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Identifying life periods during which social conditions have the highest impact on risk of common cancers in a population may help to reveal their underlying shared social mechanisms. We used the life course framework to estimate the extent to which life course SEP is associated with risk of nine cancers. In addition, we tested whether these associations conform to a critical period or cumulative life course model. Data were from a population-based case–control study of occupational exposures and cancer conducted in Montreal, Canada. Participants were males aged 35–70 years (n = 2,547) residing in the Montreal metropolitan area with primary, histologically confirmed cancers diagnosed between 1979 and 1985. Population controls (n = 512) were sampled from electoral lists. SEP was measured at three different periods of life based on respondent's report: during childhood, young adulthood and mid-life. We used a structured modeling approach using a series of unconditional logistic regressions to test which models best fit the data. Life course SEP increased the risk of all cancers. SEP in childhood was identified as a critical period for prostate and all gastrointestinal tract cancers except for esophagus cancer. In addition, the accumulation model best explained the data for melanoma and lung squamous cell carcinoma. Our findings suggest that childhood social circumstances are a common risk factor for several cancers among men; our results provide insights into the mechanisms involved in the etiology of nine cancers.  相似文献   
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INTRODUCTION: Dystrophic epidermolysis bullosa is a hereditary heterogeneous blistering disease. Clinical examination and additional tests are not always sufficient to identify the subtype or mode of transmission. We describe a case of de novo dominant inherited dystrophic epidermolysis bullosa localised strictly to the knees. CASE REPORT: A 3-year-old boy presented symmetrical lesions on the anterior aspect of the knees since starting to walk. No nail, dental or mucous dystrophy was observed and the parents presented no clinical abnormalities. Optical microscopy, electron microscopy and immunofluorescence analysis suggested dystrophic epidermolysis bullosa. The genealogical tree allowed no distinction between the dominant de novo and mitis recessive forms. Genetic analysis identified a missense G 1776W mutation at exon 61 of gene COL 7A1 in the child's DNA but not the parents'. DISCUSSION: Dystrophic epidermolysis bullosa may present in generalized or localized forms and the disease may be inherited in either autosomal dominant or recessive mode. Genetic analysis shows mutations in COL 7A1. While the clinical features often allow different types to be distinguished when the parents do not have the disease (with the recessive forms being more severe), genetic analysis is essential to confirm the mode of inheritance. In the dominant forms, and more recently in recessive cases, glycine substitutions have been implicated, although the precise role of glycine substitution has yet to be clarified. Localised involvement of the skin alone, as seen in our case report, is very rare. CONCLUSION: Genetic analysis is important for genetic counselling and determination of risk of recurrence.  相似文献   
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In order to investigate a putative weight loss in patients with Parkinson's disease, an anthropometric and biochemical study was undertaken. We compared body weight and indexes of fat [body mass index (BMI), tricipital skinfold] and lean [midarm muscle area (MMA), calf circumference] mass in men and women suffering from idiopathic Parkinson's disease with normal controls. We found that women suffering from Parkinson's disease exhibited a significant weight loss (–8.5%) and decreased calf circumference when compared with controls. A decrease (–4.3%) in total body weight was also found in men with Parkinson's disease but the difference did not reach the level of significance. Protein biochemical markers of nutritional status (albumin, prealbumin, retinol binding protein, transferrin) were normal in Parkinson's disease patients. The present study demonstrates the occurrence of weight loss in a large population of patients with Parkinson's disease. The putative mechanisms involved in the weight loss are discussed.  相似文献   
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