PubMed · 8280260
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J Walston, T Finucane. 1993-10-21. Abdominal aortic aneurysm.. https://pubmed.ncbi.nlm.nih.gov/8280260/
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PURPOSE: To test the effectiveness of our Canadian retinopathy of prematurity (ROP) screening guidelines as applied to high-risk premature infants. STUDY DESIGN: Retrospective longitudinal cohort study. SUBJECTS: A total of 969 infants were examined longitudinally between 1991 and 2000 and 46 of these infants screened were treated for severe ROP. METHODS: Data from weekly ROP screening examination results were collected from a geographical area and analysed. RESULTS: The average incidence of severe ROP requiring treatment in the population of premature infants eligible for screening was 48.3 per 1000. In all, 46 infants were treated in this cohort. The mean gestational age (GA) was 25.5 weeks of age and the mean birth weight was 750 g. The mean chronological age (CA) and postmenstrual age (PMA) at the time of first screening was 36 days and 30.7 weeks, respectively. The first identification of any ROP in this group was at a mean CA 60 days and PMA of 34.1 weeks. The mean CA and PMA of the first observation of stage 3 were 74 days and 36.3 weeks. The mean CA and PMA at the time of treatment were 86 days and 37.7 week. CONCLUSIONS: Our observations and analysis indicate the following ROP screening recommendations: infants of 28 weeks of GA or less, infants with a GA between 28 weeks and 30 weeks should have a single 'spot examination' at approximately 37 weeks of PMA (or prior to discharge from hospital) to include possible outliers; infants born with a birth weight of 1250 g or less; initial screening examination should be at 31 weeks of PMA or 4 weeks of CA, whichever is later; in the presence of any active ROP, the infant should be followed every 1-2 weeks; and stage 3 should be followed at least every 7 days.
PURPOSE: The aim of this study was to evaluate routine ophthalmic data to identify clinically useful risk factors for progressive visual field loss in patients with primary open-angle glaucoma (POAG) already receiving intraocular pressure-lowering treatments. METHODS: A retrospective cohort study design was used. Routine ophthalmic data for all subjects were obtained from case records with the knowledge that baseline clinical data had been collected in a standardised manner. Progression was defined according to the AGIS visual field defect scoring system. Variables evaluated as candidate risk factors for progression were assessed by survival analysis. Factors exerting a significant effect on survival were subsequently tested in a Cox proportional hazards model. RESULTS: A cohort of 108 eligible POAG patients was followed over an average of 3.6 years, with an average visual field intertest interval of 8 months. The incidence rate of progressive loss among the cohort was 5.4 cases per 100 person years. Increasing age was found to be independently associated with a small but significantly increased risk of glaucomatous visual field defect progression (hazard ratio 1.07, P=0.022), and a borderline association was also demonstrated with being male (hazard ratio 2.76, P=0.057). CONCLUSIONS: This retrospective investigation has provided preliminary information on factors associated with increased risk of progressive glaucomatous visual field loss that may inform clinical care strategies. Lack of concordance with other studies suggests that further prospective investigations are needed if risk stratification strategies are to be employed in caring for patients with chronic open-angle glaucoma.
O6-methylguanine methyltransferase, Mgmt, constitutes the first line of defense against O6-alkylguanine, which can result in G : C to A : T transitions upon DNA replication. Mgmt has been found in organisms as diverse as archaebacteria and mammals. This evolutionary conservation suggests that all organisms may be exposed to either endogenous or environmental alkylating agents. We thus hypothesized that tissues of Mgmt-/- mice would exhibit elevated mutant frequencies. Employing the Big Blue trade mark transgenic system, we evaluated lacI mutants rescued from liver and small intestinal DNA of young Mgmt-/- mice. Interestingly, while there was a small difference between Mgmt-/- mice and controls with respect to lacI mutant frequency, no differences attributable to Mgmt deficiency were apparent in the mutational spectra. Although mutations stemming from O6-guanine alkylations would be predicted to be cumulative, we found no evidence of an Mgmt-dependent alteration in mutation spectrum in DNA samples from 12 month-old mice. To optimize our ability to detect mutations resulting from O6-alkylguanine-induced G : T mismatches, mice with combined deficiencies of Mgmt and the DNA mismatch repair molecule, Msh6, were analysed. In spite of this strategy, we observed no significant differences between Mgmt-/- Msh6-/- and Msh6-/- mouse lacI mutations, except for a trend towards a greater percentage (of total transitions) of G : C to A : T changes in Mgmt-/-Msh6-/- livers. Therefore, despite the striking evolutionary conservation of Mgmt, deficiency of this gene did not significantly impact the spontaneous lacI mutational spectrum in vivo.