Review: Selected by Blood Research on July 9, 2020

!----Three aspirin treatments in the optimization of icharacteristic platelet hyperplasia patients with antiplatelet treatment comparison https://doi.org/10.1182/blood.2019004596 ispecial-hairplatelet hypertrophy (ET) is characterized by abnormal nucleocell production and increased risk of thrombosisdaily (od) small-dose aspirin is the recommended antithrombotic treatment, but platelet production acceleration may shorten the time of platelet cyclooxidation (COX)-1 inhibitionrecently, researchers compared the efficacy of three aspirin treatment sexist treatments to optimize platelet COX-1 inhibition while retaining COX-2-dependent vascular anticoagulant function245 patients with long-term od low-dose aspirin were randomly given 100 mg aspirin, od, 2 times a day (bid) or 3 times a day (tid) for 2 consecutive weeksthe main alternative endpoint sezer serothrombotin B2 (sTXB2) (effective biomarker of platelet COX-1 activity) and urethra cyclin metabolites (PGIM) was determined in randomized groupings and after 2 weeksstudies found that patients with bid and tid treatment regimens had significantly lower individual variability, and the median of sTXB2 was lower, with od group (n-85), bid group (n-79) and tid group (n-79) sTXB2 being 19.3, 4 and 2.5 ng/ml, respectivelyurine levels were comparable in three groups of patientstapriors in both groups significantly reduced TXM in their urine by 35%the tid group had a higher score of abdominal discomfort2Aging-induced IL27Ra signals can damage hematopoietic stem cells https://doi.org/10.1182/blood.201903910 hematopoiatestema stem cell (HSC) aging is associated with bone marrow growth-related diseases and an increased risk of immune agingrecent researchers found that the inflammatory response associated with aging can promote the aging process of HSC through the TNF alpha/ETS1/IL27Ra signaling pathwayin the aging process, the expression level of TNf alpha, a well-known inflammatory biomarker, increased and the expression of IL27Ra in HSC was induced through the ERK/ETS1 signaling pathwayknockout of il27Ra can save HSC functional decline and bone marrow differentiation bias, and reverse the inhibition of TNf alpha on HSCthe proportion of myelin differentiation bias HSC decreased in older mice that il27Ra had been struck, but there was no change in wild micecompared to IL27Ra-HSC, IL27Ra-HSC has impaired reconstruction capacity and bone marrow differentiation bias, and can be used as a myelin recovery bank after inflammation damage , inflammatory-related genes are enriched in IL27Ra-HSC, and their expression levels increase with age 3 Integrated protein alpha 6 and acute B lymphoblastic leukemia resistance https://doi.org/10.1182/blood.2019001417 previous studies have found that the fusion protein alpha6 is associated with small residual lesions in ALL and ALL cells migrate to the central nervous system but no studies have been studied to assess it in the context of chemotherapy resistance recently found that the anti-human alpha 6 blocking antibody P5G10 can induce in vitro primary ALL cell apoptosis, and can make primary ALL cells in vivo and outside the body sensitive to chemotherapy or tyrosine kinase inhibition analyzed the potential mechanism of alpha6-associated apoptosis by conditional knockout of the alpha 6 of BCR-ABL1-B-ALL cells in mice, and found that alpha6-ischemic ALL cells had apoptosis knocking out alpha6 in the body, plus tyrosine kinase inhibitors (TKI) therapy are more effective at removing ALL cells than using TKI (Niletini) treatment alone proteomics analysis showed that the loss of alpha 6 in all cells in mice was associated with changes in Src signals, including phosphorylation of Lyn (pTyr507) and Fyn (pTyr530) 4 Atypical 3q26/MECOM Rearrangement of Acute Myeloid Leukemia is comparable to inv (3)/t (3) https://doi.org/10.1182/blood.201 Acute myeloid leukemia (AML) that carries inv (3)/t (3;3) (q21q26) is recognized by WHO as a unique subtype characterized by invasive sexually transmitted diseases and poor prognosis in this AML subtype, GATA2 enhancer (3q21) translocation to MECOM (3q26), resulting in the meCOM subtype EVI1 overexpression, and GATA2 another unaffected allele gene is single alleling gene expression Because of the 3q26 rearrangement, MECOM full-length transcription, MDS1-EVI1 expression is blocked many other 3q26/ MECOM rearrangements associated with poor treatment response were reported in Patients with AML, in addition to the classic inv (3)/t(3;3) recent lying, researchers found that meCOM participated in EVI1 overexpression in 33 atypical 3q26 rearrangement cases, but no MDS1-EVI1 expression was detected in addition, these AML patients' 3q26 translocations typically involve super-enhancers of genes active in myelin development (e.g CD164, PROM1, CDK6, or MYC) in more than 50% of cases, alleles specific GATA2 expression was observed, due to an imbalance in alleles lost or unexplained by the number of copies Source: MedSci Original 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