At least 175 food plants and 52 beverage plants were gathered by Native Peoples in eastern Canada. Iroquoian agriculturalists of southern Ontario cultivated corn, beans, squash, tobacco, and sunflowers, and gathered the greatest variety of food plants. Southern and eastern Algonkian hunters and gatherers ate a wide variety of wild plant foods including fleshy fruits, nuts, greens, and underground parts. Little is known about the use of wild food plants by northern Cree and Naskapi.Nutritional data for gathered plants indicate that many of these species exceed conventional plant sources for vitamins and minerals. Vitamin A, vitamin C, calcium, iron, and fibre are particularly well represented in certain gathered plants. Some wild plant foods require special preparation or must be consumed in limited quantities because they contain toxic secondary metabolites.Over 400 plants are used in native medicine. Native medicine consists of rational and ritualistic components. Treatment of physical disorders, whose origin could be determined, was effective. At least 105 medicinal plants have a real effectiveness based on phytochemical constituents. Conifers were the most widely used group of plants in this category. Antibiotic monoterpenes, polyacetylenes and alkaloids, astringent tannins, and analgesic monoterpenes and salicylates are among the most rationally and widely used plant constituents.There is need for more research into nutritional constituents and pharmacological properties to assess the value and potential of plants used by Native People of eastern Canada.

Gene expression profiles were examined in freshly isolated peripheral blood mononuclear cells (PBMC) from two independent cohorts (training and test sets) of glucocorticoid (GC)-sensitive (n ‫؍‬ 64) and GC-resistant (n ‫؍‬ 42) asthma patients in search of genes that accurately predict responders and nonresponders to inhaled corticosteroids. A total of 11,812 genes were examined with high-density oligonucleotide microarrays in both resting PBMC (106 patients) and cells treated in vitro with IL-1␤ and TNF-␣ combined (88 patients), with or without GC. A total of 5,011 genes were expressed at significant levels in the PBMC, and 1,334 of those were notably up-regulated or down-regulated by IL-1␤͞TNF-␣ treatment. The expression changes of 923 genes were significantly reversed in GC responders in the presence of GC. The expression pattern of 15 of these 923 genes that most accurately separated GC responders (n ‫؍‬ 26) from the nonresponders (n ‫؍‬ 18) in the training set, based on the weighted voting algorithm, predicted the independent test set of equal size with 84% accuracy. The expression accuracy of these genes was confirmed by real-time-quantitative PCR, wherein 11 of the 15 genes predicted GC sensitivity at baseline with 84% accuracy, with one gene predicting at 81% in an independent cohort of 79 patients. We conclude that we have uncovered gene expression profiles in PBMC that predict clinical response to inhaled GC therapy with meaningful accuracy. Upon validation in an independent study, these results support the development of a diagnostic test to guide GC therapy in asthma patients.

Asthma is a complex genetic disorder with a heterogeneous phenotype, largely attributed to the interactions among many genes and between these genes and the environment. Numerous loci and candidate genes have been reported to show linkage and association to asthma and atopy. Although some studies reporting these observations are compelling, no gene has been mapped that confers a sufficiently high risk of asthma to meet the stringent criteria for genomewide significance. Using 175 extended Icelandic families that included 596 patients with asthma, we performed a genomewide scan with 976 microsatellite markers. The families were identified by cross-matching a list of patients with asthma from the Department of Allergy/Pulmonary Medicine of the National University Hospital of Iceland with a genealogy database of the entire Icelandic nation. We detected linkage of asthma to chromosome 14q24, with an allele-sharing LOD score of 2.66. After we increased the marker density within the locus to an average of one microsatellite every 0.2 cM, the LOD score rose to 4.00. We designate this locus "asthma locus one" (AS1). Taken together, these results provide evidence of a novel susceptibility gene for asthma on chromosome 14q24.

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Numerous asthma and atopy loci have been reported in studies demonstrating associations of the asthma-related phenotypes atopy, elevated IgE levels, and bronchial hyperresponsiveness with alleles of microsatellite markers and single-nucleotide polymorphisms (SNPs) within specific cytokine/chemokine and IgE-regulating genes. Although the studies reporting these observations are compelling, most of them lack statistical power. We assessed the nature, pattern, and frequency of SNPs in 24 candidate genes in Iceland and looked for associations with asthma and atopy. We identified 42 SNPs with an average minor allele frequency of 20.3% (asthma) and 20.7% (control). Twenty SNPs (48%) were within coding sequences and 90% of those led to a predicted change in protein sequence. No differences were detected in the allelic frequencies of SNPs in any of these candidate genes between control subjects and the patients with atopic asthma. Moreover, linkage analysis that included 269 patients with atopic asthma uncovered no evidence of linkage to markers associated with these genes. We conclude that this study has failed to produce evidence in support of the notion that variations within these 24 candidate atopy and asthma genes significantly influence the expression of the atopic asthmatic phenotype or contribute to the susceptibility of atopic asthma.