Multidisciplinary teams: common goals and communication.
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Biomedical subjects
Publications and source records attributed to M B Davis.
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Detailed chromosome studies on early-passage skin fibroblast cultures from 17 patients with familial polyposis coli (FPC) showed an increase in all classes of chromosome aberrations compared with controls. The most striking difference was in the number of cytogenetically abnormal clones, some of which reached 80-100% in early cultures, suggesting either presence in vivo or considerable proliferative advantage. The occasional occurrence of very high levels of tetraploidy in these cultures was thought to be a manifestation of clone formation. The same type of chromosome instability was found to extend to colon fibroblasts and lymphocytes but without evidence of clone formation, apart from high tetraploidy in the former. Chromosomes in colon epithelial-like cultures were remarkably stable initially, despite the time span of several months required to establish them. However, from the outset one of these cultures was composed of three abnormal clones. After approximately 18 months in culture, stable and unstable chromosome rearrangements clearly increased in all tested cultures, although the cells were not senescent, suggesting a possible shift toward malignancy.
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Human infection with the dog heartworm (Dirofilaria immitis) may lead to focal pulmonary infarction with granuloma formation. The resulting roentgenographic coin lesion may require a diagnostic thoracotomy in consideration of malignancy. Because of sometimes enigmatic histopathological characteristics, this process may not be receiving the recognition it deserves. Furthermore, the dramatic increase of primary (canine) host infections in the United States presages an increase of secondary (human) host infections. Many thoracotomies will be performed for this innocuous process unless the dirofilarial agent can be controlled or the human pulmonary lesion can be reliably identified without operation.
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The objective of this study was to compare the cost and effectiveness of nafarelin versus leuprolide in the treatment of endometriosis. To compare the economic impact of treating endometriosis with leuprolide or nafarelin and to facilitate cost comparisons between the two, we statistically analyzed information concerning the costs of medications for the treatment of endometriosis, outpatient services, and management of adverse effects, as well as other related costs. A national claims database, MarketScan, was used to obtain data on patients with a principal diagnosis of endometriosis who were treated with either leuprolide or nafarelin. During the calendar years 1992-1994, 114 patients with endometriosis had claims for nafarelin, and 343 had claims for leuprolide. There were no significant differences between nafarelin and leuprolide recipients with respect to demographic variables, types of concomitant drug used, types of outpatient service received, or major outpatient diagnostic categorization. In 1994 dollars, the cost of using leuprolide was $326.7 greater than that of using nafarelin. The results of this study suggest that nafarelin is a less expensive alternative to leuprolide for the treatment of endometriosis.
In childhood malignancies such as retinoblastoma and Wilms tumour, of which both familial and sporadic forms exist, recessive mutations of presumed differentiation genes have been implicated in tumorigenesis. A proportion of cases appear with microscopically visible chromosome deletions which indicate the regions where the genes concerned are located. Mutation or loss of one allele causes a cancer predisposition. For tumour development functional loss of the remaining normal allele is also required. In cancers with both familial and sporadic forms, molecular-genetic studies have shown that deletion is often one of the mutational events. Although familial and sporadic forms have never been distinguished in lung cancer, deletions of the short arm of chromosome 3 have been described for small cell lung cancer (SCLC), but their general occurrence in SCLC has been disputed. Using a molecular-genetic approach, we here present evidence for a consistent deletion at the chromosomal region 3p21, not only in SCLC, but in all major types of lung cancer.