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G Kauffman

Publications and source records attributed to G Kauffman.

16 recordsLinked to original sources
PubMed1995

Water-clear cell adenoma of the parathyroid. A case report with immunohistochemistry and electron microscopy.

We report a water-clear cell adenoma of the parathyroid gland, a lesion which to our knowledge has not been described previously. Like its rare but well-described hyperplastic counterpart, water-clear cell hyperplasia, this adenoma is composed of cells with abundant foamy-to-granular cytoplasm and mild nuclear pleomorphism. The cells form glandular structures and cell nests separated by fine fibrovascular septae. The tumor cells stain positively with anti-parathyroid hormone and show characteristic glassy and flocculate material by electron microscopy. Unlike water-clear cell hyperplasia, water-clear cell adenoma is a solitary lesion that compresses the residual nonneoplastic parathyroid gland.

Adenoma↗
PubMed1991

Role of central prostaglandin E2 in the regulation of gastric acid secretion in the rat.

The central action of prostaglandin E2 (PGE2) on gastric acid secretion was investigated in rats by comparing the effects of intracisternal (i.ci.) and i.v. administration of PGE2 and the influence of i.ci. injection of indomethacin on acid secretion and PGE2 generation in the brain and stomach. I.ci. injections of PGE2 (1-10 micrograms) or the stable analog, 16,16-dimethyl PGE2, (0.01-0.1 micrograms) induced a dose dependent inhibition of baclofen-stimulated gastric acid secretion by 0-82% and by 7-87% respectively. I.v. infusion of PGE2 also induced a dose related inhibition of baclofen-stimulated acid secretion, but 10 fold higher doses were required. I.ci. or i.v. injection of indomethacin in doses ranging from 50 to 500 micrograms/rat, produced a similar dose dependent inhibition of the PGE2 generation in both the gastric mucosa and brain cortex measured 1 h post injection. I.ci. injection of indomethacin (500 micrograms) increased within 10 min acid secretion with a peak response at 20-30 min; 60-120 min post injection, when prostaglandin synthesis was inhibited by 90%, basal and baclofen-stimulated acid output were not altered. These results further establish that PGE2 acts in the brain to inhibit vagally stimulated gastric acid secretion in rats, and do not support a tonic inhibitory influence of endogenous brain PGE2 in the regulation of gastric acid secretion. In addition, these data showed that indomethacin injected i.ci. at 500 micrograms does not induce a selective inhibition of prostaglandin synthesis in the brain.

16,16-Dimethylprostaglandin E2↗
PubMed1991

Abrupt vessel closure following platelet transfusion post-PTCA.

A successful PTCA was complicated by abrupt closure following a platelet transfusion which was given for control of local bleeding. Possible mechanisms of abrupt closure are discussed. Recommendation is made to avoid giving platelet transfusion following PTCA.

Aged↗
PubMed1991

Localization of central prostaglandin E2 antisecretory effects.

Intracerebroventricular prostaglandin E2 (PGE2) inhibits stimulated gastric acid secretion; however, the central site of action is unknown. Specific PGE2 binding sites have been localized to the ventromedial hypothalamic nucleus and central amygdala (A). The nuclear accumbens has been shown to play a role in central neurotensin-induced antisecretory effects. These studies tested the hypothesis that microinjections of PGE2 into the ventromedial hypothalamic nucleus, central amygdala, and nuclear accumbens inhibit stimulated gastric acid secretion. The hippocampus served as a cerebral control region. Two days before the experiments, metal cannulas were stereotaxically positioned bilaterally into specific areas of the brain, and metal gastric cannulas were operatively implanted, under nembutal anesthesia, in male 250-g Sprague-Dawley rats. On the experimental day, the rats, fasted for 14 hours, were given saline or PGE2 (0.1-1.0 micrograms in 0.2 microL/side) through the central cannulas 10 minutes before administering pentagastrin (40 micrograms/kg SC). Gastric secretion was measured at 30-minute intervals and expressed as acid output, micromoles per hour. Acid output (mean +/- SE) in control animals was 161 +/- 14 mumol/h. Prostaglandin E2 administration at doses of 0.10, 0.50, and 1.0 micrograms/side (a) into ventromedial hypothalamic nucleus reduced acid output to 53 +/- 11,* 36 +/- 10,* and 27 +/- 11* mumol/h regularly; (b) into NACB reduced acid output to 157 +/- 36, 60 +/- 12,* and 38 +/- 12* mumol/h; and (c) into A reduced acid output to 144 +/- 31, 141 +/- 26, and 90 +/- 19* mumol/h, respectively (*P less than 0.05 by Neuman-Keuls test). Prostaglandin E2 (0.50 micrograms/side) administration into hippocampus had no significant effect on acid output (134 +/- 28 mumol/h). Although central PGE2 administration was associated with hyperthermia, this occurred at lower doses than those required to inhibit acid secretion. Prostaglandin E2 administration into specific brain areas known to have PGE2 receptors, the central amygdala and ventromedial hypothalamic nucleus, and into nuclear accumbens inhibits stimulated gastric acid secretion. These observations suggest that PGE2 may have a physiological role in the central control of gastric acid secretion.

Amygdala↗
PubMed1991

Mesolimbic dopamine mediates gastric mucosal protection by central neurotensin.

Bilateral microinjection (1.0 microliter/side) of neurotensin (NT; 0.3, 1.5, and 3.0 micrograms/side) into the nucleus accumbens (NACB) and ventral tegmental area (VTA) but not in substantia nigra and striatum reduced gastric mucosal injury produced by 2 h of cold-water restraint (CWR). The minimal effective dose for NT-induced protection was 10-100 times lower when administered directly into NACB than into the lateral ventricle. These effects were blocked by pretreatment with the dopamine (DA) receptor antagonist, haloperidol (Hal; 0.5 microgram/side) given directly into NACB. Injection of 6-hydroxydopamine into VTA depleted endogenous DA and inhibited gastric mucosal protection against CWR-induced injury afforded by NT pretreatment. NT, given into either VTA and NACB, inhibited pentagastrin-stimulated gastric acid secretion. These results suggest that VTA and NACB, which represent the mesolimbic DA system, are important locations for interaction between NT and DA receptors to produce gastric mucosal protection against CWR-induced injury.

Animals↗
PubMed1990

Monoamine oxidase B inhibition reduces gastric mucosal blood flow, basal acid secretion, and cold water restraint-induced gastric mucosal injury in rats.

Inhibition of monoamine oxidase B (MAO B) by selective inhibitors pargyline and L-deprenyl increases dopamine (DA) and norepinephrine (NE) concentrations in nucleus accumbens (NACB) and is associated with reduction in cold water restraint-induced gastric mucosal injury, inhibition of basal gastric acid output, and regional gastric mucosal blood flow. Similar effects were not observed with administration of MAO A inhibitors. These observations suggest that activation of central dopamine and norepinephrine receptors, particularly in NACB, are involved in the control of gastric mucosal function.

Animals↗
PubMed1989

Aspirin-induced gastric mucosal injury: lessons learned from animal models.

This review of the mechanisms by which aspirin causes gastric mucosal damage points to the involvement of two potential mechanisms. Aspirin, which inhibits cyclooxygenase, is rapidly deacetylated to salicylate. Salicylate is toxic to cells and affects mucosal barrier function, reduces cytosolic adenosine triphosphate, stimulates sodium transport, and increases proton dissipation from surface epithelial cells. Cyclooxygenase inhibition makes the gastric mucosa more susceptible to injury, inhibits mucus and bicarbonate secretion, alters the physicochemical nature of mucus, stimulates fundic but not antral [3H]thymidine incorporation, and reduces epithelial surface hydrophobicity. No single mechanism seems to be involved. It is likely, instead, that the toxic effects of salicylate and the effect of cyclooxygenase inhibition work in concert to render the mucosa more susceptible to injury, resulting in mucosal damage.

Animals↗
PubMed1989

Prostaglandin E2 production by dispersed canine fundic mucosal cells. Contribution of macrophages and endothelial cells as major sources.

Endogenous prostaglandins (PGs) influence resistance of the gastric mucosa to injury, but the source of PGs is unknown. Using radioimmunoassay, we studied PG production by dispersed canine fundic mucosal cells. PGE2 production, stimulated by bradykinin, epidermal growth factor, zymosan, and calcium ionophore, was greater in the small-cell elutriator fraction (SCEF) than in the medium and large cell fractions, which contained mucous, chief, and parietal cells. Linear density gradients of SCEF cells revealed maximal PGE2 production in cells of light density. Mast, endocrine, and endothelial cells did not account for this PGE2 production. Macrophages, identified by uptake of acetylated-LDL, immunoreactivity with antibodies to the human Ia antigen, and phagocytosis of fluorescent latex particles, were enriched in the SCEF and correlated with PGE2 production in the density gradient. Magnetic separation of cells in the SCEF-ingesting iron particles enriched PGE2 production. Fractions enriched in endothelial cells present in intact capillary fragments, but depleted of macrophages, also produced PGE2. Regulation of PGE2 production differed among cell types. Fibroblasts were easily cultured from submucosa, but were not detected in the SCEF. We conclude that macrophages and capillary endothelial cells are major producers of PGE2 in the canine fundic mucosa.

Animals↗
PubMed1987

Potent CNS action of calcitonin to inhibit cysteamine-induced duodenal ulcers in rat.

Intracisternal injection of calcitonin (0.01-5 micrograms) dose dependently prevented the development of duodenal ulcers induced by cysteamine in female rats. By contrast, intravenous infusion of the peptide at a dose 50 times higher than an effective intracisternal dose, had no effect. Intracisternal injection of calcitonin increased by three fold the generation of 6-keto-PGF1 alpha, the stable hydrolysis product of PGI2, in the duodenal mucosa. These studies demonstrated that calcitonin acts within the brain to potently suppress duodenal ulcers induced by cysteamine. The mechanisms of the antiulcer effect may involve changes in prostaglandin generation along with alterations of gastrointestinal secretion and motility associated the central injection of calcitonin. Growing evidence suggests that salmon calcitonin may act as a neuromodulator or neurotransmitter in the central nervous system. Specific binding sites have been demonstrated for calcitonin in the hypothalamus, brain stem and dorsal horn of the spinal cord using homogenate and membrane preparations or in vitro autoradiography methods. The peptide injected into the cerebrospinal fluid (CSF) produces a wide spectrum of biological effects including analgesia, hyperthermia, changes in pituitary hormone release, decrease in food and water intake, locomotor activity, and blood pressure. Numerous studies also demonstrated that calcitonin acts within the brain to markedly influence gastrointestinal secretory and motor function in rats and dogs and gastric ulceration in rats. In particular, intracisternal injection of salmon calcitonin was found very potent to selectively inhibit gastric ulcers elicited by stress, aspirin and central thyrotropin-releasing factor but not by necrotizing agents. In the present study, we further investigated the antiulcer effect of salmon calcitonin using the well established cysteamine experimental model to induce duodenal ulcers in rats. Part of this work has been reported in abstract form.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Interaction of thiamin diphosphate and thiamin thiazolone diphosphate with wheat germ pyruvate decarboxylase.

The interactions of the apoenzyme of wheat germ pyruvate decarboxylase with thiamin diphosphate and with thiamin thiazolone diphosphate have been investigated. The results test hypotheses concerning the structure of the transition state for decarboxylation of the enzyme-bound adduct of pyruvate and thiamin diphosphate. Thiamin thiazolone diphosphate, a possible transition state analogue, binds to the apoenzyme by a two-step process. The first is slow and reversible (k = 200 M-1 s-1; K = 5 X 10(-7) M). The second step is irreversible (k = 1 X 10(-6) s-1). The rate constant for activation by thiamin diphosphate is 160 M-1 s-1. Thiamin diphosphate is released very slowly from the holoenzyme (k = 2 X 10(-5) s-1). Thiamin thiazolone diphosphate competitively inhibits activation of the apoenzyme by thiamin diphosphate, Ki = 2 X 10(-6) M. Km for thiamin diphosphate is only 3 times larger. Thiamin thiazolone is solvated preferentially to thiamin in 2-butanol, a medium whose polarity should resemble that of the binding site. It is concluded that the observed high affinity of thiamin thiazolone diphosphate for the apoenzyme is the result of a combination of effects which do not require the assumption that it is an analogue of the transition state for the decarboxylation of enzyme-bound 2-(2-lactyl) thiamin diphosphate.

Carboxy-Lyases↗
PubMed1983

A reproducible canine model of esophageal varices.

One of the most promising nonoperative techniques for control of variceal hemorrhage is sclerosis via the fiberoptic endoscope. Many questions remain, however, about sclerosing agents, guidelines for effective use, and limitations of endoscopic techniques. A reproducible large animal model of esophageal varices would facilitate the critical evaluation of techniques for variceal hemostasis or sclerosis. Our purpose was to develop a large animal model of esophageal varices. Studies in pigs and dogs are described which led to the development of a reproducible canine model of esophageal varices. For the final model, mongrel dogs had laparotomy, side-to-side portacaval shunt, inferior vena cava ligation, placement of an ameroid constrictor around the portal vein, and liver biopsy. The mean (+/- SE) pre- and postshunt portal pressure increased significantly from 12 +/- 0.4 to 23 +/- 1 cm saline. Weekly endoscopies were performed to grade the varix size. Two-thirds of animals developed medium or large sized esophageal varices after the first operation. Three to six weeks later, a second laparotomy with complete ligation of the portal vein and liver biopsy were performed in animals with varices (one-third of the animals). All dogs developed esophageal varices and abdominal wall collateral veins of variable size 3-6 wk after the first operation. After the second operation, the varices became larger. Shunting of blood through esophageal varices via splenic and gastric veins was demonstrated by angiography. Sequential liver biopsies were normal. There was no morbidity or mortality. Ascites, encephalopathy, or spontaneous variceal bleeding did not occur. We have documented the lack of size change and the persistence of medium to large esophageal varices and abdominal collateral veins in all animals followed for more than 6 mo. Variceal bleeding could be induced by venipuncture for testing endoscopic hemostatic and sclerosis methods. We suggest other potential uses of this reproducible canine model of esophageal varices.

Abdominal Muscles↗
PubMed1981

Search for resistances controlling canine gastric emptying of liquid meals.

Previous work has indicated that a chemoselective resistance controls gastric emptying. By use of meals of glucose or oleate, which were shown to empty spontaneously from dogs' stomachs half as fast as saline, we sought to locate this resistance by studying flow under controlled pressures in various regions of the gastrointestinal tract. In intact dogs, gastric outflow of glucose or oleate rose one-third as fast as outflow of saline as gastric pressure was raised, and this increased resistance to outflow of nutrients was unaffected by truncal vagotomy and pyloroplasty. In fistula dogs, gastroduodenal outflow rose linearly with gastroduodenal pressure gradients; outflow was markedly inhibited in a dose-related manner by intestinal oleate but not glucose. Inhibition by oleate was abolished by pyloroplasty. Glucose or oleate flowed into the small bowel from a barostat only slightly slower than saline. However, there was a strong inhibition of intestinal inflow of all three meals by gastric distension, an effect unaltered by truncal vagotomy. The findings suggest that gastric emptying is controlled by complex interactions among pressures and resistances, both within and beyond the stomach.

Animals↗
PubMed1980

[Percutaneous nephropyelostomy in combination with sonography and x-ray technology (author's transl)].

Sonography guarantees in a simple manner visualisation of the kidneys and of the renal tract independent of functioning. Besides enabling an exact localisation, sonography yields accurate data on the spatial depth. Hence, it must be considered the method of choice for antegrade pyelography and percutaneous nephropyelostomy, especially if the kidney is inactive. The requisite puncture is performed according to a modified Seldinger technique. The article reports on technical details, indication and results based on a study of 20 patients.

Adolescent↗
PubMedDate not supplied

Development of a patient education program for new amputees.

In this article, the authors describe how the needs of the patient with a new amputation were assessed and how behavioral objectives were developed for an educational program that would address the knowledge, motor skills, and attitudes necessary for self-care. Two teaching techniques are described. An evaluation process that identifies the patient's or family's achievement of the objectives is discussed.

Amputees↗
PubMedDate not supplied

Fatality resulting from methylphenidate overdose.

A case involving an accidental overdose fatality resulting from an intravenous injection of crushed Ritalin (methylphenidate) tablets is presented. The drug was quantified by gas chromatography/nitrogen-phosphorus detection and confirmed by gas chromatography/mass spectrometry. Concentrations of drug were as follows: blood, 2.8 mg/L; bile, 5.7 mg/L; kidney, 3.0 mg/kg; liver, 2.1 mg/kg; and stomach contents, 1.6 mg total. Other drugs and volatile substances were not detected.

Adult↗