11,380 research outputs found

    Additive effect involving a new locus of benomyl resistance in Aspergillus nidulans

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    Most of the fungicides based on the benzimidazole nucleus, including benomyl, thiabendazole and thiophanate, are systemic and because they control many important fungal diseases

    The levels of mRNA expressed by gene palF of A. nidulans do not appear to be pH regulated

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    Although pal genes are putative members of a signaling cascade involved in ambient pH sensing and in the consecutive activation of PacC protein, recent findings show that most of them (palA, B, C, H and I) do not respond to ambient pH at the transcriptional level. Here, we show that mRNA levels of the remainding palF gene are also constant at various growth pH values

    pH and acid phosphatase determinations after growth of Aspergillus nidulans on solid medium

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    pH and acid phosphatase determinations after growth of Aspergillus nidulans on solid mediu

    Heavy-flavour production in Pb-Pb collisions at the LHC, measured with the ALICE detector

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    We present the first results from the ALICE experiment on the nuclear modification factors for heavy-flavour hadron production in Pb-Pb collisions at sqrt{s_NN}=2.76 TeV. Using proton-proton and lead-lead collision samples at sqrt{s}=7 TeV and sqrt{s_NN}=2.76 TeV, respectively, nuclear modification factors R_AA(pt) were measured for D mesons at central rapidity (via displaced decay vertex reconstruction), and for electrons and muons, at central and forward rapidity, respectively.Comment: 8 pages, 5 figures, plenary talk at Quark Matter 2011, Annecy, Franc

    One-Liners

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    One liners from: N.M. Martinez-Rossi, C. Andrade-Monteiro and S.R.C. Pombeiro; M. Orbach ; H. Liu and TJ. Schmidhauser; P.A. Hubbard and C.H. Wilso

    Protein Kinase C-beta Dictates B Cell Fate by Regulating Mitochondrial Remodeling, Metabolic Reprogramming, and Heme Biosynthesis

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    PKCβ-null (Prkcb−/−) mice are severely immunodeficient. Here we show that mice whose B cells lack PKCβ failed to form germinal centers and plasma cells, which undermined affinity maturation and antibody production in response to immunization. Moreover, these mice failed to develop plasma cells in response to viral infection. At the cellular level, we have shown that Prkcb−/−B cells exhibited defective antigen polarization and mTORC1 signaling. While altered antigen polarization impaired antigen presentation and likely restricted the potential of GC development, defective mTORC1 signaling impaired metabolic reprogramming, mitochondrial remodeling, and heme biosynthesis in these cells, which altogether overwhelmingly opposed plasma cell differentiation. Taken together, our study reveals mechanistic insights into the function of PKCβ as a key regulator of B cell polarity and metabolic reprogramming that instructs B cell fate. Lymphocyte activation is associated with major changes in metabolism. Tsui and colleagues demonstrate that PKCβ promotes metabolic reprogramming to drive effector fate decision in B cells

    Oral chondroitin sulfate and prebiotics for the treatment of canine Inflammatory Bowel Disease: a randomized, controlled clinical trial

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    BACKGROUND Canine inflammatory bowel disease (IBD) is a chronic enteropathy of unknown etiology, although microbiome dysbiosis, genetic susceptibility, and dietary and/or environmental factors are hypothesized to be involved in its pathogenesis. Since some of the current therapies are associated with severe side effects, novel therapeutic modalities are needed. A new oral supplement for long-term management of canine IBD containing chondroitin sulfate (CS) and prebiotics (resistant starch, β-glucans and mannaoligosaccharides) was developed to target intestinal inflammation and oxidative stress, and restore normobiosis, without exhibiting any side effects. This double-blinded, randomized, placebo-controlled trial in dogs with IBD aims to evaluate the effects of 180 days administration of this supplement together with a hydrolyzed diet on clinical signs, intestinal histology, gut microbiota, and serum biomarkers of inflammation and oxidative stress. RESULTS Twenty-seven client-owned biopsy-confirmed IBD dogs were included in the study, switched to the same hydrolyzed diet and classified into one of two groups: supplement and placebo. Initially, there were no significant differences between groups (p > 0.05) for any of the studied parameters. Final data analysis (supplement: n = 9; placebo: n = 10) showed a significant decrease in canine IBD activity index (CIBDAI) score in both groups after treatment (p < 0.001). After treatment, a significant decrease (1.53-fold; p < 0.01) in histologic score was seen only in the supplement group. When groups were compared, the supplement group showed significantly higher serum cholesterol (p < 0.05) and paraoxonase-1 (PON1) levels after 60 days of treatment (p < 0.01), and the placebo group showed significantly reduced serum total antioxidant capacity (TAC) levels after 120 days (p < 0.05). No significant differences were found between groups at any time point for CIBDAI, WSAVA histologic score and fecal microbiota evaluated by PCR-restriction fragment length polymorphism (PCR-RFLP). No side effects were reported in any group. CONCLUSIONS The combined administration of the supplement with hydrolyzed diet over 180 days was safe and induced improvements in selected serum biomarkers, possibly suggesting a reduction in disease activity. This study was likely underpowered, therefore larger studies are warranted in order to demonstrate a supplemental effect to dietary treatment of this supplement on intestinal histology and CIBDAI

    Measurement of Exclusive π0\pi^0 Electroproduction Structure Functions and their Relationship to Transversity GPDs

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    Exclusive π0\pi^0 electroproduction at a beam energy of 5.75 GeV has been measured with the Jefferson Lab CLAS spectrometer. Differential cross sections were measured at more than 1800 kinematic values in Q2Q^2, xBx_B, tt, and ϕπ\phi_\pi, in the Q2Q^2 range from 1.0 to 4.6 GeV2^2,\ t-t up to 2 GeV2^2, and xBx_B from 0.1 to 0.58. Structure functions σT+ϵσL,σTT\sigma_T +\epsilon \sigma_L, \sigma_{TT} and σLT\sigma_{LT} were extracted as functions of tt for each of 17 combinations of Q2Q^2 and xBx_B. The data were compared directly with two handbag-based calculations including both longitudinal and transversity GPDs. Inclusion of only longitudinal GPDs very strongly underestimates σT+ϵσL\sigma_T +\epsilon \sigma_L and fails to account for σTT\sigma_{TT} and σLT\sigma_{LT}, while inclusion of transversity GPDs brings the calculations into substantially better agreement with the data. There is very strong sensitivity to the relative contributions of nucleon helicity flip and helicity non-flip processes. The results confirm that exclusive π0\pi^0 electroproduction offers direct experimental access to the transversity GPDs.Comment: 6 pages, 2 figure

    Autophagy modulates endothelial junctions to restrain neutrophil diapedesis during inflammation

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    The migration of neutrophils from the blood circulation to sites of infection or injury is a key immune response and requires the breaching of endothelial cells (ECs) that line the inner aspect of blood vessels. Unregulated neutrophil transendothelial cell migration (TEM) is pathogenic, but the molecular basis of its physiological termination remains unknown. Here, we demonstrated that ECs of venules in inflamed tissues exhibited a robust autophagic response that was aligned temporally with the peak of neutrophil trafficking and was strictly localized to EC contacts. Genetic ablation of EC autophagy led to excessive neutrophil TEM and uncontrolled leukocyte migration in murine inflammatory models, while pharmacological induction of autophagy suppressed neutrophil infiltration into tissues. Mechanistically, autophagy regulated the remodeling of EC junctions and expression of key EC adhesion molecules, facilitating their intracellular trafficking and degradation. Collectively, we have identified autophagy as a modulator of EC leukocyte trafficking machinery aimed at terminating physiological inflammation
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