A Long-term Survivor after Congenital Acute Myeloid Leukemia with t(8 ; 16)(p11 ; p13)

The treatment of patients with congenital leukemia is difficult and often results in a poor prognosis. We present here the case of a female child with congenital acute myeloid leukemia (AML) with t(8 ; 16) (p11 ; p13) who received chemotherapy and survived for more than 10 years without relapse. A novel MOZ-CBP chimera was found in her diagnostic sample. Although adult AML patients with MOZ-CBP have mainly been reported as having therapy-related AML and showed poor prognoses, the present case supports the idea that AML with MOZ-CBP in the pediatric population might show better prognoses

Dense Molecular Clumps associated with the LMC Supergiant Shells LMC 4 \& LMC 5

We investigate the effects of Supergiant Shells (SGSs) and their interaction on dense molecular clumps by observing the Large Magellanic Cloud (LMC) star forming regions N48 and N49, which are located between two SGSs, LMC 4 and LMC 5. $^{12}$CO ($J$=3-2, 1-0) and $^{13}$CO ($J$=1-0) observations with the ASTE and Mopra telescopes have been carried out towards these regions. A clumpy distribution of dense molecular clumps is revealed with 7 pc spatial resolution. Large velocity gradient analysis shows that the molecular hydrogen densities ($n({\rm H}_2)$) of the clumps are distributed from low to high density ($10^3$-$10^5$ cm$^{-3}$) and their kinetic temperatures ($T_{\rm kin}$) are typically high (greater than $50$ K). These clumps seem to be in the early stages of star formation, as also indicated from the distribution of H$\alpha$, young stellar object candidates, and IR emission. We found that the N48 region is located in the high column density HI envelope at the interface of the two SGSs and the star formation is relatively evolved, whereas the N49 region is associated with LMC 5 alone and the star formation is quiet. The clumps in the N48 region typically show high $n({\rm H}_2)$ and $T_{\rm kin}$, which are as dense and warm as the clumps in LMC massive cluster-forming areas (30 Dor, N159). These results suggest that the large-scale structure of the SGSs, especially the interaction of two SGSs, works efficiently on the formation of dense molecular clumps and stars.Comment: 26 pages, 7 tables, 16 figure

SARS-CoV-2 disrupts respiratory vascular barriers by suppressing Claudin-5 expression

臓器チップ技術を用いて新型コロナウイルスが血管へ侵入するメカニズムを解明 --Claudin-5発現抑制による呼吸器の血管内皮バリア破壊--. 京都大学プレスリリース. 2022-09-22.A study using an organ-on-a-chip reveals a mechanism of SARS-CoV-2 invasion into blood vessels --Disruption of vascular endothelial barrier in respiratory organs by decreasing Claudin-5 expression--. 京都大学プレスリリース. 2022-09-27.In the initial process of coronavirus disease 2019 (COVID-19), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infects respiratory epithelial cells and then transfers to other organs the blood vessels. It is believed that SARS-CoV-2 can pass the vascular wall by altering the endothelial barrier using an unknown mechanism. In this study, we investigated the effect of SARS-CoV-2 on the endothelial barrier using an airway-on-a-chip that mimics respiratory organs and found that SARS-CoV-2 produced from infected epithelial cells disrupts the barrier by decreasing Claudin-5 (CLDN5), a tight junction protein, and disrupting vascular endothelial cadherin–mediated adherens junctions. Consistently, the gene and protein expression levels of CLDN5 in the lungs of a patient with COVID-19 were decreased. CLDN5 overexpression or Fluvastatin treatment rescued the SARS-CoV-2–induced respiratory endothelial barrier disruption. We concluded that the down-regulation of CLDN5 expression is a pivotal mechanism for SARS-CoV-2–induced endothelial barrier disruption in respiratory organs and that inducing CLDN5 expression is a therapeutic strategy against COVID-19