In addition, these models illustrate that the processes of cholangiocyte differentiation and polarity are separable. Furthermore, these results reveal that epistatic relationships between HNF6, Selleckchem Barasertib HNF1β, and cystin-1 are even more complicated at the transcriptional and translational levels than previously reported. Published work indicates that Hnf6 and Hnf1b are involved in the same transcriptional program.6, 7 However, in their report, Raynaud et al. use defined steps in biliary tubulogenesis to expose that these genes are not exclusively regulated by each other, based on the observed phenotypic differences. Astonishingly, bile duct lumina still form in all cases. These data indicate

that bile duct

lumen formation is a very early event in tubulogenesis and occurs independent of cholangiocyte polarity. At present, the proteins and their localization required to drive lumen formation remain unknown. This initial study will allow investigators to more explicitly MAPK Inhibitor Library manufacturer define the requirement of additional genes and provide a more in-depth understanding of the mechanism behind biliary tubulogenesis. The therapeutic implication of delineating DPM classifications in clinical medicine, based on initial biopsies, will hopefully begin to improve diagnostic and prognostic stratification of patients with DPM in the diverse group of congenital and acquired cholangiopathies. In the future, this may allow for more individualized monitoring and intervention strategies. “
“It is important for anyone involved in the care of a child post liver transplant to be aware of the complications that can develop. Surgical complications are most common immediately post transplant. Acute rejection is most common in the early transplant period. Chronic rejection can occur at any time following transplant. Other serious complications which require immediate management and discussion with the transplant ADAMTS5 centre are infection and post transplant lymphoproliferative

disease. “
“We enthusiastically saw the consistent interest given by HEPATOLOGY to the importance of lifestyle interventions in the treatment of both nonalcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Johnson et al.1 have shown that a 4-week aerobic exercise training per se results in a significant reduction in both hepatic lipids and visceral adipose tissue (VAT). Beside this, Promrat et al.2 have demonstrated that a 48-week program based on both physical activity and diet-induced weight loss is able to also improve liver histology of patients with NASH. Indeed, these two trials complement each other in clarifying the role of behavioral treatment in the management of chronic fatty liver disease. Along with this, the importance of combined lifestyle therapy (diet plus physical activity) is strongly supported.

2b). The dart was buoyant in water and floated with the dart tail upright. We used a collapsible 1.2–3.7 m long pool net to retrieve darts in the water from the helicopter. We used tree click here marking paint or livestock marking solution (LA-CO Industries, Inc., Elk Grove, IL) for marking bears with this dart. We used an MK24C 0.745 projector (Paxarms N.Z. Ltd.) to fire the PX darts. For all dart types, we cleaned darts with soap and boiling water and used a 10% bleach solution as a disinfectant. When biopsy darting polar bears, we attempted to fire darts perpendicular to the body around the upper shoulder, similar to immobilization darting (Stirling et al. 1989). This approach

was used to help ensure darts would immediately bounce out from the large muscle upon impact. We typically darted Lumacaftor bears when they were approximately 3–6 m below the helicopter. Upon recovery of darts, we examined whether tissue samples had been collected and if not, we re-darted individuals when feasible. We examined the amount of time required to dart bears using the time at which bears were first observed

to the time the helicopter landed to recover fired darts. We weighed entire samples obtained in spring 2011 and September 2011. In August and September 2011, we separated adipose tissue from hair and skin and only submitted the hair and skin portion of the sample for genotyping. We air dried all genetic samples prior to DNA extraction. DNA was extracted from tissue samples using QIAGEN DNeasy Tissue Kits

according to manufacturer’s instructions by Wildlife Genetics International (WGI) Inc. (Nelson, British Columbia, Canada). WGI amplified DNA extracts at 20 microsatellite loci and the ZFX/ZFY sex identification marker (Aasen and Medrano 1990) using methods and primers as described in detail by Paetkau (2003) and Kendall et al. (2009). We considered genotyping successful if the DNA extract amplified at the full suite of microsatellite Cyclooxygenase (COX) loci and ZFX/ZFY. We extracted lipids from adipose, derivatized fatty acids to their fatty acid methyl ester (FAME) analogues using the Hilditch reagent, and quantified individual FAMEs by gas chromatography with flame ionization detection (Budge et al. 2006). We considered fatty acid analysis of the remote biopsies successful if we were able to quantify all fatty acids routinely determined in larger biopsies from captured or harvested polar bear samples (Thiemann et al. 2008; McKinney et al. 2009, 2011). We tested for normality in data sets using Shapiro-Wilk tests in the R programming language (http://cran.r-project.org/). We tested for differences in the mean wet weight of samples (the entire sample: hair, skin, and adipose tissue), mean adipose weight of samples, and adipose percent lipid content of samples obtained using the PC 5 mm heads, PX 5 mm heads, and PX 7 mm heads.

Radiofrequency energy was delivered with a 17-G, Cool-Tip electrode with a 2-cm (nodules ≤ 1.5 cm in diameter) or 3-cm (nodules 1.5–2.5 cm) exposed metallic tip (Radionics) introduced into the center of the nodule. For nodules greater than 2.5 cm, multiple needle this website punctures were performed with a 3-cm exposed metallic tip. In the 70 (80%) of 88 patients with hypervascular HCC nodules confirmed on CT during hepatic arteriography, TACE was performed an average 3 days before RFA. TACE was performed through the femoral artery using the technique of Seldinger under local anesthesia.

An angiographic catheter was inserted selectively into the hepatic feeding artery of a segment or subsegments containing the target tumor. We used cisplatinum (Randa; Nippon Kayaku, Tokyo, Japan) as an anticancer drug mixed with iodized oil (Lipiodol; Nihon Schering, Tokyo, Japan) at a concentration of 10 mg/mL and injected at a dose of 10–40 mg/body. The Carfilzomib concentration selected dose was based on tumor size. Injection was discontinued upon full accumulation of iodized oil in the tumor vessels. No gelatin sponge or coil embolization was used after TACE in the present study. To evaluate the efficacy of RFA, dynamic CT was performed at 2–3 days after each treatment session using the protocol described for pretreatment imaging studies. CT findings were confirmed by consensus between the two radiologists. On dynamic CT images, the non-enhancing

area was measured as the ablated area. When the diameter of the non-enhancing area was greater than that of the ablated nodule, RFA was considered to have produced a complete effect and the treatment was terminated. When the diameter of the necrotic area was closely similar to that of the tumor without any ablated margin or when the only partial enhancement of a portion of the tumor was seen, RFA was considered to have produced an incomplete effect, and an additional session of ablation was accordingly performed 3–5 days

later, and in principle repeated until a complete effect was confirmed. The outcome of RFA was evaluated in CT images taken 3–4 weeks after the final RFA session. Follow-up US and dynamic CT were performed at 3- to 4-month intervals using protocols similar to those applied Phospholipase D1 in the pretreatment studies. Serum HCC-specific tumor markers, including α-fetoprotein (AFP), its lectin fraction 3, and des-γ-carboxy prothrombin (DCP), were measured every 1–2 months. Local tumor progression was determined when a subsequent follow-up CT demonstrated any tumor growth or enhancement in the ablation zone, where complete primary effectiveness (i.e. no evidence of residual tumor) was previously obtained. Secondary effectiveness was evaluated in patients who underwent follow-up CT 1 year or more after RFA,19 and included tumors that underwent successful repeat RFA after the identification of local tumor progression.

Detection of phytoplasmas using universal primer pair P1A/P7A followed by primer pair R16F2n/R16R2 in nested PCR confirmed association of phytoplasmas with diseased pear trees. However, PCR using group-specific primer pairs R16(X)F1/R16(X)R1 and rp(I)F1A/rp(I)R1A showed that Iranian PI3K inhibitor pear phytoplasmas are related to apple proliferation and aster yellows groups. Moreover, PCR results using primer pair ESFYf/ESFYr specific to 16SrX-B subgroup indicated that ‘Ca. Phytoplasma prunorum’ is associated with pear decline disease in the north of Iran. RFLP analyses using HaeIII, HhaI, HinfI, HpaII and RsaI restriction enzymes confirmed the PCR results.

Partial 16S rRNA, imp, rp and secY genes sequence analyses approved that ‘Ca. Phytoplasma pyri’ and ‘Ca. Phytoplasma Maraviroc nmr asteris’ cause pear decline disease in the centre of Iran, whereas ‘Ca. Phytoplasma prunorum’ causes disease in the north of Iran. This is the first report of the association of

‘Ca. Phytoplasma asteris’ and ‘Ca. Phytoplasma prunorum’ with pear decline disease worldwide. “
“DNA sequence analysis of the nuclear ribosomal internal transcribed spacer region (ITS) was performed to determine phylogenetic relationship between 49 isolates of rusts infecting grain and forage legumes. Isolates were collected from different hosts and distinct geographic origins and represent eight species of Uromyces: U. anthyllidis, U. appendiculatus, U. ciceris-arietini,

U. minor, U. pisi, U. striatus, U. viciae-fabae and U. vignae. ITS sequences revealed length polymorphisms and variation in DNA sequence that were used to characterize phylogenetic MycoClean Mycoplasma Removal Kit relationships by maximum parsimony, maximum likelihood and Bayesian analyses which in general agreed revealing the presence of four clearly distinct clades. Clade one included the isolates causing rust on chickpea, fenugreek and alfalfa. Clade two was composed by rust isolates of field clover and pea plants, while the third clade was formed by bean and cowpea isolates. Clade four was the largest and included all the rust isolates infecting faba bean. Within this clade, the highly supported subclusters of U. viciae-fabae collected on Lens culinaris, U. viciae-fabae collected on Vicia sativa and U. viciae-fabae collected on Lathyrus palustris suggest an ongoing process of host specialization. “
“Leaf rust, caused by the fungus Puccinia triticina, is considered one of the most important foliar diseases in durum wheat. Hypersensitive resistance (HR) may be rapidly overcome by the pathogen when resistant cultivars are grown on a large acreage or following changes in virulence in the pathogen population. Prolonging the durability of the resistance requires uses of other types of resistance such as partial resistance (PR).

“
“The burden

of migraine significantly impacts the individual sufferer, their families, the workplace, and society. The World Health Organization has identified migraine as an urgent public health priority and has initiated a global initiative to reduce the burden of migraine. Underlying the World Health Organization initiative is the need to discover means of optimizing migraine treatments and make them accessible to the broader portion of the world population. Development of acute migraine medications over the past several decades has largely centered on engineering highly specific receptor molecules that alter migraine Adriamycin cost pathophysiological mechanisms to abort or reverse the acute attack of migraine. The first product of this line of discovery GSK-3 inhibition was sumatriptan and heralded as a landmark therapeutic

breakthrough. Sumatriptan is a 5-HT-1B/D receptor agonist considered to activate receptors involved in the pathophysiology specific to migraine. Large-scale regulatory/clinical studies demonstrated statistical superiority for sumatriptan over placebo in reduction or elimination of headache, nausea, photophobia, and phonophobia. Since the introduction of sumatriptan, 6 other triptan products have been released in the United States as acute treatments for migraine, all having the same mechanism of action and similar efficacy. Despite their utility as migraine abortive medications, the triptans do not successfully treat all attacks of migraine or necessarily treat all migraine associated symptoms. In fact, in less than 25% of attacks do subjects

obtain and maintain a migraine-free response to treatment for at least beyond 24 hours. A wide range of non-triptan medications also have demonstrated efficacy in acute migraine. These include non-steroidal anti-inflammatory drugs (NSAIDs), opioids, phenothiazines, and valproic acid to name a few. Given the distinctly different mechanisms of actions of these various medications, it is likely that several unique pathophysiological mechanisms are involved in terminating acute episodes of migraine. Clinicians now capitalize on this observation and use migraine tuclazepam medication in combination with another to improve patient outcomes, for example, using an antiemetic with an opioid or a triptan and NSAIDs. More recently, the Food and Drug Adminstration has approved a combination product containing 85 mg of sumatriptan plus 500 mg of naproxen sodium for acute treatment of migraine. Clinical trials conducted prior to approval demonstrated that the combination of sumatriptan and naproxen was more effective as a migraine abortive than either of its components but that each component and the combination were more effective than placebo.

(HEPATOLOGY 2011;) “
“The aim of this study was to elucidate the risk of subsequent biliary malignancy in patients undergoing cyst excision for congenital choledochal cysts. A retrospective analysis of 94 patients who had undergone cyst excision for congenital choledochal cysts was conducted. The median age at the time

of cyst excision and median follow-up time after cyst excision were 7 years and 181 months, respectively. Biliary tract cancer developed in four patients at 13, 15, 23, and 32 years after cyst excision. The cumulative incidences of biliary tract cancer at 15, 20, and 25 years after cyst excision were 1.6%, 3.9%, and 11.3%, respectively. The sites of biliary tract cancer were the intrahepatic (n = 2), hilar (n = 1), and intrapancreatic (n = 1) Ceritinib bile ducts. Of the four patients with biliary tract cancer after cyst excision, three patients underwent surgical resection and one patient received chemo-radiotherapy. The overall cumulative survival rates after treatment in the four patients with biliary tract cancer were 50% at 2 years and 25% at 3 years, with a median survival time of 15 months. The risk of subsequent biliary malignancy in patients undergoing cyst excision for congenital choledochal cysts seems to be relatively high in the

PD-1 antibody inhibitor long-term. The risk of biliary malignancy in the remnant bile duct increases more than 15 years after cyst excision. Despite an aggressive treatment approach for this condition, subsequent biliary malignancy following cyst excision for congenital choledochal cysts shows an unfavorable outcome. “
“We aimed to determine whether pretreatment serum interferon-γ-inducible protein (IP)-10 concentration can predict response to telaprevir (TVR)-based triple therapy in patients with genotype 1 chronic hepatitis C (CHC), and to examine the effects of IP-10 concentration on liver histology. Baseline IP-10 concentrations were measured in 97 patients with genotype 1 CHC treated with TVR-based

triple therapy, and the associations between baseline IP-10 and treatment outcome were assessed Glutamate dehydrogenase by univariate and multivariate analyses. Associations between baseline serum IP-10 concentration and laboratory data and liver histological findings were also investigated. Median IP-10 concentration in these patients was 461.83 pg/mL (range, 151.35–4297.62). Multivariate analysis showed that IL28B genotype (P = 0.025) and IP-10 level (P = 0.004) were factors significantly predictive of rapid virological response (RVR), whereas in pretreatment factors only, IL28B genotype (P = 0.001) and liver fibrosis (P = 0.035) were independent predictors of sustained virological response. Using a cut-off IP-10 concentration of 460 pg/mL, patients with IL28B risk allele and low IP-10 had a significantly higher RVR rate than those with high IP-10 (P = 0.005). IP-10 concentration was significantly correlated with liver fibrosis (P = 0.001) and inflammation activity (P = 0.

Vaccine prevalence exceeded 70% in those ≥65 years and was only 27.8% in survivors 19–44 years. Selleck ITF2357 increasing age, being without a spouse,

having poor self-rated health, and having a shorter duration since cancer diagnosis were significant predictors of vaccination status among cancer survivors <65 years. Shorter duration since cancer diagnosis was the only factor associated with vaccination status in cancer survivors ≥65 years. Conclusion: Influenza vaccine coverage remains much lower than recommended among cancer survivors, particularly in younger age groups. These results may help better target preventive health care efforts to increase vaccination prevalence and reduce health risks for cancer survivors. Key Word(s): 1. influenza; 2. human; 3. influenza vaccines; 4. neoplasms; 5. survivors Presenting Author: YOU JIN HAN Additional Authors: SUNG EUN KIM, MOO IN PARK, SEUN JA PARK, WON MOON Corresponding Author: YOU JIN HAN Affiliations: Kosin University College of Medicine, Kosin University College of Medicine, Kosin University College of Medicine, Kosin University College of Medicine Objective: Endoscopic ultrasound (EUS) is widely used in recent days. However, there was no definite guideline for the management and the follow up

period of small subepithelial tumor (SET) in upper gastrointestinal tract (GIT). Therefore, we evaluated the natural course of SELs using EUS and the characteristics of growing SETs. Methods: From October 2004 to June 2014, we

retrospectively investigated the size changes, echogenicity, echogenic foci, and origin layer of SETs less than 30 mm in EUS findings. The significant growth of SET defined as increasing more than 25% of the longest diameter in the last EUS finding comparing the initial study. Results: A total of 131 upper GIT SETs in 122 patients were examined two more times using EUS. The median follow up interval for SETs was 25 months (range, 3 to 124 months). The location of SETs was 31 (23.7%), 93 (71.0%), Thymidylate synthase 7 (5.3%) in esophagus, stomach, and duodenum, respectively. The majority of SETs were located in the 4th layer (90/131, 68.7%), and 117 SETs (89.3%) had hypogenicity and 107 SETs (81.1%) had homogenecity. Among 131 SETs, 28 SETs (21.4%) showed significant increase in follow up EUS. However, initial size, echogenicity, presence of echogenic foci, layer of origin, and marginal regularity were not significantly associated with the growth of the tumor. Conclusion: Although there were no significant relative factors about the SETs growth, however, about one fifth of the SETs showed the size changes. Therefore, regular observation of SETs by using EUS might be needed. Key Word(s): 1. subepithelial lesions; 2. endoscopic ultrasound; 3.

24 Until recently, our understanding of PBC has been limited by the

absence of appropriate animal models. Based upon a rigorous quantitative analysis of the epitope of PDC-E2, our laboratory has identified several organic compounds that resemble the immunodominant epitope of PDC-E2. In particular, 2-octynoic acid (2OA), a compound found in perfumes, lipstick, and many common food flavorings, reacts equally or even better than lipoic acid to AMAs.25-26 Importantly, immunization with 2OA when coupled with bovine serum albumin (BSA), induces high-titer AMAs and portal inflammation strikingly click here similar to human PBC.27-29 We report herein that treatment of this xenobiotic induced murine model of human PBC with either anti-CD20 or anti-CD79

monoclonal antibodies (mAbs) exacerbates liver pathology, even though it successfully depletes B cells and diminishes the production of AMAs. These findings have important clinical implications for the treatment of PBC and other autoimmune diseases in which B cell regulatory function may be critical. 2OA, 2-octynoic acid; ALP, alkaline phosphatase; ALT, alanine aminotransferase; AMA, antimitochondrial antibody; APC, antigen-presenting cell; AST, aspartate aminotransferase; BSA, bovine serum albumin; dnTGF-βRII, transforming growth factor β receptor II dominant negative; EAE, autoimmune encephalomyelitis; IFN-γ, interferon-γ; Ig, immunoglobulin; IL, interleukin; mAb, monoclonal learn more antibody; MCP-1, monocyte chemotactic protein-1; PBC, primary biliary Pifithrin �� cirrhosis; PBS, phosphate-buffered

saline; PDC-E2, E2 subunit of the pyruvate dehydrogenase complex; TLR, Toll-like receptor. Female C57BL/6J (B6) mice were obtained from The Jackson Laboratory (Bar Harbor, ME) and maintained in ventilated cages under specific pathogen-free conditions at the animal facilities of the University of California at Davis. The Animal Care and Use Committee in University of California Davis approved all studies. To deplete B cells in vivo, four independent groups of 6-week-old mice were injected intraperitoneally weekly with either sterile murine immunoglobulin (IgG) 2a anti-mouse CD20 antibody (n = 8) (250 μg/250 μL in phosphate-buffered saline [PBS]), hamster IgG2 anti-mouse CD79b antibody (n = 10) (1 mg/100 μL in PBS), or isotype-matched control mAbs. The anti-mouse CD20 IgG2a (Biogen Idec, San Diego, CA) and the Armenian hamster anti-mouse CD79b IgG used herein have been described elsewhere.30, 31 The non–cross-reactive mouse anti-human CD20 antibody (250 μg/250 μL in PBS) and an Armenian hamster normal IgG (1 mg/mL) (Innovative Research, Novi, MI) were used as controls. One week after the beginning of B cell depletion therapy, autoimmune cholangitis was induced as described.

We report the validity of a segmentation pipeline for the detection of MS-related brain atrophy with 3T MRI. Longitudinal studies are warranted to extend these results. “
“PRES is a reversible neurotoxic state presenting with headache, altered mental status, visual DNA Damage inhibitor loss, and seizures. Delayed diagnosis can be avoided if radiological patterns could distinguish PRES from cerebral ischemia. Clinical and radiological data were collected on all hospitalized patients who had (1) discharge diagnosis

of PRES and (2) acute CTP/CTA. Data were compared with 10 TIA patients with proven cytotoxic edema on MRI. Of the four PRES patients found, three were correlated with acute blood pressure and one with chemotherapy. At the radiological level, quantitative analyses of the CTP parameters showed that 2 out of 4 patients had bilaterally reduced CBF-values (23.2-47.1 ml/100g/min) in occipital regions, as seen in the pathological regions of TIA patients (27.3 ± 13.5 ml/100g/min). When compared with TIA patients, the pathological ROI’s demonstrated decreased CBV-values (3.4-5.6 ml/100g). Vasogenic edema on MRI FLAIR imaging was seen in only one PRES patient, and cytotoxic edema on DWI-imaging was never found. CT angiography showed in one PRES patient a vasospasm-like unilateral posterior cerebral artery. If confirmed by other groups, CTP and CTA imaging in patients with acute

visual loss and confusion may help to distinguish PRES from bi-occipital

ischemia. These radiological selleck products Acalabrutinib molecular weight parameters may identify PRES patients at risk for additional tissue infarction. “
“We report a patient with abnormal diffusion tensor imaging (DTI) and tractography of the corticospinal tract caused by mass effect from adjacent enlarged Virchow–Robin spaces. DTI was performed using 25 noncollinear directions. Fractional anisotropy (FA) and mean diffusivity (MD) maps were generated. Region-of-interest measurements of the corticospinal tracts were organized in histograms, and comparisons were made between sides. Statistical analysis consisted of a Wilcoxon rank-sum nonparametric test and a two-sample test of proportions to compare the relative percentage of voxels >.8. The patient had no signs or symptoms of motor weakness. The corticospinal tract adjacent to the enlarged Virchow–Robin spaces showed significant changes in the proportion of FA > .8, distribution of FA and distribution of MD (P < .001). Diffusion tensor changes may be caused by enlarged Virchow–Robin spaces in the absence of clinical signs or symptoms. We hypothesize that the DTI changes are due to alterations in the extravascular extracellular space. Tensor changes should be interpreted with caution in patients with space occupying mass lesions such as brain tumors. Enlarged Virchow–Robin spaces are extensions of the subpial cerebrospinal space surrounding small penetrating arteries and veins.

Dynamics of the gene expression profiles responsible for the carcinogenesis are not fully understood.

The current study was designed to determine the serial changes of gene expression profiles and genetic and epigenetic modifications responsible for hepatocarcinogenesis in the model of chronic immune-mediated hepatitis. METHODS: Three-month-old HBV transgenic mice were immunologically reconstituted with bone marrow cells and splenocytes from syngeneic nontransgenic donors. Liver tissues were obtained every Selleckchem GSK126 three months until 18 months at which time all mice developed multiple liver tumors. Oxi-dative DNA damage and hepatocyte turnover were assessed immunohistochemically. Gene expression profiles were developed by extracting total RNA from the tissues and analyzing by microarray (44 K genes, Agilent). Genomic DNA was enriched for methylated fragments and the epigenetic changes were detected, and targeted gene exomes were captured and sequenced using next-generation sequencing technology (HiSeq 2000, Illumina). RESULTS: Oxidative DNA damage (8-OHdG and 4-HNE) and hepatocyte turnover (PCNA) were increased during the progression of chronic liver disease. In a gene expression profile analysis of liver samples, nine of

gene groups with different time courses were identified by K-means clustering (P < 0.01). Although the expression levels of one group with 119 genes (cluster #2) were not changed selleck in inflamed tissue at early time points (< 3 months) and chronic selleck chemicals phases (6 – 12 months), the levels were decreased in noncan-cerous tissues in the late phase (15 – 18 months) and further

reduced in liver tumors. Of the cluster #2 genes, the hyper-methylated sites were seen at CpG islands around the coding sequences and multiple non-synonymous mutations above 1% frequency were detected in Cyp26a1, Nr2f6 and Hsd3b7 genes, all of which were involved in the catalytic and binding activity of iron, DNA or steroid. CONCLUSIONS: Chronic immune-mediated hepatitis enhances oxidative DNA damage and hepatocellular turnover in which hypermethylation and non-synonymous mutations were induced in three genes with catalytic properties of a cluster down-regulated in the late phase of liver disease. The resulting molecules may be primarily involved in malignant transformation of hepatocytes in the process of tumor development. Disclosures: Shuichi Kaneko – Grant/Research Support: MDS, Co., Inc, Chugai Pharma., Co., Inc, Toray Co., Inc, Daiichi Sankyo., Co., Inc, Dainippon Sumitomo, Co., Inc, Ajinomoto Co., Inc, MDS, Co., Inc, Chugai Pharma., Co., Inc, Toray Co., Inc, Daiichi Sankyo., Co., Inc, Dainippon Sumitomo, Co., Inc, Ajinomoto Co.