Therapeutic applications of bone marrow-derived stem cells in liver transplantation for end-stage liver diseases

Today, liver transplantation (LT) is the only established treatment for end-stage liver diseases. The de- velopment of LT, including OLT, cadaveric LT, split LT, living donor LT (LDLT), brings hopes to patients with these diseases. However, increasing donor shortage, rejection and life-long immunosuppression with its side effects are the major limitations of this therapy strategy. Bone marrow-derived stem cells (BMDSCs) are capable of differentiating into hepatocyte-like cells and contribute to liver injury repair. The microenvironment of liver injury caused by rejection, ischemia/reperfusion, loss of liver mass, recurrence of HCV and "small-for-size syndrome" after LT can attract a variety of bone marrow-derived stem cell population to the peripheral circulation and then migration to the injury liver to promote the hepatic function restoration. Additionally, BMDSCs can also take part in the functional regeneration of living donor liver after LDLT. This participation in liver regeneration may be associated to the interac- tion between SDF-1and its receptor CXCR4, involving HGF, IL-8, MMP9, and VEGF/VEGFR-2. BMDSC with its bio-characteristics could maintain the allograft tolerance from different angles and in different ways. In conclusion, BMDSCs transplantation, as a new assistant therapeutic method for LT, will ex- pand the space of LT, and provide more survival opportunities for the patients suffering liver diseases in the future.     

骨髓干细胞的可塑性及其在栓塞性疾病中的应用

栓塞性血管阻塞在急性心肌梗死、脑梗塞、血栓闭塞性脉管炎、糖尿病足等发病过程中起着重要作用。目前临床上针对这些疾病的治疗手段主要有：药物溶栓、血管旁路移植和介入手术等,多年来其治疗方法无实质性进展。上个世纪九十年代人们发现了干细胞新的生物学特性—可塑性,对干细胞可塑性的研究以及相关技术的发展为心脏病、老年痴呆、帕金森等的治疗带来了希望,也为栓塞性疾病的治疗开辟了新途径,有望成为治疗手段之一。     

骨髓干细胞与急性心肌梗死的血管新生

骨髓干细胞可分化为心肌细胞、血管内皮细胞、平滑肌细胞等，能再生心肌和血管，可用于心肌梗死的治疗。本文就骨髓干细胞在血管新生方面的生物学特性及其对心梗后的血管新生作用作一综述。     

Inhibitory effect of the adenovirus type 5 E1A protein expressed in the yeast system of the human tumor cell growth

Adenovirus 5 type E1A as a tumor suppressor gene can inhibit tumor growth and enhance the censitivity of chemotherapy and radiotherapy.E1A have the ability to integrate into the host genome,resulting in long-time expres-sion that induces Rb gene inactivation and animal cells im-mortalization.This prompted us to select the E1A protein for treatment of cancer in order to overcome the limitations of E1A gene therapy.Thus,we firstly comstructed E1A eu-caryotic expression vector (pPIC9/E1A),transformated the pichia pastoris yeast cells(GS115) and screened the high-expressing recombinant strains.The positive yeast strains were cultured in the shake flask,and induced for 3d.The crude E1A protein was purified using two steps of col-umu chromatography on HiTrap Q and HiTrap SP.The pu-rified E1A protein was identified by SDS-PAGE and Western blot.E1A protein was mostly located at cellular unclear when Cheriot delivered E1A protein into cells.The analysis in vitro indicated that the E1A protein arrested LN686 cell cycle at G2/M phase,and significantly inhibited the growth of LN686 tumor cells.The current studies firstly provided an experimental basis to further develop E1A protein for tumor treatment.     

密度梯度离心法检测脱落肿瘤细胞对恶性胸腔积液的诊断价值

胸腔积液是临床常见征象，其良恶性质的临别是临床上尚未解决的难题之一。本试验对３６例恶性胸腔，３０例结核性胸腔积液分别用密度梯度离心法，常规离心涂片法检测脱落肿瘤细胞，并对其中２２例恶性胸液患者行胸膜活组织检查。     

虫草菌提取物对HL-60细胞的抑制作用及G2/M期阻滞的诱导

对人工培养的虫草菌菌丝体提取物进行了体外抗肿瘤活性及其作用机理的研究．依次用石油醚、乙酸乙酯、乙醇和水提取人工培养的虫草菌菌丝体，分别得到石油醚、乙酸乙酯、乙醇和水提取物．采用MTT比色法检测发现乙酸乙酯提取物显著抑制类前骨髓白血病细胞HL-60的增殖活性，半数抑制质量浓度（IC50）约为25μg／mL．并采用流式细胞术和Western blotting等方法进一步研究虫草菌乙酸乙酯提取物抑制HL-60细胞生长的作用机理．用流式细胞仪检测HL-60细胞DNA含量发现，25μg／mL虫草菌乙酸乙酯提取物作用12～2Ah后，S期细胞减少，而G2／M期细胞增多，表明细胞周期中G2／M检验点被阻滞．Western blotting分析结果表明，在虫草菌乙酸乙酯提取物作用后，HL-60细胞中G2／M检验点相关周期蛋白p34^cdc2表达量降低．     

大黄素等游离型蒽醌诱导肿瘤细胞凋亡的信号转导通路

以大黄素、芦荟大黄素、大黄酸的药理作用为基础，综合分析了它们诱导多种肿瘤细胞凋亡的信号转导通路．并且对有关问题给予说明．结论是，大黄素、芦荟大黄素、大黄酸可诱导多种肿瘤细胞的凋亡响应，但仍有许多细节有待于进一步探讨．     

生血康对特发性血小板减少性紫癜患者骨髓巨核细胞的影响

目的：观察生血康治疗特发性血小板减少性紫癜（ITP）患者骨髓巨核细胞的变化．方法：治疗组30例，采用生血康（蒙药制剂）3g，每日3次口服，对照组30例，强的松1mg／（ks．d），每日1次顿服（或每日分3次口服）．两组均以6周为一个疗程，6周后强的松逐减量．并观察骨髓象的变化．结果：治疗组治疗后原、幼巨核和颗粒型巨核细胞明显减少，产板型巨核细胞明显增多，与对照组比较具有显著性差异（P〈0．05）．结论：生血康具有促进骨髓巨核细胞的成熟，使原、幼巨核和颗粒型巨核细胞减少，产板型巨核细胞增多致使升高血小板之功能。     

一例遗传性骨髓衰竭综合征中RTEL1基因新突变的研究

本研究旨在探究端粒酶RTEL1(regulator of telomere length 1)突变导致遗传性骨髓衰竭综合征发生的机制以及RTEL1的生物学功能.本研究基于临床上一例男性儿童先天性角化不良患者展开，通过对患者外周血样本进行外显子测序确定存在RTEL1突变.我们成功构建了过表达野生型RTEL1(RTEL1-WT)以及突变型RTEL1(RTEL1-MUT)的293细胞系.通过细胞计数试剂盒8(cell counting kit-8,CCK-8)探究该突变对细胞增殖的影响，并发现RTEL1-MUT的表达影响细胞的增殖.通过免疫沉淀以及质谱技术寻找到了与RTEL1相互作用的蛋白HSP90,通过western blot对相互作用进行了验证，并发现该突变导致二者的相互作用减少.使用HSP90抑制剂STA-9090处理过表达RTEL1-WT以及RTEL1-MUT的293细胞系，发现HSP90的活性影响RTEL1的稳定性.因此，该患儿的RTEL1突变可能通过影响细胞增殖而导致先天性角化不良的发生，而RTEL1功能的改变可能源于突变影响了与HSP90的相互作用，从而影响了RTEL1的稳定性...