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The article discusses the research that investigates the association with creatine kinase muscle (CKM) and leukocyte immunoglobulin-like receptor subfamily B member 5 (LILRB5) gene with serum levels of creatine kinase. It states that the research was conducted on patients recruited in Quebec, Canada. It mentions the underlying genetic determinants of CK variation in statin users.

The Génome Québec and Montreal Heart Institute Pharmacogenomics Centre (Montreal, Canada), created in 2006, is a translational pharmacogenomics platform whose main objectives are to conduct pharmacogenomics research, provide pharmacogenomics services to the academic, biotechnology and pharmaceutical sectors, and integrate pharmacogenomics solutions into the healthcare system. The Centre has brought together a multidisciplinary team of researchers with expertise in genomics, bioinformatics and clinical trial research. All the Centre's clinical research studies are supported by the Centre's unique Good Laboratory Practice facility framework, which has the ability to perform pharmaceutical clinical trials and deliver clinical diagnostics under the highest standards. The Centre has successfully leveraged its experience and expertise in technology development and pharmacogenomics clinical trial work to attract funding and collaborative partnerships in both the public and private sectors. [ABSTRACT FROM AUTHOR]

HED is an autosomal dominant skin disorder that is particularly common in the French Canadian population of south-west Quebec. We previously mapped the HED gene to the pericentromeric region of chromosome 13q using linkage analysis in eight French Canadian families. In this study, we extend our genetic analysis to include a multiethnic group of 29 families with 10 polymorphic markers spanning 5.1 cM in the candidate region. Two-point linkage analysis strongly suggests absence of genetic heterogeneity in HED in four families of French, Spanish, African and Malaysian origins. Multipoint linkage analysis in all 29 families generated a peak lod score of 53.5 at D13S1835 with a 1 lod unit support interval spanning 1.8 cM. Recombination mapping placed the HED gene in a 2.4 cM region flanked by D13S1828 proximally and D13S1830 distally. We next show evidence for a strong founder effect in families of French Canadian origin thereby representing the first example of a founder disease in the south-west part of the province of Quebec. Significant association was found between HED in these families and all markers analysed (Fisher's exact test, P < 0.001). Complete allelic association was detected at D13S1828, D13S1827, D13S1835, D13S141 and D13S175 (P[sub excess] = 1) spanning 1.3 cM. A major hapIotype including all 10 associated alleles was present on 65% of affected chromosomes. This haplotype most likely represents the founder hapIotype that introduced the HED mutation into the French Canadian population. Luria-Delbrück equations and multipoint likelihood linkage disequilibrium analysis positioned the gene at the D13S1828 locus (likely range estimate: 1.75 cM) and 0.58 cM telomeric to this marker (support interval: 3.27 cM) respectively. [ABSTRACT FROM AUTHOR]