Journal of Gastroenterology (J GASTROENTEROL)

Publisher: Nihon Shōkakibyō Gakkai

Journal description

The Journal of Gastroenterology which is the official publication of the Japanese Society of Gastroenterology publishes original papers case reports reports of multi-center trials review articles short and rapid communications and other articles on all aspects of the field of gastroenterology. Significant contributions relating to basic research theory and practice are welcomed. This publication is designed to disseminate knowledge in this field to a worldwide audience and accordingly its editorial board has an international membership.

Current impact factor: 4.02

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 4.02
2012 Impact Factor 3.788
2011 Impact Factor 4.16
2010 Impact Factor 3.61
2009 Impact Factor 2.909
2008 Impact Factor 3.117
2007 Impact Factor 2.052
2006 Impact Factor 1.927
2005 Impact Factor 1.532
2004 Impact Factor 1.209
2003 Impact Factor 1.179
2002 Impact Factor 1.504
2001 Impact Factor 1.199
2000 Impact Factor 0.99
1999 Impact Factor 0.819
1998 Impact Factor 0.796
1997 Impact Factor 0.466
1996 Impact Factor 0.484
1995 Impact Factor 0.287

Impact factor over time

Impact factor
Year

Additional details

5-year impact 3.69
Cited half-life 5.40
Immediacy index 0.68
Eigenfactor 0.01
Article influence 1.05
Website Journal of Gastroenterology website
Other titles Journal of gastroenterology (Online)
ISSN 0944-1174
OCLC 43041933
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: The efficacy and safety of pharmacotherapies are determined by the complex processes involved in the interactions between drugs with the human body, including pharmacokinetic aspects. Among pharmacokinetic factors, it has been recognized that drug transporters play critical roles for absorption, distribution and excretion of drugs, regulating the membrane transport of drugs. The vast amounts of information on drug transporters collected in the past 20 years have been organized according to biochemical, molecular, genetic, and clinical analyses. Novel technologies, public databases, and regulatory guidelines have advanced the use of such information in drug development and clinical practice. In this review, we selected some clinically important drug transporters expressed in the intestine and liver, and introduced the research history and current knowledge of their pharmacokinetic, pathophysiological, and pharmacogenetic implications.
    Journal of Gastroenterology 03/2015; DOI:10.1007/s00535-015-1061-4
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    ABSTRACT: Fatty liver is an important clinical feature not only in alcoholic and non-alcoholic fatty liver diseases, but in other chronic liver diseases as well. Our aim was to elucidate the effect and relationship between habitual alcohol intake and obesity in the development of fatty liver disease. We enrolled 8,029 subjects undergoing abdominal ultrasonography with general medical examinations, and analyzed the factors associated with fatty liver based on daily alcohol intake, body mass index (BMI), and waist circumference. For fatty liver, BMI, waist circumference, total cholesterol, triglycerides, and fasting plasma glucose were significant and independent risk factors. Heavy alcohol intake (50 g/day) was a significant risk factor for fatty liver in women (odds ratio [OR], 3.35). Analysis based on the presence or absence of obesity revealed that moderate alcohol intake was a significant negative risk factor for fatty liver in both male and female obese (BMI ≥25 kg/m(2)) subjects (OR, 0.74 for non-obese and 0.39 for obese patients, respectively). Heavy alcohol intake was also a significant negative risk factor in obese males (0.62). In contrast, heavy alcohol intake was a risk factor in non-obese males (OR, 1.29) and in all females (OR, 2.22 for non-obese and 6.6 for obese patients, respectively). The influence of alcohol intake on fatty liver differed depending on the level of alcohol consumption, gender, and the presence of obesity, and showed biphasic effects.
    Journal of Gastroenterology 03/2015; DOI:10.1007/s00535-015-1058-z
  • Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1045-4
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    ABSTRACT: Nonalcoholic fatty liver disease (NAFLD) is currently the most common cause of chronic liver disease in industrialized countries worldwide, and has become a serious public health issue not only in Western countries but also in many Asian countries including Japan. Within the wide spectrum of NAFLD, nonalcoholic steatohepatitis (NASH) is a progressive form of disease, which often develops into liver cirrhosis and increases the risk of hepatocellular carcinoma. In turn, a large proportion of NAFLD/NASH is the liver manifestation of metabolic syndrome, suggesting that NAFLD/NASH plays a key role in the pathogenesis of systemic atherosclerotic diseases. Currently, a definite diagnosis of NASH requires liver biopsy, though various noninvasive measures are under development. The mainstays of prevention and treatment of NAFLD/NASH include dietary restriction and exercise; however, pharmacological approaches are often necessary. Currently, vitamin E and thiazolidinedione derivatives are the most evidence-based therapeutic options, although the clinical evidence for long-term efficacy and safety is limited. This practice guideline for NAFLD/NASH, established by the Japanese Society of Gastroenterology in cooperation with The Japan Society of Hepatology, covers lines of clinical evidence reported internationally in the period starting from 1983 to January 2012, and each clinical question was evaluated using the GRADE system. Based on the primary release of the full version in Japanese, this English summary provides the core essentials of this clinical practice guideline comprising the definition, diagnosis, and current therapeutic recommendations for NAFLD/NASH in Japan.
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1050-7
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    ABSTRACT: Bile acids are the end product of cholesterol metabolism. Synthesized in the liver, primary bile acids are secreted by hepatocytes and are transformed by intestinal microbiota into secondary bile acids. In addition to their role in cholesterol and lipid absorption, bile acids act as signaling molecules activating a family of nuclear and G-protein-coupled receptors collectively known as bile acid activated receptors (BARs). These receptors are expressed at high density in enterohepatic tissues, but their expression occurs throughout the body and their activation mediates regulatory functions of bile acids on lipids and glucose metabolism and immunity. In the gastrointestinal tract, BARs maintain intestinal integrity, and their deletion makes the intestine more susceptible to the damage caused by acetylsalicylic acid and nonsteroidal anti-inflammatory drugs (NSAIDs). Deficiency in farnesoid X receptor and G-protein-coupled bile acid receptor 1 genes alters the expression/activity of cystathione γ-lyase and endothelial nitric oxide synthase, two genes involved in the synthesis of hydrogen sulfide and nitric oxide, i.e., two gaseous mediators that have been shown to be essential in maintaining the intestinal homeostasis. In addition, farnesoid X receptor regulates the expression of transporters required for secretion of phospholipid by hepatocytes. Because phospholids attenuate intestinal injury caused by acetylsalicylic acid and NSAIDs, BAR agonism could be exploited to protect the intestinal mucosa against injury caused by anti-inflammatory medications. This approach might be useful in the prevention of so-called NSAID enteropathy, a common clinical condition occurring in long-term users of NSAIDs, which is not effectively prevented either by cotreatment with proton pump inhibitors or by the use of coxibs.
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1041-8
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    ABSTRACT: The levels of serum HER2 extracellular domain (ECD) are highly correlated with tissue HER2 status in metastatic gastric cancer (AGC). We sought to explore whether serum HER2 ECD could predict the efficacy of trastuzumab-treated HER2-positive AGC. From 2011 to 2013, trastuzumab-treated AGC patients were enrolled. Serum HER2 ECD was centrally measured by chemiluminescence immunoassays (CLIA) method in available samples at baseline and after two cycles of trastuzumab combined with chemotherapy. The correlation between serum HER2 ECD and overall response rate (ORR) and progression-free survival (PFS) was analyzed. Sixty-five patients were analyzed with a median age of 58 years (range, 27-80 years). A significant difference of serum HER2 ECD levels was found between patients with HER2 IHC 3+ and those with HER2 IHC 2+ and FISH positive (p = 0.014). There was a significantly better ORR (80.00 vs. 50.00 %, p = 0.017) and PFS (median PFS, 268 vs. 139 days, p = 0.039) for patients with abnormal baseline serum HER2 ECD than for patients with normal serum HER2 ECD. Change in serum HER2 ECD during chemotherapy was significantly correlated with response to chemotherapy (79.17 vs. 51.52 %, p = 0.033) and PFS (median PFS, 303 vs. 147 days, p = 0.005) in patients with HER2-positive tumor tissue. Our results support the clinical utility of measuring serum HER2 ECD levels in patients with advanced gastric cancer. Baseline and early changes in serum HER2 ECD could be useful for monitoring clinical outcome in HER2-positive AGC patients receiving trastuzumab-combined chemotherapy.
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1046-3
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    ABSTRACT: We investigated the effects of proton-pump inhibitors (PPIs) on lower gastrointestinal bleeding (LGIB) and of their interactions with nonsteroidal anti-inflammatory drugs (NSAIDs), low-dose aspirin, clopidogrel, and warfarin on LGIB risk. We prospectively studied 355 patients emergently hospitalized for LGIB and 8,221 nonbleeding patients. All patients underwent colonoscopy. Smoking, alcohol drinking, drug exposure, and the Charlson comorbidity index score were assessed before colonoscopy. Adjusted odds ratios (AOR) of LGIB were estimated. LGIB was significantly associated with older age, higher comorbidity index, and NSAID, aspirin, clopidogrel, or warfarin use. PPI use was significantly associated with older age, male sex, being a current alcohol drinker, higher comorbidity index, and NSAID, aspirin, clopidogrel, warfarin, acetaminophen, or corticosteroid use. Multivariate analysis adjusted by the confounding factors revealed LGIB was not significantly associated with PPI use (AOR 0.87; 95 % confidence interval 0.68-1.13; p = 0.311), or specifically with omeprazole (AOR 1.18; p = 0.408), esomeprazole (AOR 0.76; p = 0.432), lansoprazole (AOR 0.93; p = 0.669), or rabeprazole (AOR 0.63; p = 0.140). In the interaction model, no significant interactions were observed between PPIs and NSAIDs (AOR 1.40; p = 0.293), aspirin (AOR 1.09; p = 0.767), clopidogrel (AOR 0.99, p = 0.985), or warfarin (AOR 1.52; p = 0.398). This large case-control study demonstrated that PPI use did not lead to an increased risk of LGIB, regardless of the type of PPI used. Further, LGIB risk was not affected by PPI use, irrespective of concomitant therapy with NSAIDs, low-dose aspirin, clopidogrel, or warfarin.
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1055-2
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    ABSTRACT: It is a great honor to pen few words for the recent dramatic evolution of the Journal of Gastroenterology (JG). JG is the official journal of the Japanese Society of Gastroenterology (JSGE). It was launched in 1966 as Gastroenterologia Japonica, and then the journal name was changed to Journal of Gastroenterology in 1994, and has completed 50 years of publication in 2015.Only 10 years ago, no one could have imagined the current situation of JG. When I joined in the editorial team of JG in 2003, the journal had approximately 350 manuscript submissions per year. It was substantially a Japanese journal with 80 % of the submitted manuscripts and 90 % of the accepted manuscripts coming from Japanese gastroenterologists. Very few foreign researchers even know the name of the journal. I would like to let you know indispensable decisions and efforts of former Presidents of the JSGE, Editorial Directors, Editor-in-Chief, Deputy Editor-in-Chief, associate editors and editorial stuffs of JG to ma ...
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1047-2
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    ABSTRACT: Epidemiological studies have indicated that patients with chronic Helicobacter pylori infection have an increased risk of developing type 2 diabetes mellitus, but the underlying mechanisms remain largely unknown. This study aimed to investigate whether H. pylori infection contributes to the development of insulin resistance, as well as the underlying mechanisms both in vivo and in vitro. The effect of H. pylori infection on glucose metabolism was evaluated in humans and mouse models. The role of the c-Jun/miR-203/suppressor of cytokine signaling 3 (SOCS3) pathway in H. pylori-induced insulin resistance was determined in vitro and was validated in vivo. Average fasting glucose levels were increased in patients (P = 0.012) and mice (P = 0.004) with H. pylori infection. Diabetic mice with H. pylori infection showed impaired glucose metabolism and insulin tolerance and hyperinsulinemia. Furthermore, H. pylori infection impaired insulin signaling in primary hepatocytes. H. pylori infection could upregulate SOCS3, a well-known insulin signaling inhibitor, by downregulating miR-203. SOCS3 overexpression interfered with insulin signaling proteins, and knockdown of SOCS3 alleviated H. pylori-induced impairment of insulin signaling. The transcription factor c-Jun, which affects gene expression, was induced by H. pylori infection and suppressed miR-203 expression. Our results demonstrated that H. pylori infection induced hepatic insulin resistance by the c-Jun/miR-203/SOCS3 signaling pathway and provide possible implications with regard to resolving insulin resistance.
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1051-6
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    ABSTRACT: The "resect and discard" strategy is beneficial for cost savings on screening and surveillance colonoscopy, but it has the risk to discard lesions with advanced histology or small invasive cancer (small advanced lesion; SALs). The aim of this study was to prove the principle of new "resect and discard" strategy with consideration for SALs using magnifying narrow-band imaging (M-NBI). Patients undergoing colonoscopy at a tertiary center were involved in this prospective trial. For each detected polyp <10 mm, optical diagnosis (OD) and virtual management ("leave in situ", "discard" or "send for pathology") were independently made using non-magnifying NBI (N-NBI) and M-NBI, and next surveillance interval were predicted. Histological and optical diagnosis results of all polyps were compared. While the management could be decided in 82 % of polyps smaller than 10 mm, 24/31 (77 %) SALs including two small invasive cancers were not discarded based on OD using M-NBI. The sensitivity [90 % confidence interval (CI)] of M-NBI for SALs was 0.77 (0.61-0.89). The risk for discarding SALs using N-NBI was significantly higher than that using M-NBI (53 vs. 23 %, p = 0.02). The diagnostic accuracy (95 % CI) of M-NBI in distinguishing neoplastic from non-neoplastic lesions [0.88 (0.86-0.90)] was significantly better than that of N-NBI [0.84 (0.82-0.87)] (p = 0.005). The results of our study indicated that our "resect and discard" strategy using M-NBI could work to reduce the risk for discarding SALs including small invasive cancer (UMIN-CTR, UMIN000003740).
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1048-1
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    ABSTRACT: Patients with hypoalbuminemia often fail to respond to increased doses of loop diuretics. We therefore performed a post hoc analysis to investigate the pharmacological action of tolvaptan and whether it is dependent on the serum albumin level. This analysis was based on four previous clinical trials of tolvaptan in patients with liver cirrhosis who exhibited insufficient response to conventional diuretics. We analyzed the correlation between the change in the initial 24-h cumulative urine volume from baseline and the serum albumin level at baseline, and assessed potential predictive factors of response to tolvaptan. The correlation coefficient was 0.029 in the placebo group and -0.112 in the 7.5 mg tolvaptan group of patients with liver cirrhosis. Administration of tolvaptan provoked a stable response regardless of the serum albumin level. Tolvaptan use was identified as a significant predictor of pharmacological action, and was shown to change the initial urine volume by 885 mL (P < 0.0001) in liver cirrhosis patients. In this post hoc analysis, tolvaptan increased the initial urine volume from baseline regardless of serum albumin levels. Use of tolvaptan as an add-on therapy to loop diuretics can be considered an optimal therapeutic option in patients with insufficient response to loop diuretics.
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1052-5
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    ABSTRACT: This research was conducted is to assess the effect of booster doses of the trivalent influenza vaccine in adult inflammatory bowel disease (IBD) patients treated with anti-tumor necrosis factor (TNF)-α agents and/or immunomodulators. Adult IBD patients and healthy individuals were subcutaneously administered the trivalent influenza vaccine. They were randomized into two groups: the single vaccination group and the two vaccination booster group. Blood samples were collected, and the antibody titers against each influenza strain were determined by hemagglutination inhibition at 3 different time points (pre-vaccination, 3 weeks post-vaccination, and after the flu season) in the single vaccination group and at 4 time points (pre-vaccination, 3 weeks post-first vaccination, 3 weeks post-second vaccination, and after the flu season) in the booster vaccination group. Seventy-eight IBD patients and 11 healthy controls were randomized into the single vaccination group and the booster vaccination group. Twenty-nine patients received immunomodulators; 21 received anti-TNF-α agents; and 28 received a combination of both. No significant differences were observed in the evaluated immune response parameters between 3 weeks post-vaccination in the single vaccination group and 3 weeks post-second vaccination in the booster vaccination group (geometric mean titers: H1N1, p = 0.09; H3N2: p = 0.99; B: p = 0.94). A higher pre-vaccination titer was significantly associated with sufficient seroprotection rate after vaccination for the H1N1 strain (odds ratio 11.93, p = 0.03). The second booster of trivalent influenza vaccination did not improve the immune response in adult IBD patients who were treated with immunomodulators and/or anti-TNF-α agents.
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1042-7
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    ABSTRACT: The letter to the editor by Carol Brotherton raises the question of the interaction among insoluble fiber (specifically cellulose and wheat bran), the microbiome, and human disease. We agree that this is an interesting and poorly understood area worthy of review and appreciate her comments. However, the author of the letter misstates components of our review, as well the literature she cites.Our only mention of insoluble fiber is the definition of fermentable carbohydrates that can produce short-chain fatty acids (SCFAs) (emphasis added):Fermentable carbohydrates include pectins, hemicelluloses, gums, and prebiotic substances including fructose and galactose-oligosaccharides that are not responsive to mammalian enzymes, but not what we typically think of as dietary fiber, such as cellulose or wheat bran [1].We do not believe, as the letter writer states, that there is a misconception that wheat bran and cellulose “are not fermentable carbohydrates,” as in general, human microbial comm ...
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1044-5
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    ABSTRACT: Goldsmith and Sartor [1] recently published in your journal an original paper entitled “The role of diet on intestinal microbiota metabolism: downstream impacts on host immune function and health, and therapeutic implications.” The authors reviewed the current knowledge of potential diet and gut microbiota-mediated pathophysiology. Most interestingly, they reported evidence that short-term diet manipulation has little effect on microbial composition, but very rapidly shifts microbial gene expression in mice.I write to suggest publication of a comprehensive review of cellulose and wheat bran mechanisms related to microbiota metabolism. The authors repeated a growing misconception [2] by stating that these two insoluble fibers are not fermentable carbohydrates—further obscuring the benefits of insoluble fiber. In 1984, Denis Burkitt [3] described a lack of cereal fibers as “predominantly incriminated” in the prevalence of gastrointestinal diseases associated with Western diets, and ensui ...
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1043-6
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    ABSTRACT: Milk fat globule-epidermal growth factor 8 (MFG-E8) promotes phagocytic clearance of apoptotic cells to maintain normal tissue homeostasis. However, its functions in intestinal inflammation and carcinogenesis are unknown. Experimental colitis was induced in MFG-E8 knockout (KO) and wild-type (WT) mice by dextran sodium sulfate (DSS) administration. Colon tissues were used for assessments of colitis activity and epithelial proliferation. A mouse colitis-associated cancer (CAC) model was induced by intraperitoneal injection of azoxymethane (AOM) and then the animals were given a single administration of DSS. A sporadic colon cancer model was established by repeated intraperitoneal injections of AOM. The role of MFG-E8 in epithelial proliferation with or without treatment of siRNA targeting αv-integrin was examined in vitro using a WST-1 assay. The severity of colitis in KO mice was greater than that in WT mice, while the proliferative potential of colonic epithelial cells in KO mice was lower during the regenerative phase. In both CAC and sporadic models, tumor size in KO was lower as compared to WT mice, while decreased tumor incidence was only found in the CAC model. In vitro findings showed that MFG-E8 promotes epithelial cell proliferation, and treatment with a siRNA targeting αv-integrin reduced the proliferation of Colon-26 cells stimulated with recombinant MFG-E8. MFG-E8 promotes tumor growth regardless of the presence or absence of colonic inflammation, whereas colon tumor development is initiated by MFG-E8 under inflammatory conditions. These MFG-E8 functions may be dependent on integrin-mediated cellular signaling.
    Journal of Gastroenterology 01/2015; DOI:10.1007/s00535-014-1036-x
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    ABSTRACT: Low-dose aspirin, alone or combined with other antiplatelet agents, is increasingly prescribed for cardiovascular prevention. However, the cardiovascular benefits should be evaluated together with the gastrointestinal risks. Low-dose aspirin is associated with upper and lower gastrointestinal injury, although lower gastrointestinal effects are poorly characterized. This gastrointestinal risk differs among antiplatelets drugs users. The most important risk factors are history of peptic ulcer, older age, and concomitant use of non-steroidal anti-inflammatory drugs or dual antiplatelet therapy. Effective upper gastrointestinal prevention strategies are available and should be used in at-risk patients taking low-dose aspirin or clopidogrel. Proton pump inhibitors seem to be the best gastroprotective agents, whereas the benefits of Helicobacter pylori eradication are still unclear. Low-dose aspirin has additional effects in the gastrointestinal tract. A large body of evidence indicates that it can protect against different cancers, in particular colorectal cancer. This effect could modify the future indications for use of low-dose aspirin and the risk-benefit balance.
    Journal of Gastroenterology 01/2015; DOI:10.1007/s00535-015-1038-3