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Biomedical subjects

J A Moore

Publications and source records attributed to J A Moore.

At least 163 records · Page 9Linked to original sources
PubMed1981

Gene flow and the geographical distribution of a molecular polymorphism in Drosophila pseudoobscura.

This paper discusses the relation between the geographical distribution of an enzyme polymorphism and population structure in Drosophila pseudoobscura. California populations of this species living in very different montane and lowland habitats separated by several kilometers are similar to each other in the frequency of an esterase allele. Previous estimates suggest that gene flow is too limited to account for this homogeneity of genetic structure, so that it must reflect some balancing force of natural selection. We slow, however, that dispersal over unfavorable habitats is much greater than earlier supposed. Isolated populations of D. pseudoobscura separated by 15 km from other populations are subject to large amounts of immigration. This is shown by changes in the seasonal abundance of this species and in the annual pattern of lethal alleles in such populations. The genetic structure of an experimentally perturbed isolated population in an oasis returned to normal within a single year, suggesting that such populations are ephemeral and that the oasis is subject to annual recolonization by distant migrants. Direct assessment of marked flies shows that they can move at least 10 10 km in 24 hours over a desert. Such extensive gene flow may help explain the distribution of the esterase allele, and is relevant to the high level of molecular polymorphism and its general lack of geographic differentiation throughout the range of D. pseudoobscura.

Alleles↗
PubMed1981

Anorexia nervosa: the patient, her family and key family therapy interventions.

In a nation in which jogging, diets, and weight consciousness are so prevalent, it is easy to understand why middle class teenage girls want to become or stay thin. It is harder for us all to understand why some of these young women become so emaciated that they may die. We have tried to present information that will enable health care professionals to achieve a broader understanding of the clinical syndrome of anorexia nervosa and the family of the anorexic. Some key family therapy interventions that will enable the family system to become more adaptive to change have been highlighted and explained through the use of actual case material.

Adolescent↗
PubMed1980

Examination of bone marrow, immunologic parameters and host susceptibility following pre- and postnatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).

The effects of pre/postnatal exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on various immunological, bone marrow and host susceptibility assays were examined in B6C3F1 hybrid mice. Exposure was accomplished by maternal dosing on Day 14 of gestation and again on Days 1, 7, and 14 following birth, employing dosages of 0, 1.0, 5.0 or 15.0 micrograms/kg body weight. The 15.0 micrograms/kg dosage was lethal to 70% of the offspring with the remainder of that dosage group revealing overt toxicity. Bone marrow toxicity occurred in both the 15.0 and 5.0 micrograms/kg dosage groups as evidenced by bone marrow hypocellularity and depressed colony formation of macrophage-granulocyte progenitor cells and pleuripotent stem cells. Evidence was presented that depression of lymphoproliferative responses following mitogen stimulation in TCDD-immunosuppressed mice was due to a functional defect of lymphocyte activation rather than suppressor cell activity. Administration of either Listeria monocytogenes or syngeneic PYB6 tumor cells in mice exposed to relatively low levels of TCDD during pre- and postnatal development increased their susceptibility to either bacterial or tumor challenge.

Animals↗
PubMed1980

Role of the endocrine system in the action of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on the thymus.

Several experiments were conducted to study the involvement of the adrenal and the pituitary gland in the acute toxic effects of TCDD. Adrenalectomized or hypophysectomized rats were treated with a single oral dose of 10 or 20 microgram of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)/kg body weight. The reduced growth rate, the hepatotoxic effects and thymic involution induced by TCDD were not prevented by the adrenalectomy. The pituitary gland did not appear to be involved in causing thymic involution. In fact, the thymic effects of TCDD intoxication were even somewhat increased in hypophysectomized rats. Treatment with growth hormone failed to prevent thymic involution or the influence of TCDD on the liver.

Adrenal Cortex Hormones↗
PubMed1980

Dose response of 1,2-dimethylhydrazine and methylazoxymethanol acetate in the F 344 rat.

Weanling male and female F 344 rats were given various doses of 1,2-dimethylhydrazine (DMH) or methylazoxymethyl acetate (MAMAc), and were then held for 46-64 weeks in an effort to determine a dose response and establish a dose level which would produce a low level of intestinal neoplasia with a minimal number of tumors in other organs. DMH proved superior to MAM in this respect, although liver lesions were still observed with both compounds at the lowest carcinogenic intestinal dose.

Animals↗
PubMed1980

Endocrine effects of meternal alcoholization: plasma and brain testosterone, dihydrotestosterone, estradiol, and corticosterone.

Maternal ethanol consumption was associated with reduced levels of dihydrotestosterone in the brains of 1--2-day-old male rats when compared to those of sex-matched pups obtained from dames that were fed sucrose. In contrast, brain levels of corticosterone were increased significantly in the pups of ethanol-fed animals when compared to those from sucrose-fed controls. Brain and plasma estradiol did not differ between groups. These results suggest that maternal ethanol consumption may influence the central nervous system and plasma levels of certain steroidal hormones in the offspring.

Alcoholism↗
PubMed1980

Long-term hazards of polychlorinated dibenzodioxins and polychlorinated dibenzofurans.

During January 10-11, 1978 in Lyon, France, a joint National Institute of Environmental Health Sciences/International Agency for Research on Cancer ad hoc Working Group considered and discussed the feasibility of coordinating epidemiological studies on the long-term hazards associated with the chlorinated dibenzo-p-dioxins and chlorinated dibenzofurans (PCDDs and and PCDFs). Nineteen invited scientists from eight countries presented introductory working papers summarizing the most up-to-date and relevant information available from their individual programs. This report represents the collective views and scientific opinions of the Working Group. The greater part of this document comprises epidemiological studies related to episodes of human exposures. The review begins with a brief section concerning possible routes of human exposure, an overview of the pertinent chemical characteristics, and the salient toxicological properties of the structurally similar PCDDs/PCDFs. The Working Group report ends with recommendations for future activities.

Abnormalities, Drug-Induced↗
PubMed1980

Studies on the use of activated charcoal and cholestyramine for reducing the body burden of polybrominated biphenyls.

Weanling male rats were exposed to a polybrominated biphenyl (PBB) mixture (Firemaster FF-1) in their diet so that they received 1 mg/kg/day for 6 months. They were then fed a normal diet for 4 months. Following this they were placed on diets containing either activated charcoal (AC) or cholestyramine (CSA) for 6 months to evaluate the usefulness of these compounds in reducing the body burdens of the retained PBBs. Periods of restricted caloric intake were also used in an effort to mobilize PBBs stored in fat. Neither compound nor restricted caloric intake was found to be effective in reducing tissue bromine levels but CSA proved useful in preventing the progression of chronic progressive nephropathy, a spontaneous lesion of aging rats.

Animals↗
PubMed1980

Brain corticosterone in lactating rats: possible relation to the attenuation of the pituitary-adrenocortical response to stress.

In an attempt to elucidate the mechanism of suppression of the plasma corticosterone stress response in the lactating female rats, nonstress levels of corticosterone in plasma and hypothalamus, cerebral cortex, hippocampus and pituitaries were determined in the lactating and nonlactating Sprague-Dawley rats at 1600-1700 hr by the protein binding assay. The brain corticosterone levels were significantly higher (64-92%) in the lactating than in nonlactating rats, while the plasma corticosterone levels were identical. We conclude that the suppression of the stress response in the lactating female rats is directly or indirectly related to the high basal levels of corticosterone in the brain, which result from a chronic hyperactivation of the endocrine axis.

Animals↗