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Results of a new study contradict previous research suggesting mice do not make suitable models for human inflammatory conditions.
The original study, published in PNAS in February 2013, indicated that genomic responses to different acute inflammatory stressors—trauma, burns, sepsis, and infection—are highly similar in humans but poorly reproduced in corresponding mouse models.
The new study, published in PNAS yesterday, suggests that is not the case.
The original study was conducted by Junhee Seok, PhD, of Northwestern University, and his colleagues. It garnered a lot of attention from the scientific community and the general public, reigniting the debate over mouse models’ suitability for medical research.
Tsuyoshi Miyakawa, PhD, of Fujita Health University in Japan, was among those who argued that mice are suitable models, and Dr Seok’s findings were likely incorrect.
So Dr Miyakawa and his colleague, Keizo Takao, PhD, of the National Institute for Physiological Sciences in Japan, reanalyzed the data from Dr Seok’s study using the bioinformatics tool NextBio.
Dr Seok’s group had compared the expression levels of genes that were altered in a particular human condition between humans and mice.
A comparison of the genomic response between humans and mice, including those genes altered in one species but not in another, obscures the correlation between homologous genes of humans and mice to nearly 0, as the team showed.
The group’s comparison of the gene expression patterns between human burn victims and mouse models of burns, trauma, sepsis, and infection revealed a Pearson’s correlation coefficient (R) that ranged from 0.14 to 0.28. And the percentage of genes whose expression changed in the same direction was 55% to 61%.
In the new analysis based on the same data, Drs Miyakawa and Takao found the R values ranged from 0.36 to 0.59. And 77% to 93% of the genes changed in the same directions between the human condition and the mouse models.
Non-parametric ranking analysis using NextBio showed the pattern of the gene expression changes in mouse models was highly similar to that in human burn conditions—a significant correlation (P = 6.5 x 10-11 to 1.2 x 10-35).
Drs Miyakawa and Takao noted that many molecular pathways are commonly dysregulated in human diseases and mouse models. And focusing on the commonalities between human diseases and mouse models will allow us to derive useful information for studying the pathophysiology and pathogenesis of human diseases, as well as aid treatment development. 
Results of a new study contradict previous research suggesting mice do not make suitable models for human inflammatory conditions.
The original study, published in PNAS in February 2013, indicated that genomic responses to different acute inflammatory stressors—trauma, burns, sepsis, and infection—are highly similar in humans but poorly reproduced in corresponding mouse models.
The new study, published in PNAS yesterday, suggests that is not the case.
The original study was conducted by Junhee Seok, PhD, of Northwestern University, and his colleagues. It garnered a lot of attention from the scientific community and the general public, reigniting the debate over mouse models’ suitability for medical research.
Tsuyoshi Miyakawa, PhD, of Fujita Health University in Japan, was among those who argued that mice are suitable models, and Dr Seok’s findings were likely incorrect.
So Dr Miyakawa and his colleague, Keizo Takao, PhD, of the National Institute for Physiological Sciences in Japan, reanalyzed the data from Dr Seok’s study using the bioinformatics tool NextBio.
Dr Seok’s group had compared the expression levels of genes that were altered in a particular human condition between humans and mice.
A comparison of the genomic response between humans and mice, including those genes altered in one species but not in another, obscures the correlation between homologous genes of humans and mice to nearly 0, as the team showed.
The group’s comparison of the gene expression patterns between human burn victims and mouse models of burns, trauma, sepsis, and infection revealed a Pearson’s correlation coefficient (R) that ranged from 0.14 to 0.28. And the percentage of genes whose expression changed in the same direction was 55% to 61%.
In the new analysis based on the same data, Drs Miyakawa and Takao found the R values ranged from 0.36 to 0.59. And 77% to 93% of the genes changed in the same directions between the human condition and the mouse models.
Non-parametric ranking analysis using NextBio showed the pattern of the gene expression changes in mouse models was highly similar to that in human burn conditions—a significant correlation (P = 6.5 x 10-11 to 1.2 x 10-35).
Drs Miyakawa and Takao noted that many molecular pathways are commonly dysregulated in human diseases and mouse models. And focusing on the commonalities between human diseases and mouse models will allow us to derive useful information for studying the pathophysiology and pathogenesis of human diseases, as well as aid treatment development.
Results of a new study contradict previous research suggesting mice do not make suitable models for human inflammatory conditions.
The original study, published in PNAS in February 2013, indicated that genomic responses to different acute inflammatory stressors—trauma, burns, sepsis, and infection—are highly similar in humans but poorly reproduced in corresponding mouse models.
The new study, published in PNAS yesterday, suggests that is not the case.
The original study was conducted by Junhee Seok, PhD, of Northwestern University, and his colleagues. It garnered a lot of attention from the scientific community and the general public, reigniting the debate over mouse models’ suitability for medical research.
Tsuyoshi Miyakawa, PhD, of Fujita Health University in Japan, was among those who argued that mice are suitable models, and Dr Seok’s findings were likely incorrect.
So Dr Miyakawa and his colleague, Keizo Takao, PhD, of the National Institute for Physiological Sciences in Japan, reanalyzed the data from Dr Seok’s study using the bioinformatics tool NextBio.
Dr Seok’s group had compared the expression levels of genes that were altered in a particular human condition between humans and mice.
A comparison of the genomic response between humans and mice, including those genes altered in one species but not in another, obscures the correlation between homologous genes of humans and mice to nearly 0, as the team showed.
The group’s comparison of the gene expression patterns between human burn victims and mouse models of burns, trauma, sepsis, and infection revealed a Pearson’s correlation coefficient (R) that ranged from 0.14 to 0.28. And the percentage of genes whose expression changed in the same direction was 55% to 61%.
In the new analysis based on the same data, Drs Miyakawa and Takao found the R values ranged from 0.36 to 0.59. And 77% to 93% of the genes changed in the same directions between the human condition and the mouse models.
Non-parametric ranking analysis using NextBio showed the pattern of the gene expression changes in mouse models was highly similar to that in human burn conditions—a significant correlation (P = 6.5 x 10-11 to 1.2 x 10-35).
Drs Miyakawa and Takao noted that many molecular pathways are commonly dysregulated in human diseases and mouse models. And focusing on the commonalities between human diseases and mouse models will allow us to derive useful information for studying the pathophysiology and pathogenesis of human diseases, as well as aid treatment development.