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T M Smith

Publications and source records attributed to T M Smith.

118 records · Page 7Linked to original sources
PubMedDate not supplied

The use of logit models to investigate social and biological factors in infant mortality. I: Methodology.

Infant mortality data for England and Wales, cross classified by mother's age, parity and social class, have been published on two occasions, the first giving the relevant data for 1949/50, the second for 1975, some 25 years later. Published analyses of these separate data sets have been based on graphical and tabular methods. This paper describes the statistical methodology appropriate to the use of logit models to investigate these data sets and shows how such models may be used to supplement the more informal approach. The stillbirth data for 1975 are used for illustration. Paper II, which follows, explores the stillbirth data in greater detail, with emphasis on the changes between 1949/50 and 1975. Subsequent papers describe neonatal and post-neonatal deaths using the same framework. A final paper summarizes the overall changes in infant mortality by means of a multilogit model.

Adolescent↗
PubMedDate not supplied

The use of logit models to investigate social and biological factors in infant mortality. II: Stillbirths.

Infant mortality data for England and Wales cross-classified by mother's age, parity and social class have only been published for 1949/50 and 1975. Appropriate statistical methodology for the analysis of such data has been described in Paper I, which used the 1975 stillbirth data for illustration. This paper examines the stillbirth data from both years by formally incorporating the year of data collection into the statistical model, enabling changes in the age, parity and social class effects with time to be investigated. Despite a marked reduction in stillbirth mortality from 21.1 to 10.1 per thousand over the period, the relative contribution of social class has increased. In particular there has been a relative increase in risk for mothers in the lower social classes. By contrast the effects of age and parity, although remaining important, have diminished over the period.

Adolescent↗
PubMedDate not supplied

The use of logit models to investigate social and biological factors in infant mortality. III. Neonatal mortality.

Infant mortality data for England and Wales, cross-classified by mother's age, parity and social class have been published on two occasions, the first giving the relevant data for 1949/50, the second for 1975, some 25 years later. Published analyses of these separate data sets have been based on graphical and tabular analysis. This paper develops the methodology from an earlier paper by Murrells et al. to the analysis of the neonatal data.

Adolescent↗
PubMedDate not supplied

The use of logit models to investigate social and biological factors in infant mortality. IV: Post-neonatal mortality.

Infant mortality data for England and Wales, cross-classified by mother's age, parity and social class have been published on two occasions, the first giving the relevant data for 1949/50, the second for 1975, some 25 years later. Published analyses of these separate data sets have been based on graphical and tabular analysis. This paper describes the application of logit models using the methodology presented by Murrells et al. to investigate post-neonatal deaths.

Adolescent↗
PubMedDate not supplied

Cholinergic role in alcohol's effects on evoked potentials in visual cortex of the albino rat.

Photic evoked potentials were recorded from the visual cortex of chronically implanted albino rats. Since photic evoked potential components are representations of neural pathways which are activated during photic stimulation, study of the effects of alcohol on these components may help to trace pathways which are affected by alcohol. In the present study, evoked potentials were recorded at 5, 20, and 40 min following IP injections of saline, ethanol (2.0 g/kg), physostigmine (0.6 mg/kg) or atropine (15.0 mg/kg) on separate days. Ethanol depressed the amplitudes of most evoked potential components in comparison to saline administration. Component P2, however, was increased in amplitude. Physostigmine briefly reduced the amplitude of most components, including P2. In contrast, atropine increased the amplitudes of components P1 and P2, while decreasing components N1, N2 and N3 for varying durations of time. Physostigmine pretreatment augmented the depressant effect of alcohol on the early components P1 and N1, while attenuating alcohol's influence on components P2 and P3. Pretreatment with atropine likewise further reduced the amplitudes of components P1 and N1, and produced a similar effect on component N3. Atropine, either alone or in combination with alcohol, produced approximately the same degree of enhancement of component P2. In comparison to saline values, all three agents produced reliable increases in peak latency for most of the components, with only N3 showing no effects. The amplitude data from this study suggest that ethanol's augmentation of component P2 may result, at least in part, from alterations in cholinergic functions.

Animals↗
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Hyperammonemia in neonates receiving intravenous nutrition.

Inadequate arginine intake has been suggested as an etiology for hyperammonemia in neonates on parenteral nutrition. We randomized 26 nonasphyxiated neonates to receive amino acid solutions containing either 3.6 or 10.4% of total nitrogen as arginine when intravenous nutrition (IVN) therapy was initiated. Neonates in both amino acid solution study groups were observed to have significantly elevated blood ammonia (BA) concentrations during IVN (p less than 0.01) as compared to pre-IVN levels. Blood ammonia concentrations tended to be higher in infants receiving the 3.6% arginine amino acid solution. Septic infants were at particular risk for hyperammonemia as compared to nonseptic patients (p less than 0.025). Other clinical parameters including birth weight, gestational age, oxygen requirements, enteral nutritional intake, congenital anomalies, and heart disease did not appear to be related to BA concentration.

Amino Acids↗
PubMedDate not supplied

Pharmacokinetics of bupropion and metabolites in plasma and brain of rats, mice, and guinea pigs.

Recent reports indicate that bupropion, a novel non-tricyclic antidepressant, is metabolized differently in certain species of animals. To further define the disposition of bupropion, a study was done involving three species, the rat, mouse, and guinea pig, as animal models to evaluate bupropion metabolism. The pharmacokinetic profiles of bupropion and its major basic metabolites, BW 306U and BW A494U, were determined following the ip administration of 40 mg/kg bupropion to these animals. Pharmacokinetic profiles of the parent drug and metabolites from plasma and brain samples were obtained using a liquid chromatographic procedure. Further investigation of the reduced bupropion metabolite BW A494U was carried out by the ip administration of this metabolite to these animals and assaying the plasma and brain samples 90 min after dosing. Analysis of the pharmacokinetic data revealed that the rat quickly metabolized bupropion, but no basic metabolites accumulated. The mouse metabolized bupropion predominantly to BW 306U, whereas the guinea pig converted bupropion to reduced bupropion (BW A494U) as well as BW 306U. Brain/plasma ratios of bupropion among these animals did not vary significantly. However, both metabolites showed dramatic differences in their brain/plasma ratios among these species. When reduced bupropion (BW A494U) was injected, almost 3% of the plasma concentration of BW A494U was determined to be bupropion in the rat. Lesser amounts were converted in the mouse and guinea pig. Therefore, we have demonstrated that distinct differences exist in the metabolism of bupropion in various species of animals. The guinea pig, when compared to the rat or mouse, appears to constitute a model that most closely resembles that of human bupropion metabolism.

Animals↗
PubMedDate not supplied

Isolation of avian influenza virus (subtype H5N2) from chicken eggs during a natural outbreak.

Avian influenza virus (A/Chicken/Pennsylvania/83; H5N2) was recovered from the yolk, albumen, and shell surface of eggs obtained from naturally infected chicken flocks in Pennsylvania and Virginia. These findings represent the first reported isolation of avian influenza virus from the internal contents of eggs from naturally infected flocks. The need for adequate safeguards to prevent spread of the virus during commercial movement of table and hatching eggs, cracked and "checked" eggs, and egg flats and other materials is emphasized.

Animals↗
PubMedDate not supplied

Comparison of the clastogenic and carcinogenic effects of intravenous beta-propiolactone and benzo(a)pyrene in rats.

Scored at 24 hours, the LD-50 of a solution of beta-propiolactone administered intravenously to young rats was 225 +/- 55 mg/kg. Twenty-four hours after a single intravenous injection (100 mg/kg = 1.4 m mole/kg) of beta-propiolactone into male and female rats of both the Long-Evans and Sprague-Dawley strains, the incidence of breaks found in the chromosomes of metaphase marrow cells was low (8.8 percent vs. 5.0 percent in controls). The s5 chromosomes were preferentially damaged. A 200 mg/kg dose increased the incidence modestly to 11.3 percent. In comparison, a single intravenous dose of benzo(a)pyrene (40 mg/kg = 0.16 m mole/kg) produced a break incidence of 19 percent. In long-term experiments multiple (five) intravenous injections (100 mg/kg each) of beta-propiolactone given in a 6 week period elicited only two neoplasms (a chloro-leukemia and a mammary fibroadenoma) among 37 animals during the following 12-13 months. In contrast, four injections of benzo(a)pyrene (40 mg/kg) produced a 14-times greater mammary tumor incidence in the Sprague-Dawley female rat than did beta-propiolactone. Marrow cell chromosome examination indicated no significant chromosomal changes due to the earlier beta-propiolactone treatment except for one animal with a consistent 43-chromosome karyotype resulting from S1 trisomy; no neoplasm was evident in that animal. Earlier treatment with benzo(a)pyrene produced a persistent and significant elevation in break incidence. Both the carcinogenic and clastogenic effects of intravenous beta-propiolactone are low in rats and are not comparable in magnitude to those produced by benzo(a)pyrene.

Animals↗