Reviewer's report
Title:Bax Inhibitor-1 down-regulation in the progression of chronic liver diseases
Version: 2Date:26 January 2010
Reviewer: Yusuf Yilmaz
Reviewer's report:
Overview
In an effort to study the implications of hepatocyte apoptosis in chronic liver
diseases, the authors examined Bax and BI-1 mRNA and protein expressions in
liver tissues from 39 patients with chronic hepatitis (CH) (31 HCV-related and 8
HBV-related); 7 with cirrhosis (6 HCV-related and 1 HBV-related); 13 with
hepatocellular carcinoma (HCC) (7 in viral cirrhosis [6 HCV- and 1 HBV-related],
6 in non-viral cirrhosis); and 3 controls. Bax and BI-1 mRNAs were quantified by
real-time PCR; in addition, BI-1 protein expression was determined by Western
blot. The authors observed that high BI-1 mRNAs levels observed in early liver
disease may protect virus-infected cells against apoptosis, while their
progressive downregulation may facilitate hepatocellular carcinogenesis. HCV
genotype seems to have a relevant role in Bax transcript expression.
Major Compulsory Revisions
- The study was mainly focused on virus-related chronic liver disease. Therefore
the inclusion of 6 patients with non-viral cirrhosis is questionable here and may
complicate data analysis and interpretation. This is especially true inasmuch as
the authors did not include patients with NAFLD in this study. Therefore, data on
patients with non-viral cirrhosis should be deleted and the paper re-arranged
accordingly.
- The inclusion of only three controls is another problematic issue. Although the
main comparisons were between liver disease with different severities, this is a
caveat that needs to be highlighted. The addition of more controls is desirable.
- Another interesting research direction is to study Bax and BI-1 mRNAs in the
spectrum of NAFLD. This is a caveat of this study that should be highlighted. The
authors should briefly introduce this concept and refer to the paper by Beatrice
Bailly-Maitre d coworkers (Hepatic Bax-inhibitor (BI)-1 inhibits IRE1# and
protects from obesity-associated insulin resistance and glucose intolerance. J.
Biol. Chem. jbc.M109.056648) that may represent an important starting point for
the study of BI-1 in NAFLD.
Minor Essential Revisions
- Was normality of the data checked?
- "A 2P value of < 0.05 was required for significance" should be changed in
"Two-tailed P values < 0.05 were deemed to be significant".
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Needs some language corrections before being
published
Statistical review: Yes, and I have assessed the statistics in my report.
Declaration of competing interests:
I declare that I have no competing interests.
Reviewer's report
Title:Bax Inhibitor-1 down-regulation in the progression of chronic liver diseases
Version: 2Date:26 January 2010
Reviewer: Yusuf Yilmaz
Reviewer's report:
Overview
In an effort to study the implications of hepatocyte apoptosis in chronic liver
diseases, the authors examined Bax and BI-1 mRNA and protein expressions in
liver tissues from 39 patients with chronic hepatitis (CH) (31 HCV-related and 8
HBV-related); 7 with cirrhosis (6 HCV-related and 1 HBV-related); 13 with
hepatocellular carcinoma (HCC) (7 in viral cirrhosis [6 HCV- and 1 HBV-related],
6 in non-viral cirrhosis); and 3 controls. Bax and BI-1 mRNAs were quantified by
real-time PCR; in addition, BI-1 protein expression was determined by Western
blot. The authors observed that high BI-1 mRNAs levels observed in early liver
disease may protect virus-infected cells against apoptosis, while their
progressive downregulation may facilitate hepatocellular carcinogenesis. HCV
genotype seems to have a relevant role in Bax transcript expression.
Major Compulsory Revisions
- The study was mainly focused on virus-related chronic liver disease. Therefore
the inclusion of 6 patients with non-viral cirrhosis is questionable here and may
complicate data analysis and interpretation. This is especially true inasmuch as
the authors did not include patients with NAFLD in this study. Therefore, data on
patients with non-viral cirrhosis should be deleted and the paper re-arranged
accordingly.
- The inclusion of only three controls is another problematic issue. Although the
main comparisons were between liver disease with different severities, this is a
caveat that needs to be highlighted. The addition of more controls is desirable.
- Another interesting research direction is to study Bax and BI-1 mRNAs in the
spectrum of NAFLD. This is a caveat of this study that should be highlighted. The
authors should briefly introduce this concept and refer to the paper by Beatrice
Bailly-Maitre d coworkers (Hepatic Bax-inhibitor (BI)-1 inhibits IRE1# and
protects from obesity-associated insulin resistance and glucose intolerance. J.
Biol. Chem. jbc.M109.056648) that may represent an important starting point for
the study of BI-1 in NAFLD.
Minor Essential Revisions
- Was normality of the data checked?
- "A 2P value of < 0.05 was required for significance" should be changed in
"Two-tailed P values < 0.05 were deemed to be significant".
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Needs some language corrections before being
published
Statistical review: Yes, and I have assessed the statistics in my report.
Declaration of competing interests:
I declare that I have no competing interests.
Please review this paper.
user
Reviewer's report
Title:Bax Inhibitor-1 down-regulation in the progression of chronic liver diseases
Version: 2Date:26 January 2010
Reviewer: Yusuf Yilmaz
Reviewer's report:
Overview
In an effort to study the implications of hepatocyte apoptosis in chronic liver
diseases, the authors examined Bax and BI-1 mRNA and protein expressions in
liver tissues from 39 patients with chronic hepatitis (CH) (31 HCV-related and 8
HBV-related); 7 with cirrhosis (6 HCV-related and 1 HBV-related); 13 with
hepatocellular carcinoma (HCC) (7 in viral cirrhosis [6 HCV- and 1 HBV-related],
6 in non-viral cirrhosis); and 3 controls. Bax and BI-1 mRNAs were quantified by
real-time PCR; in addition, BI-1 protein expression was determined by Western
blot. The authors observed that high BI-1 mRNAs levels observed in early liver
disease may protect virus-infected cells against apoptosis, while their
progressive downregulation may facilitate hepatocellular carcinogenesis. HCV
genotype seems to have a relevant role in Bax transcript expression.
Major Compulsory Revisions
- The study was mainly focused on virus-related chronic liver disease. Therefore
the inclusion of 6 patients with non-viral cirrhosis is questionable here and may
complicate data analysis and interpretation. This is especially true inasmuch as
the authors did not include patients with NAFLD in this study. Therefore, data on
patients with non-viral cirrhosis should be deleted and the paper re-arranged
accordingly.
- The inclusion of only three controls is another problematic issue. Although the
main comparisons were between liver disease with different severities, this is a
caveat that needs to be highlighted. The addition of more controls is desirable.
- Another interesting research direction is to study Bax and BI-1 mRNAs in the
spectrum of NAFLD. This is a caveat of this study that should be highlighted. The
authors should briefly introduce this concept and refer to the paper by Beatrice
Bailly-Maitre d coworkers (Hepatic Bax-inhibitor (BI)-1 inhibits IRE1# and
protects from obesity-associated insulin resistance and glucose intolerance. J.
Biol. Chem. jbc.M109.056648) that may represent an important starting point for
the study of BI-1 in NAFLD.
Minor Essential Revisions
- Was normality of the data checked?
- "A 2P value of < 0.05 was required for significance" should be changed in
"Two-tailed P values < 0.05 were deemed to be significant".
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Needs some language corrections before being
published
Statistical review: Yes, and I have assessed the statistics in my report.
Declaration of competing interests:
I declare that I have no competing interests.
assistant