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A Multicenter Prospective Observational Study of the Efficacy and Safety of Rehabilitation for Pediatric Blood Cancer Patients - Pediatric Blood Cancer Rehabilitation Multicenter Study

开始日期2023-09-27

申办/合作机构

Shiga University of Medical Science

JPRN-UMIN000049604

/ RecruitingN/AIIT

Intervention study on the effectiveness of a new nipple care cream focusing on aloe ingredients. - Intervention study on the effectiveness of a new nipple care cream focusing on aloe ingredients.

开始日期2023-08-01

申办/合作机构

Shiga University of Medical Science

JPRN-UMIN000051872

/ RecruitingN/AIIT

Measurement of Nardilysin concentration in synovial fluid - Measurement of Nardilysin concentration in synovial fluid

开始日期2023-07-14

申办/合作机构

Shiga University of Medical Science

100 项与 Shiga University of Medical Science 相关的临床结果

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0 项与 Shiga University of Medical Science 相关的专利（医药）

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13,640

项与 Shiga University of Medical Science 相关的文献（医药）

2025-06-01·Acta Histochemica

The significance of Itga8 and Vangl2 in kidney development: Insights from yotari mice

Article

作者: Katsuyama, Yu ; Filipović, Natalija ; Gelemanović, Andrea ; Vukojević, Katarina ; Kelam, Nela ; Bajt, Patricija ; Racetin, Anita ; Pavlović, Nikola

The permanent kidney develops from the metanephros through the interaction of the ureteric bud (UB) and metanephric mesenchyme (MM). Congenital anomalies of the kidney and urinary tract (CAKUT) are common prenatal diagnoses, and genetic factors play a critical role in their development. This study explores the involvement of Integrin alpha-8 (Itga8) and Van Gogh-like 2 (Vangl2) proteins in kidney development, using the yotari (yot) mouse model, which harbors a mutation in the Dab1 gene, disrupting Reelin signaling. Immunofluorescence was employed to analyze the spatiotemporal expression patterns of these proteins in embryonic and postnatal kidney samples. Our results show that Itga8 and Vangl2 expression is significantly higher in the embryonic kidneys of yot mice than those of wt mice. However, the two groups observed no significant differences in the temporal expression of these proteins in postnatal kidneys. Spatially, Itga8 was most strongly expressed in the metanephric mesenchyme and renal vesicles/immature glomeruli. At the same time, Vangl2 showed the highest expression in the metanephric mesenchyme, renal vesicles/immature glomeruli, and collecting ducts in yot mice. Our findings suggest that the Dab1 mutation disrupts the expression of Itga8 and Vangl2, contributing to kidney developmental defects associated with CAKUT phenotypesThis increased expression suggests a disruption in the normal regulation of these proteins, likely due to the Dab1 mutation, which impairs Reelin signaling. Still, the exact mechanism through which the Reelin/Dab1 pathway influences the expression of examined markers remains to be elucidated. These results offer valuable insights into the factors associated with kidney malformations and suggest potential therapeutic targets for CAKUT abnormalities.

2025-06-01·Molecular Therapy Nucleic Acids

Correcting tau isoform ratios with a long-acting antisense oligonucleotide alleviates 4R-tauopathy phenotypes

Article

作者: Watanabe, Hirohisa ; Sahashi, Kentaro ; Watanabe, Eri ; Mohammad, Moniruzzaman ; Ishigaki, Shinsuke ; Kanamitsu, Kayoko ; Okada, Yohei ; Hirai, Shinobu ; Ishibashi, Minaka ; Iwade, Nobuyuki ; Neya, Masahiro ; Katsuno, Masahisa ; Okado, Haruo ; Tuerde, Dilina ; Sobue, Gen ; Aldoghachi, Asraa Faris ; Fujiwara, Tsuyoshi ; Fujioka, Yusuke ; Kawai, Kaori ; Iwata-Endo, Kuniyuki

Tau, a microtubule-binding protein linked to tauopathies like Alzheimer's disease and frontotemporal lobar degeneration (FTLD), has 3-repeat (3R) and 4-repeat (4R) isoforms. Accumulation of the 4R-tau is associated with FTLD, progressive supranuclear palsy (PSP), and cortico-basal degeneration (CBD). We previously showed that a loss of fused in sarcoma (FUS) or splicing factor, proline- and glutamine-rich (SFPQ) promoted 4R-tau accumulation, which induced FTLD-like behaviors and neurodegeneration in mice. Here, we developed antisense oligonucleotides (ASOs) modified with 2'-O, 4'-C-ethylene-bridged nucleic acids (ENAs), reducing the 4R-tau/3R-tau ratio while maintaining total tau expression from the MAPT gene. In vitro screening identified EN-06 as the most effective ENA. Intracerebroventricular (ICV) administration of EN-06 corrected the 4R/3R-tau ratio in FUS-silenced humanized tau mice and human iPSC-derived neurons. This treatment ameliorated disease phenotypes, including aberrant behaviors, spine dysmorphology, and neurodegeneration. The half-life of EN-06 after a single ICV administration was approximately 6 months in the brain, with splicing correction effects that persisted for 2 years. The efficacy of EN-06 was higher than that of 2'-O-methoxyethyl (MOE)-modified ASO (MO-06). These findings highlight the potential of ENA-modified ASOs to reduce 4R-tau while preserving total MAPT expression, thus offering a safe and long-acting treatment for 4R-tau-associated tauopathies.

2025-05-01·Redox Biology

ROS-dependent SOCS3 upregulation disrupts regulatory T cell stability during autoimmune disease development

Article

作者: Satooka, Hiroki ; Nakamura, Yuzuki ; Hirata, Takako

Autoimmune diseases including rheumatoid arthritis (RA) are often associated with high levels of reactive oxygen species (ROS); however, the ROS targets in autoimmunity are diverse and unclear. Using collagen-induced arthritis (CIA) mice as a model for RA, we report that antioxidants markedly suppress joint inflammation, antibody production, and effector T cell responses. We found that the frequency of CD4⁺ regulatory T cells (Tregs) was reduced in CIA mice, which was reversed by antioxidant treatment, and SOCS3, known to be associated with Treg instability, was upregulated in Tregs from both RA patients and CIA mice. Mechanistically, SOCS3 upregulation was induced by ROS-dependent PTEN oxidation and the resultant Akt/mTOR/STAT3 activation. We further showed that the source of ROS involved in this pathway is NADPH oxidase 2 (Nox2). Nox2 expression was upregulated in Tregs from CIA mice, and Nox2 transduction induced a decrease in Treg frequency that depended on SOCS3 upregulation. This study thus provides a mechanistic understanding of ROS-induced Treg instability and suggests that ROS-dependent disruption of Treg homeostasis underlies the development and progression of autoimmune diseases.

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