Crystallicutis gen. nov. (Irpicaceae,Basidiomycota), including C. damiettensis sp. nov., found on Phoenix dactylifera (date palm) trunks in the Nile Delta of Egypt

The taxonomy of Polyporales is complicated by the variability in key morphological characters across families and genera, now being gradually resolved through molecular phylogenetic analyses. Here a new resupinate species, Crystallicutis damiettensis sp. nov. found on the decayed trunks of date palm (Phoenix dactylifera) trees in the fruit orchards of the Nile Delta region of Egypt is reported. Multigene phylogenetic analyses based on ITS, LSU, EF1α, RPB1 and RPB2 loci place this species in Irpicaceae, and forming a distinct clade with Ceraceomyces serpens and several other hitherto unnamed taxa, which we also incorporate into a new genus Crystallicutis. We name two of these species, Crystallicutis huangshanensis sp. nov. and Crystallicutis rajchenbergii sp. nov. The distinctive feature of Crystallicutis gen. nov. is the presence of crystal-encrusted hyphae in the hymenium and subiculum. Basidiomes are usually honey-yellow with white margins but there is variability in the presence of clamp connections and cystidia, as noted for other genera within Irpicacae. C. damiettensis is hitherto consistently associated with date palms killed by the red palm weevil Rhynchophorus ferrugineus, a highly damaging and invasive pest, recently spread to the Mediterranean region. C. damiettensis causes rapid wood decay by a potentially unusual white-rot mechanism and may play a role in the damage caused by R. ferrugineus.     

Effects of congenital stationary night blindness type 2 mutations R508Q and L1364H on Cav1.4 L-type Ca2+ channel function and expression

At least 48 mutations in the CACNA1F gene encoding retinal Ca(v)1.4 L-type Ca(2+) channels have been linked to X-linked recessive congenital stationary night blindness type 2 (CSNB2). A large number of these are missense mutations encoding full-length alpha1-subunits that can potentially form functional channels. We have previously shown that such missense mutations can confer their phenotype by different pathological mechanisms, such as complete lack of alpha1 subunit protein expression or dramatic changes in channel gating. Here we investigated the functional consequences of CSNB2 missense mutations R508Q and L1364H. We found no (R508Q) or only minor (L1364H) changes in the gating properties of both mutants after heterologous expression in Xenopus laevis oocytes (at 20 degrees C). However, both mutants resulted in altered expression density of Ca(v)1.4 currents. When expressed in the mammalian cell line tsA-201, the current amplitude of L1364H channels was reduced when cells were grown at 30 degrees C and both mutations affected total alpha1 protein expression. This effect was temperature dependent. Our data provide evidence that, in contrast to previously characterized CSNB2 missense mutations, the clinical phenotype of R508Q and L1364H is unlikely to be explained by changes in channel gating. Instead, these mutations affect the protein expression of Ca(v)1.4 Ca(2+) channels.     

Yoga for Multiple Sclerosis: A Systematic Review and Meta-Analysis

While yoga seems to be effective in a number of neuropsychiatric disorders, the evidence of efficacy in multiple sclerosis remains unclear. The aim of this review was to systematically assess and meta-analyze the available data on efficacy and safety of yoga in patients with multiple sclerosis. Medline/PubMed, Scopus, the Cochrane Central Register of Controlled Trials, PsycINFO, CAM-Quest, CAMbase, and IndMED were searched through March 2014. Randomized controlled trials (RCTs) of yoga for patients with multiple sclerosis were included if they assessed health-related quality of life, fatigue, and/or mobility. Mood, cognitive function, and safety were defined as secondary outcome measures. Risk of bias was assessed using the Cochrane tool. Seven RCTs with a total of 670 patients were included. Evidence for short-term effects of yoga compared to usual care were found for fatigue (standardized mean difference [SMD] = −0.52; 95% confidence intervals (CI) = −1.02 to −0.02; p = 0.04; heterogeneity: I² = 60%; Chi² = 7.43; p = 0.06) and mood (SMD = −0.55; 95%CI = −0.96 to −0.13; p = 0.01; heterogeneity: I² = 0%; Chi² = 1.25; p = 0.53), but not for health-related quality of life, muscle function, or cognitive function. The effects on fatigue and mood were not robust against bias. No short-term or longer term effects of yoga compared to exercise were found. Yoga was not associated with serious adverse events. In conclusion, since no methodological sound evidence was found, no recommendation can be made regarding yoga as a routine intervention for patients with multiple sclerosis. Yoga might be considered a treatment option for patients who are not adherent to recommended exercise regimens.     

Whole genome comparisons of serotype 4b and 1/2a strains of the food-borne pathogen Listeria monocytogenes reveal new insights into the core genome components of this species

The genomes of three strains of Listeria monocytogenes that have been associated with food-borne illness in the USA were subjected to whole genome comparative analysis. A total of 51, 97 and 69 strain-specific genes were identified in L.monocytogenes strains F2365 (serotype 4b, cheese isolate), F6854 (serotype 1/2a, frankfurter isolate) and H7858 (serotype 4b, meat isolate), respectively. Eighty-three genes were restricted to serotype 1/2a and 51 to serotype 4b strains. These strain- and serotype-specific genes probably contribute to observed differences in pathogenicity, and the ability of the organisms to survive and grow in their respective environmental niches. The serotype 1/2a-specific genes include an operon that encodes the rhamnose biosynthetic pathway that is associated with teichoic acid biosynthesis, as well as operons for five glycosyl transferases and an adenine-specific DNA methyltransferase. A total of 8603 and 105 050 high quality single nucleotide polymorphisms (SNPs) were found on the draft genome sequences of strain H7858 and strain F6854, respectively, when compared with strain F2365. Whole genome comparative analyses revealed that the L.monocytogenes genomes are essentially syntenic, with the majority of genomic differences consisting of phage insertions, transposable elements and SNPs.     

Dominant Renin Gene Mutations Associated with Early-Onset Hyperuricemia, Anemia, and Chronic Kidney Failure

Through linkage analysis and candidate gene sequencing, we identified three unrelated families with the autosomal-dominant inheritance of early onset anemia, hypouricosuric hyperuricemia, progressive kidney failure, and mutations resulting either in the deletion (p.Leu16del) or the amino acid exchange (p.Leu16Arg) of a single leucine residue in the signal sequence of renin. Both mutations decrease signal sequence hydrophobicity and are predicted by bioinformatic analyses to damage targeting and cotranslational translocation of preprorenin into the endoplasmic reticulum (ER). Transfection and in vitro studies confirmed that both mutations affect ER translocation and processing of nascent preprorenin, resulting either in reduced (p.Leu16del) or abolished (p.Leu16Arg) prorenin and renin biosynthesis and secretion. Expression of renin and other components of the renin-angiotensin system was decreased accordingly in kidney biopsy specimens from affected individuals. Cells stably expressing the p.Leu16del protein showed activated ER stress, unfolded protein response, and reduced growth rate. It is likely that expression of the mutant proteins has a dominant toxic effect gradually reducing the viability of renin-expressing cells. This alters the intrarenal renin-angiotensin system and the juxtaglomerular apparatus functionality and leads to nephron dropout and progressive kidney failure. Our findings provide insight into the functionality of renin-angiotensin system and stress the importance of renin analysis in families and individuals with early onset hyperuricemia, anemia, and progressive kidney failure.     

Homogeneous oxidative coupling catalysts. Mechanism of conversion of 2,6-dimethylphenol [DMP] to 3,3′,5,5′-tetramethyl-4,4′-diphenoquinone [DPQ] by [(Pip)nCuX]4O2 (n = 1 or 2, Pip = piperidine, X = Cl, Br or I) in aprotic media

This paper represents the mechanism of the second half of the catalytic cycle, Scheme 1, which represents the conversion of 2,6-dimethylphenol [DMP] to 3,3′,5,5′-tetramethyl, 4,4′-diphenoquinone [DPQ] by homogenous oxidative coupling catalysts [(Pip)_nCuX]₄O₂ in aprotic media. The mechanism can be represented as a pre-equilibrium, K, between the catalyst and 2,6-dimethylphenol to form a complex intermediate which is converted into the activated complex through the rate determining step, k₂, to form the final products. The observed pseudo first-order rate constant is given by k_obs = K k₂[DMP]^y/(1 + K[DMP]^y). When the coordination number around copper(II) is equal to five as in [(Pip)CuX]₄O₂, the system suffers from kinetic saturation due to strong complex formation between catalyst and [DMP] and therefore K[DMP]^y > 10 and k_obs = k₂. Kinetic saturation has been avoided by using six coordinate copper(II) as in [(Pip)₂CuX]₄O₂. The influence of the coordination saturation of copper(II) in [(Pip)₂CuX]₄O₂ helps to evaluate both thermodynamic and kinetic parameters for the system as well as for the structure of the activated complex, (y = 2), which consists of one [(Pip)₂CuX]₄O₂ and two [DMP]. Reduction of copper(II) to copper(I) has been suggested as a rate determining step due to halogen, X, and solvent effects.     

Opposite effects of a single IIIS5 mutation on phenylalkylamine and dihydropyridine interaction with L-type Ca2+ channels

Replacement of L-type Ca(2+) channel alpha(1) subunit residue Thr-1066 in segment IIIS5 by a tyrosine residue conserved in the corresponding positions of non-L-type Ca(2+) channels eliminates high dihydropyridine sensitivity through a steric mechanism. To determine the effects of this mutation on phenylalkylamine interaction, we exploited the availability of Ca(v)1.2DHP(-/-) mice containing the T1066Y mutation. In contrast to dihydropyridines, increased protein-dependent binding of the phenylalkylamine (-)-[(3)H]devapamil occurred to Ca(v)1.2DHP(-/-) mouse brain microsomes. This effect could be attributed to an at least 2-fold increase in affinity as determined by saturation analysis and binding inhibition experiments. The latter also revealed a higher affinity for (-)-verapamil but not for (-)-gallopamil. The mutation caused a pronounced slowing of (-)-[(3)H]devapamil dissociation, indicating a stabilization of the drug-channel complex. The increased affinity of mutant channels was also evident in functional studies after heterologous expression of wild type and T1066Y channels in Xenopus laevis oocytes. 100 mum (-)-verapamil inhibited a significantly larger fraction of Ba(2+) inward current through mutant than through WT channels. Our results provide evidence that phenylalkylamines also interact with the IIIS5 helix and that the geometry of the IIIS5 helix affects the access and/or binding of different chemical classes of Ca(2+) channel blockers to their overlapping binding domains. Mutation of Thr-1066 to a non-L-type tyrosine residue can be exploited to differentially affect phenylalkylamine and dihydropyridine binding to L-type Ca(2+) channels.