A selection of Blood research highlights from July 30, 2020.

Platelet-VWF prevents plasma leakage when it penetrates by stimulating Tie-2 to endalyssgets with white blood cells https://doi.org/10.1182/blood.2019003442 neutrophone ooztomy requires opening the endothelial barrier of blood vessels, but does not automatically cause plasma to leak.
shrinking actin filaments surround the outer seepage of blood cells, keeping the opening tightly enclosed around the migrating neutrophils, thus preventing plasma leakage.
recently, researchers have discovered a receptor system that is responsible for preventing plasma leakage.
through fluorescent microspheres, the researchers found that The Tie-2 of silent or inactivated endothelial cells can lead to microvesine seepage at the epiliac area of neutrophils after capillaries.
plasma leakage depends on the outer osteocyte oozing, because plasma leakage does not exist when neutrophils are depleted.
, the researchers also found that the Cdc42 GTPase exchange factor FGD5 is a downstream target for Tie-2 and plays a key role in preventing plasma leakage from the plasma leakage process of the neutrophil seisphon, which is essential for preventing leakage caused by neutrophils.
blocking angiogenic hemophilia factor (VWF) can lead to blood vessel stoice leakage during white blood cell migration, indicating that the interaction between platelets and endothelial VWF activates Tie-2 by secreting angiogenesis-1, thereby preventing plasma leakage induced by osteophile.
a new method for predicting the survival rate of allo-HCT in sickle cell patients at https://doi.org/10.1182/blood.2020005687 Researchers recently developed a risk score to predict the event-free survival rate (EFS;
the study population (n-1425) was randomly divided into training groups (n-1070) and validation groups (n-355).
of the nine risk factors assessed, two biological risk factors had a predictive effect on EFS: the age at the time of transplantation and the type of donor.
the training queue, if the patient is 12 years old and the donor is a brother and sister with HLA match, the patient has the lowest risk, with a 3-year survival rate of 92%, and a risk score of 0.
siblings with HLA-matched age of 13 years were donors, and non-relative donors with HLA matches were at medium risk (score s 1; 3 years EFS s 87%).
other groups, including patients of any age, relatives with monoploids or non-relative donors with A mismatch edimajority, and non-kinship donors with HLA matching age of 13 years and HLA matching were all at high risk (score: 2 or 3; 57 percent of 3 years EFS).
3. Targeting bone marrow niches can save the function of hematopoietic stem cells impaired by beta-thalassemia at https://doi.org/10.1182/blood.2019002721 hematopoionstemostemogene stem cells (HSCs) are regulated by bone marrow (BM) wall signals and regulate blood cell production in stable conditions and in blood diseases.
researchers studying mouse models of beta-thalassemia found that secondary changes in primary hemoglobin defects had potential effects on HSC-niche cross-linking.
HSC's self-renewal defects were repaired after transplanting to a normal microenvironment, thus proving the positive effects of BM matrix.
consistent with common findings in patients with osteoporosis, the researchers found that bone deposition decreased as levels of parathyroid initavirus (PTH) decreased;
in the body, activating the PTH signal through reconstructed Jagged1 and bone bridge protein levels is associated with saving the functional pool of th3 HSCs by correcting HSC-niche crosslinking.
confirmed a decrease in the resting state of HSC in patients with thalassemia, accompanied by a change in the properties of BM matrix niches.
The study on the correlation between the rare variant of STAB2 and VTE https://doi.org/10.1182/blood.2019004161 deep vein thrombosis and pulmonary embolism, collectively known as venous thromboembolism (VTE), is the third leading cause of cardiovascular death in the United States.
Genome-wide Association Study (GWAS) has identified common genetic variants that contribute to increased risk of venous thromboembolism in varying degrees. Rare mutations in the
anticoagulant genes PROC, PROS1, and SERP INC1 lead to fatal thrombosis during the perinatal period of pure heron, and significantly increase the Risk of VTE of heterogeneics.
To identify new rare VTE risk variants, the researchers performed an exon sequencing analysis of 393 patients with causeless VTE.
researchers identified four new VTE risk genes, proS1, STAB2, PROC and SERP INC1.
, such as STAB2, 7.8 percent of VTE patients carry a rare mutation in the gene, while only 2.4 percent of individuals in the control carried the gene's rare mutation.
in cell culture, cell surface expression levels of STAB2 carrying VTE-related variants decreased compared to control STAB2. The common variations in
STAB2 were associated with plasma angiogiomophilia factors and coagulation factor VIII levels in GWAS, suggesting that insufficient single dose of stabilin-2 may increase the risk of VTE through elevated levels of these coagulants.
, the researchers found in an independent queue that individuals carrying a rare variant of STAB2 had higher levels of vascular hemophilia factor and equivalent pre-peptide levels than the control group. the relationship between the energy metabolism and dryness of hematopoietic stem cells (HSCs) at different stages of development is largely unclear at the
. MDH1 and the active maintenance of fetal liver HSC https://doi.org/10.1182/blood.2019003940.
researchers recently established a genetically modified mouse lineage with the genetically coded NADH/NAD-plus sensor (SoNar) and demonstrated the presence of three different fetal liver hematopoietic cell groups based on SoNar fluorescence ratios.
the mitochondrial breathing levels of low-lying soNar cells increased, but the levels of glycolyses were similar to those of cells with high SoNar.
interesting, 10% of low SoNar cells contain 65% of immune phenopharycin hematopoietic stem cells (FL-HSCs) and contain about five times as many functional HSCs as high SoNar cells.
SoNar can sensitively monitor changes in the dynamics of energy metabolism of HSCs in vivo and outside the body.
mechanism, STAT3 transactivation MDH1 to maintain the malic acid-tine NADH shuttle activity and HSC self-renewal and differentiation.
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