A selection of Blod research on September 17, 2020.

The study of the mechanism by which malaria parasites develop in human red blood cells and affect the production of host red blood cells https://doi.org/10.1182/blood.2019004746 The malaria parasite has two hosts, which are found in liver cells and red blood cells in the human body, and are used for cleavage proliferation (schizogony).
in red blood cells, in addition to the proliferation of cleavage, the division of the proliferatives to form a liturgy, began the initial development of sexual reproduction.
in mosquitoes, complete the gametogony, and then spore proliferation (sporogony).
plasmodium falciparum ligation cells are the sexual stage that causes the spread of plasmodium falciparum from humans to mosquitoes and are the main goal in the elimination of malaria.
immature matchocytes develop in the human bone marrow tissue and gather around the red blood cell-producing island.
, however, the interaction between ligation cells and hematocytes has not been studied.
Recently, researchers found that late-stage erythocytes are new host cells in the plasmodium falciparum phase, and that ligation cells can fully develop (both in and out of the body) in these nucleocytes, leading to infectious mature lithosomes in meshed red blood cells.
surprising, extracellular vesicular vesicle infections derived from ligation cells and parasites can slow the differentiation of the red line, allowing the mater to mature at the same time as its host cells are released from the bone marrow.
. Effects of arginine therapy on mitochondrial function during vascular ocular aches and pain in children with sickle cell disease https://doi.org/10.1182/blood.2019003672 sickle cell disease (SCD) have changed, in part due to low biodetilization of nitric oxide (NO).
is the substrate that produces NO and becomes severely lacking in SCD patients with vascular reforestation pain events (VOEs).
To determine whether arginine improved mitochondrial function, the researchers randomly divided 12 children with SCD who were hospitalized with VOE (age 13.6 to 3 years old, 67% male, 75% HbSS) into 3 groups (4 people in each group) to receive different doses of arginine treatment: 1) 100 mg/kg intravenous drip, 3 times/day; 2) load dose 200 mg/kg, then 100 mg/kg, 3 times/day; 3) load dose 200 mg/kg, then continuous infusion 300 mg/kg/day until discharge.
results showed that the activity of compound V was significantly reduced in all VOE children compared to the stable queue.
, the activity of complex V increased significantly when discharged from the hospital in subjects treated with three arginine doses;
although the activity of plateplate complex IV and citric acid synthase in children with VOE was similar to that in stable condition, the activity of enzymes increased significantly in children with VOE after the treatment of arginine load dose.
addition, arginine therapy reduced the protein niobium levels of all children, indicating a reduction in oxidative stress.
genomics and functional genetic analysis of the subsysmsters of cellular lymphoma https://doi.org/10.1182/blood.2020005289 Cell lymphoma (MCL) is a mature B-cell tumor, initially driven by CND1 rearm, with two molecular subsypes, conventional (cMCL) and non-lymph node leukemia (nnMCL), which have different clinical biological behaviors.
To determine the genetic/exogenous genetic changes that determine this diversity, the researchers analyzed 82 MCL samples (74% cMCL, 26% nnMCL) using genome-wide sequencing (61 cases) and exon sequencing (21 cases) combined with transcription groups and DNA methylation spectrometry.
analysis found that open and active chromatin at the main contigation cluster gene base may promote t(11; 14) (q13; 32), thus modifying the 3D structure of the region in question.
this sub-type is mainly obtained in two MCL subsypes of RAJ-mediated pregenuity B cells, and 8% of the cases occur in AID-mediated mature B cells.
researchers identified new relapsed MCL-driven genes, including CDKN1B, SAMHD1, BCOR, SYNE1, HNRNPH1, SMARCB1, and DAZAP1.
mechanism associated with structural changes in complexes as MCLs targeting key driver genes.
fault fusion bridge circulation and sublocation activation cancer genes (BMI1, MIR17HG, TERT, MYC, and MYCN) to produce gene amplification and reconstruction of regulatory regions.
cMCL carries significantly more structural variation, copy number variation, and drive gene changes than nnMCL, but cMCL does not have ATM variation, and TP53 and TRT variants are rich in nnMCL.
drive genes have an effect on prognostics, but only TP53 and MYC distortions can increase prognostic significance independently of genetic complexity.
4: The treatment of titration glutides for acute graft anti-host disease https://doi.org/10.1182/blood.2020005957 Acute graft anti-host disease (GVHD) is a life-threatening complication after allo-HCT transplantation of allo-HCT.
current GVHD treatment is primarily targeted at the immune system of the provider, and researchers recently explored a way to protect and regenerate Paneth cells (PCs) and intestinal stem cells (ISCs).
researchers observed that acute GVHD reduced intestinal GLP-2 levels in mice and GVHD patients.
In multiple mouse models, the use of GLP-2 agonists, teduglutide, was used to reduce the occurrence of acute GVHD and steroid refraortic GVHD in new hairstyles without affecting the role of grafts in anti-leukemia (GVL).
mechanism, GLP-2 substitution promotes pc and ISC regeneration, thereby enhancing the production of antimicrobial peptides and causing changes in the microbiome.
GLP-2 to expand intestinal organs and reduce the expression of apoptosis-related genes.
patients receiving allo-HCT, low number of L cells in intestinal tissue biopsies and high serum GLP-2 levels were associated with high non-recurrence mortality.
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