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Biomedical subjects

D E Wilson

Publications and source records attributed to D E Wilson.

At least 19 recordsLinked to original sources
PubMed1995

Caremap management in low-severity surgery: a comparative trial.

BACKGROUND: Caremap management refers to the management of defined patient groups using multidisciplinary clinical guidelines developed through literature review and expert opinion. STUDY DESIGN: Using a prospective preintervention and postintervention comparison model, this controlled study compared caremap management and traditional treatment in patients undergoing inguinal herniorrhaphy. Preintervention (n = 141) and postintervention (n = 110) groups were compared for hospital length of stay, resource consumption, and outcomes. RESULTS: Patients cared for by caremap management compared with traditional treatment showed a significant reduction in average length of stay (0.6 compared to 1.6 days, p < 0.01). Laboratory testing decreased by 60 percent in the caremap management group relative to traditional treatment (p < 0.01) and standardization of medication profiles was achieved. There were no significant differences in readmission rate, reutilization of health care services, or complications. Patients in the caremap management group indicated a preference for additional length of stay. CONCLUSIONS: Caremap management offers the potential for achieving effective patient care while using resources efficiently. Further evidence is required to demonstrate that caremap management can fulfill the promise of improving health status outcomes in varied types of patients.

Adult↗
PubMed1994

Effect of the pSV2-neo plasmid on NIH 3T3 cell motion detected electrically.

Advantage was taken of DNA transfection techniques to investigate the effect of the pSV2-neo plasmid and its derivatives on recipient NIH 3T3 cell motion. Cell spreading and motion were followed by a newly developed electrical method to monitor cell morphology, referred to as electric cell-substrate impedance sensing. Using this method, we found that the eukaryotic-prokaryotic shuttle vector pSV2-neo had a strong effect on the recipient NIH 3T3 cell spreading and cell motion. However, two new neo plasmids, pSK-neo and pSP-neo, which were constructed by modifying the pSV2-neo plasmid, did not have a significant effect on the recipient cell activities. The results suggest that there may be some sequences in pSV2-neo which affect recipient cell behavior.

3T3 Cells↗
PubMed1994

Diabetes increases hepatic hydroxymethyl glutaryl coenzyme A reductase protein and mRNA levels in the small intestine.

Previous studies have shown that both cholesterol synthesis and the activity of hepatic hydroxymethyl glutaryl coenzyme A (HMG CoA) reductase, the rate-limiting enzyme in cholesterol synthesis, are increased in the small intestine of a wide variety of different animal models of diabetes. In the present study, we demonstrate that the mass of HMG CoA reductase protein is increased in the small intestine of both streptozocin-induced diabetic rats (2.5-fold) and streptozocin/alloxan-induced diabetic dogs (2.4-fold). These increases in HMG CoA reductase protein mass are of a magnitude similar to the previously observed increases in either HMG CoA reductase activity and/or cholesterol synthesis in the small intestine of diabetic animals. Furthermore, mRNA levels for HMG CoA reductase in the small intestine of diabetic rats and diabetic dogs are increased 2.1- and 1.7-fold, respectively. These results suggest that the increase in HMG CoA reductase protein levels in the small intestine of diabetic animals is due to an increase in mRNA levels. In contrast, mRNA levels for HMG CoA reductase in the liver of diabetic rats are not increased. Additionally, mRNA levels for the low-density lipoprotein (LDL) receptor are also increased in the small intestine of diabetic animals (rats, 43%; dogs, 59%). The increase in small-intestinal cholesterol synthesis has the potential for adversely affecting lipoprotein metabolism and increasing the risk of atherosclerosis in diabetes.

Animals↗
PubMed1994

Molecular screening of the lipoprotein lipase gene in hypertriglyceridemic members of familial noninsulin-dependent diabetes mellitus families.

Hypertriglyceridemia is common among individuals with noninsulin-dependent diabetes mellitus (NIDDM), and heterozygous lipoprotein lipase (LPL) mutations may result in the syndrome of familial hypertriglyceridemia and low levels of high density lipoprotein (HDL) cholesterol. To test the hypothesis that heterozygous LPL mutations predispose to the hypertriglyceridemia and low HDL cholesterol levels observed among members of familial NIDDM families, we examined 36 members and 3 unrelated spouses selected from members of 20 pedigrees for triglyceride levels exceeding the age- and sex-specific 95th percentile. Eighteen pedigree members and 2 spouses were diabetic. LPL exons 1-9 were screened by single strand conformation polymorphism analysis. Six different variants were detected in exons 2, 3, 4, 8, and 9, including 4 (exons 3, 4, and 8) silent nucleotide substitutions. A common nonsense mutation (exon 9; Ser-->Ter) was present in 2 pedigrees, and a missense mutation (exon 2; Asp-->Asn) was also present in members of 2 pedigrees. Analysis of members of these families suggested an association of the exon 2 variant with hypertriglyceridemia, although this trend was no longer significant when individuals with diabetes were excluded from the analysis. The variant enzyme was not present among 83 random control individuals, and when expressed in COS-1 cells, it was similar to the wild type with respect to specific activity, heparin binding, and heat stability. Our data suggest that coding region mutations of the LPL gene cannot account for the elevated triglyceride and low HDL levels noted in diabetic individuals and their relatives in most NIDDM pedigrees, but the exon 2 Asn variant may contribute to the hypertriglyceridemia in some families.

Adult↗
PubMed1994

Effect of positive genetic trend for mature size on age-of-dam adjustment factors for weaning weight in Angus field records.

Weaning weight and postweaning gain field data from the American Angus Association were used to estimate age-of-dam adjustment factors for 205-d weaning weight. A two-trait model was used to take into account all genetic information available in the breed. Correction factors were developed for age-of-dam categories by sex of calf and management (creep or no creep) within maternal-grandsire birth-year groups. The maternal-grandsire birth-year groups were included to determine the need for updating age-of-dam adjustment factors for weaning weight. The mathematical model for 205-d weight included an overall mean, weaning contemporary group, age of dam by sex of calf and management code within maternal-grandsire birth-year group, animal direct effect, maternal genetic effect, permanent environmental effect, and residual error. The model for postweaning gain included an overall mean, postweaning contemporary group, animal direct effect, and residual error. Age-of-dam additive adjustment factors differed from the current factors used for the Angus breed. Young dams did not receive as large an adjustment as the current Angus adjustments recommended. Grouping the age-of-dam categories by birth year of maternal grandsire yielded different additive adjustment factors for 205-d weight. Noncreep calves tended to have larger age-of-dam adjustments than creep-fed calves did. Results indicate the need to consider including age of dam as a fixed effect in the animal model evaluation, so that adjustment factors may be specific to the genetic changes for growth in the breed.

Age Factors↗
PubMed1994

Genetic predisposition to hyperlipidaemia in diabetes: the end of the beginning?

Diabetes mellitus leads to disturbances in lipoprotein homeostasis particularly when there is poor glycaemic control. The resulting abnormalities in concentration and composition of the circulating lipoproteins are modified by inherited variation in the genes coding for apolipoproteins, for the lipoprotein-processing enzymes, and possibly for lipoprotein receptors. Thus, poorly controlled diabetes provides an opportunity to observe the phenotypic effects of recessive mutant alleles that would otherwise be silent. This phenomenon should be considered when one attempts to understand the pathogenesis of variant phenotypes, ones differing from those typical of diabetes mellitus alone. Our understanding of how genetic variation modulates the expression of hyperlipidaemia in diabetes is still rudimentary--it now seems probable that many other genetic conditions affecting lipoprotein metabolism in diabetes will eventually be brought to light.

Alleles↗
PubMed1994

Gastrointestinal bleeding in patients with chronic liver disease: a review.

Most patients with decompensated liver disease who bleed from the gastrointestinal tract bleed from gastroesophageal varices or gastritis (congestive gastropathy). While a variety of pharmacologic and physical therapies are available, optimal treatment and effective prevention of gastrointestinal bleeding have yet to be delineated. In this review, current therapies are compared, as is the effectiveness of prophylaxis. A major problem with evaluating the literature continues to be the disparity between "comparable control groups" using similar protocols.

Esophageal and Gastric Varices↗
PubMed1992

Concanavalin A microspheres for a self-regulating insulin delivery system.

A self-regulating insulin delivery system based on the competitive binding of glucose and p-succinylamidophenyl-alpha-D-glycopyranoside-insulin (SAPG-insulin) to crosslinked concanavalin A (Con A) microspheres (MSs) has been investigated. Con A MSs prepared by a water-in-oil emulsion technique demonstrated properties of binding to glucose and SAPG-insulin (binding constants of 1.25 x 10(3) and 1.28 x 10(4) M-1, respectively) that are similar to the literature values of these properties for unmodified Con A. The retained binding capacity (number of binding sites per molecule) of Con A MSs, produced with 20% of the epsilon-amino groups crosslinked, was approximately 28% that of intact Con A. As a new device, Con A MSs loaded with SAPG-insulin was enclosed in a heat-sealed, surface-modified, porous poly(vinylidene difluoride) membrane pouch. This system showed a pulsatile release pattern for insulin with a short lag time in response to glucose challenges of 50-500 mg/dL. The pattern of release of SAPG-insulin from the devices was studied with varying design parameters, such as surface area, membrane pore size, and loading content of SAPG-insulin.

Binding, Competitive↗
PubMed1992

5,8,11,14-eicosatetraynoic acid-induced destruction of mitochondria in human prostate cells (PC-3).

Culturing human prostate PC-3 cells for 4, 24, or 72 h in the presence of 5,8,11,14-eicosatetraynoic acid (ETYA), an inhibitor of arachidonic acid metabolism and cholesterol biosynthesis, markedly altered the morphology and reduced the number of mitochondria in the treated cells. Using quantitative electron microscopic morphometry, we documented changes in the number, form, area, matrix density, and integrity of the cristae and limiting membranes of mitochondria in cells cultured with ETYA. The inhibition of cholesterol synthesis or the substitution of ETYA for polyunsaturated fatty acids in the inner membrane may participate in the disruption of the mitochondria, which resembles the morphologic sequelae of oxidative stress. If sufficiently extensive, these changes could contribute to the inhibition of cellular proliferation by ETYA.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1992

Application of ultrasound for genetic improvement.

Genetic improvement programs for livestock would be enhanced by the ability to accurately and easily measure body composition of live animals or to make measurements at anatomical reference points that can be used to accurately predict body composition. Advances in ultrasonic technology, such as real-time imagery and portable ultrasound units, have renewed interest among animal scientists working with genetic improvement programs and the livestock industry groups they serve. Ultrasound has been used for more than 30 yr and, for swine, has been demonstrated to improve significantly the accuracy of predicting body composition. However, many studies have shown less success in improving prediction of body composition from the use of ultrasonics to measure live beef cattle and sheep. The swine industry probably will be the first to benefit measurably from use of ultrasound technology in large-scale genetic improvement programs for carcass merit. Considerable research and development is needed before ultrasound technology can be effectively used in similar large-scale programs in the beef cattle and sheep industries.

Animals↗
PubMed1992

Adjusting weight for body condition score in Angus cows.

Weight, height, and body condition score data supplied by the American Angus Association were used to determine the effect of body condition score on cow weight and to compute condition score adjustment factors. Single records on 11,301 cows for weight and 7,769 cows for height were collected at or near weaning, at which time a subjective condition score (9-point scale) was taken. Limited information on extreme scores 1 and 9 allowed only scores 2 through 8 to be included in the analysis. Cows were grouped into age classes corresponding to 2, 3, 4, 5, 6, 7 to 10, and 11+ yr of age. The mathematical model for a weight record included effects of fixed herd, year-month the record was collected, cow age, body condition score, and a random residual error term. The model for height excluded the condition score effect. Effects of herd, year-month, and cow age were highly significant (P less than .0001) for weight and height. Body condition score was a significant source of variation in weight (P less than .0001) and accounted for 16% of the total variation. Adjustment factors for weight (kilograms) by condition score were +116 (score 2), +91 (score 3), +69 (score 4), +39 (score 5), 0 (score 6), -40 (score 7), and -86 (score 8).

Analysis of Variance↗
PubMed1992

Familial dyslipidaemic hypertension and other multiple metabolic syndromes.

Data from several different studies are reviewed suggesting that a subset of hypertension is associated with metabolic abnormalities involving lipids, insulin, and often obesity, all aggregating strongly in families. Persons with 'familial dyslipidaemic hypertension (FDH)' have an especially high risk of early coronary disease. The clinical and biochemical features of FDH are compared with Reaven's Syndrome X, familial combined hyperlipidaemia, dense LDL subfractions, diabetes, impaired glucose tolerance, central and general obesity, pre-diabetes, pre-hypertension, and heterozygous lipoprotein lipase deficiency. Some contribution from major gene effects is suggested in specific subsets reported in several different genetic studies reviewed in this report. It seems likely that multiple metabolic abnormalities are genetically heterogeneous. The data also suggest significant contributions from environmental factors such as diet and physical activity.

Coronary Disease↗
PubMed1991

Successful hyperlipemic pregnancy.

Women with hypertriglyceridemia are prone to gestational pancreatitis, a condition carrying substantial maternal and fetal risk. We describe a 33-year-old woman with familial hypertriglyceridemia who had recurrent hyperlipidemic abdominal crises during previous pregnancies despite dietary fat restrictions. A fifth pregnancy was carried to term without complications after aggressive dietary therapy and intermittent intravenous feeding, administered whenever her triglyceride levels exceeded an arbitrarily selected threshold concentration of 28 mmol/L. The efficacy of this approach may be explained by the published observation that low-fat (high-carbohydrate) isocaloric diets elevate serum triglyceride levels by the oral, but not the intravenous, route in normal individuals. Reduction of this patient's serum triglyceride concentrations by interrupting oral intake and administering intravenous glucose appeared to prevent late-pregnancy pancreatitis and culminated in uncomplicated full-term delivery.

Adult↗
PubMed1991

Elevation of synovial plasminogen activator activity after injection of interleukin-1 alpha into rabbit knee joint.

We investigated production of plasminogen activator (PA) and cartilage degradation induced by injection of recombinant human interleukin-1 (rhIL-1 alpha) in rabbit knees. Rabbits were injected intra-articularly (i.a.) with 100 ng rhIL-1 alpha and necropsied at 0, 3, 6, 18 and 54 h and synovial lavage and articular cartilage were collected. PA activity in the joint lavage was measured using Z-Lys-thiobenzyl ester as a substrate. Cartilage degradation was assessed by quantitating sulfated glycosaminoglycan (S-GAG) to hydroxyproline (Hyp) and appearance of keratan sulfate (KS) in synovial lavage by and ELISA. The PA activity in the lavage of IL-1 injected knees at 3, 6, and 18 h was elevated 8 to 10 fold compared to vehicle controls. At 54 h the activity declined to approximately one third of that seen at the earlier time points. KS in the joint lavage was highest at 18 h, suggesting proteoglycan degradation. The maximal loss of cartilage proteoglycan (S-GAG/Hyp) occurred by 54 h. These observations demonstrate that i.a. injection of IL-1 stimulated the production of PA activity within the rabbit joint. Since elevation of PA activity is followed by cartilage degradation, we investigated effect of anti-inflammatory agents on PA activity and cartilage degradation in this model. We found that triamcinolone, indomethacin and dexamethasone were able to suppress PA activity but not the cartilage degradation. These observations suggest that in this model of cartilage degradation suppression of PA is not sufficient to inhibit cartilage degradation.

Animals↗
PubMed1991

Anxiolytic properties of certain annelated [1,2,4]triazolo[1,5-c]pyrimidin-5(6H)-ones.

Modification of the benzodiazepine (BZ) receptor binding template 2-aryl[1,2,4]triazolo[1,5-c]quinazolin-5(6H)-one by replacement of the annelated benzene ring with various alicyclic and heterocyclic moieties led to novel structures with potent BZ receptor binding affinity. High affinity was found in some cycloalkyl-annelated [1,2,4]triazolo[1,5-c]pyrimidin-5(6H)-ones and in some 7,8,9,10-tetrahydropyrido[3,4-e][1,2,4]triazolo[1,5-c]pyrimidin- 5(6H)-ones, in which the degree of activity was strongly dependent on the N-substituent in the 9-position. Nine compounds with BZ receptor IC50 binding affinity values equal or superior to diazepam were evaluated in secondary screening. One of these, 9-benzyl-2-phenyl-7,8,9,10-tetrahydropyrido[3,4-e] [1,2,4]triazolo[1,5-c]pyrimidin-5(6H)-one, showed good activity in rats as a potential anxiolytic agent without sedative liability. However, it increased the rotorod deficit produced by ethanol at anxiolytic doses, an indication of alcohol interaction. Thus, none of the compounds showed an advantage over CGS 9896 (Yokoyama et al. J. Med. Chem. 1982, 25, 337-339), which is free of sedative and alcohol interaction potential as measured by the test procedures described.

Aggression↗
PubMed1991

Role of prostaglandins in gastroduodenal mucosal protection.

Prostaglandins protect the gastroduodenal mucosa from damage caused by diverse noxious agents. This protection (cytoprotection) occurs under experimental conditions where intraluminal acid is required for maximal expression of damage (e.g., stress, aspirin, and bile acids), as well as where damage occurs irrespective of the presence of acid (e.g., 100% ethanol, boiling water, and lye). Prostaglandins stimulate several factors felt to be important in maintaining normal mucosal integrity, such as mucus synthesis and secretion, mucosal bicarbonate secretion, mucosal blood flow, and cellular repair. Inhibition of the prostaglandin synthetic enzyme, cyclooxygenase, by nonsteroidal anti-inflammatory drugs (NSAIDs), is associated with increased gastroduodenal mucosal damage and ulceration. This damage is primarily the result of decreased tissue levels of prostaglandins, but may also be due to direct NSAID actions on the mucosa, as well as with shifting of arachidonic acid metabolism from synthesizing protective prostaglandins to increased production of injurious leukotrienes. There is also evidence that patients with peptic ulcer disease have a deficiency of gastroduodenal mucosal prostaglandin synthesis, so that prostaglandins may play a pathophysiologic role in this disorder. Prostaglandins have a unique ability to prevent NSAID-induced gastric damage in humans, and also appear to improve ulcer healing during the continuation of NSAID therapy.

Anti-Inflammatory Agents, Non-Steroidal↗
PubMed1991

Intestinal and hepatic cholesterogenesis in hypercholesterolemic dyslipidemia of experimental diabetes in dogs.

We previously reported that dog diabetes results in hypercholesterolemia and the accumulation of a high-density lipoprotein (HDL) subclass, HDL1. Hypercholesterolemic diabetic rodents exhibit hyperphagia, intestinal hypertrophy, and increased intestinal cholesterol synthesis and absorption; intestinal 3-hydroxy-3-methylglutaryl (HMG) CoA reductase activity is increased, whereas hepatic activity is unchanged or reduced. To determine whether similar mechanisms operate in the hypercholesterolemic diabetic dog, we measured hepatic and intestinal cholesterologenesis. Streptozocin-alloxan-induced diabetic dogs allowed access to food ad libitum were hyperphagic and hypercholesterolemic (10.1 vs. 4.47 mM) but normotriglyceridemic. Plasma HDL1 concentrations were markedly increased. Differences in renal and hepatic function were not statistically significant, except serum alkaline phosphatase, which was elevated 4-fold (P = 0.0003). Urinary mevalonate, an index of whole-body cholesterol synthesis, was increased 6-fold. Intestinal and hepatic weights were both increased, and direct measurements showed crypt and villus thickening. The activity of HMG CoA reductase per gram organ weight was increased 1.7-fold in liver and 2.1-fold in intestine. Calculated whole-organ activity in intestine was nearly twice that in liver. These observations provide strong evidence that intestinal cholesterogenesis is involved in the pathogenesis of hypercholesterolemia in dog diabetes and support the conclusion that increased cholesterol synthesis plays a role in the hypercholesterolemia of diabetes.

Animals↗