[Subjects and disciplines: redoubts restraining renovation in medical teaching].
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Biomedical subjects
Publications and source records attributed to C Pera.
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The role of diet in carcinogenesis has received much attention in recent years. The incidence of oesophageal cancer varies widely in different geographical regions and oesophageal cancer shows one of the greatest correlations between the diet type and eventual malignant development. Oesophageal carcinogenesis involves the combined action of predispositional, initiatory, and promotional factors. Specific dietary deficiencies (vitamins and minerals) may create a sensitized "environment" for the combined activities of initiatory and promotional factors. Other predispositional factors include physical abrasion (irritant vegetal components, thermal injury) and chemical injuries (alcohol, tobacco). Initiatory factors such as nitrosamines or their precursors in the diet are also considered.
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We used polymerase chain reaction amplification and hybridization with specific oligonucleotides to analyze the distribution of DPB1, DQA1, DQB1, and DRB1 allelic variants in 48 patients with rheumatoid arthritis (RA) and compared our results with those from 109 randomly chosen, healthy control subjects. Our work confirms a previously reported increase in DR4 specificity in RA: in particular, we found a statistically significant positive association of the DRB1*0401 and DRB1*0404 alleles with RA. When we compared the DR4 groups, however, none of the DRB1*04 alleles were increased in the RA group. Molecular analysis of the other DRB1 polymorphic variants disclosed the trend of a positive association of DRB1*0101 (DR1) in DR4 negative patients vs DR4 negative healthy control subjects, and an increase in DRw6 (DRB1*13,*14) in the DR4 and/or DR1 negative patient group. Moreover, analysis of the association between RA and a heptapeptide motif (positions 67-74) in the third hypervariable region confirmed that this epitope confers enhanced risk for the development of RA with respect to the allele DRB1*0404 (etiologic fraction = 0.53 vs 0.12). We also observed a statistically significant increase in DQA1*0301 and DQB1*0302 accompanied by a significant decrease in DQA1*0202, DQA1*0501 and DQB1*0201 in RA patients. Analysis of DPB1 alleles disclosed no significant differences between RA patients and healthy control subjects.