Based on the preferential elevation of MCP-1 among other CC-chemokines in alcoholic hepatitis patients4, 5 and its importance in the modulation of proinflammatory cytokines,9, 10 we hypothesized that MCP-1 contributes to chronic alcoholic liver injury and steatosis via the modulation of inflammatory cytokines. Using MCP-1-deficient mice, we sought to investigate whether MCP-1 and its receptor, chemokine (C-C motif) receptor 2 (CCR2), play a causative role in alcoholic liver injury. ACOX, acyl coenzyme A oxidase; ALD, alcoholic liver disease; ALT, alanine aminotransferase; CCL2, chemokine (C-C motif) ligand 2; CCR2, chemokine (C-C motif) receptor 2; CD, cluster of differentiation; CoA, coenzyme Quizartinib chemical structure A; CPT-1,

carnitine palmitoyl transferase 1A; CYP2E1, cytochrome P450 2E1; ELISA, enzyme-linked immunosorbent assay; EMSA, electrophoretic mobility shift analysis; H&E, hematoxylin and eosin; ICAM-1, intercellular adhesion molecule 1; IL, interleukin; IP, intraperitoneal; KCs, Kupffer cells; KO, knockout; LCAD, long-chain acyl-CoA dehydrogenase; LPS, lipopolysaccharide; MCAD, medium-chain acyl-CoA dehydrogenase; MCP-1, monocyte chemoattractant protein-1; MIP-1, macrophage inflammatory Napabucasin order protein 1; mRNA, messenger RNA; NF-κB, nuclear factor kappa light-chain enhancer of activated B cells; PPARα, peroxisome proliferator-activated receptor

alpha; PPARγ, peroxisome proliferator-activated receptor gamma; PPRE, peroxisome proliferator response element; qPCR, quantitative polymerase chain reaction; SEM, standard error of the mean; TBARS, thiobarbituric acid-reactive substances; TLR4, Toll-like receptor 4; TNFα, tumor necrosis factor alpha; VCAM-1, vascular cell adhesion molecule 1; WT, wild type. Additional descriptions medchemexpress of methods are available

in the Supporting Information. All animals received proper care in agreement with animal protocols approved by the Institutional Animal Use and Care Committee of the University of Massachusetts Medical School (Worcester, MA). Six- to eight-week-old female wild-type (WT) (C57BL/6) and MCP-1-deficient and CCR2-deficient mice (all generated on a C57BL/6 background; The Jackson Laboratory, Bar Harbor, ME) received Lieber-DeCarli diet (Bio-Serv, Frenchtown, NJ) with 5% (v/v) ethanol (36% ethanol-derived calories) for 6 weeks; pair-fed control mice received an equal amount of calories as their alcohol-fed counterparts with the alcohol-derived calories substituted with dextrin maltose. All strains of mice consumed comparable daily calories. In some cases, mice from both the alcohol-fed and pair-fed groups were administered an intraperitoneal (IP) injection of either 0.2 mL of 0.9% saline (phosphate-buffered, pH 7.4) alone as a vehicle control or 0.2 mL 0.9% saline containing 0.5 mg/kg of nonpurified lipopolysaccharide (LPS; from Escherichia coli 0111:B4; Sigma-Aldrich, St. Louis, MO) and sacrificed 2 hours later.

Key Word(s): 1. Postcholecystectomy; 2. diarrhoea; 3. Diagnosis criteria; 4. Prediction; Presenting Author: HIROYUKI TAMAKI Additional Authors: AKIKO NOGAMI, TERUYO NODA, YUMIKO MORIOKA, SOUICHI ARASAWA, YUKIKO MIYAMOTO, MASAKO IZUTA, TETSURO ISHIKAWA, TOSHIHIRO MATSUNAKA, CHIKARA OGAWA, MITSUSHIGE SHIBATOGE Corresponding Author: HIROYUKI TAMAKI Affiliations: Takamatsu Redcross Hospital Objective: Although some studies have reported the efficacy of percutaneous transhepatic gallbladder aspiration (PTGBA) as alternative therapy for the treatment of acute cholecystitis

with fewer Temsirolimus manufacturer complications, the clinical usefulness of PTGBA has not yet been fully examined. We evaluated the efficacy and safety of PTGBA for the treatment of acute cholecystitis compared with percutaneous transhepatic gallbladder INCB018424 purchase drainage (PTGBD) and surgical treatment. Methods: A total of 76 patients, median age 67 years old, with acute cholecystitis was included to this study. PTGBA was performed in

36 patients and 30 patients were treated with PTGBD. Remaining 10 patients were performed an emergency surgery. Results: PTGBA were successful in all patients and achieved improvement in 30 of 36 patients (83.4%). In 3 (8.3%) of the remaining 6 patients, PTGBD was undergone because of recurrence. Biliary peritonitis was occurred in 3 patients (8.3%) and treated with emergency surgery. One of them showed high viscosity of the bile and open surgery revealed that the bile

leaked out to the surface of the liver through puncture hole. In the remaining two, torsion of gallbladder and rupture of necrotic gallbladder were observed. PTGBD were successful in 29 of 30 patients and all cases of success were improved without any complications. All patients treated by emergency surgery were improved without any complications. There was no difference in the improvement of WBC and CRP in 5 days after treatment between each group. Mean length of hospital stay was 上海皓元 significantly shorter in patients treated with PTGBA than others (p < 0.05). In patients treated with PTGBA, there was no correlation between the volumes of puncture fluid or bacterial strain cultured from removed bile and the effect of treatment. Recurrence was tending to observe more frequently in patients with biliary sludge and no gallstones than patients with both of them or only with gallstones. Although abdominal pain was ameliorated within 12 hours after PTGBA in successfully treated patients, was not ameliorated in patients with biliary peritonitis even after 12 hours. Conclusion: PTGBA is a simple and useful therapy for the treatment of acute cholecystitis. However, it is important to pay attention to development of complications especially in patients with high bile viscosity, torsion of gallbladder, and necrotic cholecystitis. Key Word(s): 1. acute cholecystitis; 2.