Publications by authors named "Kazuhiko Azuma"

Article Synopsis
  • - Notch signaling is a crucial communication method between cells that influences how they develop and differentiate, relying on receptor-ligand interactions on cell surfaces.
  • - The study finds that overexpression of a protein called TM2D3, similar to a Drosophila protein, activates Notch1 by binding to it and enhancing its presence on the cell surface.
  • - Without TM2D3, Notch1 and Notch2 levels drop on the cell surface, leading to deficiencies in cell signaling and endocytosis in developing Drosophila embryos.
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Introduction: Kawasaki disease (KD) is an acute systemic vasculitis that predominantly afflicts children. KD development is known to be associated with an aberrant immune response and abnormal platelet activation, however its etiology is still largely unknown. Myosin light chain 9 (Myl9) is known to regulate cellular contractility of both non-muscle and smooth muscle cells, and can be released from platelets, whereas any relations of Myl9 expression to KD vasculitis have not been examined.

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The mortality of coronavirus disease 2019 (COVID-19) is strongly correlated with pulmonary vascular pathology accompanied by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection-triggered immune dysregulation and aberrant activation of platelets. We combined histological analyses using field emission scanning electron microscopy with energy-dispersive X-ray spectroscopy analyses of the lungs from autopsy samples and single-cell RNA sequencing of peripheral blood mononuclear cells to investigate the pathogenesis of vasculitis and immunothrombosis in COVID-19. We found that SARS-CoV-2 accumulated in the pulmonary vessels, causing exudative vasculitis accompanied by the emergence of thrombospondin-1-expressing noncanonical monocytes and the formation of myosin light chain 9 (Myl9)-containing microthrombi in the lung of COVID-19 patients with fatal disease.

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Regarding vascularized lymph node transfer (VLNT) for lymphedema, partial blood flow impairment in transferred lymph node (LN) flaps may adversely affect the therapeutic results. We investigated the clinical and histological effects of partial blood flow impairment in LN flaps. In upper extremity lymphedema cases, based on ultrasonographic examination at 2 weeks after VLNT, we compared the treatment results depending on whether the postoperative blood flow in transferred LNs was good (Group G) or poor (Group P).

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Article Synopsis
  • In bronchial asthma patients, changes such as mucous cell metaplasia and fibrosis are detected in lung tissue using specific staining techniques, but current methods for observing these changes under a scanning electron microscope (SEM) are limited.
  • This study introduces a new technique using osmium thin film coating applied via plasma chemical vapor deposition, which enhances the clarity of SEM images for better visualization of these pathological changes.
  • The research also reveals that while Amphiregulin (Areg) influences mucous cell metaplasia in asthma, the associated interstitial fibrosis is independent of Areg, highlighting different mechanisms at play in the disease's progression.
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In addition to the symptoms of aging, the main symptoms in Werner syndrome (WS), a hereditary premature aging disease, include calcification of subcutaneous tissue with solid pain and refractory skin ulcers. However, the mechanism of calcification in WS remains unclear. In this study, the histological analysis of the skin around the ulcer with calcification revealed an accumulation of calcium phosphate in the lymphatic vessels.

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Background: Increased skin and subcutaneous tissue stiffness in patients with early-stage lymphedema has been reported. The purpose of this study was to examine the use of shear wave elastography (SWE) for evaluating lower extremity lymphedema (LEL).

Methods: For 10 lower extremities of normal controls and 72 limbs of patients with gynecological cancer whose lymphatic function was categorized into six stages based on the range of dermal backflow (DBF) observed in indocyanine green (ICG) lymphography, SWE was performed and shear wave velocity (SWV) of the dermis and three layers of subcutaneous tissue at the thigh and calf were recorded.

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It is not always possible to detect nonpalpable small lymph nodes (LNs) surrounded by adipose tissue under the wavelength of visible light. A newly developed near-infrared camera with InGaAs element was able to capture photographs using light at >1000-nm wavelength, at which the difference in absorbance between water and lipids is large. This study investigated the ability to detect nonvisible small LNs using light at 1300-nm wavelength.

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Article Synopsis
  • * In HeLa-S3 cells, knocking down HAS2 led to decreased spontaneous chemokinesis, suggesting that HA production is linked to cell movement, but adding external high molecular weight HA didn't enhance this movement.
  • * The study found that reducing HYAL2 or CD44 also diminished chemokinesis, while low molecular weight HA was able to reverse these effects, indicating a self-regulating mechanism in which HMW-HA contributes to
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Medial-to-intimal migration of SMCs is critical to atherosclerotic plaque formation and remodeling of injured arteries. Considerable amounts of the shed soluble form of the LDL receptor relative LR11 (sLR11) produced by intimal SMCs enhance SMC migration in vitro via upregulation of urokinase-type plasminogen activator receptor (uPAR) expression. Here, we show that circulating sLR11 is a novel marker of carotid intima-media thickness (IMT) and that targeted disruption of the LR11 gene greatly reduces intimal thickening of arteries through attenuation of Ang II-induced migration of SMCs.

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Adhesion molecules can initiate intracellular signaling. Engagement of CD44 either by its natural ligand hyaluronan or a specific antibody on a cell line induced tyrosine phosphorylation and activation of focal adhesion kinase (FAK), which then associated with phosphatidylinositol 3-kinase (PI3K) and activated mitogen-activated protein kinase at its downstream. However, the introduction of dominant negative Rho into the cells inhibited the CD44-stimulated FAK phosphorylation.

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