Publications by authors named "Y Mizutani"

Background: A psoriasis (PSO) diagnosis may pose specific treatment challenges for women of childbearing age (WoCBA) who are considering pregnancy, are pregnant, or have just given birth.

Objective: To report perspectives of WoCBA with PSO regarding pregnancy and dermatologists about the disease management of these women in Australia and Japan.

Methods: Online surveys were completed by women aged 18 to 45 years who were pregnant within the past 5 years with moderate to severe PSO and dermatologists.

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Objectives: Sudden death in multiple system atrophy (MSA) is caused by decreased serotonergic innervation, but there is no routine test method for this decrease. In addition to dopamine transporters, iodine-123-labelled N-(3-fluoropropyl)-2β-carbomethoxy-3β-(4-iodophenyl) nortropane (I-FP-CIT) binds serotonin transporters (SERTs). We noted a binding potential to quantify the total quantity of I-FP-CIT binding to its receptors.

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Introduction: Progressive supranuclear palsy (PSP) involves midbrain structures, including the red nucleus (RN), an iron-rich region that appears as a high-contrast area on quantitative susceptibility mapping (QSM). RN may serve as a promising biomarker for differentiating parkinsonism. However, RN deformation in PSP remains elusive.

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Proton-pumping rhodopsins, which consist of seven transmembrane helices and have a retinal chromophore bound to a lysine side chain through a Schiff base linkage, offer valuable insights for developing unidirectional ion transporters. Despite identical overall structures and membrane topologies of outward and inward proton-pumping rhodopsins, these proteins transport protons in opposing directions, suggesting a rational mechanism that enables protons to move in different directions within similar protein structures. In the present study, we clarified the chromophore structures in early intermediates of inward and outward proton-pumping rhodopsins.

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Objective: Loss-of-function mutations in the GIRDIN/CCDC88A gene cause developmental epileptic encephalopathy (DEE) in humans. However, its pathogenesis is largely unknown. Global knockout mice of the corresponding orthologous gene (gKOs) have a preweaning lethal phenotype with growth failure, preventing longitudinal analysis.

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