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Objective: To determine the incidence and case fatality of seven distinct subtypes of stroke in Perth, Western Australia., Design and Setting: A population-based descriptive epidemiological study., Subjects: All residents of a geographically defined segment of the Perth metropolitan area (estimated population 138,708 persons) who had a stroke or transient ischaemic attack between 20 February 1989 and 19 August 1990, inclusive., Main Outcome Measures: The following subtypes of stroke were classified according to standard clinical, radiological and pathological criteria: types of cerebral infarction, namely, large artery (thrombotic) occlusive infarction (LAOI), cerebral embolic infarction (EMBI), lacunar infarction (LACI) and boundary zone infarction (BZI); primary intracerebral haemorrhage (PICH); subarachnoid haemorrhage (SAH); and stroke of undetermined cause., Results: Over the 18-month study period 536 stroke events were registered, of which 86% (95% confidence interval, 83%-89%) had a defined "pathological" diagnosis on the basis of computed tomographic scanning, magnetic resonance imaging or necropsy. Cerebral infarction accounted for 71% of cases (95% CI, 68%-75%), PICH 11% (95% CI, 9%-14%) and SAH 4% (95% CI, 2%-5%). The 382 cases of cerebral infarction included LAOI (in approximately 71%), EMBI (15%), LACI (10%) and BZI (5%). While the incidence of all subtypes of stroke increased with age, there were age and sex differences in their proportional frequency, management and prognosis: patients with PICH, SAH and EMBI were more likely to be admitted to hospital, and these conditions carried the highest early case fatality. Over all, the 28-day case fatality was 24% (95% CI, 20%-28%), but varied from 0 for LACI and BZI, to 37% (95% CI, 15%-59%) for SAH and 35% (CI, 23%-47%) for PICH., Conclusions: In this study, we found considerable differences in incidence rates, the effect of age and sex on incidence rates, and prognosis for the different subtypes of stroke. Hospital-based studies are likely to be selectively biased by emphasising strokes that are severe and require admission to hospital. These data have important implications in the design and evaluation of clinical trials of therapy for stroke.

A ninth-grade alcohol education program aimed at reducing drinking, drinking and driving, and riding with a drinking driver was developed on the basis of problem behavior theory, social cognitive theory and role theory. In Year 1 the program was taught by Social Studies teachers to half of the eighty-four ninth-grade classes in all nine junior high schools in a single school system; the other half served as controls. In Year 2 the program was taught to the ninth-grade students of the same school system by English teachers. Students' knowledge, skills and practices were measured before and four-six weeks and one year after the program. Results indicated significant increases in knowledge and perceived ability to resist pressures to drink among experimental students. No significant differences were noted for the drinking or the drinking and driving practices of either group. One year after the program, significantly fewer students in the experimental classes reported riding with a driver who had been drinking. Results suggested that English teachers were more effective than Social Studies teachers in teaching this program.

Survival is the most fundamental measure of the outcome from stroke, the magnitude of the burden being strongly reflected in case-fatality and survival rates. Although the literature is rich with follow-up studies examining survival after stroke, most are based on selected series of patients and factors which correlated with time to death have usually been determined in univariate analyses. We examined the factors associated with a high risk of death during the acute phase of stroke. Analyses were based on data from a population based study of acute cerebrovascular disease undertaken in Perth, Western Australia, during an 18 month period 1989-1990. Using logistic regression modelling techniques only 2 factors, severe loss of consciousness, odds ratio 14.7 [95% confidence limits (CL), 4.0-53.6], and severe paresis, odds ratio 7.2 [95% CL, 1.6-32.0], independently predicted death by 28 days after the onset of stroke. The implication is that 2 simple measures, level of consciousness and motor power, may help direct management. Furthermore, age is not an independent risk factor for death early after stroke. Therefore the elderly should not be denied therapy purely on the basis of their age.

The mutagenic potential of two soils amended with a municipal sewage sludge at two application rates was monitored over a 2-year period using Salmonella/microsome mutagenicity assay. Samples were collected from undisturbed monolith lysimeters of Weswood sandy clay (Fluventic Ustochrept) and Padina sandy loam (Grossarenic Paleustalf) amended with dried sewage sludge at 50 and 100 Mg/ha. Soil samples were collected and sequentially extracted with methylene chloride and methanol. The residues from these extracts were tested for mutagenicity at five doses with and without metabolic activation in Salmonella strain TA98. In general, the mutagenic potential of the amended soils of both application rates for the first 8 weeks following sludge application increased and then slowly decreased. The maximum mutagenic response observed in the soil extracts was 222 revertants at a dose of 10 mg of residue. This response was induced by the methanol extract from the Weswood soil collected 56 days after the application of 50 Mg/ha sewage sludge as compared to the 100 Mg/ha application which induced 202 revertants/mg. The mutagenicity of all fractions extracted from the sludge-amended soil at both application rates collected 717 days after application were not appreciably different from extracts from the unamended soils. The data indicate that chemicals that were mutagenic in bacteria persist in the soil and that at the higher application rates, as much as 2 years may be required for the mutagenic potential of the soil to return to background levels.

Binding assays with secretory component (SC) were used to detect polymeric IgA antibody to E. coli lipopolysaccharide and to estimate total polymeric IgA in sera from 14 patients with alcoholic liver disease and eight normal controls. Radioiodinated human SC was shown to bind to polymeric IgA and IgM but not to monomeric IgA, secretory IgA or IgG. Serum aliquots (0.5 ml) were totally depleted of IgM using 2 ml anti-IgM affinity columns and the effluent sera were titrated in microtitre plates coated with lipopolysaccharide, the binding of polymeric IgA being detected by adding 10 ng radiolabelled SC. Total polymeric IgA was measured via its capacity to inhibit the binding of 5 ng labelled SC to IgM coated wells, quantitation being achieved by comparison with the inhibition produced by purified polymeric IgA. Total lipopolysaccharide-specific IgA antibody was detected by ELISA in sera from both patients and controls, 1185 +/- 793 and 56 +/- 19 U/100 microliters (mean +/- SD), respectively; but polymeric IgA antibody was detected only in patients' sera (131 +/- 214 U/100 microliters). The concentration of total polymeric IgA was higher in patients' sera than in control sera (488 +/- 333 and less than 120 micrograms/ml respectively).

Hypercalcemia is a common cause of morbidity in cancer patients. The mechanism of malignancy-associated hypercalcemia includes increased bone resorption and decreased renal calcium clearance which also occur in primary hyperparathyroidism. Norethisterone can inhibit bone resorption and has recently been shown to be effective treatment for mild hyperparathyroidism in post menopausal women. We report the successful use for the first time of norethisterone (5 mg daily) in a case of malignancy-associated hypercalcemia after other standard agents failed.

The clinical and pathological associations of hepatic granulomas in patients who presented to the Royal Adelaide Hospital between January 1, 1968 and February 29, 1984 were reviewed retrospectively. Cases of primary biliary cirrhosis were excluded. Of 59 patients with hepatic granulomas, clear associations with diseases were identified in 42 (71%) patients. These were sarcoidosis (seven cases), chronic liver disease (12 cases), biliary tract disease (three cases), tuberculosis (four cases), Q-fever (three cases), other infections (four cases), drug hypersensitivity (four cases) and neoplasms (five cases). Ten patients had multiple associations and five other patients presented without any clearly defined cause for granulomas. Three of these latter patients presented with an acute febrile illness, showed hepatomegaly and had abnormal results of liver function tests. These cases may represent the entity that is labeled "idiopathic granulomatous hepatitis". Two other patients abused alcohol. Granulomas were categorized morphologically as microgranulomas, macrogranulomas and lipogranulomas according to their size, organization and the presence of fat droplets. Microgranulomas were associated with diseases of short duration and less architectural disturbance of the liver parenchyma. The presence of granulomas did not confer any prognostic implication over and above that of the associated disease.