Myeloid/natural killer cell precursor acute leukemia (MNKPL) is a rare leukemia subtype characterized by a high incidence of extramedullary infiltration. No appropriate treatment strategy has so far been developed. Acute myelogenous leukemia-type chemotherapy combined with L-Asparaginase is an effective treatment for MNKPL. Hematopoietic cell transplantation is a second option in refractory cases.

https://www.onlinelibrary.wiley.com/doi/pdf/10.1002/ccr3.1506

Hematopoietic cell transplantation for myeloid/NK cell precursor acute leukemia in second remission.

Objective To identify whether histologically confirmed chorioamnionitis (hCAM) is associated with development of retinopathy of prematurity (ROP). Study design We retrospectively analyzed two different cohorts. Cohort 1 was the national database of newborns in Japan born at ≤1500g or <32 weeks' gestation (January 2003 through April 2021, n=38,013). Cohort 2 was babies born at <1500g from a single institution in Tsuchiura, Japan, (April 2015 through March 2018, n=118). Results For Cohort1, after adjusting for potential confounders, stage III CAM (n=5,554) was associated with lower odds of severe ROP (stage ≥3 or required peripheral retinal ablation) by 14% (odds ratio [OR]: 0.86; 95% confidence interval [CI]: 0.78–0.94]. CAM of stage I (n=3,277) and II (N=4,319) was not associated with the risk of ROP. For Cohort 2, the odds of severe ROP were significantly reduced in moderate to severe hCAM groups (stage II, OR: 0.06, 95% CI: 0.05–0.82; stage III, OR: 0.10, 95% CI: 0.01-0.84). Neonates with funisitis, comorbidity of hCAM, and a finding of fetal inflammatory response had lower odds of severe ROP (OR: 0.11; 95% CI: 0.01–0.93). Conclusions After adjusting for confounders, severe hCAM with fetal inflammatory response was associated with reduced risk of ROP. 

Stage III Chorioamnionitis Is Associated with Reduced Risk of Severe Retinopathy of Prematurity.

Effectiveness of venetoclax and azacytidine against myeloid/natural killer cell precursor acute leukemia

A 21-year-old man was diagnosed with myeloid/natural killer precursor leukemia (MNKPL) with bone marrow infiltration of blasts of cyCD3 

Successful Cord Blood Transplantation for Myeloid/Natural Killer Precursor Acute Leukemia: A Case Report and Literature Review



Hypoxia-inducible factor-1 alpha (HIF-1α) is a transcription factor that plays a crucial role in cellular responses to hypoxia, such as in the development of intimal hyperplasia, a common complication in arteriovenous fistula (AVF) creation. While the application of umbilical cord mesenchymal stem cells (UC-MSCs) has shown promise in various regenerative medicine applications, including tissue repair and angiogenesis, the effect of UC-MSCs on HIF-1α level in the AVF has not been tested. Therefore, the aim of this study was to evaluate the effect of UC-MSCs administration on HIF-1α levels in the AVF animal model. An experimental study was conducted on 28 local male rabbits (Lepus domestica) using a post-test-only design. The rabbits were divided randomly into four groups: normal rabbit group (negative control), placebo-treated AVF rabbit group (positive control), AVF rabbits treated with in-situ UC-MSCs injection (one dose, 106 UC-MSCs/kg body weight), and AVF rabbits treated with intravenous UC-MSCs (one dose, 106 UC-MSCs/kg body weight (BW). HIF-1α level was measured using ELISA method after 28 days post- treatment. All data were analyzed using the one-way analysis of variance (ANOVA) and continued with the Duncan’s post-hoc test. The data indicated that the levels of HIF-1α were different among all four groups (p<0.001). The post-hoc analysis revealed that the HIF-1α levels in both UC-MSC treated groups were significantly lower compared to untreated AVF rabbits(p<0.05). This study suggests that UC-MSCs could be a promising therapy to prevent and reduce intimal hyperplasia in AVF. 



pdf/effect-of-umbilical-cord-mesenchymal-stem-cells-on-hypoxia-3zwxjs4tdn.pdf

Effect of umbilical cord mesenchymal stem cells on hypoxia-inducible factor-1 alpha (HIF-1α) production in arteriovenous fistula (AVF) animal model: A preliminary study

Although chorioamnionitis (CAM) has been demonstrated to be associated with numerous short- and long-term morbidities, the precise mechanisms remain unclear. One of the reasons for this is the lack of appropriate models for analyzing the relationship between the fetal environment and chorioamnionitis and fetal programming in humans. In this study, we aimed to clarify the fetal programming caused by CAM using the gene expression profiles of UCMSCs. From nine preterm neonates with CAM (n = 4) or without CAM (n = 5), we established UCMSCs. The gene expression profiles obtained by RNA-seq analysis revealed distinctive changes in the CAM group USMSCs. The UCMSCs in the CAM group had a myofibroblast-like phenotype with significantly increased expression levels of myofibroblast-related genes, including α-smooth muscle actin (p < 0.05). In the pathway analysis, the genes involved in DNA replication and G1 to S cell cycle control were remarkably decreased, suggesting that cellular proliferation was impaired, as confirmed by the cellular proliferation assay (p < 0.01-0.05). Pathway analysis revealed that genes related to white fat cell differentiation were significantly increased. Our results could explain the long-term outcomes of patients who were exposed to CAM and revealed that UCMSCs could be an in vitro model of fetal programming affected by CAM. 

https://www.nature.com/articles/s41598-022-10258-0.pdf

Transcriptome analysis of umbilical cord mesenchymal stem cells revealed fetal programming due to chorioamnionitis

Pediatrics InternationalVolume 64, Issue 1 e15027 Clinical Notes A suspected case of heterotopic glia in an MM-twin discordant for anencephaly Yusuke Noguchi, Yusuke Noguchi orcid.org/0000-0003-0633-4573 Department of Pediatrics, Tokyo Medical and Dental University Hospital, Tokyo, JapanSearch for more papers by this authorTsunanori Shidei, Tsunanori Shidei Department of Pediatrics, Tokyo Medical and Dental University Hospital, Tokyo, JapanSearch for more papers by this authorChikako Morioka, Corresponding Author Chikako Morioka cmorped@tmd.ac.jp Department of Pediatrics, Tokyo Medical and Dental University Hospital, Tokyo, Japan Correspondence: Chikako Morioka, MD PhD, Department of Pediatrics, Tokyo Medical and Dental University Hospital, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan. Email: cmorped@tmd.ac.jpSearch for more papers by this authorKenichi Kashimada, Kenichi Kashimada orcid.org/0000-0003-2505-5932 Department of Pediatrics, Tokyo Medical and Dental University Hospital, Tokyo, JapanSearch for more papers by this authorTomohiro Morio, Tomohiro Morio Department of Pediatrics, Tokyo Medical and Dental University Hospital, Tokyo, JapanSearch for more papers by this author Yusuke Noguchi, Yusuke Noguchi orcid.org/0000-0003-0633-4573 Department of Pediatrics, Tokyo Medical and Dental University Hospital, Tokyo, JapanSearch for more papers by this authorTsunanori Shidei, Tsunanori Shidei Department of Pediatrics, Tokyo Medical and Dental University Hospital, Tokyo, JapanSearch for more papers by this authorChikako Morioka, Corresponding Author Chikako Morioka cmorped@tmd.ac.jp Department of Pediatrics, Tokyo Medical and Dental University Hospital, Tokyo, Japan Correspondence: Chikako Morioka, MD PhD, Department of Pediatrics, Tokyo Medical and Dental University Hospital, 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan. Email: cmorped@tmd.ac.jpSearch for more papers by this authorKenichi Kashimada, Kenichi Kashimada orcid.org/0000-0003-2505-5932 Department of Pediatrics, Tokyo Medical and Dental University Hospital, Tokyo, JapanSearch for more papers by this authorTomohiro Morio, Tomohiro Morio Department of Pediatrics, Tokyo Medical and Dental University Hospital, Tokyo, JapanSearch for more papers by this author First published: 08 April 2022 https://doi.org/10.1111/ped.15027Read the full textAboutPDF ToolsRequest permissionExport citationAdd to favoritesTrack citation ShareShare Give accessShare full text accessShare full-text accessPlease review our Terms and Conditions of Use and check box below to share full-text version of article.I have read and accept the Wiley Online Library Terms and Conditions of UseShareable LinkUse the link below to share a full-text version of this article with your friends and colleagues. Learn more.Copy URL Share a linkShare onFacebookTwitterLinked InRedditWechat No abstract is available for this article. Volume64, Issue1January/December 2022e15027 RelatedInformation 

A suspected case of heterotopic glia in an MM-twin discordant for anencephaly.

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Yusuke Noguchi

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Papers

Hematopoietic cell transplantation for myeloid/NK cell precursor acute leukemia in second remission.

Transcriptome analysis of umbilical cord mesenchymal stem cells revealed fetal programming due to chorioamnionitis

A suspected case of heterotopic glia in an MM-twin discordant for anencephaly.