Spinal cord injury (SCI) can disrupt neural connections and impair locomotion and sensation function. Currently, biomaterials containing neural progenitor cells (NPCs) are widely used to replace damaged tissue or provide support for neural regeneration following SCI. Immunosuppressive drugs (ISDs) are commonly utilized to ensure the survival of transplanted NPC in SCI. However, the potential benefits and risks of using ISDs in NPC transplantation with biomaterials for SCI repair has not been deeply studied. Herein, an orderly aligned collagen sponge scaffold (ACSS) combined with human embryonic spinal cord neural progenitor cells (hscNPCs) was transplanted into SCI rats, with or without ISDs. Results showed that ISDs suppressed cell-mediated immune and inflammatory responses, maintained early survival and differentiation capacity of transplanted cells, and promoted early functional recovery of SCI rats. However, ISDs did not influence endogenous nerve regeneration, angiogenesis, glial scarring or long-term functional recovery after ACSS and hscNPC transplantation. Additionally, ISDs can induce toxicity in multiple organ and impact the survival of animals after SCI. Thus, careful evaluation of the benefits and risks is necessary to maximize therapeutic efficiency when administrating ISD in combination with scaffold-loaded NPCs for SCI repair.

Abstract GATA2, a principal member of the GATA family, plays important roles in the generation and maintenance of hematopoietic stem/progenitor cells. Among the three mRNA transcripts, the distal first exon of GATA2 (IS exon) is specific for hematopoietic and neuronal cells. GATA2 mutants with abnormal expression are often present in acute myeloid leukemia-related familial diseases and myelodysplastic syndrome, indicating the crucial significance of GATA2 in the proper maintenance of blood system functions. This article offers an overview of the regulation dynamics and function of GATA2 in the generation, proliferation, and function of hematopoietic stem cells in both mouse and human models. We acknowledge the current progress in the cell fate determination mechanism by dynamic GATA2 expression. The gene modification approaches for inspecting the role of GATA2 in definitive hematopoiesis demonstrate the potential for acquiring hPSC-derived hematopoietic stem cells via manipulated GATA2 regulation.

Protein modification by ubiquitin and ubiquitin-like proteins (UBLs) regulates numerous biological functions. The UFM1 system, a novel UBL conjugation system, is implicated in mouse development and hematopoiesis. However, its broad biological functions and working mechanisms remain largely elusive. CDK5RAP3, a possible ufmylation substrate, is essential for epiboly and gastrulation in zebrafish. Herein, we report a crucial role of CDK5RAP3 in liver development and hepatic functions. Cdk5rap3 knockout mice displayed prenatal lethality with severe liver hypoplasia, as characterized by delayed proliferation and compromised differentiation. Hepatocyte-specific Cdk5rap3 knockout mice suffered post-weaning lethality, owing to serious hypoglycemia and impaired lipid metabolism. Depletion of CDK5RAP3 triggered endoplasmic reticulum stress and activated unfolded protein responses in hepatocytes. We detected the in vivo interaction of CDK5RAP3 with UFL1, the defined E3 ligase in ufmylation. Notably, loss of CDK5RAP3 altered the ufmylation profile in liver cells, suggesting that CDK5RAP3 serves as a novel substrate adaptor for this UBL modification. Collectively, our study identifies CDK5RAP3 as an important regulator of ufmylation and suggests the involvement of ufmylation in mammalian development.

Abstract Radiotherapy is used to treat approximately 50% of all cancer patients, with varying prognoses. Intrinsic radiosensitivity is an important factor underlying the radiotherapeutic efficacy of this precise treatment. During the past decades, great efforts have been made to improve radiotherapy treatment through multiple strategies. However, invaluable data remains buried in the extensive radiotherapy literature, making it difficult to obtain an overall view of the detailed mechanisms leading to radiosensitivity, thus limiting advances in radiotherapy. To address this issue, we collected data from the relevant literature contained in the PubMed database and developed a literature-based database that we term the cancer radiosensitivity regulation factors database (dbCRSR). dbCRSR is a manually curated catalogue of radiosensitivity, containing multiple radiosensitivity regulation factors (395 coding genes, 119 non-coding RNAs and 306 chemical compounds) with appropriate annotation. To illustrate the value of the data we collected, data mining was performed including functional annotation and network analysis. In summary, dbCRSR is the first literature-based database to focus on radiosensitivity and provides a resource to better understand the detailed mechanisms of radiosensitivity. We anticipate dbCRSR will be a useful resource to enrich our knowledge and to promote further study of radiosensitivity. Database URL: http://bioinfo.ahu.edu.cn:8080/dbCRSR/

Core binding factor (CBF) leukemia represents an individual subgroup of the disease, which accounts for 20% of acute myeloid leukemia (AML), characterized by the special t(8;21)(q22;q22) translocation most in AML-M2 variant (CBFα leukemia) or inv(16) (p13q22)/t(16;16) rearrangement in AML-M4 with eosinophilia (CBFβ leukemia), respectively. 1Chimerical fusion genes AML1-ETO and CBF-MYH11 are formed by these two cytogenetic changes, respectively, which finally lead to the leukemogenesis. 2Generally, CBF leukemias are considered to have favorable treatment outcome and prognosis and most centers regard CBF markers as 'good' cytogenetic factor, with a 5-year overall survival (OS) rate over 50%. 3 However, given using similar treatment strategy, such as '3+7' regimen in induction and high-dose Ara-C in consolidation, the treatment outcome of CBF leukemia in Chinese patients were not as good as reported by western groups. 4Interestingly, the incidence of CBFβ leukemia is even significantly lower than the western countries, as shown in our previous report; in 1185 AML patients, only 18 M4 with eosinophilia patients were identified.The difference of genetic background between Chinese and western population may be the reason, however, until now, evidence remains unavailable. 5n mouse model, stepwise leukemogenesis in AML with t(8;21)/ AML1-ETO is proved by the phenomena that coexpression of C-KIT N822K and AML1-ETO induces the full development of AML, whereas single or C-KIT is not sufficient to lead to the leukemia.Similarly, transgenic mice of CBF-MYH11 only induce a myeloid maturation block. 6Therefore, it could be concluded that additional mutations, especially kinase-associated mutations, providing a second 'hit' 7 may play a crucial role in the evolving of the disease.In this study, we included 205 newly diagnosed AML patients, including 180 patients with CBFα and 25 patients with CBFβ leukemia, to investigate the potential role of additional mutations beyond AML1-ETO and CBF-MYH11 in these diseases.All the patients received standard first-line treatment of DNR (daunorubicin), A (Ara-c(cytarabine))-like regimen.In the consolidation therapy, young patients were treated with high-dose cytarabine-based chemotherapy.Allogenetic stem cell transplantation was not used as first-line treatment in first time to complete remission.This study was approved by the ethnic board of the participating centers.All patients were given informed consent for both treatment and cryopreservation of bone marrow and peripheral blood according to the Declaration of Helsinki.Genomic DNA and total RNA were extracted as previously reported. 8We had screened the mutational status of FLT3-ITD and -TKD, C-KIT, N-RAS, CEPBA, WT1, ASXL1, DNMT3A, NPM1, MLL, IDH2 and TET2 genes by distinct approaches.A chip-based matrixassisted laser desorption/ionization time-of-flight mass spectrometry analysis system (iPLEXTM, Sequenom, San Diego, CA, USA) was used to assess the mutational status of FLT3-TKD, N-RAS, NPM1, IDH1 and IDH2.For mutations of FLT3-ITD, and those in C-KIT, CEPBA, WT1, ASXL1, DNMT3A and TET2 genes, samples were analyzed by whole-gene sequencing.Six MLL-related common fusion genes, including MLL-AF9, MLL-AF10, MLL-AF6, MLL-ELL,

Objective To explore the effects of evidence-based medicine(EBM) course on improvement of information consciousness and information morality for medical students Methods A total of 288 medical undergraduates and postgraduates,who took EBM as an elective course in Sichuan University,were surveyed with 'information consciousness and information morality questionnaire' before and after that course.Results After the EBM course,the number of students surfing the Internet increased by 5%,of which postgraduates increased by 24% with significant differences(P0.05),while their purpose for specialized knowledge increased by 7%;the number of students making plans in advance increased by 7%,and the number of students learning intellectual property and copyright law increased by 7%;the number of postgraduates knowing how to cite articles increased by 12% with significant differences(P0.05);and the number of students not knowing how to get legitimate information decreased by 12% with significant differences(P0.05).Conclusion Evidence-based medicine course is positive for the information consciousness and information morality of medical students.

It is well known that terminally differentiated cells derived from mesenchymal stem cells (MSCs) will lose the immunomodulation capacity. NANOG is known to be a core transcription factor in the maintenance of stem cell specific features or stemness. To evaluate whether NANOG was involved in the immunomodulation effects of MSCs, MSCs' immunomodulation capacity on lymphocyte activation and proliferation before or after endogenous NANOG interference was investigated. We found that MSCs' inhibitory effects on lymphocyte activation and proliferation was significantly weakened after NANOG knockdown. In addition, NANOG RNAi and chromatin immunoprecipitation experiments showed that NANOG suppressed the expression and secretion of DKK-1, transforming growth factor-beta1 (TGF-β1), TGF-β2, and TGF-β3, which are all important factors mediating MSCs' immunomodulation capacity. Based on these data, we propose that NANOG plays an important role in maintaining the immunomodulation functions of MSCs by regulating the expression and secretion of TGF-β1, TGF-β2, TGF-β3, and DKK-1.

The aim of this study is to find a suitable alternative to fetal bovine serum for amplification of mesenchymal stem cells products and study the differentiation potential of the amplication products.Adherent screening adult bone marrow mesenchymal stem cells were isolated and cultured,and different passages of the expanded cells were used to differentiate into osteoblasts and fat cells.Osteoblasts were identified by Vonkossa,alkaline phosphatase staining of osteoblasts,and fat cells by oil red staining of adipogenic.In the configuration with 2% adult serum complete medium,different passages of adult bone marrow mesenchymal stem cells still had a bone,adipogenic differentiation potential.The adult bone marrow mesenchymal stem cells expanded in this medium can be incuced into osteoblasts,fat cells.The proposed method may be ideal for expansion of adult bone marrow mesenchymal stem cells in vitro.The amplication products may be useful to bone tissue engineering.

BACKGROUND:Many research articles on medical education have been published in Chinese-language journals, the majority within the past few years. However, there have been no objective studies to look at the quality of these, and their contribution to present day thinking.AIM:This study explored the areas of focus, and the quality, of published research on Chinese undergraduate medical education.METHOD:We searched three major Chinese databases, including Chinese Biology Medicine in electronic form, Chinese Journals Full-text Database, and Chinese Technological Periodicals Database, to trace the research themes and methodologies of Chinese-language research papers published from January 2000 to December 2008.RESULTS:The annual number of published articles on undergraduate medical education research has increased over time in China, with 70% of the articles in our 9-year study published in the past 4 years; the most popular theme was curriculum and teaching. Non-comparative studies accounted for the majority of the literature (84.6%); and comparative studies were rare.CONCLUSIONS:Although an increase in the number of articles on medical education research in China is encouraging, more methodologically rigorous designs are needed to improve research quality. Generic and focused training on research methodology is essential to convert quantity into quality.

Loss of function of tumor suppressor genes, such as PTEN, CEBPAlpha, and CTNNA1 (encoding the alpha-catenin protein), has been found to play an essential role in leukemogenesis. However, whether these genes genetically interact remains largely unknown. Here, we show that PTEN-mammalian target of rapamycin signaling acts upstream to dictate the ratio of wild-type p42 C/EBPalpha to its dominant-negative p30 isoform, which critically determines whether p30 C/EBPalpha (lower p42/p30 ratio) or p42 C/EBPalpha (higher p42/p30 ratio) binds to the proximal promoter of the retained CTNNA1 allele. Binding of p30 C/EBPalpha recruits the polycomb repressive complex 2 to suppress CTNNA1 transcription through repressive H3K27me3 modification, whereas binding of p42 C/EBPalpha relieves this repression and promotes CTNNA1 expression through activating H3K4me3 modification. Loss of Pten function in mice and zebrafish induces myelodysplasia with abnormal invasiveness of myeloid progenitors accompanied by significant reductions in both wild-type C/EBPalpha and alpha-catenin protein. Importantly, frame-shift mutations in either PTEN or CEBPA were detected exclusively in the primary LICs with low CTNNA1 expression. This study uncovers a novel molecular pathway, PTEN-C/EBPalpha-CTNNA1, which is evolutionarily conserved and might be therapeutically targeted to eradicate LICs with low CTNNA1 expression.

背景:间充质干细胞的免疫调节作用是被大家普遍认可的,在以往实验中也对Flk-1~+骨髓间充质干细胞体外抑制T/B淋巴细胞增殖的能力进行了确认.目的:验证Flk-1~+骨髓间充质干细胞对胶原诱导性关节炎小鼠的治疗作用.方法:健康10周龄雄性DBA-1(H-2K~q)小鼠18只,随机分为3组:初次免疫后细胞移植组、加强免疫后细胞移植组、模型对照组,3组小鼠均通过尾皮下注射牛Ⅱ型胶原进行初次免疫,21 d后同法进行加强免疫,建立胶原诱导性关节炎模型.密度梯度离心法和贴壁筛选法体外分离DBA-1(H-2K~q)小鼠Flk-1~+骨髓间充质干细胞,初次免疫后细胞移植组小鼠在初次免疫后立即经尾静脉输注Flk-1~+骨髓间充质干细胞(1～2)×10~6个/只,加强免疫后细胞移植组小鼠在加强免疫时同法输注等量Flk-1~+骨髓间充质干细胞,模型对照组小鼠于初次免疫后0或21 d尾静脉输注等量生理盐水.观察初次免疫后和加强免疫后各组小鼠的爪垫增厚情况、临床评分,检测小鼠关节病理学变化及血清因子质量浓度的动态变化.结果与结论:与模型对照组比较,初次免疫后细胞移植组爪垫增厚程度及平均临床疾病得分均无明显差异(P > 0.05),均可见明显的滑膜组织损伤和炎症细胞浸润,各血清细胞因子质量浓度基本相似;而加强免疫后细胞移植组爪垫明显增厚(P < 0.01),平均临床疾病得分高达3.35分,滑膜损伤严重,毛细血管增生,在初次免疫后28 d白细胞介素6血清浓度急剧上升(P < 0.1),初次免疫后35 d白细胞介素6血清浓度又明显下降(P < 0.1).提示在胶原诱导性关节炎小鼠模型中,Flk-1~+骨髓间充质干细胞移植不但未取得预期的治疗效果,还在加强免疫后细胞移植组观察到显著地关节炎症状恶化现象,其可能通过上调白细胞介素6血清浓度加重类风湿关节炎小鼠的行为症状.

目的 调查分析医学生批判性思维的现状,为探索建立"核心能力为导向,循证医学为载体,终身学习为目的 "的医学人才培养模式提供依据.方法 采用中文版批判性思维能力测量表(Chinese Version of CriticalThinking Disposition Inventory,CTDI-CV)调查分析四川大学617名医学本科生和研究生批判性思维现状.结果 该组医学生批判性思维素质平均总分均高于280分,批判性思维呈正性.亚组分析结果显示,平均总分由高到低依次为8年制(309分)、研究生(298分)、7年制(287分)和5年制(286分).平均总分两两比较,除5年制和7年制之间无明显差异外,其余各组平均相差均≥10分.5年制和7年制医学生"寻找真相"、"系统化能力"、"批判性思维自信心"三项≤40分,其中"批判性思维自信心"最低.不同性别和年龄间批判性思维总分和7项特质无差异.结论 影响我国学生批判性思维的因素主要包括:教学理念、教学氛围、教学方式和教学评价体系.

[Objective] To learn the existing circumstances how the medicos in Sichuan understand the standardized training system of residents and specialists and the factors affecting them,so that we can provide the health administrations and hospitals suggestions on how to promote the training system.[Methods] We organized a sampling inquiry of 1 800 medicoes in Sichuan to collect data and use statistical software SPSS16 to analyze the data.[Results] The study showed that a lot of students didn' t known the standardized training system of residents and specialists and there was differences between the students in different schools and grades and the students whose parents had different jobs.Most of the students chose postgraduate medical education or work directly after graduating while a few students chose to be a resident receiving the training and the factors affecting it included which schools students were in,the grades students had,gender,parents' jobs and how student known about the reformation.[Conclusion] It is essential to improve the medicos' and the social understanding to the standardized training of residents and specialists and make more students attend the training by the propaganda and education,which is helpful to promote the development of postgraduate medical education.

OBJECTIVE:To explore the relationship between TNF-alpha, transcriptional co-activator with PDZ-binding motif (TAZ) and bone disease of multiple myeloma.METHODS:The biological characteristics, especially the osteogenic potential of marrow MSCs from myeloma patients and normal subjects were studied. Real-time RT-PCR and Western-blot were employed to detect mRNA and protein expression of TAZ in MSCs. The concentration of TNF-alpha in the marrow plasma was detected using ELISA method. CD138(+) myeloma cells were cocultured with normal MSCs with or without anti-human TNF-alpha monoclonal antibody in the Transwell system. Real-time RT-PCR was employed to detect the mRNA expressions of ALP, Cbfa1 and TAZ in MSCs two weeks later. von Kossa staining was used to detect the mineral deposition. TNF-alpha was added into the culture media of normal marrow MSCs and real-time RT-PCR and Western-blot were employed to detect mRNA and protein expression of TAZ in MSCs one week later.RESULTS:Real-time RT-PCR revealed that the mRNA of osteogenic markers was decreased in comparison with that of normal controls after cultured in the osteogenic medium. von Kossa staining showed weakened mineral deposition in MSCs from multiple myeloma patients compared with that in normal subjects after osteogenic differentiation for two weeks. The mRNA and protein levels of TAZ in the MSCs from myeloma patients were decreased. TNF-alpha concentration in the marrow plasma of myeloma patients was higher than that in the normal controls [(355.4 +/- 49.1) vs. (92.3 +/- 17.2) pg/ml]. CD138(+) myeloma cells inhibited mRNA expressions of ALP, Cbfal1 and TAZ in MSCs, which could be partially reversed by anti-human TNF-alpha monoclonal antibody.CONCLUSION:The osteogenic potential of MSCs from myeloma patients is significantly decreased in comparison with that in normal subjects, which may play an important role in the pathology of myeloma bone disease. TAZ expression inhibited by TNF-alpha may play an important role in this inhibition effect.

Severe graft-versus-host disease (GVHD) and graft rejection still remain major complications of haploidentical nonmyeloablative (NMA) stem cell transplantation. Recent studies have shown that bone marrow-derived mesenchymal stem cells (MSCs) possess immunomodulatory capacity and may promote hematopoietic engraftment. The purpose of this study was to observe if the new strategy, which included a haploidentical peripheral blood stem cell transplantation (PBSCT) combined with MSCs, modified NMA conditioning, and GVHD prophylaxis would improve donor engraftment and prevent severe GVHD. The modified conditioning approach consisted of fludarabine (Flu), low-dose total body irradiation (TBI), cyclophosphamide (Cy), cytarabine, and anti-Tcell-lymphocyte globulin, whereas the GVHD prophylaxis consisted of cyclosporin A (CsA), mycophenolate mofetil (MMF), anti-CD25 antibody and intrabone marrow injection of MSCs. Thirty-three patients with high-risk acute leukemia underwent transplantation with PBSC from HLA-haploidentical donors without T cell depletion. All of the patients achieved full donor chimerisms, including 6 who switched to full donor chimerisms from mixed chimerisms in 1 to 2 months after the transplantations. Rapid hematological engraftment was observed with neutrophils >0.5×109/L at day 11 and platelets >20×109/L at day 14. Fifteen patients (45.5%) developed grade I–IV acute GVHD (aGVHD) and only 2 (6.1%) developed grade III to IV aGVHD. Nine (31%) of 29 evaluable patients experienced chronic GVHD (cGVHD). Upon follow-up for 1.5 to 60 months, 20 (60.6%) patients were alive and well and 6 (18.2%) had relapsed leukemia in the 33 patients. The probability of 3-year survival was 57.2%. The results indicate that this new strategy is effective in improving donor engraftment and preventing severe GVHD, which will provide a feasible option for the therapy of high-risk acute leukemia.

医学生就业问题是影响我国医学教育和卫生事业长远、健康发展的重要因素.面对医学生严峻的就业形势,结合国内外已有研究,本文从社会、教育、家庭个人三个层面对医学本科生就业困难的原因进行分析,并提出相应对策.

The immunomodulatory ability of mesenchymal stem cells (MSCs) may be used to develop therapies for autoimmune diseases. Flk-1(+) MSCs are a population of MSCs with defined phenotype and their safety has been evaluated in Phase 1 clinical trials. We designed this study to evaluate whether Flk-1(+) MSCs conferred a therapeutic effect on collagen-induced arthritis (CIA), an animal model of rheumatic arthritis, and to explore the underlying mechanisms. Flk-1(+) MSCs, 1-2 x 10(6), were injected into CIA mice on either day 0 or day 21. The clinical course of arthritis was monitored. Serum cytokine profile was determined by cytometric bead array kit or enzyme-linked immunosorbent assay. Flk-1(+) MSCs and splenocytes co-culture was conducted to explore the underlying mechanisms. Flk-1(+) MSCs did not confer therapeutic benefits. Clinical symptom scores and histological evaluation suggested aggravation of arthritis in mice treated with MSCs at day 21. Serum cytokine profile analysis showed marked interleukin (IL)-6 secretion immediately after MSC administration. Results of in vitro culture of splenocytes confirmed that the addition of Flk-1(+) MSCs promoted splenocyte proliferation and increased IL-6 and IL-17 secretion. Moreover, splenocyte proliferation was also enhanced in mice treated with MSCs at day 21. Accordingly, MSCs at low concentrations were found to promote lipopolysaccharide-primed splenocytes proliferation in an in vitro co-culture system. We propose that Flk-1(+) MSCs aggravate arthritis in CIA model by at least up-regulating secretion of IL-6, which favours Th17 differentiation. When Flk-1(+) MSCs are used for patients, we should be cautious about subjects with rheumatoid arthritis.

目的:通过对医学本科生关于择业意向的调查,了解医学本科生择业意向的整体情况及其影响因素,为医学院校开展就业指导和解决医学生就业问题提供科学的决策依据.方法:以四川大学华西临床医学院临床医学(五年制)学生为调查对象;利用统一自制的问卷进行调查;用Epidata3.0输录数据,采用SPSS16.0分析.结果:共下发问卷400份,回收有效问卷359份(有效回收率89.8%),调查结果显示:医学本科生在工作地点、工作单位及月薪期望方面定位均较高;生源地是影响医学生就业地区选择的重要因素;生源地、助学贷款和担任职务是学生月薪期望的重要影响因素.结论:加强对医学本科生择业观的教育,端正医学生的择业观念,重视医学生职业生涯规划的指导,扩大医学生的就业范围及其可能性,对解决医学本科生就业问题有重要作用;同时,加大对西部医学教育的支持,通过政策鼓励,引导医学本科生到西部和农村服务,不但可以解决医学生就业问题,而且对提高我国医疗服务公平性具有重要意义.

Objective:To investigate the reality of community health service system after earthquake in Mianzhu,the satisfaction of community residents to the community health service as well as the post-disaster emergency response capability of community hospital in order to provide decision-making suggestions on better reconstruction of community health service system.Methods:Jiannan and Tianhe community hospital were randomly selected for visiting and 2.4‰ of community residents in the city zone of Mianzhu were selected by convenience sampling for a face-to-face interview using a questionnaire.Data entry and statistically analysis were completed by Epidata3.0 and SPSS13.0 respectively.Results:A total of 240 questionnaires were conducted to face-to-face interviews,and 229 questionnaires were returned (response rate 95.4%).The community health service system was badly injured.Residents' satisfactory degree of the community health service after earthquake was 45.4%.The proportions of disaster /disaster prevention education was 33.6%,medicine supply for familiar diseases and the chronic were the main factors which influenced judgements of residents to the emergency response capabilities of community hospitals(P=0.033,P=0.001,respectively).Conclusion:The community health services after earthquake had not been widely satisfied and the emergency response capability of community hospital was far from enough.The proportions of disaster /disaster prevention education were far from enough.The effectiveness of emergency response work of community hospitals can be enhanced by reinforcing medicine preparation.In the course of the reconstruction,community health service system should pay attention to the resumance of basic community health service,reconstruction of basic establishment and construction of first-aid system.

Background: Whether the transplantation of mesenchymal stem cells (MSCs) is successful or not depends on homing. However, the molecular mechanism of regulating and controlling MSC homing is still unclear. Objective: To explore the homing mechanism of fetal bone marrow Flk1+ MSCs into bone marrow, to observe effects of stromal cells-derived growth factor-1 and its receptor CXCR4 on homing efficiency of stem cells, and to investigate the method of elevating the homing and long-term implantation efficiency. Design, Time and Setting: The cytology in vivo study was performed at the Center of Tissue Engineering, Peking Union Medical College, Chinese Academy of Medical Sciences from September 2005 to July 2006. Materials: Flk+ MSCs were isolated from human fetal bone marrow obtained from aborted fetus, which was provided by the Department of Gynaecology and Obstetrics, Second Affiliated Hospital, Tianjin Medical University. NOD/SCID mice aged 6 to 8 weeks old were purchased from the Animal Experimental Institute, Chinese Academy of Medical Sciences. Methods: The expression of CXCR4 in Flk1+ MSCs stimulated with a cytokine cocktail and the migration capacity to stromal cell-derived factor-1 in vitro were investigated. NOD/SCID mice were sublethally irradiated prior to transplantation with Flk1+ MSCs stimulated with cytokines or not. Control mice received the same volume of saline. At 24 hours after transplantation, the presence of donor cells were analyzed by flow cytometry. Blood was obtained from the mouse caudal vein after transplantation to analyze the changes in number of leukocytes, erythrocytes and thrombocyte in peripheral blood. Human specific DNA content was measured in mouse bone marrow using real-time PCR at 6 months after transplantation to understand the implantation of human-derived cells. Results: Flk1+ MSCs harbored intracellular CXCR4 which could be rapidly induced to cell surface within a few hours. Short-term (24 hours) stimulation with the cocktail cytokines resulted in up-regulation of both cell surface and intracellular CXCR4, increasing in vitro migration capacity to stromal cell-derived factor-1 and homing to the bone marrow of irradiated NOD/SCID mice. Moreover, transplantation of cytokine-treated Flk1+ MSCs resulted in faster hematological recovery and higher levels of donor chimerism in bone marrow than non-treated cells. Neutralization of CXCR4 significantly reduced homing and engraftment of Flk1+ MSCs in murine bone marrow. Conclusion: Stromal cell-derived factor-1/CXCR4 axis plays an important role in the regulation of motility of Flk1+ MSCs. Increasing CXCR4 expression might be a potential strategy to improve homing of Flk1 +MSCs in bone marrow and accelerate hematopoiesis recovery.