1E). Comparison of other lymphocyte subsets between IL-10 KO and check details IL-10/IL-4 KO mice revealed only a slight and variable decrease in CD8+ T cell numbers in IL-10 KO animals (data not shown). Overall, the data supported the contention that IL-10 prevented hepatocyte

injury and accumulation of intestinally-derived CD4+ cells, whereas IL-4 was required for the development of hepatic necrosis. To investigate further the role of IL-4 in the liver during infection, we sought to determine which cell type(s) produced it. The majority of IL-4+ cells were CD4+; however, the percentage of CD4+IL-4+ cells in IL-10 KO mice was approximately twice that in WT mice (Fig. 2A). Most CD4+ cells in the liver are conventional CD4+ T cells, but some classical natural killer (NK) T cells also express CD4. To distinguish between contributions from these two cell

types, we stained cells for CD4, IL-4, and NK1.1. IL-4+ cells were gated, and the percentages of IL-4 expressing conventional CD4+ T cells versus NK T cells are shown in Fig. 2B. Almost all of the IL-4+ cells colocalized with AZD2281 the CD4+NK1.1− population. Thus, CD4+ T cells were the major source of IL-4. Additionally, this population was expanded in IL-10 KO animals in comparison with WT mice. Because we previously discovered that an intestinal immune response was a prerequisite for hepatic Dolichyl-phosphate-mannose-protein mannosyltransferase inflammation, we asked if any CD4+NK1.1−IL-4+ cells were gut-derived. CCR9, like α4β7, is up-regulated on lymphocytes after activation within gut-associated lymphoid tissue (GALT) and is used as a marker of intestinal origin. 15 Infected IL-10 KO animals had significantly more IL-4+, intestinally

derived CD4+ T cells than WT mice (Fig. 2C). Previously, we noted that lesions in infected IL-10 KO mice contained an abundance of granulocytes, including neutrophils and eosinophils. IL-4 promotes eosinophil proliferation, recruitment, and effector functions, and its expression is elevated by T. spiralis infection. 16 This led us to ask if eosinophils were involved in the development of hepatic necrosis. We compared eosinophil infiltration in singly and doubly deficient mice after infection (Fig. 3A). As expected, IL-4 KO mice displayed reduced eosinophilia in comparison with WT animals. In contrast, eosinophil numbers were higher in infected IL-10 KO mice compared to WT animals. The hepatic eosinophil content in IL-10/IL-4 KO mice was similar to that in WT mice. Hence, eosinophil accumulation in the liver was inhibited by IL-10 and promoted by IL-4. We tested whether eosinophils were essential in the development of hepatic necrosis by mating IL-10 KO animals to eosinophil-deficient (PHIL) mice to generate mice lacking both IL-10 and eosinophils.

1E). Comparison of other lymphocyte subsets between IL-10 KO and selleck products IL-10/IL-4 KO mice revealed only a slight and variable decrease in CD8+ T cell numbers in IL-10 KO animals (data not shown). Overall, the data supported the contention that IL-10 prevented hepatocyte

injury and accumulation of intestinally-derived CD4+ cells, whereas IL-4 was required for the development of hepatic necrosis. To investigate further the role of IL-4 in the liver during infection, we sought to determine which cell type(s) produced it. The majority of IL-4+ cells were CD4+; however, the percentage of CD4+IL-4+ cells in IL-10 KO mice was approximately twice that in WT mice (Fig. 2A). Most CD4+ cells in the liver are conventional CD4+ T cells, but some classical natural killer (NK) T cells also express CD4. To distinguish between contributions from these two cell

types, we stained cells for CD4, IL-4, and NK1.1. IL-4+ cells were gated, and the percentages of IL-4 expressing conventional CD4+ T cells versus NK T cells are shown in Fig. 2B. Almost all of the IL-4+ cells colocalized with BMN 673 in vitro the CD4+NK1.1− population. Thus, CD4+ T cells were the major source of IL-4. Additionally, this population was expanded in IL-10 KO animals in comparison with WT mice. Because we previously discovered that an intestinal immune response was a prerequisite for hepatic see more inflammation, we asked if any CD4+NK1.1−IL-4+ cells were gut-derived. CCR9, like α4β7, is up-regulated on lymphocytes after activation within gut-associated lymphoid tissue (GALT) and is used as a marker of intestinal origin. 15 Infected IL-10 KO animals had significantly more IL-4+, intestinally

derived CD4+ T cells than WT mice (Fig. 2C). Previously, we noted that lesions in infected IL-10 KO mice contained an abundance of granulocytes, including neutrophils and eosinophils. IL-4 promotes eosinophil proliferation, recruitment, and effector functions, and its expression is elevated by T. spiralis infection. 16 This led us to ask if eosinophils were involved in the development of hepatic necrosis. We compared eosinophil infiltration in singly and doubly deficient mice after infection (Fig. 3A). As expected, IL-4 KO mice displayed reduced eosinophilia in comparison with WT animals. In contrast, eosinophil numbers were higher in infected IL-10 KO mice compared to WT animals. The hepatic eosinophil content in IL-10/IL-4 KO mice was similar to that in WT mice. Hence, eosinophil accumulation in the liver was inhibited by IL-10 and promoted by IL-4. We tested whether eosinophils were essential in the development of hepatic necrosis by mating IL-10 KO animals to eosinophil-deficient (PHIL) mice to generate mice lacking both IL-10 and eosinophils.

Similarly, it has been noted by others that some hiPS cell lines appear to be incompletely reprogrammed, and

still others maintain expression of exogenous transgenes, which appear to interfere with VX-770 molecular weight differentiation protocols.32 With this in mind, we believe it is crucial that standards for the generation and characterization of hiPS cells are adopted throughout the community to ensure reproducibility of formation of differentiated cells from hiPS cells from different patients and tissue sources. Although several groups have been able to produce hepatocyte-like cells from huES cells, we believe that the current protocol used to produce hepatocytes from either huES or hiPS cells offers a number of advances. Differentiation is extremely efficient and reproducible, with between 80% and 85% of cells expressing YAP-TEAD Inhibitor 1 hepatic markers, including albumin. In most other procedures, the differentiation of

cells relies on embryoid body formation, includes interactions with primary feeder cells, or requires the inclusion of serum during the differentiation procedure. Although using such approaches to produce hepatocytes can be successful, the inherent variability associated with use of undefined factors reduces reproducibility. The approach we have described relies on well-defined culture conditions. We believe that using such conditions will facilitate accurate analyses of molecular pathways that control human hepatocyte differentiation, comparative studies between iPS cells derived from patients suffering 6-phosphogluconolactonase from various congenital liver diseases, and development of screens for novel pharmaceutical approaches to correct liver disease. Although the efficiency of generating cells that exhibit most hepatocyte characteristics is high, we noted that the repertoire of mRNAs encoding phase I and phase II enzymes, which have important roles in controlling drug metabolism and xenobiotic responses, is

incomplete when compared with cadaveric livers. Loss of CYP450 enzyme expression is common when hepatocytes are grown under normal culture conditions, and this reflects the complex control of CYP450 expression and activity by several environmental and physiological parameters that are lacking in the tissue culture environment.33, 34 We believe our data support the conclusion that both huES and hiPS cells are competent to differentiate toward the hepatocyte lineage; however, we also believe that to use iPS cells as a source of hepatocytes for toxicological and drug metabolic studies will require the establishment of culture conditions that more fully support expression of a full panel of phase I and II enzymes.

e., total daily dose 240 mg), failed to achieve an intragastric milieu consistent

with dual PPI plus amoxicillin therapy being an effective anti-H. pylori regimen. “
“Levofloxacin has been proposed to replace clarithromycin for Helicobacter pylori treatment. Seven- and 10-day fluoroquinolone triple therapies have generally failed to achieve cure rates of ≥90%, whereas 14-day therapy has achieved 95% success. The aim was to assess the efficacy and effect of fluoroquinolone resistance on 14-day levofloxacin-containing triple therapy with or without the addition of bismuth. Helicobacter pylori-positive patients with functional selleck inhibitor dyspepsia or healed peptic ulcers were randomized to receive lansoprazole 30 mg b.i.d., amoxicillin 1000 mg b.i.d., and levofloxacin 500 mg daily with (B-LAL) or without (LAL) bismuth potassium citrate 220 mg b.i.d. for 14 days. Eradication was assessed by 13C-urea breath testing 4 weeks after completing treatment. Antimicrobial susceptibility was by the agar dilution method. Success was defined as PP success ≥90%. A total of 152 of 161 patients (81 LAL and 80 B-LAL) enrolled completed treatment. The PP rates were 94.6% (70/74; 95% CI, 86.9–97.9%)

with B-LAL and 85.9% (95% CI, 76.5–91.9%) with LAL (p = .07); the ITT eradication rates were 87.5% (95% CI, 78.5–93.1%) with B-LAL and 82.7% (95% CI, 73–89.4%) with LAL (p = .39). Levofloxacin resistance was present in 30.3%. Treatment success was excellent with susceptible strains (97.5%) versus resistant strains (70.6%) for B-LAL and 97.3% versus 37.5% for LAL, respectively. Fourteen-day

fluoroquinolone therapy was highly effective when fluoroquinolone resistance rates are <12%. The EGFR inhibitor review addition Methamphetamine of bismuth maintained effectiveness with fluoroquinolone resistance as high as 25%. “
“Background: Helicobacter pylori produces γ-glutamyltranspeptidase (GGT), a potential virulence factor involved in induction of host cell apoptosis. Regulation of the production of this protein is not known. Methods:  The transcription start sites were determined by primer extension analysis. Transcription level of the GGT gene was examined by measuring the mRNA by RT-PCR and expression level of GGT protein was examined by Western blot analysis under different conditions. Results:  Two transcription start sites were identified; thymine at 78-bp upstream and adenine at 79-bp upstream from the ATG codon of the GGT gene. There was a possible -10 consensus promoter sequence (ATTAAT), but no apparent -35 consensus sequence was found. The transcription of the mRNA and the expression of the protein were at almost constant level during the course of culture. The mRNA level increased by exposure to low pH; however, the actual protein expression level remained almost constant. Addition of glutamine or glutamate did not affect the mRNA level and the protein expression level to a remarkable degree, nor did co-culture with AGS cells affect the GGT activity level. Conclusion:  It was suggested that H.

These results suggest 3-deazaneplanocin A solubility dmso that in Japanese haemophilia patients, the type of clotting factor preparations used for therapy has not influenced the incidence of inhibitor formation. “
“This chapter contains sections titled:

Introduction Structure and function of the factor VIII gene (F8) and protein F8 gene defects found in hemophilia A Conclusion Public databases Mutation nomenclature Acknowledgment References “
“Summary.  The most common severe hereditary bleeding disorder phenotype in humans, the coagulation factor VIII (F8) deficiency haemophilia A (HEMA), maps on Xq28 band, a region that comprises 11.7% of genes and 14.2% of phenotypes on X chromosome. Information about the distribution and extent of gametic disequilibrium (GD) covering the F8 gene is scarce, despite its relevance for linkage and association studies. The aim of this study was to determine the patterns, by frequency and strength, of non-random multiallelic interallelic associations between two-locus combinations of seven microsatellite loci (REN90833, F8Int25.2, F8Int22, F8Int13.2, HEMA154311.3, TMLHEInt5 and HEMA154507.3, in that

physical order) spanning 0.813 Mb on distalmost Xq28. We measured sign-based interallelic D′ coefficients in 106 men and in 100 women drawn from a single unrelated Brazilian population. Significance and patterns of GD using haploid and phased diploid sample probabilities were close to conformity. Only 9.18% of the variance of D′ could be accounted for by changes in length, indicating that GD is not a monotonically decreasing function of length. We defined Daporinad two regions of overlapping long-range GD extending 698 735 base pairs (bp) (REN90833/TMLHEInt5

block) and 689 900 bp (F8Int13.2/HEMA154507.3 block) The extent of GD overlap is 575 637 bp (F8Int13.2/TMLHEInt5 interstice). Extended haplotype homozygosity analysis centred at the F8 intronic loci revealed that the most frequent core haplotypes decay the least in the flanking GD. The F8 intronic loci attend distinct non-random association forces; F8Int13.2 serves at maintenance of the long-range overlapping pattern of GD, whereas F8Int25.2 and F8Int22 serve at lessening it in force or effect. “
“Children’s Hospital of Philadelphia, Philadelphia, PA, USA Department of Pediatrics and Medicine, Division of Hematology, Johns Hopkins School of PAK5 Medicine, Baltimore, MD, USA All Children’s Research Institute, All Children’s Hospital – Johns Hopkins Medicine (ACH-JHM), St. Petersburg, FL, USA Department of Pediatrics, Section of Pediatric Hematology/Oncology, Rush University Medical Center, Chicago, IL, USA Division of Blood Diseases and Resources at the National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA Congenital factor VII (FVII) deficiency is characterized by genotypic variability and phenotypic heterogeneity. Traditional screening and factor assays are unable to reliably predict clinical bleeding phenotype and guide haemorrhage prevention strategy.

These results suggest Vadimezan that in Japanese haemophilia patients, the type of clotting factor preparations used for therapy has not influenced the incidence of inhibitor formation. “
“This chapter contains sections titled:

Introduction Structure and function of the factor VIII gene (F8) and protein F8 gene defects found in hemophilia A Conclusion Public databases Mutation nomenclature Acknowledgment References “
“Summary.  The most common severe hereditary bleeding disorder phenotype in humans, the coagulation factor VIII (F8) deficiency haemophilia A (HEMA), maps on Xq28 band, a region that comprises 11.7% of genes and 14.2% of phenotypes on X chromosome. Information about the distribution and extent of gametic disequilibrium (GD) covering the F8 gene is scarce, despite its relevance for linkage and association studies. The aim of this study was to determine the patterns, by frequency and strength, of non-random multiallelic interallelic associations between two-locus combinations of seven microsatellite loci (REN90833, F8Int25.2, F8Int22, F8Int13.2, HEMA154311.3, TMLHEInt5 and HEMA154507.3, in that

physical order) spanning 0.813 Mb on distalmost Xq28. We measured sign-based interallelic D′ coefficients in 106 men and in 100 women drawn from a single unrelated Brazilian population. Significance and patterns of GD using haploid and phased diploid sample probabilities were close to conformity. Only 9.18% of the variance of D′ could be accounted for by changes in length, indicating that GD is not a monotonically decreasing function of length. We defined selleck chemical two regions of overlapping long-range GD extending 698 735 base pairs (bp) (REN90833/TMLHEInt5

block) and 689 900 bp (F8Int13.2/HEMA154507.3 block) The extent of GD overlap is 575 637 bp (F8Int13.2/TMLHEInt5 interstice). Extended haplotype homozygosity analysis centred at the F8 intronic loci revealed that the most frequent core haplotypes decay the least in the flanking GD. The F8 intronic loci attend distinct non-random association forces; F8Int13.2 serves at maintenance of the long-range overlapping pattern of GD, whereas F8Int25.2 and F8Int22 serve at lessening it in force or effect. “
“Children’s Hospital of Philadelphia, Philadelphia, PA, USA Department of Pediatrics and Medicine, Division of Hematology, Johns Hopkins School of Thalidomide Medicine, Baltimore, MD, USA All Children’s Research Institute, All Children’s Hospital – Johns Hopkins Medicine (ACH-JHM), St. Petersburg, FL, USA Department of Pediatrics, Section of Pediatric Hematology/Oncology, Rush University Medical Center, Chicago, IL, USA Division of Blood Diseases and Resources at the National Heart, Lung and Blood Institute, National Institutes of Health, Bethesda, MD, USA Congenital factor VII (FVII) deficiency is characterized by genotypic variability and phenotypic heterogeneity. Traditional screening and factor assays are unable to reliably predict clinical bleeding phenotype and guide haemorrhage prevention strategy.

The increase in quasispecies complexity after LMV in genotype A and HBeAg(+) cases suggests lower sensitivity to this treatment. Funding Instituto CarlosIII (PI 12/1893) cofinanced by ERDF (<)Less than 0.25%; (*)No viral breakthrough (Λ)No identity between 4nt and ASDR1 sequences The variability in TA1 and TA2 does

not include variability of positions 1753 and 1762   %TATA boxes(TA1-TA4) %DR1 Case Sample Genotype HBe 1 (1753) 2 (1762) 3 4 Total (Λ) 1 Basal A/D N 1 1.00 < 27.9 < < 2.4 <   Untreated A P < < < 19.1 < < < <   After LMV Fulvestrant research buy A P < < < 16.6 < < < < 2 Basal A P 1.9 < 0.3 87.5 0.4 < < 0.38   Untreated A P < < < 92.9 < < < 1.74   After LMV A P < < < 13.9 < 14 < 5.84 3 Basal A/D N < < < 27.6 < < < <   Untreated A/D N 2.1 < < 23.2 < < < <   After LMV * A/D N < 88.00 < 84.3 < < 1.5 1.51 4 Basal D P < < < < < < 0.4 0.60   Untreated D P < <

< 1.2 < < 2.9 2.30   After LMV* D P 0.3 < < 18.5 < < < < 5 Basal D P 0.8 < < < 0.3 0.3 2.9 1.05   Untreated find more D P 0.3 < 0.3 < 0.3 < 0.6 0.29   After LMV D P < < < < < < 1.2 0.88 6 Basal A P < < < 0.9 < 0.3 0.5 0.77   Untreated A P 0.5 0.50 < < < 0.4 15 0.42   After LMV A P < < < < 0.3 < 0.4 2.64 7 Basal A/D N 6.6 6.60 < 18 < < < <   Untreated D N < < < < < < < <   After LMV * D N < < < < < < 2.5 < 8 Basal A P < < < 98 < < < < Oxalosuccinic acid   untreated D N < < < < < < < <   After LMV A P < < < 4 < < < < 9 Basal D P 0.4 < 6.3 0.65 0.4 0.6 0.6 0.53   Untreated A P < < < 99.4 < < < <   After LMV A P < 7.50 < < < < < < 10 Basal D P/N < < < 63.5 < < < <   Untreated D N 1.9 < < 100 < < < <   After LMV A N/P < < < < < <

3 < Disclosures: Rafael Esteban – Speaking and Teaching: MSD, BMS, Novartis, Gilead, Glaxo, MSD, BMS, Novartis, Gilead, Glaxo, Janssen Maria Buti – Advisory Committees or Review Panels: Boerhinger Inghelm, Boer-hinger Inghelm; Speaking and Teaching: MSD, Bristol-Myers Squibb, Novartis, Gilead, Janssen, MSD, Bristol-Myers Squibb, Novartis, Gilead, Janssen The following people have nothing to disclose: Andrea Caballero, Josep Gregori, Maria Homs, David Tabernero, Maria Blasi, Rosario Casillas, Leonardo Nieto, Irene Belmonte Mula, Xose Costa, Carolina Gonzalez, Francisco Rodriguez-Frias Background & aims. MicroRNAs (miRs) are implicated in viral immune control: we studied their serum dynamics in chronic inactive HBsAg carriers (IC) and chronic hepatitis B (CHB) patients with different responses to antiviral therapy. Methods. Sera (143) were obtained from 75 (male/female 48/27, median age 43, 18-67 y.) HBeAg negative chronic genotype-D-HBV carriers followed for 8-13 y. IC (15) had persistently serum HBV-DNA levels ≤2000 IU/ml and normal ALT. CHB patients (60) were treated with peg-IFN or nucleos(t)ide-analogs.

In the treatment of the hepatorenal syndrome, many strategies have been used, with liver transplantation often the only viable alternative. Pentoxifylline (PTX), which inhibits TNF production, has been suggested Trichostatin A as an adjunct in the treatment of these patients,38 and an important clinical study was done in 2000

by the University of Southern California Liver Unit, using PTX to treat patients with alcoholic hepatitis.39 The results demonstrated a short-term survival improvement in the PTX group, felt to be related to a significant decrease in the risk of developing the hepatorenal syndrome. An interesting and well-designed clinical study on the effect of probiotics was recently published.40 It included a controlled study of gut flora, endotoxin levels, and Child-Pugh severity score in patients with cirrhosis. Using Escherichia coli Nissle strain or a placebo, the E. coli Nissle seemed to be effective in the

restoration of normal colonic colonization and can probably lower endotoxemia in patients with cirrhosis. With the presumed role of endotoxin in the hyperdynamic circulatory state in cirrhosis, selective intestinal decontamination was studied using oral norfloxacin in 14 patients with alcohol-related cirrhosis and 14 controls.41 This 4-week regimen of the antibiotic partially reversed the hyperdynamic circulatory state, further supporting the role of intestinal endotoxin in its pathogenesis. However, in contrast to the above studies was a randomized, double-blinded, placebo-controlled study of etanercept, in which the TNF-lowering receptor binding compound was used to lower TNFα in the treatment of INCB024360 mouse alcoholic hepatitis.42 Unfortunately, despite lowering of TNF levels, there was a significantly higher mortality in the etanercept group. Rates of infection were significantly higher in the treated group, indicating it to be

an ineffective therapy in acute alcoholic hepatitis. Thus, even though TNF is established as a major agent in causing liver damage, it also has an important role in immune protection. Because patients with alcoholic liver disease are more susceptible to serious infection, the whole concept of therapy to lower TNF levels may not be feasible. Table 4 lists Nitroxoline potential additional strategies developed thus far in attempts to lessen the damage from enteric LPS in toxic liver injury, and can be compared to the list of potential modifiers in Table 3 from 1981. Few investigators have the privilege to contribute to and then to follow a novel idea in disease causation through some 35 years of halting but substantial progress. In 1975, on the basis of our studies and those of other investigators, we postulated a key role for enteric endotoxin in injury from a variety of toxins. It was also postulated that, in chronic liver disease, the spillover of LPS into the systemic circulation resulted in many of the extrahepatic manifestations observed.

Junko Kishimoto for technical assistance with the HPLC analysis. We also thank Dr. Atsushi Takabayashi for helping Temozolomide price in PAM method. Our thanks go to Dr. Stuart D. Sym for reading the manuscript. We also thank Dr. Ryuta Terada and Captain M. Uchiyama and the crew of T/S Nansei-maru, Faculty of Fisheries, Kagoshima University, for their kind help in collecting the underwater samples. This work was partly supported by the Grant-in-Aid by the Ministry of Education, Culture, Sports, Science and Technology (No. 24370034). One of the specimens used in this study was collected during the visit to South Africa for the project

entitled ‘Biodiversity and evolution of algae in the Indo-Pacific: a Japan/South Africa comparison’ (Strategic International Research Cooperative Program)

supported by Japan Science and Technology Agency. “
“Endogenous auxins and cytokinins were quantitated in 24 axenic microalgal strains from the Chlorophyceae, Trebouxiophyceae, Ulvophyceae, and Charophyceae. These strains were in an exponential growth phase, being harvested on day 4. Acutodesmus acuminatus Mosonmagyaróvár Algal Culture Collection-41 (MACC) produced the highest biomass and Chlorococcum ellipsoideum MACC-712 the lowest biomass. The auxins, indole-3-acetic acid (IAA) and indole-3-acetamide (IAM) were present in all microalgal strains. No other auxin conjugates were detected. IAA and IAM concentrations varied greatly, ranging from 0.50 to 71.49 nmol IAA · g−1 DW and 0.18 to 99.83 nmol IAM · g−1 DW, respectively. In 19 strains, IAA occurred in higher concentrations than IAM. Nineteen cytokinins were CDK inhibitor identified in the microalgal strains. Total cytokinin concentrations varied, Flucloronide ranging from 0.29 nmol · g−1 DW in Klebsormidium flaccidum MACC-692 to 21.40 nmol · g−1 DW in Stigeoclonium nanum MACC-790. The general trend was that cis-zeatin types were the predominant cytokinins; isopentenyladenine-type cytokinins were present in moderate concentrations, while low levels of trans-zeatin-type and very low levels of dihydrozeatin-type cytokinins were

detected. Ribotides were generally the main cytokinin conjugate forms present with the cytokinin free bases and ribosides present in similar but moderate levels. The levels of O-glucosides were low. Only one N-glucoside was detected, being present in nine strains in very low concentrations. In 15 strains, the auxin content was 2- to 4-fold higher than the cytokinin content. “
“Dinoflagellates are a group of eukaryotic microalgae that have many unusual cytological and genomic characteristics. Here, we report the detection of a novel catalase–peroxidase (KatG) gene from the dinoflagellate Prorocentrum minimum, and its transcript levels under copper sulfate (CuSO4) treatment. cDNA analysis yielded a 1,293 bp complete open reading frame (ORF) encoding a 431-amino acid (aa) polypeptide (46.6 kDa).

Junko Kishimoto for technical assistance with the HPLC analysis. We also thank Dr. Atsushi Takabayashi for helping GSK126 in vitro in PAM method. Our thanks go to Dr. Stuart D. Sym for reading the manuscript. We also thank Dr. Ryuta Terada and Captain M. Uchiyama and the crew of T/S Nansei-maru, Faculty of Fisheries, Kagoshima University, for their kind help in collecting the underwater samples. This work was partly supported by the Grant-in-Aid by the Ministry of Education, Culture, Sports, Science and Technology (No. 24370034). One of the specimens used in this study was collected during the visit to South Africa for the project

entitled ‘Biodiversity and evolution of algae in the Indo-Pacific: a Japan/South Africa comparison’ (Strategic International Research Cooperative Program)

supported by Japan Science and Technology Agency. “
“Endogenous auxins and cytokinins were quantitated in 24 axenic microalgal strains from the Chlorophyceae, Trebouxiophyceae, Ulvophyceae, and Charophyceae. These strains were in an exponential growth phase, being harvested on day 4. Acutodesmus acuminatus Mosonmagyaróvár Algal Culture Collection-41 (MACC) produced the highest biomass and Chlorococcum ellipsoideum MACC-712 the lowest biomass. The auxins, indole-3-acetic acid (IAA) and indole-3-acetamide (IAM) were present in all microalgal strains. No other auxin conjugates were detected. IAA and IAM concentrations varied greatly, ranging from 0.50 to 71.49 nmol IAA · g−1 DW and 0.18 to 99.83 nmol IAM · g−1 DW, respectively. In 19 strains, IAA occurred in higher concentrations than IAM. Nineteen cytokinins were www.selleckchem.com/Caspase.html identified in the microalgal strains. Total cytokinin concentrations varied, Phosphoprotein phosphatase ranging from 0.29 nmol · g−1 DW in Klebsormidium flaccidum MACC-692 to 21.40 nmol · g−1 DW in Stigeoclonium nanum MACC-790. The general trend was that cis-zeatin types were the predominant cytokinins; isopentenyladenine-type cytokinins were present in moderate concentrations, while low levels of trans-zeatin-type and very low levels of dihydrozeatin-type cytokinins were

detected. Ribotides were generally the main cytokinin conjugate forms present with the cytokinin free bases and ribosides present in similar but moderate levels. The levels of O-glucosides were low. Only one N-glucoside was detected, being present in nine strains in very low concentrations. In 15 strains, the auxin content was 2- to 4-fold higher than the cytokinin content. “
“Dinoflagellates are a group of eukaryotic microalgae that have many unusual cytological and genomic characteristics. Here, we report the detection of a novel catalase–peroxidase (KatG) gene from the dinoflagellate Prorocentrum minimum, and its transcript levels under copper sulfate (CuSO4) treatment. cDNA analysis yielded a 1,293 bp complete open reading frame (ORF) encoding a 431-amino acid (aa) polypeptide (46.6 kDa).