Publications by authors named "Yudai Kabata"

Article Synopsis
  • Atopic dermatitis (AD) is a chronic skin disease characterized by intense itching, and new treatments like dupilumab have been developed but predicting the right treatment for each patient is challenging.
  • A study involving 110 AD patients aimed to identify factors and biomarkers that could indicate how well patients might respond to dupilumab, using various scales for assessment.
  • Findings showed that higher baseline serum LDH levels and certain comorbidities, like food allergies, were linked to poorer treatment outcomes, suggesting these could help guide treatment decisions for AD patients.
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Article Synopsis
  • * Researchers evaluated objective (Eczema Area and Severity Index - EASI) and subjective (Patient-Oriented Eczema Measure - POEM and pruritis-NRS) symptoms of AD and found strong associations between various biomarkers and these assessments.
  • * Key findings suggest that CCL26/eotaxin-3 and SCCA2 are the most effective biomarkers for measuring AD severity via EASI, while lactate dehydrogenase is best for assessing symptoms on POEM and pruritis-NRS. *
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The Lamc2jeb junctional epidermolysis bullosa (EB) mouse model has been used to demonstrate that significant genetic modification of EB symptoms is possible, identifying as modifiers Col17a1 and six other quantitative trait loci, several with strong candidate genes including dystonin (Dst/Bpag1). Here, CRISPR/Cas9 was used to alter exon 23 in mouse skin specific isoform Dst-e (Ensembl GRCm38 transcript name Dst-213, transcript ID ENSMUST00000183302.5, protein size 2639AA) and validate a proposed arginine/glutamine difference at amino acid p1226 in B6 versus 129 mice as a modifier of EB.

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Article Synopsis
  • Atopic dermatitis (AD) is a common skin disorder causing intense itching, and dupilumab, an anti-IL-4 receptor antibody, has shown significant success in improving symptoms and reducing inflammation associated with this condition.
  • * In a study involving over 130 patients with moderate-to-severe AD, researchers will assess clinical symptoms and measure 18 blood biomarkers to find potential predictors for treatment outcomes with dupilumab.
  • * The main goal is to explore if initial levels of these biomarkers are linked to changes in skin severity scores after 16 weeks of treatment.
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Loss-of-function mutations in dystonin () can cause hereditary sensory and autonomic neuropathy type 6 (HSAN-VI) or epidermolysis bullosa simplex (EBS). Recently, -related diseases were recognized to be more complex than previously thought because a patient exhibited both neurological and skin manifestations, whereas others display only one or the other. A single locus produces at least three major isoforms: (neuronal isoform), (muscular isoform) and (epithelial isoform).

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Recessive dystrophic epidermolysis bullosa (RDEB) is a severe inherited skin disorder caused by mutations in the gene encoding type VII collagen (C7). The spectrum of severity depends on the type of mutation in the gene. C7 is the major constituent of anchoring fibrils (AFs) at the basement membrane zone (BMZ).

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The touch domes of mammalian hairy skin are mechanoreceptors characterized by the accumulation of Merkel cell-neurite complexes at the epidermal base. In this study, we examined the shape, size, and density of the touch dome of human skin of the forearm and the abdomen through scanning electron microscopy (SEM). Human skin samples were obtained from donated bodies, as well as a patient who underwent biopsy.

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