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Biomedical subjects

M R Adams

Publications and source records attributed to M R Adams.

At least 109 records · Page 6Linked to original sources
PubMed1994

Comparison of laparoscopic and minilap cholecystectomy for acute cholecystitis.

The charts of all patients with acute cholecystitis undergoing either laparoscopic or minilap cholecystectomy at the Chinle Comprehensive Health Care Facility between October 1, 1991, and August 15, 1993, were retrospectively reviewed. During that period, 54 patients underwent laparoscopic cholecystectomy and 45 patients had minilap procedures. The two groups had similar mean age, sex distribution, temperature, leukocyte count, gallbladder wall thickness, and duration of preoperative symptoms. While laparoscopic cholecystectomy took an average of 16 min longer to perform than minilap cholecystectomy, patients who had laparoscopic cholecystectomy had less blood loss, reduced postoperative narcotic needs, and shorter hospital stays.

Acute Disease↗
PubMed1994

The effects of hormonal replacement therapy on insulin sensitivity in surgically postmenopausal cynomolgus monkeys (Macaca fascicularis).

OBJECTIVE: Our purpose was to evaluate the effect of hormone replacement therapy on insulin resistance in postmenopausal cynomolgus monkeys (Macaca fascicularis). STUDY DESIGN: We studied 37 surgically postmenopausal cynomolgus monkeys that were fed a moderately atherogenic diet for 12 weeks with either no treatment (control), conjugated equine estrogens, medroxyprogesterone acetate, combination conjugated equine estrogens and medroxyprogesterone acetate, or tamoxifen. Insulin sensitivity and glucose effectiveness were determined by the frequent-sampling intravenous tolerance test by means of the minimal model analysis. RESULTS: There were no differences in body weight, total plasma cholesterol, or body fat distribution between control and conjugated equine estrogens, medroxyprogesterone acetate, or combination treatment groups. However, compared with control animals (insulin sensitivity = 5.9 +2- 1.2 x 10(-4) min-1 microU-1 ml) or conjugated equine estrogens treatment (6.3 +/- 1.1 x 10(-4) min-1 microU-1 ml) insulin sensitivity was significantly decreased in animals treated with medroxyprogesterone acetate (2.9 +/- 0.4 x 10(-4) min-1 microU-1 ml, p < 0.001) or conjugated equine estrogens and medroxyprogesterone acetate (2.8 +/- 0.6 x 10(-4) min-1 microU-1 ml, p < 0.001). Although insulin sensitivity was shown to be decreased in the tamoxifen-treated animals (insulin sensitivity = 4.6 +/- 0.6 x 10(-4) min-1 microU -1 ml), the difference was not statistically significant compared with the control or conjugated equine estrogens-treated animals. No significant differences were seen for glucose effectiveness comparing control animals (glucose effectiveness = 0.043 +/- 0.006 min-1) to animals treated with medroxyprogesterone acetate (glucose effectiveness = 0.046 +/- 0.009 min-1), conjugated equine estrogens and medroxyprogesterone acetate (0.048 +/- 0.008 min-1) or tamoxifen (0.039 +/- 0.006 min-1). CONCLUSION: These results suggest that progestins alone or in combination with estrogens can induce insulin resistance in postmenopausal monkeys while having no effect on plasma lipid concentrations or glucose effectiveness.

Animals↗
PubMed1994

Application of a log-logistic model to describe the survival of Yersinia enterocolitica at sub-optimal pH and temperature.

A log-logistic model previously used to describe the thermal inactivation of microorganisms has been applied to predict accurately the survival of Yersinia enterocolitica under conditions of sub-optimal temperatures (0-23 degrees C) and growth inhibitory pH values for a number of different acidulants. Predictions from the model were also compared to observed survival times of Y. enterocolitica in mayonnaise and were found to be in excellent agreement. However in yoghurt the model overestimated survival of this organism at both 20 and 4 degrees C but would 'fail safe' if used for predictive purposes. The discrepancy in yoghurt is discussed.

Food Microbiology↗
PubMed1994

Resistance of Listeria monocytogenes to the bacteriocin nisin.

Listeria monocytogenes NCTC 5105 and F6861 were evaluated for sensitivity to nisin. The results confirmed those previously published indicating marked differences in the sensitivity of the two strains. Mutants with increased resistance to nisin could be isolated from the less sensitive F6861 strain at a frequency of 10(-6) to 10(-7). Using a nisin specific enzyme-linked immunosorbent assay, the adsorption of nisin to the different strains and the resistant mutant were studied. At a range of nisin concentrations the amount adsorbed was found to reflect the sensitivity of the strain to nisin, with the more sensitive cells showing greater adsorption. In resistant cells, K+ efflux increased at a slower rate with increasing nisin concentration and had a lower maximum rate indicating that the mechanism of resistance involves a reduction in the accessibility or presence of suitable adsorption sites.

Adsorption↗
PubMed1994

Production and viability of coccoid forms of Campylobacter jejuni.

Studies were conducted into the formation and physiological state of coccoid cells of a strain of the human and animal pathogen Campylobacter jejuni. It was found that growth phase and the presence of chloramphenicol did not affect the rate of shape transformation from spiral to coccoid, while nutrient limitation, aeration of the medium and the presence of free-radical scavengers had profound effects. Coccoid cells were found to reduce the tetrazolium salts INT (2-(p-iodophenyl)-3-(p-nitrophenyl)-5-phenyl tetrazolium chloride) and CTC (5-cyano-2,3-ditolyl tetrazolium chloride) to their respective formazans and this was linked to cellular respiration. However, respiring coccoid cells could not sustain their existence in prolonged adverse conditions, and it was concluded that they represent a degenerative stage rather than a dormant state of the organism.

Campylobacter jejuni↗
PubMed1994

Probabilistic health risk assessment for exposures to estuary sediments and biota contaminated with polychlorinated biphenyls, polychlorinated terphenyls and other toxic substances.

A Latin Hypercube probabilistic risk assessment methodology was employed in the assessment of health risks associated with exposures to contaminated sediment and biota in an estuary in the Tidewater region of Virginia. The primary contaminants were polychlorinated biphenyls (PCBs), polychlorinated terphenyls (PCTs), polynuclear aromatic hydrocarbons (PAHs), and metals released into the estuary from a storm sewer system. The exposure pathways associated with the highest contaminant intake and risks were dermal contact with contaminated sediment and ingestion of contaminated aquatic and terrestrial biota from the contaminated area. As expected, all of the output probability distributions of risk were highly skewed, and the ratios of the expected value (mean) to median risk estimates ranged from 1.4 to 14.8 for the various exposed populations. The 99th percentile risk estimates were as much as two orders of magnitude above the mean risk estimates. For the sediment exposure pathways, the stability of the median risk estimates was found to be much greater than the stability of the expected value risk estimates. The interrun variability in the median risk estimate was found to be +/- 1.9% at 3000 iterations. The interrun stability of the mean risk estimates was found to be approximately equal to that of the 95th percentile estimates at any number of iterations. The variation in neither contaminant concentrations nor any other single input variable contributed disproportionately to the overall simulation variance. The inclusion or exclusion of spatial correlations among contaminant concentrations in the simulation model did not significantly effect either the magnitude or the variance of the simulation risk estimates for sediment exposures.

Adult↗
PubMed1994

Estrogen modulates the expression of tumor necrosis factor alpha mRNA in phorbol ester-stimulated human monocytic THP-1 cells.

Monokines, including tumor necrosis factor alpha (TNF-alpha), have been implicated in the pathogenesis of several pathologic processes, including atherosclerosis. Because estrogen has been found to offer a certain degree of protection against atherosclerotic progression, we examined the effect of estrogen on the expression of TNF-alpha mRNA in a monocyte-macrophage cell line, THP-1. Cells were exposed to 12-O-tetradecanoylphorbol 13-acetate (TPA, 50 ng/ml) for 48 or 96 h to induce differentiation. Some of the cells were treated with lipopolysaccharide (LPS, 10 micrograms/ml) in the last 3 h and/or ethinyl estradiol (estrogen, 10(-9) M) in the last 20 h. Total cellular RNA was isolated and cDNA synthesized and than coamplified using the polymerase chain reaction (PCR) in the presence of two sets (pairs) of 32P-labeled primers, one for TNF-alpha (product size 325 bp) and the second for the internal control, glyceraldehyde 3-phosphate dehydrogenase (G3PDH; 983 bp). The resultant PCR products were separated by agarose gel electrophoresis, and the ratios of radioactivity incorporated into TNF-alpha PCR products to G3PDH products were used to assess the relative changes in the levels of TNF-alpha mRNA abundance in response to various substances. Treatment with TPA for 48 h induced the expression of TNF-alpha mRNA. Treatment of these TPA-stimulated cells with estrogen caused a 62% decrease in TNF-alpha message abundance (p < 0.01). Similar results were obtained with cells stimulated with TPA for 96 h.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriosclerosis↗
PubMed1994

Effects of estrogen on cardiovascular responses of premenopausal monkeys.

Exogenous estrogen administration has been shown to reduce the risk of coronary heart disease in women. However, there are limited data in regard to the effects of estrogen on cardiovascular function and hemodynamics. This experiment sought to determine the effect of exogenous estrogen administration on systemic hemodynamic variables and cardiovascular responses to adrenergic and vasodilator agonists in premenopausal cynomolgus monkeys. Adult female monkeys were given weekly i.m. injections of 1) saline (control, n = 6), 2) estradiol cypionate (100 micrograms/kg, n = 6) or 3) estradiol cypionate (700 micrograms/kg, n = 5) for 6 weeks. A Swan-Ganz thermodilution catheter and arterial catheters were used to measure cardiovascular hemodynamic parameters in anesthetized monkeys before and during i.v. infusion of 1, 2, 4 and 8 micrograms kg-1 min-1 of isoproterenol, phenylephrine and nitroprusside. The high-dose estradiol group had a higher cardiac output index (0.6 +/- 0.1 versus 0.25 +/- 0.1 liter min-1 kg-1, mean +/- S.E.M.) and lower systemic vascular resistance index (628 +/- 160 versus 2630 +/- 872 dyne x cm-5 x sec-2 kg-1) than the control group at base line before infusion of agonists (P < .05). High-dose estradiol administration attenuated the mean arterial blood pressure, cardiac output and systemic vascular resistance changes in response to infusions of phenylephrine, isoproterenol and nitroprusside (P < .05 versus control). It was concluded that the administration of high-dose estradiol resulted in systemic arterial dilation, although changes in hemodynamic variables (systemic vascular resistance and cardiac output) were attenuated during adrenergic stimulation and vasodilation.

Animals↗
PubMed1994

The inducible expression of THP-1 cell interleukin-1 mRNA: effects of estrogen on differential response to phorbol ester and lipopolysaccharide.

Monokines, such as interleukin-1, have been implicated in the pathogenesis of several pathologic processes, including the initiation and progression of atherosclerosis. Since estrogen has been identified as a modulator of atherosclerosis progression, we sought to examine the effect of estrogen on the inducible expression of interleukin-1 beta (IL-1 beta) and interleukin-1 alpha (IL-1 alpha) mRNA in the monocytic cell line, THP-1. Cells were treated with 12-O-tetradecanoylphorbol-13-acetate (TPA) (50 ng/ml) for 48 or 96 h to induce differentiation. Some cells were treated with lipopolysaccharide (LPS) (10 micrograms/ml) in the last 3 h and/or 10(-9) M ethinyl estradiol (estrogen) in the last 20 h. Total cellular RNA was isolated, and cDNA was synthesized and amplified using the polymerase chain reaction (PCR) using two sets (pairs) of 32P-labeled primers, one for IL-1 beta (product size 388 bp) and the second for the internal control, beta-actin (1126 bp), or to detect another cytokine mRNA, a set of primers for IL-1 alpha (product size 420 bp) and beta-actin. The PCR products were separated on a 3.0% agarose gel and the ratio of radioactivity incorporated into cytokine PCR products and beta-actin products was determined to assess the relative changes in the relative levels of cytokine to beta-actin mRNA abundance in response to various inducers. Treatment with TPA for 48 h induced expression of IL-1 beta mRNA, an effect that was enhanced two fold by LPS.(ABSTRACT TRUNCATED AT 250 WORDS)

Arteriosclerosis↗
PubMed1993

Immunolocalization of noncollagenous bone matrix proteins in lumbar vertebrae from intact and surgically menopausal cynomolgus monkeys.

The noncollagenous matrix proteins, composing about 10% of the organic matrix of bone, are considered important for cell matrix organization and regulation of mineralization in bone. In the present study, seven of the major noncollagenous bone matrix proteins were localized immunohistochemically in serial sections of lumbar vertebrae from 24 (12 intact and 12 ovariectomized) adult female cynomolgus monkeys (Macaca fascicularis). Osteocalcin was the only protein restricted to bone cells and mineralized bone matrix. Bone sialoprotein was present in both bone and calcified cartilage, and all the other proteins were distributed in soft tissues as well as bone. Staining for both osteocalcin and bone sialoprotein was present diffusely throughout the bone matrix, but osteonectin, osteopontin, matrix gla protein, decorin, and biglycan staining was concentrated along bone surfaces. Osteoid was negative for osteocalcin and bone sialoprotein, but all other proteins had areas of positive immunostaining within osteoid. All proteins except biglycan exhibited strong immunostaining of a subset of active osteoblasts, suggesting that they may be markers of osteoblast maturity or state of activation. The pattern of immunostaining in intact and surgically menopausal monkeys was similar, except that staining for matrix proteins concentrated along bone surfaces appeared to be more widely distributed in the surgically menopausal monkeys, probably due to the higher rate of bone formation in these animals.

Animals↗
PubMed1993

A conjugated equine estrogen with differential effects on uterine weight and plasma cholesterol in the rat.

OBJECTIVE: Our purpose was to determine the effect of Premarin (conjugated estrogens) and three of its component estrogens on uterine weight and plasma cholesterol concentrations in surgically menopausal female rats. STUDY DESIGN: A randomized trial of Premarin and three component estrogens--estrone sulfate, 17 alpha-estradiol sulfate, and 17 alpha-dihydroequilenin sulfate--in female rats after oophorectomy. RESULTS: High-dose Premarin and high- and middle-dose estrone sulfate significantly increased uterine weight relative to untreated controls (high-dose Premarin, 243.34 +/- 0.15 mg; high-dose estrone sulfate, 376.1 +/- 9.36 mg; middle-dose estrone sulfate, 249.0 +/- 6.34 mg; untreated controls, 124.63 +/- 3.17 mg; for all, p < 0.05). 17 alpha-Dihydroequilenin sulfate had no effect on uterine weight relative to controls. All 17 alpha-dihydroequilenin sulfate doses markedly reduced total plasma cholesterol concentrations versus controls (34.02 +/- 3.44 mg/dl, 32.49 +/- 1.08 mg/dl, and 71.55 +/- 5.16 mg/dl vs 90.44 +/- 1.06 mg/dl; for all, p < 0.02). 17 alpha-Dihydroequilenin sulfate had a more pronounced effect on low- or very-low-density lipoprotein cholesterol than total plasma cholesterol or high-density lipoprotein cholesterol concentrations. CONCLUSIONS: 17 alpha-Dihydroequilenin sulfate reduced total plasma cholesterol concentrations without inducing uterine growth in rats after oophorectomy.

Animals↗
PubMed1993

Plaque changes and arterial enlargement in atherosclerotic monkeys after manipulation of diet and social environment.

To study the effects of dietary and social manipulations on lesion progression in male monkeys with established atherosclerosis, 83 animals fed a diet containing 1 mg cholesterol per kcal for 14 months were either necropsied (baseline group, n = 21) or assigned to one of three experimental conditions: 1) a diet containing a high amount of fat and cholesterol and a stressful social situation (HiFC-stress, n = 18); 2) a diet lower in fat and cholesterol and a stressful social situation (LoFC-stress, n = 21); or 3) the low-fat, low-cholesterol diet and a nonstressful social situation (LoFC-no stress, n = 23). After 28 months, all animals were necropsied. Coronary atherogenesis was arrested among monkeys in the LoFC-stress and LoFC-no stress conditions compared with that of animals in the baseline condition (plaque areas of 0.35 mm2, 0.30 mm2, and 0.38 mm2, respectively). Lesions in animals fed the LoFC diet (both stress and no-stress groups) were significantly smaller than those in monkeys in the HiFC-stress condition (0.96 mm2). Furthermore, aortic cholesterol content was significantly decreased and luminal areas were relatively larger among monkeys in both LoFC conditions compared with animals in the baseline and HiFC-stress conditions (p < 0.05 for all). The results demonstrate that a low-fat, low-cholesterol diet can halt plaque development, reduce arterial cholesterol content, and permit compensatory arterial enlargement, processes that were unaffected by social stress in this investigation.

Animals↗
PubMed1993

Oral contraceptive treatment decreases arterial low density lipoprotein degradation in female cynomolgus monkeys.

The effect of oral contraceptive therapy on early events in atherogenesis was studied in female cynomolgus monkeys. After a 1-month dietary challenge, monkeys were randomized into three groups stratified by total plasma cholesterol and high density lipoprotein cholesterol concentrations. The monkeys were then fed a cholesterol-containing diet for 16 weeks. This relatively short period ensured that studies were done before any treatment-induced differences in arterial morphology occurred. Monkeys were treated with either diet alone (control group), with the addition of a monophasic oral contraceptive (equivalent to a human dose of 50 micrograms ethinyl estradiol and 500 micrograms norgestrel per day), or with a triphasic oral contraceptive (equivalent to a human dose of 30-40 micrograms ethinyl estradiol and 50-125 micrograms levonorgestrel per day). Twenty-four hours before necropsy, low density lipoproteins (LDLs) labeled with 131I and LDLs labeled with the residualizing label 125I-tyramine cellobiose were injected into the animals. The arterial LDL degradation rate, amount of undegraded LDLs, and total LDL accumulation were then determined. Although there were regional differences in LDL metabolism, both treatments decreased the rate of LDL degradation and LDL accumulation in the coronary arteries and other arterial sites. Treatment also resulted in significantly lower LDL molecular weights. Despite a trend toward a more atherogenic lipid profile (decreased high density lipoprotein cholesterol and increased total plasma/high density lipoprotein cholesterol ratio), oral contraceptive treatment may inhibit atherogenesis by decreasing arterial LDL degradation.

Animals↗
PubMed1992

Short-term administration of estrogen and vascular responses of atherosclerotic coronary arteries.

OBJECTIVES: This experiment sought to determine the effect of short-term administration of estrogen on endothelium-dependent dilation in the coronary arteries of 13 surgically postmenopausal female cynomolgus monkeys. BACKGROUND: Long-term estrogen replacement therapy prevents impaired endothelium-dependent dilation of atherosclerotic coronary arteries in postmenopausal female monkeys. However, it remains unclear whether this action of estrogen is due to long-term effects on plasma lipids and atherogenesis or to direct short-term effects on the endothelium. METHODS: The monkeys consumed an atherogenic diet for 18 months after bilateral ovariectomy. Vascular responses were measured just before euthanasia and necropsy. Dextrose in water (control), acetylcholine, 10(-6)M, and nitroglycerin were infused for 2.5 min each both before and 20 min after intravenous injection of 54 ng ethinyl estradiol. RESULTS: Quantitative coronary angiography revealed that the arteries constricted (-17 +/- 3%) in response to intracoronary infusion of acetylcholine before estrogen treatment but dilated (+5 +/- 3%) 20 min after intravenous injection of ethinyl estradiol (p less than 0.05). Coronary arteries dilated in response to nitroglycerin both before and after administration of estrogen (p greater than 0.05). Vascular responses of coronary arteries, both before and after administration of estrogen, were not associated with variation in plasma lipid concentrations, blood pressure, heart rate or plaque size. CONCLUSIONS: Estrogen affects endothelium-dependent coronary dilation within 20 min of administration and may have rapid direct effects on the vascular endothelium.

Acetylcholine↗
PubMed1992

Cross-reactivity of bacteriocins from lactic acid bacteria and lantibiotics in a nisin bioassay and ELISA.

A number of bacteriocins from lactic acid bacteria and lantibiotics were tested for cross-reactivity in a nisin ELISA and bioassay. The bacteriocins showed no cross-reactivity, reflecting their structural dissimilarity from nisin. The lantibiotic subtilin which shares many common structural features with nisin, showed a high cross-reactivity in both the ELISA and the bioassay suggesting possible modifications to nisin to enhance its activity. Gallidermin did not cross react in the ELISA but did produce a zone of inhibition in the less specific bioassay. Other lantibiotics tested did not react in either assay.

Anti-Bacterial Agents↗
PubMed1992

Regional differences in arterial low density lipoprotein metabolism in surgically postmenopausal cynomolgus monkeys. Effects of estrogen and progesterone replacement therapy.

To determine if arterial lipoprotein metabolism may be involved in mediating well-known anatomic regional differences in susceptibility to atherosclerosis, arterial low density lipoprotein (LDL) metabolism and extent of atherosclerosis were studied in 17 ovariectomized female cynomolgus monkeys. The animals were fed an atherogenic diet for 18 weeks, during which time one group received 17 beta-estradiol and cyclic progesterone treatment (n = 9) and the controls received no hormone replacement therapy (n = 8). As reported previously, hormone replacement markedly reduced the accumulation of LDL in coronary arteries without affecting plasma lipoprotein patterns. We report here that LDL metabolism differed among arterial sites. LDL accumulation, LDL degradation rate, and the concentration of undegraded LDL were greatest in the coronary arteries and carotid bifurcations compared with the aorta, iliac arteries, and cerebral arteries. Although hormone replacement decreased indexes of LDL metabolism, there was no effect on intimal thickness or indexes of endothelial injury, such as leukocyte adhesion and endothelial cell turnover rate. There were, however, regional differences in these morphological parameters. The intima was thickest in the aorta, and leukocyte adhesion and endothelial cell turnover rates were greatest in the carotid bifurcation and thoracic aorta. The decreased accumulation and metabolism of LDL caused by hormone replacement therapy was specific to the arterial system and did not occur in the liver or other peripheral tissues.

Animals↗