阵发性睡眠性血红蛋白尿症异常克隆特征研究

阵发性睡眠性血红蛋白尿症(PNH)是一类源于造血干细胞PIGA基因突变的获得性克隆性疾病,临床表现主要为溶血、骨髓衰竭等。该文通过流式细胞术和体外集落形成等实验检测比较经典型PNH(cPNH)患者与健康对照组外周血细胞、骨髓中血细胞及造血干祖细胞(hemopoietic stem progenitor cells,HSPCs)的数量和功能,探究PNH异常克隆特征。结果显示,cPNH患者外周血细胞中T细胞、B细胞和NK细胞数明显降低,髓系细胞数无明显改变。骨髓各类血细胞中,cPNH患者单核细胞比例明显高于对照组,中性粒细胞、有核红细胞以及淋系细胞比例无明显改变。cPNH患者骨髓HSPCs均为CD59~–的PNH异常克隆;患者HSPCs出现大量耗竭,向B-NK祖细胞分化明显受阻,该结果与外周血和骨髓中B、NK细胞变化一致,提示cPNH患者淋系细胞受损最为严重。CFU实验结果表明,cPNH患者HSPCs形成髓系克隆的能力与健康对照组无差异;而在红系克隆种类中,cPNH患者形成的偏小的红系克隆代偿性增多。综上,该研究解析了PNH异常克隆的生物学特征,为PNH的诊治提供了一定的理论依据。     

大口黑鲈外周血细胞显微结构、细胞化学特征及吞噬作用的研究

通过对大口黑鲈外周血细胞的显微结构及细胞化学染色特征和吞噬作用的研究,为大口黑鲈免疫学研究积累资料。Wright's染色表明:大口黑鲈外周血细胞分为红细胞、粒细胞、单核细胞、淋巴细胞和血栓细胞,其中粒细胞又分为Ⅰ型、Ⅱ型和Ⅲ型。外周血中成熟红细胞最多,占血细胞总数的98.12%,其次为淋巴细胞和血栓细胞,占白细胞中的比例分别为60.92%和22.99%;单核细胞最大,大小为(9.89±0.70)μm×(8.72±0.68)μm;小淋巴细胞最小,大小为(3.88±0.46)μm×(3.48±0.40)μm。大口黑鲈外周血细胞的免疫相关酶ACP、AKP、PO、POX及细胞成分PAS反应、SBB染色的结果表明,所有红细胞的细胞化学染色均呈阴性,不同白细胞的细胞化学染色特征存在差异。其中所有白细胞的AKP、POX染色均呈阴性,PAS反应均呈阳性,除Ⅱ型粒细胞外所有白细胞的PO、ACP染色均呈阳性,除单核细胞外所有白细胞的SBB染色均呈阳性。大口黑鲈外周血细胞吞噬酵母菌的实验表明,红细胞能够吞噬酵母菌,其吞噬率为(15.70±1.07)%,也观察到部分白细胞吞噬酵母的现象。PO和ACP及脂类和糖类可能是大口黑鲈外周血细胞吞噬作用的重要酶类和能量来源。     

史氏鲟外周血细胞的显微及超微结构

采用血细胞计数、光学显微及电子显微技术对二龄史氏鲟外周血细胞的数目、形态及结构进行了研究。二龄史氏鲟红细胞的数目为47.75×104个/mm3,白细胞数目为2.9万个/mm3,其中淋巴细胞所占比率最高。史氏鲟的外周血中除正常红细胞外,还有处于分裂状态及未成熟的红细胞。史氏鲟外周血中的白细胞有四种类型,分别为淋巴细胞、粒细胞、血栓细胞和单核细胞。其中粒细胞有两种,即嗜中性粒细胞和嗜酸性粒细胞。嗜中性粒细胞含有多种形状的核,其中分叶的核数目较多,粒细胞及淋巴细胞均类似于哺乳动物。对史氏鲟外周血细胞细微结构的观察显示:红细胞中具有少量的细胞器;淋巴细胞结构典型;单核细胞较粒细胞稍小且具有较多线粒体;血栓细胞具有梭形和圆形两种,胞质较少,其中梭形的血栓细胞胞质几乎透明;对粒细胞的颗粒按照形状和电子密度进行了分类。     

乌龟外周血细胞的显微和超微结构

乌龟血细胞的显微和超微结构研究表明;在外周血细胞中,可分辨出红细胞、单核细胞、淋巴细胞、血栓细胞、嗜酸性粒细胞、嗜碱性粒细胞、嗜中性粒细胞等7种细胞.红细胞核圆形,胞质均匀无细胞器.单核细胞的特征是核内异染色质多聚集于周边,胞质中含有许多囊泡.淋巴细胞的核质比例大.血栓细胞以具细长的指状突起,基本无细胞器为其特征.嗜酸性粒细胞仅含一种圆形颗粒,颗粒质地均匀,电子致密,大小不等.嗜碱性粒细胞颗粒环绕在胞核周围,有三种电子密度、颗粒大小不一的类型.嗜中性粒细胞含有两种电子密度、形态不一的颗粒.       

北部湾棱皮树蛙外周血细胞显微结构观察

本文以人们极少关注的两栖动物北部湾棱皮树蛙(Thelodermacorticale)为研究对象,采用瑞氏-姬姆萨混合染色法与血细胞计数法观察并统计了北部湾棱皮树蛙外周血细胞的形态特征和数量比例。结果显示,北部湾棱皮树蛙的外周血由红细胞、嗜中性粒细胞、嗜碱性粒细胞、嗜酸性粒细胞、淋巴细胞(包括大、小淋巴细胞)和单核细胞、血栓细胞7种细胞组成。其中,红细胞的数量最多,平均含量为2.43×10⁵个/mm³,多呈椭圆形或卵圆形,少数呈泪滴形、梨形、逗号形、梭形,具椭圆或圆形核,核染色质密集,偶尔可观察到正在进行直接分裂或有丝分裂的红细胞。白细胞的数量比红细胞少,平均含量为1.74×10⁴个/mm³,其中,小淋巴细胞占40.02%±1.77%、大淋巴细胞占10.83%±2.53%、单核细胞占23.17%±3.16%、嗜中性粒细胞占10.08%±4.62%、嗜碱性粒细胞占9.25%±2.69%、嗜酸性粒细胞占6.72%±1.50%。血栓细胞呈纺锤形和梭形,常单独存在,或者呈圆形和不规则圆形,数个集合在一起。     

CXCR1和CXCR2在系统性红斑狼疮中的表达及意义

目的:检测白介素-8受体CXCR1和CXCR2在系统性红斑狼疮(SLE)患者外周血CD14+单核细胞上的表达,探讨其与SLE疾病活动的相关性和可能涉及的SLE炎症发病机制.方法:36例活动期SLE患者和34例健康志愿者,采用流式细胞术(FCM)检测CXCR1、CXCR2在SLE患者和健康志愿者外周血CD14+单核细胞上的MFI表达.结果:CXCR2在SLE组外周血CD14+单核细胞上MFI表达(195.75±52.76)与对照组(298.82±51.86)相比明显降低(P＜0.01);CXCR2在SLE患者外周血CD14+单核细胞上MFI表达下降与C3存在着正相关关系(rs=0.421,P=0.022),与dsDNA、SLEDAI存在着负相关关系(分别为rs=-0.390,P=0.032;rs=-0.463,P=0.011).结论:SLE患者外周血CD14+单核细胞CXCR2的表达异常,提示CXCR2可能参与了SLE的发病过程.检测SLE患者外周血CD14+单核细胞的CXCR2表达水平,可能是评价SLE疾病活动性有价值的潜在的生物学标志之一.     

中性粒细胞CD64指数、PCT及NLR在感染性疾病诊断中的价值

目的 探讨中性粒细胞CD64指数、降钙素原（PCT）和中性粒细胞与淋巴细胞比值（NLR）在感染性疾病诊断和鉴别诊断中的临床价值。方法 选取确诊的感染性疾病患者127例和同期健康对照者54例为研究对象,感染性疾病患者按照血培养和微生物检测结果分为病毒感染组（51例）和细菌感染组（76例）。分别检测每一位受试对象的外周血中性粒细胞CD64指数、PCT水平和NLR,应用受试者工作特征曲线（ROC）研究这3项指标在感染性疾病诊断和鉴别中的临床价值。结果 感染性疾病患者中性粒细胞CD64指数、PCT水平和NLR明显高于健康对照组（P<0.01）。细菌感染组患者中性粒细胞CD64指数、PCT水平和NLR明显高于病毒感染组（P<0.01）。ROC曲线显示：当用于诊断感染性疾病时,中性粒细胞CD64指数、PCT和NLR的AUC值分别为0.799、0.655、0.622,灵敏度分别为75.4%、63.5%、60.3%,特异度分别为79.6%、67.4%、60.0%,3项指标联合检测的AUC值为0.812;当用于鉴别诊断细菌感染和病毒感染时,中性粒细胞CD64指数、PCT和NLR的AUC值分别为0.931、0.728、0.551,灵敏度分别为89.1%、70.3%、60.9%,特异度分别为80.0%、64.6%、57.2%,3项指标联合检测的AUC值为0.935。结论 在感染性疾病的诊断和鉴别感染类型中,中性粒细胞CD64指数明显优于PCT和NLR。3项指标联合检测优于任何一个单项指标的检测效果。     

湘华鲮外周血细胞形态特征及嗜中性粒细胞吞噬与杀菌能力

采用血涂片、显微测量、血细胞计数及嗜中性粒细胞吞噬功能和氯化硝基四氮唑蓝还原试验方法,于光学显微镜下观察分析三种水体湘华鲮(Sinilabeo decorus tungting)外周血细胞形态结构、大小、种类及数量。结果表明,湘华鲮外周血细胞中有红细胞、血栓细胞、粒细胞、淋巴细胞和单核细胞,红细胞比例最高,达80%以上,白细胞中血栓细胞最多,占70%～74%。大水面网箱养殖的湘华鲮外周血红细胞数量显著低于水泥池和土池养殖个体(0.01

0.05),但水泥池湘华鲮嗜中性粒细胞的吞噬与杀菌能力较其他两种养殖方式显著下降(0.01

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CD44~+/CD24~-和CK5/6在乳腺浸润性导管癌、乳腺普通型导管增生和低级别导管原位癌中的表达

目的探讨乳腺浸润性导管癌、普通型导管增生和低级别导管原位癌组织中CD44~+/CD24~-和CK5/6的表达和意义。方法采用免疫组织化学染色检测30例乳腺浸润性导管癌中CD44~+/CD24~-、CK5/6和P63的表达、30例乳腺普通型导管增生组织中CD44~+/CD24~-、CK5/6、34βE12和CK8的表达和30例低级别导管原位癌中CD44~+/CD24~-、CK5/6的表达。结果 30例乳腺浸润性导管癌中24例呈CD44~+/CD24~-,30例普通型导管增生中9例呈CD44~+/CD24~-和30例低级别导管原位癌中19例呈CD44~+/CD24~-,3组相比具有统计学意义。浸润性导管癌中CD44~+/CD24~-表型与患者的年龄、月经状况、肿瘤大小、淋巴结转移、组织学分级、ER、PR和HER~-2无相关性。30例乳腺浸润性导管癌中6例表达CK5/6,30例乳腺普通型导管增生中全部表达CK5/6,30例低级别导管原位癌中8例表达CK5/6,3组相比具有统计学意义。结论 CD44~+/CD24~-和CK5/6联合使用可用于鉴别乳腺浸润性导管癌、普通型导管增生和低级别导管原位癌。     

玳瑁和绿海龟幼体外周血细胞的观察与比较

对玳瑁(Eretmochelys imbricata)和绿海龟(Chelonia mydas)外周血细胞形态特征及其数量进行了观察、测定与比较.结果表明,在2种海龟外周血都观察到7种血细胞:红细胞、淋巴细胞、单核细胞、嗜中性粒细胞、嗜酸性粒细胞、嗜碱性粒细胞和血栓细胞,除了绿海龟观察到大、小2种嗜酸性粒细胞外,另外几种血细胞的形态结构与其他爬行动物相似.白细胞分类计数表明,2种海龟白细胞中以嗜中性粒细胞数量最多,其次是淋巴细胞和单核细胞,嗜酸性粒细胞仅有少数,嗜碱性粒细胞极少,并且此类细胞在玳瑁的白细胞分类计数中为零.玳瑁红细胞数量为(346.7±68.4)×10~3个/μl,比绿海龟红细胞含量少,绿海龟为(403.3±170.6)×10~3/μl;玳瑁白细胞及血栓细胞数分别为(7.7±1.9)×10~3个/μl和(9.6±2.2)×10~3个/μl,绿海龟分别为(7.3±2.8)×10~3个/μl和(7.5±3.7) ×10~3个/μl.     

Flow cytometric analysis of glycosylphosphatidyl-inositol-anchored proteins to assess paroxysmal nocturnal hemoglobinuria clone size

Paroxysmal nocturnal hemoglobinuria (PNH) is characterized by total or partial deficiency of membrane proteins anchored to the cell surface through a glycosylphosphatidyl-inositol (GPI) moiety. The relationship between the size of the PNH clone, determined by the expression of GPI-anchored proteins (AP; CD14, CD48, CD55, CD59, and CD66b) on erythrocytes, lymphocytes, monocytes, and granulocytes using forward and side scatter analysis, and severity of the disease was evaluated in 19 PNH patients. CD55 antigen expression did not delineate abnormal erythrocytes as well as did anti-CD59.The proportion of monocytes deficient in CD55, CD59, CD48, and CD14 (48-97%) and of granulocytes deficient in CD55, CD59, and CD66b (60-99%) was greater than the proportion of erythrocytes deficient in CD59 (24-95%) and the proportion of lymphocytes deficient in CD55 and CD59 (30-98%). There were no significant correlations among reticulocyte, leukocyte, and platelet counts and GPI-AP-deficient immunophenotypes in red and white blood cells. However, high coefficients of determination were seen between hemoglobin levels and granulocytes deficient in CD59 (r(2) = 0.76), CD55 (r(2) = 0.74), and CD66b (r(2) = 0.74) antigens and between hemoglobin and monocytes deficient in CD55 (r(2) = 0.73), CD59 (r(2) = 0.80), and CD14 (r(2) = 0.75) antigens. These results are interpreted as indicating that the size of PNH clone is better assessed by immunophenotypic analysis of monocytes and granulocytes rather than of lymphocytes and erythrocytes.     

Analysis of PI (phosphatidylinositol)-anchoring antigens in a patient of paroxysmal nocturnal hemoglobinuria (PNH) reveals deficiency of 1F5 antigen (CD59), a new complement-regulatory factor.

FACS analysis together with PIPLC treatment was applied to PI-anchoring antigens such as DAF (decay-accerelating factor, CD55), 1F5 antigen (CD59), CD14 and CD16 on the cell surfaces of blood cells from a normal adult and a male patient with paroxysmal nocturnal hemoglubinuria (PNH). Through the extensive analysis, this patient proved to be completely defective in 1F5 antigen, a newly found complement-regulatory protein, on all the blood cells tested. In normal blood cells such as lymphocytes, monocytes and granulocytes, 1F5 antigen was expressed as one of PI-anchoring proteins. In contrast to most of PNH patients, this patient reserved DAF, CD14 and CD16 at normal levels in his erythrocytes, monocytes and granulocytes. Also, there were no significant differences between the normal adult and the patient in the activities of erythrocyte acetylcholinesterase and granulocyte alkaline phosphatase which were also known to be PI-anchoring enzymes. Thus, deficiency of 1F5 antigen must be deeply related to the clinical symptoms of PNH in this patient.     

Flow cytometric analysis of CD55 and CD59 expression on blood cells in paroxysmal nocturnal haemoglobinuria

PNH is a rare clonal disorder of hematopoietic stem cells, therefore all blood cells lineages are involved. The main feature is an increased sensitivity of erythrocytes to complement-mediated cell lysis due to deficiency of membrane-bound GPI (glycosylphosphatidylinositol)-anchored proteins which normally function as inhibitors of reactive hemolysis. In the present study, we performed flow cytometric analysis using monoclonal antibodies against CD55 and CD59 for the detection of PNH-type clone in the blood of 50 patients (28 females and 22 males, age range 7-67 yrs). In one patient only we found a large population (95%) of granulocytes with decreased expression of both CD55 and CD59 molecules (type I PNH) and in two others with partial loss of CD55 expression (type II PNH). The expression was determined chiefly on granulocytes which in the control group showed reliable and high expression of CD55 and CD59.     

Aurin Tricarboxylic Acid Protects against Red Blood Cell Hemolysis in Patients with Paroxysmal Nocturnal Hemoglobinemia

Objectives

Paroxysmal nocturnal hemoglobinemia (PNH) is a rare but serious condition characterized by complement-mediated red blood cell (RBC) hemolysis and episodic thrombotic attack. It results from decay accelerating factor (CD55), and protectin (CD59), becoming attached to RBC and other cell surfaces. Absence of these protective proteins leaves such cells vulnerable to self attack at the C3 convertase and membrane attack complex (MAC) stages of complement activation. We have previously reported that aurin tricarboxylic acid (ATA) is an orally effective agent that selectively blocks complement activation at the C3 convertase stage as well as MAC formation at the C9 insertion stage.

Design and Methods

We used a CH50 assay method and western blot analysis to investigate the vulnerability to complement attack of PNH RBCs compared with normal RBCs. Zymosan was used as the activator of normal serum and PNH serum. ATA was added to the sera to determine the concentration necessary to protect the RBCs from lysis by the zymosan-activated sera.

Results

We found that erythrocytes from PNH patients on long term treatment with eculizumab were twice as vulnerable as normal erythrocytes to lysis induced by complement activated serum. Western blot data showed the presence of both C3 and C5 convertases on the PNH patient erythrocyte membranes. These data indicate persistent vulnerability of PNH erythrocytes to complement attack due to deficiencies in CD55 and CD59. ATA, when added to serum in vitro, protected PNH erythrocytes from complement attack, restoring their resistance to that of normal erythrocytes.

Conclusions

We conclude that ATA, by protecting PNH erythrocytes from their decay accelerating factor (CD55) and protectin (CD59) deficiencies, may be an effective oral treatment in this disorder.     

成人t(8;21)急性髓系白血病患者初诊Ki-67的表达特征及预后意义

目的:研究成人t(8; 21)急性髓系白血病(AML)初诊Ki-67抗原的表达特征及预后意义。方法:采集2012年7月至2019年2月本院57例成人初诊t(8; 21) AML患者的新鲜骨髓标本,采用流式细胞术(FCM)检测CD34和Ki-67抗原,分析Ki-67表达与患者初诊生物学特征、疗效及复发的关系。结果:全部患者中,CD34~+Ki-67~+细胞比例的中位值为30. 5%(范围:10. 0%～65. 8%);通过受试者工作特征(ROC)曲线确定CD34~+Ki-67~+细胞比例的最适分界阈值,CD34~+Ki-67~+细胞高比例与初诊c-KIT基因突变阳性及WT1转录本低水平均明显相关(P=0. 001; P=0. 042)。随访的36例患者中,CD34~+Ki-67~+高比例比低比例患者具有明显更高的1年累积复发(CIR)率(P=0. 035);此外,初诊WT1转录本低水平和微小残留病(MRD)高水平(2个疗程巩固治疗后RUNX1-RUNX1T1转录本水平下降3-log)均与更高的1年CIR率明显相关(P 0. 0001;P=0. 041),初诊c-KIT基因突变阳性和白细胞计数 10×109/L的患者分别有较高的1年CIR率趋势(P=0. 091; P=0. 054)。联合分组显示,MRD高水平同时CD34~+Ki-67~+细胞高比例的患者比其他患者具有明显更高的1年CIR率(P 0. 0001)。结论:初诊骨髓高比例的CD34~+Ki-67~+可能是成人t(8; 21) AML患者预后不良因素,MRD联合初诊CD34~+Ki-67~+细胞比例可能比单纯MRD更好地预测复发。     

H19, a surface membrane molecule involved in T-cell activation, inhibits channel formation by human complement.

Here we compare the properties of leukocyte antigens H19 and CD59 with those of the PI-linked 18,000-20,000 Mr molecules which inhibit lysis of human cells by the autologous terminal complement components C5b-9. H19, a 19,000 Mr protein found on human erythrocytes, monocytes, neutrophils, T-lymphocytes and other cells, is one of the ligands involved in the spontaneous rosette formation between human T-lymphocytes and erythrocytes. Recent evidence indicates that H19 also participates in T-cell activation. CD59 is a widely distributed 18,000-25,000 Mr protein anchored to the cell membrane by phosphatidylinositol (PI). The function of CD59 is unknown. Affinity-purified H19 incorporates into cell membranes and inhibits channel formation by human C5b-9 on guinea pig erythrocytes. Significant inhibition is achieved with picogram quantities of H19, corresponding to approximately 600 molecules per erythrocyte. H19 is most effective when C9 is limiting but quite active when C5b-7 or C8 are limiting, indicating that it may interact with several of the structurally related terminal complement components. The inhibitory activity is blocked by mAbs to either CD59 or to H19. H19 is PI-anchored: it is released from the cell membrane by treatment with PI-specific phospholipase C, and it is absent from cells from a patient with paroxysmal nocturnal hemoglobinuria (PNH). Analysis of PNH erythrocytes after treatment with terminal complement proteins shows that the H19-negative erythrocytes are more susceptible to C5b-9-mediated lysis. Treatment of normal human erythrocytes with either anti-H19 or anti-CD59 renders them more susceptible to lysis by human C5b-9. We conclude that H19 and CD59 are probably the same molecule and are identical or closely related to the recently described inhibitors of C5b-9 channel formation.     

CD11c在慢性淋巴细胞白血病诊断中的意义

目的:探讨CD11c抗原在慢性淋巴细胞白血病(chronic lymphocytic leukemia,CLL)中的表达及在临床诊断中的价值,以及CD11c抗原表达与患者的遗传学异常及预后参数的相关性。方法:采用多参数流式细胞术(flow cytometry,FCM)检测200例CLL患者、49例套细胞淋巴瘤(mantle cell lymphoma,MCL)患者CD11c的表达率和平均荧光强度(mean fluorescence intensity,MFI);并比较CLL患者CD11c的表达与预后参数ZAP-70和CD38表达的关系;同时采用荧光原位杂交(fluorescence in situ hybridization,FISH)技术检测CLL患者的P53缺失、13q14缺失、ATM缺失、6q23缺失、+12以及IGH重排,比较CD11c~+CLL患者与CD11c~-CLL患者遗传学特点。结果:CLL患者中CD11c阳性率为49.5%(99/200),MFI中位值为2.06(1.00～7.34);而MCL患者中CD11c阳性率为6.12%(3/49),MFI中位值为2.00(1.97～2.54)。CD11c在CLL中的表达率明显高于MCL,(x~2=30.62,P0.05)。CD11c~+CLL患者的ZAP-70和CD38阳性率均明显高于CD11c~-CLL患者(x~2=15.472,P0.05;x~2=11.556,P0.05),差异有统计学意义。而CLL患者的CD11c表达率与P53缺失、13q14缺失、ATM缺失、6q23缺失、+12、IGH重排的结果均无统计学差异。结论:CD11c对于辅助诊断CLL有重要价值,尤其有助于CLL和MCL的诊断和鉴别诊断。     

自噬抑制肿瘤坏死因子α诱导人胎盘胎儿来源间充质干细胞发生凋亡

目的:探讨TNF-α诱导人胎盘胎儿来源间充质干细胞(hfPMSCs)发生凋亡和自噬的作用,以及自噬对细胞凋亡的调控作用。方法:利用流式细胞术检测无血清培养hfPMSCs中CD73、CD90、CD105、CD14、CD34、CD45的表达;用终浓度20μg/L的TNF-α处理hfPMSCs 24h,以未处理细胞作为对照组。Annexin V/PI双染色检测TNF-α对hfPMSCs凋亡程度的影响;分别提取各组总蛋白,Western blot检测自噬标志基因LC3Ⅰ/Ⅱ的表达;利用mRFP-GFP-LC3腺病毒感染细胞,观察胞内点状聚集形成的情况;利用Atg5干扰慢病毒(si-Atg5)及阴性对照慢病毒(si-NC)感染hfPMSCs,Annexin V/PI双染色检测TNF-α对慢病毒感染后hfPMSCs凋亡程度的影响。结果:所培养细胞具有典型的MSCs形态,呈CD73~+CD90~+CD105~+/CD14~-CD34~-CD45~-细胞; Annexin V/PI染色结果显示,TNF-α作用24 h后,hfPMSCs凋亡数和凋亡率均高于对照组(P 0. 05);Western blot检测自噬标志蛋白表达结果表明,TNF-α可增加LC3Ⅱ的表达(P 0. 05);荧光共聚焦显微境观察到TNF-α可显著提高细胞中的点状聚集。利用si-Atg5感染细胞,抑制hfPMSCs自噬的发生,与对照慢病毒si-NC感染细胞比较,可显著促进TNF-α诱导hfPMSCs凋亡的发生(P 0. 05)。结论:TNF-α诱导的自噬抑制人胎盘胎儿来源MSCs凋亡的发生,具有一定的保护性作用。     

长薄鳅外周血细胞的显微结构和细胞化学特征研究

长薄鳅外周血细胞可分为红细胞、中性粒细胞、单核细胞、淋巴细胞和血栓细胞.在数量上,中性粒细胞、单核细胞、淋巴细胞和血栓细胞占白细胞总数的百分比分别是17.06%、5.83%、28.16%和48.94%.细胞化学染色显示所有白细胞均含有糖原物质,所有红细胞均不含酸性磷酸酶,中性粒细胞、单核细胞、淋巴细胞和血栓细胞均含有酸性磷酸酶.非特异件酯酶染色显示单核细胞呈阳性反应,中性粒细胞、淋巴细胞和血栓细胞均为部分呈阳性反应.所有细胞的碱性磷酸酶、过氧化物酶、苏丹黑显色反应均呈阴性.