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Biomedical subjects

A P Bell

Publications and source records attributed to A P Bell.

7 recordsLinked to original sources

Screening for smokers in four Sydney teaching hospitals.

BACKGROUND: Cardiovascular disease is a major cause of death and a reason for hospital admissions. The hospital stay is a window of opportunity to assist smokers to quit. METHODS: Patients from selected wards in four teaching hospitals in Sydney, Australia were screened using a self-completed general health questionnaire. The questionnaire included questions on demographic variables, tobacco and alcohol consumption, attitudes towards tobacco and alcohol use, and a measure of readiness to charge high-risk lifestyle behaviors, based on that proposed by Prochaska and DiClemente [1]. RESULTS: The total number of screening questionnaires completed was 2,815: 78% men and 22% women. The average age of the sample was 44 years, 48% were married or living in a de facto relationship whilst 35% never married, with the rest widowed, separated or divorced. A total of 877 (31%) patients reported smoking: 33% of men and 24% of women screened. Predictors of smoking were sex, age, marital status, education level and socio-economic status. A significant association was found between excessive drinking and smoking. Among the smoking patients, 157 (18%) planned no change in smoking (precontemplation), 379 (43%) were ambivalent about smoking (contemplation), and 334 (38%) were serious about quitting. CONCLUSION: As about one third of patients in hospital are smokers, the hospital is an ideal setting for the delivery of brief interventions by a range of health personnel at the patients bedside. The use of a detection instrument measuring levels of intake and readiness to change tobacco use is described, as a practical method for targeting patients in hospital who are at risk or have already developed cigarette-related diseases, such as cardiovascular disease.

Adolescent↗

Familiality of female and male homosexuality.

We examined data from a large cohort of homosexual and heterosexual females and males concerning their siblings' sexual orientations. As in previous studies, both male and female homosexuality were familial. Homosexual females had an excess of homosexual brothers compared to heterosexual subjects, thus providing evidence that similar familial factors influence both male and female homosexuality. Furthermore, despite the large sample size, homosexual females and males did not differ significantly from each other in their proportions of either homosexual sisters or homosexual brothers. Thus, results were most consistent with the possibility that similar familial factors influence male and female sexual orientation. However, because results conflicted with those of some other studies, and because siblings' sexual orientations were obtained in a manner likely to yield more errors than in these other, smaller studies, further work is needed using large samples and more careful methods before the degree of cofamiliality of male and female homosexuality can be resolved definitively. We also examined whether some parental influences comprised shared environmental effects on sexual orientation. Scales attempting to measure such influences failed to distinguish subjects with homosexual siblings from subjects with only heterosexual siblings and, thus, did not appear to measure shared environmental determinants of sexual orientation.

Adult↗

Avian sarcoma virus gag precursor polypeptide is not processed in mammalian cells.

We studied intracellular avian gag proteins (internal structural proteins of virions) in several mammalian cell lines transformed by Rous sarcoma virus. All lines examined contain gag antigens as determined by radioimmune assay. We used the techniques of protein blotting from polyacrylamide gels, which detects nanogram quantities of viral protein, to investigate the size of intracellular viral polypeptides. All of the lines that contained enough viral protein to be amenable to this type of analysis synthesized Pr76, the avian sarcoma virus gag precursor polypeptide, but failed to process it into mature virion proteins. In some cell lines, the recovery of Pr76 was greatly enhanced by the addition of a mixture of protease inhibitors, including the sulfhydryl-blocking reagent N-ethylmaleimide, to the lysis buffer. At least several of the mammalian cells also synthesized a viral polypeptide the size of Pr180, the precursor to reverse transcriptase. Since Rous sarcoma virus does not replicate or replicates extremely poorly in mammalian cells, the lack of processing suggests that cleavage and virion assembly are invariably associated.

Animals↗