Low scale Seesaw model and Lepton Flavor Violating Rare B Decays

We study lepton flavor number violating rare B decays, $b \to s l_h^{\pm} l_l^{\mp}$, in a seesaw model with low scale singlet Majorana neutrinos motivated by the resonant leptogenesis scenario. The branching ratios of inclusive decays $b \to s l_h^{\pm} \bar{l_l}^{\mp}$ with two almost degenerate singlet neutrinos at TeV scale are investigated in detail. We find that there exists a class of seesaw model in which the branching fractions of $b \to s \tau \mu$ and $\tau \to \mu \gamma$ can be as large as $10^{-10}$ and $10^{-9}$ within the reach of Super B factories, respectively, without being in conflict with neutrino mixings and mass squared difference of neutrinos from neutrino data, invisible decay width of $Z$ and the present limit of $Br(\mu \to e \gamma)$.Comment: 19 pages, 6 figure

Modeling Interaction of Fluid and Salt in an Aquifer/Lagoon System

Auther Posting. ©The Authers 2009 The full text of this article is published in GROUND WATER, 47, 1, 35-48. It is available online from Blackwell-Synergy at https://doi.org/10.1111/j.1745-6584.2008.00482.xArticleGROUND WATER. 47(1):35-48 (2009)journal articl

Colletotrichum orbiculare FAM1 Encodes a Novel Woronin Body-Associated Pex22 Peroxin Required for Appressorium-Mediated Plant Infection

ABSTRACT The cucumber anthracnose fungus Colletotrichum orbiculare forms specialized cells called appressoria for host penetration. We identified a gene, FAM1, encoding a novel peroxin protein that is essential for peroxisome biogenesis and that associates with Woronin bodies (WBs), dense-core vesicles found only in filamentous ascomycete fungi which function to maintain cellular integrity. The fam1 disrupted mutants were unable to grow on medium containing oleic acids as the sole carbon source and were nonpathogenic, being defective in both appressorium melanization and host penetration. Fluorescent proteins carrying peroxisomal targeting signals (PTSs) were not imported into the peroxisomes of fam1 mutants, suggesting that FAM1 is a novel peroxisomal biogenesis gene (peroxin). FAM1 did not show significant homology to any Saccharomyces cerevisiae peroxins but resembled conserved filamentous ascomycete-specific Pex22-like proteins which contain a predicted Pex4-binding site and are potentially involved in recycling PTS receptors from peroxisomes to the cytosol. C. orbiculare FAM1 complemented the peroxisomal matrix protein import defect of the S. cerevisiae pex22 mutant. Confocal microscopy of Fam1-GFP (green fluorescent protein) fusion proteins and immunoelectron microscopy with anti-Fam1 antibodies showed that Fam1 localized to nascent WBs budding from peroxisomes and mature WBs. Association of Fam1 with WBs was confirmed by colocalization with WB matrix protein CoHex1 (C. orbiculare Hex1) and WB membrane protein CoWsc (C. orbiculare Wsc) and by subcellular fractionation and Western blotting with antibodies to Fam1 and CoHex1. In WB-deficient cohex1 mutants, Fam1 was redirected to the peroxisome membrane. Our results show that Fam1 is a WB-associated peroxin required for pathogenesis and raise the possibility that localized receptor recycling occurs in WBs. IMPORTANCE Colletotrichum orbiculare is a fungus causing damaging disease on Cucurbitaceae plants. In this paper, we characterize a novel peroxisome biogenesis gene from this pathogen called FAM1. Although no genes with significant homology are present in Saccharomyces cerevisiae, FAM1 contains a predicted Pex4-binding site typical of Pex22 proteins, which function in the recycling of PTS receptors from peroxisomes to the cytosol. We show that FAM1 complements the defect in peroxisomal matrix protein import of S. cerevisiae pex22 mutants and that fam1 mutants are completely defective in peroxisome function, fatty acid metabolism, and pathogenicity. Remarkably, we found that this novel peroxin is specifically localized on the bounding membrane of Woronin bodies, which are small peroxisome-derived organelles unique to filamentous ascomycete fungi that function in septal pore plugging. Our finding suggests that these fungi have coopted the Woronin body for localized receptor recycling during matrix protein import

Recombinant variant fibrinogens substituted at residues γ326Cys and γ339Cys demonstrated markedly impaired secretion of assembled fibrinogen

ArticleThrombosis Research. 124(3):368-372 (2009)journal articl

Asymptotic analysis of the model for distribution of high-tax payers

The z-transform technique is used to investigate the model for distribution of high-tax payers, which is proposed by two of the authors (K. Y and S. M) and others. Our analysis shows an asymptotic power-law of this model with the exponent -5/2 when a total ``mass'' has a certain critical value. Below the critical value, the system exhibits an ordinary critical behavior, and scaling relations hold. Above the threshold, numerical simulations show that a power-law distribution coexists with a huge ``monopolized'' member. It is argued that these behaviors are observed universally in conserved aggregation processes, by analizing an extended model.Comment: 5pages, 3figure

Functional analysis of recombinant B beta 15C and B beta 15A fibrinogens demonstrates that B beta 15G residue plays important roles in FPB release and in lateral aggregation of protofibrils

The definitive version is available at www.blackwell-synergy.com.ArticleJOURNAL OF THROMBOSIS AND HAEMOSTASIS. 3(5): 983-990 (2005)journal articl

Complex Relationship of Body Mass Index with Mortality in Patients with Critical Limb Ischemia Undergoing Endovascular Treatment

ObjectiveTo investigate the relationship between body mass index (BMI) and long-term outcomes of patients with CLI after endovascular treatment (EVT).DesignRetrospective multicenter study.Subjects1088 consecutive patients (1306 limbs, mean age 72 ± 10 years) with CLI who underwent EVT for isolated infrapopliteal artery lesions were evaluated. These subjects were identified in the J-BEAT III registry.MethodsThe patients were divided into groups based on BMI <18.5 kg/m2 (underweight, n = 188; 219 limbs), 18.5 to 24.9 kg/m2 (normal weight, n = 718; 868 limbs), and >25.0 kg/m2 (overweight/obese, n = 182; 219 limbs). The endpoints were overall survival and freedom from major adverse limb events (MALE).ResultsThe median follow up period was 1.5 years (range: 1 month–8.7 years). The 3 year overall survival rates were 33.3%, 61.2%, and 69.8% in underweight, normal, and overweight/obese patients, respectively. The survival rate was significantly lower in underweight patients and significantly higher in overweight/obese patients compared with patients of normal weight (both p < .0001). The 3 year rates of freedom from MALE did not differ significantly among the three groups (36.4%, 45.4%, and 52.3%, respectively, p = .32). Age, BMI <18.5 kg/m2, heart failure, aortic valve stenosis, renal failure, triglyceride levels, serum albumin <3.0 g/dL, anticoagulant treatment, non-ambulatory status, and Rutherford 6 classification all were significantly associated with overall survival.ConclusionsBMI has a complex correlation with mortality in patients with CLI after EVT for isolated infrapopliteal artery lesions. Underweight patients with CLI have an extremely poor prognosis. Such patients have many other factors associated with mortality, but low BMI was identified as an independent predictor of a poor prognosis in patients with CLI. Similarly, normal weight patients had a small but significant increase in mortality compared with overweight/obese patients

QRDR mutations, efflux system &amp; antimicrobial resistance genes in enterotoxigenic Escherichia coli isolated from an outbreak of diarrhoea in Ahmedabad, India

Background &amp; objectives: Diverse mechanisms have been identified in enteric bacteria for their adaptation and survival against multiple classes of antimicrobial agents. Resistance of bacteria to the most effective fluoroquinolones have increasingly been reported in many countries. We have identified that most of the enterotoxigenic Escherichia coli (ETEC) were resistant to several antimicrobials in a diarrhoea outbreak at Ahmedabad during 2000. The present study was done to identify several genes responsible for antimicrobial resistance and mobile genetic elements in the ETEC strains. Methods: Seventeen ETEC strains isolated from diarrhoeal patients were included in this study. The antimicrobial resistance was confirmed by conventional disc diffusion method. PCR and DNA sequencing were performed for the identification of mutation in the quinolone resistance-determining regions (QRDRs). Efflux pump was tested by inhibiting the proton-motive force. DNA hybridization assay was made for the detection of integrase genes and the resistance gene cassettes were identified by direct sequencing of the PCR amplicons. Results: Majority of the ETEC had GyrA mutations at codons 83 and 87 and in ParC at codon 80. Six strains had an additional mutation in ParC at codon 108 and two had at position 84. Plasmid-borne qnr gene alleles that encode quinolone resistance were not detected but the newly described aac(6')-Ib-cr gene encoding a fluoroquinolne-modifying enzyme was detected in 64.7 per cent of the ETEC. Class 1 (intI1) and class 2 (intI2) integrons were detected in six (35.3%) and three (17.6%) strains, respectively. Four strains (23.5%) had both the classes of integrons. Sequence analysis revealed presence of dfrA17, aadA1, aadA5 in class 1, and dfrA1, sat1, aadA1 in class 2 integrons. In addition, the other resistance genes such as tet gene alleles (94.1%), catAI (70.6%), strA (58.8%), bla TEM-1 (35.2%), and aphA1-Ia (29.4%) were detected in most of the strains. Interpretation &amp; Conclusions: Innate gene mutations and acquisition of multidrug resistance genes through mobile genetic elements might have contributed to the emergence of multidrug resistance (MDR) in ETEC. This study reinforces the necessity of utilizing molecular techniques in the epidemiological studies to understand the nature of resistance responsible for antimicrobial resistance in different species of pathogenic bacteria

In vitro transcription of compound heterozygous hypofibrinogenemia Matsumoto IX; first identification of FGB IVS6 deletion of 4 nucleotides and FGG IVS3-2A > G causing abnormal RNA splicing

ArticleClinica Chimica Acta. 411(17-18):1325-1329 (2010)journal articl

B : b interactions are essential for polymerization of variant fibrinogens with impaired holes 'a'

This is an electronic version of an Article published in Journal of Thrombosis and Haemostasis 2007; 5(12): 2352-2359.ArticleJOURNAL OF THROMBOSIS AND HAEMOSTASIS. 5(12): 2352-2359 (2007)journal articl