不同分期老年COPD患者Th17、Treg细胞比例及炎性因子水平研究

目的探讨不同分期老年慢性阻塞性肺病(COPD)患者外周血Th17、调节T细胞(Treg)细胞及相关炎症因子水平的变化及其与患者肺功能的关系。方法选取2012年1月至2014年1月在本院呼吸内科就诊的68例COPD患者(其中稳定期32例,急性期36例)为研究对象,另选取30例健康体检者为对照组。应用流式细胞仪测定两组外周血CD+4Th17、CD+4CD+25 Treg细胞的比率。应用ELISA法测定两组白细胞介素-6,10,17,21,22(IL-6,10,17,21,22)及转化生长因子β(TGF-β)水平。结果急性期组患者FEV1、FEV1/FVC水平显著低于稳定期及对照组(P0.05),而稳定期组低于对照组(P0.05)。急性期组CD+4Th17细胞比率高于稳定期及对照组,CD+4CD+25Treg细胞的比率则低于稳定期及对照组,差异有统计学意义(P0.05)。急性期组IL-6,17,21,22水平高于稳定期及对照组,而IL-10、TGF-β水平低于稳定期及对照组,差异有统计学意义(P0.05)。FEV1与IL-6,17,21,22呈负相关,而与IL-10、TGF-β水平呈正相关,FEV1/FVC与IL-6,17,21,22呈负相关,而与IL-10、TGF-β水平呈正相关。结论 Th17/Treg比例失衡可导致机体促炎因子生成增多,抑制炎症作用不足,促进气道炎症反应,导致患者呼吸功能障碍,加重COPD病情。     

青蒿素对 AECOPD 患者外周血中炎症因子及 Th17/Treg 失衡的调控

目的：通过检测青蒿素干预前后慢性阻塞性肺疾病急性加重期(AECOPD)患者外周血中 Th17细胞,Treg 细胞占 CD4+ T 细胞的比例,炎症因子 IL-6、IL-21、转化生长因子β(TGF-β)的含量,初步探讨青蒿素对 COPD 患者外周血中炎症因子和 Th17/Treg 失衡的调控机制。方法随机收集 AECOPD 20例,将其分为1640干预组和青蒿素干预组,收集同一时期肺功能正常健康体检者20例作为对照组,抽取清晨空腹静脉血,采用流式细胞术检测所有实验对象 CD4+ Th17细胞和 Treg 细胞占 CD4+ T 细胞的比例;采用 ELISA 方法检测所有实验对象血清中炎症因子 IL-6、IL-21、TGF-β的水平。结果①CD4+ Th17细胞/CD4+ T 细胞和 Th17/CD4+ Treg 细胞的比例1640干预组高于青蒿素干预组和对照组,青蒿素干预组高于对照组,差异有统计学意义(P <0.05)。Treg 细胞/CD4+ T 细胞的比例1640干预组则低于青蒿素干预组和对照组,青蒿素干预组低于对照组,差异有统计学意义(P <0.05)。炎症因子 IL-6和 IL-21的水平1640干预组高于青蒿素干预组和对照组;青蒿素干预组高于对照组,差异有统计学意义(P <0.05)。④炎症因子 TGF-β的水平1640干预组则低于青蒿素干预组和对照组,青蒿素干预组低于对照组,差异有统计学意义(P <0.05)。⑤Th17/Treg 细胞的比值与炎症因子 IL-6(r =0.095,P <0.05),IL-21(r =0.051,P <0.05)的水平呈正相关,与 TGF-β(r =-0.002,P <0.05)的水平呈负相关;炎症因子 TGF-β的水平与炎症因子 IL-6(r =-2.075,P <0.05),IL-21(r =-2.869,P <0.05)的水平呈负相关。结论 AECOPD 患者外周血中存在 Th17/Treg 的失衡,炎症因子 IL-6、IL-21、TGF-β与 Th17/Treg 的失衡密切相关,青蒿素可能能够通过下调 IL-6和 IL-21的表达,上调 TGF-β的表达来调节其失衡。     

参麦注射液对支气管哮喘患者外周血Th17/Treg细胞的影响

目的 探讨参麦注射液对支气管哮喘(简称哮喘)患者外周血Th17/Treg细胞的影响及其意义.方法 选取山西医科大学第一医院呼吸科急性发作期、缓解期哮喘患者各25例,选取山西医科大学第一医院体检中心肺功能正常、激发或者舒张试验阴性的健康人25例作为对照组,分别使用1640培养液及参麦注射液进行干预处理.抽取晨起空腹静脉血5 ml,运用流式细胞仪对各组外周血Th17细胞、Treg细胞分别占CD4+的比例及Th17/Trcg细胞的比值进行比较,同时检测血清中IL-10因子的水平.结果 ①各组间干预前CD4+ Th17细胞/CD4+T细胞、CD4+ Th17细胞/CD4+ Treg细胞的比值,急性发作期组(3.05±1.27、1.49±1.78)高于缓解期组(2.38±0.93、0.61±0.24)及对照组(1.19±0.39、0.30±1.14),差异有统计学意义(P＜0.05),缓解期高于对照组,差异有统计学意义(P＜0.05);CD4+Treg细胞/CD4+T细胞的比值,对照组(5.20±3.26)高于缓解期组(3.99±0.90)及急性发作期组(2.76±0.93),差异有统计学意义,(P＜0.05),缓解期组高于急性发作期组,差异有统计学意义(P ＜0.05).血清中IL-10因子的水平,对照组(5,28±1.31)高于缓解期组(4.46±0.83)及急性发作期组(3.90±0.64),差异有统计学意义(P＜0.05),缓解期组高于急性发作期组,差异有统计学意义(P ＜0.05).②同一组间CD4+ Th17细胞/CD4+T细胞、CD4+Th17细胞/CD4+ Treg细胞的比值,干预前高于干预后,差异有统计学意义(P＜0.05).CD4+ Treg细胞/CD4+T细胞的比值,干预后高于干预前,差异有统计学意义(P＜0.05).血清中IL-10因子水平,干预后高于干预前,差异有统计学意义(P ＜0.05).结论 哮喘患者外周血中存在Th17/Treg细胞失衡,参麦注射液可以改善哮喘患者的Th17/Treg细胞失衡.     

急性冠状动脉综合征患者Th17细胞检测及意义

目的:探讨急性冠状动脉综合征患者外周血辅助性T细胞(T help,Th)17的水平及意义.方法:将85例患者分为4组:急性心肌梗死(AMI)组26例,不稳定型绞痛(UA)组17例,稳定型心绞痛(SA)组22例和胸痛综合征(CPS)组20例.采用流式细胞分析法,检测各组患者外周血Th17细胞占CD4 T细胞比例.应用酶联免疫吸附方法(ELISA)检测患者外周血血浆Th17相关细胞因子白细胞介素(IL)-17和IL-23的表达.结果:AMI组和UA组患者外周血Th17/CD4 T细胞比例分别为(2.3±1.3)%、(2.1±1.1)%,明显高于SA组(0.5±0.3)%和CPS组的(0.3±0.2)%(P＜0.01).AMI组和UA组患者IL-17和IL-23水平[IL-17:AMI组(72.3±50.2)ng/L、UA组(64.6±38.7)ng/L;IL-23:AMI组(615±254)ng/L,UA组(571±252)ng/L]亦明显高于SA组[IL-17;(24.2±15.3)ng/L,IL-23:(136±67)ng/L]和CPS组[IL-17:(20.8±13.3)ng/L,IL-23:(128±70)ng/L],P＜0.05;而SA组和CPS组间差异无统计学意义(P＞0.05).患者血浆IL-17水平与血浆IL-23水平呈正相关(r＝0.631,P＜0.01).结论:急性冠状动脉综合征患者外周血Th17细胞比例增加,IL-17、IL-23水平升高,Th17细胞可能参与动脉粥样斑块不稳定和急性冠状动脉综合征的发病.     

外周血TNF-α、Th17、Treg水平与COPD患者病情程度的关联性及临床意义

目的探讨外周血肿瘤坏死因子-α(TNF-α)、辅助性T细胞17(Th17)、调节性T细胞(Treg)水平与慢性阻塞性肺疾病(COPD)患者病情程度的关联性及临床意义。方法 COPD患者70例为观察组,另选同期健康体检者40例为对照组。均行外周血TNF-α、Th17、Treg检测。比较两组外周血TNF-α、Th17、Treg、Th17/Treg水平,并分析其与COPD病情程度相关性。结果经单因素方差分析,观察组外周血TNF-α、Th17、Treg、Th17/Treg水平与对照组比较,差异有统计学意义(P0.05);AECOPD患者外周血TNF-α、Th17、Th17/Treg水平高于COPD稳定期患者,Treg水平低于COPD稳定期患者(P0.05);COPD稳定期患者外周血TNF-α、Th17、Th17/Treg水平高于对照组,Treg水平低于对照组(P0.05);经Pearson检验,外周血TNF-α、Th17水平与COPD病情程度呈正相关(P0.05);Treg水平与COPD病情程度呈负相关(P0.05)。结论外周血TNF-α、Th17水平在COPD中异常升高,且随病情程度逐渐上升;Treg水平在COPD中异常下降,并随病情程度逐渐下降,有助于判断病情,为制定治疗方案提供依据,还可监测疗效及评估预后。     

调节性T细胞和辅助性T细胞17的平衡变化在慢性乙型肝炎病毒感染中的作用

目的 研究调节性T细胞(Treg)和辅助性T细胞17(Th17)的平衡变化在慢性HBV感染中的作用.方法 应用ELISA法和流式细胞术分别对34例慢性乙型肝炎(CHB)患者、20例HBV相关慢加急性肝功能衰竭(ACHBLF)患者和20例健康对照者外周血中Treg和Th17分化相关细胞因子及外周血Th17和Treg细胞水平进行检测.计数资料应用Fisher's确切概率法,计量资料应用单因素方差分析和Tukey's多重比较检验.结果 ACHBLF组Th17分化相关因子IL-1β为(3.97±2.85) pg/mL,IL-6为(12.75±8.87)pg/mL,IL-21为(360.0±335.7)pg/mL,比健康对照组的IL-1β[(1.87±0.94)pg/mL,q=4.559,P＜0.01)、IL-6[(5.28±o.72)pg/mL,q=7.309,P＜0.01)和IL-21[(46.68±20.17) pg/mL,q=6.946,P＜0.01)均明显上调.ACHBLF组外周血Th17细胞比例明显高于健康对照组(q=3.972,P＜0.05).与健康对照组和ACHBLF组相比,CHB组Treg细胞分化相关因子TGF-β明显升高(q=4.536、5.323,均P＜0.01),外周血Treg比例也明显升高.ACHBLF组Th17细胞效应因子IL-17A水平最高,ACHBLF患者外周血Th17细胞比例与血清TBil水平呈正相关(γ=0.74,P＜0.01).结论 慢性HBV感染中,宿主免疫存在Th17和Treg失衡,ACHBLF组以Th17细胞活动为主,CHB组以Treg细胞活动为主.     

慢性阻塞性肺疾病患者辅助性T细胞17/调节性T细胞变化及其与肺功能的相关性研究

目的观察慢性阻塞性肺疾病(COPD)患者辅助性T细胞17(Th17细胞)/调节性T细胞(Treg细胞)变化,探讨其与肺功能的相关性。方法选取2013年9月—2015年9月四川省成都市西区医院收治的老年COPD稳定期患者36例作为稳定期组,COPD急性加重期患者29例作为急性加重期组;另选取同期在本院体检健康者50例作为对照组,其中吸烟者22例作为吸烟对照组,不吸烟者28例作为正常对照组。比较4组受试者外周血Th17细胞分数、Treg细胞分数、Th17细胞/Treg细胞比值,血清IL-17、IL-10水平及肺功能指标〔第1秒用力呼气容积占预计值百分比(FEV1%)、用力肺活量占预计值百分比(FVC%)及第1秒用力呼气容积与用力肺活量比值(FEV1/FVC)〕,并分析外周血Th17细胞分数、Treg细胞分数及Th17细胞/Treg细胞比值与肺功能指标的相关性。结果急性加重期组和稳定期组患者外周血Th17细胞分数、Th17细胞/Treg细胞比值及血清IL-17水平高于吸烟对照组和正常对照组,外周血Treg细胞分数及血清IL-10水平低于吸烟对照组和正常对照组(P0.05);急性加重期组患者外周血Th17细胞分数、Th17细胞/Treg细胞比值及血清IL-17水平高于稳定期组,外周血Treg细胞分数及血清IL-10水平低于稳定期组(P0.05);吸烟对照组受试者外周血Th17细胞分数、Th17细胞/Treg细胞比值高于正常对照组(P0.05)。4组受试者FVC%比较,差异无统计学意义(P0.05);急性加重期组和稳定期组患者FEV1%、FEV1/FVC低于吸烟对照组和正常对照组,急性加重期组患者FEV1%、FEV1/FVC低于稳定期组(P0.05)。Pearson相关性分析结果显示,外周血Th17细胞分数与FEV1、FEV1%/FVC呈负相关(r值分别为-0.736、-0.694,P0.05),Th17/Treg细胞比值与FEV1、FVC%、FEV1%/FVC呈负相关(r值分别为-0.892、-0.222、-0.748,P0.01),而外周血Treg细胞分数与FEV1、FVC%、FEV1%/FVC呈正相关(r值分别为0.837、0.368、0.822,P0.01)。结论 COPD患者存在Th17/Treg细胞失衡,而Th17/Treg细胞失衡与吸烟、COPD病情变化及肺功能损伤等密切相关。     

抗结核治疗对肺结核患者Th17/Treg的影响

目的分析抗结核治疗前后肺结核患者外周血(CD3+CD4+IL-17+)辅助性T细胞17(Th17)和(CD4+CD25+Foxp3+)调节性T细胞(Treg)平衡状态的变化及其临床意义。方法收集本院2014年10月至2015年5月感染科收治的肺结核患者80例,选择30例健康体检者作为对照组。流式细胞术检测患者抗结核药物治疗前、治疗6个月以及对照组的外周血Th17细胞和Treg细胞的表达,ELISA检测外周血中IL-17A的表达。结果流式结果显示,治疗前肺结核患者外周血Th17细胞,Treg细胞表达率为分别为(1.18±0.74)%、(7.68±0.92)%,均明显低于健康体检者((3.95±1.17)%,(4.17±1.12)%,P0.05);治疗6个月后肺结核患者外周血Th17细胞,Treg细胞表达率分别为(2.98±1.42)%,(5.26±0.72)%,均明显高于治疗前、但仍显著低于健康体检者(P0.05)。治疗前肺结核患者Th17/Treg为0.15±0.21,明显低于健康体检者(0.95±0.45,P0.05);治疗6个月后肺结核患者Th17/Treg为0.56±0.39,明显高于治疗前、但仍显著低于健康体检者(P0.05)。ELISA检测结果显示,治疗6个月后肺结核患者外周血IL-17A表达水平为39.06±5.83 pg/m L,明显高于治疗前、但仍显著低于健康体检者(P0.05)。结论结核分枝杆菌可破坏肺结核患者机体Th17/Treg平衡,抗结核治疗可缓解患者外周血Th17/Treg失衡状态。     

抗病毒治疗对慢性丙型肝炎患者Treg/Th17细胞比例变化的影响

目的 了解抗病毒治疗对慢性丙型肝炎患者调节性T细胞(Treg) /Th17细胞比例变化的影响.方法 32例慢性丙型肝炎患者进行聚乙二醇干扰素α-2a联合利巴韦林治疗,20例健康人作为对照.在抗病毒治疗前和随访24周时,采用流式细胞仪检测患者外周血Treg和Th17细胞频率,ELISA法检测患者IL-17的水平,观察Treg/Th17细胞比例变化与患者获得持续性病毒学应答(SVR)的关系.统计学处理采用t检验.结果 抗病毒治疗前患者外周血中Th 17、Treg细胞频率和Treg/Th17比例明显高于对照组[(4.58±0.86)％与(2.48±0.60)％,t=2.399,P＜0.05;(8.58±2.20)％与(4.70±1.30)％,t=7.990,P＜0.01;(1.82±0.40)与(1.60±0.35),t=2.088,P＜0.05].抗病毒治疗后Th 17、Treg细胞频率和Treg/Th17比例分别为(5.35±0.79)％、(6.46±1.29)％、(1.25±0.21).获得SVR患者Th17细胞频率为(6.27±1.15)％,明显高于未获得SVR的(4.05±0.82)％(t=10.103,P＜0.01).获得SVR患者Treg细胞频率和Treg/Th17比例为(4.90±1.39)％、(0.80±0.15),明显低于未获得SVR的(7.42±1.95)％、(1.83±0.42)(t=5.718,8.752,P＜0.01).获得SVR患者IL-17水平为(143.5±31.2)pg/mL,明显高于未获得SVR患者组的(121.4±30.1 )pg/mL(t=2.028,P＜0.05).结论 慢性丙型肝炎患者Treg/Th 17细胞比例高于对照组,抗病毒治疗后Treg/Th17细胞比例下降,获得SVR患者下降更为明显.     

系统性红斑狼疮患者外周血白细胞介素-17与辅助T细胞17的检测及其意义

目的 研究系统性红斑狼疮(SLE)患者外周血白细胞介素(IL)-17蛋白和mRNA水平、辅助T细胞(Th17)细胞表达比例,探讨其临床意义.方法 用酶联免疫吸附试验检测SLE患者及对照者血浆中IL-17的蛋白水平;采用实时荧光定量反转录-聚合酶链式反应(RT-PCR)检测2组外周血中IL-17 mRNA表达水平;运用流式细胞术检测SLE患者外周血单个核细胞(PBMCs)中Th17细胞比例,进一步分析IL-17/Th17细胞与SLE临床实验室指标的相关性.计量资料组间比较采用t检验,相关性分析采用Spearman秩和相关分析.结果 SLE组患者血浆IL-17含量明显高于健康对照组,SLE组患者外周血IL-17 mRNA表达水平[(28.3±11.7)×10-5]高于对照组[(9.8±2.2)×10-5](P均＜0.01).SLE患者PBMCs中Th17细胞比例(2.5±1.5)%及IL-17荧光强度(1937±1022)显著高于对照组[(1.5±0.7)%,(1245±413)],且SLE活动期患者Th17细胞百分比高于非活动组,SLE肾病组Th17细胞比例较无肾病组明显升高(P均＜0.05).SLE患者血浆IL-17水平、Th17细胞数与SLE疾病活动性指数(SLEDAI)呈正相关(r=0.681,P＜0.01;r=0.426,P=0.034).结论 SLE患者体内IL-17蛋白分泌及基因表达水平存在明显异常,外周血Th17细胞比例亦显著升高,且与疾病活动性有明显相关,提示IL-17/Th17细胞可能在SLE发病中起着重要作用.     

Liver cell adenoma and liver cell adenomatosis

During the last three decades liver cell adenoma and liver cell adenomatosis have emerged as new clinical entities in hepato-logical practice due to the widespread use of oral contraceptives and increased imaging of the liver. On review of published series there is evidence that 10% of liver cell adenomas progress to hepatocellular carcinoma, diagnosis is best made by open or laparoscopic excision biopsy, and the preferred treatment modality is resection of the liver cell adenoma to prevent bleeding and malignant transformation. In liver cell adenomatosis, the association with oral contraceptive use is not as high as in solitary liver cell adenomas. The risk of malignant transformation is not increased compared with solitary liver cell adenomas. Treatment consists of close monitoring and imaging, resection of superficially located, large (>4 cm) or growing liver cell adenomas. Liver transplantation is the last resort in case of substantive concern about malignant transformation or for large, painful adenomas in liver cell adenomatosis after treatment attempts by liver resection.     

胆红素对肝星状细胞-T6增殖及细胞周期的影响

[目的]观察胆红素对肝星状细胞(HSC)-T6增殖及细胞周期影响.[方法]将培养细胞分成正常组和胆红素不同浓度(10 μmol/L、30 umol/L、50 /μmol/L、70 μmol/L、100 μmol/L)干预组,采用MTT法观察胆红素对HSC-T6增殖的影响,流式细胞仪观察各组细胞周期的变化.[结果]①不同浓度胆红素对HSC-T6均有促进增殖作用,且呈一定的量效关系,与正常组比较差异有统计学意义(P＜0.05);②10 μmol/L、50 μmol/L、100 μmol/L浓度胆红素作用HSC-T6后,G0/G1期减少,S期增加,G2/M期增加,与正常组比较均P＜0.05.[结论]胆红素对HSC-T6均有促进增殖作用.     

Actin filament debranching regulates cell polarity during cell migration and asymmetric cell division

The formation of the branched actin networks is essential for cell polarity, but it remains unclear how the debranching activity of actin filaments contributes to this process. Here, we showed that an evolutionarily conserved coronin family protein, the Caenorhabditis elegans POD-1, debranched the Arp2/3-nucleated actin filaments in vitro. By fluorescence live imaging analysis of the endogenous POD-1 protein, we found that POD-1 colocalized with Arp2/3 at the leading edge of the migrating C. elegans neuroblasts. Conditional mutations of POD-1 in neuroblasts caused aberrant actin assembly, disrupted cell polarity, and impaired cell migration. In C. elegans one-cell−stage embryos, POD-1 and Arp2/3, moved together during cell polarity establishment, and inhibition of POD-1 blocked Arp2/3 motility and affected the polarized cortical flow, leading to symmetric segregation of cell fate determinants. Together, these results indicate that F-actin debranching organizes actin network and cell polarity in migrating neuroblasts and asymmetrically dividing embryos.

Cell polarity is a fundamental feature of virtually all eukaryotic cells and plays crucial roles in a wide range of cellular processes, including cell motility, asymmetric cell division, and cell signaling (1). The establishment of cell polarity involves the asymmetric assembly of distinct cellular components to perform specialized functions. The actin-related protein (Arp) 2/3 complex-dependent branched actin networks and the pushing force they produce provide the principal means for cells to remodel the plasma membrane during cellular polarization (2). For example, in the leading edge of a migrating cell, the local Arp2/3-nucleated actin polymerization powers asymmetric projections of the plasma membrane (3). During asymmetric cell division of the Caenorhabditis elegans zygote, an actomyosin flow is central to the transport of the polarity PAR proteins into defined subcellular domains (4).Actin filaments'' continuous assembly must be balanced by actin depolymerization to ensure a constant supply of actin monomers for new growth. The Arp2/3 complex potency in actin nucleation empowers this complex as an essential regulator to organize the actin cytoskeleton. While Arp2/3 by itself is biochemically inactive, interactions with nucleation-promoting factors (NPFs) such as the Wiskott Aldrich syndrome protein (WASP)/WASP family verproline-homologous (WASP/WAVE) family proteins shift the Arp2/3 complex from its open, inactive conformation to a closed, active conformation (5, 6). The conformationally activated Arp2/3 complex then binds to the side of preexisting actin filaments to nucleate a branch from the mother filament (7–12). Conversely, nucleation by Arp2/3 can be inhibited by several binding partners, including glia maturation factor (GMF), Gadkin, Arpin, and Coronin, whose activities replenish available pools of actin monomers and Arp2/3 complexes for sustained actin assembly (13–18).The coronin family proteins are conserved actin regulators (19). The phylogenetic analysis grouped coronin genes into three types (19, 20). The best-characterized coronin is the Type I coronin (e.g., Coronin 1B) that binds to actin filaments through the β-propeller structure and to the Arp2/3 complex via its N terminus. These interactions block the docking of Arp2/3 onto actin filaments or facilitate debranching the existing actin network (20). Coronin 1B simultaneously interacts with the Slingshot phosphatase to dephosphorylate and activate ADF/Cofilin proteins that sever actin filaments, thereby promoting the actin network disassembly (13). Despite significant progress on Type I coronin, the activity and function of other coronins remain unclear. In particular, Type III coronins, known as POD-1 in C. elegans and Drosophila or Coronin7 in Dictyostelium and humans, contain two tandem coronin repeats, making them distinct from other coronins (19–21). POD-1 was biochemically isolated from C. elegans oocytes (22), and its mutations disrupted the polarity and architecture in early C. elegans embryos and impaired midlife touch sensitivity of the nematode (21, 23). However, it remains unclear how the Type III coronin functions. The Drosophila homolog of POD-1 is required for correct axon guidance, and the purified Dpod-1 cross-links the actin and microtubule cytoskeletons (24), whereas the mammalian Coronin7 was implicated in the Golgi morphology and function (25, 26), demonstrating the functional divergence of this family of coronin. Here, we show that the C. elegans POD-1 debranches Arp2/3-nucleated actin filaments in vitro and that POD-1 regulates cell polarity by remodeling the actin cytoskeleton during cell migration and asymmetric cell division.     

Measurement of adherent cell mass and growth

The characterization of physical properties of cells such as their mass and stiffness has been of great interest and can have profound implications in cell biology, tissue engineering, cancer, and disease research. For example, the direct dependence of cell growth rate on cell mass for individual adherent human cells can elucidate the mechanisms underlying cell cycle progression. Here we develop an array of micro-electro-mechanical systems (MEMS) resonant mass sensors that can be used to directly measure the biophysical properties, mass, and growth rate of single adherent cells. Unlike conventional cantilever mass sensors, our sensors retain a uniform mass sensitivity over the cell attachment surface. By measuring the frequency shift of the mass sensors with growing (soft) cells and fixed (stiff) cells, and through analytical modeling, we derive the Young's modulus of the unfixed cell and unravel the dependence of the cell mass measurement on cell stiffness. Finally, we grew individual cells on the mass sensors and measured their mass for 50+ hours. Our results demonstrate that adherent human colon epithelial cells have increased growth rates with a larger cell mass, and the average growth rate increases linearly with the cell mass, at 3.25%/hr. Our sensitive mass sensors with a position-independent mass sensitivity can be coupled with microscopy for simultaneous monitoring of cell growth and status, and provide an ideal method to study cell growth, cell cycle progression, differentiation, and apoptosis.     

Childhood CML in blastic stage: an analysis of cell markers and cell kinetics

The clinical course of Ph+CML and their terminal blastic stage is described in the following case histories. During blastic phase, cell surface markers, terminal deoxynucleotidyl transferase (TdT) activity, and flow cytometric measurements were used or determination of the blast cell phenotype which was undifferentiated by morphological and cytochemical criteria. A high proportion of blast cells expressed Fc receptors for IgG, TdT activity was normal in both children and RNA measurements of single cells flow cytometry showed a high RNA content in the majority of blasts. These findings are compatible with the phenotype seen in the myelomonocytic leukemias. Flow cytometry appears to be a useful adjunct to immunological methods and TdT activity for the rapid characterization of CML in blastic phase.     

回转器模拟失重对静脉内皮细胞形态、增殖和周期的影响

目的:探讨回转器模拟失重对人脐静脉内皮细胞(HUVECs)形态、增殖和周期的影响。方法: 以HUVECs为研究对象,采用回转器模拟失重,在倒置显微镜下观察模拟失重后细胞形态的变化,用细胞计数法测定细胞的增殖情况,用流式细胞仪(FCM)测定细胞周期。结果: 模拟失重后,HUVECs多呈圆形,可见细胞重叠或聚集生长。回转器模拟失重后12 h、24 h和36 h,细胞周期明显阻滞在G0+G1期（P<0.05）,而细胞计数则无明显改变。结论: 模拟失重可使HUVECs的形态发生一定改变,使HUVECs的细胞周期阻滞。     

Efficacy of high-dose therapy and hematopoietic stem cell transplantation for mantle cell lymphoma

Conventional treatment of mantle cell lymphoma (MCL) yields modest responses and short remissions. We report 30 hematopoietic stem cell transplants (HSCT) for MCL: 13 autologous, 10 allogeneic myeloablative, and 7 nonablative. After a median 1.2 years from diagnosis (range 0.5 to 4.7) and a median of 2 pre-HSCT chemotherapeutic regimens (range 1 to 5), their median age at HSCT was 52 years (range 37 to 67). Eleven patients (41%) were in first remission, 11 (41%) were in second remission, and 7 (25%) had resistant disease. Four died early. Nineteen achieved CR (83%) and 4 PR (17%). With median 2.7 years of follow-up, 5-year overall survival (OS) was 42% (95% CI 11-73%) after autologous versus allogeneic at 49% (95% CI 22-76%). Five-year progression-free survival (PFS) was 31% (95% CI 3-59%) and 50% (95% CI 24-76%) for autologous and allogeneic HSCT, respectively. Fourteen died: 3 from sepsis, 1 acute GVHD, 10 MCL. No autologous transplant-related deaths occurred. Allogeneic transplant-related mortality was 29% (95% CI 6-52%) at 1 and 5 years. HSCT for MCL can yield extended disease control and long-term survival.     

COVID-19 outcomes in sickle cell disease and sickle cell trait

Throughout the Coronavirus Disease 2019 (COVID-19) pandemic, understanding the effects of COVID-19 on persons with Sickle Cell Disease (SCD) and Sickle Cell Trait (SCT) has garnered interest. Patients with SCD diagnosed with COVID-19 utilize the emergency department and are hospitalized at significantly higher rates compared to the general population, with vaso-occlusive crisis and acute chest syndrome as the leading presentations. Whether SCD alone increases the likelihood of severe COVID-19 illness remains uncertain; however, potential risk factors for severe disease among patients with SCD include older age, frequent acute care visits for pain, haemoglobin SC disease, and pre-existing end-organ disease. SCT status may also influence COVID-19 outcomes, particularly among those with pre-existing co-morbidities. Corticosteroids in patients with SCD and COVID-19 should be used with extreme caution given strong associations between corticosteroid exposure and severe vaso-occlusive crisis, with prophylactic transfusion administered if corticosteroids are deemed necessary. Hydroxyurea may be protective in COVID-19.     

Establishment and characterization of four new squamous cell carcinoma cell lines derived from oral tumors

Summary Four cell lines were established from squamous cell carcinomas (SCC) of the oral cavity. Cell lines AW 13516 and AW 8507 were derived from poorly differentiated SCC and epidermoid carcinoma of the tongue respectively. Cell line AW 10498 was derived from moderately differentiated SCC of the lower alveolus, and AW 9803 grew from a well-differentiated SCC of a retromolar trigone. The cultures showed typical epithelial cell morphology, numerous mitotic figures, occasional multinucleated giant cells, individual cell diskeratosis and nuclear and nucleolar abnormalities. The cell lines AW 13516 and AW 8507 were fast growers with a doubling time of 35.5 h and 31.9 h, respectively, which was independent of the initial seeding density. Cell lines AW 10498 (doubling time 52.2 h) and AW 9803 (doubling time 66 h) showed slower growth and had shorter doubling times at higher seeding densities. The presence of cytokeratins was detected in all the four cell lines by using polyclonal antikeratin antisera in indirect immunofluorescence and in Western blotting. None of the cell lines expressed major histocompatibility complex (MHC) class II antigens. MHC class I antigens were expressed by three cell lines but not by AW 9803. Flow cytometric analysis of DNA content and chromosomal studies suggested the presence of polyploidy and aneuploidy in all the four cell lines. Ultrastructural studies revealed typical epithelial cell features, such as the presence of desmosomes, tonofilaments and keratin bundles.Abbreviations SCC squamous cell carcinoma - PBS phosphatebuffered saline - MHC major histocompatibility complex