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R McGinnis

Publications and source records attributed to R McGinnis.

9 recordsLinked to original sources

Further support for the association of CCR5 allelic variants with asthma susceptibility.

English and German nuclear families containing multiple asthmatic children and asthmatic parents were analysed to retest a recently reported association between resistance to asthma and the delta32 allele of chemokine receptor 5 (CCR5). Analysis of the families by the transmission-disequilibrium test (TDT) revealed a non-significant trend in the English families that provided marginal confirmation of the association (P < 0.125), but no similar trend was observed in the German families. Case-control comparison of delta32 allele and genotype frequencies in asthmatic vs. non-asthmatic parents revealed a significantly lower frequency of delta32 in asthmatic English parents (P < 0.009) and a similar but non-significant trend in German parents (P < 0.265). Taken together, the pattern of results provides confirmation for the previously observed delta32-asthma association and indicates that susceptibility to asthma may be influenced by CCR5 or another gene in chromosomal region 3p21.

Alleles↗

General equations for Pt, Ps, and the power of the TDT and the affected-sib-pair test.

Several equations are highlighted here, whose algebraic symmetries and generality make them very useful for understanding and comparing the properties of the transmission disequilibrium test (TDT) and affected sib-pair test. Methods using the equations are also presented that yield precise estimates of sample sizes needed for genome scans or for testing a single candidate gene, and these power methods are shown to compare favorably with alternative approaches recently described by Knapp (1999) and by Tu and Whittemore (1999). Simple relationships are also noted that summarize the relative sample sizes required for equivalent power to detect association by the TDT or case-control designs. As single-nucleotide polymorphism (SNP) maps revolutionize the search for disease-causing genes, the equations should prove useful for planning and evaluating studies of linkage and association across a broad range of possible disease models and relationships between markers and linked disease loci.

Alleles↗

What price quality? Assuring the quality of case-managed in-home care.

Case managed community-based long-term care has now become an established component of the service delivery system in the United States. As case management has developed, it has gone through an evolutionary process. In the initial phase of case management, considerable attention was placed on gaining access to resources by the case manager. This article addresses issues of assuring the quality of case-managed care. It focuses on the current concerns and potential problems associated with evaluating the effectiveness of services arranged by case managers, and describes a model, developed in Ohio, to ensure the quality of care. In addition, it discusses the continued challenges for and costs of quality assurance and notes the difficulty of obtaining empirical data in the effort to assure quality.

Cost Control↗

Genetically obese (ob/ob) mice are hypersensitive to glucocorticoid stimulation of feeding but dramatically resist glucocorticoid-induced weight loss.

The genetically obese (ob/ob) mouse is hyperphagic and hypercorticosteronemic; both hyperphagia and excessive weight gain are ameliorated by adrenalectomy. We report here that corticosterone or dexamethasone stimulate feeding in obese mice at one-fifth the dose needed to increase feeding in lean littermates. Metabolic weight loss, a measure of carbon dioxide and water lost due to respiration, is stimulated by glucocorticoids. Yet we find that obese mice are only one-seventh as sensitive as lean mice to the enhancement of metabolic weight loss following corticosterone. Therefore, hypersensitivity to glucocorticoid-induced feeding and hyposensitivity to glucocorticoid-stimulated weight loss may act in tandem to produce the ob/ob's exaggerated weight gain.

Animals↗