Reviewer's report
Title:Change of nitric oxide synthase neurons in ileal myenteric plexus of rat
severe acute pancreatitis
Version: 1Date:18 April 2011
Reviewer: Axel Brehmer
Reviewer's report:
The study investigates the gastrointestinal motility disturbances following
experimental acute pancreatitis. The authors found enlarged transit time in the
small intestine, increased numbers of nitrergic neurons in the myenteric plexus
and enhanced mRNA expression of nNOS. However, there are some important
points limiting the impact of the study.
Major compulsory revision:
(1) Background: The authors should clearly give reasons for their decision to
select acute pancreatitis as experimental model for studying gastrointestinal
motility. As the authors state (Page 15, last paragraph: “Masolo et al showed that
many situations such as pancreatitis could induce paralytic ileus”), other
abdominal inflammations may reach the intended purpose by less technical
effort. Thus, the connection between pancreatitis and impaired gastrointestinal
motility is a rather unspecific one.
(2) Material and Methods: There are some insufficient descriptions, e.g.:
preparation of wholemounts (“tissue … pinned … with mucosal surface down …
prepared with peeling off the circle muscle …”), method of counting
NOS-neurons (how many neurons per specimen were recorded etc.).
(3) Results: Table 3 is not sufficient for presentation of quantitative results. Some
more original data are needed (transit time delay, pathologic score, numbers of
NOS-neurons).
Further comments:
Abstract and elsewhere: NOS-neurons were “bigger” in pancreatitis animals.
There was no measurement of cell body sizes. The authors should provide the
reader with results of measurements or rather omit these passages.
Pathological scoring criteria should shortly be explained.
There are redundancies between Introduction and Discussion (e.g., page 13 last
paragraph/page 14 first paragraph: “ENS is a complex of intrinsic neurons …”
Page 14, second paragraph: “smooth muscle cells … are innervated by hundreds
of… motor neurons…” How was this estimated?
Same paragraph: ICCs are the primary (!) targets of innervation, they are
intercalated between neuron and muscle. What does the statement mean: “The
ICC … have receptors … for excitatory tachykinin transmitters such as
muscarinic”?
Page 16, first paragraph: “upregulation of NOS-neurons”: If there are more
NOS-neurons in SAP-intestines as compared to controls the question arises
which neurons change their nNOS-expression from negative to positive?
Page 16, last but one paragraph: “The upregulation of NOS-neurons in our study
most likely represents a neuronal reaction to SAP” This is what should be
explained more concisely by the authors, also in light of the citation of Masolo et
al. (see point 1)!
Page 17, second paragraph. “In our previous study…” (quotation is missing)
Page 17/18: paragraph is not related to the main strength of the study
(Discussion should be shortened with focus on more relevant passages).
Level of interest: An article of limited interest
Quality of written English: Not suitable for publication unless extensively edited
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
Reviewer's report
Title:Change of nitric oxide synthase neurons in ileal myenteric plexus of rat
severe acute pancreatitis
Version: 1Date:18 April 2011
Reviewer: Axel Brehmer
Reviewer's report:
The study investigates the gastrointestinal motility disturbances following
experimental acute pancreatitis. The authors found enlarged transit time in the
small intestine, increased numbers of nitrergic neurons in the myenteric plexus
and enhanced mRNA expression of nNOS. However, there are some important
points limiting the impact of the study.
Major compulsory revision:
(1) Background: The authors should clearly give reasons for their decision to
select acute pancreatitis as experimental model for studying gastrointestinal
motility. As the authors state (Page 15, last paragraph: “Masolo et al showed that
many situations such as pancreatitis could induce paralytic ileus”), other
abdominal inflammations may reach the intended purpose by less technical
effort. Thus, the connection between pancreatitis and impaired gastrointestinal
motility is a rather unspecific one.
(2) Material and Methods: There are some insufficient descriptions, e.g.:
preparation of wholemounts (“tissue … pinned … with mucosal surface down …
prepared with peeling off the circle muscle …”), method of counting
NOS-neurons (how many neurons per specimen were recorded etc.).
(3) Results: Table 3 is not sufficient for presentation of quantitative results. Some
more original data are needed (transit time delay, pathologic score, numbers of
NOS-neurons).
Further comments:
Abstract and elsewhere: NOS-neurons were “bigger” in pancreatitis animals.
There was no measurement of cell body sizes. The authors should provide the
reader with results of measurements or rather omit these passages.
Pathological scoring criteria should shortly be explained.
There are redundancies between Introduction and Discussion (e.g., page 13 last
paragraph/page 14 first paragraph: “ENS is a complex of intrinsic neurons …”
Page 14, second paragraph: “smooth muscle cells … are innervated by hundreds
of… motor neurons…” How was this estimated?
Same paragraph: ICCs are the primary (!) targets of innervation, they are
intercalated between neuron and muscle. What does the statement mean: “The
ICC … have receptors … for excitatory tachykinin transmitters such as
muscarinic”?
Page 16, first paragraph: “upregulation of NOS-neurons”: If there are more
NOS-neurons in SAP-intestines as compared to controls the question arises
which neurons change their nNOS-expression from negative to positive?
Page 16, last but one paragraph: “The upregulation of NOS-neurons in our study
most likely represents a neuronal reaction to SAP” This is what should be
explained more concisely by the authors, also in light of the citation of Masolo et
al. (see point 1)!
Page 17, second paragraph. “In our previous study…” (quotation is missing)
Page 17/18: paragraph is not related to the main strength of the study
(Discussion should be shortened with focus on more relevant passages).
Level of interest: An article of limited interest
Quality of written English: Not suitable for publication unless extensively edited
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
Please review this paper.
user
Reviewer's report
Title:Change of nitric oxide synthase neurons in ileal myenteric plexus of rat
severe acute pancreatitis
Version: 1Date:18 April 2011
Reviewer: Axel Brehmer
Reviewer's report:
The study investigates the gastrointestinal motility disturbances following
experimental acute pancreatitis. The authors found enlarged transit time in the
small intestine, increased numbers of nitrergic neurons in the myenteric plexus
and enhanced mRNA expression of nNOS. However, there are some important
points limiting the impact of the study.
Major compulsory revision:
(1) Background: The authors should clearly give reasons for their decision to
select acute pancreatitis as experimental model for studying gastrointestinal
motility. As the authors state (Page 15, last paragraph: “Masolo et al showed that
many situations such as pancreatitis could induce paralytic ileus”), other
abdominal inflammations may reach the intended purpose by less technical
effort. Thus, the connection between pancreatitis and impaired gastrointestinal
motility is a rather unspecific one.
(2) Material and Methods: There are some insufficient descriptions, e.g.:
preparation of wholemounts (“tissue … pinned … with mucosal surface down …
prepared with peeling off the circle muscle …”), method of counting
NOS-neurons (how many neurons per specimen were recorded etc.).
(3) Results: Table 3 is not sufficient for presentation of quantitative results. Some
more original data are needed (transit time delay, pathologic score, numbers of
NOS-neurons).
Further comments:
Abstract and elsewhere: NOS-neurons were “bigger” in pancreatitis animals.
There was no measurement of cell body sizes. The authors should provide the
reader with results of measurements or rather omit these passages.
Pathological scoring criteria should shortly be explained.
There are redundancies between Introduction and Discussion (e.g., page 13 last
paragraph/page 14 first paragraph: “ENS is a complex of intrinsic neurons …”
Page 14, second paragraph: “smooth muscle cells … are innervated by hundreds
of… motor neurons…” How was this estimated?
Same paragraph: ICCs are the primary (!) targets of innervation, they are
intercalated between neuron and muscle. What does the statement mean: “The
ICC … have receptors … for excitatory tachykinin transmitters such as
muscarinic”?
Page 16, first paragraph: “upregulation of NOS-neurons”: If there are more
NOS-neurons in SAP-intestines as compared to controls the question arises
which neurons change their nNOS-expression from negative to positive?
Page 16, last but one paragraph: “The upregulation of NOS-neurons in our study
most likely represents a neuronal reaction to SAP” This is what should be
explained more concisely by the authors, also in light of the citation of Masolo et
al. (see point 1)!
Page 17, second paragraph. “In our previous study…” (quotation is missing)
Page 17/18: paragraph is not related to the main strength of the study
(Discussion should be shortened with focus on more relevant passages).
Level of interest: An article of limited interest
Quality of written English: Not suitable for publication unless extensively edited
Statistical review: Yes, but I do not feel adequately qualified to assess the
statistics.
assistant