Publications by authors named "I Tanida"

Background: Adipose-derived stem cells (ADSCs) are widely used in the field of regenerative medicine because of their various functions, including anti-inflammatory effects. ADSCs are considered to exert their anti-inflammatory effects by secreting anti-inflammatory cytokines and extracellular vesicles. Although recent studies have reported that metabolites have a variety of physiological activities, whether those secreted by ADSCs have anti-inflammatory properties remains unclear.

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SNCA/PARK1 encodes α-synuclein, which is associated with familial Parkinson's disease. Despite its abundance in presynaptic terminals, the aggregation mechanism of α-synuclein and its relationship with Parkinson's disease have not yet been elucidated. Moreover, the ultrastructures of α-synuclein localization sites in neuronal presynaptic terminals remain unclear.

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Introduction: Administration of adipose-derived stem cells (ADSCs) into the joint cavity has been shown to alleviate the symptoms of knee osteoarthritis (OA) by releasing exosomes and anti-inflammatory cytokines. However, the therapeutic effect of these cells is limited by their rapid disappearance after administration. Thus, it is necessary to prolong cell survival in the joint cavity.

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Article Synopsis
  • Pneumolysin (Ply) is a critical protein for the infection process of pneumococci, but its effectiveness can also harm bacterial survival by causing excessive disruptions in host cells.
  • A novel assay using NanoBiT-Nanobody was developed to measure the endosomal disruption effects of Ply, revealing that the pneumococcal sialidase NanA regulates Ply activity by modifying cell membrane sugars.
  • Also, the sialidase inhibitor oseltamivir amplifies Ply's destructive effects in vitro and increases tissue damage and bacterial clearance in vivo, suggesting new treatment approaches for severe pneumococcal infections that leverage Ply’s dual role.
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Neuronal ceroid lipofuscinosis is a group of pediatric neurodegenerative diseases. One of their causative genes, CLN10/CtsD, encodes cathepsin D, a major lysosomal protease. Central nervous system (CNS)-specific CtsD-deficient mice exhibit a neurodegenerative disease phenotype with accumulation of ceroid lipofuscins, granular osmiophilic deposits, and SQSTM1/p62.

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