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1. The fate of the new mechanism of bone marrow reconstruction after transplantation is strictly regulated by its bone marrow (BM) micro-environment (ME) at https://doi.org/10.1182/blood.2020005399.
bone marrow transplantation (BMT) often requires radiation pre-treatment to remove endologic hematologic cells.
so far, it is not clear whether the mesotherapic ME is damaged after radiotherapy and how it will recover.
researchers recently found that BM interstuming stem cells (MSCs) severely impaired mitochondrial function after radiotherapy.
healthy HSPC transfers functional mitochondrials to the substiter ME, thereby improving the mitochondrial activity of the subject MSC.
specifically, mitochondrial transfer from healthy HSPC to MSC depends on cell contact and is mediated by HSPC-connected protein 43 (Cx43).
chisel mice with
hematocyte Cx43 defects showed a decrease in mitochondrial metastasis, which was saved by re-expression of Cx43 in HSPC or by adding mitochondrials isolated from the HSPC of Cx43 defects to the medium.
increase in ATP levels in HSPC cells activates the pyrethride-energy-insulated P2RX7, resulting in reduced AMPK activity, which significantly increases the transport of mitochondrials to BM MSC.
mitochondrial metastasis, the host substation ME is restored and the supply HSPC implantation increases.
Cx43 delays the regeneration of interstate and osteoblasts, while AMPK inhibition in the body promotes interstate recovery.
, the reconstruction of the hemast chambers has also been improved as a result of the recovery of the supportive substation ME.
. 2. Venetok combination therapy to treat recurring/refracticable folytic lymphoma https://doi.org/10.1182/blood.2020005588CONTRALTO trial is an open label Phase 2 studies aimed at evaluating the efficacy and safety of BCL-2 inhibitors Ven)Vitoxy monoantigen (R), VEN combined with benzodiamostin (B) and R, compared to the treatment of recurring/refractic follicle lymphoma with BR alone.
patients without chemotherapy arms (Group A: VEN-R) received Venetok 800 mg/day and lytoxi monoantigen 375 mg/m2 (on the first day, 8 days, 15 days and 22 days of the first course of treatment ( C) ( D ) and 4/6/8/10/12 on the first day of treatment.
patients with a queue containing chemotherapy were randomly assigned to VEN-BR (Group B: VEN 800 mg/day for 1 year, and 6 courses of BR (Benzamostin 90 mg/m2 D1), after safe contact with Venetok, 2 and lysoxi monoanti-resistant 375 mg/m2 D1)) or 6 courses of BR (Group C).
total, 163 patients were included: 9 in safety tests, 52 in groups A, B and C, and 51 in groups A, 51 and 51, respectively.
metabolic/remission rates in groups A, B and C were 17%, 75% and 69%, respectively.
only 61 per cent of patients with the B treatment arm received ≥90 per cent of the planned dose of benzomostin, and 96 per cent of patients with the C treatment arm.
blood toxicity in group B led to a reduction or suspension of the dose compared to Group C.
rate of adverse reactions in groups A, B and C was 51.9%, 93.9% and 60.0%, respectively.
, compared with Group C, the toxicity of VEN-BR increased and the dose of medication decreased, but the efficacy was similar.
Optimize dosages and programmes to maintain the dose strength of benzomostin and lysoxi monoantigen or improve the efficacy and toeration of VEN combined benzodiamic and lytoxides monoantigen, while data on VEN Unitoxy monoantigens need to be further studied.
( 3) Monoclonal immunoglobulin promotes bone loss in patients with multiple myeloma https://doi.org/10.1182/blood.2020006045 Most patients with multiple myeloma develop severe bone-soluble diseases.
myeloma cells secrete immunoglobulin, the presence of monoclonal immunoglobulin in the patient's serum is an important diagnostic criterion.
Recently, researchers demonstrated that adding immunoglobulins isolated from myeloma to human bone-breaking precellular cells cultured in-body can promote bone-breaking cell differentiation, while immunoglobulins isolated from myeloma patients who never combine osteopathy have no effect.
this effect is mainly mediated by immune complexes or aggregates.
and aggregation behavior of immunoglobulins depends in part on differences in glycosylation in the immunoglobulin Fc part.
glycosylation analysis showed that there was a significant reduction in semi-lactose on IgG in myeloma patients with combined osteopathy and a decrease in salivary acid on IgG compared to healthy people.
, the researchers also observed a significant reduction in IgG saliva acidification in the serum of myeloma patients in the event of osteopathy.
In the 5TGM1 mouse myeloma model, the researchers found that in mice treated with the salivary acid preluptogen N-acetyl glycosamine (ManNAc), the number of bone-soluble injuries decreased and the level of CTX-1, a marker of bone-breaking cell activity, decreased.
manNAc therapy increased saliva acidification of IgG-Fc in mice.
: Study on the mechanism of glucosal hormone-induced eosinophil reduction https://doi.org/10.1182/blood.2020005161 Glucosteroids is considered a first-line drug for the treatment of various eosinophil diseases.
can cause a brief and significant reduction in eosinophils in the blood within a few hours of taking.
Saccharide corticosteroid-induced reduction in eosinophils is the basis for the treatment of eosinophil disease using glucosticosteroids, which have attracted the interest of clinicians for 70 years, but the underlying mechanisms are not yet fully defined.
researchers recently studied the response of circulating acidic granulocytes to glucosal hormones in three animals for the first time, and found that the response in rhesus monkeys was similar to that in humans, not in mice.
Then, the researchers developed a separation technique to purify acidic granulocytes from the outer blood of rhesus monkeys and to track acidic granulocytes labeled before and after glucoticoids through a series of PET/CT imaging.
results showed that glucosal hormones can quickly induce the return of bone marrow to acid-addicted granulocytes.
The dynamics of acidic granulocyte reduction and bone marrow migration induced by glucosal corticosteroids are consistent with the induced dynamics of Glucosteroid-reactive chimogenic factor subject CXCR4, and selective blocking of CXCR4 can reduce or eliminate the early hemophilic acidophil reduction induced by glucostetin.
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