abstract format for haligi
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WRITING REQUIREMENTS OF ABSTRACT
1 Title Title should be less than 12 words.2 Running Title: A short running title of less than 6 words should be provided.
3 Authorship: Authorship credit should be in accordance with the standard proposed by
International Committee of Medical Journal Editors, based on (1) substantial contributions
to conception and design, acquisition of data, or analysis and interpretation of data; (2)
drafting the article or revising it critically for important intellectual content; and (3) final
approval of the version to be published. Authors should meet conditions 1, 2, and 3.
4 Received: Fill out by S-editor; Revised: Fill out by S-editor; Accepted: Fill out by S-
editor; Published online: Fill out by E-editor.
5 Abstract: There are unstructured abstracts (no more than 256 words) and
structured abstracts (no more than 480). The specific requirements for structured
abstracts are as follows:
An informative, structured abstracts of no more than 480 words should accompany
each manuscript. Abstracts for original contributions should be structured into thefollowing sections. AIM (no more than 20 words): Only the purpose should be
included. Please write the aim as the form of To investigate/study/; MATERIALS
AND METHODS(no more than 140 words); RESULTS (no more than 294 words): You
should present P values where appropriate and must provide relevant data to illustrate
how they were obtained, e.g. 6.92 3.86 vs 3.61 1.67, P < 0.001; CONCLUSION (no
more than 26 words). Available from:http://www.wjgnet.com/wjg/help/8.doc
6 Keywords: Please list 5-10 key words for each manuscript, selected mainly from Index
Medicus, which reflect the content of the study. Each key word is separated by a
semicolon.
7 Peer reviewer: Fill out by S-editor.
8 Tables and illustrations: Each table or illustration should be made on a separate
sheet and should be self-explanatory (sufficient to be intelligible without reference to
the text). Avoid repetitions of data in the text, tables, and illustration. Explain tersely the
symbols, letters, or number used. Indicate the number and character of observations and
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subjects. Identify statistical significance by superscripts in front of the probabilities ( P),
e.g. aP
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lowercased while the first one be capitalized. An interval should be inserted between
numbers and units. Photos or figures that are obtained at different time or places must
not be grouped into one, unless those photos or figures are arranged in a time order.
There are intervals between photos or figures of the same group. Photographs or figures
should be put in an independent file.
8.2.3 Authors should list the names of tools they use to obtain and edit the image file.
Images must be edited equally and contrast must be reasonable. Editing that is far
beyond the contents is forbidden. It is not allowed to over-emphasize the difference
between experiment data and control data, or over-emphasize a certain part of the
photos by ignoring some other parts. (A) Electrophoresis and blotting images: mustinclude negative, positive controls and molecular Marker; provide the reference of the
identified antibodies; explain the specificity and active spectrum of the agents not
identified; band should be clear; important bands must not be deleted; leave six-band
space around the blotting bands; we suggest not use high-contrast blotting, for over-
display may conceal the other bands. Authors should try to exhibit the bands on the gray
background. Black frame may be used if the background is weak. (B) Microscopic or
endoscopic images: cells from different field must not be put in the same field; images
should be adjusted at a whole; avoid pseudo-color and nonlinear adjustment (e.g.
transformation ), and give an explanation in the legend if necessary.
8.3 Tables: A decomposable table is required. Each table should be put in an
independent page, with a bold title no more than a row long. Tables should be put at the
end of the article.
9 References : Pleased provide PubMed citation numbers to the reference list, e.g. PMID
and DOI, which can be found at http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmed
and http://www.crossref.org/SimpleTextQuery/ , respectively. The numbers will be used in
E-version of this journal. Thanks very much for your co-operation.
10 S- Editor, L- Editor and E- Editor: Fill out by responsible person.
11 Abstract Contents
11.1 UNSTRUCTURED ABSTRACT FORMAT FOR EDITORIAL 411.2 UNSTRUCTURED ABSTRACT FORMAT FOR TOPIC HIGHLIGHT 6
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http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmedhttp://www.crossref.org/SimpleTextQuery/http://www.ncbi.nlm.nih.gov/sites/entrez?db=pubmedhttp://www.crossref.org/SimpleTextQuery/ -
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11.3 UNSTRUCTURED ABSTRACT FORMAT FOR OBSERVER 8
11.4 UNSTRUCTURED ABSTRACT FORMAT FOR REVIEW 10
11.5 STRUCTURED ABSTRACT FORMAT FOR ORIGINAL ARTICLES 12
11.6 UNSTRUCTURED ABSTRACT FORMAT FOR CASE REPORT 16
11.7 UNSTRUCTURED ABSTRACT FORMAT FOR LETTERS TO THE EDITOR 18
11.1 UNSTRUCTURED ABSTRACT FORMAT FOR EDITORIAL
Role of cannabinoids in chronic liver diseases
Anna Parfieniuk, Robert Flisiak
Anna Parfieniuk, Robert Flisiak, Department of Infectious Diseases and
Hepatology, Medical University of Bialystok, Zurawia Str 14, Bialystok 15-540,
Poland
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Author contributions: Parfieniuk A was responsible for the review of the
literature and initial preparation of the paper, Flisiak R prepared final version
of the manuscript.
Correspondence to: Robert Flisiak, Department of Infectious Diseases and
Hepatology, Medical University of Bialystok, Zurawia Str 14, Bialystok 15-540,
Poland. [email protected]
Telephone: +48-85-7416921 Fax: +48-85-7416921Received: April 2, 2008 Revised: June 30, 2008
Accepted: July 7, 2008
Published online: October 28, 2008
Abstract (256 words)
Cannabinoids are a group of compounds acting primarily via CB1 and CB2
receptors. The expression of cannabinoid receptors in normal liver is low or
absent. However, many reports have proven up-regulation of the expression
of CB1 and CB2 receptors in hepatic myofibroblasts and vascular endothelial
cells, as well as increased concentration of endocannabinoids in liver in the
course of chronic progressive liver diseases. It has been shown that CB1
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receptor signalling exerts profibrogenic and proinflammatory effects in liver
tissue, primarily due to the stimulation of hepatic stellate cells, whereas the
activation of CB2 receptors inhibits or even reverses liver fibrogenesis.
Similarly, CB1 receptor stimulation contributes to progression of liver
steatosis. In end-stage liver disease, the endocannabinoid system has been
shown to contribute to hepatic encephalopathy and vascular effects, such as
portal hypertension, splanchnic vasodilatation, relative peripheral
hypotension and probably cirrhotic cardiomyopathy. So far, available evidence
is based on cellular cultures or animal models. Clinical data on the effects of
cannabinoids in chronic liver diseases are limited. However, recent studieshave shown the contribution of cannabis smoking to the progression of liver
fibrosis and steatosis. Moreover, controlling CB1 or CB2 signalling appears to
be an attractive target in managing liver diseases.
2008 The WJG Press. All rights reserved.
Key words: Hepatic fibrosis; Endocannabinoids; Endocannabinoid receptors;
CB1; CB2
Peer reviewer:
Parfieniuk A, Flisiak R. Role of cannabinoids in chronic liver diseases. World J
Gastroenterol 2008; 14(40): 6109-6114Available from: URL: http://www.wjgnet.com/1007-9327/14/6109.asp
DOI: http://dx.doi.org/10.3748/wjg.14.6109
11.2 UNSTRUCTURED ABSTRACT FORMAT FOR TOPIC
HIGHLIGHT
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http://dx.doi.org/10.3748/wjg.14.6109http://dx.doi.org/10.3748/wjg.14.6109 -
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Effects of ghrelin on interdigestive contractions of
the rat gastrointestinal tract
Hiroshi Taniguchi, Hajime Ariga, Jun Zheng, Kirk Ludwig, Toku Takahashi
Hiroshi Taniguchi, Hajime Ariga, Jun Zheng, Kirk Ludwig, Toku
Takahashi, Department of Surgery, Medical College of Wisconsin and
Zablocki VA Medical Center, Milwaukee, WI 53295, United States
Author contributions: Taniguchi H, Ariga H and Zheng J performed
research; Taniguchi H, Ludwig K and Takahashi T analyzed the data; Taniguchi
H and Takahashi T wrote the paper.
Correspondence to: Toku Takahashi, MD, PhD, Department of Surgery,
Medical College of Wisconsin and Zablocki VA Medical Center, 5000 West
National Avenue, Milwaukee, WI 53295, United States. [email protected]
Telephone: +1-414-3842000-41472 Fax: +1-414-3825374
Received: October 15, 2008 Revised: October 30, 2008
Accepted: November 6, 2008
Published online: November 7, 2008
Abstract (256 words)
Ghrelin causes interdigestive contractions of the stomach in rats. However, it
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remains unknown whether ghrelin causes interdigestive contractions in the
small intestine. Four strain gauge transducers were implanted on the antrum,
duodenum, proximal and distal jejunum. After an overnight fast,
gastrointestinal (GI) contractions were recorded in freely moving conscious
rats. Spontaneous phase -like contractions were observed at every 13-16
min in rat GI tract. The fasted motor patterns were replaced by the fed motor
pattern immediately after food intake. Two minutes after finishing the
spontaneous phase -like contractions in the antrum, acyl ghrelin (0.8, 2.4
and 8.0 mg/kg per min) was continuously infused for 30 min. Three-five
minutes after the starting ghrelin infusion, augmented phase -likecontractions were observed at the antrum, duodenum, and jejunum. Ghrelin
infusion (0.8, 2.4 and 8.0 mg/kg per min) significantly increased motility index
of phase -like contractions at the antrum and jejunum in a dose dependent
manner, compared to that of saline injection. Thus, it is likely that
exogenously administered ghrelin causes phase -like contraction at the
antrum, which migrates to the duodenum and jejunum. The possible role of 5-
HT, in addition to ghrelin, in mediating intestinal migrating motor complex
(MMC), is discussed.
2008 The WJG Press. All rights reserved.
Key words: Phase -like contractions; Strain gage transducers; Motility index
Taniguchi H, Ariga H, Zheng J, Ludwig K, Takahashi T. Effects of ghrelin on
interdigestive contractions of the rat gastrointestinal tract. World J
Gastroenterol 2008; 14(41): 6299-6302
Available from: URL: http://www.wjgnet.com/1007-9327/14/6299.asp
DOI: http://dx.doi.org/10.3748/wjg.14.6299
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11.3 UNSTRUCTURED ABSTRACT FORMAT FOR OBSERVER
Segmental colitis associated with diverticulosis
syndrome
Hugh James Freeman
Hugh James Freeman, Department of Medicine (Gastroenterology),
University of British Columbia, Vancouver V6T 1W5, Canada
Author contributions: Freeman HJ contributed all to this paper.
Correspondence to: Dr. Hugh James Freeman, MD, FRCPC, FACP,
Department of Medicine (Gastroenterology), University of British Columbia
Hospital, 2211 Wesbrook Mall, Vancouver V6T 1W5, Canada.
Telephone: +1-604-8227216 Fax: +1-604-8227236
Received: July 24, 2008 Revised: September 12, 2008
Accepted: September 19, 2008
Published online: November 14, 2008
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Abstract (256 words)
An inflammatory process that involves the sigmoid colonic segment
associated with diverticular disease (SCAD) appears to be a distinct clinical
and pathological disorder. It has been described in older adults, often
presenting with rectal bleeding. Most of the patients seem to respond to
treatment only with a 5-aminosalicylate, but some spontaneously resolve with
no treatment. Endoscopic evaluation usually shows a non-specific
inflammatory process localized in the sigmoid colon alone that may resolve
completely with histologically normal colonic mucosa. Repeated symptomatic
events with discrete episodes of segmental colitis may occur, but most
patients have an entirely benign clinical course. Definition of the underlying
molecular events that occur with SCAD may be critically important in
understanding the critical elements present in a colonic inflammatory process
that can completely resolve without pharmacological or biological treatment.
2008 The WJG Press. All rights reserved.
Key words: Segmental colitis; Diverticulosis; Crohns disease; Natural
history; Ulcerative colitis; Colon cancer
Peer reviewer:
Freeman HJ. Segmental colitis associated with diverticulosis syndrome. World
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J Gastroenterol 2008; 14(42): 6442-6443
Available from: URL: http://www.wjgnet.com/1007-9327/14/6442.asp
DOI: http://dx.doi.org/10.3748/wjg.14.6442
11.4 UNSTRUCTURED ABSTRACT FORMAT FOR REVIEW
Ste20-related proline/alanine-rich kinase: A novel
regulator of intestinal inflammation
Yutao Yan, Didier Merlin
Yutao Yan, Didier Merlin, Department of Medicine, Division of Digestive
Diseases, Emory University School of Medicine, 615 Michael Street, Atlanta,
GA 30322, United States
Author contributions: Yan Y and Merlin D contributed equally to this work.
Correspondence to: Didier Merlin, PhD, Associate Professor, Emory
University Department of Medicine Division of Digestive Diseases 615 Michael
Street Atlanta GA 30322, United States. [email protected]
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Telephone: +01-404-7276454 Fax: +01-404-727-5767
Received: May 14, 2008 Revised: July 28, 2008
Accepted: August 3, 2008
Published online: October 28, 2008
Abstract (256 words)
Recently, inflammatory bowel disease (IBD) has been the subject of
considerable research, with increasing attention being paid to the loss of
intestinal epithelial cell barrier function as a mechanism of pathogenesis.
Ste20-related proline/alanine-rich kinase (SPAK) is involved in regulating
barrier function. SPAK is known to interact with inflammation-related kinases
(such as p38, JNK, NKCC1, PKC, WNK and MLCK), and with transcription
factor AP-1, resulting in diverse biological phenomena, including cell
differentiation, cell transformation and proliferation, cytoskeleton
rearrangement, and regulation of chloride transport. This review examines
the involvement of Ste20-like kinases and downstream mitogen-activated
protein kinases (MAPKs) pathways in the pathogenesis and control of
intestinal inflammation. The primary focus will be on the molecular features
of intestinal inflammation, with an emphasis on the interaction between SPAK
and other molecules, and the effect of these interactions on homeostatic
maintenance, cell volume regulation and increased cell permeability in
intestinal inflammation.
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2008 The WJG Press. All rights reserved.
Key words: Inflammatory bowel diseases; WNK; NKCC1; Barrier function;
Ste20-related proline/alanine-rich kinase
Peer reviewer:
Yan Y, Merlin D. Ste20-related proline/alanine-rich kinase: A novel regulator of
intestinal inflammation. World J Gastroenterol 2008; 14(40): 6115-6121Available from: URL: http://www.wjgnet.com/1007-9327/14/6115.asp
DOI: http://dx.doi.org/10.3748/wjg.14.6115
11.5 STRUCTURED ABSTRACT FORMAT FOR ORIGINAL
ARTICLES
Preventive effect of gelatinizedly-modified chitosan
film on peritoneal adhesion of different types
Xie-Lai Zhou, Shan-Wen Chen, Guo-Dong Liao, Zhou-Jun Shen, Zhi-Liang
Zhang, Li Sun, Yi-Jun Yu, Qiao-Ling Hu, Xiao-Dong Jin
Xie-Lai Zhou, Shan-Wen Chen, Guo-Dong Liao, Xiao-Dong Jin,
Department of Urology, The First Affiliated Hospital, College of Medicine,Zhejiang University, Hangzhou 310003, Zhejiang Province, China
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Zhou-Jun Shen, Department of Urology, Ruijin Hospital, School of Medicine,
Shanghai Jiao Tong University, Shanghai 200025, China
Xie-Lai Zhou, Zhi-Liang Zhang, Yi-Jun Yu, Surgical Department, Clinical
Medical College of Hangzhou Teachers College, Hangzhou 310036, Zhejiang
Province, China
Li Sun, Experimental Center of Medical Science, Hangzhou Teachers College,
Hangzhou 310036, Zhejiang Province, China
Qiao-Ling Hu, Institute of Polymer Composites, Zhejiang University,
Hangzhou 310027, Zhejiang Province, China
Author controbutions: The format of this section should be like this: Author
contributions: Zhou XL and Chen SW contributed equally to this work; Zhou
XL, Chen SW, Liao GD, Shen ZJ, Zhang ZL, Sun L, Yu YJ, Hu QL and Jin XD
designed research; Zhou XL, Chen SW, Liao GDand Yu YJ performed research;
Zhou XL and Chen SW contributed new reagents/analytic tools; Zhang ZL, Hu
QL and Jin XD analyzed data; and Zhou XL, Chen SW,and Jin XD wrote the
paper.
Supported by The National Natural Science Foundation of China, No.
50173023
Correspondence to: Xiao-Dong Jin, Professor, Department of Urology, The
First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou
310003, Zhejiang Province, China. [email protected]
Telephone: +86-571-87236833 Fax: +86-571-87236628
Received: Revised:
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Accepted: Published online:
Abstract ( 480 words)
AIM (no more than 20 words) : To comparatively study the preventive effect of
gelatinizedly-modified chitosan film on peritoneal adhesions induced by four
different factors in rats.
METHODS (no more than 140 words) : Chitosan was chemically modified by
gelatinization, and made into films of 60 m in thickness, and sterilized. Two
hundred Sprague-Dawley rats were randomly divided into five groups, Sham-
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operation group (group A), wound-induced adhesion group (group B), purified
talc-induced adhesion group (group C), vascular ligation-induced adhesion
group (group D), and infection-induced adhesion group (group E),
respectively. In each group, the rats were treated with different adhesion-
inducing methods at the cecum of vermiform processes and then were
divided into control and experimental subgroups. Serous membrane surface
of vermiform processes were covered with the films in the experimental
subgroups, and no films were used in the control subgroups. After 2 and 4 wk
of treatments, the abdominal cavities were reopened and the adhesive
severity was graded blindly according to Bhatias method. The cecum of vermiform processes were resected for hydroxyproline (OHP) measurement
and pathological examination.
RESULTS (no more than 294 words. You should present P value where necessary and
must provide relevant data to illustrate how it is obtained, e.g. 2 wk: 0.199 0.026 vs
0.285 0.041 g/mg pr, P < 0.001 ): Adhesion severity and OHP level: After 2 and
4 wk of the treatments, in the experimental subgroups, the adhesions were
significantly lighter and the OHP levels were significantly lower than those of
the control subgroups in group B (2 wk: 0.199 0.026 vs 0.285 0.041
g/mg pr, P < 0.001; 4 wk: 0.183 0.034 vs 0.276 0.03 g/mg pr, P