Publications by authors named "Jun Kanamune"

Article Synopsis
  • - The emergence of the Omicron subvariant BA.5 of SARS-CoV-2 requires urgent investigation due to its rapid spread and the need for ongoing control measures.
  • - BA.5 exhibits enhanced fusogenicity and a greater ability to disrupt respiratory barriers compared to earlier subvariants BA.1 and BA.2, even though its in vitro growth rates are similar.
  • - In a hamster model, BA.5 shows slightly higher pathogenicity than other Omicron variants but less than the ancestral strain, along with improved virus spread and immune response activation.
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Article Synopsis
  • The emergence of various subvariants of the SARS-CoV-2 Omicron BA.2, such as BA.2.9.1, BA.2.11, BA.2.12.1, BA.4, and BA.5, shows that they have higher effective reproduction numbers compared to the original BA.2 strain.
  • Neutralization experiments indicate that immunity from previous BA.1/2 infections is less effective against the newer BA.4/5 subvariants, which also replicate more efficiently and exhibit greater cell fusion than BA.2.
  • Research using hamsters and structural analysis of the BA.4/5 spike protein suggests that these subvariants are more pathogenic and pose a greater risk to global health
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Recent studies have profiled the innate immune signatures in patients infected with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and suggest that cellular responses to viral challenge may affect disease severity. Yet the molecular events that underlie cellular recognition and response to SARS-CoV-2 infection remain to be elucidated. Here, we find that SARS-CoV-2 replication induces a delayed interferon (IFN) response in lung epithelial cells.

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Beta cell replacement by islet transplantation is a promising clinical therapy for patients with type 1 diabetes because it satisfies safety issues and offers reliability in controlling blood glucose levels. One remaining problem is that it requires islets from two to three donor pancreases to achieve insulin independence, thus aggravating the donor shortage. Islet regeneration in vivo and generation of beta cells ex vivo followed by transplantation represent attractive therapeutic methods to restore the beta cell mass.

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Since donor T-cells' allorecognition of host antigens is a prerequisite for the onset of graft-versus-host disease (GVHD), blocking their cellular signaling pathways can decrease the severity of GVHD. We hypothesized that epigallocatechin-3-gallate (EGCG), due to its strong affinity to macromolecules, would adhere to surface molecules of donor T cells, inhibit their allorecognition, and attenuate GVHD in the recipient. We tested the hypothesis by treating donor splenocytes with EGCG in both in vitro and in vivo murine GVHD models.

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We investigated the hibernation effect of epigallocatechin-3-O-gallate (EGCG) on neonatal human tarsal fibroblasts (nHTFs) by analyzing the expression of cell cycle-related genes. EGCG application to culture media moderately inhibited the growth of nHTFs, and the removal of EGCG from culture media led to complete recovery of cell growth. EGCG resulted in a slight decrease in the cell population of the S and G(2)/M phases of cell cycle with concomitant increase in that of the G(0)/G(1) phase, but this cell cycle profile was restored to the initial level after EGCG removal.

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