22 research outputs found

    Pressure challenge test and histopathological inspections for 17 Japanese cases with clinically diagnosed delayed pressure urticaria

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    Delayed pressure urticaria (DPU) is characterized by deep dermal wheals that appear in response to a local continuous pressure. Although it has been reported to complicate as many as 40% of cases of Caucasian patients with chronic urticaria, no definitive cases of Asian/Japanese patients have been reported in English literature. Here, we identified 17 cases of DPU, among 540 Japanese patients with urticaria (3.1%), based on careful history taking, pressure challenge test and, ideally, skin biopsy. Twelve out of 17 patients (70.5%) who undertook pressure challenge test developed wheal and erythema in the area of pressure 1-12 h later. Six out of 15 patients (40%) were positive for the autologous serum skin test. All cases were complicated with ordinary chronic urticaria, and all specimens of skin biopsies performed for 12 patients showed substantial eosinophil infiltration. All cases were resistant to antihistamines with or without other non-steroidal medications and eventually treated with 0.25-1.5 mg/day of betamethasone. However, 12 of them (70.6%) were able to cease steroid use because of cure or remission. For those cured or in remission, the duration of steroid administration and that from the onset to diagnosis was 11.2 +/- A 11.0 and 54.8 +/- A 60.2 months (mean +/- A SD), respectively. DPU may be identified as a relatively rare complication of Japanese patients with chronic idiopathic urticaria. A proper diagnosis and a small amount of steroid may be beneficial for the treatment of DPU

    Effect of Sequence-Directed Nucleosome Disruption on Cell-Type-Specific Repression by α2/Mcm1 in the Yeast Genome

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    In Saccharomyces cerevisiae, a-cell-specific genes are repressed in MATα cells by α2/Mcm1, acting in concert with the Ssn6-Tup1 corepressors and the Isw2 chromatin remodeling complex, and nucleosome positioning has been proposed as one mechanism of repression. However, prior studies showed that nucleosome positioning is not essential for repression by α2/Mcm1 in artificial reporter plasmids, and the importance of the nucleosome positioning remains questionable. We have tested the function of positioned nucleosomes through alteration of genomic chromatin at the a-cell-specific gene BAR1. We report here that a positioned nucleosome in the BAR1 promoter is disrupted in cis by the insertion of diverse DNA sequences such as poly(dA) · poly(dT) and poly(dC-dG) · poly(dC-dG), leading to inappropriate partial derepression of BAR1. Also, we show that isw2 mutation causes loss of nucleosome positioning in BAR1 in MATα cells as well as partial disruption of repression. Thus, nucleosome positioning is required for full repression, but loss of nucleosome positioning is not sufficient to relieve repression completely. Even though disruption of nucleosome positioning by the cis- and trans-acting modulators of chromatin has a modest effect on the level of transcription, it causes significant degradation of the α-mating pheromone in MATα cells, thereby affecting its cell type identity. Our results illustrate a useful paradigm for analysis of chromatin structural effects at genomic loci

    Data-Retention-Voltage-Based Analysis of Systematic Variations in SRAM SEU Hardness: A Possible Solution to Synergistic Effects of TID

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    Single-event upset (SEU) hardness varies across dies, wafers, and lots—even just after fabrication and further across time. Mechanisms of postfabrication variations include total ionizing dose (TID) effects, which are caused by long-term radiation exposure. This synergistic effect of TID on SEU hardness is a particular concern in integrated circuits used in space and nuclear radiation environments. This article shows that an electrical parameter called the data-retention voltage is useful in dealing with such TID effects on the SEU hardness of static random access memories (SRAMs), which are known to be particularly radiation-sensitive. Experiments showed that TID-induced variations in SRAM SEU hardness, i.e., variations in SEU cross sections, were predicted by measuring the data-retention voltage. In addition, these variations were canceled out by adjusting the power supply voltage according to its interesting relationship to the data-retention voltage. Results suggest that it might be possible in flight to predict and cancel out SEU hardness variations caused by TID and other synergistic effects

    Low Infection of Phelipanche aegyptiaca in Micro-Tom Mutants Deficient in CAROTENOID CLEAVAGE DIOXYGENASE 8

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    Strigolactones (SLs), a group of plant hormones, induce germination of root-parasitic plants and inhibit shoot branching in many plants. Shoot branching is an important trait that affects the number and quality of flowers and fruits. Root-parasitic plants, such as Phelipanche spp., infect tomato roots and cause economic damage in Europe and North Africa—hence why resistant tomato cultivars are needed. In this study, we found carotenoid cleavage dioxygenase 8-defective mutants of Micro-Tom tomato (slccd8) by the “targeting induced local lesions in genomes” (TILLING) method. The mutants showed excess branching, which was suppressed by exogenously applied SL. Grafting shoot scions of the slccd8 mutants onto wild-type (WT) rootstocks restored normal branching in the scions. The levels of endogenous orobanchol and solanacol in WT were enough detectable, whereas that in the slccd8 mutants were below the detection limit of quantification analysis. Accordingly, root exudates of the slccd8 mutants hardly stimulated seed germination of root parasitic plants. In addition, SL deficiency did not critically affect the fruit traits of Micro-Tom. Using a rhizotron system, we also found that Phelipanche aegyptiaca infection was lower in the slccd8 mutants than in wild-type Micro-Tom because of the low germination. We propose that the slccd8 mutants might be useful as new tomato lines resistant to P. aegyptiaca
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