Key Word(s): 1. Helicobacter pylori; 2. outer-membrane protein; 3. HomB Presenting Author: YONG XIE Additional Authors: ZHI RONG p38 MAPK apoptosis MAO, NAN JIN ZHOU, DONG SHENG LIU, FU CAI WANG Corresponding Author: YONG XIE Affiliations: The First Affiliated Hospital of Nanchang University, Institute of Medical Sciences of Jiangxi Province, The First Affiliated Hospital of Nanchang University, The First Affiliated Hospital of Nanchang

University Objective: Macrophages play an important role in H. pylori infection. Toll-like receptor 4 (TLR4) activated macrophages to secrete plenty of cytokines which regulated inflammation and immunity reaction; T-cell immunoglobulin and mucin-domain-containing molecule-3 (Tim-3) , an important member of TIM family, was also expressed on macrophages and could impact macrophages function through interacting

with TLR4 pathways. Until now, It is unclear that how H. pylori impacts Tim-3 and TLR4 pathways in macrophages. Methods: ①RAW264.7 cells were co-cultured with H.pylori CP-673451 nmr SS1 at different bacteria/cell ratio (MOI) at 3h, 6h, 12h, 24h and 48h were detected by MTT assay, respectively. At 12h, the mRNA expressions of Tim-3\TLR4\MyD88 were measured by RT-PCR; ②Tim-3-overexpressing RAW264.7 cells were constructed by transfer pLVX-IRES-ZsGreen-Tim-3 and co-cultured with H.pylori. The mRNA and protein expressions 上海皓元 of Tim-3\TLR4\MyD88 were determined

by RT-PCR and Western Blot. The concentrations of cytokines (TNF-α, IL-6, IFN-γ and IL-10) in supernatants were measured by ELISA. Results: ①RAW264.7 cells were co-cultured with H.pylori SS1 at different bacteria/cell ratio (MOI) at 3h, 6h, 12h, 24h and 48h were detected by MTT assay, respectively. At 12h, the mRNA expressions of Tim-3\TLR4\MyD88 were measured by RT-PCR; ②Tim-3-overexpressing RAW264.7 cells were constructed by transfer pLVX-IRES-ZsGreen-Tim-3 and co-cultured with H.pylori. The mRNA and protein expressions of Tim-3\TLR4\MyD88 were determined by RT-PCR and Western Blot. The concentrations of cytokines (TNF-α, IL-6, IFN-γ and IL-10) in supernatants were measured by ELISA. Conclusion: Over-expression of Tim-3 reduces H. pylori-induced inflammation through down-regulating TLR4 pathways expressions and pro-inflammatory cytokines release from RAW264.7 infected with H. pylori. Key Word(s): 1. Helicobacter pylori; 2. RAW264.7; 3. Tim-3; 4.

, MD (Early Morning Workshops) Advisory Committees or Review Panels: Janssen, Merck, Genentech, BMS, Gilead, Boehinger Ingelheim, AbbVioe Consulting: Genentech, Lumena, Regulus, Beckman Coulter, RMS Grant/Research Support: Novartis, Intercept, Janssen, Genentech, BMS, Gilead, Vertex, selleck screening library Boehinger Ingelheim, Lumena, Beckman Coulter, AbbVie, RMS, Novartis, Merck Speaking and Teaching: Genentech, BMS, Gilead Podskalny, Judith, PhD (Career Development Workshop) Nothing to disclose Poelstra, Klaas, PhD (Basic Research Workshop) Consulting: BiOrion Technologies BV Grant/Research Support: BiOrion Technologies

BV Stock Shareholder: BiOrion Technologies BV Pomposelli, James, MD, PhD (Parallel Session) Nothing to disclose Poordad, Fred, MD (General Hepatology Update) Advisory Committees or Review Panels: Abbott, Achillion, BMS, Inhibitex, Boeheringer Ingelheim, Pfizer, Genentech, Idenix, Gilead, Merck, Vertex, SCH727965 in vitro Salix, Janssen, Novartis Grant/Research Support: Abbott, Anadys, Achillion, BMS, Boehringer Ingelheim, Genentech, Idenix, Gilead, Merck, Pharmassett, Vertex, Salix, Tibotec/Janssen, Novartis Porte, Robert J., MD, PhD, FEBS (AASLD/ILTS Transplant Course) Advisory Committees or Review Panels: Organ Assist Quigley, Eamonn M., MD (AASLD Postgraduate Course) Advisory Committees

or Review Panels: Salix, Shire, Almirall, Ironwood/Forest Board Membership: Alimentary Health Consulting: Alimentary Health, Vibrant Grant/Research Support: Ironwood/Forest, Rhythm, Norgine Speaking and Teaching: Procter and Gamble, Janssen, Shire, Almirall Stock Shareholder: Alimentary Health Rafii, Shahin, MD (Basic Research Workshop) Consulting: Angiocrine Bioscience Ramsay, Michael A., MD (Transplant Surgery Workshop) Grant/Research Support: Masimo Inc Reddy, K. Gautham, MD (Competency Training Workshop) Advisory Committees or Review Panels: AASLD Transplant Hepatology Pilot Steering MCE Committee, ACG Training Committee, Program Director’s

Caucus Steering Committee Grant/Research Support: Intercept, Ocera, Merck, Lumena Reddy, K. Rajender, MD (Advances for Practitioners, Meet-the-Professor Luncheon) Advisory Committees or Review Panels: Genentech-Roche, Merck, Janssen, Vertex, Gilead, BMS, Novartis, Abbvie Grant/Research Support: Merck, BMS, Ikaria, Gilead, Janssen, AbbVie Rehermann, Barbara, MD (AASLD Postgraduate Course, Early Morning Workshops, Parallel Session) Nothing to disclose Reich, David J., MD (Plenary Session) Consulting: VTI Grant/Research Support: VTI Speaking and Teaching: neuwave Renz, John F., MD, PhD (AASLD/ILTS Transplant Course) Nothing to disclose Reuben, Adrian, MBBS, FRCP, FACG (Early Morning Workshops, State-of-the-Art Lecture) Nothing to disclose Rex, Douglas K.

RNA was isolated using RNeasy FFPE Mini Kit (QIAGEN, BAY 73-4506 in vivo Hilden, Germany) according to

the manufacturer’s instructions with modification for copurification of miRNA, then stored at −80°C. Contaminating genomic DNA was removed using Turbo DNase digestion (Ambion Life Technologies, Carlsbad, CA, USA) according to the manufacturer’s instructions. MicroRNA expression was determined applying the following TaqMan MicroRNA Assays (Applied Biosystems, Carlsbad, CA, USA): miR-21 (ID:000397), miR-23a (ID:000399), miR-34a (ID:000426), miR-96 (ID:000186), miR-99a* (ID:002141), miR-122 (ID:002245), miR-125b (ID:000449), miR-181a-2* (ID:002317), miR-194 (ID:000493), miR-195 (ID:000494), miR-217 (ID:002337), miR-221 (ID000524), and miR-224 (ID:002099). RT

was performed using TaqMan BGJ398 cost MicroRNA Reverse Transcription Kit (Applied Biosystems) according to the manufacturer’s instructions in 7.5 μL final volume containing 10 ng total RNA. TaqMan Universal PCR Master Mix No AmpErase UNG (Applied Biosystems) was applied for real-time PCR, also carried out according to the manufacturer’s instructions, in 10 μL final volume containing 0.65 μL RT product. The reaction was run on an ABI PRISM 7000 system (Applied Biosystems). The samples were measured in duplicates. Relative expression level in samples was determined by 2ΔCq method using the mean Cq value of miR-23a and miR-34a as reference. These MCE公司 reference miRs showing the overall least variation among samples were selected using NormFinder[20] as U6 snRNA (ID:001973) proved to be highly variable in the samples. SPSS 15. version (SPSS, Inc., Chicago, IL, USA) was used for the statistical analysis. Continuous variables

are shown as mean values and standard deviations. Student’s t-test, anova test with Scheefe and Bonferroni post hoc tests, as well as Mann–Whitney U-test were utilized for univariate analyses, after examining population homogeneity of the variables (Levene test). The anova method was used to compare microRNA expression before and after IFN therapy, when therapy response (SVR vs NR) was taken into account. The connections between continuous variables were evaluated by correlation analysis, using Pearson correlation coefficient. P < 0.05 was considered significant. Baseline characteristics of patients are shown in Table 1. Examination of the clinical data revealed that post-treatment viral load decreased significantly only in the SVR group when compared with pretreatment levels (12 × 106 /mL ± 15.7 vs 0/mL, P = 0.003). HAI decreased in both NR (3.74 ± 1 vs 1.6 ± 1, P < 0.0001) and SVR groups (4 ± 1 vs 1 ± 1.3, P = 0.002) after administering IFN/RBV therapy. After finishing antiviral therapy fibrosis score was analyzed, and no correlation was found between fibrosis being above or below the median (fibrosis score 1) and the investigated miRs. High viral load (above median 3.

RNA was isolated using RNeasy FFPE Mini Kit (QIAGEN, selleck chemical Hilden, Germany) according to

the manufacturer’s instructions with modification for copurification of miRNA, then stored at −80°C. Contaminating genomic DNA was removed using Turbo DNase digestion (Ambion Life Technologies, Carlsbad, CA, USA) according to the manufacturer’s instructions. MicroRNA expression was determined applying the following TaqMan MicroRNA Assays (Applied Biosystems, Carlsbad, CA, USA): miR-21 (ID:000397), miR-23a (ID:000399), miR-34a (ID:000426), miR-96 (ID:000186), miR-99a* (ID:002141), miR-122 (ID:002245), miR-125b (ID:000449), miR-181a-2* (ID:002317), miR-194 (ID:000493), miR-195 (ID:000494), miR-217 (ID:002337), miR-221 (ID000524), and miR-224 (ID:002099). RT

was performed using TaqMan Ulixertinib manufacturer MicroRNA Reverse Transcription Kit (Applied Biosystems) according to the manufacturer’s instructions in 7.5 μL final volume containing 10 ng total RNA. TaqMan Universal PCR Master Mix No AmpErase UNG (Applied Biosystems) was applied for real-time PCR, also carried out according to the manufacturer’s instructions, in 10 μL final volume containing 0.65 μL RT product. The reaction was run on an ABI PRISM 7000 system (Applied Biosystems). The samples were measured in duplicates. Relative expression level in samples was determined by 2ΔCq method using the mean Cq value of miR-23a and miR-34a as reference. These 上海皓元 reference miRs showing the overall least variation among samples were selected using NormFinder[20] as U6 snRNA (ID:001973) proved to be highly variable in the samples. SPSS 15. version (SPSS, Inc., Chicago, IL, USA) was used for the statistical analysis. Continuous variables

are shown as mean values and standard deviations. Student’s t-test, anova test with Scheefe and Bonferroni post hoc tests, as well as Mann–Whitney U-test were utilized for univariate analyses, after examining population homogeneity of the variables (Levene test). The anova method was used to compare microRNA expression before and after IFN therapy, when therapy response (SVR vs NR) was taken into account. The connections between continuous variables were evaluated by correlation analysis, using Pearson correlation coefficient. P < 0.05 was considered significant. Baseline characteristics of patients are shown in Table 1. Examination of the clinical data revealed that post-treatment viral load decreased significantly only in the SVR group when compared with pretreatment levels (12 × 106 /mL ± 15.7 vs 0/mL, P = 0.003). HAI decreased in both NR (3.74 ± 1 vs 1.6 ± 1, P < 0.0001) and SVR groups (4 ± 1 vs 1 ± 1.3, P = 0.002) after administering IFN/RBV therapy. After finishing antiviral therapy fibrosis score was analyzed, and no correlation was found between fibrosis being above or below the median (fibrosis score 1) and the investigated miRs. High viral load (above median 3.

Zhao et al. [32] analyzed the expression of the transmembrane protein CD133 in GC, because it was described that CD133 is overexpressed in various solid tumors [33]. They found that CD133 PD98059 mouse was overexpressed in more than 55% of GC and has a positive correlation with the expression of Ki-67. In another study, Anami et al. [34] found an overexpression

of the membrane protein desmocollin-2 (DSC2) in intestinal-type GC. Interestingly, they showed that expression of DSC2 was induced by CDX2, suggesting that expression of desmocollin-2 could be a key regulator for GC with intestinal phenotype. One transmembrane protein for which a new targeted compound is being studied in clinical trials on solid tumors is P-cadherin. Kim et al. [35] reported recently that P-cadherin is not expressed in normal

gastric mucosa but is overexpressed in GC, especially in tumors of the intestinal type. The authors reported that the increased expression of P-cadherin in GC was found to be significantly correlated with promoter hypomethylation. Another member of the cadherin superfamily, CDH17, was also reported by Lee et al. [36] as a promising marker for early-stage gastric cancer. Also according to Lee et al., CDH17 expression was positively check details associated with a good prognosis. Hyaluronic acid (HA) is a component of the extracellular matrix. In cancerous tissue, HA is greatly secreted from stromal fibroblasts in response to factors MCE derived from tumor cells [37]. The two most well-known cell receptors for HA are CD168 and CD44 [38]. In a recent study, Ishigami et al. [39] reported the overexpression of CD168 in a panel of GC cases. According to these authors, CD168 positivity was significantly associated with the depth of invasion and metastasis of GC, an association that was previously reported for other types of cancer [40].

In a different study, da Cunha et al. [41] described the de novo expression of a CD44 variant (CD44v6) in GC. Noteworthy, they observed that CD44v6 was rarely expressed in normal gastric mucosa but was increasingly expressed in premalignant and malignant lesions. A recent study by Ishimoto et al. [42] sheds light about some roles of CD44 variants (CD44v) expression in gastrointestinal tumors. Ishimoto et al. found that CD44v controls the intracellular level of reduced glutathione (GSH), and cancer cells that express more CD44v showed an enhanced capacity for GSH synthesis and defence against reactive oxygen species, promoting tumor growth. Matrix metalloproteinases (MMP), a family of zinc-dependent endopeptidases, are involved in various physiological and pathological processes, such as extracellular matrix degradation, tissue remodeling, inflammation, and tumor invasion and metastasis [43].

Zhao et al. [32] analyzed the expression of the transmembrane protein CD133 in GC, because it was described that CD133 is overexpressed in various solid tumors [33]. They found that CD133 Ibrutinib ic50 was overexpressed in more than 55% of GC and has a positive correlation with the expression of Ki-67. In another study, Anami et al. [34] found an overexpression

of the membrane protein desmocollin-2 (DSC2) in intestinal-type GC. Interestingly, they showed that expression of DSC2 was induced by CDX2, suggesting that expression of desmocollin-2 could be a key regulator for GC with intestinal phenotype. One transmembrane protein for which a new targeted compound is being studied in clinical trials on solid tumors is P-cadherin. Kim et al. [35] reported recently that P-cadherin is not expressed in normal

gastric mucosa but is overexpressed in GC, especially in tumors of the intestinal type. The authors reported that the increased expression of P-cadherin in GC was found to be significantly correlated with promoter hypomethylation. Another member of the cadherin superfamily, CDH17, was also reported by Lee et al. [36] as a promising marker for early-stage gastric cancer. Also according to Lee et al., CDH17 expression was positively find more associated with a good prognosis. Hyaluronic acid (HA) is a component of the extracellular matrix. In cancerous tissue, HA is greatly secreted from stromal fibroblasts in response to factors medchemexpress derived from tumor cells [37]. The two most well-known cell receptors for HA are CD168 and CD44 [38]. In a recent study, Ishigami et al. [39] reported the overexpression of CD168 in a panel of GC cases. According to these authors, CD168 positivity was significantly associated with the depth of invasion and metastasis of GC, an association that was previously reported for other types of cancer [40].

In a different study, da Cunha et al. [41] described the de novo expression of a CD44 variant (CD44v6) in GC. Noteworthy, they observed that CD44v6 was rarely expressed in normal gastric mucosa but was increasingly expressed in premalignant and malignant lesions. A recent study by Ishimoto et al. [42] sheds light about some roles of CD44 variants (CD44v) expression in gastrointestinal tumors. Ishimoto et al. found that CD44v controls the intracellular level of reduced glutathione (GSH), and cancer cells that express more CD44v showed an enhanced capacity for GSH synthesis and defence against reactive oxygen species, promoting tumor growth. Matrix metalloproteinases (MMP), a family of zinc-dependent endopeptidases, are involved in various physiological and pathological processes, such as extracellular matrix degradation, tissue remodeling, inflammation, and tumor invasion and metastasis [43].

3) 382 (98.5) <0.0001* More than one comarbidites (%) 23 (9.5) 283 (72.9) <0.0001* Hematemesis (%) 40 (16.6) 51 (25.5) 0.009* Initial SBP < 100 mmHg (%) 49 (20.3) 136 (35.1) <0.0001* In-hospital bleeders (%) 3 (1.2) 88 (22.7) <0.0001* H pylori (%) 190 (78.8) 103 (26.5) <0.0001* Rebleeding (%) 6 (2.5) 66 (17.0) <0.0001* Nees for surgery (%) 0 (0) 9 (2.3) 0.015* selleck Presenting Author: ARIFAHRIAL SYAM Additional Authors: ARIANI SETIAWATI Corresponding

Author: ARIFAHRIAL SYAM Affiliations: Department of Internal Medicine, Faculty of Medicine University of Indonesia; Department of Pharmacology and Therapeutics, Faculty of Medicine University of Indonesia Objective: This study was a multicenter observational postmarketing study of lansoprazole injection to assess its safety and effectiveness in patients with upper gastrointestinal

bleeding due to peptic ulcers or erosive gastritis. Methods: Patients with upper gastrointestinal bleeding due to peptic ulcers or erosive gastritis were given intravenous lansoprazole for a maximum of 7 days or until the bleeding stopped and the patients were able to take oral lansoprazole. Primary outcome of the study was stopped bleeding. Some laboratory parameters were also measured. Results: Among a total of 204 patients evaluable for safety, there was no adverse event reported during the study. A total of 200 patients were eligible for efficacy evaluation, 125 patients (62.5%) were males. Among these patients, upper GI bleeding stopped selleck chemicals in 20 patients (10.0%) on day 1, in 71 patients (35.5%) on day 2, 75 patients (37.5%) on day 3, 24 patients (12.0%) on day 4, and 7 patients (3.5%) on day 5, making a cumulative of 197 patients (98.5%) on day 5. The hemostatic effect was rated as “excellent” if the bleeding stopped within 3 days, and “good” if the bleeding stopped within 5 days. Thus, the results were “excellent” in 166 patients (83.0%) and “good” in 31 patients (15.5%). These results were not different between males and females, between age below 60 years and 60 years and above, and between baseline Hb below medchemexpress 10 g/dL and 10 g/dL and above.

Conclusion: The results of this observational postmarketing study in 200 patients with upper gastrointestinal bleeding due to peptic ulcers or erosive gastritis demonstrated that intravenous lansoprazole twice a day was well tolerated and highly effective. Key Word(s): 1. postmarketing; 2. lansoprazole; 3. gastrointestinal; 4. bleeding; Presenting Author: ALI KHAWAJA Additional Authors: SHAHAB ABID, AMBREEN SONAWALLA, SANAFARHAD SOMANI Corresponding Author: ALI KHAWAJA Affiliations: The Aga Khan University Hospital Objective: Gastric variceal bleeding, one of the most feared complications of portal hypertension is usually more severe and difficult to control than esophageal variceal bleeding. Hence, it is imperative to identify the optimal therapy for its management.

We selected the HepG2, SNU368,

and SNU449 cells as they were found to express little or no HDAC6 by northern and western blot analysis (Fig. 1E), and transfected with pcDNA_HDAC6. As expected, ectopic expression of HDAC6 caused growth retardation and elicited increased LC3B-II conversion in these liver cancer cells as compared with control (non- or empty vector-transfected) cells (Fig. 5A-F). In contrast, for PLC/PRF/5 and SNU423 cells that exhibit relatively high expression of HDAC6 among liver cancer cell lines (Fig. 1E), the knockdown of HDAC6 significantly enhanced growth rates of these cell R788 clinical trial lines (Supporting Fig. 3). Similarly, when the same experimental approach was applied to newly established HDAC6-overexpressing Hep3B cell lines (Hep3B_HDAC6 Clone #1 and Clone #2), resilencing of HDAC6 also caused an increased growth rate compared to control cells (scramble sequence of siRNA transfectants). Lastly, to investigate whether tumor suppressor activity of HDAC6 is HCC-specific,

we selleck screening library analyzed HDAC6 gene expressions of colon, gastric, and breast cancer patients from the NCBI GEO database. We selected two sets of microarray data for each colon, gastric, or breast cancer, and compared HDAC6 expression in cancer patients with that of nontumor tissues. There were no significant differences of HDAC6 expression between the normal and tumor group in both colon and gastric cancer datasets (Supporting Fig. 5A-D), whereas the HDAC6 expression in breast cancer was variable depending on cohort study (Supporting Fig. 5E,F). However, when ectopic overexpression of HDAC6 was performed in each of three different colon, gastric, or breast cancer cell lines, all cell lines exhibited no changes in growth rate and LC3B-II conversion (Supporting Figs. 6-8). These results clearly indicated 上海皓元 that HDAC6 functions as a tumor

suppressor by activating autophagic cell death, and tumor suppressor activity is specific to HCC. To investigate whether the stable overexpression of HDAC6 suppresses liver tumorigenesis, we established two cell lines stably overexpressing HDAC6 (Hep3B_HDAC6 Clone #1 and Clone #2). The functional HDAC6 expression was confirmed by detecting the hypoacetylated α-tubulin in these cell lines (Fig. 6A). These cells also exhibited lower growth rates than mock-transfected cells (Hep3B_Mock; Fig. 6B). The immunofluorescence analysis revealed the apparent accumulation of LC3B in Hep3B_HDAC6 cells, whereas almost no accumulation of LC3B was observed in Hep3B_Mock cells (Fig. 6C). In addition, when cells were examined ultrastructures by transmission electron microscopy, ≈40%-45% of Hep3B_HDAC6 cells exhibited autophagic vacuoles, some of which accumulated to form larger cytoplasmic vacuoles (Fig. 6D-b), and at higher magnifications most vacuoles were found to contain electron-dense material and degraded organelles (Fig. 6D-c,d).

Multiple factor scoring systems (Ranson’s criteria and APPACHE II classification system) and individual laboratory tests of pancreatitis

injury and inflammatory response were compared using ANOVA one way test of variances for the degree of pancreatic damage. P value < 0.001 was considered statistically significant. Results: Fourty- six patients (67.6%) were males selleckchem and twenty two (32.4%) females. AP was associated with gallstone disease in 33 patients (48.5%), due to alcohol abuse in 29 (42.6%), and due to other causes of unknown origin in 6 (8.9%). M ± SD value of age, white cells and the number of positive Ranson and APACHE II variables were significantly higher in patients included in the group III compared with those of click here group I, 58.89 ± 16.93 years vs 42.21 ± 16.55 years (p < 0.001), 17800 ± 7000 vs 11143 ± 5692 (p < 0.001), 3.63 ± 1.26 vs 1.79 ± 1.25 (p < 0.001) and 14.47 ± 4.3 vs 8.07 ± 1.14 (p < 0.001), respectively. There were futhermore significant differences in Ranson's criteria and APACHE II classification system between the patients of the group II and III. Although without significant difference, M ± SD of hematocrit and fasting blood sugar were higher in the patients of the group III compared to those of the group I, 35.12 ± 10.71 vs 32.69 ± 14.65 and 157.82 ± 48.42 vs 153.90 ± 108.90, respectively. Conclusion: The early detection of pancreatic necrosis signifies severe disease and is being

used as a grave prognostic indicator in the initial evaluation of these patients. Balthazar grade score plus necrosis score in combination with age, white blood cells and multiple factor score systems may be largely used to asses the severity of AP. Key Word(s): 1. 上海皓元医药股份有限公司 AP; 2. Balthazar score; 3. pancreatic necrosis; 4. severity; Presenting Author: XUE LIU Corresponding Author: XUE LIU Affiliations: Ganzhou City People’s Hospital Objective: To analysis clinical feature of the different etiology of acute pancreatitis (AP), offer information about prevention and

cure of acute pancreatitis. Methods: The clinical data of 82 patients with AP admitted to our hospital from January 2011 to January 2013 were reviewed and were divided into 4 groups according to etiology, analysise the difference from gender, age, clinical symptoms, tiology of pathogenesis of acute pancreatitis. Results: The constituent ratio of etiology of acute pancreatitis the 4 groups were was biliary tract diease (67.1%), alcoholic pancreatitis (6.1%), hyperlipidemic acute pancreatitis (4.9%), and others reason (21.9%). The average age of four group was no significant difference (P > 0.05), The number of female were significantly less in the alcoholic pancreatitis group (P < 0.01). The cause of Mild Acute Pancreatitis and Sereve Acute Pancreatitis was no significant difference. All the acute pancreatitis patients had belly ache. The blood calcium and the blood albumin of the four groups were no significant difference (P > 0.05).

Multiple factor scoring systems (Ranson’s criteria and APPACHE II classification system) and individual laboratory tests of pancreatitis

injury and inflammatory response were compared using ANOVA one way test of variances for the degree of pancreatic damage. P value < 0.001 was considered statistically significant. Results: Fourty- six patients (67.6%) were males learn more and twenty two (32.4%) females. AP was associated with gallstone disease in 33 patients (48.5%), due to alcohol abuse in 29 (42.6%), and due to other causes of unknown origin in 6 (8.9%). M ± SD value of age, white cells and the number of positive Ranson and APACHE II variables were significantly higher in patients included in the group III compared with those of selleck chemicals group I, 58.89 ± 16.93 years vs 42.21 ± 16.55 years (p < 0.001), 17800 ± 7000 vs 11143 ± 5692 (p < 0.001), 3.63 ± 1.26 vs 1.79 ± 1.25 (p < 0.001) and 14.47 ± 4.3 vs 8.07 ± 1.14 (p < 0.001), respectively. There were futhermore significant differences in Ranson's criteria and APACHE II classification system between the patients of the group II and III. Although without significant difference, M ± SD of hematocrit and fasting blood sugar were higher in the patients of the group III compared to those of the group I, 35.12 ± 10.71 vs 32.69 ± 14.65 and 157.82 ± 48.42 vs 153.90 ± 108.90, respectively. Conclusion: The early detection of pancreatic necrosis signifies severe disease and is being

used as a grave prognostic indicator in the initial evaluation of these patients. Balthazar grade score plus necrosis score in combination with age, white blood cells and multiple factor score systems may be largely used to asses the severity of AP. Key Word(s): 1. 上海皓元医药股份有限公司 AP; 2. Balthazar score; 3. pancreatic necrosis; 4. severity; Presenting Author: XUE LIU Corresponding Author: XUE LIU Affiliations: Ganzhou City People’s Hospital Objective: To analysis clinical feature of the different etiology of acute pancreatitis (AP), offer information about prevention and

cure of acute pancreatitis. Methods: The clinical data of 82 patients with AP admitted to our hospital from January 2011 to January 2013 were reviewed and were divided into 4 groups according to etiology, analysise the difference from gender, age, clinical symptoms, tiology of pathogenesis of acute pancreatitis. Results: The constituent ratio of etiology of acute pancreatitis the 4 groups were was biliary tract diease (67.1%), alcoholic pancreatitis (6.1%), hyperlipidemic acute pancreatitis (4.9%), and others reason (21.9%). The average age of four group was no significant difference (P > 0.05), The number of female were significantly less in the alcoholic pancreatitis group (P < 0.01). The cause of Mild Acute Pancreatitis and Sereve Acute Pancreatitis was no significant difference. All the acute pancreatitis patients had belly ache. The blood calcium and the blood albumin of the four groups were no significant difference (P > 0.05).