Search PubMed⌕ Search

Biomedical subjects

D E Wilson

Publications and source records attributed to D E Wilson.

At least 145 records · Page 8Linked to original sources
PubMed1982

Babesia, Theileria and Anaplasma spp. infecting sable antelope, Hippotragus niger (Harris, 1838), in southern Africa.

Some observations are recorded on blood parasites of sable antelopes. Blood smears of 124 of these antelopes from South Africa and Zimbabwe were examined and 7 were found to be positive for a Babesia sp., identified as Babesia irvinesmithi Martinaglia 1936. A total of 70 of the smears were positive for theilerial piroplasms, while 1 smear had macroschizonts (with cytomeres) and microschizonts of a Theileria (= Cytauxzoon) sp. One blood smear was positive for an Anaplasma sp. Attempts to isolate the Babesia sp. by subinoculating blood from sable to splenectomized and intact sable and splenectomized cattle were unsuccessful. Attempts to infect sable with Babesia bovis and Babesia bigemina were likewise unsuccessful. Theilerial piroplasms reached high levels in a splenectomized sable but could not be transmitted with blood to cattle. The Anaplasma sp. was found to be infective for sheep but not for cattle.

Anaplasma↗
PubMed1981

Comparison of intravenous and intramuscular sincalide (C-terminal octapeptide of cholecystokinin) on gallbladder contraction in man.

The effects of intramuscular and intravenous sincalide on gallbladder contraction and visualization of the bile ducts were compared in a group of 37 subjects referred for oral cholecystography. The maximum reduction in gallbladder size observed after sincalide 400 ng/kg intramuscular, 54.7 +/- 7.2% (mean +/- SEM), occurred 25 min after injection and was significantly greater than that observed after sincalide 20 ng/kg intravenous, 26.5 +/- 8.2%. Maximum reduction after sincalide 100 ng/kg intramuscular was 47.3 +/- 8.2%. The common bile duct was visualized in 60 and 45% of subjects after intramuscular and intravenous sincalide, respectively. The use of intramuscular sincalide 400 ng/kg intramuscular is an effective and convenient adjunct to oral cholecystography when significant gallbladder contraction and visualization of the common bile duct is desired.

Adolescent↗
PubMed1981

A new prostaglandin E1 analogue (CL115,574). I. antisecretory and cytoprotective effects in the rat.

The effects of a new analogue of PGE1 (CL115,574) on gastric acid secretion, mucus secretion and protection against stress and indomethacin-induced ulcers were studied in the rat. CL115,574 was more potent than PGE1 and cimetidine in inhibiting acid secretion. CL115,574 protected against the development of stress and indomethacin-induced ulcers and prevented the indomethacin-induced decrease in hematocrit at an ED50 (3 micrograms/kg) far below the antisecretory ED50 (1 microgram/kg). While inhibiting acid secretion, CL115,574 increased the volume of gastric secretion indicating a stimulation of nonparietal cell secretion by the rat stomach. In addition the compound stimulated the secretion of mucus into the gastric juice. On the basis of its potency as an inhibitor of acid secretion and these additional effects which are indicative of cytoprotective activity, CL115,574 should be further studied as a possible anti-ulcer agent in man.

Alprostadil↗
PubMed1981

A new prostaglandin E1 analogue (CL-115,574) II. Effects on gastric acid secretion in the dog.

The efficacy of CL-115,574, a prostaglandin E1 analogue, as an acid antisecretory agent was evaluated in dogs. CL-115,574 inhibited acid secretion maximally at an oral dose of 20 micrograms/kg causing 100% inhibition of acid secretion up to one hour after administration, with significant inhibition of secretion (30%) still present nearly four hours after drug administration. The wide disparity between the maximally effective antisecretory dose 20 micrograms/kg and the dose at which reproducible side effects occurred (1 mg/kg) suggests that this compound may be developed as an antisecretory compound for use in man.

Administration, Oral↗
PubMed1981

The clinical laboratory and hyperlipidemia: a clinician's view.

Many patients with hyperlipidemia are without symptoms, thus laboratory data are often the sole index of therapeutic success or failure. Aggressive laboratory investigation of patient and family may identify inherited hyperlipidemia long before the clinical manifestations of atherosclerosis. The classification system of Fredrickson et al and Goldstein et al are reviewed from an historical and a clinician's point of view. Specific phenotypes and phenocopies, their causes, clinical manifestations, and management are presented. The basic laboratory assessment of hyperlipidemia is described, specialized testing is reviewed, and promising new methodologies are discussed.

Cholesterol↗
PubMed1980

Association of the herpes simplex-1 viral gene for thymidine kinase with the human gene for adenylate kinase-1 in biochemically transformed cells.

The herpes simplex type 1 biochemically transformed human cell line, HB-1, was fused with thymidine kinase deficient rodent cells, and 18 hybrids were isolated using the HAT-ouabain selection system. The selected enzyme, viral thymidine kinase, was present in all 18 hybrids. In 16 of 18 hybrids the viral gene for thymidine kinase cosegregated with the human gene for adenylate kinase-1 (AK-1). Thirty-six bromodeoxyuridine (BrdUrd) resistant sublines were isolated from the 16 human AK-1 positive hybrids. Each BrdUrd-resistant subline was examined for the presence of the viral TK gene by back-selection in HAT medium, and for human AK-1. In all 36 BrdUrd-resistant sublines the viral TK gene cosegregated with the human AK-1 gene. These results indicate that the transforming viral DNA fragment was associated with a specific human chromosomal region in HB-1 cells.

Adenylate Kinase↗
PubMed1980

Association of herpes simplex thymidine kinase gene with chromosome No. 18 in transformed human cells.

The herpes simplex virus type-2 (HSV-2)-transformed human cell line HB-2-3 was fused with thymidine kinase (TK)-deficient mouse cells [LM(TK-)], and 12 independent hybrids were isolated with the use of the HAT (hypoxanthine, amethopterin, and thymidine)-ouabain selection system. Discontinuous polyacrylamide gel electrophoresis studies demonstrated that the HSV-2-specific TK was the selected enzyme in the hybrids. Isoenzyme analysis and karyotyping were used in the analysis of the hybrids for the presence of human chromosomes. All 12 hybrids contained human chromosome No. 18 and the enzyme peptidase A, which is encoded by a gene on this chromosome. Hybrids were exposed to bromodeoxyuridine (BrdUrd) as a means of selection for cells that had lost HSV-2 TK activity. Isoenzyme and karyotyping data obtained from 33 BrdUrd-resistant sublines were consistent with the hypothesis that the HSV-2 TK gene is associated with chromosome No. 18 in the HB-2-3 cell line.

Animals↗
PubMed1980

Antagonism of prostanoid-induced contractions of rat gastric fundus muscle by SC-19220, sodium meclofenamate, indomethacin or trimethoquinol.

1 The effects of SC-19220, sodium meclofenamate, indomethacin or trimethoquinol were studied on contractions of the rat stomach longitudinal muscle to prostaglandin D2 (PGD2), PGE2, PGF2 alpha, PGH2, epoxymethano PGH2 analogues, PGI2, 6-keto-PGF1 alpha, 6,15-diketo-PGF1 alpha and thromboxane B2. All the drugs reduced contractions to all the prostanoids, but the degree of reduction differed widely. Selectivity of blockade was assessed by comparison with acetylcholine (ACh). 2 With SC-19220 5 micrograms/ml the effect on thromboxane B2, PGD2 or PGH2 and its epoxymethano analogues was not significantly different from the small effect on ACh, but the other prostanoids were blocked to greater extents. 3 The effect of the cyclo-oxygenase inhibitor sodium meclofenamate, 1 or 2 micrograms/ml, on 6,15-diketo-PGF1 alpha or thromboxane B2 was similar to the small antagonism of ACh, whereas the other prostanoids were blocked to greater extents. Indomethacin, 1 microgram/ml, also reduced contractions to the prostanoids, but antagonism of the PGH2 epoxymethano analogues was considerably less than with meclofenamate. 4 The beta-adrenoceptor stimulant trimethoquinol, 50 ng/ml, was the most potent prostanoid antagonist tested; all the prostanoids except PGE2 were antagonized more than ACh.

Acetylcholine↗
PubMed1979

Cyclic nucleotides and the regulation of canine gastric acid secretion.

The response of the cyclic nucleotide system (cAMP, cGMP, adenylate cyclase, guanylate cyclase, and specific phosphodiesterases) to two gastric acid secretagogues, histamine and acetylcholine, and two secretory inhibitors, prostaglandin E2 and secretin, was studied in vivo and in vitro in canine gastric fundic mucosa. Histamine and acetylcholine in vivo failed to stimulate cAMP but significantly increased cGMP; in vitro they affected neither adenylate cyclase nor guanylate cyclase. Prostaglandin E2 and secretin, however, increased cAMP in vivo and significantly stimulated adenylate cyclase in vitro. Specific phosphodiesterases were unaffected by these compounds. The changes, while not specifically localized to the acid-producing cells, are consistent with the suggestion that the control of canine gastric acid secretion may be mediated by changes in mucosal cAMP and cGMP.

Acetylcholine↗
PubMed1979

The effects of a prostaglandin endoperoxide analogue on canine gastric acid and mucus secretion.

The effects of U-46619, a stable analogue of the prostaglandin endoperoxide PGH2, were studied on canine gastric acid secretion, gastric mucosal blood flow, and secretion of mucus into gastric juice and compared to those of PGE2. U-46619 was approximately four and three times as potent as PGE2 in inhibiting acid secretion and stimulating mucus secretion, respectively. When infused at a low dose, U-46619 inhibited acid secretion directly without causing a decrease in the ratio of mucosal blood flow to volume rate of secretion (R), this effect being similar to that observed for PGE2. However, unlike PGE2, U-46619 when administered in a higher dose caused a decline in R while decreasing acid secretion and mucosal blood flow, suggesting a primary restriction of blood flow. The antisecretory effects of arachidonic acid may be due in part to the endogenous formation of prostaglandin endoperoxides as opposed solely to prostaglandin formation. Considering the antisecretory and mucogenic actions of U-46619, nontoxic analogues of prostaglandin endoperoxides may be of value as antiulcer agents.

Aminopyrine↗
PubMed1978

Heparin resistance and decreased hepatic triglyceride hydrolase release during long-term estrogen-progestin treatment.

These studies were undertaken to define the mechanism for the depression of post-heparin triglyceride hydrolase activity in women treated with estrogen-progestin oral contraceptives. Six treated and six control women were studied. Total, protamine-inhibited, and protamine-resistant triglyceride hydrolase activities were measured after six different intravenous doses of heparin in each subject in order to determine the dose-response relationships for lipase release. As has been reported during short-term treatment with estrogens, long-term treatment with oral contraceptive agents is accompanied by selective depression of protamine-resistant (hepatic) lipase activity. This depression can be partly reversed by the administration of large heparin doses, but maximally releasing heparin does fail to restore postheparin protamine-resistant activity to control values. These data are compatible with the idea that the releasable pool of hepatic triglyceride hydrolase activity is diminished in women who receive oral contraceptive agents and that the pharmacokinetics of its release are altered in such a way that only relatively high concentrations of heparin displace the enzyme from this pool.

Adult↗
PubMed1978

Postheparin plasma lipase activities in obesity: failure to increase with adipose organ enlargement.

Published studies have shown that overproduction of very low density lipoproteins is a major factor leading to hypertiglyceridemia in obesity. Few systematic studies of triglyceride removal or postheparin lipoprotein lipase activity (LPLA) in obesity have appeared. We have examined heparin-released lipoprotein triglyceride hydrolase activities in 12 lean and 12 obese age- and sex-matched volunteers after overnight fasting. Heparin doses were calculated to compensate for the disproportionality between body mass and plasma volume in obesity. Triglyceride hydrolase activities of hepatic (HTGLA) and extrahepatic (LPLA) origin were distinguished by in vitro inhibition of LPLA with protamine sulfate. Incremental heparin doses were given to each subject to determine lipase activities under conditions of maximal release and to define sensitivity to heparin-facilitated lipase release. Maximal postheparin LPLA and HTGLA (u/ml plasma or u/total plasma vol) were similar in lean and obese individuals despite a nearly three-fold increase in calculated adipose tissue mass in the obese. Since adipose tissue LPLA has been reported to increase in proportion to adipocyte size, the lack of difference in maximal postheparin LPLA was expected. There was an inverse correlation between plasma triglyceride concentration and LPLA/kg adipose tissue. These empirical observations may reflect relatively decreased heparin-releaseable (functional) LPLA in relation to adipose organ mass in obese subjects. The mechanism of this relationship has not been established.

Adipose Tissue↗
PubMed1978

The effects of 11-methyl 16,16 dimethyl prostaglandin E2 on canine gastric acid secretion.

11-Methyl 16,16 dimethyl Prostaglandin E2 (TM-PGE2) at peak effectiveness inhibited acid output stimulated submaximally by histamine in the dog by 95 and 84% when administered by the intravenous and oral routes, respectively. Inhibition of secretion was maintained for 1-1/2 hours following intravenous administration while with the oral route, secretory inhibition was still present at the end of two hours after administration of the drug. The degree of inhibition of acid secretion caused by TM-PGE2, its duration of action and the lack of side effects observed following administration of this drug makes it a suitable compound for evaluation as an anti-secretory agent in man.

Administration, Oral↗
PubMed1978

The effects of 11-methyl 16,16 dimethyl prostaglandin E2 on gastric acid secretion in man.

11-Methyl 16,16 Dimethyl Prostaglandin E2 (TM-PGE) was administered orally to man in dosages of 2.5, 5,7.5 and 10 microgram/kg. Maximal inhibition of basal secretion was 52 and 78% and submaximal histamine-stimulated secretion 45 and 70% for volume and acid output, respectively. Secretory inhibition was observed for approximately two hours after ingestion of the drug. No effect was observed on serum gastrin levels. Side effects occurred with equal frequency in the placebo and drug groups. TM-PGE is well tolerated and inhibits both basal and submaximal histamine-stimulated acid secretion in man. Further evaluation may prove it to be helpful in the clinical treatment of acid hypersecretory states and peptic ulcer disease.

Adult↗