ABSTRACT
Objective To observe the CALR mutation in patients with Ph negative chronic myeloproliferative neoplasms(MPNs) and its clinical significance. Methods From January 2012 to January 2015,the clinical data of ninety-seven patients with chronic myeloproliferative neoplasms was retrospectively analyzed and followed up to analyze different types of MPNs, including the clinical characteristics and gene mutation of polycythemia vera(PV),essential thrombocythemia(ET)and primary myelofibrosis (PMF).The hematological parameters and prognosis of patients with different mutation types were compared ( Cox regression model). Results Among the patients,the incidence of JAK2 mutation was the highest,64. 95% (63/97), followed by CALR mutation ( 19. 59% ( 19/97 ) ) and triple negative ( 10. 31% ( 10/97 ) ) . The incidence of MPL mutation was 5. 15% (5/97),which was the lowest and CALR mutations in ET and PMF were 28. 57%(10/35) and 28. 13% (9/32),respectively. The difference was not statistically significant (χ2 =1. 616,P>0. 05);the CALR gene mutation was not detected in PV patients. Compared with the JAK2 mutation, the hemoglobin,leukocyte and neutrophils in the patients with CALR mutation were lower (P<0. 05),PLT levels were lower in CALR-mutant ET patients ( P<0. 017) ,whereas platelet levels in CALR-mutant PMF patients were higher (P<0. 017). The incidence of disease progression in JAK2 and CALR mutation was 47. 62% (30/63)and 31. 58% (6/19) (χ2=1. 525,P>0. 05). The risk of disease progression in patients with CALR mutation was significantly lower than that of JAK2 mutation ( HR=0. 46,95%CI 0. 26-0. 98,P<0. 05) . Conclusion The clinical characteristics of MPNs patients with different gene mutations are different. The prognosis of MPNs patients with CALR mutation is better than that of JAK2 mutation.
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Objective To investigate the potential and underlying molecular mechanism of salidroside in ameliorating radiation-induced bone marrow adipogenesis and stimulating hematopoiesis.Methods The female BALB/c mice aged 6-7 weeks were randomly divided into normal control group,radiation group and salidroside group.The radiation group and salidroside group were irradiated with 6.0 Gy of 60Co γ-rays.The salidroside group was intraperitoneally injected with 30 mg· kg-1 · d-1 salidroside at 12 h and then every day until 8th d after radiation.The normal control group and radiation group were treated with equal volume of saline as control of salidroside.At 14 d after radiation,the mice weight,peripheral blood count,femur bone marrow histology,and the proportion of adipocyte area were measured,and the expressions of PPAR-γ and FABP4 were detected by q-PCR.Results After irradiation,the numbers of white blood cells,hemoglobin and platelet in peripheral blood were reduced obviously,and the percentage of adipocyte area was increased significantly.Compared with mice in the radiation group,salidroside inhibited adipogenesis and reduced the proportion of adipocyte area (t =13.31,P ＜ 0.05) by reducing the expressions of PPAR-γ and FABP4 (t =8.64,13.19,P ＜ 0.05).The number of white blood cells was partly recovered at 7 d after irradiation (t =5.80,P ＜ 0.05).Both white blood cells and hemoglobinin in peripheral blood of the salidroside group were higher than those in the radiation group at 14 d after irradiation.Conclusions Salidroside could inhibit radiation-induced bone marrow adipogenesis and regulate bone marrow microenvironment,thereby promotes hematopoietic recovery in mice after radiation injury.
ABSTRACT
Objective To investigate the protective effect of 1,25-(OH) 2D3 on radiation-induced bone marrow microenvironment injury and to explore the related molecular mechanism.Methods Sixty 7-week old male BALB/c mice were randomly divided into control group without any treatment; radiation group exposed to 6.0 Gy 60Co γ-rays with DMSO,and 1,25-(OH)2 D3 + radiation group treated with 1,25-(OH)2D32.5 μg/kg dissolved in DMSO each day and 6 Gy of γ-rays.The body weight and peripheral white blood cells,femur bone marrow histology,and the proportion of adipocyte area were measured.The expression of peroxisome proliferator-activated receptor-gamma (PPARγ) was detected immunohistochemistrically at 8 d after irradiation.Results After irradiation,the number of white blood cells and the body weight decreased obviously,and the percentage of adipocyte area was increased significantly.Compared with radiation group,1,25-(OH)2D3 reduced the decrease rate of body weight (t =-2.23,-2.34,P ＜ 0.05),partly recovered the number of white blood cells at 4 or 8 d after irradiation(t =-4.99,-4.46,P ＜ 0.05),and reduced the proportion of adipocyte area (t =-3.75,-2.10,P ＜ 0.05).With immunohistochemistrical assay,it was found that 1,25-(OH) 2D3 inhibited adipogenesis by reducing the expression of PPARγ.Conclusions 1,25-(OH) 2 D3 decreases radiationinduced adipogenesis and hence protects the bone marrow microenvironment from radiation damage.