Bench-to-bedside review: Association of genetic variation with sepsis

Abstract Susceptibility and response to infectious disease is, in part, heritable. Initial attempts to identify the causal genetic polymorphisms have not been entirely successful because of the complexity of the genetic, epigenetic, and environmental factors that influence susceptibility and respons...
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Gespeichert in:

Autor*in:	Sutherland, Ainsley M [verfasserIn] Walley, Keith R

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2009

Schlagwörter:	Genetic Association Study Allelic Expression Predictive Genetic Test Candidate Gene Association Study PMP22 Gene

Anmerkung:	© BioMed Central Ltd 2009

Übergeordnetes Werk:	Enthalten in: Critical care - London : BioMed Central, 1997, 13(2009), 2 vom: 29. Apr.
Übergeordnetes Werk:	volume:13 ; year:2009 ; number:2 ; day:29 ; month:04

Links:	Volltext

DOI / URN:	10.1186/cc7702

Katalog-ID:	SPR029803128

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spelling	10.1186/cc7702 doi (DE-627)SPR029803128 (SPR)cc7702-e DE-627 ger DE-627 rakwb eng Sutherland, Ainsley M verfasserin aut Bench-to-bedside review: Association of genetic variation with sepsis 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2009 Abstract Susceptibility and response to infectious disease is, in part, heritable. Initial attempts to identify the causal genetic polymorphisms have not been entirely successful because of the complexity of the genetic, epigenetic, and environmental factors that influence susceptibility and response to infectious disease and because of flaws in study design. Potential associations between clinical outcome from sepsis and many inflammatory cytokine gene polymorphisms, innate immunity pathway gene polymorphisms, and coagulation cascade polymorphisms have been observed. Confirmation in large, well conducted, multicenter studies is required to confirm current findings and to make them clinically applicable. Unbiased investigation of all genes in the human genome is an emerging approach. New, economical, high-throughput technologies may make this possible. It is now feasible to genotype thousands of tag single nucleotide polymorphisms across the genome in thousands of patients, thus addressing the issues of small sample size and bias in selecting candidate polymorphisms and genes for genetic association studies. By performing genome-wide association studies, genome-wide scans of nonsynonymous single nucleotide polymorphisms, and testing for differential allelic expression and copy number polymorphisms, we may yet be able to tease out the complex influence of genetic variation on susceptibility and response to infectious disease. Genetic Association Study (dpeaa)DE-He213 Allelic Expression (dpeaa)DE-He213 Predictive Genetic Test (dpeaa)DE-He213 Candidate Gene Association Study (dpeaa)DE-He213 PMP22 Gene (dpeaa)DE-He213 Walley, Keith R aut Enthalten in Critical care London : BioMed Central, 1997 13(2009), 2 vom: 29. Apr. (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:13 year:2009 number:2 day:29 month:04 https://dx.doi.org/10.1186/cc7702 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2009 2 29 04
allfields_unstemmed	10.1186/cc7702 doi (DE-627)SPR029803128 (SPR)cc7702-e DE-627 ger DE-627 rakwb eng Sutherland, Ainsley M verfasserin aut Bench-to-bedside review: Association of genetic variation with sepsis 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2009 Abstract Susceptibility and response to infectious disease is, in part, heritable. Initial attempts to identify the causal genetic polymorphisms have not been entirely successful because of the complexity of the genetic, epigenetic, and environmental factors that influence susceptibility and response to infectious disease and because of flaws in study design. Potential associations between clinical outcome from sepsis and many inflammatory cytokine gene polymorphisms, innate immunity pathway gene polymorphisms, and coagulation cascade polymorphisms have been observed. Confirmation in large, well conducted, multicenter studies is required to confirm current findings and to make them clinically applicable. Unbiased investigation of all genes in the human genome is an emerging approach. New, economical, high-throughput technologies may make this possible. It is now feasible to genotype thousands of tag single nucleotide polymorphisms across the genome in thousands of patients, thus addressing the issues of small sample size and bias in selecting candidate polymorphisms and genes for genetic association studies. By performing genome-wide association studies, genome-wide scans of nonsynonymous single nucleotide polymorphisms, and testing for differential allelic expression and copy number polymorphisms, we may yet be able to tease out the complex influence of genetic variation on susceptibility and response to infectious disease. Genetic Association Study (dpeaa)DE-He213 Allelic Expression (dpeaa)DE-He213 Predictive Genetic Test (dpeaa)DE-He213 Candidate Gene Association Study (dpeaa)DE-He213 PMP22 Gene (dpeaa)DE-He213 Walley, Keith R aut Enthalten in Critical care London : BioMed Central, 1997 13(2009), 2 vom: 29. Apr. (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:13 year:2009 number:2 day:29 month:04 https://dx.doi.org/10.1186/cc7702 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2009 2 29 04
allfieldsGer	10.1186/cc7702 doi (DE-627)SPR029803128 (SPR)cc7702-e DE-627 ger DE-627 rakwb eng Sutherland, Ainsley M verfasserin aut Bench-to-bedside review: Association of genetic variation with sepsis 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2009 Abstract Susceptibility and response to infectious disease is, in part, heritable. Initial attempts to identify the causal genetic polymorphisms have not been entirely successful because of the complexity of the genetic, epigenetic, and environmental factors that influence susceptibility and response to infectious disease and because of flaws in study design. Potential associations between clinical outcome from sepsis and many inflammatory cytokine gene polymorphisms, innate immunity pathway gene polymorphisms, and coagulation cascade polymorphisms have been observed. Confirmation in large, well conducted, multicenter studies is required to confirm current findings and to make them clinically applicable. Unbiased investigation of all genes in the human genome is an emerging approach. New, economical, high-throughput technologies may make this possible. It is now feasible to genotype thousands of tag single nucleotide polymorphisms across the genome in thousands of patients, thus addressing the issues of small sample size and bias in selecting candidate polymorphisms and genes for genetic association studies. By performing genome-wide association studies, genome-wide scans of nonsynonymous single nucleotide polymorphisms, and testing for differential allelic expression and copy number polymorphisms, we may yet be able to tease out the complex influence of genetic variation on susceptibility and response to infectious disease. Genetic Association Study (dpeaa)DE-He213 Allelic Expression (dpeaa)DE-He213 Predictive Genetic Test (dpeaa)DE-He213 Candidate Gene Association Study (dpeaa)DE-He213 PMP22 Gene (dpeaa)DE-He213 Walley, Keith R aut Enthalten in Critical care London : BioMed Central, 1997 13(2009), 2 vom: 29. Apr. (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:13 year:2009 number:2 day:29 month:04 https://dx.doi.org/10.1186/cc7702 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2009 2 29 04
allfieldsSound	10.1186/cc7702 doi (DE-627)SPR029803128 (SPR)cc7702-e DE-627 ger DE-627 rakwb eng Sutherland, Ainsley M verfasserin aut Bench-to-bedside review: Association of genetic variation with sepsis 2009 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © BioMed Central Ltd 2009 Abstract Susceptibility and response to infectious disease is, in part, heritable. Initial attempts to identify the causal genetic polymorphisms have not been entirely successful because of the complexity of the genetic, epigenetic, and environmental factors that influence susceptibility and response to infectious disease and because of flaws in study design. Potential associations between clinical outcome from sepsis and many inflammatory cytokine gene polymorphisms, innate immunity pathway gene polymorphisms, and coagulation cascade polymorphisms have been observed. Confirmation in large, well conducted, multicenter studies is required to confirm current findings and to make them clinically applicable. Unbiased investigation of all genes in the human genome is an emerging approach. New, economical, high-throughput technologies may make this possible. It is now feasible to genotype thousands of tag single nucleotide polymorphisms across the genome in thousands of patients, thus addressing the issues of small sample size and bias in selecting candidate polymorphisms and genes for genetic association studies. By performing genome-wide association studies, genome-wide scans of nonsynonymous single nucleotide polymorphisms, and testing for differential allelic expression and copy number polymorphisms, we may yet be able to tease out the complex influence of genetic variation on susceptibility and response to infectious disease. Genetic Association Study (dpeaa)DE-He213 Allelic Expression (dpeaa)DE-He213 Predictive Genetic Test (dpeaa)DE-He213 Candidate Gene Association Study (dpeaa)DE-He213 PMP22 Gene (dpeaa)DE-He213 Walley, Keith R aut Enthalten in Critical care London : BioMed Central, 1997 13(2009), 2 vom: 29. Apr. (DE-627)331258269 (DE-600)2051256-9 1364-8535 nnns volume:13 year:2009 number:2 day:29 month:04 https://dx.doi.org/10.1186/cc7702 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 13 2009 2 29 04
language	English
source	Enthalten in Critical care 13(2009), 2 vom: 29. Apr. volume:13 year:2009 number:2 day:29 month:04
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author	Sutherland, Ainsley M
spellingShingle	Sutherland, Ainsley M misc Genetic Association Study misc Allelic Expression misc Predictive Genetic Test misc Candidate Gene Association Study misc PMP22 Gene Bench-to-bedside review: Association of genetic variation with sepsis
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topic_title	Bench-to-bedside review: Association of genetic variation with sepsis Genetic Association Study (dpeaa)DE-He213 Allelic Expression (dpeaa)DE-He213 Predictive Genetic Test (dpeaa)DE-He213 Candidate Gene Association Study (dpeaa)DE-He213 PMP22 Gene (dpeaa)DE-He213
topic	misc Genetic Association Study misc Allelic Expression misc Predictive Genetic Test misc Candidate Gene Association Study misc PMP22 Gene
topic_unstemmed	misc Genetic Association Study misc Allelic Expression misc Predictive Genetic Test misc Candidate Gene Association Study misc PMP22 Gene
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title	Bench-to-bedside review: Association of genetic variation with sepsis
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title_full	Bench-to-bedside review: Association of genetic variation with sepsis
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title_sort	bench-to-bedside review: association of genetic variation with sepsis
title_auth	Bench-to-bedside review: Association of genetic variation with sepsis
abstract	Abstract Susceptibility and response to infectious disease is, in part, heritable. Initial attempts to identify the causal genetic polymorphisms have not been entirely successful because of the complexity of the genetic, epigenetic, and environmental factors that influence susceptibility and response to infectious disease and because of flaws in study design. Potential associations between clinical outcome from sepsis and many inflammatory cytokine gene polymorphisms, innate immunity pathway gene polymorphisms, and coagulation cascade polymorphisms have been observed. Confirmation in large, well conducted, multicenter studies is required to confirm current findings and to make them clinically applicable. Unbiased investigation of all genes in the human genome is an emerging approach. New, economical, high-throughput technologies may make this possible. It is now feasible to genotype thousands of tag single nucleotide polymorphisms across the genome in thousands of patients, thus addressing the issues of small sample size and bias in selecting candidate polymorphisms and genes for genetic association studies. By performing genome-wide association studies, genome-wide scans of nonsynonymous single nucleotide polymorphisms, and testing for differential allelic expression and copy number polymorphisms, we may yet be able to tease out the complex influence of genetic variation on susceptibility and response to infectious disease. © BioMed Central Ltd 2009
abstractGer	Abstract Susceptibility and response to infectious disease is, in part, heritable. Initial attempts to identify the causal genetic polymorphisms have not been entirely successful because of the complexity of the genetic, epigenetic, and environmental factors that influence susceptibility and response to infectious disease and because of flaws in study design. Potential associations between clinical outcome from sepsis and many inflammatory cytokine gene polymorphisms, innate immunity pathway gene polymorphisms, and coagulation cascade polymorphisms have been observed. Confirmation in large, well conducted, multicenter studies is required to confirm current findings and to make them clinically applicable. Unbiased investigation of all genes in the human genome is an emerging approach. New, economical, high-throughput technologies may make this possible. It is now feasible to genotype thousands of tag single nucleotide polymorphisms across the genome in thousands of patients, thus addressing the issues of small sample size and bias in selecting candidate polymorphisms and genes for genetic association studies. By performing genome-wide association studies, genome-wide scans of nonsynonymous single nucleotide polymorphisms, and testing for differential allelic expression and copy number polymorphisms, we may yet be able to tease out the complex influence of genetic variation on susceptibility and response to infectious disease. © BioMed Central Ltd 2009
abstract_unstemmed	Abstract Susceptibility and response to infectious disease is, in part, heritable. Initial attempts to identify the causal genetic polymorphisms have not been entirely successful because of the complexity of the genetic, epigenetic, and environmental factors that influence susceptibility and response to infectious disease and because of flaws in study design. Potential associations between clinical outcome from sepsis and many inflammatory cytokine gene polymorphisms, innate immunity pathway gene polymorphisms, and coagulation cascade polymorphisms have been observed. Confirmation in large, well conducted, multicenter studies is required to confirm current findings and to make them clinically applicable. Unbiased investigation of all genes in the human genome is an emerging approach. New, economical, high-throughput technologies may make this possible. It is now feasible to genotype thousands of tag single nucleotide polymorphisms across the genome in thousands of patients, thus addressing the issues of small sample size and bias in selecting candidate polymorphisms and genes for genetic association studies. By performing genome-wide association studies, genome-wide scans of nonsynonymous single nucleotide polymorphisms, and testing for differential allelic expression and copy number polymorphisms, we may yet be able to tease out the complex influence of genetic variation on susceptibility and response to infectious disease. © BioMed Central Ltd 2009
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title_short	Bench-to-bedside review: Association of genetic variation with sepsis
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