Objective:To evaluate the impact of donor characteristics on the prognosis of myelodysplastic syndrome (MDS) patients undergoing haplo-identical transplantation (HIDT) .Methods:A retrospective analysis of 203 MDS patients who received HIDT was conducted to evaluate how donor factors influenced transplant outcomes.Results:In MDS patients undergoing haploidentical transplantation, donors over 50 years were associated with higher EBV reactivation (2-year cumulative incidence 42.9% vs 22.0% for <50 years old; P=0.010). Female donors were linked to increased severe chronic GVHD compared with male donors (2-year incidence 11.9% vs 4.0% ; P=0.017). Additionally, 2-year overall survival (OS) was slightly lower with female donors than male donors (56.6% vs 69.7% ), but the difference was not statistically significant ( P=0.073). Donor-recipient blood type did not affect post-transplant OS or cumulative relapse rates. Donor-recipient kinship analysis revealed that child donors, compared to haploidentical sibling or parent donors, had lower rates of grade Ⅱ–Ⅳ acute GVHD (27.2% vs 45.7% vs 53.5%, P=0.007) and 2-year EBV reactivation (13.9% vs 29.3% vs 38.9%, P=0.001). For donors under 20 years, donor gender did not significantly affect 2-year OS ( P=0.913), relapse-free survival ( P=0.716), or 100-day incidence of grade Ⅱ–Ⅳ acute GVHD ( P=0.359) . Conclusion:For MDS patients undergoing HIDT, donors over 50 should be avoided. Male and child donors are preferred, while donor gender does not significantly affect outcomes if the donor is under 20 years old.

Objective:To evaluate the impact of donor characteristics on the prognosis of myelodysplastic syndrome (MDS) patients undergoing haplo-identical transplantation (HIDT) .Methods:A retrospective analysis of 203 MDS patients who received HIDT was conducted to evaluate how donor factors influenced transplant outcomes.Results:In MDS patients undergoing haploidentical transplantation, donors over 50 years were associated with higher EBV reactivation (2-year cumulative incidence 42.9% vs 22.0% for <50 years old; P=0.010). Female donors were linked to increased severe chronic GVHD compared with male donors (2-year incidence 11.9% vs 4.0% ; P=0.017). Additionally, 2-year overall survival (OS) was slightly lower with female donors than male donors (56.6% vs 69.7% ), but the difference was not statistically significant ( P=0.073). Donor-recipient blood type did not affect post-transplant OS or cumulative relapse rates. Donor-recipient kinship analysis revealed that child donors, compared to haploidentical sibling or parent donors, had lower rates of grade Ⅱ–Ⅳ acute GVHD (27.2% vs 45.7% vs 53.5%, P=0.007) and 2-year EBV reactivation (13.9% vs 29.3% vs 38.9%, P=0.001). For donors under 20 years, donor gender did not significantly affect 2-year OS ( P=0.913), relapse-free survival ( P=0.716), or 100-day incidence of grade Ⅱ–Ⅳ acute GVHD ( P=0.359) . Conclusion:For MDS patients undergoing HIDT, donors over 50 should be avoided. Male and child donors are preferred, while donor gender does not significantly affect outcomes if the donor is under 20 years old.

Objective To find the differentially expressed long non-coding RNA (lncRNA) between db/db mice that with nephropathy (DN) or not (DM).Methods In this study,3 DM db/db mice and 2 DN db/db mice proven by renal biopsy were randomly selected,and 3 healthy db/m mice as normal control group.Then,differentially expressed lncRNAs,mRNAs and their fragments per kilobase million (FPKM) in kidney samples were detected by high-throughput next generation sequencing technology.Sequencing data were analyzed to filter out the differentially expressed lncRNA,and theirfunction was preliminarily investigated by bioinformatics analysis and functional enrichment analysis to predict their target genes.Total RNAs of kidneys from these 8 mice were extracted to run real time PCR (RT-qPCR) for verifying the outcomes of the high-throughput sequencing.Results The urinary microalbumin/creatinine ratio (UACR),serum creatinine,and glomerular basement membrane thickness of DN db/db mice were higher than those of DM db/db mice (all P ＜ 0.05),while there was not significant difference in glucose between DM and DN mice.Totally 160 lncRNAs were up-regulated and 99 lncRNAs were down-regulated in kidneys of DN mice compared with those of DM mice,in which the differentially expressed lncRNAs with FPKM value≥2 and differential expression≥ 1 fold between groups were screened and verified by RT-qPCR.Finally three lncRNAs whose variation trend were consistent with the outcomes of the high-throughput sequencing were obtained.Conclusion There was a significantly different expression pattern of lncRNA between the kidneys of DN and DM mice,which may be involved in the progress of DN.

Objective To explore the protective effect of heme oxygenase-1 (HO-1) on lung injury induced by seawater drowning in mice,so as to provide a new strategy for the treatment of lung injury induced by seawater drowning.Methods Forty-eight healthy adult male BALB/c mice were randomly divided into the normal control group (n =8),the zinc protoporphyrin (ZnPP) treatment group(n =8),the seawater drowning group (3-d,7-d and 15-d treatment) (n =24) and the seawater drowning + ZnPP treatment group (n =8).The mice were immersed in the artificial seawater with a water depth of 6 cm and water temperature of (25 ± 2) ℃ for 28 seconds.Then,the moment after the mice were taken out from the water,in-time cardio-pulmonary resuscitation was perfromed and a mouse seawater drowning model was thus established.Gross morphology of the lung tissue was observed,and lung wet/dry weight (W/D) ratio,lactate dehydrogenase (LDH) and superoxide dismutase (SOD) levels were detected accordingly.At the same time,changes in the histopathology of the pulmonary tissue,pulmonary fibrosis,apoptosis and proliferation of lung epithelial cells were also observed.HO-1 protein expression and activity in the lung tissue were measured as well.Results Three and 7 days after seawater drowning,there was pulmonary hemorrhage in the lung tissue.The lung wet/dry ratio and serum LDH level significantly increased,as compared with those of the normal control group (P ＜ 0.05),and the SOD level significantly decreased,as compared with that of the normal control group (P ＜ 0.05).Furthermore,alveolar cavity was damaged,alveolar wall thickened,red blood cells and inflammatory cells were infiltrated.HO-1 protein expression level and activity in the lung tissue significantly increased as compared with those of the normal control group (P ＜ 0.05).The expression levels of HO-1 protein in the normal control group,the 3-d and 7-d seawater drowning groups were respectively (0.313 ± 0.027),(0.604 ± 0.092) and (0.945 ± 0.252),and HO-1 activity in these groups were respectively (75.0 ± 45.6),(220.0 ± 109.5) and (350.0 ± 218.9).Fifteen days after seawater drowning,the above pathological changes in the groups significantly alleviated,and no significant differences could be noted,as compared with those of the normal control group (P ＞0.05).The HO-1 protein expression in the lung tissue was (1.367 ±0.284),which was significantly higher as compared with that of the normal control group (P ＜ 0.05),while HO-1 activity was (125.0 ±50.0),and there were no significant differences,as compared with that of the normal control group (P ＞0.05).Seven days after seawater drowning,the expression of HO-1 protein in the lung tissue for the ZnPP treatment group was (1.192 ± 0.341),which displayed no significant differences from that of the seawater drowning group (1.070 ± 0.119) (P ＞ 0.05),while HO-1 activity was (40.0 ± 22.4),which was significantly lower than that of the seawater drowning group (135.0 ± 51.8) (P ＜ 0.05).As compared with the seawater drowning group,pathological changes in the ZnPP treatment group all obviously worsened 7 days after seawater drowning (P ＞ 0.05),the pulmonary fibrosis and lung epithelial cell apoptosis increased (P ＜ 0.05),and lung epithelial cell proliferation decreased.Conclusion HO-1 could alleviate lung injury induced by seawater drowning through the access of enzyme activity,and it might play an important role in the the course of lung self-repair.

Objective To explore the protective effect of heme oxygenase-1 (HO-1) on lung injury induced by seawater drowning in mice,so as to provide a new strategy for the treatment of lung injury induced by seawater drowning.Methods Forty-eight healthy adult male BALB/c mice were randomly divided into the normal control group (n =8),the zinc protoporphyrin (ZnPP) treatment group(n =8),the seawater drowning group (3-d,7-d and 15-d treatment) (n =24) and the seawater drowning + ZnPP treatment group (n =8).The mice were immersed in the artificial seawater with a water depth of 6 cm and water temperature of (25 ± 2) ℃ for 28 seconds.Then,the moment after the mice were taken out from the water,in-time cardio-pulmonary resuscitation was perfromed and a mouse seawater drowning model was thus established.Gross morphology of the lung tissue was observed,and lung wet/dry weight (W/D) ratio,lactate dehydrogenase (LDH) and superoxide dismutase (SOD) levels were detected accordingly.At the same time,changes in the histopathology of the pulmonary tissue,pulmonary fibrosis,apoptosis and proliferation of lung epithelial cells were also observed.HO-1 protein expression and activity in the lung tissue were measured as well.Results Three and 7 days after seawater drowning,there was pulmonary hemorrhage in the lung tissue.The lung wet/dry ratio and serum LDH level significantly increased,as compared with those of the normal control group (P ＜ 0.05),and the SOD level significantly decreased,as compared with that of the normal control group (P ＜ 0.05).Furthermore,alveolar cavity was damaged,alveolar wall thickened,red blood cells and inflammatory cells were infiltrated.HO-1 protein expression level and activity in the lung tissue significantly increased as compared with those of the normal control group (P ＜ 0.05).The expression levels of HO-1 protein in the normal control group,the 3-d and 7-d seawater drowning groups were respectively (0.313 ± 0.027),(0.604 ± 0.092) and (0.945 ± 0.252),and HO-1 activity in these groups were respectively (75.0 ± 45.6),(220.0 ± 109.5) and (350.0 ± 218.9).Fifteen days after seawater drowning,the above pathological changes in the groups significantly alleviated,and no significant differences could be noted,as compared with those of the normal control group (P ＞0.05).The HO-1 protein expression in the lung tissue was (1.367 ±0.284),which was significantly higher as compared with that of the normal control group (P ＜ 0.05),while HO-1 activity was (125.0 ±50.0),and there were no significant differences,as compared with that of the normal control group (P ＞0.05).Seven days after seawater drowning,the expression of HO-1 protein in the lung tissue for the ZnPP treatment group was (1.192 ± 0.341),which displayed no significant differences from that of the seawater drowning group (1.070 ± 0.119) (P ＞ 0.05),while HO-1 activity was (40.0 ± 22.4),which was significantly lower than that of the seawater drowning group (135.0 ± 51.8) (P ＜ 0.05).As compared with the seawater drowning group,pathological changes in the ZnPP treatment group all obviously worsened 7 days after seawater drowning (P ＞ 0.05),the pulmonary fibrosis and lung epithelial cell apoptosis increased (P ＜ 0.05),and lung epithelial cell proliferation decreased.Conclusion HO-1 could alleviate lung injury induced by seawater drowning through the access of enzyme activity,and it might play an important role in the the course of lung self-repair.