Abstract format for haligi

8/7/2019 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


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.


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


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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.

[email protected]

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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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.


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


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


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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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


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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mailto:[email protected]:[email protected]


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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

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Abstract format for haligi