[Pathological sigificance of hypochromic anemia].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to J Rouleau.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
PURPOSE: To examine the pattern of testicular cancer incidence by age, time period and birth cohort since 1969 in Canada. METHODS: In addition to analyses of the secular trends by age group and birth cohort separately, an age-period-cohort model and the submodels with standard Poisson assumptions were fitted to the data. RESULTS: The overall age-adjusted incidence of testicular cancer increased in Canada, from 2.8 per 100,000 males in 1969-71 to 4.2 in 1991-93. The younger age groups showed much higher absolute incidence rates in the recent period compared with those in the early period. Age-period-cohort modelling of data restricted to males aged 20-84 years suggested that the observed increase in testicular cancer could be largely attributed to a birth cohort effect. A steady increase in risk was observed among men born since 1945; those born between 1959 and 1968 were 2.0 (95% CI, 1.5-2.6) times as likely to develop testicular cancer as those born between 1904 and 1913. CONCLUSION: The risk of testicular cancer has increased over time and changing exposure to environmental factors early in life may be responsible for this.
To assess the quality and appropriateness of Canadian Congenital Anomalies Surveillance System (CCASS), a system based on routine hospital admission/separation records, we compared the congenital anomalies ascertained by CCASS for the period of January 1, 1990 to December 31, 1993 in the province of Alberta with corresponding figures obtained from Alberta Congenital Anomalies Surveillance System (ACASS), a specific-purpose surveillance program collecting information on congenital anomalies from multiple sources with mechanisms to evaluate diagnosis. Rates of congenital anomalies estimated by CCASS tended to be higher. Agreement between CCASS and ACASS depended on diagnosis: for the International Clearinghouse for Birth Defects Monitoring System standard categories of congenital anomalies (except for anomalies of abdominal wall), agreement usually exceeded 50%; for less clear-cut diagnoses, it was well below 50%. We conclude that routine medical records can be used for surveillance purposes for major congenital anomalies with clear-cut diagnosis.
The intrinsic metabolic capacity of the liver at end-stage heart failure in the pacing overdrive dog model of congestive heart failure was evaluated ex vivo. Congestive heart failure was induced in seven adult mongrel dogs (20-30 kg) by cardiac electrical pacing at a frequency of 240 stimuli/min until the development of overt heart failure; seven other dogs served as controls. The animals were then anesthetized and the right ventricular papillary muscles and samples from the left lateral hepatic lobes were collected. The degree of myocardial dysfunction as well as the total amount and the activities of cytochromes P-450 were evaluated. Tension, maximum rate of tension rise, and Vmax were significantly lower (40-60%) in the paced than in the control dogs, indicating a marked myocardial dysfunction. Moreover, significant decreases in total cytochrome P-450 (0.31 +/- 0.04 vs. 0.53 +/- 0.03 nmol/mg of microsomal protein, p less than 0.01) and in the intensity of four different electrophoretic protein bands (molecular masses of 46, 48, 50, and 59 kDa) occurred in the dogs with congestive heart failure. The decrease in total cytochrome P-450 was accompanied by a significant reduction in aminopyrine N-demethylase activity (1.74 +/- 0.25 vs. 2.91 +/- 0.40 nmol/min/mg of microsomal protein, p less than 0.05). Immunoblot analysis using antibodies to two different dog liver phenobarbital-inducible cytochromes P-450 demonstrated that PBD-1 (a P-450IIIA) was not affected by congestive heart failure, whereas PBD-2 (a P-450IIB) was markedly decreased.(ABSTRACT TRUNCATED AT 250 WORDS)
The aim of this study was to develop a model for predicting clinically significant deterioration in the left ventricular ejection fraction due to chronic doxorubicin administration. Twenty-six patients were monitored during their courses of doxorubicin chemotherapy with serial gated equilibrium radionuclide angiography. Multiple linear regression analysis was used to derived the best combination of clinical and radionuclide angiographic predictors of resting left ventricular ejection fraction at any point during the course of chemotherapy. The final model consisted of five variables: left ventricular ejection fraction at the previous monitoring point; cumulative dose of doxorubicin achieved at the previous monitoring point; increment in dose from the previous monitoring point; age of the patient; and time to peak left ventricular emptying at the previous monitoring point. The cumulative dose, the ejection fraction at the previous monitoring point and the final model, respectively, explained 11%, 33% and 53% of the variability in ejection fraction determinations during the 26 patient courses. The final model also forecast a potentially very low resting left ventricular ejection fraction (less than 35%) at the cumulative doses of doxorubicin which provoked serious clinical cardiotoxicity in two patients. A multivariate model is a useful aid in timing discontinuation of doxorubicin prior to the development of a clinically significant deterioration in left ventricular ejection fraction.
The Canadian Congenital Anomalies Surveillance System monitors birth defects reported for stillborns, newborns and infants during the first year of life. Data are available through the 1980s and early 1990s for Ontario, Manitoba and Alberta, and since 1984 for an additional four provinces. Fifty-seven routine monitoring categories and 15 summary categories were examined for temporal trends. Comparing the period 1979-1981 with 1991-1993, the reported birth defect case birth prevalence increased by 0.2% and the total birth defects birth prevalences by 2.5%. The birth prevalence of central nervous system defects decreased by 8.2%; the reported birth prevalence increased for congenital heart defects by 41%, urinary defects by 127%, Down syndrome by 13% and other chromosomal defects by 47%. Further investigation of individual defects would be required to evaluate the degree to which changes in reported birth prevalence reflect changes including the availability and use of specific diagnostic procedures. The work highlights the need to expand the surveillance system to include all affected pregnancies where an anomaly has been detected antenatally.