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

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

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

Development of Time- and Energy-Resolved Synchrotron-Radiation-Based Mössbauer Spectroscopy

14th International Conference on Synchrotron Radiation Instrumentation (SRI 2021) 28.03.2022 - 01.04.2022 OnlineSynchrotron-radiation based Mössbauer spectroscopy has become a useful technique capable for investigating various Mössbauer isotopes. For a typical experimental setup, the information associated with the pulse height (that is, energy) in an avalanche photodiode (APD) detector has not been used effectively. By using a system for simultaneous measurement system of time and energy associated with the APD signal, a system for the time- and energy-resolved Mössbauer spectroscopy has been developed. In this system, the pulse height information was converted to the time information through an amplitude-to-time converter applied to one of the divided signals from the APD. The corresponding time information was processed separately from another one of the divided signals. Both signals are recorded by a multi-channel scaler in an event-by-event data acquisition process. The velocity information from the Mössbauer transducer was also recorded as a tag for each signal event. Thus, the Mössbauer spectra with any time- and energy-window can be reconstructed after the data collection process. This system can be used for many purposes in time- and energy-resolved Mössbauer spectroscopy, and shows significant promise for use with other fast detectors and for various types of experiments

Disruption of the leptomeningeal blood barrier in neuromyelitis optica spectrum disorder

OBJECTIVE: To describe leptomeningeal blood-barrier impairment reflected by MRI gadolinium-enhanced lesions in patients with aquaporin-4 immunoglobulin G (AQP4-IgG)-positive neuromyelitis optica spectrum disorder (NMOSD). METHODS: A retrospective case series of 11 AQP4-IgG-positive NMOSD patients with leptomeningeal enhancement (LME) were collected from 5 centers. External neuroradiologists, blinded to the clinical details, evaluated MRIs. RESULTS: LME was demonstrated on postcontrast T1-weighted and fluid-attenuated inversion recovery images as a sign of leptomeningeal blood-barrier disruption and transient leakage of contrast agent into the subarachnoid space in 11 patients, 6 in the brain and 6 in the spinal cord. The patterns of LME were linear or extensive and were accompanied by periependymal enhancement in 5 cases and intraparenchymal enhancement in all cases. The location of LME in the spinal cord was adjacent to intraparenchymal contrast enhancement with involvement of a median number of 12 (range 5-17) vertebral segments. At the time of LME on MRI, all patients had a clinical attack such as encephalopathy (36%) and/or myelopathy (70%) with median interval between symptom onset and LME of 12 days (range 2-30). LME occurred in association with an initial area postrema attack (44%), signs of systemic infection (33%), or AQP4-IgG in CSF (22%) followed by clinical progression. LME was found at initial clinical presentation in 5 cases and at clinical relapses leading to a diagnosis of NMOSD in 6 cases. CONCLUSION: This study suggests that altered leptomeningeal blood barrier may be accompanied by intraparenchymal blood-brain barrier breakdown in patients with AQP4-IgG-positive NMOSD during relapses