tailieunhanh - báo cáo khoa học: " Genetic discovery: the prescription for chronic pain"

Tuyển tập báo cáo các nghiên cứu khoa học quốc tế ngành y học dành cho các bạn tham khảo đề tài: Genetic discovery: the prescription for chronic pain | Zheng and Peltz Genome Medicine 2010 2 82 http content 2 11 82 w Genome Medicine MINIREVIEW L__ Genetic discovery the prescription for chronic pain Ming Zheng and Gary Peltz Abstract A recent publication that combined rat gene expression data and a human genetic association study has identified the first genetic risk factor for chronic pain in humans. In four of the five cohorts studied there was a significant association of an allele within a gene KCNS1 encoding a potassium channel with an increased risk for chronic pain. Identification of genetic risk factors for chronic pain could catalyze new advances in this difficult clinical area that has become a major public health problem. Genomic-medicinebased advances for chronic pain could include the development of a mechanism-based classification system for chronic pain new treatment options improved methods for treatment selection and targeted prevention strategies for high-risk individuals. There is tremendous inter-individual variation in the response to painful stimuli. A level of pain that completely incapacitates one individual may cause only a minor annoyance in another. Characterizing the genetic factors affecting susceptibility to chronic pain could lead to novel treatment or prevention strategies which are desperately needed. A recent paper by Costigan et al. 1 presents a bold step toward understanding these differences. The authors performed a multi-dimensional analysis using rat gene expression and human genetic association that identified a new genetic factor affecting susceptibility to chronic pain. This study 1 was initiated by analysis of gene expression changes within rat dorsal root ganglia obtained after nerve damage was induced in three different models of chronic pain. The mRNA for a potassium channel alpha subunit Kcnsi was constitutively expressed in sensory neurons but was downregulated after three types of nerve injury in these models. Correspondence .

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