1,103 research outputs found
Development of Real Time Personal Neutron Dosimeter with Two Silicon Detectors
開始ページ、終了ページ: 冊子体のページ付
Voltammetry and single-molecule in situ scanning tunneling microscopy of laccases and bilirubin oxidase in electrocatalytic dioxygen reduction on Au(111) single-crystal electrodes
Tissue-Specific Expression of the Gene for a Putative Plasma Membrane H+-ATPase in a Seagrass
Peripheral CD103+ dendritic cells form a unified subset developmentally related to CD8α+ conventional dendritic cells
Although CD103-expressing dendritic cells (DCs) are widely present in nonlymphoid tissues, the transcription factors controlling their development and their relationship to other DC subsets remain unclear. Mice lacking the transcription factor Batf3 have a defect in the development of CD8α(+) conventional DCs (cDCs) within lymphoid tissues. We demonstrate that Batf3(−/−) mice also lack CD103(+)CD11b(−) DCs in the lung, intestine, mesenteric lymph nodes (MLNs), dermis, and skin-draining lymph nodes. Notably, Batf3(−/−) mice displayed reduced priming of CD8 T cells after pulmonary Sendai virus infection, with increased pulmonary inflammation. In the MLNs and intestine, Batf3 deficiency resulted in the specific lack of CD103(+)CD11b(−) DCs, with the population of CD103(+)CD11b(+) DCs remaining intact. Batf3(−/−) mice showed no evidence of spontaneous gastrointestinal inflammation and had a normal contact hypersensitivity (CHS) response, despite previous suggestions that CD103(+) DCs were required for immune homeostasis in the gut and CHS. The relationship between CD8α(+) cDCs and nonlymphoid CD103(+) DCs implied by their shared dependence on Batf3 was further supported by similar patterns of gene expression and their shared developmental dependence on the transcription factor Irf8. These data provide evidence for a developmental relationship between lymphoid organ–resident CD8α(+) cDCs and nonlymphoid CD103(+) DCs
Phosphorylation of GFAP is associated with injury in the neonatal pig hypoxic-ischemic brain
Glial fibrillary acidic protein (GFAP) is an intermediate filament protein expressed in the astrocyte cytoskeleton that plays an important role in the structure and function of the cell. GFAP can be phosphorylated at six serine (Ser) or threonine (Thr) residues but little is known about the role of GFAP phosphorylation in physiological and pathophysiological states. We have generated antibodies against two phosphorylated GFAP (pGFAP) proteins: p8GFAP, where GFAP is phosphorylated at Ser-8 and p13GFAP, where GFAP is phosphorylated at Ser-13. We examined p8GFAP and p13GFAP expression in the control neonatal pig brain and at 24 and 72 h after an hypoxic-ischemic (HI) insult. Immunohistochemistry demonstrated pGFAP expression in astrocytes with an atypical cytoskeletal morphology, even in control brains. Semi-quantitative western blotting revealed that p8GFAP expression was significantly increased at 24 h post-insult in HI animals with seizures in frontal, parietal, temporal and occipital cortices. At 72 h post-insult, p8GFAP and p13GFAP expression were significantly increased in HI animals with seizures in brain regions that are vulnerable to cellular damage (cortex and basal ganglia), but no changes were observed in brain regions that are relatively spared following an HI insult (brain stem and cerebellum). Increased pGFAP expression was associated with poor neurological outcomes such as abnormal encephalography and neurobehaviour, and increased histological brain damage. Phosphorylation of GFAP may play an important role in astrocyte remodelling during development and disease and could potentially contribute to the plasticity of the central nervous system
Detection of a novel locus involved in non-seed-shattering behaviour of Japonica rice cultivar, Oryzasativa ‘Nipponbare’
Asian cultivated rice, Oryzasativa, was domesticated from its wild ancestor, O.rufipogon. Loss of seed shattering is one of the most recognisable traits selected during rice domestication. Three quantitative trait loci (QTLs), qSH1, qSH3, and sh4, were previously reported to be involved in the loss of seed shattering of Japonica cultivated rice, O.sativa ‘Nipponbare’. However, the introgression line (IL) carrying ‘Nipponbare’ alleles at these three loci in the genetic background of wild rice, O.rufipogon W630, showed a lower value for detaching a grain from the pedicel than ‘Nipponbare’. Here, we investigated abscission layer formation in the IL and found a partially formed abscission layer in the central region between the epidermis and vascular bundles. Based on QTL-seq analysis using the F2 population obtained from a cross between ‘Nipponbare’ and the IL, we detected two novel loci qCSS3 and qCSS9 (QTL for the Control of Seed Shattering in rice on chromosomes 3 and 9), which were found to be involved in the difference in seed-shattering degree between ‘Nipponbare’ and W630. Then, we further focused on qCSS3 in order to understand its potential role on the loss of seed shattering. The candidate region of qCSS3 was found to be located within a 526-kb region using substitution mapping analysis. Interestingly, the qCSS3 candidate region partially overlaps the selective sweep detected for Japonica but not for Indica rice cultivars, suggesting that this region harbours the mutation at a novel seed-shattering locus specifically selected for non-seed-shattering behaviour in Japonica cultivars
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