Recent studies showed that repositioning the hands in visible space, or making visual events more distant, can modulate such crossmodal extinction. Here, in a detailed single-case study, we implemented a novel spatial manipulation when assessing crossmodal extinction. This was designed not only to hold somatosensory inputs and hand/arm-posture

constant, but also to hold (retinotopic) visual inputs constant, yet while still changing the spatial relationship of tactile and visual events in the external world. Our right hemisphere patient extinguished left-hand touches due to visual stimulation of the right visual learn more field (RVF) when tested in the usual default posture with eyes/head directed straight ahead. But when her eyes/head were turned to the far left (and any visual events shifted along with this), such that the identical RVF retinal stimulation now fell at the same external location as the left-hand touch, crossmodal extinction was selleck eliminated. Since only proprioceptive postural cues could signal this changed spatial relationship for the critical condition, our results show for the first time that such postural cues alone are sufficient to modulate crossmodal extinction. Identical somatosensory and retinal inputs can lead to severe crossmodal extinction, or none, depending on current

posture. “
“Both real action control and execution and motor imagery abilities require knowledge MCE公司 of the spatial location of body parts, in other words efference copy information and feedbacks from the sensory system (Frith et al., 2000, Philos. Trans. R. Soc. Lond. B. Biol. Sci., 355, 1771). Spinal cord injuries induce severe motor disability, due to a

damage of the descending motor pathways (Cramer et al., 2007, Exp. Brain. Res., 177, 233). Patients’ motor imagery competences are variably reported as either normal or defective (Decety & Boisson, 1990, Eur. Arch. Psychiatry Clin. Neurosci., 240, 39; Lacourse et al., 1999, Behav. Brain Sci., 104, 73). We explored biomechanical constraint effects in Spinal Cord Injury (SCI) patients, as they are considered the most reliable indexes of motor imagery abilities (Parsons, 1987b, Cogn. Psychol., 19, 178). Sixteen spinal cord injuries patients and 16 neurologically unimpaired subjects have been administered with (1) the Hand Laterality Task (HLT), in which subjects were asked to judge the laterality of a rotated hand; and (2) the Mirror Letter Discrimination Task (MLD), in which subjects were asked to judge if a rotated character was in its correct upright position or mirror-reversed form. Our patients did not present the effect of stimulus orientation, neither did they show any effect related to biomechanical constraints. Based on these data, the hypothesis is that SCI patients’ performance may be ascribed to the use of a different strategy to solve the tasks, based on memory rather than on mental rotation.

Recent studies showed that repositioning the hands in visible space, or making visual events more distant, can modulate such crossmodal extinction. Here, in a detailed single-case study, we implemented a novel spatial manipulation when assessing crossmodal extinction. This was designed not only to hold somatosensory inputs and hand/arm-posture

constant, but also to hold (retinotopic) visual inputs constant, yet while still changing the spatial relationship of tactile and visual events in the external world. Our right hemisphere patient extinguished left-hand touches due to visual stimulation of the right visual check details field (RVF) when tested in the usual default posture with eyes/head directed straight ahead. But when her eyes/head were turned to the far left (and any visual events shifted along with this), such that the identical RVF retinal stimulation now fell at the same external location as the left-hand touch, crossmodal extinction was Paclitaxel datasheet eliminated. Since only proprioceptive postural cues could signal this changed spatial relationship for the critical condition, our results show for the first time that such postural cues alone are sufficient to modulate crossmodal extinction. Identical somatosensory and retinal inputs can lead to severe crossmodal extinction, or none, depending on current

posture. “
“Both real action control and execution and motor imagery abilities require knowledge 上海皓元 of the spatial location of body parts, in other words efference copy information and feedbacks from the sensory system (Frith et al., 2000, Philos. Trans. R. Soc. Lond. B. Biol. Sci., 355, 1771). Spinal cord injuries induce severe motor disability, due to a

damage of the descending motor pathways (Cramer et al., 2007, Exp. Brain. Res., 177, 233). Patients’ motor imagery competences are variably reported as either normal or defective (Decety & Boisson, 1990, Eur. Arch. Psychiatry Clin. Neurosci., 240, 39; Lacourse et al., 1999, Behav. Brain Sci., 104, 73). We explored biomechanical constraint effects in Spinal Cord Injury (SCI) patients, as they are considered the most reliable indexes of motor imagery abilities (Parsons, 1987b, Cogn. Psychol., 19, 178). Sixteen spinal cord injuries patients and 16 neurologically unimpaired subjects have been administered with (1) the Hand Laterality Task (HLT), in which subjects were asked to judge the laterality of a rotated hand; and (2) the Mirror Letter Discrimination Task (MLD), in which subjects were asked to judge if a rotated character was in its correct upright position or mirror-reversed form. Our patients did not present the effect of stimulus orientation, neither did they show any effect related to biomechanical constraints. Based on these data, the hypothesis is that SCI patients’ performance may be ascribed to the use of a different strategy to solve the tasks, based on memory rather than on mental rotation.

There was an approximate 30% increase in MDZ AUC when co-administered with MK-5172, suggesting that MK-5172 is a weak CYP3A4 inhibitor. There was an approximate 3-fold increase in atorvastatin AUC when co-administered with MK-5172, due to CYP3A4 inhibition and potentially BCRP inhibition. MK-5172 PK was not significantly impacted by co-administration with pitavastatin or atorvastatin. Disclosures: Luzelena Caro – Employment: Merck & Co., Inc. Jennifer E. Talaty- Employment: Merck, Sharp, & Dohme Zifang Guo – Employment: Merck & Co., Inc. Christina Reitmann – Employment: Merck, Sharp & Dohme, Corp Iain click here P. Fraser – Employment:

Merck & Co.; Stock Shareholder: Merck & Co. Raymond Evers – Employment: Merck Wendy W. Yeh – Employment: Merck & Co. Joan R. Butterton – Employment: Merck Sharp & Dohme Corp.; Stock Shareholder: Merck Sharp & Dohme Corp.

The following people have nothing to disclose: Dennis Swearingen Background: MK-5172, a once-daily competitive inhibitor of the hepatitis C virus (HCV) NS3/4A protease with improved potency compared with the approved first generation protease inhibitors, and MK-8742, a HCV NS5A replication complex inhibitor with improved potency compared to first generation NS5A inhibitors, are selleck products being developed for the treatment of chronic HCV infection. Since these agents may be coadministered as a combination regimen for HCV, the present study evaluated the pharmacokinetic interactions and tolerability of MK-5172 and MK-8742 co-administration in healthy subjects. Methods: This was an open-label, multiple-dose study in 10 healthy adult male and female volunteers, ages 19-55 years. Since MK-5172 in

HCV-infected patients demonstrates ∼2-fold higher exposure compared to healthy subjects, a 200 mg dose of MK-5172 in healthy subjects was used in this study to match the exposure of 100 mg dose (the intended Phase 3 dose) in HCV-infected patients. In Period 1, subjects received oral doses of 200 mg MK-5172 once medchemexpress daily on Days 1 to 7. Following a 7 day washout, subjects received oral doses of 20 mg MK-8742 once daily on Days 1 to 7 in Period 2. In Period 3, subjects were co-administered once daily oral doses of 200 mg MK-5172 and 20 mg MK-8742 on Days 1 to 8. Plasma PK samples were collected for the pharmacokinetic assessment of MK-5172 and MK-8742. Safety assessments included ECGs, vital signs, clinical laboratory tests, physical examination, and adverse event monitoring. Results: Co-administration of MK-5172 with MK-8742 was generally well-tolerated. Multiple oral doses of MK-5172 did not meaningfully change the steady-state AUC0-24h, Cmax, or C24h of MK-8742 with geometric mean ratios (GMRs) [90% confidence intervals (CIs)] for MK-8742 (MK-8742+MK-5172/MK-8742) of 1.01 [0.83, 1.24], 0.93 [0.76, 1.13], and 1.02 [0.83, 1.24], respectively. Multiple oral doses of MK-8742 did not meaningfully change AUC0-24h, Cmax, or C24h of MK-5172 (MK-5172+MK-8742/MK-5172) with GMRs [90% CIs] of 0.90 [0.

Here, the phenotype was characterized during

the progression of acute and chronic liver injury. Results: In 8 week old NemoΔhepa/CREM-α compared with NemoΔhepa mice, we found significantly reduced serum AST and ALT levels. These findings were associated with lower absolute numbers of infiltrating CD11 b+ and F4/80 cells in NemoΔhepa /CREM-α livers. In addition, we found significantly elevated mRNA expression levels of cytokines IL-10 and IL-4 in both T-cells and liver tissue in NemoΔhepa/CREM-α compared with NemoΔhepa and WT mice suggesting that the CREM-α transgene in T-cells influences click here liver inflammation towards a protective environment. Liver histology and sirius red staining revealed that fibrosis was

significantly reduced in NemoΔhepa/CREM-α compared to NemoΔhepa livers in 13 weeks old animals. This was further confirmed by studying extracellular matrix deposition showing significantly reduced Collagen IA1 and fiber deposition in NemoΔhepa/CREM-α livers, which was accompanied by decreased desmin-associated activation of Hepatic Stellate cells. In 52 weeks old NemoΔhepa/CREM-α livers, a significantly reduced liver-body-weight ratio and significantly selleck chemical less nodules in comparison to NemoΔhepa mice were evident. Additionally, c-myc mRNA levels and protein levels of glutamine synthetase revealed lower cancer related-metabolism in NemoΔhepa/CREM-α livers. Conclusion: Our results demonstrate that overexpression of CREM-a in T-cells in NemoΔhepa mice attenuates disease progression as shown by reduced liver fibrosis

and growth of HCC. This finding is the result of changing inflammation in these livers towards a protective milieu by enhancing the expression of distinct cytokines (IL-4, IL-10) and by reducing immune cell infiltration and IL-17 production. The present findings suggest a new molecular approach to reduce 上海皓元 disease progression in chronic liver diseases. Disclosures: Christian Trautwein – Grant/Research Support: BMS, Novartis, BMS, Novartis; Speaking and Teaching: Roche, BMS, Roche, BMS The following people have nothing to disclose: Nadine Hermanns, Francisco Javier Cubero, Antje Mohs, Kim Ohl, Malika Al Masaoudi, Christian Liedtke, Klaus Tenbrock Background/Aims: We investigated the nature of ASCs here by direct ex vivo assays in patients with acute hepatitis A (AHA) which is caused by the primary infection of hepatitis A virus (HAV). Methods : The study included 39 patients diagnosed with AHA infection who were hospitalized at Chung-Ang University Hospital. All patients were seropositive for anti-HAV IgM, and all had clinical features of acute hepatitis. Peripheral blood samples at the acute stage were collected on the day of admission from all of the 39 patients. Follow-up sampling was performed at the subacute stage (5–14 days) or at the convalescent stage (35–150 days).

It is not unreasonable to hypothesize that HA patients with certain HLA class II alleles and/or haplotypes will be more susceptible to T-cell stimulation by particular variant sequences in therapeutic FVIII than patients with other alleles and/or haplotypes. Indeed, the identification of HLA-restricted T-cell responses

in mild HA patients against peptides with the wild-type FVIII sequence at the region corresponding to a haemophilic missense site [45–47] serves as proof-of-principle that even a single amino acid change can cause T-cell stimulation leading to inhibitor development when the patient is infused with FVIII that AZD1208 datasheet differs at this site. Some higher-risk HLA haplotypes (i.e., those encoding HLA class II molecules that can effectively bind and present particular FVIII sequence variants) may be more prevalent in some racial/ethnic groups than in others. We are currently investigating associations of genetic variations with inhibitor prevalence. Cell-based assays are also being used to directly test the immunogenicity check details of FVIII sequence variations due to both haemophilic missense mutations and non-haemophilic ns-SNPs. It is hoped that the results of these and similar

studies will identify immunodominant epitopes in FVIII and thus motivate the development of new therapeutic FVIII products targeted to particular populations. We expect that susceptible patient populations will increasingly be defined

by the results of genetic tests that are more specific, i.e. predictive of potential immune responses. We also expect that some genetic determinants of risk – such as large F8 deletions involving multiple exons, 上海皓元医药股份有限公司 which occur with comparable frequencies in all human populations – will not correlate with racial self-identification. Future genetic markers will be more predictive of inhibitor risk in more precisely defined sub-populations and they will be more useful than, for example, the general assumption of a higher inhibitor risk in black HA patients. It is important to note that only a subset of HA patients with any racial heritage is likely to be at higher risk for inhibitor development, and the relevant genetic risk factors need to be better defined. Increasing knowledge of immune mechanisms leading to neutralizing antibodies will also suggest new therapeutic approaches targeted to specific at-risk populations. We anticipate that genotyping of HA patients will eventually include testing for the presence of particular SNPs in both F8 and immune regulatory genes, e.g. those encoding the HLA class II antigen-presentation repertoire, in addition to the HA-causing F8 mutation. Appropriate genetic testing will allow better matching of HA patients with FVIII products that are likely to be less immunogenic.

It is not unreasonable to hypothesize that HA patients with certain HLA class II alleles and/or haplotypes will be more susceptible to T-cell stimulation by particular variant sequences in therapeutic FVIII than patients with other alleles and/or haplotypes. Indeed, the identification of HLA-restricted T-cell responses

in mild HA patients against peptides with the wild-type FVIII sequence at the region corresponding to a haemophilic missense site [45–47] serves as proof-of-principle that even a single amino acid change can cause T-cell stimulation leading to inhibitor development when the patient is infused with FVIII that Ganetespib in vitro differs at this site. Some higher-risk HLA haplotypes (i.e., those encoding HLA class II molecules that can effectively bind and present particular FVIII sequence variants) may be more prevalent in some racial/ethnic groups than in others. We are currently investigating associations of genetic variations with inhibitor prevalence. Cell-based assays are also being used to directly test the immunogenicity Compound Library molecular weight of FVIII sequence variations due to both haemophilic missense mutations and non-haemophilic ns-SNPs. It is hoped that the results of these and similar

studies will identify immunodominant epitopes in FVIII and thus motivate the development of new therapeutic FVIII products targeted to particular populations. We expect that susceptible patient populations will increasingly be defined

by the results of genetic tests that are more specific, i.e. predictive of potential immune responses. We also expect that some genetic determinants of risk – such as large F8 deletions involving multiple exons, medchemexpress which occur with comparable frequencies in all human populations – will not correlate with racial self-identification. Future genetic markers will be more predictive of inhibitor risk in more precisely defined sub-populations and they will be more useful than, for example, the general assumption of a higher inhibitor risk in black HA patients. It is important to note that only a subset of HA patients with any racial heritage is likely to be at higher risk for inhibitor development, and the relevant genetic risk factors need to be better defined. Increasing knowledge of immune mechanisms leading to neutralizing antibodies will also suggest new therapeutic approaches targeted to specific at-risk populations. We anticipate that genotyping of HA patients will eventually include testing for the presence of particular SNPs in both F8 and immune regulatory genes, e.g. those encoding the HLA class II antigen-presentation repertoire, in addition to the HA-causing F8 mutation. Appropriate genetic testing will allow better matching of HA patients with FVIII products that are likely to be less immunogenic.

Figure 7 depicts molecular mechanisms by which the ASC/caspase-1/IL-1β-HMGB1

axis may regulate the liver IRI immune cascade. ASC contributes to inflammatory responses through the activation of inflammasomes, which in turn activate caspase-1 and catalyze pro–IL-1β/pro–IL-18 into mature IL-1β/IL-18. IL-18 is closely related to and shares a similar dimensional structure with IL-1β. ASC/caspase-1/IL-1 promotes HMGB1 induction through the activation of p38 MAPK, which triggers TLR4 and NF-κB to program proinflammatory mediators. In addition, HMGB1 might provide a positive feedback mechanism to regulate caspase-1 activation. ASC/caspase-1–mediated elaboration of IL-1β and COX2 downstream are required for inflammatory development in the course www.selleckchem.com/products/OSI-906.html of hepatic IRI. In conclusion, ASC/caspase-1/IL-1β signaling promotes HMGB1 induction to facilitate a TLR4-dependent inflammatory phenotype leading to IR hepatocellular damage. By identifying HMGB1 as a novel mediator in ASC/caspase-1/IL-1β–triggered inflammation, Selleckchem ICG-001 our findings provide a rationale for refined therapeutic strategies against liver IRI. Additional Supporting Information may be found in the online version of this article. “
“Taking nucleoside/nucleotide analogs is a major antiviral

therapy for chronic hepatitis B infection. The problem with this treatment is the selection for drug-resistant mutants. Currently, identification of genotypic drug resistance is conducted by molecular cloning sequenced by the Sanger method. However, this methodology is complicated and time-consuming.

These limitations can be overcome by deep sequencing technology. Therefore, we performed MCE公司 sequential analysis of the frequency of drug resistance in one individual, who was treated with lamivudine on-and-off therapy for 2 years, by deep sequencing. The lamivudine-resistant mutations at rtL180M and rtM204V and the entecavir-resistant mutation at rtT184L were detected in the first subject. The lamivudine- and entecavir-resistant strain was still detected in the last subject. However, in the deep sequencing analysis, rt180 of the first subject showed a mixture in 76.9% of the methionine and in 23.1% of the leucine, and rt204 also showed a mixture in 69.0% of the valine and 29.8% of the isoleucine. During the treatment, the ratio of resistant mutations increased. At rt184, the resistant variants were detectable in 58.7% of the sequence, with the replacement of leucine by the wild-type threonine in the first subject. Gradually, entecavir-resistant variants increased in 82.3% of the leucine in the last subject. In conclusion, we demonstrated the amino acid substitutions of the serial nucleoside/nucleotide analog resistants.

Results: In contrast to the g-c, liver fibrosis in the g-TAA was remarkable and portal pressure was increased from 9.43 ± 1.42 mmHg to 15.03 ± 0.79 mmHg, p < 0.01. The hepatic tissue levels of Collagen I, Collagen III, α-SMA, TGF-β1 were increased 1.5–6.3 folds individually, while

E-cadherin was decreased to 39%. Compared with g-TAA, both Ishak’s score (5.42 ± 0.84 vs. 3.33 ± 1.41, p < 0.05) and portal pressure (15.03 ± 0.79 mmHg vs. 12.03 ± 1.06 mmHg, p < 0.05) of the g-TAA + O were significantly decreased. Moreover, the hepatic tissue levels of cytokines, Collagen proteins, α-SMA, TGF-β1 and Smad2/3 were decreased to 31–53% separately, E-cadherin was increased 0.64 fold, after octreotide treatment, p < 0.05 or p < 0.01. Conclusion: Octreotide relieved hepatic fibrogenesis and decreased portal pressure properly through inhibition of Dasatinib manufacturer chronic inflammation and TGF-β1 pathway in the TAA cirrhotic rats. These findings suggest octreotide may benefit the prevention of hepatic cirrhosis and portal hypertension. Key Word(s): 1. hepatic fibrosis; 2. portal hypertension; 3. octreotide; 4. TGF beta-1; Presenting Author: RADAN BRUHA Additional Authors: JAROMIR PETRTYL, LIBOR VITEK, PETR URBANEK, KAREL DVORAK Corresponding Author: RADAN BRUHA Affiliations: Charles University

in Prague, 1st Faculty of Medicine, 4th Internal clinic; Charles University in Prague, 1st Faculty of Medicine, Internal clinic of Central Military Hospital Objective: Portal hypertension is an unavoidable consequence of Sotrastaurin datasheet liver cirrhosis leading 上海皓元 to major complications of this disease. Non-selective betablockers like propranolol play a crucial role in the prevention of variceal bleeding. Carvedilol is a new promising combined alfa and nonselective betablocker used in the treatment of portal hypertension. The data from long-term use of carvedilol are scarce in literature. The aim was to determine 1. The efficacy

of carvedilol in the lowering the portal pressure in patients with liver cirrhosis; 2. The safety of carvedilol treatment in patients with liver cirrhosis. Methods: 67 patients with liver cirrhosis (47 ethylic, 47 men, age 36–72 years) indicated for the treatment by betablockers in the prevention of variceal bleeding were given carvedilol 12, 5 mg twice a day. HVPG measurement was performed before and 1 month after the treatment initialisation. The treatment response was evaluated as the drop in HVPG for more than 20% or below 12 mm Hg. Results: HVPG decreased from 17 ± 4, 3 to 15 ± 4, 5 mmHg (p < 0.001) in the whole group of cirrhotics. Complete response was observed in 33 patients (49% of all patients). HVPG decreased to from 18 ± 4, 2 mm Hg to 13 ± 4, 1 mm Hg in responders (-33%; p < 0.001). The heart rate decreased from 82.4 ± 10.5 to 71.2 ± 11.

The three HP+ patient who were resistant to fluoroquilolones were HetEM (*2/*1).

Eradication with 14 days regime (PPI+clarithromycin+amoxycilin) was near 96%. Conclusion: More epidemiological data in Greek population are needed to establish the real prevalence of the CYP2C19 polymorphisms which, combined with the antibiotic resistant molecular test could be useful for difficult to treat patients. Key Word(s): 1. CYP2C19; 2. Helicobacter Protein Tyrosine Kinase inhibitor pylori; 3. Resistance; 4. Eradication; Presenting Author: LIAOSHENG YIN Additional Authors: CHENJIAN YONG, HUJIAN FANG Corresponding Author: CHENJIAN YONG Affiliations: The People’s Hospital of JianXi Province; The People’s Hospital of JianXI Province; The People’s Hospital of Jianxi Province

Objective: To Study the gastric mucosal proteins expression in chronic gastictis rat with damp-heat Opaganib datasheet syndrome of spleen-stomach and investigate the pathogenesis related to the chronic gastictis. To observe the differential expression of gastric mucosal protein in chronic gastictis rat model with damp-heat syndrome of spleen-stomach after treatment with sanren decoction and investigate the mechanism of sanren decoction in chronic gastictis Methods: The rats models were reproduced by quantified method. Proteomic two-dimensional gel electrophoresis technique was used to separate total gastric mucosal protein. The two-dimensional gel electrophoresis maps were analysised to decect protein spots expressed differently by

PDquest 8.0 software, the protein spots expressed differently was identified by MALDI-TOF/TOF-MS. Results: the protein spots were 1025 ± 39, 994 ± 51, 1087 ± 33, deteced from two-dimensional gel electrophoresis profiles of normal control group, model group and sanren decoction group respectively. The protein spots of differential expression were 74 between model group and normal control group,30 spots up-regulated in model group while 44 spots down-regulated; The protein spots of differential expression were 75 between sanren decoction group and model group,49 spots up-regulated in sanren decoction group while 26 spots down- regulated. 上海皓元医药股份有限公司 Five protein spots of differential expression were identified successfully. The identificated results are: heat shock protein 72, heat shock protein 60, protein disulfide-isomerase, malate dehydrogenase, unnamed protein Conclusion: The pathogenesis of chronic gastictis with damp-heat syndrome of spleen-stomach may be related to energy metabolism disorders and stress, the mechanism of sanren decoction in the chronic gastritis with damp-heat syndrome of spleen-stomach may adjust the differential expression of gastric mucosal protein. Key Word(s): 1. chronic gastritis; 2. Damp-heat syndrome; 3. proteome; 4. Sanren decoction; Presenting Author: YINGLIAN XIAO Additional Authors: FRÉDÉRIC NICODÈME, ZHIYUE LIN, SABINE ROMAN, PETER J.

The three HP+ patient who were resistant to fluoroquilolones were HetEM (*2/*1).

Eradication with 14 days regime (PPI+clarithromycin+amoxycilin) was near 96%. Conclusion: More epidemiological data in Greek population are needed to establish the real prevalence of the CYP2C19 polymorphisms which, combined with the antibiotic resistant molecular test could be useful for difficult to treat patients. Key Word(s): 1. CYP2C19; 2. Helicobacter selleck screening library pylori; 3. Resistance; 4. Eradication; Presenting Author: LIAOSHENG YIN Additional Authors: CHENJIAN YONG, HUJIAN FANG Corresponding Author: CHENJIAN YONG Affiliations: The People’s Hospital of JianXi Province; The People’s Hospital of JianXI Province; The People’s Hospital of Jianxi Province

Objective: To Study the gastric mucosal proteins expression in chronic gastictis rat with damp-heat LDE225 syndrome of spleen-stomach and investigate the pathogenesis related to the chronic gastictis. To observe the differential expression of gastric mucosal protein in chronic gastictis rat model with damp-heat syndrome of spleen-stomach after treatment with sanren decoction and investigate the mechanism of sanren decoction in chronic gastictis Methods: The rats models were reproduced by quantified method. Proteomic two-dimensional gel electrophoresis technique was used to separate total gastric mucosal protein. The two-dimensional gel electrophoresis maps were analysised to decect protein spots expressed differently by

PDquest 8.0 software, the protein spots expressed differently was identified by MALDI-TOF/TOF-MS. Results: the protein spots were 1025 ± 39, 994 ± 51, 1087 ± 33, deteced from two-dimensional gel electrophoresis profiles of normal control group, model group and sanren decoction group respectively. The protein spots of differential expression were 74 between model group and normal control group,30 spots up-regulated in model group while 44 spots down-regulated; The protein spots of differential expression were 75 between sanren decoction group and model group,49 spots up-regulated in sanren decoction group while 26 spots down- regulated. MCE公司 Five protein spots of differential expression were identified successfully. The identificated results are: heat shock protein 72, heat shock protein 60, protein disulfide-isomerase, malate dehydrogenase, unnamed protein Conclusion: The pathogenesis of chronic gastictis with damp-heat syndrome of spleen-stomach may be related to energy metabolism disorders and stress, the mechanism of sanren decoction in the chronic gastritis with damp-heat syndrome of spleen-stomach may adjust the differential expression of gastric mucosal protein. Key Word(s): 1. chronic gastritis; 2. Damp-heat syndrome; 3. proteome; 4. Sanren decoction; Presenting Author: YINGLIAN XIAO Additional Authors: FRÉDÉRIC NICODÈME, ZHIYUE LIN, SABINE ROMAN, PETER J.