All non-steroidal anti-inflammatory drugs (NSAIDs), such as ibuprofen, diclofenac, and naproxen, now carry a black box label from the US Food and Drug Administration (FDA) because of their association with increased risk of heart attack. NSAIDs do vary in the amount of risk to the heart, with naproxen

the safest. Other NSAIDs vary in their heart risk, mostly seen in those who use them frequently. Using NSAIDs not more than 2 days a week is generally safe in most individuals who have never had a heart attack. Other acute, as-needed medications that may help CX-4945 dial down the migraine pain without causing blood vessel narrowing include metoclopramide, prochloperazine, diphenhydramine, baclofen, acetaminophen, and gabapentin. Trigger point injections and nerve blocks may also be used. Migraine preventive strategies become very important LY2109761 in individuals with vascular

disease and migraine, as acute treatment options are limited. Topiramate, venlafaxine, and blood pressure medications such as propranolol and candesartan, as well as onabotulinumtoxinA, can be highly effective in decreasing both the intensity and frequency of migraine. In summary, the link of cardiovascular disease and peripheral artery disease with migraine may be present, but it is difficult to separate out from other risk factors often present at the same time such as smoking, diabetes, uncontrolled blood pressure, and other common vascular risks. The presence of coronary artery disease or peripheral vascular disease limits the

use of certain acute and preventive migraine treatments. All medicines that cause artery narrowing should be avoided in the presence of cardiovascular or peripheral vascular disease, but there remain multiple effective treatments to reduce migraine pain and frequency. To find more resources, please visit the American Migraine Foundation (http://kaywa.me/ir2eb) “
“This chapter features an approach to both headache classification and diagnosis. The history of headache classification and the current classification system for headache disorders are first described, Isotretinoin followed by an overview on the approach to the evaluation of a patient with recurrent or daily headache. Then, an outline of a 3 step diagnostic process is presented. First, we emphasize the identification or exclusion of secondary headache disorders by history, physical examination and judicious use of diagnostic tests. Second, 4 groups of primary headache disorders defined based on headache frequency and duration are delineated, and referred to as primary headache syndromes. Finally, the identification of specific disorders within syndromic groups is discussed. “
“A 13-year-old previously healthy female presented at our institution following an acute episode of altered mental status characterized by impairment of speech, urinary incontinence, and emesis.

pylori eradication. “
“Rifabutin has been known to be effective in multidrug-resistant Helicobacter pylori-harboring patients undergoing treatment failure for H. pylori infection. To evaluate the efficacy of 7-day treatment regimen consisting rifabutin daily but increasing the dose of amoxicillin and lansoprazole in patients who have failed first and second eradication and to assess the side effect profiles in South Korea. From December 2007 to May 2013, 59 H. pylori-infected patients with two previous eradication

failures were enrolled for this study prospectively. The eligible patients were randomly assigned to either group A or B. Group A received lansoprazole 30 mg bid, amoxicillin 1.0 g tid and rifabutin 150 mg bid during 7 days, whereas group B received

lansoprazole 60 mg bid, amoxicillin AZD1152-HQPA datasheet 1.0 g tid and rifabutin 150 mg bid during 7 days. In group A, H. pylori eradication was achieved in 25 (78.1%) of the 32 patients in the ITT analysis and in 25 (80.6%) of the 31 patients in the PP analysis. In group B, H. pylori eradication was achieved in 26 (96.3%) of the 27 patients in the ITT analysis and in 27 (100%) of the 26 patients in the PP analysis. There was statistically significant difference between the two groups in terms of the eradication rates in PP analysis (p = .047), whereas a marginally statistical significance was found in terms of the eradication rates in ITT analysis (p = .051). Reported side effects were mild, and treatment was well tolerated. No major changes

in physical examination or in standard laboratory EGFR cancer parameters were observed after treatment. Rifabutin-based high-dose proton-pump inhibitor (PPI)-combined therapy as empirical rescue treatment is more effective than standard dose PPI-combined rifabutin-based therapy, safe and best tolerable in third-line therapy in the Korean population. The key to successful rescue therapy with rifabutin–amoxicillin–PPI regimen may be to increase doses of PPI. “
“Over the Urease last decades, it has become evident that chronic infection by Helicobacter pylori is achieved by colonizing an almost exclusive niche and hiding from many of the host’s cellular immune defense mechanisms. Although recent years have seen progress in our understanding of the innate and adaptive immune response against H. pylori, it is still uncertain how to promote the development of immunity with the final goal of a successful vaccine. Research published in the last year revealed an intriguing mutual regulation of innate response mechanisms of mucosal epithelial cells by the host and H. pylori, respectively. A further focus was put on the interaction between H. pylori and dendritic cells, with some emphasis on the inflammasome and the resulting T-cell responses. Moreover, the function of microRNAs in macrophages and gastric MALT lymphoma development has been studied in more detail. Several novel antigens and adjuvants have been tested as vaccination strategies, primarily in mice.

pylori eradication. “
“Rifabutin has been known to be effective in multidrug-resistant Helicobacter pylori-harboring patients undergoing treatment failure for H. pylori infection. To evaluate the efficacy of 7-day treatment regimen consisting rifabutin daily but increasing the dose of amoxicillin and lansoprazole in patients who have failed first and second eradication and to assess the side effect profiles in South Korea. From December 2007 to May 2013, 59 H. pylori-infected patients with two previous eradication

failures were enrolled for this study prospectively. The eligible patients were randomly assigned to either group A or B. Group A received lansoprazole 30 mg bid, amoxicillin 1.0 g tid and rifabutin 150 mg bid during 7 days, whereas group B received

lansoprazole 60 mg bid, amoxicillin STAT inhibitor 1.0 g tid and rifabutin 150 mg bid during 7 days. In group A, H. pylori eradication was achieved in 25 (78.1%) of the 32 patients in the ITT analysis and in 25 (80.6%) of the 31 patients in the PP analysis. In group B, H. pylori eradication was achieved in 26 (96.3%) of the 27 patients in the ITT analysis and in 27 (100%) of the 26 patients in the PP analysis. There was statistically significant difference between the two groups in terms of the eradication rates in PP analysis (p = .047), whereas a marginally statistical significance was found in terms of the eradication rates in ITT analysis (p = .051). Reported side effects were mild, and treatment was well tolerated. No major changes

in physical examination or in standard laboratory SAHA HDAC clinical trial parameters were observed after treatment. Rifabutin-based high-dose proton-pump inhibitor (PPI)-combined therapy as empirical rescue treatment is more effective than standard dose PPI-combined rifabutin-based therapy, safe and best tolerable in third-line therapy in the Korean population. The key to successful rescue therapy with rifabutin–amoxicillin–PPI regimen may be to increase doses of PPI. “
“Over the Etofibrate last decades, it has become evident that chronic infection by Helicobacter pylori is achieved by colonizing an almost exclusive niche and hiding from many of the host’s cellular immune defense mechanisms. Although recent years have seen progress in our understanding of the innate and adaptive immune response against H. pylori, it is still uncertain how to promote the development of immunity with the final goal of a successful vaccine. Research published in the last year revealed an intriguing mutual regulation of innate response mechanisms of mucosal epithelial cells by the host and H. pylori, respectively. A further focus was put on the interaction between H. pylori and dendritic cells, with some emphasis on the inflammasome and the resulting T-cell responses. Moreover, the function of microRNAs in macrophages and gastric MALT lymphoma development has been studied in more detail. Several novel antigens and adjuvants have been tested as vaccination strategies, primarily in mice.

For RT-PCR, 1 μg of total RNA, M-MLV RTase

(ReverTra Ace, Toyobo, Tokyo, selleckchem Japan) and oligo-dT primers were used. Polymerase chain reaction (PCR) amplification was performed using DNA polymerase (Takara EX Taq, Takara, Tokyo, Japan) and specific primers for human mRNA sequences (Table 1). The glyceraldehyde 3-phosphate dehydrogenase mRNA was used as a housekeeping gene. Following After PCR, an annealing of primers for 1 minute, and an extension at 72°C for 2 minutes (the annealing temperature and cycle number are shown in Table 1), PCR products were subjected to agarose gel electrophoresis. Approximately 1 × 104 HuCCT1 cells per well in 96-well plates were cultured for 24 hours. Supernatants were then tested for human IL-10 via enzyme-linked immunosorbent assay (ELISA) (R&D Systems). Data were analyzed using the Welch t test; P

< 0.05 was considered statistically significant. Immunohistochemistry revealed that IgG4-positive plasma cells were scattered within and around cancerous nests to various degrees in most cases (Fig. 1). In the cases with marked infiltration, the IgG4-positive cells were prominent with intermingling of other inflammatory cells. Figure 1C shows the number of IgG4-positive cells/HPF in extrahepatic cholangiocarcinomas from common bile ducts, gallbladder, and the Papilla of Vater, but there was no significant difference in IgG4-positive cell counts among anatomical locations of extrahepatic cholangiocarcinomas. Therefore,

they were integrated as shown in Fig. 1D. Consequently, the combined quantitative evaluation revealed that 23 (43%) of 54 cholangiocarcinoma ACP-196 ic50 patients had ≥10 IgG4-positive cells/HPF. PIK3C2G There was no correlation between the density of IgG4-positive cells and any clinicopathological factor including age, sex, anatomical location (common bile ducts, gallbladder, and the Papilla of Vater), or the histological differentiation (well, moderate, and poor) of extrahepatic cholangiocarcinoma. Representative images of immunostaining are shown in Fig. 2. Expression of HLA-DR was found in some infiltrating immunocompetent cells. Moreover, HLA-DR–positive cholangiocarcinoma cells were also found in 33 of 54 cases. HLA-DR expression in tumor cells showed uniformity and metastatic foci in lymph nodes as well as main tumors expressing HLA-DR. In contrast, the expression of costimulatory molecules (CD80 and CD86) was mostly faint or absent. Only four cases were clearly positive for CD86 in cholangiocarcinoma cells, and all of them were positive for HLA-DR. No cases evidently expressed CD80. Cholangiocarcinoma cells expressing HLA-DR but lacking costimulatory molecules (CD80 and CD86) were found in 29 of 54 cases (54%) and suggested to act as nonprofessional APCs inducing IL-10–producing anergy T cells. The relation between IgG4 reactions and HLA-DR and costimulatory molecules in cancer cells is shown in Fig. 3.

Peroxidase activity was demonstrated using the ImmPact DAB (diaminobenzidine-based) peroxidise substrate kit (Vector Laboratories). Slides were counterstained with hematoxylin. Data are expressed as mean ± standard error of the mean (SEM), unless otherwise stated. Multiple comparisons on data sets were performed using one-way analysis of variance (ANOVA), followed by Tukey’s post-hoc test. P ≤ 0.05 was regarded as significant. Influence of maternal obesity and postnatal diet as well as any interaction between them were investigated

using two-way ANOVA (GraphPad Prism 5.0; GraphPad Software, Inc., Cary, NC). The statistical unit was considered the number of dams (n = 5 per group), with one offspring

studied per litter per time point. Ab, antibody; α-SMA, alpha smooth muscle actin; ALT, alanine aminotransferase; ANOVA, analysis of variance; Col1-α2, collagen type 1 Vincristine order alpha 2; FACS, fluorescence-activated cell sorting; FCA, flow cytometric analysis; HBSS, Hank’s balanced salt solution; H&E, hematoxylin and eosin; Ig, immunoglobulin; IHC, immunohistochemical; IL, interleukin; IR, insulin resistance; KCs, Kupffer cells; LPS, lipopolysaccharide; mAb, monoclonal Ab; MNC, mononuclear cell; mRNA, messenger RNA; NAFLD, nonalcoholic fatty liver disease; Seliciclib mw NAS, NAFLD Activity Score; NASH, nonalcoholic steatohepatitis; NKT, natural killer T cells; PBS, phosphate-buffered saline; PCR, polymerase chain reaction; ROS, reactive oxygen species; SEM, standard error of the mean; TGs, triglycerides; TGF-β, transforming growth factor beta; Th-1/2, T-helper cells; TNF-α, tumor necrosis factor alpha Both maternal

obesity and postnatal diet were independent predictors of offspring body weight, inguinal fat mass, and hepatic TG, and there was an apparent interaction between maternal and postnatal environments. Body weight (Fig. 1A) was significantly increased in OffCon-OD, compared to OffCon-SC. Body weight was further increased by exposure to maternal obesity during gestation and lactation. A similar pattern was observed for inguinal fat pad mass (Fig. 1B) and for hepatic TG content (Fig. 1C). Therefore, the postnatal high-fat diet induced increases in body weight, adiposity, and hepatic fat content and was exacerbated by previous exposure to maternal obesity. There was an independent MYO10 effect of both maternal obesity and postnatal high-fat diet on TNF-α, TGF-β and Col1-α2 expression as well as a significant interaction apparent between maternal obesity and the postnatal diet for TGF-β and Col1-α2. IL-6 and TNF-α, as markers of liver injury, were significantly up-regulated in OffCon-OD (Fig. 2A,B) and further significantly increased in OffOb-OD. Similarly, relative expression of α-SMA, TGF-β, and Col1-α2, as markers of hepatic fibrogenesis (Fig. 2C-E), were up-regulated in OffCon-OD and OffOb-OD, compared to OffCon-SC.

Also, hepato-cytes from Alb-Lpin1−/− mice had normal rates of triglyceride synthesis. In mice receiving high fat diet for 10 weeks, there was no difference between WT and Alb-Lpin1−/− in total body weight gain, plasma chemistries, glucose tolerance, or insulin signaling. Liver histology and the mRNA expression of markers of inflammation or stellate cell activation in the liver were also not different between genotypes. Conclusion: Collectively these data demonstrate that lipin 1 accounts for the inducible component of hepatic PAP activity, 3-deazaneplanocin A but that marked deficits in PAP activity do not impair hepatic triglyceride synthesis

nor does it affect insulin signaling or expression of markers of NASH in the liver in mice fed high fat diet. These data likely suggest that lipin 2-mediated PAP activity is more than sufficient for robust triglyceride

synthesis and development of fatty liver. Disclosures: The following people have nothing to disclose: Nisreen Soufi, George G. Schweitzer, Zhouji Chen, Connie Gan, Kyle McCommis, Brian Finck Background: Elevated circulating levels of free fatty acids are found in patients with Daporinad mouse metabolic syndrome is are associated with increased cell death and liver inflammation promoting the pathologic features of non-alcoholic fatty liver disease. Recently, we demonstrated that free fatty acids caused lipoapoptosis in cholangiocytes. Purpose: The purpose of this study was to test whether free fatty acids induced cholangio-cyte inflammatory cytokine production. Methods: Cultured human cholangiocyte and cholangiocarcinoma cell lines (H69, Mz-ChA-1, and KMCH) were used. The saturated free fatty acid palmitic acid was complexed with BSA and cells were treated for 2-24 hours. Cells were imaged by transmission electron microscopy. Cytokines were detected in the supernatant using a cytokine protein array while cytokine mRNA was quantified by RT-PCR. Inhibition of p38 mitogen activated protein kinase was achieved by treatment with SB203580. Results: Treatment of cultured cholangiocyte cell

lines with palmitic acid did not increase lipid droplet formation in PD184352 (CI-1040) cells but did cause a rapid increase in secreted IL-6, IL-8, and GM-CSF. This increase in secreted cytokine proteins was accompanied by an increase in mRNA for IL-6, IL-8, and GM-CSF. Additionally, TNF-α mRNA was also increased by palmitic acid treatment. A time course experiment of IL-6 and IL-8 mRNA in palmitic acid-treated cells showed rapid activation at 1-4 hours that returned to baseline by 8 hours. Activation of MAPKs occurred rapidly upon addition of palmitic acid so we tested the dependence of cytokine production on p38 activation. Cells pretreated with the p38 inhibitor SB203580 were protected against increased IL-6 and IL-8 production.

Interestingly, a second CRP determination obtained ∼6 weeks later in the validation cohort, and therefore post-TACE in most cases, retained the

predictive value. The mean CRP levels increased with increasing Barcelona Clinic Liver Cancer (BCLC) stage. CRP levels also stratified patients within the same BCLC stage into long- and short-term survivors. Within BCLC stage B and C, patients with elevated CRP had a shorter survival than patients with low CRP. Within the BCLC C stage, Child B patients with a normal CRP had a survival comparable to Child A patients with an elevated CRP (median survival 15 and 14 months, respectively). Peck-Radosavljevic and co-workers further considered the Navitoclax concentration presence/absence

of clinically evident infection. When unrelated selleck chemical to infection, elevated CRP levels correlated directly with tumor characteristics, in particular with tumor burden. This suggests that elevation of CRP might be tumor-related. The authors also compared the proportion of patients with CRP elevation from unknown origin and from infectious origin, in their cohort as well as in a group of 104 non-HCC patients undergoing a transjugular intrahepatic portosystemic shunt (TIPS) placement. Elevated CRP was more frequently of unknown origin in HCC patients than in non-HCC patients (38% versus 17%). Nevertheless, elevated CRP in both groups was associated with poor prognosis. Similarly, Cervoni et al.12 recently reported a benefit of CRP determination in predicting short-term mortality in patients with advanced cirrhosis. What pathophysiological mechanisms trigger CRP elevation in HCC? Low-grade inflammation promotes tumor development. Mdr2−/− mice show defective biliary secretion of phospholipids, spontaneous cholangitis, and eventually develop HCC.13 Transgenic mice that express lymphotoxin α:β develop a chronic parenchymal inflammation with the production of cytokines and eventually HCC.14 IL-6, which is the principal regulator of CRP production, is produced by Kupffer

cells. In the diethylnitrosamine (DEN) rodent model for HCC, IL-6 rises in response to IL-1a, which is released from necrotic hepatocytes.15 This IL-6 production is gender-specific and may partly enough explain the male predominance of HCC.16 In fact, IL-6 expression is elevated in patients with cirrhosis and HCC.17 Moreover IL-6 levels were reported to correlate with the development of HCC.18, 19 This suggests that the hepatocellular signaling pathway of IL-6 might be a therapeutic target. The transcription factor STAT3 mediates the IL-6 effects. STAT3 was found to be activated in the majority of HCCs and seems to identify more aggressive tumors.20 Inactivation of the negative feedback loop of the JAK/STAT pathway by methylation of the SCOCS genes is frequent in HCC.

Interestingly, a second CRP determination obtained ∼6 weeks later in the validation cohort, and therefore post-TACE in most cases, retained the

predictive value. The mean CRP levels increased with increasing Barcelona Clinic Liver Cancer (BCLC) stage. CRP levels also stratified patients within the same BCLC stage into long- and short-term survivors. Within BCLC stage B and C, patients with elevated CRP had a shorter survival than patients with low CRP. Within the BCLC C stage, Child B patients with a normal CRP had a survival comparable to Child A patients with an elevated CRP (median survival 15 and 14 months, respectively). Peck-Radosavljevic and co-workers further considered the learn more presence/absence

of clinically evident infection. When unrelated Fulvestrant price to infection, elevated CRP levels correlated directly with tumor characteristics, in particular with tumor burden. This suggests that elevation of CRP might be tumor-related. The authors also compared the proportion of patients with CRP elevation from unknown origin and from infectious origin, in their cohort as well as in a group of 104 non-HCC patients undergoing a transjugular intrahepatic portosystemic shunt (TIPS) placement. Elevated CRP was more frequently of unknown origin in HCC patients than in non-HCC patients (38% versus 17%). Nevertheless, elevated CRP in both groups was associated with poor prognosis. Similarly, Cervoni et al.12 recently reported a benefit of CRP determination in predicting short-term mortality in patients with advanced cirrhosis. What pathophysiological mechanisms trigger CRP elevation in HCC? Low-grade inflammation promotes tumor development. Mdr2−/− mice show defective biliary secretion of phospholipids, spontaneous cholangitis, and eventually develop HCC.13 Transgenic mice that express lymphotoxin α:β develop a chronic parenchymal inflammation with the production of cytokines and eventually HCC.14 IL-6, which is the principal regulator of CRP production, is produced by Kupffer

cells. In the diethylnitrosamine (DEN) rodent model for HCC, IL-6 rises in response to IL-1a, which is released from necrotic hepatocytes.15 This IL-6 production is gender-specific and may partly Digestive enzyme explain the male predominance of HCC.16 In fact, IL-6 expression is elevated in patients with cirrhosis and HCC.17 Moreover IL-6 levels were reported to correlate with the development of HCC.18, 19 This suggests that the hepatocellular signaling pathway of IL-6 might be a therapeutic target. The transcription factor STAT3 mediates the IL-6 effects. STAT3 was found to be activated in the majority of HCCs and seems to identify more aggressive tumors.20 Inactivation of the negative feedback loop of the JAK/STAT pathway by methylation of the SCOCS genes is frequent in HCC.

Results: Compared with the baseline (W0), at the end of the eighth week (W8) two group without anxiety and depression, anxiety and depression in patients with mild to moderate SAS, SDS score decreased significantly, the difference PI3K inhibitor was statistically significant (P < 0.05). Houever, severe anxiety and depression in patients with SAS, SDS score were not significantly decreased, no significant differences (P < 0.05). After the treatment, the total curative effect of patients with mild to moderate anxiety and depression in the study group were higher than those in the control group (97.32% VS 17.98%, P < 0.001). However,

no statistical significance in the two group without anxiety and depression, severe anxiety and severe depression patients with

different total curative effect (P > 0.05). Conclusion: Low dose of Flupentixol and melitracen can effectively alleviate the symptoms of FD patients, significantly improve the without anxiety and depression, mild to moderate anxiety and depression in patients with psychological score. Key Word(s): 1. functional dyspepsia; 2. deanxit; 3. anxiety; 4. depression; Presenting Author: XUE HAN Additional Authors: KUI JIANG, BANGMAO WANG, LU ZHOU, XIN CHEN, SHU LI Corresponding check details Author: KUI JIANG Affiliations: General Hospital of Tianjin medical university Objective: To investigate the clinical effect of rebamipide in chronic gastritis patients. Methods: 180 patients with chronic gastritis were randomly divided into the experimental group and the control group. The experimental group were treated with

rebamipide 0.1 g tid and optimization of life style, and the control group were only optimized their life style for 26 weeks. Upper gastrointestinal endoscopy was performed in all patients to evaluate the severity of gastritis by modified Lanza score (MLS) and the histology by the updated Sydney system before and after treatment. Histamine H2 receptor Results: compare experimental group and control group in the differences of clinical symptoms, gastric mucosal lesions and inflammation grade scores between pre-treatment and post-treatment respectively (2.62 ± 1.86 vs. 1.55 ± 1.61, 0.57 ± 1.05 vs. 0.16 ± 0.90, 0.43 ± 0.96 vs. 0.01 ± 0.72), and the differences have statistical significance (P < 0.05). Conclusion: Rebamipide can improve clinical symptoms, gastric mucosal lesions, and pathologic grade (inflammation) of chronic gastritis safely, and hence it is and worthy of applying in clinical practice. Key Word(s): 1. Rebamipide; 2. chronic gastritis; 3. clinical effect; 4.

Results: Compared with the baseline (W0), at the end of the eighth week (W8) two group without anxiety and depression, anxiety and depression in patients with mild to moderate SAS, SDS score decreased significantly, the difference learn more was statistically significant (P < 0.05). Houever, severe anxiety and depression in patients with SAS, SDS score were not significantly decreased, no significant differences (P < 0.05). After the treatment, the total curative effect of patients with mild to moderate anxiety and depression in the study group were higher than those in the control group (97.32% VS 17.98%, P < 0.001). However,

no statistical significance in the two group without anxiety and depression, severe anxiety and severe depression patients with

different total curative effect (P > 0.05). Conclusion: Low dose of Flupentixol and melitracen can effectively alleviate the symptoms of FD patients, significantly improve the without anxiety and depression, mild to moderate anxiety and depression in patients with psychological score. Key Word(s): 1. functional dyspepsia; 2. deanxit; 3. anxiety; 4. depression; Presenting Author: XUE HAN Additional Authors: KUI JIANG, BANGMAO WANG, LU ZHOU, XIN CHEN, SHU LI Corresponding selleckchem Author: KUI JIANG Affiliations: General Hospital of Tianjin medical university Objective: To investigate the clinical effect of rebamipide in chronic gastritis patients. Methods: 180 patients with chronic gastritis were randomly divided into the experimental group and the control group. The experimental group were treated with

rebamipide 0.1 g tid and optimization of life style, and the control group were only optimized their life style for 26 weeks. Upper gastrointestinal endoscopy was performed in all patients to evaluate the severity of gastritis by modified Lanza score (MLS) and the histology by the updated Sydney system before and after treatment. many Results: compare experimental group and control group in the differences of clinical symptoms, gastric mucosal lesions and inflammation grade scores between pre-treatment and post-treatment respectively (2.62 ± 1.86 vs. 1.55 ± 1.61, 0.57 ± 1.05 vs. 0.16 ± 0.90, 0.43 ± 0.96 vs. 0.01 ± 0.72), and the differences have statistical significance (P < 0.05). Conclusion: Rebamipide can improve clinical symptoms, gastric mucosal lesions, and pathologic grade (inflammation) of chronic gastritis safely, and hence it is and worthy of applying in clinical practice. Key Word(s): 1. Rebamipide; 2. chronic gastritis; 3. clinical effect; 4.