenum. The incisions were closed with one or two silk sutures. The animals were killed 4-10 months after DMBA implantation, and nodules were removed and routinely prepared for light and/or electron microscopic study. Histologic organization varied from normal, through areas of tubule-like structures, to sheets of pleomorphic tumor cells. Electron microscopic study of tumor cells revealed large electron-lucent nuclei that frequently had irregular outlines and prominent nucleoli. The predominant feature of the cytoplasm was abundant rough endoplasmic reticulum. Zymogen granules were rare. Adjacent cells sometimes were jointed by an apical junctional complex to form a lumen into which projected irregular microvilli. A basal lamina sometimes occurred at the bases of the tumor cells. The fine structural similarity of these tumor cells to acinar cells was noted.

9,10-Dimethyl-1,2-benzanthracene↗
PubMed1973

Hormonal control of pancreatic growth.

Investigations have outlined pancreatic secretory and synthetic responses to gastrointestinal hormones. However, there is little information concerning hormonal influences on pancreatic growth. These studies were designed to examine effects of chronic administration of bethanechol and cholecystokinin-pancreozymin (CCK-PZ) on the pancreas. Male albino rats were given saline, bethanechol, 6 mg/kg, or CCK-PZ, 20 U/kg, intraperitoneally twice daily and killed after 5 days. The following changes were studied; pancreatic weight; RNA, DNA, and protein content; and [(14)C]thymidine incorporation into DNA. Bethanechol administration was associated with a 20% increase in pancreatic weight and a 33% increase in mg protein/100 mug DNA. In bethanechol-treated groups, amounts of DNA/gram body weight and incorporation of [(14)C]thymidine into DNA were similar to controls. CCK-PZ administration was associated with a 71% increase in pancreatic weight and a 38% increase in mg protein/100 mug DNA. In CCK-PZ-treated groups, amounts of DNA/gram body weight were increased by 42% and [(14)C]thymidine incorporation into DNA was increased by 185%. These studies indicate that bethanechol administration was associated with increases in pancreatic cell mass (hypertrophy). CCK-PZ administration was associated with increases in cell mass and cell numbers (hypertrophy and hyperplasia). This information suggests the importance of CCK-PZ in maintaining pancreatic functional integrity. Although bethanechol and CCK-PZ elicit similar secretory responses, their mode of action on the cell, at least as far as growth influences are concerned, appears to be different.

Animals↗