In the present research, a novel MOF-containing Zn(II) ions as nodes were created via the reaction between Zn salt and 2-hydroxy-4-(pyridin-4-yl)benzaldehyde (HL), a N,O-hetrodonor ligand under a solvothermal reaction condition, and its chemical formula is [Zn(L)2]·2DMA·CH3OH (1). The structural analysis results show that complex 1 has a 3D porous framework with 1D channels running along the c axis, and its network could be simplified into a four-linked nbo-type topological network. Complex 1 possesses outstanding luminescent performances and it can determine selectively the Fe3+ ions with a high Ksv value of 3.5 × 104 M−1 and a low LOD (limit of detection) of 0.3 µM. Its treatment on the primary immune thrombocytopenia (ITP) was evaluated in this present research, and its specific mechanism was also studied in the meantime. Firstly, the levels of lgG and lgA on the platelets were determined via the enzyme-linked immunosorbent assay detection kit. Furthermore, the PD-L1 relative expression on the platelets was detected employing the real-time RT-PCR (reverse transcription-polymerase chain reaction) assay.

OBJECTIVE:To investigate the effect of kaempferol on proliferation of acute myeloid leukemia (AML) KG1a cells and its mechanism.METHODS:Human AML KG1a cells in logarithmic growth stage were taken and set at 25, 50, 75 and 100 μg/ml kaempferol group, another normal control group (complete medium without drug) and solvent control group (add dimethyl sulfoxide) were also set. After 24 and 48 hours of intervention, the cell proliferation rate was detected by CCK-8 assay. In addition, interleukin-6 (IL-6) combined with kaempferol group (Plus 20 μg/l IL-6 and 75 μg/ml kaempferol) was set up, 48 hours after culture, the cell cycle and apoptosis of KG1a cells were detected by flow cytometry, the mitochondrial membrane potential (MMP) of KG1a cells was detected by MMP detection kit (JC-1 method), and the expression of Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway related proteins in KG1a cells were detected by Western blot.RESULTS:The cell proliferation rate of 25, 50, 75 and 100 μg/ml kaempferol group decreased significantly (P<0.05), and with the increase of kaempferol dose (r24 h=-0.990, r48 h= -0.999), the cell proliferation rate decreased gradually (P<0.05). The inhibitory effect of 75 μg/ml kaempferol on cell proliferation reached half of effective dose after 48 hours of intervention. Compared with normal control group, the G0/G1 phase cell proportion and apoptosis rate of cells in 25, 50 and 75 μg/ml kaempferol group increased, while the S phase cell proportion, MMP, phosphorylated JAK2 (p-JAK2)/JAK2 and phosphorylated STAT3 (p-STAT3)/STAT3 protein expression decreased in a dose-dependent manner (r=0.998, 0.994, -0.996, -0.981, -0.997, -0.930). Compared with 75 μg/ml kaempferol group, the G0/G1 phase cell proportion and apoptosis rate of cells in IL-6 combined with kaempferol group decreased, while the S phase cell proportion, MMP, p-JAK2/JAK2 and p-STAT3/STAT3 protein expression increased significantly (P<0.05).CONCLUSION:Kaempferol can inhibit KG1a cell proliferation and induce KG1a cell apoptosis, its mechanism may be related to the inhibition of JAK2/STAT3 signal pathway.

目的:探讨弥漫大B细胞淋巴瘤(DLBCL)患者辅助性T细胞(Th)22细胞及其细胞因子的表达及临床意义.方法:选择2019年6月到2021年6月河北北方学院附属第一医院收治的121例DLBCL患者(DLBCL组)和70例健康志愿者(对照组).治疗前、后检测外周血Th22细胞百分比及其细胞因子-白细胞介素(IL)-22、IL-13、IL-6、肿瘤坏死因子(TNF)-α水平.比较DLBCL组和对照组及不同AnnArbor临床分期、国际预后指数(IPI)评分、Hans免疫分型以及疗效的DLBCL患者外周血Th22百分比及血清IL-22、IL-13、IL-6、TNF-α水平差异.结果:DLBCL组外周血Th22细胞百分比、血清IL-22、IL-13、IL-6、TNF-α水平高于对照组(P＜0.05).Ⅲ～Ⅳ期组、高中危组和高危组、非GCB型组治疗前外周血Th22细胞百分比、血清IL-22、IL-13、IL-6、TNF-α水平分别高于Ⅰ～Ⅱ期组、低危组和低中危组、GCB型组(P均＜0.05).121例患者中判定治疗无效者有39例,根据疗效将患者分为无效组(39例)和有效组(82例),无效组治疗后外周血Th22细胞百分比、血清IL-22、IL-13、IL-6、TNF-α水平与治疗前比较无显著变化(P＞0.05),且无效组治疗前、后高于有效组(P＜0.05).结论:DLBCL患者外周血中Th22百分比以及血清IL-22、IL-13、IL-6、TNF-α水平升高,且与高AnnArbor临床分期、高IPI评分、非GCB型以及临床治疗效果较差有关.临床可通过监测上述指标水平以调整治疗方案,提高治疗的有效率.

目的 探讨益中生血片联合输血治疗重度与极重度缺铁性贫血的临床效果.方法 选取自2018年1月至2022年1月河北北方学院附属第一医院收治的100例重度与极重度缺铁性贫血患者为研究对象.按照随机数字表法将患者分为A组与B组,每组各50例.给予A组患者输血治疗,B组在A组的基础上给予益中生血片治疗.比较两组患者的临床疗效、血常规指标(血红蛋白、红细胞计数、平均红细胞体积、平均红细胞血红蛋白量、平均红细胞血红蛋白浓度、红细胞分布宽度)、铁四项指标(血清铁、铁蛋白、总铁结合力、可溶性转铁蛋白受体)、免疫功能指标(CD4+、CD4+/CD8+、Th1/Th2)及不良反应发生情况.结果 B组治疗总有效率为100.00％(50/50),与A组的98.00％(49/50)比较,差异无统计学意义(P>0.05).B组治疗后血红蛋白、红细胞计数、平均红细胞体积、平均红细胞血红蛋白量、平均红细胞血红蛋白浓度高于A组,红细胞分布宽度低于A组,差异均有统计学意义(P<0.05).B组治疗后血清铁、铁蛋白高于A组,总铁结合力、可溶性转铁蛋白受体低于A组,差异均有统计学意义(P<0.05).B组治疗后CD4+、CD4+/CD8+高于A组,Th1/Th2低于A组,差异均有统计学意义(P<0.05).A组不良反应发生率为28.00％(14/50),与B组的34.00％(17/50)比较,差异无统计学意义(P>0.05).结论 益中生血片联合输血治疗重度与极重度缺铁性贫血疗效可观,有助于提高患者血红蛋白水平,改善铁代谢,增强免疫功能,且无明显不良反应.

目的 探讨成人原发免疫性血小板减少症(ITP)患者外周血CD4+、CD8+T淋巴细胞表面程序性死亡受体1(PD-1)及程序性死亡配体1(PD-L1)的表达.方法 选取自2016年1月至2022年1月河北北方学院附属第一医院血液科收治的120例成人ITP患者纳入B组.根据血小板计数(PLT)及是否有出血,将B组患者分为有效组(n=83)与无效组(n=37).另选取120例健康体检者纳入A组.比较各组CD4+、CD8+T淋巴细胞表面PD-1与PD-L1表达水平、PLT、ITP出血评分.结果 有效组与无效组治疗前后CD4+、CD8+T淋巴细胞表面PD-1与PD-L1表达率、出血评分均高于A组,PLT均低于A组,差异均有统计学意义(P＜0.05).有效组治疗后CD4+、CD8+T淋巴细胞表面PD-1与PD-L1表达率均低于无效组,差异均有统计学意义(P＜0.05).有效组治疗后PLT高于无效组,出血评分低于无效组,差异均有统计学意义(P＜0.05).PLT与CD4+、CD8+T淋巴细胞表面PD-1、PD-L1表达率具有极强负相关性(P＜0.05);而出血评分与CD4+、CD8+T淋巴细胞表面PD-1、PD-L1表达率具有中等强度正相关性(P＜0.05).结论 PD1/PD-L1信号通路可能与成人ITP的发生发展相关,PD1/PD-L1可能为ITP的治疗及预后评估提供新的思路.

目的 探究血清微小RNA-326(miR-326)水平与治疗相关性血液系统恶性肿瘤患者化疗敏感性和预后的关系.方法 选取2012年1月—2021年1月河北北方学院附属第一医院收治的50例治疗相关性血液系统恶性肿瘤患者(研究组),以同期40例无原发实体瘤的血液系统恶性肿瘤患者为对照组.采用实时荧光定量聚合酶链反应(RT-qPCR)检测所有患者血清miR-326相对表达量.研究组入院后均接受化疗,根据肿瘤评估情况分为化疗有效组和化疗无效组,比较2个组化疗前后血清miR-326相对表达量.采用Spearman相关分析评估血清miR-326相对表达量与治疗相关性血液系统恶性肿瘤患者化疗敏感性的相关性.对研究组患者进行随访,根据随访终点事件(全因死亡)将研究组患者分为存活组和死亡组,收集2个组患者的临床资料,采用Logistic回归分析评估治疗相关性血液系统恶性肿瘤患者预后的影响因素.采用受试者工作特征(ROC)曲线评估血清miR-326预测治疗相关性血液系统恶性肿瘤患者预后的价值.结果 研究组血清miR-326相对表达量低于对照组(P<0.001).化疗有效组化疗后血清miR-326相对表达量高于化疗前(P<0.05);化疗无效组化疗前后血清miR-326相对表达量差异无统计学意义(P>0.05).血清miR-326相对表达量与治疗相关性血液系统恶性肿瘤患者化疗敏感性呈正相关(r=0.641,P<0.05).死亡组高血压、感染、凝血功能异常、再发肿瘤化疗周期(≥5个)、脏器功能损伤所占比例均高于存活组,血清miR-326相对表达量低于存活组(P<0.05).感染、凝血功能异常、脏器功能损伤、低血清miR-326相对表达量是治疗相关性血液系统恶性肿瘤患者预后不良的危险因素(P<0.05).以0.44为最佳临界值,血清miR-326相对表达量预测治疗相关性血液系统恶性肿瘤患者预后的敏感性为86.80％,特异性为78.10％,曲线下面积为0.868.结论 血清miR-326在治疗相关性血液系统恶性肿瘤患者中异常低表达,其与患者化疗敏感性关系密切,对患者预后有较高的预测价值.

目的:探究血清微小 RNA-4731-5p(miR-4731-5p)和间皮素(MSLN)水平与需治疗原发免疫性血小板减少症(ITP)发生的相关性.方法:选择 ITP患者 118 例,根据血小板(PLT)计数及是否伴有出血分为需治疗组(62例)和需观察组(56 例).另选取体检健康者 60 例为对照组.采用全自动血液分析仪检测白细胞计数、血红蛋白、PLT及平均血小板体积(MPV)水平.采用实时荧光定量 PCR 和酶联免疫吸附法分别对血清 miR-4731-5p 和MSLN 水平进行测定.比较三组血常规及血清 miR-4731-5p、MSLN 水平.分析 ITP 患者血清 miR-4731-5p、MSLN、PLT、MPV间的相关性,影响需治疗 ITP发生的因素,以及血清 miR-4731-5p、MSLN 对需治疗 ITP 发生的预测价值.结果:对照组、需观察组、需治疗组 PLT、血清 miR-4731-5p 水平依次降低,MPV、血清 MSLN 水平依次升高(均P<0.05).ITP患者血清 miR-4731-5p与 MSLN 呈负相关(r=-0.683,P<0.05);miR-4731-5p 与 PLT呈正相关,与 MPV呈负相关(r=0.401、-0.564,均P<0.05);MSLN 与 PLT 呈负相关,与 MPV 呈正相关(r=-0.429、0.460,均P<0.05).低水平PLT、高水平 MPV、低水平 miR-4731-5p、高水平 MSLN 是需治疗 ITP 发生的独立危险因素(均P<0.05).血清miR-4731-5p、MSLN联合预测的AUC大于单项预测(均P<0.05).结论:ITP患者血清 miR-4731-5p水平降低,MSLN水平升高,两者与血常规指标密切相关,对需治疗 ITP 的发生有较高预测价值.

Aim To analyze the levels of helper T cell 22(Th22)cells and interleukin-22(IL-22)in patients with diffuse large B-cell lymphoma(DLBCL),and the effects of IL-22 on the proliferation and invasion of DLBCL cell lines.Methods Forty patients with DLBCL(DLBCL group)were selected and divided into different subgroups ac-cording to clinical staging,and another 40 healthy individuals who underwent physical examination during the same period were selected as the control group.Flow cytometry was used to detect the level of Th22 cells in each group,and ELISA was used to detect the level of IL-22 protein in each group.MTT assay was used to detect the proliferation of DLBCL cells,and Transwell assay was used to detect the invasion of DLBCL cells.Results Compared with the control group,the levels of Th22 cells and IL-22 in the DLBCL group were increased.Compared with stages Ⅰ-Ⅱ,the levels of T22 cells and IL-22 in stages Ⅲ-Ⅳ were increased(P<0.05).The proportion of Th22 after chemotherapy was lower than that before,while the proportion of Th22 in relapsed patients was higher than that in newly diagnosed patients and the con-trol group(P<0.05).The results of MTT and Transwell experiments showed that IL-22 promoted the proliferation and in-vasion of DLBCL cells(P<0.05).Conclusion The levels of Th22 cells and their cytokine IL-22 in DLBCL patients are elevated,and IL-22 promotes the proliferation and invasion of DLBCL cells,providing a new strategy for DLBCL research.

Objective:To investigate the clinical relationship between homocysteine (Hcy) metabolizing enzyme gene polymorphism and poor prognosis of multiple myeloma (MM) in Han nationality.Methods:One hundred and twenty-eight MM patients of Han nationality admitted to the First Affiliated Hospital of Hebei North University from February 2018 to March 2020 were selected as the disease group, and 120 healthy volunteers of Han nationality were recruited as the control group at the same time. Blood samples were taken to detect plasma Hcy level and Hcy metabolizing enzyme gene polymorphism, including methylenetetrahydrofolate reductase(MTHFR) C677T, MTHFRA1298C, methionine synthase reductase(MTRR) A66G, cystathionine beta-synthase(CBS) 844ins68 and methionine synthase (MS) A2756G. The patients in the disease group were treated with conventional methods , followed up for 1 year after treatment, and the incidence of poor prognosis was counted. Plasma Hcy level, genotype distribution and allele frequency of Hcy metabolic enzymes were compared between the two groups. Logistic multiple regression analysis was used to analyze the association of Hcy metabolizing enzyme gene polymorphism with MM poor prognosis in Han nationality.Results:The plasma Hcy level in the disease group was higher than that in the control group: (15.01 ± 2.98) μmol/L vs. (8.45 ± 1.69) μmol/L, there was statistical difference ( P<0.05). The frequency of TT genotype and T allele of MTHFRC677T locus in the disease group were higher than those in the control group : 26.56% vs. 6.67% , 29.30 vs. 16.25%; while the frequency of CT genotype in the disease group was lower than that in the control group: 5.47% vs. 19.17% , there were statistical differences ( P<0.05). There were no significant differences in genotype distribution and allele frequency of other gene loci between the two groups ( P>0.05). The incidence of poor prognosis in the disease group was 49.22%(63/128). Age, platelet count, serum β 2 microglobulin level, serum κ light chain level, plasma Hcy level and TT genotype of MTHFRC677T locus were the influencing factors of poor prognosis in the disease group ( OR = 7.286, 0.545, 6.841, 6.284, 8.117 and 8.440; P<0.05). Conclusions:The plasma Hcy level, TT genotype and T allele frequency of MTHFRC677T locus in MM patients of Han nationality are higher than those in healthy people, while the CT genotype frequency is lower than that in healthy people. The poor prognosis of MM in Han nationality is related to plasma Hcy level and TT genotype of MTHFRC 677T locus.

目的 探讨白细胞介素-1受体相关激酶(IRAK1)/肿瘤坏死因子受体相关因子6(TRAF6)通路影响急性髓系白血病(AML)发生发展的作用机制.方法 选取54例AML患者为研究对象(AML组),30例于本院治疗的缺铁性贫血患者作为对照组,分离所有受试者骨髓单核细胞;体外常规培养人AML细胞系HL-60、KG-1、U937和人正常单核细胞系THP-1;将HL-60细胞分为空白组(转染Lipofectamine 3000试剂)、阴性对照(NC)组(转染空质粒)、IRAK1短发夹RNA(IRAK1 shRNA)组(转染IRAK1 shRNA);实时荧光定量PCR(qPCR)法检测单核细胞及不同细胞系各组中IRAK1、TRAF6 mRNA表达水平;CCK-8法检测各组细胞增殖抑制率;流式细胞术检测各组细胞凋亡率;蛋白免疫印迹法检测各组细胞β-连环蛋白(β-catenin)、细胞周期蛋白D1(CyclinD1)、B淋巴细胞瘤-2(Bcl-2)、Bcl-2相关X蛋白(Bax)及IRAK1/TRAF6通路蛋白表达水平.结果 与对照组比较,AML组单核细胞中IRAK1、TRAF6 mRNA表达水平显著升高(P＜0.05).与THP-1细胞比较,KG-1、U937、HL-60细胞中IRAK1、TRAF6mRNA表达水平显著升高,且HL-60细胞最高(P＜0.05).与空白组和NC组比较,IRAK1 shRNA组细胞增殖抑制率、凋亡率及Bax蛋白表达显著升高,IRAK1 mRNA、TRAF6 mRNA、β-catenin、CyclinD1、Bcl-2、磷酸化-IRAK1(p-IRAK1)/IRAK1、TRAF6、核因子-κB(NF-κB)蛋白表达显著降低(P＜0.05).结论 IRAK1/TRAF6通路与AML的发生发展有关,抑制IRAK1/TRAF6通路可抑制人AML细胞系HL-60增殖,促进其凋亡,IRAK1/TRAF6可能是AML治疗的潜在靶点.

OBJECTIVE:To observe the expression level of serum homocysteine (Hcy) and methylenetetrahydrofolate reductase (MTHFR) gene polymorphism in patients with hematological diseases complicated with coronary heart disease, and analyze the relationship between serum Hcy level, MTHFR gene polymorphism and coronary heart disease. METHODS:The medical records of 80 patients with coronary heart disease who completed treatment of hematological diseases during the period from March 2018 to March 2020 were selected as observation group. In addition, the medical records of 92 patients with hematological diseases who completed treatment in our hospital during the same period were selected as control group. Venous blood samples of the two groups were collected to detect serum Hcy level and MTHFR gene polymorphism. The serum Hcy levels of the two groups with different MTHFR genotypes were compared, and the effects of the above indicators on hematological diseases complicated with coronary heart disease were analyzed. RESULTS:The detection rates of MTHFR gene TT and TC in the observation group were higher than those in the control group, while the distribution frequency of MTHFR genotype CC was lower (P<0.05). The serum Hcy levels of the patients with MTHFR genotype TT and TC in the observation group was higher than the control group (P<0.05). Binary logistic regression analysis showed that MTHFR gene TC/CC genotype serum Hcy overexpression may be influencing factor which induced coronary heart disease in patients with hematological diseases (OR=2.107/OR=1.634, P<0.05). ROC curves showed that the AUC of serum Hcy level of MTHFR gene TC/CC genotype and hematological disease complicated with coronary heart disease were both > 0.8. When MTHFR gene TC reaching the optimal threshold of 22.165 μmol/L, the sensitivity was 0.950 and the specificity was 0.837, While MTHFR gene CC reached the optimal threshold of 19.630 μmol/L, the sensitivity was 0.938 and the specificity was 0.826, the best predictive value could be obtained. CONCLUSION:The changes of serum Hcy and MTHFR gene polymorphisms may be involved in the pathological process in patients with hematological diseases complicated with coronary heart disease. In the future, early detection of serum Hcy levels and MTHFR gene polymorphisms in patients with hematological diseases can be used to predict the risk of coronary heart disease.

目的 探讨益中生血片联合琥珀酸亚铁片治疗重度缺铁性贫血的临床疗效.方法 选择2019年1月-2020年1月于河北北方学院附属第一医院就诊的120例重度缺铁性贫血患者作为研究对象,采用随机数字表法将患者分为对照组和观察组,每组60例.对照组患者餐后服用琥珀酸亚铁片,1片/次,3次/d.观察组在对照组基础上餐后服用益中生血片,2片/次,3次/d,4周为1个疗程,两组患者均治疗1个疗程.观察两组患者的临床疗效,同时比较两组治疗前后的中医证候积分,外周血红细胞(RBC)、血红蛋白(Hb)、平均红细胞体积(MCV)、平均红细胞血红蛋白量(MCH)、红细胞平均血红蛋白浓度(MCHC)、网织红细胞血红蛋白(Ret-He)含量,以及血清铁离子(Fe)和血清铁蛋白(SF)水平.结果 治疗后,对照组和观察组的总有效率分别为83.33％、95.00％,两组总有效率比较差异具有统计学意义(P＜0.05).治疗后,两组患者中医证候积分均降低(P＜0.05),且观察组明显低于对照组(P＜0.05).治疗后,两组患者RBC、Hb、MCV、MCH、MCHC、Ret-He水平均显著升高(P＜0.05);且观察组外周血象水平明显高于对照组(P＜0.05).治疗后,两组患者血清Fe、SF水平均升高(P＜0.05),且观察组血清Fe、SF水平明显高于对照组(P＜0.05).结论 益中生血片联合琥珀酸亚铁片对重度缺铁性贫血患者疗效较好,可有效改善患者外周血象,提高网织红细胞血红蛋白含量并改善铁代谢水平.

目的 探讨多发性骨髓瘤(Multiple Myeloma,MM)患者亚甲基四氢叶酸还原酶(Methylenetetrahydrofo-late reductase,MTHFR)基因C677T的多态性与化疗并发症及感染的相关性.方法 选择河北北方学院附属第一医院血液科2018年3月-2019年3月收治的多发性骨髓瘤患者100例作为研究对象,根据MTHFR基因型将其分为CC组、CT组和TT组,收集患者一般资料,化疗期间及治疗结束3个月内血液系统并发症中骨髓抑制、血小板减少、中性粒细胞减少、贫血及非血液系统并发症血栓形成(深静脉血栓及肺栓塞)、胃肠道反应、肾损害、疲劳、心肌梗死、周围神经病变发生率和感染发生情况.结果 100例MM患者共包含野生型CC 34例,CT突变型47例,TT突变型19例,C、T位点分布符合Hardy-Weinbery平衡;不同MTHFR基因型MM患者骨髓抑制、中性粒细胞发生率比较差异无统计学意义;TT组患者血小板减少、贫血发生率高于CT、CC组(P＜0.05),CT组血小板减少、贫血发生率与CC组差异无统计学意义;不同MTHFR基因型MM患者肾损害、疲劳、周围神经病变发生率比较差异无统计学意义;TT组血栓形成、胃肠道反应、心肌梗死发生率高于CT、CC组(P＜0.05),CT组血栓形成、胃肠道反应、心肌梗死发生率与CC组差异无统计学意义;不同MTHFR基因型MM患者真菌感染发生率比较差异无统计学意义;TT组病毒感染发生率高于CC、CT组,差异均具有统计学意义(P＜0.05),TT组和CT组细菌感染发生率均高于CC组(P＜0.05).结论 MTHFR基因C677T的多态性与多发性骨髓瘤患者化疗期间血小板减少、贫血、血栓形成、胃肠道反应、心肌梗死等并发症及细菌、病毒感染发生存在相关性.

目的 探讨蔗糖铁联合促红细胞生成素(erythropoietin,EPO)治疗晚期肺癌患者贫血的疗效及其对生存预后的影响.方法 66例晚期肺鳞癌伴轻度-中度贫血且预估生存时间大于3个月的患者,采用单药(吉西他宾或紫杉类)非铂类化疗方案者47(71.2％)例,联合铂类(顺铂或卡铂)化疗者19例(28.8％);完成化疗<4周期者31(47.0％)例,完成化疗≥4个周期者35(53.0％)例;部分Ⅲb期、Ⅳ期患者联合姑息性放疗;所有患者化疗均不少于3个周期.采用蔗糖铁联合EPO治疗贫血.结果 蔗糖铁联合EPO治疗后48(72.7％)例有效,18(27.3％)例铁剂治疗无效.2例患者出现低热,1例出现血压轻度升高,整个贫血治疗过程中无血栓性事件、喉头水肿及休克等情况发生.单因素分析中TNM分期、KPS评分、联合疗法是否有效、化疗方式、化疗周期数、近期疗效与预后相关.联合疗法的疗效与肿瘤近期疗效显著相关(φ=0.686,P<0.001).Cox比例风险回归模型分析结果显示TNM分期、KPS评分、联合疗法是否有效、近期疗效是影响患者生存时间的独立因素.结论 蔗糖铁联合EPO能有效改善恶性肿瘤相关性贫血,提高肿瘤对治疗的反应,延长生存时间.

目的 探讨亚甲基四氢叶酸还原酶(MTHFR)C677T基因多态性及同型半胱氨酸(Hcy)水平与急性淋巴细胞白血病(ALL)患者血栓发生风险的相关性.方法 选择2019年1月至2020年4月于河北北方学院附属第一医院就诊的ALL患者140例,其中发生静脉血栓者43例,未发生者97例.患者入院时均测定血清同型半胱氨酸(Hcy)水平,并分析MTHFR C677T基因多态性.收集患者临床基线资料及实验室检查资料,并进行倾向性评分匹配后采用Logistic回归分析评价MTHFR C677T基因多态性及Hcy与患者血栓发生之间的关系.结果 倾向性评分匹配后,发生血栓组患者纤维蛋白原、D-二聚体、纤维蛋白原降解产物及Hcy水平均显著高于未发生血栓组[(0.94±0.21)g/L比(0.86±0.19)g/L、(0.41±0.09)mg/L 比(0.37±0.07)mg/L、(2.1±0.7)mg/L 比(1.9±0.5)mg/L、(15±6)μmol/L 比(13±4)μmol/L](均P＜0.05),2组患者MTHFR C677T基因多态性分布及CT基因型频率差异均有统计学意义(均 P＜0.05).Logistic 回归分析结果显示,Hcy(比值比=1.217,95％置信区间:1.063～1.393,P=0.005)为影响血栓发生的危险因素;MTHFR C677T基因多态性为血栓发生的独立影响因素(比值比=7.857,P=0.022),其中与TT基因型比较,CC基因型为影响血栓发生的保护因素(比值比=0.092,95％置信区间:0.017～0.493,P=0.005).结论 MTHFR C677T基因多态性及Hcy水平均与ALL患者血栓发生显著相关.

目的 检测原发免疫性血小板减少症(ITP)患者外周血CD4+T淋巴细胞表面程序性死亡因子-1(PD-1)的表达水平,探讨PD-1在ITP发病过程中的作用.方法 选取河北北方学院附属第一医院(以下简称"我院")血液科2015年12月—2017年12月收治的100例ITP患者作为研究组,给予0.15 mg/(kg·d)的地塞米松静脉输注,1次/d或0.8 mg/(kg·d)的甲泼尼龙静脉输注,1次/d,病情好转后改为1 mg/(kg·d)泼尼松顿服,一共连续治疗4周.选择同期在我院门诊进行体检的50名健康者作为对照组.采用流式细胞术检测外周血CD4+T淋巴细胞表面PD-1表达情况.观察研究组治疗前后血小板计数及CD4+T淋巴细胞表面PD-1阳性表达率的变化,按治疗效果将研究组分成完全反应组、有效组和无效组,比较不同治疗效果组CD4+T淋巴细胞表面PD-1阳性表达率的差异.结果 治疗后,研究组血小板计数高于治疗前,但仍低于对照组,差异均有统计学意义(均P<0.05).治疗后,研究组CD4+T淋巴细胞表面PD-1阳性表达率低于治疗前,但仍高于对照组,差异均有统计学意义(均P<0.05).治疗后,完全反应组和有效组CD4+T淋巴细胞表面PD-1阳性表达率均较治疗前降低,差异均有统计学意义(均P<0.05),无效组治疗前后CD4+T淋巴细胞表面PD-1阳性表达率比较,差异无统计学意义(P>0.05).完全反应组CD4+T淋巴细胞表面PD-1阳性表达率低于有效组和无效组,有效组低于无效组,差异均有统计学意义(均P<0.05).结论 外周血CD4+T淋巴细胞表面PD-1表达上调可能与ITP患者疾病发展程度及预后有关.

目的 探讨骨髓涂片和骨髓活检同步检测对骨髓转移瘤的诊断价值.方法 100例疑似骨髓转移瘤患者同步行骨髓涂片及骨髓活检检查,查看已浸润的骨髓转移瘤细胞的阳性检出率.结果 全部患者中,骨髓涂片查见癌细胞78例(临床诊断符合率为78.0％),骨髓活检查见癌细胞92例(临床诊断符合率为92.0％),骨髓活检阳性检出率显著高于骨髓涂片(P<0.05).结论 骨髓涂片与骨髓活检均对骨髓转移瘤有较高敏感性,但骨髓活检阳性检出率更高.

慢性粒细胞白血病(CML)是一种造血干细胞的恶性克隆增殖性疾病,以分子生物学、免疫学为基础的生物治疗手段成为新的研究方向.生物治疗主要包括分子靶向治疗、基因治疗和过继免疫治疗.基因治疗主要通过基因转染使肿瘤细胞抗原标志过度表达而增加机体的免疫识别;或通过下调相关原癌基因表达,抑制细胞增殖,诱导细胞凋亡等方式发挥抗肿瘤作用.过继免疫治疗是将CIK、NK等免疫活性细胞注入肿瘤宿主体内的一种治疗方法.基于K562细胞系的相关研究为深入进行生物治疗研究奠定了基础,但因缺乏合适靶标等原因,生物治疗尚不能取代传统的治疗方法.

患者，男，69岁，主因腹胀伴消瘦1月余入院。1个月前患者无明显诱因出现腹胀，以左侧腹部为著，伴消瘦，体质量下降约5 kg，有乏力、多汗，无腹痛、腹泻，无发热，无骨及关节疼痛，未予重视。1 d前患者因行白内障手术来我院门诊，查血WBC 42．92×109／L，RBC 4×1012／L，Hb 109 g／L，PLT 149×109／L，拟诊为“白血病”收入院。6年前患高血压最高达170／110 mm Hg，现服药血压控制在120／80 mm Hg左右。查体：轻度贫血貌，全身皮肤黏膜未见出血点、肝掌及蜘蛛痣。全身浅表淋巴结未触及。胸骨无压痛。心肺未见异常。左上腹膨隆，无腹壁静脉曲张，未见肠型、蠕动波。全腹无压痛及反跳痛，肝肋下未触及，脾脐下约4 cm，过中线4 cm，质硬，无压痛。实验室检查：血WBC 30．38×109／L，RBC 3．25×1012／L，Hb 92 g／L，PLT 119×109／L。骨髓象：骨髓增生活跃，粒系增生，原始粒细胞2％，中幼粒细胞4％，晚幼粒细胞12％，杆状核粒细胞15％，分叶核粒细胞38％，红系增生，以中晚红为主。 BCR－ABL P210阴性， BCR－ABL P190阴性。染色体示：46，XY，del（13）（q32）［20］。CSF3R基因EXON14未见突变， JAK2基因 V617F 突变阳性。上腹部CT：肝脏、脾脏增大，脾内斑片状低密度影，考虑脾梗死可能，脾内不规则高密度影，不除外出血机化，腹水，层面肋骨、椎体、骨盆骨质改变。腹部超声：肝内中强回声，胆囊壁增厚，脾大，脾内中强回声，建议进一步检查。前列腺增大伴钙化。诊断为：（1）慢性中性粒细胞白血病；（2）原发性高血压3级，极高危。给予口服羟基脲1 g，每天3次，碳酸氢钠片碱化尿液、降压及改善循环等治疗，10 d后白细胞下降，脾脏较前轻度缩小，羟基脲减量至1 g，每天2次，患者症状好转出院，因患者不同意应用干扰素治疗，嘱其定期门诊复查，目前正在随访中。

目的：探讨温热刺激对bcr/abl融合基因阳性的慢性粒细胞白血病（chronic myeloid leukemia，CML）细胞gp96转录水平的影响，为CML热疗研究提供理论基础。方法通过骨髓涂片对初选患者进行诊断，荧光原位杂交（ FISH）技术检测bcr/abl融合基因，采集病例血细胞分为4组，对照组采用37℃温热刺激30 min，试验组分别经40℃、42℃、44℃进行温热刺激各30min，采用RT-PCR技术检测gp96 mRNA的转录水平。结果骨髓涂片表现为CML骨髓像，FISH检测bcr/abl融合基因阳性。温热刺激后，随着刺激温度的提高，gp96的转录水平也升高。结论在CML病例中开展热疗，可能通过gp96参与的机体免疫调节，有助于病情的缓解。