To address this hypothesis, we treated CcnE1−/− and CcnE2−/− mice acute or chronically with CCl4 and analyzed the effect on the proliferative response of hepatocytes and nonparenchymal liver cells. Ubiquitous ablation of CcnE1 in this fibrosis model revealed several unexpected findings defining CcnE1 as an essential profibrotic mediator. After acute toxic liver injury, the overall proliferative response of CcnE1-deficient hepatic cells was dramatically impaired. Several studies, including our own work, demonstrated that CcnE1

is dispensable for the proliferation of continuously cycling cells and regenerating hepatocytes after surgical partial liver resection.9, 11, 19 From our present data, it is now evident that the requirement of proliferating hepatocytes for CcnE1 depends on the proliferation stimulus. Though CcnE1 is dispensable for hepatocyte proliferation in a proinflammatory environment (e.g., hepatectomy), www.selleckchem.com/products/Rapamycin.html it is apparently essential after toxic liver injury (i.e., CCl4) in vivo. In agreement with this hypothesis, we recently observed a prolonged cell-cycle arrest of CcnE1−/−

hepatocytes in vivo after treatment with the hepatotoxic agent, diethylnitrosamine (data not shown). Intriguingly, constitutive ablation of CcnE1—but not inhibition of CcnE2—protected from CCl4-mediated liver fibrosis, which was related to impaired cell-cycle activity of nonparenchymal liver cells. Hence, we focused on HSCs because this cell population is central for the process of liver fibrosis Target Selective Inhibitor Library concentration as the major source of ECM proteins.20 A recent study suggested that down-regulation of CcnE1 is related to the delayed cell-cycle progression of the human HSC 上海皓元医药股份有限公司 line, LX-2.21 In line with these findings, we demonstrated that complete ablation of CcnE1 induces a dramatic cell-cycle arrest of HSCs and hypersensitivity to apoptosis and overall poor survival. Although the mechanism triggering apoptosis in CcnE1-deficient cells remains elusive, HSC apoptosis clearly acts as an

antifibrotic.22 Thus, reduced liver fibrosis in CCl4-treated CcnE1−/− mice is most likely explained by impaired viability and cell-cycle arrest of HSCs after profibrogenic stimulation. Our study also revealed an unexpected role of CcnE2 for liver fibrogenesis. In line with our earlier studies,11 loss of CcnE2 resulted in accelerated gene activation of CcnE1 in hepatocytes and HSCs, suggesting that CcnE2 is an inhibitor of CcnE1 expression. At present, the underlying mechanism is unclear; however, CcnE2 was shown to be 1.5- to 10-fold more highly expressed, compared to CcnE1, in at least three independent studies.23 We speculate that CcnE2 might sequester, and thus inactivate, transcriptional activators of CcnE1. Besides up-regulating CcnE1, loss of CcnE2 resulted in early liver fibrogenesis and, more important, in accelerated HSC activation and proliferation.

HULC was discovered as the first IGF2BP substrate that is not stabilized or translationally regulated, but destabilized by way of CNOT1-mediated deadenylation recruited by IGF2BP1. Sixty human HCCs were analyzed for HULC expression using microarray analysis. Median age at surgery was 57 years (range 16-78), and the male/female ratio was 4:1. All diagnoses were confirmed by histological reevaluation, and use of the samples was approved by the local Ethics Committee.

The cohort contained a balanced repertoire of relevant underlying etiologies: hepatitis B virus (HBV) (n = 15), HCV (n = 12), alcohol (n = 10), cryptogenic (presumably mostly nonalcoholic fatty liver disease [NAFLD]; n = 19) or genetic hemochromatosis learn more (n = 3). The patients’ characteristics are

check details shown in Supporting Table 1. For in vitro transcription, the Megascript T7 kit (Life Technologies, Carlsbad, CA) was used according to the manufacturer’s recommendations. Briefly, 1 μg linearized plasmid template was used and reactions were incubated for 16 hours in the presence or absence of Biotin-16-UTP (Epicentre, Madison, WI). The ratio between UTP and Biotin-16-UTP was 20:1. The reaction was stopped by addition of 1 μL Turbo-DNase. RNA was precipitated with LiCl. RNA integrity and size were controlled using agarose gel electrophoresis. Beads were preblocked with 1 mg/mL BSA (Roche), 0.2 mg/mL yeast tRNA (Roche), and 0.2 mg/mL Glycogen (Carl 上海皓元 Roth, Karlsruhe, Germany) in low salt wash buffer (20 mM Hepes, pH 7.9; 100 mM KCl; 10 mM MgCl2; 0.01% NP40; 1 mM DTT) before addition of RNA. RNA was incubated with 50 μL Streptavidine-Sepharose beads (GE Healthcare, Little Chalfont, UK) in 500 μL HS-WB300 (20 mM Hepes, pH 7.9; 300 mM KCl; 10 mM MgCl2; 0.01% NP40; 1 mM DTT) for 4 hours. Unbound RNA was washed away with 3× 1 mL HS-WB400 (20 mM Hepes, pH 7.9; 400 mM KCl; 10 mM

MgCl2; 0.01% NP40; 1 mM DTT). Cytoplasmic cell extract (2-3 mg) was added and incubated overnight at 4°C. The next day the extract was removed and beads were washed 6 times with 1 mL HS-WB400. Beads were resuspended in 50 μL 6 M urea; 1 mM DTT; 0.01% NP-40 and incubated at room temperature for 30 minutes in a shaking block at 900 rpm. Then the supernatant was transferred into a new tube and proteins were precipitated with 5 volumes of prechilled acetone for 1 hour at −20°C. Proteins were pelleted by way of centrifugation at 13,000g at room temperature. Pellets were washed twice with 1 mL 80% ethanol, dried for 5 minutes, and resuspended in 20 μL protein sample buffer. HepG2 cells were transfected with small interfering RNAs (siRNAs) as stated above. After 48 hours, alpha-amanitine (AppliChem, Darmstadt, Germany) was added (10 μg/mL f.c.) and cells were harvested at the indicated timepoints. All experiments were done in biological triplicates.

HULC was discovered as the first IGF2BP substrate that is not stabilized or translationally regulated, but destabilized by way of CNOT1-mediated deadenylation recruited by IGF2BP1. Sixty human HCCs were analyzed for HULC expression using microarray analysis. Median age at surgery was 57 years (range 16-78), and the male/female ratio was 4:1. All diagnoses were confirmed by histological reevaluation, and use of the samples was approved by the local Ethics Committee.

The cohort contained a balanced repertoire of relevant underlying etiologies: hepatitis B virus (HBV) (n = 15), HCV (n = 12), alcohol (n = 10), cryptogenic (presumably mostly nonalcoholic fatty liver disease [NAFLD]; n = 19) or genetic hemochromatosis CP-673451 cost (n = 3). The patients’ characteristics are

NVP-BGJ398 shown in Supporting Table 1. For in vitro transcription, the Megascript T7 kit (Life Technologies, Carlsbad, CA) was used according to the manufacturer’s recommendations. Briefly, 1 μg linearized plasmid template was used and reactions were incubated for 16 hours in the presence or absence of Biotin-16-UTP (Epicentre, Madison, WI). The ratio between UTP and Biotin-16-UTP was 20:1. The reaction was stopped by addition of 1 μL Turbo-DNase. RNA was precipitated with LiCl. RNA integrity and size were controlled using agarose gel electrophoresis. Beads were preblocked with 1 mg/mL BSA (Roche), 0.2 mg/mL yeast tRNA (Roche), and 0.2 mg/mL Glycogen (Carl MCE公司 Roth, Karlsruhe, Germany) in low salt wash buffer (20 mM Hepes, pH 7.9; 100 mM KCl; 10 mM MgCl2; 0.01% NP40; 1 mM DTT) before addition of RNA. RNA was incubated with 50 μL Streptavidine-Sepharose beads (GE Healthcare, Little Chalfont, UK) in 500 μL HS-WB300 (20 mM Hepes, pH 7.9; 300 mM KCl; 10 mM MgCl2; 0.01% NP40; 1 mM DTT) for 4 hours. Unbound RNA was washed away with 3× 1 mL HS-WB400 (20 mM Hepes, pH 7.9; 400 mM KCl; 10 mM

MgCl2; 0.01% NP40; 1 mM DTT). Cytoplasmic cell extract (2-3 mg) was added and incubated overnight at 4°C. The next day the extract was removed and beads were washed 6 times with 1 mL HS-WB400. Beads were resuspended in 50 μL 6 M urea; 1 mM DTT; 0.01% NP-40 and incubated at room temperature for 30 minutes in a shaking block at 900 rpm. Then the supernatant was transferred into a new tube and proteins were precipitated with 5 volumes of prechilled acetone for 1 hour at −20°C. Proteins were pelleted by way of centrifugation at 13,000g at room temperature. Pellets were washed twice with 1 mL 80% ethanol, dried for 5 minutes, and resuspended in 20 μL protein sample buffer. HepG2 cells were transfected with small interfering RNAs (siRNAs) as stated above. After 48 hours, alpha-amanitine (AppliChem, Darmstadt, Germany) was added (10 μg/mL f.c.) and cells were harvested at the indicated timepoints. All experiments were done in biological triplicates.

Using this technique, changes in regional tissue volume can be detected on the basis of the deformation field derived from the warping subject to the template image. A voxelwise estimation of the morphological differences Veliparib clinical trial between the two groups can be acquired after applying a threshold (P < .001, uncorrected) to the statistic maps. Regions with enlarged volume in the brains of blind subjects are mainly localized in the left associated visual cortex, posterior cingulated cortex, and cerebellum,

whereas volume reductions are primarily localized in the left early visual cortex. DBM is an effective method for detecting entire brain structural changes in blindness. Visual deprivation actually alters the local structural organization

during the early critical periods of neurodevelopment. Volume increases outside the occipital lobe detected with DBM may suggest compensatory adaptations. Blindness provides a rare model to investigate the effects of visual experience on the functional and structural organization of the human brain.[1] Many studies have demonstrated that the human brain can adapt to changes in the environment through functional reorganization rather than structural plastic changes. The cross-modal plasticity in functional reorganization induced by vision deprivation has also been reported in previous selleck chemicals neuroimaging. Plastic changes have been reported in the visual cortex both in the resting state and imaginary, auditory, and tactile tasks,[1-3] and in the early sensory areas of spared modalities after visual deprivation in early life.[4] Compared with functional studies, investigations on the structural reorganization of the brain in blind subjects are few and have only attracted MCE research attention in recent years. Evidence from the nonhuman primate literature proves that early visual deprivation leads

to changes in the structural anatomy of the visual cortex at the microscopic level.[5], [6] With the development of the imaging technique, the identification of structural changes in the brain on magnetic resonance imaging (MRI) scans is becoming increasingly important in the study of neurological science. Using voxel-based morphometry (VBM) method,[7] previous MRI studies on blindness have reported decreased gray matter (GM) density and increased white matter (WM) density in the sensory–motor system.[8-10] Another useful tool aside from VBM for the analysis of brain morphology from MRI is the deformation-based morphometry (DBM) method which provides an unbiased automated examination of the entire brain with high regional sensitivity.[11] Unlike VBM which focuses on an analysis of differences in GM and WM, DBM can detect the differences in local structures using high-dimensional nonrigid registration. Leporé and colleagues used this technique with fast fluid registration to examine whole brain volumetric changes in both early- and late-onset blind subjects.

Using this technique, changes in regional tissue volume can be detected on the basis of the deformation field derived from the warping subject to the template image. A voxelwise estimation of the morphological differences Barasertib supplier between the two groups can be acquired after applying a threshold (P < .001, uncorrected) to the statistic maps. Regions with enlarged volume in the brains of blind subjects are mainly localized in the left associated visual cortex, posterior cingulated cortex, and cerebellum,

whereas volume reductions are primarily localized in the left early visual cortex. DBM is an effective method for detecting entire brain structural changes in blindness. Visual deprivation actually alters the local structural organization

during the early critical periods of neurodevelopment. Volume increases outside the occipital lobe detected with DBM may suggest compensatory adaptations. Blindness provides a rare model to investigate the effects of visual experience on the functional and structural organization of the human brain.[1] Many studies have demonstrated that the human brain can adapt to changes in the environment through functional reorganization rather than structural plastic changes. The cross-modal plasticity in functional reorganization induced by vision deprivation has also been reported in previous Venetoclax chemical structure neuroimaging. Plastic changes have been reported in the visual cortex both in the resting state and imaginary, auditory, and tactile tasks,[1-3] and in the early sensory areas of spared modalities after visual deprivation in early life.[4] Compared with functional studies, investigations on the structural reorganization of the brain in blind subjects are few and have only attracted 上海皓元医药股份有限公司 research attention in recent years. Evidence from the nonhuman primate literature proves that early visual deprivation leads

to changes in the structural anatomy of the visual cortex at the microscopic level.[5], [6] With the development of the imaging technique, the identification of structural changes in the brain on magnetic resonance imaging (MRI) scans is becoming increasingly important in the study of neurological science. Using voxel-based morphometry (VBM) method,[7] previous MRI studies on blindness have reported decreased gray matter (GM) density and increased white matter (WM) density in the sensory–motor system.[8-10] Another useful tool aside from VBM for the analysis of brain morphology from MRI is the deformation-based morphometry (DBM) method which provides an unbiased automated examination of the entire brain with high regional sensitivity.[11] Unlike VBM which focuses on an analysis of differences in GM and WM, DBM can detect the differences in local structures using high-dimensional nonrigid registration. Leporé and colleagues used this technique with fast fluid registration to examine whole brain volumetric changes in both early- and late-onset blind subjects.

At different times after a single dose of DEN in 15-day-old animals, liver was collected and analyzed. The appearance of tumors was observed microscopically in all male mice at 9 months of age, but clear macroscopic observation of relevant tumor masses was not observed until 12 months (Supporting Fig. 5). Real-time PCR analysis revealed a progressive increase in the expression of TGFB1,

this website TGFBR1, and CXCR4 in livers from mice of 9 to 12 months of age (Fig. 5A). Increased expression of TGFB1 correlated with a higher percentage of cells showing nuclear localization of phospho-SMAD2 and phospho-SMAD3 in immunohistochemical studies (Fig. 5B). Cells in the border of the tumor presented the maximal level of CXCR4 expression (Fig. 5C). Importantly, it was possible to observe some CXCR4-positive cells invading the stroma. The expression of CXCL12/SDF-1α was concentrated in perivascular or ductal cells, which could induce the stimulus for cells to migrate toward these areas. Furthermore, we found that immortalized Selleckchem HDAC inhibitor mice hepatocytes in culture were able to respond to TGF-β by inducing CXCR4 expression, a process that was SMAD2/3-dependent (Fig. 5D). In summary, tumor cells in the DEN-induced mice model of liver tumorigenesis show increased activation of the TGF-β pathway, which correlates with enhanced CXCR4 levels

that concentrates particularly in the cells of the tumor border line. Finally, we wanted to know whether TGF-β1 signaling and CXCR4 expression 上海皓元 correlated in human HCC tissues. We analyzed tissues from 17 patients with HCC from different etiologies (Table 1). Heterogeneity among HCC tumors, with variable expression of TGFB1 and its receptor TGFBR1, was observed. Nevertheless, when calculated as the mean among the patients, the expression was significantly increased in tumor tissues versus their surrounding nontumoral tissues. Analysis of CXCR4 was also variable, but again the tendency was to an increased expression in the tumor tissues (Fig. 6A). However, the most interesting

way to dissect the results was individually (Fig. 6B), considering each patient independently. In all the patients showing increased expression of CXCR4, TGFB1 expression was also enhanced, with the exception of patient 8, who presented CXCR4 expression mainly in areas of infiltration (results not shown). This patient suffered from an autoimmune disease. This direct correlation was not necessarily true the other way around, since some patients with increased expression of TGFB1 did not show higher expression of CXCR4 (patients 9, 10, 13, 17). Of note, the increased expression of TGFB1 at the mRNA level correlated with higher levels of TGFB1 protein in the tissues from these patients, not only in the tumoral cells but also in the surrounding stroma and perivascular areas (Fig. 6B,C).

At different times after a single dose of DEN in 15-day-old animals, liver was collected and analyzed. The appearance of tumors was observed microscopically in all male mice at 9 months of age, but clear macroscopic observation of relevant tumor masses was not observed until 12 months (Supporting Fig. 5). Real-time PCR analysis revealed a progressive increase in the expression of TGFB1,

PD0325901 price TGFBR1, and CXCR4 in livers from mice of 9 to 12 months of age (Fig. 5A). Increased expression of TGFB1 correlated with a higher percentage of cells showing nuclear localization of phospho-SMAD2 and phospho-SMAD3 in immunohistochemical studies (Fig. 5B). Cells in the border of the tumor presented the maximal level of CXCR4 expression (Fig. 5C). Importantly, it was possible to observe some CXCR4-positive cells invading the stroma. The expression of CXCL12/SDF-1α was concentrated in perivascular or ductal cells, which could induce the stimulus for cells to migrate toward these areas. Furthermore, we found that immortalized HM781-36B research buy mice hepatocytes in culture were able to respond to TGF-β by inducing CXCR4 expression, a process that was SMAD2/3-dependent (Fig. 5D). In summary, tumor cells in the DEN-induced mice model of liver tumorigenesis show increased activation of the TGF-β pathway, which correlates with enhanced CXCR4 levels

that concentrates particularly in the cells of the tumor border line. Finally, we wanted to know whether TGF-β1 signaling and CXCR4 expression MCE公司 correlated in human HCC tissues. We analyzed tissues from 17 patients with HCC from different etiologies (Table 1). Heterogeneity among HCC tumors, with variable expression of TGFB1 and its receptor TGFBR1, was observed. Nevertheless, when calculated as the mean among the patients, the expression was significantly increased in tumor tissues versus their surrounding nontumoral tissues. Analysis of CXCR4 was also variable, but again the tendency was to an increased expression in the tumor tissues (Fig. 6A). However, the most interesting

way to dissect the results was individually (Fig. 6B), considering each patient independently. In all the patients showing increased expression of CXCR4, TGFB1 expression was also enhanced, with the exception of patient 8, who presented CXCR4 expression mainly in areas of infiltration (results not shown). This patient suffered from an autoimmune disease. This direct correlation was not necessarily true the other way around, since some patients with increased expression of TGFB1 did not show higher expression of CXCR4 (patients 9, 10, 13, 17). Of note, the increased expression of TGFB1 at the mRNA level correlated with higher levels of TGFB1 protein in the tissues from these patients, not only in the tumoral cells but also in the surrounding stroma and perivascular areas (Fig. 6B,C).

A possible explanation for this apparent lack of improvement in clinical management of cirrhosis is the 47% prevalence among our patients of comorbidities or complications other than those we considered in our analysis. Comorbidity has recently been demonstrated to increase both all-cause and cirrhosis-related mortality,27 and its importance is corroborated by the observation see more that a quarter of our patients did not die from cirrhosis, compared with 15%–20% in the older studies.3, 7 Differences in alcohol consumption also may be of importance; the proportion of abstainers in our cohort matched that in the older studies, but in those studies only complete

teetotalers counted as abstainers.3, 7 Among patients in our study, mortality increased further following the development Smoothened Agonist clinical trial of complications, in accordance with the existing

literature.28 Probably the higher proportion of persistent drinkers among patients with complications contributed to this association. Mortality among patients with variceal bleeding has previously been found to be similar in those with and without a history of ascites,28 but our results and those from a recent German study demonstrate that this is not the case.29 A likely explanation for the emerging importance of ascites among patients with variceal bleeding is that bleeding is less fatal now than it was in the past.30 In fact, the mortality of patients with complications was consistently lower in our study than in older studies.3, 6, 7, 10, 31 The largest earlier study, including 122 Spanish patients with alcoholic cirrhosis and 171 patients with nonalcoholic cirrhosis,11 reported that the risk of developing ascites, variceal bleeding, or hepatic encephalopathy increased steadily by 7%–10% per year in the cohort as a whole.11–14 This is consistent with our finding that 49% of patients without complications at cirrhosis diagnosis developed 上海皓元医药股份有限公司 complications within 5 years. At the same time, the risk in our study was much higher during

the first year (22%) than during the following 4 years (27%, or about 7% per year). In the Spanish study, patients were not included when the clinical diagnosis was made, but when it had been confirmed by a liver biopsy in a specialist unit.11 However, patients at highest risk of complications may not have survived from clinical diagnosis to inclusion, and the risk of complications could therefore have been underestimated. Furthermore, although our study corroborates previous findings that ascites is usually the first complication to appear,11, 28 we also found a high risk of variceal bleeding or hepatic encephalopathy as the first complication. This indicates that patients with alcoholic liver cirrhosis should always be considered at risk of all three complications.

A possible explanation for this apparent lack of improvement in clinical management of cirrhosis is the 47% prevalence among our patients of comorbidities or complications other than those we considered in our analysis. Comorbidity has recently been demonstrated to increase both all-cause and cirrhosis-related mortality,27 and its importance is corroborated by the observation PD98059 clinical trial that a quarter of our patients did not die from cirrhosis, compared with 15%–20% in the older studies.3, 7 Differences in alcohol consumption also may be of importance; the proportion of abstainers in our cohort matched that in the older studies, but in those studies only complete

teetotalers counted as abstainers.3, 7 Among patients in our study, mortality increased further following the development check details of complications, in accordance with the existing

literature.28 Probably the higher proportion of persistent drinkers among patients with complications contributed to this association. Mortality among patients with variceal bleeding has previously been found to be similar in those with and without a history of ascites,28 but our results and those from a recent German study demonstrate that this is not the case.29 A likely explanation for the emerging importance of ascites among patients with variceal bleeding is that bleeding is less fatal now than it was in the past.30 In fact, the mortality of patients with complications was consistently lower in our study than in older studies.3, 6, 7, 10, 31 The largest earlier study, including 122 Spanish patients with alcoholic cirrhosis and 171 patients with nonalcoholic cirrhosis,11 reported that the risk of developing ascites, variceal bleeding, or hepatic encephalopathy increased steadily by 7%–10% per year in the cohort as a whole.11–14 This is consistent with our finding that 49% of patients without complications at cirrhosis diagnosis developed 上海皓元 complications within 5 years. At the same time, the risk in our study was much higher during

the first year (22%) than during the following 4 years (27%, or about 7% per year). In the Spanish study, patients were not included when the clinical diagnosis was made, but when it had been confirmed by a liver biopsy in a specialist unit.11 However, patients at highest risk of complications may not have survived from clinical diagnosis to inclusion, and the risk of complications could therefore have been underestimated. Furthermore, although our study corroborates previous findings that ascites is usually the first complication to appear,11, 28 we also found a high risk of variceal bleeding or hepatic encephalopathy as the first complication. This indicates that patients with alcoholic liver cirrhosis should always be considered at risk of all three complications.

Methods: Patients who failed previous H. pylori treatment at least once were enrolled. They were given RTFB (rabeprazole 20 mg+ tetracycline 750 mg+furazolidone 100 mg+ colloidal bismuth subcitrate 220 mg. bid) for 14 days. The adverse effects were recorded. Eradication of H. pylori was determined by 13C-urea breath test at least 4 weeks after treatment. Results: 67 patients were recruited with 17 males and their average age is 51.33 ± 11.02Y. H. pylori eradication rate (PP) was 97.0% (65/67). Side effects had been recorded

as follows: mild nausea and dizziness in 14 patients, mild gastrointestinal discomfort in 2 patients, mild skin itch in 2 patients and urticaria recurrence in 1 patient. They all got relieve LBH589 ic50 after treatment. But, 3 patients stopped the treatment due to Pirfenidone mw fever. Conclusion: The 14-day tetracycline, furazolidone -containing quadruple rescue therapy can achieve a high eradication rate. The adverse effects are usually mild, but it can cause drug fever. Clinicians should pay close attention to the adverse effects of patients during the treatment with this regimen.

Once the fever symptom is found in patients, treatment should be stopped immediately. Key Word(s): 1. H. pylori; 2. tetracycline; 3. furazolidone; 4. safety; Presenting Author: SHEW-MEEI SHEU Additional Authors: CHENG-YEN KAO, SHING CHENG, YAO-JONG YANG, YI-CHUN YEH, BOR-SHYANG SHEU Corresponding Author: BOR-SHYANG SHEU Affiliations: National Cheng-Kung University Objective: Diabetes patients have higher glucose level and prevalence rate of H. pylori infection, which is significantly associated with chronic gastritis. The detail mechanism is still unknown. We try to investigate whether higher glucose concentration change bacterial growth, adhesion or virulence to stimulate stronger inflammation. Methods: Strain 43504 was used to determine the glucose effect on H. pylori. In the presence

of different glucose concentration (0, 100, 150, 200 mg/dl), growth curves of strain 43504 were detected and mRNA was extracted to perform RT-PCR to detect the expression of cagA, medchemexpress csrA, napA and vacA. Adhesion assay was analyzed by counting the colony number of strain 43504 after adhering to AGS cells. Results: Under glucose concentrations (100 and 200 mg/dl), the growth curves of H. pylori were similar. Glucose (150 mg/dl) could decrease mRNA expression of carbon storage regulator (csrA), a global transcriptional regulator and vacuolating cytotoxin (vacA) of H. pylori. However, cytotoxin-associated gene A (cagA) and neutrophil activating protein (napA) and adhesion ability of H. pylori did not have obvious change under the treatment of different glucose concentrations. The glucose effect on H. pylori infected cells will be further analyzed. Conclusion: Higher glucose decreases the expression of virulence genes, csrA and vacA, may contribute to the pathogenesis of H. pylori in diabetes patients. Key Word(s): 1.