Biomedical subjects
Publications and source records attributed to A J Dobson.
In the structure of the title compound, C10H6O4, there is a single intramolecular hydrogen bond. In addition, there are a number of significant intermolecular C-H...O attractive interactions. These interactions account in part for the rather high density for an ordinary monocarboxylic acid, 1.522 Mg m(-3).
In biphenyl-3-carboxylic acid, C13H10O2, hydrogen bonding is of the cyclic-dimer type about a center of symmetry. The carboxyl H atom is ordered. The dihedral angle between the planar phenyl rings is 31.78(8) degrees at 296 K and 31.27(6) degrees at 203 K. The data show that the larger-than-average magnitudes of the displacement parameters of the carboxylic O atoms are due to thermal motion rather than static disorder.
In xanthene-9-carboxylic acid, C14H10O3, hydrogen bonding is of the cyclic dimer type but involves two crystallographically inequivalent molecules and does not occur about a center of symmetry. The carboxylic H atoms are ordered. The dihedral angle (fold angle) of the xanthene core is 14.2 (1) degree for molecule A and 11.3 (2) degrees for molecule B. The planes of the carboxyl groups are almost perpendicular to the xanthene cores.
The structures of two phases of fluorene-4-carboxylic acid, C14H10O2, from room-temperature growths have been determined. In the alpha phase, O-H...O hydrogen bonding occurs via cyclic dimers about a center of symmetry; in the beta phase, cyclic dimers with O-H...O hydrogen bonds are formed between two crystallographically inequivalent molecules and do not involve a center of symmetry, though centers of symmetry are present in the crystal. The present evidence strongly suggests that the beta phase is metastable with respect to the alpha phase at room temperature, but the regions of stability have not been determined.
3-Aminopyrazine-2-carboxylic acid, C5H5N3O2, displays an extensive network of intra- and intermolecular hydrogen bonds which are undoubtedly responsible for the modest values of the displacement parameters. H-atom transfer to the ring N atoms did not occur and the carboxy and amino H atoms are ordered. The virtually planar molecules lie very nearly in planes parallel to (102) and are stacked along the a direction with separations of 3.324 (2) A indicating pi-pi interactions.
The central rings of 1,2,3,4,7,8,9,10-octahydrochrysene, C18H20, are essentially planar, with the r.m.s. deviation of the atoms defining the plane from the best-fit plane being 0.013 (2) A. The outer rings are found to be substantially non-planar, contrary to the conclusion of an earlier study based on photographic data [Ferrier & Iball (1958). Acta Cryst. 11, 325-329]. The C-C single-bond distances in the outer rings are quite uniform, with the range of observed values varying by only 0.017 (6) A. There are no notably close intermolecular approaches.
In fluorene-1-carboxylic acid, C14H10O2, the sole hydrogen bond is of the cyclic dimer type about a center of symmetry. The carboxyl H atom is ordered. Distances in the fluorene core are very similar to those in fluorene itself; the fluorene core dihedral angle is, however, larger than in fluorene.
Choosing a measure instrument for a study raises the question of whether instruments designed for the same purpose produce the same results. We investigated this question for two instruments designed to measure subjective quality of life (QOL) in cancer clinical trials: the Functional Living Index-Cancer (FLIC) and the Quality of Life Questionnaire Core module (QLQ-C30). These were administered concurrently to 98 cancer patients. Four patient groups were defined: (1) well, no chemotherapy (n = 23); (2) adjuvant chemotherapy (n = 24); (3) stable disease, active chemotherapy (n = 24); (4) progressive disease (n = 27). Both instruments have global, role, social, emotional, pain, and nausea scales; QLQ-C30 also assesses physical function, cognitive function, and fatigue, while FLIC assesses hardship. Correlation analysis indicated convergent validity for the global, role, emotional, pain and nausea dimensions, but not the social dimension. Both instruments indicated that groups 1 and 2 had better QOL than group 4 in at least one dimension. However, different dimension-specific results meant that qualitatively different conclusions would have been drawn if either instrument had been used singly: FLIC indicated that group 1 had better role function that group 4 and suffered less hardship and that group 1 suffered less nausea than group 3, while the QLQ-C30 data indicated that group 2 had better physical function than group 4. The only consistent result was for pain: both instruments indicated group 4 had more pain than either groups 1 or 2. Thus the choice of QOL instrument for use in a particular trial will affect both the results and conclusions. It is important, therefore, to consider carefully which instrument is most likely to detect important differences relevant to the patients' lives in that setting.
OBJECTIVES: This study sought to examine whether lipoprotein(a) concentrations were risk factors for a first acute and recurrent myocardial infarction. BACKGROUND: There is conflicting evidence concerning the risk of acute myocardial infarction from lipoprotein(a). No studies have examined the risk of recurrent acute myocardial infarction from lipoprotein(a), and few have addressed the risk in women. METHODS: This was a population-based case-control study of 893 men and women 35 to 69 years old participating in the World Health Organization Monitoring Trends and Determinants in Cardiovascular Disease (MONICA) Project in Newcastle, Australia in 1993 to 1994. Case and control patients were classified into those with and without a previous myocardial infarction, and median lipoprotein(a) concentrations were compared after adjusting for other variables. Quintiles of lipoprotein(a) concentration were also examined. RESULTS: Compared with control subjects without a previous myocardial infarction, median lipoprotein(a) concentrations increased from case patients with a first myocardial infarction (15 mg/liter higher, 95% confidence interval [CI] -36 to 60) to control patients with a previous myocardial infarction (159 mg/ liter higher, 95% CI 40 to 278) and case patients with a previous myocardial infarction (60 mg/liter higher, 95% CI -16 to 136, p < 0.01, test for trend). Women had significantly higher lipoprotein(a) concentrations than men (median 71 mg/liter higher, 95% CI 23 to 118). The highest quintile of lipoprotein(a) (>550 mg/liter) was a significant risk factor for a first acute myocardial infarction (odds ratio [OR] 1.77, 95% CI 1.03 to 3.03); but in those with a previous myocardial infarction, the highest quintile was not associated with recurrent myocardial infarction (OR 0.84, 95% CI 0.30 to 2.37). CONCLUSIONS: High lipoprotein(a) concentrations may be a marker of vascular or tissue injury or may be associated with other genetic or environmental factors that cause acute myocardial infarction. Currently, lipoprotein(a) measurement cannot be recommended for assessment of risk for acute myocardial infarction.
Social and health problems among the construction workers in Thailand were studied in a multicenter cross-sectional survey. This paper documents methodological issues related to conducting the survey in the northeastern Thailand. These issues include defining suitable sampling frames for building sites and workers and collecting data. A number of practical problems and the approaches to solve them are discussed.
OBJECTIVES: To determine factors associated with cardiopulmonary resuscitation being attempted after cardiac arrest from myocardial infarction, in or outside hospital, and estimate short term and long term survival rates. DESIGN: Descriptive cross sectional and cohort study. SETTING: Community based register of all suspected heart attacks and sudden cardiac deaths in Lower Hunter region of New South Wales, Australia. SUBJECTS: 4924 men and women aged 25-69. MAIN OUTCOME MEASURES: Rates of attempted cardiopulmonary resuscitation and survival after successful resuscitation. RESULTS: Cardiopulmonary resuscitation was attempted in 41% of cases of cardiac arrest after myocardial infarction outside hospital and 63% of cases in hospital. Survival rates at 28 days were 12% and 39% respectively. Among the survivors, although 41% had another myocardial infarction (or coronary death), 81% of both groups were still alive two years later. Younger and better educated people were more likely to receive cardiopulmonary resuscitation in either setting, and being married predicted cardiopulmonary resuscitation being attempted outside hospital. Younger age predicted better survival rates after attempted resuscitation in hospital. CONCLUSIONS: The reasons for better education to predict cardiopulmonary resuscitation being attempted need explanation. The higher survival rate after cardiopulmonary resuscitation in hospital compared with outside hospital and the good long term prognosis for survivors in both settings suggest that attempts to improve success of cardiopulmonary resuscitation outside hospital may be worth while.
BACKGROUND: In Australia information on the incidence of acute myocardial infarction (AMI) is available from routinely collected morbidity and mortality data. Given that these data are used for monitoring AMI it is important to assess their quality. AIMS: This paper examines the accuracy of the hospital records and death certificates. METHODS: Morbidity and mortality data were compared with the Newcastle heart disease register which is part of the WHO MONICA Project for 1986-1991 and sensitivity and positive predictive values calculated. RESULTS: For non-fatal AMI the hospital diagnostic coding had sensitivity of 78.9% (95% confidence interval [CI] 77.1%-80.7%), and positive predictive value of 65.6% (95% CI 63.7%-67.4%). Sensitivity was higher for men than for women and decreased with increasing age. Sensitivity was higher in those with no history of either AMI or other ischaemic heart disease (IHD), higher in current smokers than ex-smokers or never smokers, and lower in those with a self-reported history of high blood pressure. Sensitivity also varied among hospitals. Positive predictive value varied only with hospital. Both sensitivity and positive predictive value were high for death certificate data--89.9% (95% CI 88.4%-91.3%) and 96.0% (95% CI 95.1%-97.0%), respectively. CONCLUSIONS: Although the mortality data appear to be quite accurate, the hospital data alone are not accurate enough to be used to estimate rates or trends of heart attacks. Additional data are required in order to determine numbers of non-fatal AMIs accurately.
OBJECTIVE: To compare two interventions for reducing dietary fat intake in first degree relatives of recent heart attack victims. DESIGN: A randomised controlled trial comparing a low cost mail-out advice program; referral to a general practitioner (GP); and no intervention (control group). PARTICIPANTS: Adult children or siblings, aged less than 70 years, of survivors of definite or suspected heart attack who had been admitted to hospitals in the Lower Hunter Region of New South Wales. MAIN OUTCOME MEASURES: Dietary fat intake (evaluated with a validated short questionnaire) and measurement of blood cholesterol levels at six months. RESULTS: Of the 342 relatives who participated (36% of those invited), 109, 120 and 113, respectively, were randomly assigned to receive a mail-out intervention, advice from their GP or to be part of a control group. The six-month follow-up questionnaire was completed by only 59% of those in the mail-out intervention group compared with 71% of the GP group and 77% of the control group. Younger participants, cigarette smokers and children (compared with siblings) were less likely to return a follow-up questionnaire. The mail-out group showed a statistically significant 20% reduction in self-reported dietary fat intake, but this was not seen in either the GP group or the controls. The low response rate meant the study had insufficient power to detect hypothesised changes in blood cholesterol. CONCLUSION: Because of the poor response rate and possible biases from a differential response to follow-up, we conclude that this low intensity intervention for relatives of people with recent heart attack produces only a modest improvement in reported dietary fat intake. Alternative strategies may be more effective in reducing the risk of heart disease.
There were substantial reductions in mortality rates for all causes of death and for cardiovascular diseases in all age groups examined and both sexes during the period 1969 to 1990. Among young and middle-aged women, cardiovascular diseases were no longer the major cause of death; cancers were. In younger men, accidents, poisonings and violence (including suicides) were the leading cause of death. In middle-aged men, cardiovascular mortality dropped to about the same level as cancer mortality. Only in older people did cardiovascular mortality still dominate. Nevertheless, the proportion of all deaths due to cardiovascular disease remained high and there are opportunities for further reductions. The relative lack of improvement in mortality from cancers suggests that these will form increasing proportions of the burden of disease and treatment costs in the next decades.
To what extent can trends in risk factor levels in populations explain trends in disease rates? Some methodological difficulties in answering this question include weaknesses of ecological studies, small sample size, time lags and multiple sources of variability. Two possible approaches are to apply predictive equations derived from longitudinal studies of individuals to average data for populations, or to use results from overviews of randomized, controlled trials and cohort studies to estimate the magnitude of effects achievable through various risk factor changes. These methods are illustrated with Australian data on trends in mortality from ischaemic heart disease and cigarette smoking, blood pressure and cholesterol during the 1980s. If it is assumed that time lags are short between reductions in risk factor levels and reductions in risk, then both methods suggest that about half the mortality decline in men, and less in women, may be related to changes in these three well-established risk factors. Improvements in population levels of blood pressure and, for men, reductions in smoking appear to be the main contributors. It is argued that such ecological analyses can provide valid results as long as care is taken to avoid various epidemiological pitfalls.
In Australia there has been a recent increase in the body mass index (BMI) of the population and a decrease in smoking prevalence. Data from the three risk factor prevalence surveys conducted by the National Heart Foundation of Australia in 1980, 1983 and 1989 were analysed to determine if the increase in BMI could be explained by the decrease in smoking. For men in all age groups and for women aged 50 years or over, there were parallel increases in mean BMI for current smokers, ex-smokers and never smokers. For women under 50 years, the pattern of increasing BMI over time was less clear. Mean BMI increased over time within each five-year age group and in age 'cohorts' and the pattern was independent of smoking status. For men and for both groups of women there were similar changes in mean BMI over time for most categories of employment status, education and physical activity. Thus the increase in body weight cannot be explained by the decrease in smoking rate, or by the other factors investigated in this paper.
OBJECTIVE: To estimate the impact of smoking on the incidence of coronary heart disease in Australia. Data collected for the WHO MONICA Project were used. DESIGN: Combined data from a community-based register of all suspected coronary events and a survey of risk factor prevalence in a random sample of the same population. SETTING AND PARTICIPANTS: All residents of the Hunter Region of New South Wales aged 35-69 years who had a first acute myocardial infarction or fatal heart attack (without a history of coronary heart disease) between 1 January 1986 and 31 December 1990. MAIN OUTCOME MEASURES: Acute myocardial infarction or coronary death, as defined by the WHO MONICA Project. RESULTS: Men who are current smokers are 2.9 times (95% CI, 2.7-3.1) more likely than non-smokers to have a first myocardial infarction or fatal heart attack, and for women the equivalent figure is 3.5 times (95% CI, 3.2-3.8), after adjusting for age. Current male smokers with a history of hypertension are 4.5 times more likely to have a coronary event (7.9 times in women) than are non-smokers without a history of hypertension. The age-adjusted excess rate was 566 per 100,000 per year in men and 373 per 100,000 per year in women. Smoking is a stronger predictor of coronary heart disease incidence than a history of hypertension (relative risk [RR] = 1.6 for men and 1.9 for women) or a known history of hypercholesterolaemia (RR not significantly different from 1). CONCLUSIONS: Cigarette smoking plays a more important role in the causation of a first myocardial infarction or fatal heart attack and appears to have more influence on the incidence of coronary heart disease in Australia than hypertension.
The hypothesis that 6 months after acute myocardial infarction, adoption of secondary prevention activities would be higher, quality of life better, and blood cholesterol lower in patients randomly allocated to a mail-out intervention program than in those receiving usual care was tested. Patients were aged < 70 years, admitted to hospitals in and around Newcastle, Australia with a suspected heart attack and discharged alive from the hospital. Cluster randomization, based on the patient's family practitioner, was used to allocate consenting patients to an intervention or usual care group. A low-cost mail-out program was designed to help patients reduce dietary fat, obtain regular exercise by walking and (for smokers only) to quit smoking. Supplementary telephone contact was also used. In addition, a letter was sent to the family doctor regarding the benefit of aspirin and beta blockers for secondary prevention. Of eligible patients, 71% participated, and 79% of the 213 intervention subjects and 87% of the 237 usual care ones returned a 6-month follow-up questionnaire. Self-reported fat intake was significantly lower, an "emotional" score obtained from a quality-of-life questionnaire was significantly higher in the intervention than in the usual care group, and "physical" and "social" scores for quality of life were slightly higher. Blood cholesterol level and other variables were not different between the groups at 6 months. Simple low-cost programs providing support and advice on lifestyle change may be beneficial, particularly in improving patients' perceived quality of life.