Search PubMed⌕ Search

Biomedical subjects

D A Lewis

Publications and source records attributed to D A Lewis.

At least 343 records · Page 19Linked to original sources
PubMed1969

Androgen sulphate formation in male and female mice.

1. After the administration of large doses of androsterone, epiandrosterone, dehydroepiandrosterone and testosterone to mice, females excreted more of the dose conjugated with sulphuric acid than did males. 2. Liver slices from female mice conjugated androgens with sulphuric acid to a greater extent than did slices from males. 3. Sulphotransferase preparations from livers of female rats and mice catalysed the formation of dehydroepiandrosterone sulphate at a faster rate than preparations from livers of the male animals. 4. A possible explanation for the observed sex differences is discussed.

Androgens↗
PubMed1968

Androgen sulphate formation in male and female rats.

1. After large doses of androsterone, epiandrosterone, dehydroepiandrosterone and testosterone, female rats excreted more of the dose conjugated with sulphuric acid than did the males. 2. Androgens were also incubated with liver slices from male and female rats. Slices from females conjugated androgens with sulphuric acid to a greater extent than did slices from males. 3. The amount of unchanged androgen present in the faeces of orally dosed animals was 4-35% of the dose.

Androgens↗
PubMed1966

The metabolism of cis- and trans-indane-1,2-diol.

1. The metabolism of cis-indane-1,2-diol, trans-indane-1,2-diol, indene epoxide and 2-hydroxyindan-1-one in rats has been studied. The substances were administered to the animals by subcutaneous injection. 2. The urine of the dosed animals was examined for the presence of free and conjugated cis- and trans-dihydrodiols, and for each compound it was possible to isolate both cis and trans forms of indane-1,2-diol from the urine. 3. The urines were also examined by paper chromatography for ketones and two ketonic metabolites were detected in the urine of rats dosed separately with cis-indane-1,2-diol, trans-indane-1,2-diol, 2-hydroxyindan-1-one and indene epoxide. The ketones were provisionally identified as (1-oxoindan-2-yl glucosid)uronic acid and 1-oxoindan-2-yl sulphuric acid. 4. (1-Oxoindan-2-yl glucosid)uronic acid was isolated as the 2,4-dinitrophenylhydrazone from the urine of rats dosed separately with cis-indane-1,2-diol and trans-indane-1,2-diol. 5. Possible mechanisms for the interconversion of cis- and trans-indane-1,2-diol are discussed.

Animals↗
PubMedDate not supplied

Reproducibility of head-up tilt-table testing in pediatric patients with neurocardiogenic syncope.

The aim of this study is to assess the reproducibility of a head-up tilt-table test protocol so it may be used to more accurately evaluate the effectiveness of a treatment protocol. Children between the ages of 10 and 18 years presenting to the cardiology department at Children's Hospital of Wisconsin with a diagnosis of neurocardiogenic syncope were eligible for the study. The patients were tilted to 70 degrees for 30 minutes or until a positive test occurred. Patients with a positive test were retilted using the same protocol. Parameters measured included heart rate, blood pressure, and the presence or absence of syncope or presyncope. Twenty-two patients were enrolled in the study. Seventeen patients had a positive test on first tilt. Fifteen had a positive tilt test on the second tilt. There were no significant differences between the two tilts with regard to mean differences of baseline heart rate, systolic blood pressure, or mean arterial pressure. There were no significant differences between the two tilts with regard to mean differences in time until symptoms, heart rate, systolic blood pressure, or mean arterial blood pressure at time of symptoms. This study shows that the head-up tilt-table test protocol used is reproducible in adolescents with the diagnosis of neurocardiogenic syncope.

Adolescent↗
PubMedDate not supplied

Axonal loss from the olfactory tracts in Alzheimer's disease.

Senile dementia of the Alzheimer type has been shown to be associated with impaired olfactory function early in the course of the disease. Neuropathology in the olfactory system is also a feature of Alzheimer's disease (AD) and it has been suggested that the disease may be caused by a pathogen entering the brain via olfactory pathways. To investigate this hypothesis, the effect of AD on the olfactory tract was investigated. There was a 40% decrease in the cross-sectional area of the olfactory tract and a 52% loss of myelinated axons from the tract in AD. These results, together with those of previous studies suggest that peripheral regions of the olfactory system, i.e., the olfactory bulb and primary sensory olfactory neurons are less affected by the pathology of AD than more central parts, i.e., cortical regions, the anterior olfactory nuclei, and olfactory tract. This less severe pathology at the periphery argues against a pathogen entering the brain via the peripheral olfactory apparatus and suggests a central pathogenesis which spreads centrifugally along olfactory pathways.

Aged↗
PubMedDate not supplied

Cortical dopamine in schizophrenia: strategies for postmortem studies.

Many of the symptoms of schizophrenia appear to involve dysfunction of the cognitive processes mediated by the neural circuitry of the cerebral cortex. The application of modern neuroscience techniques to the study of postmortem human brain specimens provides a powerful approach for exploring the manner in which cortical circuitry may be disrupted in schizophrenia. In this paper, we describe a strategy for the conduct of postmortem investigations of schizophrenia that involves (1) the use of a nonhuman primate model to guide the design and interpretation of studies in humans; (2) the detailed characterization of the normal organization of neural systems in the human cerebral cortex, and the range of inter-individual variations in that organization; and (3) the testing of specific hypotheses about the disruption of that organization in schizophrenia. The application of this strategy, and its value in overcoming some of the potential pitfalls of postmortem studies, is demonstrated in a series of investigations designed to test the hypothesis that dopamine neurotransmission is impaired in the entorhinal cortex in schizophrenia.

Animals↗
PubMedDate not supplied

Polychlorinated dibenzo-p-dioxins (PCDDs) and polychlorinated dibenzofurans (PCDFs) in human milk samples collected across Canada in 1986-87.

Monitoring of human milk samples for the presence of chemical contaminants has been carried out in Canada for several decades. In 1986-87 over 400 donations of human milk were collected nationwide and 100 of these, selected by province according to population, were analysed for the PCDDs/PCDFs. The results show the presence of about eleven different analytes all with 2,3,7,8-substitution with the PCDDs at higher and more variable concentrations than the PCDFs. On a 2,3,7,8-TCDD toxic equivalents (TEQ) basis, the mean value for the country is about 15 ng per kg milk fat. This TEQ value is similar to that from many other industrialized nations and about 50% lower than certain European states. Little or no variation was apparent in the milk content among the various Canadian provinces probably reflecting the uniformity of the general food supply across the country. Limited data over a period of five years suggest the average level of these compounds in human milk may be decreasing.

Benzofurans↗
PubMedDate not supplied

Nonphosphorylated neurofilament protein and calbindin immunoreactivity in layer III pyramidal neurons of human neocortex.

Subpopulations of pyramidal neurons in the neocortex have been shown to contain nonphosphorylated neurofilament protein (NPNFP) and calbindin D28K (Morrison et al., 1987; Campbell and Morrison, 1989; Hof et al., 1990; Kobayashi et al., 1990; Hof and Morrison, 1991; Mesulam and Geula, 1991). However, it is not known what relations, if any, exist between the pyramidal neurons containing each of these proteins. In this study, the expression of NPNFP and calbindin immunoreactivity was compared in six regions of human neocortex. Characteristic laminar patterns of immunoreactivity for each protein were seen in most regions examined, and both NPNFP- and calbindin-labeled pyramidal neurons were found in layer III. However, the pyramidal neurons labeled with NPNFP and calbindin differed in several respects. First, the sublaminar distribution of NPNFP-labeled pyramids within layer III differed across regions, ranging from an even distribution throughout the layer in a visual association region (area 18) to a predominance of labeled neurons in the deep half of that layer in a higher association region (area 20). The distribution of calbindin-immunoreactive pyramidal neurons also varied regionally, but in a different manner than that of the NPNFP-labeled neurons. Second, in every region examined, the average size of NPNFP-labeled layer III pyramids was greater than that of calbindin-immunoreactive pyramids. However, there was substantial regional heterogeneity in the extent to which the size distributions of neurons in each of the two populations overlapped. Third, in the regions in which NPNFP- and calbindin-immunoreactive neurons were most similar in size, the amount of colocalization (as identified by double-labeling studies) was also greatest. Similarly, in the regions in which there was minimal overlap in the size of the NPNFP- and the calbindin-immunoreactive neurons, there was minimal colocalization. These regional characteristics of NPNFP- and calbindin-immunoreactive layer III pyramidal neurons have implications for the involvement of these neuronal populations in Alzheimer's disease.

Adult↗