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Biomedical subjects

S Webster

Publications and source records attributed to S Webster.

At least 55 records · Page 3Linked to original sources
PubMed1991

The life shortening effects of treatment with doxorubicin and/or local irradiation on a cohort of young C3Hf/Sed mice.

The long-term consequences of treating a cohort of C3Hf/Sed mice in early life with either local-field single dose radiation, systemic doxorubicin, or both, are reported in this study. Significant life shortening was observed in all treatment groups. Median survival times (days) from time of treatment were: control, 690; 35 Gy, 560; 70 Gy, 460; 5 mg/kg doxorubicin, 580; 10 mg/kg doxorubicin, 350; 35 Gy + 5 mg/kg doxorubicin, 510; 70 Gy + 10 mg/kg doxorubicin, 310. Mice receiving hind limb irradiation died principally from induced sarcomas in a dose dependent fashion (80% after 70 Gy and 55% after 35 Gy). Those treated with doxorubicin alone showed an increase in the actuarial incidence of spontaneous malignancies but died mainly from non-malignant causes. Histological examination did not reveal any characteristic cardiac, renal or pulmonary lesions. Doxorubicin did not increase the rate of development of radiation induced sarcomas in mice treated with combined modality.

Animals↗
PubMed1990

Physiological effects of a weight loss regimen practiced by college wrestlers.

The effects of weight loss (dehydration) techniques (which mimicked techniques used prior to actual competition) used by intercollegiate wrestlers on selected physiological parameters (strength, anaerobic power, anaerobic capacity, the lactate threshold (LT), and peak aerobic power) were examined in seven intercollegiate wrestlers. During the 36 h weight loss period, subjects lost 3.3 kg (4.9% body weight), all of which occurred during the 12 h prior to weigh-in, using exercise in a rubberized sweat suit. Weight loss resulted in a reduction in upper body but not lower body strength measures (peak torque and average work per repetition). Anaerobic power and anaerobic capacity were significantly reduced in a dehydrated state (81.4 kgm.s-1, normal weight; 63.9 kgm.s-1, weight loss; 1984.3 kgm.40 s-1, normal weight; 1791.4 kgm.40 s-1, weight loss). Analyses of treadmill data revealed the following: 1) velocity was decreased at LT (4.4%) and peak (6.5%) during weight loss (P less than 0.05); 2) VO2 peak was significantly reduced with weight loss (6.7%, P less than 0.05); 3) treadmill time to exhaustion was significantly reduced in the weight loss state (12.4%) (35.7 min, normal weight; 31.3 min, weight loss). It was concluded that typical wrestling weight loss techniques result in deleterious effects on strength, anaerobic power, anaerobic capacity, the lactate threshold, and aerobic power.

Adolescent↗
PubMed1988

A controlled trial of an oral bronchodilator preparation ('Franol') in asthma.

In view of the lack of published data on the oral bronchodilator preparation 'Franol' (120 mg theophylline, 11 mg ephedrine hydrochloride and 8 mg phenobarbitone per tablet) a double-blind study was carried out to compare the effects on lung function of a single dose of 2 'Franol' tablets, 1 'Franol' plus 1 placebo tablet, or 2 placebo tablets over a period of 8 hours in 30 asthmatic patients with reversible airways resistance (mean FEV1 1.31 l increasing to 1.71 l after 200 micrograms salbutamol inhalation). 'Franol' produced dose-dependent bronchodilation. Two tablets caused significant bronchodilation from 90 minutes to 8 hours (peak change from baseline at 2.5 hours: FEV1 20.8%, PEFR 22.3%). One tablet of 'Franol' produced significant bronchodilation only between 60 minutes and 3 hours (change from baseline at 2.5 hours: FEV1 7.5%, PEFR 7.9%). There was no change in lung function with placebo (change from baseline at 2.5 hours: FEV1 5.4%, PEFR 5.9%). Median serum theophylline levels at 2.5 hours were 6.38 micrograms/ml for 2 tablets and 3.18 micrograms/ml for 1 tablet. Median peak phenobarbitone levels were 0.5 micrograms/ml. There were no clinically relevant changes in pulse rate and blood pressure during the study and no adverse events were reported.

Administration, Oral↗
PubMed1987

The effect of smoking on placental and fetal zinc status.

Previous studies have reported a cadmium/zinc interaction in cadmium-exposed pregnant animals that results in (1) increased placental cadmium levels, (2) increased placental zinc levels, and (3) decreased placental zinc transport. This study was carried out to determine whether zinc status would be affected in pregnant women exposed to cadmium through cigarette smoke. Atomic absorption spectroscopy was used to determine the levels of cadmium and zinc; 65 pregnant women who smoke and 84 who do not smoke were studied. Our data reveal that increased cadmium levels in pregnant women as the result of smoking increase placental zinc levels and decrease cord red blood cell zinc levels. Significantly higher levels of both cadmium and zinc were found in the placentas of pregnant women who smoke; moreover, stepwise multiple regression showed that maternal whole blood cadmium levels predicted placental zinc levels. In regard to cord blood, a significant 9% decrease in the red blood cell zinc level was observed in infants of mothers who smoke and this decrease was correlated with smoking activity, as evaluated by measuring plasma levels of thiocyanate. Also cord red blood cell zinc levels were found to correlate with placental zinc levels in nonsmokers but not in smokers. Overall, our data show that a cadmium/zinc interaction does take place in the maternal-fetal-placental unit of pregnant women who smoke and results in less favorable zinc status in the infants.

Adult↗
PubMed1980

Psychophysiological assessment of sex offenders in a security hospital.

A study on the sexual orientation and responsiveness of sexual offenders in a maximum security hospital who had been referred to the Psychology Department for sexual assessment is described. Correlations between "felt sexual arousal" ratings and penis diameter increase were calculated to assess validity, but a high proportion of detained patients gave results which could be interpreted as indicating defensiveness or faking. Groups of sexual offenders (against women, girls, boys, and men), nonsexual attackers of women, and typical heterosexuals were compared on their profiles of response to films showing consenting adult heterosexual, adult homosexual, and boy homosexual activity, girl abduction, and girl rape. Groups did not differ on the consenting heterosexual activity film, but typical heterosexuals and nonsexual attackers of women showed significantly less response to the film of girl abduction (p less than 0.001) and rape (p less than 0.001) than did groups of sex offenders generally.

Antisocial Personality Disorder↗
PubMed1979

Electrodermal indices of public offending and recidivism.

Three hypotheses based on the relationship between electrodermal activity and 'psychopathic' behaviour were investigated. These hypotheses are that 'psychopathic' behaviour relates to frequency of spontaneous fluctuations (Schalling, 1978), orienting response recovery time (Mednick, 1975) and orienting response amplitude (Siddle, Nicol and Foggitt, 1973). Non-recidivistic domestic offenders and highly recidivistic public offenders were compared on two test sessions. The high public risk recidivists had relatively lower rates of spontaneous fluctuation on both test sessions (p less than 0.001, p less than 0.02) and longer recovery OR(t/2)(p less than 0.05) on the first session. Reductions in fluctuation rate over sessions were significant for both groups, but were very much greater in the domestic offenders (p less than 0.001) than in the public offenders. OR amplitude did not discriminate between groups.

Antisocial Personality Disorder↗
PubMed1978

Simple behaviour rating scales for maximum security patients: development and validation.

An outline is given of objective behaviour rating scales developed for use by nurse custodians in the maximum security hospital setting. Four independent scales are described: (a) antisocial belligerence, (b) disorientation, (c) withdrawal and (d) personal hygiene. The scales gave high test-retest and inter-rater reliabilities. Various indications of validity and potential usefulness of the scales are given. In particular, a probable relationship of the scales (a) and (c) with an impulsivity/overcontrol dimension is suggested-this relating to the type of aggressive offending recorded.

Adult↗
PubMedDate not supplied

Inflammation and Alzheimer's disease pathogenesis.

Appreciation of the role that inflammatory mediators play in Alzheimer's disease (AD) pathogenesis continues to be hampered by two related misconceptions. The first is that to be pathogenically significant a neurodegenerative mechanism must be primary. The second is that inflammation merely occurs to clear the detritis of already existent pathology. The present review addresses these issues by showing that 1) inflammatory molecules and mechanisms are uniquely present or significantly elevated in the AD brain, 2) inflammation may be a necessary component of AD pathogenesis, 3) inflammation may be sufficient to cause AD neurodegeneration, and 4) retrospective and direct clinical trials suggest a therapeutic benefit of conventional antiinflammatory medications in slowing the progress or even delaying the onset of AD.

Alzheimer Disease↗
PubMedDate not supplied

Inflammation and Alzheimer's disease.

Inflammation clearly occurs in pathologically vulnerable regions of the Alzheimer's disease (AD) brain, and it does so with the full complexity of local peripheral inflammatory responses. In the periphery, degenerating tissue and the deposition of highly insoluble abnormal materials are classical stimulants of inflammation. Likewise, in the AD brain damaged neurons and neurites and highly insoluble amyloid beta peptide deposits and neurofibrillary tangles provide obvious stimuli for inflammation. Because these stimuli are discrete, microlocalized, and present from early preclinical to terminal stages of AD, local upregulation of complement, cytokines, acute phase reactants, and other inflammatory mediators is also discrete, microlocalized, and chronic. Cumulated over many years, direct and bystander damage from AD inflammatory mechanisms is likely to significantly exacerbate the very pathogenic processes that gave rise to it. Thus, animal models and clinical studies, although still in their infancy, strongly suggest that AD inflammation significantly contributes to AD pathogenesis. By better understanding AD inflammatory and immunoregulatory processes, it should be possible to develop anti-inflammatory approaches that may not cure AD but will likely help slow the progression or delay the onset of this devastating disorder.

Alzheimer Disease↗