Biomedical subjects
Publications and source records attributed to G A Richards.
Pulmonary thrombo-endarterectomy for chronic pulmonary thrombo-embolic disease is an underutilised and potentially lifesaving therapeutic manoeuvre. This case study describes the functional improvement that can be attained by such a procedure.
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The proinflammatory effects of passive inhalation of cigarette smoke were investigated by exposing a total of 16 healthy, young nonsmokers (mean age 29 +/- 1.4 yr, 11 women and five men) to actively smoking individuals in a poorly-ventilated room. Neutrophil functions were measured before and after 3 h of exposure to cigarette smoke. Passive cigarette smoking was associated with increased leukocyte counts (mean increase 33%, p less than 0.005), chemotaxis (57%, p less than 0.001), and release of reactive oxidants (71%, p less than 0.005) by stimulated neutrophils. These results were confirmed in a second study designed to eliminate the possible complicating effects of serial venepuncture. Plasma concentrations of the proinflammatory cytokines interleukin-1 (IL-1) alpha, IL-1 beta, IL-6, and tumor necrosis factor alpha (TNF alpha) were not affected by passive smoking. These results indicate that inhalation of sidestream tobacco smoke promotes systemic priming of neutrophils. These potentially proinflammatory events may induce oxidant-mediated tissue damage and carcinogenesis in the lungs of passive smokers.
Sixty asymptomatic cigarette smokers were randomly allocated into three treatment groups. Smokers in Group 1 received 900 international units of Vitamin E (VE) daily for 6 wk, whereas 40 mg of beta-carotene (BC) daily was administered to those in Group 2 for the same period. Subjects in Group 3 were treated with a matched placebo. Plasma levels of VE and BC as well as circulating leukocyte counts, sister chromatid exchanges (SCEs), and the luminol-enhanced chemiluminescence (LECL) responses of blood phagocytes activated with phorbol myristate acetate (PMA) and FMLP with cytochalasin B (FMLP/CB) were measured prior to the administration of the antioxidant/placebo after 4 and 6 wk of supplementation and 12 wk after cessation of treatment. SCEs and leukocyte counts remained unchanged throughout the trial in all three treatment groups. Administration of VE for 4 wk was accompanied by decreased FMLP/CB-activated (p less than 0.005) and PMA-activated (p less than 0.005) LECL responses. However, with PMA as stimulant, the inhibition of LECL was transient, with partial recovery observed after 6 wk despite continued administration of VE. Administration of BC was associated with progressive inhibition of both FMLP/CB-activated (p less than 0.05 and p less than 0.01 after 4 and 6 wk, respectively) and PMA-activated (p less than 0.025 after 6 wk) LECL. No alterations in LECL responses were observed in Group 3 (placebo). VE appeared to inhibit the generation of oxidants by activated phagocytes, whereas BC scavenged oxidants generated by the myeloperoxidase/H2O2/halide system.
In this study we have correlated the plasma levels of the anti-oxidant vitamins C and E, and beta-carotene with smoking histories, the release of reactive oxidants from circulating phagocytes and spirometry in asymptomatic cigarette smokers. Smoking histories, the generation of reactive oxidants by activated phagocytes and spirometric abnormalities were strongly inter-correlated. However, plasma levels of the anti-oxidant nutrients did not correlate with any of the other measured parameters. These findings indicate that plasma levels of vitamins C and E, and beta-carotene are apparently not predictive of predisposition to oxidant-mediated-spirometric abnormalities in cigarette smokers.
In this study the frequencies of sister-chromatid exchanges (SCEs) were correlated with measurements of the release of reactive oxidants by phagocytes, as determined by luminol-enhanced chemiluminescence (LECL), and levels of the anti-oxidants ascorbate, beta-carotene and vitamin E in blood specimens taken from 65 young asymptomatic cigarette smokers. Increased SCE frequencies correlated with LECL responses (p less than 0.0075) of activated blood phagocytes. Anti-oxidant levels did not correlate with either LECL or SCEs. These findings indicate that increased generation of reactive oxidants by circulating phagocytes from cigarette smokers are associated with cytogenetic changes.
Spirometric values determined from the flow-volume loops of 60 healthy young smokers (mean age, 28 +/- 0.6 yr) were correlated with measurements of the release of extracellular and intracellular reactive oxidants (RO) as determined by luminol-enhanced chemiluminescence (LECL) from peripheral blood activated with the synthetic chemotactic tripeptide FMLP combined with cytochalasin B (CB). Fractionation and reconstitution experiments revealed that LECL originated predominantly from polymorphonuclear leukocytes (PMNL). Circulating total leukocyte counts and serum thiocyanate levels were also determined. The data were analyzed using Spearman's correlation coefficient and by multiple regression analysis. Cigarette smoking was associated with elevated intracellular and especially extracellular LECL responses, the latter being strongly correlated (p less than 0.0001) with cigarettes smoked per day, serum thiocyanate levels, circulating leukocytes, and PMNL counts. Abnormalities of the spirometric parameters FEV1/FVC, FEF50/FVC, FEF25, FEF25-75, and FEF75-85 correlated best with extracellular LECL (p less than 0.0002 to p less than 0.0001), but also with pack-years (p less than 0.006 to p less than 0.0001), cigarettes smoked per day (p less than 0.008 to p less than 0.0002), thiocyanate levels (p less than 0.04 to p less than 0.002) and leukocyte counts (p less than 0.03 to p less than 0.002). According to stepwise multiple regression analysis of the data the combination of the independent variables extracellular LECL, pack-years, and numbers of circulating PMNL accounts for 35.6% of the variation in lung function in the group of cigarette smokers, with LECL being the most important contributor (26%).(ABSTRACT TRUNCATED AT 250 WORDS)
In the United States there has been an increase in mycobacterial infections that is attributable to the acquired immunodeficiency syndrome (AIDS). Since 1983, when the first case of AIDS was reported in Australia, there have been 523 patients (to June 30, 1987) notified with group-IV AIDS and, of these, 361 (69%) cases have been in New South Wales. Of these 361 notifications, 59 (16%) patients have had concurrent mycobacterial infection. Seven of these patients had Mycobacterium tuberculosis infection and five of these infections occurred in 1986. This means that, in 1986, patients with group-IV AIDS had a rate of infection with Myco. tuberculosis of 3000 per 100,000 population, compared with 5.2 cases per 100,000 population for New South Wales. We sought to determine whether or not there was any unexplained increase in notifications which might be attributable to AIDS. This paper reports cases that were notified to the AIDS and tuberculosis registers, finds that atypical mycobacterial infections are underreported by at least 19.5%, and examines trends in notifications for mycobacterial disease since the onset of the AIDS epidemic. It also raises the importance of appropriate measures to protect health workers from tuberculosis.
Early diagnosis and treatment of Wegener's granulomatosis with cyclophosphamide has considerably improved the prognosis in this previously fatal disease. Experience with this disease in an 11-year-old child is reported.
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The standardized cancer mortality ratios for selected localities in New South Wales with fluoridated and non-fluoridated water supplies were examined. The cancer mortality ratios for both fluoridated and non-fluoridated localities were spread along a continuum. Two localities (one fluoridated, one non-fluoridated) had standardized mortality ratios significantly lower than the New South Wales State average. No relationship was found between cancer deaths and whether water supplies had been fluoridated or not.
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