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Severe Fever with Thrombocytopenia Syndrome Initially Diagnosed as Diffuse Large B-cell lymphoma

Medical Science & Innovation Volume 72 Issue 1-2

A 70-year-old woman presented with acute fever, impaired consciousness, leukopenia, thrombocytopenia, and right inguinal lymphadenopathy. A lymph node biopsy was diagnosed as diffuse large B-cell lymphoma (DLBCL). However, her symptoms were consistent with severe fever with thrombocytopenia syndrome (SFTS), and RT-PCR for SFTS virus (SFTSV) RNA was positive. The patient’s condition and lymphadenopathy gradually improved with supportive measures and short-term steroid treatment and no lymphadenopathy recurrence was observed. Lymph node pathological examination revealed SFTSV-infected cells, leading to the final diagnosis of necrotizing lymphadenitis associated with SFTS. Careful consideration is required to differentiate necrotizing lymphadenitis associated with SFTS from that associated with DLBCL.

An invited review following the Soujinkai Award: Human Induced Pluripotent Stem Cell Modeling of the Blood-Brain Barrier Identifies Intrinsic Barrier Dysfunction in Multiple Sclerosis

Medical Science & Innovation Volume 72 Issue 1-2

Blood-brain barrier (BBB) dysfunction found in the multiple sclerosis (MS) cases is generally considered as a consequence of neuroinflammation. In this study we challenge this view by developing and analyzing novel BBB model from MS patients using induced pluripotent stem cells (iPSCs). We differentiated iPSCs into brain microvascular endothelial cell (BMEC)-like cells to establish an in vitro BBB model. We found that BMEC-like cells from MS patients exhibited compromised barrier integrity, characterized by weakened junctions, heightened permeability, and an elevated inflammatory profile when compared to cells from healthy individuals. Notably, the activation of the Wnt/β-catenin signaling pathway led to improvements in barrier function and a reduction in inflammatory responses, indicating potential therapeutic targets for reinforcing BBB stability in MS.

Creators : Nishihara Hideaki Publishers : Yamaguchi University School of Medicine Date Issued : 2025-06

An Invited Review following the Soujinkai Young Investigator Award: Modulating Calmodulin-Ryanodine Receptor Binding as a Strategy to Halt Pressure-Overload Induced Cardiac Hypertrophy

Medical Science & Innovation Volume 72 Issue 1-2

Cardiac hypertrophy is widely recognized as a significant risk factor contributing to adverse outcomes in individuals with cardiovascular conditions. The disruption of intracellular calcium ( Ca^{2+} ) balance has been implicated in the development of cardiac hypertrophy, though the precise mechanisms remain poorly understood. In this research, we explored whether hypertrophy induced by pressure overload may arise from the destabilization of the cardiac ryanodine receptor (RyR2) triggered by the dissociation of calmodulin (CaM), leading to subsequent Ca^{2+} leakage. We also assessed whether genetically strengthening the binding affinity between CaM and RyR2 could potentially reverse this process. In the early phases of cardiac hypertrophy caused by pressure overload—when contractile function is still intact—we observed that RyR2 destabilization mediated by reactive oxygen species (ROS) coincides with impaired relaxation. Moreover, stabilizing RyR2 through enhanced CaM binding was found to completely inhibit hypertrophic signaling and improve survival rates. Our findings reveal a crucial connection between RyR2 destabilization and the progression of cardiac hypertrophy.

Creators : Kohno Michiaki | Kobayashi Shigeki | Yamamoto Takeshi | Yano Masafumi Publishers : Yamaguchi University School of Medicine Date Issued : 2025-06

Appendix 2 Tree species identification of wooden relics at Yosida site in the 2012 fiscal year