Journal of Gastroenterology Impact Factor & Information

Publisher: Nihon Shōkakibyō Gakkai, Springer Verlag

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

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

Springer Verlag

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
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  • Conditions
    • Author's pre-print on pre-print servers such as
    • Author's post-print on author's personal website immediately
    • Author's post-print on any open access repository after 12 months after publication
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany link to published version (see policy)
    • Articles in some journals can be made Open Access on payment of additional charge
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: This nonsystematic review aims to describe recent developments in the use of functional lumen imaging in the gastrointestinal tract stimulated by the introduction of the functional lumen imaging probe. When ingested food in liquid and solid form is transported along the gastrointestinal tract, sphincters provide an important role in the flow and control of these contents. Inadequate function of sphincters is the basis of many gastrointestinal diseases. Despite this, traditional methods of sphincter diagnosis and measurement such as fluoroscopy, manometry, and the barostat are limited in what they can tell us. It has long been thought that measurement of sphincter function through resistance to distension is a better approach, now more commonly known as distensibility testing. The functional lumen imaging probe is the first medical measurement device that purports in a practical way to provide geometric profiling and measurement of distensibility in sphincters. With use of impedance planimetry, an axial series of cross-sectional areas and pressure in a catheter-mounted allantoid bag are used for the calculation of distensibility parameters. The technique has been trialed in many valvular areas of the gastrointestinal tract, including the upper esophageal sphincter, the esophagogastric junction, and the anorectal region. It has shown potential in the biomechanical assessment of sphincter function and characterization of swallowing disorders, gastroesophageal reflux disease, eosinophilic esophagitis, achalasia, and fecal incontinence. From this early work, the functional lumen imaging technique has the potential to contribute to a better and more physiological understanding of narrowing regions in the gastrointestinal tract in general and sphincters in particular.
    Journal of Gastroenterology 05/2015; DOI:10.1007/s00535-015-1087-7
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    ABSTRACT: Wisteria floribunda agglutinin positive Mac-2-binding protein (WFA(+)-M2BP) is a novel serum marker of liver fibrosis identified in glycoproteomic biomarker screening studies, and its clinicopathological characteristics have yet to be elucidated sufficiently for clinical utilization. We retrospectively analyzed the clinicopathology data and serum WFA(+)-M2BP levels in 376 hepatocellular carcinoma patients undergoing liver surgery. WFA(+)-M2BP was quantified in frozen serum samples collected at the time of surgery using the FastLec-Hepa method. Significant independent determinants of serum WFA(+)-M2BP levels included pathological diagnosis of cirrhosis, female gender, hepatitis C virus (HCV) infection, and liver dysfunction characteristics, such as abnormal indocyanine green retention rate at 15 min, platelet counts, albumin levels, alanine aminotransferase levels, and total bilirubin levels. Serum WFA(+)-M2BP levels increased with the pathological fibrosis stage and liver dysfunction severity. HCV infection significantly affected serum WFA(+)-M2BP levels throughout the pathological and functional progression of liver fibrosis, and the effect of gender was significant only in F4 stage patients with severe liver dysfunction. The diagnostic thresholds for cutoff index values for cirrhosis were 1.435 and 4.615 in HCV-negative and HCV-positive patients, respectively. Serum WFA(+)-M2BP levels at the time of operation were a significant predictor of hepatocellular carcinoma recurrence and overall survival in both HCV-negative and HCV-positive patients. Serum WFA(+)-M2BP levels reflected both the pathological and functional progression of liver fibrosis comprehensively and continuously. Elevated WFA(+)-M2BP levels were a significant risk factor for tumor recurrence and decreased overall survival after liver surgery independent of HCV infection.
    Journal of Gastroenterology 03/2015; DOI:10.1007/s00535-015-1063-2
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    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; 50(5). DOI:10.1007/s00535-015-1061-4
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    ABSTRACT: Genome-wide association studies have revealed several single-nucleotide polymorphisms around interleukin 28B (IL28B) that are strongly associated with hepatitis C virus (HCV) clearance. However, their predictive value is not perfect, which suggests that other genetic factors may also be involved in HCV clearance. We previously reported a wide variation in the length of a thymine-adenine (TA) dinucleotide repeat in the promoter region of IL28B and that the transcriptional activity of the promoter increased gradually in a TA repeat length-dependent manner. We determined the length of the TA repeats of 1,060 Japanese and 201 African-American samples to investigate the relation to spontaneous HCV clearance. The distribution of the TA repeats greatly differed between the two ethnicities. The variation ranged from 10 to 18 repeats, and the most frequent allele, 12, accounted for over 80 % for Japanese. The African-American data showed a gently sloping distribution, and the allele with six repeats was detected only in the African-American sample. The TA repeats 11 or greater were correlated with spontaneous clearance. Multiple logistic regression analysis extracted the genotype of the TA repeats as an independent factor in both the Japanese [p = 0.0004, odds ratio (OR) = 13.02 95 % confidence interval (CI) = 2.59-237.0] and African-American (p = 0.027, OR = 3.70 95 % CI = 1.16-11.8) populations. A long TA repeat in the promoter region of IL28B was associated with spontaneous HCV clearance. Although its efficacy may be limited in Japanese population because of its allele distribution, this novel genetic factor will be useful for predicting HCV clearance especially for the African Americans.
    Journal of Gastroenterology 03/2015; DOI:10.1007/s00535-015-1056-1
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    ABSTRACT: We recently demonstrated in humans that the extent of low-dose aspirin (LDA)-induced gastropathy was directly related to the individual gastric acid secretion level. We also established reliable cutoff serum pepsinogen (PG) values to predict gastric acid secretion status. In this study, we investigated the clinical usefulness of measuring the serum pepsinogen values for identifying a high-risk group for gastric mucosal injury among chronic LDA users. One hundred long-term LDA users were enrolled in this analysis. Serum from each subject was subjected to determination of H. pylori status and measurement of pepsinogen values. According to our recent report, a PG I value a parts per thousand yen 50 ng/mL was defined as estimated hyperchlorhydria in H. pylori-negative subjects, while a PG I/II a parts per thousand yen 3.3 was defined as estimated hyperchlorhydria in H. pylori-positive subjects. The grade of gastric mucosal injury was assessed endoscopically, and multiple logistic regression analyses were used to estimate the risk. Estimated hyperchlorhydria was a strong independent risk for intensive gastric mucosal injury with an OR (95 % CI): 34.0 (4.5-259) and for gastric ulcer with an OR (95 % CI): 10.2 (1.8-58.3) in H. pylori-positive subjects, while it was not a significant risk in H. pylori-negative subjects. The association persisted even after excluding those with conventional risks for LDA-gastropathy such as ulcer histories. Using simple serum measurement of H. pylori antibody and pepsinogen concentrations, an extremely high-risk group for LDA-induced gastropathy could be extracted, and these patients should become a therapeutic target for prevention of LDA-induced gastropathy.
    Journal of Gastroenterology 03/2015; 50(3):305-312. DOI:10.1007/s00535-014-0976-5
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    ABSTRACT: In this study we examined whether histopathological findings, specifically lymphatic vessel invasion identified by an anti-human podoplanin antibody, and several other factors are associated with lymph node metastasis in T1 colorectal cancer. We searched PubMed and Cochrane Library, and also handsearched relevant journals, for reports written in English and published between 1998 and 2012, utilizing combination headings, such as 'colorectal cancer,' 'lymph node metastasis,' and 'risk factors.' For the report to be included in our study, the following criteria had to be met: (1) data on the frequency of lymph node metastasis in T1 colorectal cancer in relation to histopathological factors were reported; (2) patients had undergone bowel resection and had histologically diagnosed T1 colorectal cancer; (3) lymphatic vessel invasion was identified by immunohistochemistry with an anti-human podoplanin antibody rather than by hematoxylin and eosin staining; (4) univariate and multivariate analyses were conducted. Studies investigating molecular markers were excluded. The independent predictive factors were confirmed in at least one study included in the meta-analysis in the present systematic review. Microsoft Excel 2013 for Windows was used for the statistical analysis. Initially, 369 publications were identified in the database searches and handsearches, of which five ultimately met all of the inclusion criteria and selected for this systematic review. The meta-analysis revealed that only two factors were significantly associated with T1 colorectal cancer lymph node metastasis: (1) lymphatic vessel invasion identified by an anti-human podoplanin antibody [Mantel-Haenszel odds ratio (OR) 5.19; (95 % confidence interval (CI) 3.31-8.15; P = 0.01]; (2) tumor budding (OR 7.45; 95 % CI 4.27-13.02; P = 0.0077). Our meta-analysis revealed that lymphatic vessel invasion identified by an anti-human podoplanin antibody and tumor budding were significantly associated with T1 colorectal cancer lymph node metastasis.
    Journal of Gastroenterology 03/2015; DOI:10.1007/s00535-015-1057-0
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    ABSTRACT: Sustained liver injury causes liver fibrosis and eventually cirrhosis. Understanding the pathophysiological mechanisms of liver fibrosis and interventions in the fibrotic process is crucial for improving the prognosis of patients with chronic liver diseases. Although studies have shown that splenectomy suppresses liver fibrosis, the mechanism by which this occurs is poorly understood. The present study focuses on the immunological functions of the spleen to investigate its role in liver fibrosis. BALB/c and severe combined immunodeficiency (SCID) mice underwent splenectomies or sham operations prior to induction of liver fibrosis with carbon tetrachloride or thioacetamide. Sirius red staining and hydroxyproline assays showed that splenectomy suppressed liver fibrogenesis in BALB/c mice. Reverse transcription PCR analysis of T helper type 1 (Th1) and T helper type 2 (Th2) cytokines demonstrated that splenectomy shifted the Th1/Th2 balance in the liver towards Th1 dominance. In SCID mice, the inhibitory effect on liver fibrosis was abrogated. The number of CD4(+) T helper lymphocytes in the spleen decreased after liver injury. Green fluorescent protein positive (GFP(+)) splenocytes were transplanted into the spleens of syngeneic wild-type mice to trace their destination after fibrosis induction. GFP(+)CD4(+) lymphocytes appeared in the liver after induction of fibrosis, and flow cytometry revealed the vast majority of them were Th2 lymphocytes. Transfer of splenocytes via the portal vein into syngeneic splenectomized mice cancelled the suppressive effect of splenectomy on liver fibrosis. The present study demonstrated that Th2-dominant splenic lymphocytes migrate into the liver and promote liver fibrosis by shifting the cytokine balance towards Th2 dominance. Splenectomy suppresses the progression of fibrosis at least partly by restoring the Th1/Th2 balance.
    Journal of Gastroenterology 02/2015; DOI:10.1007/s00535-015-1054-3
  • Journal of Gastroenterology 02/2015; 50(4). 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, non-alcoholic 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 non-invasive 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 through 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. © 2015 The Japan Society of Hepatology.
    Journal of Gastroenterology 02/2015; 45(4). DOI:10.1007/s00535-015-1050-7
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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; 50(3). 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: 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: 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