Reviewer's report
Title:The Helicobacter pylori duodenal ulcer promoting gene, dupA in China
Version: 3Date:2 July 2008
Reviewer: Richard Harry Argent
Reviewer's report:
MAJOR COMMENTS
A) The previous paper by Lu et al. (Gastroenterology 128, 2005; 833-48) showed
a significant correlation between dupA and DU, but an inverse correlation with
GC, in strains from Korea, Japan, and Colombia. The data presented in the new
article suggests that the situation is the same in this Chinese population.
However, the authors appear to be viewing their data from the Chinese
population in light of their previous findings, rather than looking at the new data
independently. For instance, in figure 1, the authors find a significant association
between DU and dupA but only when compared with GU or GC patients. If the
data is compared with patients with gastritis only, as it should be, there is no
significant association (p = 0.27) between DU and dupA prevalence. However,
patients with GC are significantly more likely to be infected with strains lacking
dupA (p = 0.032), but, again, this does not hold for patients with GU (p = 0.064).
B) Discussion. The discussion needs more detail. The data should be compared
in more detail to the work of Argent et al. (ref 23) who showed that dupA was not
associated with DU but was significantly associated with GC, and who also
looked at a Chinese population. The authors also need to discuss the similarities
and differences between the Shanghai population and those from Korea and
Japan from their previous study.
MINOR POINTS
1) In the abstract and results section, the chronic inflammation data does not
match that presented in Table 3.
2) It is not clear why biopsies were only taken from the antrum. If samples were
also taken from the corpus, this would allow greater sampling of the stomach.
3) The authors refer to "putative virulence factors" several times – are the cag
pathogenicity island and VacA, in particular, still considered putative?
4) A reference should be provided for the updated Sydney system in the
methods.
5) In the IL-1-beta methods section, the name of restriction enzyme "Ava" is not
complete.
6) Results – dupA typing – how many strains were only positive for one of the
two genes jhp0917 or jhp0918, and if these were present, how were they
classified?
7) Results – the GU data should be (11/47, 23.4%).
8) Discussion – the sentence "Thus, one would expect...severity of corpus
gastritis" is speculative, particularly as the authors did not look at strains from the
corpus.
9) Discussion – final sentence. The authors cannot make this claim based on
data presented on a single Chinese population.
10) Tables – no data is presented for vacA typing other than s1a – why wasn't
the prevalence of s2 and the other s1 types determined?
11) Table 3 – this is possibly incomplete (as the title suggests), and, as already
mentioned, the data presented doesn't match the text.
12) Table 4 – the data for the vacA mid-region types do not add up. vacAm2 is
mis-spelled.
13) Figure 1 – dupA is not italicised in the title, and this figure could probably be
omitted.
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
Reviewer's report
Title:The Helicobacter pylori duodenal ulcer promoting gene, dupA in China
Version: 3Date:2 July 2008
Reviewer: Richard Harry Argent
Reviewer's report:
MAJOR COMMENTS
A) The previous paper by Lu et al. (Gastroenterology 128, 2005; 833-48) showed
a significant correlation between dupA and DU, but an inverse correlation with
GC, in strains from Korea, Japan, and Colombia. The data presented in the new
article suggests that the situation is the same in this Chinese population.
However, the authors appear to be viewing their data from the Chinese
population in light of their previous findings, rather than looking at the new data
independently. For instance, in figure 1, the authors find a significant association
between DU and dupA but only when compared with GU or GC patients. If the
data is compared with patients with gastritis only, as it should be, there is no
significant association (p = 0.27) between DU and dupA prevalence. However,
patients with GC are significantly more likely to be infected with strains lacking
dupA (p = 0.032), but, again, this does not hold for patients with GU (p = 0.064).
B) Discussion. The discussion needs more detail. The data should be compared
in more detail to the work of Argent et al. (ref 23) who showed that dupA was not
associated with DU but was significantly associated with GC, and who also
looked at a Chinese population. The authors also need to discuss the similarities
and differences between the Shanghai population and those from Korea and
Japan from their previous study.
MINOR POINTS
1) In the abstract and results section, the chronic inflammation data does not
match that presented in Table 3.
2) It is not clear why biopsies were only taken from the antrum. If samples were
also taken from the corpus, this would allow greater sampling of the stomach.
3) The authors refer to "putative virulence factors" several times – are the cag
pathogenicity island and VacA, in particular, still considered putative?
4) A reference should be provided for the updated Sydney system in the
methods.
5) In the IL-1-beta methods section, the name of restriction enzyme "Ava" is not
complete.
6) Results – dupA typing – how many strains were only positive for one of the
two genes jhp0917 or jhp0918, and if these were present, how were they
classified?
7) Results – the GU data should be (11/47, 23.4%).
8) Discussion – the sentence "Thus, one would expect...severity of corpus
gastritis" is speculative, particularly as the authors did not look at strains from the
corpus.
9) Discussion – final sentence. The authors cannot make this claim based on
data presented on a single Chinese population.
10) Tables – no data is presented for vacA typing other than s1a – why wasn't
the prevalence of s2 and the other s1 types determined?
11) Table 3 – this is possibly incomplete (as the title suggests), and, as already
mentioned, the data presented doesn't match the text.
12) Table 4 – the data for the vacA mid-region types do not add up. vacAm2 is
mis-spelled.
13) Figure 1 – dupA is not italicised in the title, and this figure could probably be
omitted.
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
Please review this paper.
user
Reviewer's report
Title:The Helicobacter pylori duodenal ulcer promoting gene, dupA in China
Version: 3Date:2 July 2008
Reviewer: Richard Harry Argent
Reviewer's report:
MAJOR COMMENTS
A) The previous paper by Lu et al. (Gastroenterology 128, 2005; 833-48) showed
a significant correlation between dupA and DU, but an inverse correlation with
GC, in strains from Korea, Japan, and Colombia. The data presented in the new
article suggests that the situation is the same in this Chinese population.
However, the authors appear to be viewing their data from the Chinese
population in light of their previous findings, rather than looking at the new data
independently. For instance, in figure 1, the authors find a significant association
between DU and dupA but only when compared with GU or GC patients. If the
data is compared with patients with gastritis only, as it should be, there is no
significant association (p = 0.27) between DU and dupA prevalence. However,
patients with GC are significantly more likely to be infected with strains lacking
dupA (p = 0.032), but, again, this does not hold for patients with GU (p = 0.064).
B) Discussion. The discussion needs more detail. The data should be compared
in more detail to the work of Argent et al. (ref 23) who showed that dupA was not
associated with DU but was significantly associated with GC, and who also
looked at a Chinese population. The authors also need to discuss the similarities
and differences between the Shanghai population and those from Korea and
Japan from their previous study.
MINOR POINTS
1) In the abstract and results section, the chronic inflammation data does not
match that presented in Table 3.
2) It is not clear why biopsies were only taken from the antrum. If samples were
also taken from the corpus, this would allow greater sampling of the stomach.
3) The authors refer to "putative virulence factors" several times – are the cag
pathogenicity island and VacA, in particular, still considered putative?
4) A reference should be provided for the updated Sydney system in the
methods.
5) In the IL-1-beta methods section, the name of restriction enzyme "Ava" is not
complete.
6) Results – dupA typing – how many strains were only positive for one of the
two genes jhp0917 or jhp0918, and if these were present, how were they
classified?
7) Results – the GU data should be (11/47, 23.4%).
8) Discussion – the sentence "Thus, one would expect...severity of corpus
gastritis" is speculative, particularly as the authors did not look at strains from the
corpus.
9) Discussion – final sentence. The authors cannot make this claim based on
data presented on a single Chinese population.
10) Tables – no data is presented for vacA typing other than s1a – why wasn't
the prevalence of s2 and the other s1 types determined?
11) Table 3 – this is possibly incomplete (as the title suggests), and, as already
mentioned, the data presented doesn't match the text.
12) Table 4 – the data for the vacA mid-region types do not add up. vacAm2 is
mis-spelled.
13) Figure 1 – dupA is not italicised in the title, and this figure could probably be
omitted.
Level of interest: An article whose findings are important to those with closely
related research interests
Quality of written English: Acceptable
Statistical review: No, the manuscript does not need to be seen by a
statistician.
Declaration of competing interests:
I declare that I have no competing interests.
assistant