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Biomedical subjects

M Feldman

Publications and source records attributed to M Feldman.

At least 253 records · Page 14Linked to original sources
PubMed1988

Spontaneous pneumomediastinum and subcutaneous emphysema.

Spontaneous pneumomediastinum with subcutaneous emphysema is a well-documented phenomenon which usually follows a benign course and rarely results in circulatory collapse and death. The condition is caused by a sustained increase in the intra-alveolar and intrabronchial pressure with air dissecting along the perivascular spaces of the mediastinum. The majority of patients respond to conservative therapy and rarely require aggressive surgical intervention. Three cases are presented. The anatomy, etiology and the pathophysiology of the disease are reviewed, and the treatment options discussed.

Adolescent↗
PubMed1987

Steroid receptor antibodies in autoimmune disorders.

Sera from patients with autoimmune disorders have been analyzed for the presence of antibodies against the estrogen receptor. About 42% of the male and 34% of the female patients had measureable levels of antibody under our assay conditions. However, whereas the male patient population had significantly higher levels of anti-estrogen receptor than normal males, there was no significant difference between female patients and controls. Separation of the estrogen receptor by sucrose gradient centrifugation into the large (9-10S) and small (4S) molecular weight forms demonstrated that only the large form was antigenic, suggesting that the antibodies are not interacting with the steroid binding subunit. The clinical significance of increased levels of antibodies against the estrogen receptor in a percentage of male patients remains to be established.

Autoantibodies↗
PubMed1987

Is plasma GABA of peripheral origin?

Plasma levels of gamma-aminobutyric acid (GABA) appear to be altered in affective disorders and alcoholism. Plasma levels of GABA were not affected by menstrual cycle, exercise, gender, gut flora, nor by cholinergic stimulation by bethanechol. An obvious peripheral source for plasma GABA could not be demonstrated.

Adult↗
PubMed1987

Positive intravenous secretin test in patients with achlorhydria-related hypergastrinemia.

The intravenous secretin test is widely used to distinguish gastrinoma (Zollinger-Ellison syndrome) from other causes of fasting hypergastrinemia. We report 2 patients with fasting hypergastrinemia and a rise of greater than 200 pg/ml in serum gastrin concentration after intravenous injection of 2 CU/kg body wt of pure natural secretin. Both patients had pentagastrin-fast achlorhydria. Thus, the intravenous secretin test may be positive in patients with achlorhydria-related hypergastrinemia. Gastric acid secretion should be measured in hypergastrinemic patients before embarking on a secretin test.

Achlorhydria↗
PubMed1987

Gastrointestinal ulcer formation in rabbits immunized with prostaglandin E2.

Circulating prostaglandin E2 antibodies were produced in 12 rabbits immunized with prostaglandin E2-thyroglobulin conjugate and ulcers occurred in 10, usually in the stomach and less often in the small intestine. Immunization of rabbits with both prostaglandin E2 and 6-keto prostaglandin F1 alpha significantly increased the number of gastric ulcers compared with rabbits immunized with prostaglandin E2 alone. Gastrointestinal ulceration in prostaglandin E2-immunized rabbits was not prevented by oral enprostil. Gastrointestinal ulcers occurred as early as 6 wk after beginning immunization and often perforated with resulting fatality. Neither prostaglandin E2 antibodies nor ulcers developed in rabbits immunized with thyroglobulin vehicle (controls). Passive immunization of unimmunized rabbits with prostaglandin E2-hyperimmune plasma led to acute gastric ulcers within 9 days, whereas passive transfer of nonimmune plasma did not produce ulcers. This latter finding suggests that prostaglandin E2 antibodies per se were responsible for ulcer formation.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

Effect of cisapride on gastric emptying of indigestible solids in patients with gastroparesis diabeticorum. A comparison with metoclopramide and placebo.

Cisapride is a prokinetic agent believed to facilitate acetylcholine release from the myenteric plexus of the gut. The effect of cisapride on gastric emptying of solids was studied in 9 diabetic patients, all of whom had delayed gastric emptying of indigestible solids (gastroparesis). Six patients had chronic nausea and vomiting, and 3 had no symptoms. Cisapride (5 mg) was given intravenously 15 min before ingestion of a 400-kcal test meal and 10 indigestible solid radiopaque markers. On separate days and in random order each patient also received intravenous metoclopramide (10 mg) or placebo 15 min before ingestion of the meal and markers. Mean gastric emptying of radiopaque markers, assessed by serial radiographs of the gastric region, was accelerated by metoclopramide and cisapride, but the difference reached significance only with cisapride (p less than 0.05). There was considerable intersubject variability in gastric emptying responses to cisapride and metoclopramide. No side effects occurred with either drug. This study indicates that acute, intravenous administration of cisapride accelerates gastric emptying of indigestible solids in patients with diabetic gastroparesis.

Adult↗
PubMed1987

Variable contribution of gastrin to gastric acid secretion after a meal in humans.

The purpose of these experiments was to determine the contribution of gastrin to the acid secretory response to eating in healthy human subjects. To simulate the gastric and intestinal phases of eating, a meal was homogenized and then infused into the stomach through a nasogastric tube. At the same time, the cephalic phase of acid secretion was activated by sham feeding. With this simulated meal, mean serum gastrin concentration increased from a basal value of 43 +/- 9 pg/ml to an average postprandial gastrin concentration over 2 h of 121 +/- 25 pg/ml. Gastrin release after this simulated meal was similar to gastrin release after a normally eaten meal in the same 12 subjects. Gastric acid secretion in response to the simulated meal, which was measured by in vivo intragastric titration, averaged 24.2 +/- 2.4 mmol/h. To determine how much of this postprandial acid secretion could be attributed to gastrin, gastrin 17 I was infused intravenously in the same subjects on a separate day and acid secretion and serum gastrin concentrations were measured. By relating serum gastrin concentration during gastrin 17 infusion to concomitant acid secretion, we determined that an average postprandial serum gastrin concentration of 121 pg/ml could result in an acid secretion rate of 21.5 mmol/h, 89% of the actual acid secreted after the simulated meal in these subjects. However, in individual subjects, the amount of gastrin released after a meal could produce as little as 51% or as much as 162% of actual postprandial acid secretion. Thus, in individual human subjects the contribution of gastrin to acid secretion after a meal is variable.

Adult↗
PubMed1987

Effect of indomethacin on gastric mucosal prostaglandins in humans. Correlation with mucosal damage.

We evaluated in healthy human beings the effect of indomethacin on gastric mucosal prostaglandin concentration and on gastric mucosal damage in a placebo-controlled study. Prostaglandin E2, prostaglandin F2 alpha, and 6-keto prostaglandin F1 alpha concentrations of gastric mucosal biopsy specimens, obtained endoscopically, were measured by radioimmunoassay. Mean prostaglandin concentration of the antrum and fundus was similar. In both regions there was considerable intersubject variability in prostaglandin concentration. Repeated 50-mg oral doses of indomethacin for 4 days reduced mean prostaglandin F2 alpha and E2 concentration by 50.2% and 69.4%, respectively, in the fundus and by 40.0% and 49.7% in the antrum, but this led to no significant mucosal damage when assessed endoscopically or histologically. A single 100-mg oral dose of indomethacin reduced mean prostaglandin F2 alpha and prostaglandin E2 concentration by 81.4% and 60.9% in the fundus and by 64.2% and 57.5% in the antrum and also induced significant mucosal injury in both regions when assessed endoscopically. However, there was no correlation between degree of suppression of prostaglandin concentration by indomethacin and endoscopic evidence of mucosal damage.

Administration, Oral↗
PubMed1987

Gastroduodenal ulceration following active immunization with prostaglandin E2 in dogs. Role of gastric acid secretion.

In this study we present evidence to suggest that gastroduodenal mucosal defects may occur in gastric fistula dogs actively immunized with PGE2-thyroglobulin conjugate. One of four PGE2-immunized dogs developed a chronic pyloroduodenal ulcer with penetration into the pancreas and the other three had endoscopic evidence of gastric and/or duodenal erosions. In contrast, no gastroduodenal mucosal defects were seen in control dogs immunized with thyroglobulin alone. Occurrence of gastroduodenal ulcers or erosions was temporally related to formation of specific antibody to PGE2 suggesting that PGE2 antibody may be responsible for lesion formation. An increase in gastric acid secretion was not observed in PGE2-immunized dogs. Thus, it is likely that mucosal defects occur as a result of an impairment of PGE2-mediated mucosal defense mechanisms. Since gastroduodenal lesions can be visualized by endoscopy, the dog may prove to be useful in studying the role of endogenous PG in ulcer diseases.

Animals↗
PubMed1987

Evidence for a nonprolactin, non-growth-hormone mammary mitogen in the human pituitary gland.

To determine whether the human pituitary contains a previously unidentified, nonprolactin (non-hPRL), non-growth-hormone (non-hGH) factor capable of stimulating mammary development, we tested the effects of whole human pituitary extract (hPE) and pituitary extracts depleted of hPRL and hGH ("stripped hPE") in hypophysectomized, castrated estradiol (E2)-treated male rats and rhesus monkeys. Both whole and stripped hPE significantly stimulated rat mammary development (mean scores = 3.3 and 2.0, respectively, on a scale ranging from 0 to 4) in comparison with controls (mean score = 1.0). Mammary development was not due to minute concentrations of hGH or hPRL remaining in stripped hPE because 30- to 100-fold higher concentrations of hGH (Genentech) and 1000-fold higher concentrations of hPRL were required to stimulate significant mammary development. Non-pituitary extracts of human ovary, muscle, and serum, and bovine serum albumin did not stimulate rat mammary gland growth. Trypsin destroyed the mammary mitogenic activity of whole hPE, indicating that the unidentified factor is likely a protein. Mammary growth and development were also stimulated in hypophysectomized, E2-treated monkeys by stripped hPE (mean histological score = 3.25 vs. 1.35 in control animals). Monkeys receiving stripped hPE had undetectable levels of hGH and hPRL in serum sampled over a 24-hr period. These findings suggest that the human pituitary contains a non-hPRL, non-hGH factor that stimulates mammary growth and may be important in normal mammary growth and development and perhaps in breast cancer.

Animals↗
PubMed1987

Comparison of two antimuscarinic drugs, pirenzepine and propantheline, on gastric acid secretion, serum gastrin concentration, salivary flow and heart rate in patients with duodenal ulcer disease.

Effects of orally-administered pirenzepine and propantheline bromide on food-stimulated gastric acid secretion, serum gastrin concentration, salivary flow and heart rate were compared in 10 duodenal ulcer patients in a placebo-controlled, double-blind study. Pirenzepine inhibited acid secretion by 25, 36 and 44% at doses of 50, 100, and 150 mg, respectively, while propantheline inhibited acid secretion by 32 and 41% at doses of 15 and 45 mg, respectively. None of the doses of pirenzepine affected food-stimulated serum gastrin concentrations, whereas 45 mg propantheline increased serum gastrin concentration significantly above placebo control. Enhancement of gastrin release by propantheline was not due to its antisecretory effect since intragastric pH after the meal was held constant at 5.0 by intragastric titration in vivo. Pirenzepine had no significant effect on heart rate and little or no inhibitory effect on salivary volume, depending on the dose administered. By contrast, both doses of propantheline increased heart rate and reduced salivary volume significantly (P less than 0.05). Thus, pirenzepine and propantheline in the doses administered inhibited acid secretion to approximately the same extent but pirenzepine had fewer effects on other organs.

Adult↗
PubMed1987

Mechanism for high PCO2 in gastric juice: roles of bicarbonate secretion and CO2 diffusion.

The partial pressure of CO2 (PCO2) in gastric juice often exceeds the PCO2 of blood. CO2 in gastric juice may originate from blood and enter luminal fluid by diffusion, or CO2 may be produced in the lumen of the stomach from the reaction of HCO3- and H+. Because CO2 production from HCO3- is dependent on acid (low pH), we suppressed acid secretion with intravenous cimetidine to estimate to what extent appearance of CO2 in luminal fluid is due to production from HCO3-. When denervated fundic pouches of dogs were distended with saline, the PCO2 of the solution increased to the PCO2 of blood in approximately 20 min, with the initial rate of appearance of CO2 in the pouch solution only minimally affected by cimetidine. Thereafter, PCO2 of luminal fluid continued to increase to 50-60 mmHg in the absence of cimetidine, whereas PCO2 of luminal fluid remained approximately equal to that of blood when cimetidine was infused (P less than 0.001, cimetidine vs. control). The mean pH in the pouch solution remained between 6.3 and 6.9 during cimetidine infusion but decreased to 4.75 without cimetidine (P less than 0.001). In additional experiments, an acidic solution with high PCO2 (242 +/- 3 mmHg) was infused into the fundic pouches. PCO2 in luminal fluid decreased rather slowly toward plasma PCO2, requiring 240 min for luminal fluid PCO2 to decrease to 56 +/- 2 mmHg. Thus the permeability of the gastric mucosa to luminal CO2 was relatively low.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1987

Detailed comparison of basal and food-stimulated gastric acid secretion rates and serum gastrin concentrations in duodenal ulcer patients and normal subjects.

We measured basal and peak acid outputs, food-stimulated acid secretion, and basal and food-stimulated serum gastrin concentrations in a large group of duodenal ulcer patients and normal subjects. Basal and peak acid outputs were significantly higher in ulcer patients. In contrast, acid secretion was similar in the groups when food was infused into the stomach and when sham feeding was combined with meal infusion to simulate normal eating. Meal-stimulated acid secretion, expressed as a percentage of peak acid output to correct for differences in secretory capacity, was lower in ulcer patients (P less than 0.002). Basal serum gastrin concentrations were higher in ulcer patients, which may have contributed to higher basal acid output. However, increases in serum gastrin after food were similar in the groups. Duodenal ulcer patients, as a group, have increased basal and maximal acid secretion, but the amount of acid secreted and gastrin released after eating is normal.

Adult↗
PubMed1987

Effect of proximal gastric vagotomy on calculated gastric HCO3- and nonparietal volume secretion in man. Studies during basal conditions and gastrin-17 infusion.

We calculated gastric HCO3- and H+ secretion, as well as nonparietal and parietal volume secretion, in 15 duodenal ulcer patients who had previously undergone successful proximal gastric vagotomy, 15 unoperated duodenal ulcer patients, and 15 normal control subjects. Basal HCO3- secretion was not significantly altered after vagotomy, while basal H+ secretion, parietal volume and nonparietal volume secretion were reduced significantly. Intravenous gastrin-17 infusion reduced gastric HCO3- secretion by approximately 50% in both unoperated ulcer patients and normal subjects (P less than 0.05). Gastrin-17 infusion did not inhibit gastric HCO3- secretion after vagotomy. In fact, mean gastric HCO3- secretion increased to a nearly significant extent in response to gastrin (P = 0.06). These findings indicate that gastrin inhibits gastric HCO3- secretion in humans and that the gastrin-induced reduction in gastric HCO3- secretion is dependent upon intact vagal innervation to the oxyntic mucosa.

Bicarbonates↗
PubMed1987

Effect of sham feeding on acid secretion in patients with Zollinger-Ellison syndrome with or without proximal gastric vagotomy.

In dogs, vagal stimulation by sham feeding inhibits gastrin-stimulated gastric acid secretion from vagally denervated fundic pouches. To investigate this in humans, we sham fed patients with endogenous hypergastrinemia secondary to the Zollinger-Ellison syndrome. Whether these patients had been treated previously by proximal gastric vagotomy or not, sham feeding did not reduce basal acid secretion. Thus, sham feeding did not inhibit acid secretion in humans with hypergastrinemia, even when the fundus of the stomach had been vagally denervated.

Adolescent↗
PubMed1987

Expression of major histocompatibility class I genes in differentiating leukemic cells is temporally related to activation of c-fos proto-oncogene.

The relationship between the expression of the c-fos proto-oncogene and the expression of the class I major histocompatibility (MHC) antigens during the early stages of induced differentiation in three different leukemic cell lines was examined. In the U937 histiocytic lymphoma line TPA induced an increase in mRNA and cell surface MHC expression which followed induction of c-fos. In contrast, in the murine erythro-leukemia cell line, DMSO induced declining constitutive c-fos levels that were accompanied by declining mRNA and cell surface MHC expression. In the pluripotent HL60 promyelocytic line induction of macrophage differentiation with TPA led to c-fos induction and rising MHC levels, whereas induction of granulocyte differentiation with DMSO did not induce c-fos expression and was followed by declining MHC levels. Taken together, the results suggest that the c-fos proto-oncogene might be involved in the control of class I MHC antigen expression during differentiation.

Cell Differentiation↗