Publications by authors named "Kayoko Komatsu"
Non-vascularized pigment epithelial detachments (PED) are usually associated with dry age-related macular degeneration (AMD). In this study, we aimed to investigate the correlation between visual function and morphologic parameters. Seventeen eyes of eleven patients with non-vascularized AMD were enrolled.
View Article and Find Full Text PDFPurpose: To investigate the three-dimensional distribution and associating demographic factors of depolarization, using polarization-sensitive optical coherence tomography (PS-OCT), to evaluate melanin pigmentation in the retinal pigment epithelium (RPE) and choroid in healthy eyes.
Methods: In total, 39 unaffected healthy eyes of 39 subjects were examined using a PS-OCT clinical prototype. The degree of depolarization, expressed as the polarimetric entropy, was assessed in the RPE, the superficial and the total choroid layer, especially in the center, the inner, or the outer areas centered at the fovea.
Purpose: To evaluate cases with a retinal pigment epithelium (RPE) aperture using polarization-sensitive optical coherence tomography (PS-OCT).
Study Design: Retrospective consecutive case series.
Methods: A retrospective study that included three eyes (three patients) with RPE aperture and age-related macular degeneration (AMD) evaluated at the Macular Clinic in Tokyo University Hospital.
Article Synopsis
- The study focused on the cardiotoxic effects of combretastatin A4 disodium phosphate (CA4DP), a microtubule-disassembling agent, administered to rats.
- After a single dose, significant increases in blood biomarkers indicating cardiac injury were observed at 0.5, 24, and 72 hours post-administration, along with histopathological evidence of myocardial damage.
- The findings suggest that the rat model effectively mimics human cardiotoxicity from MDAs, highlighting the importance of this research in understanding potential heart-related side effects in cancer treatments.
The microtubule inhibitor colchicine is cardiotoxic and is suggested to impair impulse formation and conduction. However, little is known about the electrocardiographic (ECG) changes induced by colchicine in experimental animals and the detailed pathogenesis of its cardiotoxicity. Therefore, we analyzed cardiotoxicity in colchicine-treated rats using electrocardiographic, histopathological and blood-chemistry approaches.
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