Abstract:Radical resection+D2 or D3 lymphadenectomy is the standard operation for gastrointestinal tumor surgery. The appearance of total mesorectal excision（TME）and complete mesocolic excision（CME）gradually replaced the dominant position of lymphadenectomy in the colorectal cancer surgery，and the surgical treatment of gastrointestinal tumor began to enter the era of “membrane anatomy”. Membrane anatomy is a new concept of surgery and a standardized new operation paradigm under the guidance of the new concept，which is conceived by many factors such as the accumulation of clinical practice，the continuous progress of clinical basic research and medical industry science and technology. However，most clinicians lack in-depth understanding of the origin and current situation of membrane anatomy，the nature and technical composition of membrane anatomy are not very clear，and there are many complex and even wrong interpretations. More and more surgeons engaged in the research and exploration of membrane anatomy. How to condense the membrane anatomy into a systematic theory and guide the operation practice is a problem that needs special attention in the research of modern practical membrane anatomy. The purpose of this essay is to review the origin and evolution of membrane anatomy theory，define the concept of “membrane anatomy”，and help gastrointestinal surgeons to understand the basic theory and principle of membrane anatomy better. At present，the theoretical system of membrane anatomy is not perfect，and more scholars are expected to participate in the basic research or clinical exploration of membrane anatomy，especially for gastric cancer. The theoretical system of “membrane anatomy” is constantly enriched and improved to promote the development of membrane anatomy.

Abstract:Objective：To explore the distributions of PNPLA7 in different tissues of mouse under different nutritional status and its expression levels in the process of adipocyte differentiation as well as insulin or fatty acids treatment on adipocytes. Methods：The distributions of PNPLA7 in different tissues and cell lines were preliminarily analyzed using bioinformatics，and the expressions of PNPLA7 in different tissues of mouse under different nutritional status were further identified by real time PCR. In addition，3T3-L1 cells were induced for differentiation and then the PNPLA7 expressions in the process of differentiation and in the mature adipocytes treated with insulin or fatty acids were detected by real time PCR and Western blot. Results：PNPLA7 was mainly expressed in active metabolic tissues or cells. The expression level of PNPLA7 in adipocytes under starvation was higher than that in normal diet，but became lower when re-fed after starvation status. The expression level was down-regulated in insulin treatment and up-regulated in oleic acids treatment. Besides，the expression of PNPLA7 was down-regulated in the early stage and up-regulated in the later stage of 3T3-L1 cells differentiation. Conclusion：PNPLA7 is enriched in adipocytes and its expression level changes from down-regulation to up-regulation during the adipocyte differentiation. Besides，its expression is regulated by insulin and oil acids.

Abstract:Objective：To idefine the regions of the human short isoform thymic stromal lymphopoietin（sfTSLP）promoter and to predict the potential transcription factor binding sites. Methods：Original human promoter fragments were isolated by PCR，using primers generated from genomic sequences of sfTSLP. Amplified fragments were then cloned into the pGL3-basic vector. Five promoter fragments with different length were obtained by walking deletion and cloned into pGL3-basic vector. The vector expression activities were determined by measuring luciferase activity in HEK-293 cells. Its potential transcriptional binding sites were predicted by bioinformatics methods. Results：A nested series of deletion constructs of the human sfTSLP gene promoter were generated and the core promoter region was determined to be located in the -200~+25 region at the 5′ side，which may contain the binding sites of SP1/SP3，SPI1/SPIB，TCF3，ETS1 and other transcription factors. Conclusion：It is the first study on the promoter fragmentsof human sfTSLP. The core promoter region was found and the possible transcription factor binding sites were also preliminarily identified，which can be the basis of further study.

Abstract:Objective：To observe the effects of human adiponectin receptor（AdipoR1）gene overexpression and knockdown on PC9 cells proliferation and migration，and to clarify the regulatory effect of AdipoR1 on lung cancer. Methods：The expression levels of AdipoR1 in PC9 cells and control HBEC were deteceted by RT-PCR. The overexpression vector and shRNA interference vector of AdipoR1 were established by molecular clone method and transfected into PC9 cells，the expression levels of AdipoR1 mRNA and protein were detected by RT-PCR and Western blot. CCK8 method and scratch healing experiment were used to detect the effect of AdipoR1 agonist AdipoRon，AdipoR1 overexpression，and AdipoR1 knockdown on proliferation and migration ability of PC9 cells. Results：RT-PCR results showed that the expression of AdipoR1 was decreased in PC9 cells（P < 0.05）. RT-PCR and Western blot results showed that mRNA and protein expression levels of AdipoR1 were up-regulated in AdipoR1 overexpressed PC9 cells（P < 0.05），and down-regulated in AdipoR1 knockdown PC9 cells（P < 0.05）. CCK8 and scratch healing results showed that the proliferation and healing percentage of PC9 cells treated by AdipoRon for 24 or 48 h were significantly decreased when compared with the vehicle group（all P< 0.05）. The proliferation and healing percentage were also significantly lower in AdipoR1 overexpression PC9 cells and higher in AdipoR1 knockdown PC9 cells than theircontrols after cultured for 24 or 48 h（all P < 0.05）. Conclusion：AdipoR1 agonist AdipoRon，AdipoR1 overexpression can inhibit the proliferation and migration ability of lung cancer PC9 cells，while AdipoR1 knockdown can increase the proliferation and migration ability of lung cancer PC9 cells.

Abstract:Objective：To observe the effects of endotoxin tolerance induced by Porphyromonas gingivalis（P.gingivalis）on the secretion of metalloproteinase（MMP）-1 and MMP-7 in peritoneal macrophages of mice and the wound-healing abilities of L929 cells. Methods：Endotoxin tolerance in murine peritoneal macrophages was triggered by repeated 1 μg/mL P.gingivalis lipopolysaccharide（LPS）stimulations，and 1 μg/mL Escherichia coli（E.coli） LPS was served as positive control. Supernatants from tolerized macrophages were collected and levels of MMP-1 and MMP-7 were determined by ELISA. In addition，L929 cells were stimulated by supernatants from tolerized macrophages and their wound-healing abilities were evaluated by repair areas after scratch. Results：Secretion of MMP-1 in macrophages decreased significantly after repeated stimulation by P.gingivalis LPS compared with that treated by single P.gingivalis LPS stimulation（P < 0.05），while there were no differences in MMP-7 levels between the two groups（P > 0.05）. Repaired areas after scratch（12 h，24 h）in L929 cells cultured with supernatants from P.gingivalis LPS-tolerized macrophages were bigger than those from P.gingivalis LPS non-tolerized macrophages（P < 0.05）. Conclusion：Endotoxin tolerance triggered by P.gingivalis LPS contributes to the decreased secretion of MMP-1 in murine peritoneal macrophages and the enhanced migration of L929 cells.

Abstract:Objective：To explore the target and related mechanism of resveratrol in the treatment of hypertension. Methods：Using angiotensin Ⅱ to induce rat aortic smooth muscle cells A7r5 to establish a hypertensive cell model and interventing with resveratrol and miR-21-5p mimic on this basis. CCK-8 assay was used to detect cell viability of A7r5 cells，wounding healing assay was used to detect migration ability of A7r5 cells，Real-time PCR was used to detect expression of miR-21-5p，Western blot was used to detect the expression of cell proliferation-related proteins PCNA，Cyclin D1 and CDK4，and cell migration associated proteins MMP2，MMP9 and PDCD4. In addition，the targeting relationship between miR-21-5p and PDCD4 was verified by dual luciferase reporter gene detection technology in logarithmic growth phase 293T cells. Results：Compared with the NC group，the cell viability，migration ability and the expression level of proliferation and migration-related proteins PCNA，Cyclin D1，CDK4，MMP2，MMP9 and miR-21-5p were significantly up-regulated，and the expression level of PDCD4 protein was significantly decreased in the NC+ model group，and the difference was statistically significant（P < 0.01）；Compared with the NC+ model group，the cell viability，migration ability，and the expression level of proliferation and migration-related proteins PCNA，Cyclin D1，CDK4，MMP2，MMP9 and miR-21-5p were significantly down-regulated，and the expression level of PDCD4 protein was significantly up-regulated in the NC+ model+resveratrol group，and the difference was statistically significant（P < 0.01）；Compared with the NC+ model+resveratrol group，cell viability，migration ability and the expression level of proliferation and migration related proteins PCNA，Cyclin D1，CDK4，MMP2，MMP9 and miR-21-5p was significantly up-regulated，and the expression level of PDCD4 protein was significantly decreased in the miR-21-5p mimic+model+resveratrol group，and the difference was statistically significant（P < 0.01）. The dual luciferase assay miR-21-5p significantly inhibited the luciferase activity of the wild-type PDCD4 3’UTR reporter vector（P < 0.01）. Conclusion：Resveratrol inhibits the proliferation and migration of vascular smooth muscle cells by regulating the miR-21-5p/PDCD4 pathway，which in turn has a certain therapeutic effect on hypertension.

Abstract:Objective：The aim of this study was to identify the key genes and uncover the potential molecular mechanisms of lung adenocarcinoma（LAC）. Methods：In our study，three microarray data sets of LAC genes，including 156 cases of LAC and 106 cases of normal lung tissue，were used to screen the potential key genes. Results：First，341 overlapping differentially expressed genes（DEG）were found by microarray data analysis. The main biological processes of DEG enrichment were extracellular matrix tissue，regulation of chemical kinase-mediated signaling pathways，cell response to transformed growth factor stimulation，extracellular matrix assembly，and regulation of angiogenesis. Next，10 key genes were screened out by using protein protein interaction（PPI）network，including 8 genes AURKA（aurora kinase A），CDC20（cell division cycle 20），CDH5（cadherin 5），COL1α1（collagen I，α1），EDN1（endothelin 1），MMP9（matrix metalloprotein 9），PECAM1（platelet endothelial cell adhesion molecule 1），SPP1（secreted phosphoprotein 1），which were correlated with the prognosis of LAC. Additional，CDC20 has the highest correlationship with the prognosis of LAC. The subgroup analysis showed that expression of CDC20 in all age groups of LAC patients increased significantly compared with nomal control；expression of CDC20 in tumor stage Ⅰ is lower than tumor stage Ⅱ，Ⅲ，Ⅳ；expression of CDC20 in aciner subtype，solid subtype，mixed subtype，clear cell subtype was higher than other subtypes；expression of CDC20 in LAC patients with smoking was lower than the non-smokers. Furthermore，the results by immunohistochemical showed that expression of CDC20 in LAC tissues was significantly higher than that in normal lung tissues，in acinar subtype and solid subtype was higher than other subtypes. Conclusion：CDC20 is high expressed in LAC，which is correlated with poor prognosis of LAC. CDC20 might be a potential biomarker and therapeutic target for LAC.

Abstract:Objective：Combined speckle tracking imaging（STI）and myocardial contrast echocardiography（MCE）to evaluate myocardial function of left ventricular（LV）in the early stage of acute myocardial ischemia（AMI）in rabbits by measuring the LV strain and myocardial perfusion parameters. Methods：A total of 36 New Zealand white rabbits were enrolled in this experiment，the LV branch of coronary artery was ligated in order to establish an AMI model. In the low MI mode，15 cardiac cycles of parasternal LV long-axis，apical four-，three- and two-chamber views were acquired before operation（which was called the preoperation group）and 10 minutes after AMI（which was called the postoperation group）for analysis. Global and segmental peak systolic longitudinal strain（LS）of LV walls was analyzed by STI. Myocardial blood volume（A），velocity（β）and myocardial blood flow（MBF）were analyzed by MCE. Results：There were significant differences in GLS and LS of left anterior septum wall，anterior wall，lateral wall，posterior wall，inferior middle wall，and apex sections between the preoperation and postoperation groups，the values in the postoperation group were significantly lower than those in the preoperation group（P＜0.05）. The myocardial perfusion parameters of LV between the postoperation and preoperation groups had significant differences（P＜0.05）except the A value of inferior and posterior septum wall. The changes of LS percent were positively correlated with MBF of left anterior septum，anterior，lateral，inferior，posterior，and posterior septum walls（r were 0.58，0.56，0.65，0.62，0.56，0.36，P＜0.05）. Conclusion：Combined STI and MCE can reflect the changes of LV myocardial function in the early stage of acute myocardial ischemia sensitively.

Abstract:Objective：To explore the hypoglycemic effect of gastrointestinal bypass and effects on glucagon like peptide -1（GLP-1）and insulin-like growth factor -1（IGF-1）levels in diabetic rats. Methods：A total of 60 SD rats were randomly divided into the control group，the sham operation group，the duodenal bypass group，and the jejunal bypass group. The diabetic model was established by injecting of 1% streptozotocin（STZ）intraperitoneally in the sham operation group，the duodenal bypass group and the jejunal bypass group. The surgical operations were performed accordingly. The levels of blood sugar，insulin，serum GLP-1，and IGF-1 were examined before operation and 1，3 and 8 weeks after operation. Results：The survival rates of rats were 100.00% in both the control group and the sham-operated group，and were 93.33% and 86.67% in the duodenal bypass group，and the jejunal bypass group，respectively. The blood glucose，GLP-1 and IGF-1 levels of the sham operation group，the duodenal bypass group，and the jejunal bypass group before operation were significantly higher than those of the control group，and the insulin level was significantly lower than that of the control group（P < 0.05）；3 or 8 week after surgery，the body weight，and blood glucose of the duodenal bypass group and the jejunal bypass group were lower than those of the sham operation group at the same time point，and the levels of insulin，GLP-1，and IGF-1 were higher than those of the sham operation group at the same time point（P < 0.05）；meanwhile，the body weight，blood glucose of the jejunal bypass group were lower than those of the duodenal bypass group，and the levels of insulin，GLP-1，and IGF-1 were higher than those of the duodenal bypass group（P < 0.05）. Conclusion：Gastrointestinal bypass can be effective in the treatment of diabetic rats，and the effect increased with the increase of the length of small intestine. One of the mechanisms may be that gastrointestinal bypass increases the synthesis and secretion of GLP-1 and IGF-1.

Abstract:Objective：To investigate the role of long non-coding RNA（lncRNA）SNHG14 in the progression of gastric cancer（GC）. Methods：RT-qPCR was used to detect the expression level of SNHG14 in 68 pairs of gastric cancer tissues and adjacent normal tissues，3 gastric cancer cell lines（MGC-803，BGC-823，SGC-7901）and human normal gastric epithelial cell line GES-1. The correlation between the expression level of SNHG14 and the clinicopathological features in gastric cancer tissues and gastric cancer cell lines was analyzed. The function of gastric cancer cell lines was observed after SNHG14 silencing by siRNA. The effect of SNHG14 on the proliferation of gastric cancer cells was evaluated by means of CCK-8 proliferation assay. Transwell assay was used to detect the migration and invasion of gastric cancer cells. Results：The expression level of SNHG14 was significantly up-regulated in the gastric cancer cell lines and gastric cancer tissues compared with normal controls. Result of correlation analysis showed that the expression level of SNHG14 was significantly correlated with the TNM stage（P < 0.05），degree of differentiation（P < 0.001），tumor size（P < 0.01）and depth of invasion（P < 0.05）of gastric cancer tissues. The SNHG14 silencing by siRNA significantly inhibited the proliferation（P < 0.01），migration（P < 0.01）and invasion（P < 0.05）of gastric cancer cells. Conclusion：SNHG14 may play a role in promoting cancer and affect the progression of gastric cancer by promoting the proliferation and metastasis of gastric cancer cells. SNHG14 bears potential value in the treatment and diagnosis of gastric cancer，and may become a novel biomarker for the diagnosis of gastric cancer or a candidate target in the biotherapy of gastric cancer.

Abstract:Objective：To investigate the expression and significance of long non-coding RNA CBR3-AS1（LncRNA CBR3-AS1）in osteosarcoma tissue and cell lines. Methods：The pathological tissue samples and clinical data of 66 patients with osteosarcoma diagnosed and treated in our hospital from January 2012 to January 2014 were retrospectively collected. The expression of LncRNA CBR3-AS1 in pathological tissues was detected by qRT-PCR. The patients were divided into the high expression group and the low expression group. The correlation of the expression of LncRNA CBR3-AS1 and clinical parameters was analyzed by Chi-square test. Kaplan-Meier survival analysis was used to compare the survival rate of osteosarcoma patients with high or low expression of LncRNA CBR3-AS1. U-2 OS cell lines were divided into the LncRNA CBR3-AS1 silent expression group（si-CBR3-AS1 group）and the negative control group（si-NC group）. LncRNA CBR3-AS1 siRNA and si-NC sequences were transfected by LipofectamineTM 3000，respectively. Cell proliferation，cell migration and invasion were measured by MTT and colony formation assay. Apoptotic capacity was measured by cytometry. Expression of carboxyl reductase 3（CBR3）were detected by qRT-PCR and Western blot. Results：LncRNA CBR3-AS1 were highly expressed in osteosarcoma tissues and cell lines（P < 0.001）. LncRNA CBR3-AS1 high expression were significantly correlated with Enneking staging（P < 0.001），distant metastasis（P=0.004）and histological grade（P=0.036）. LncRNA CBR3-AS1 high expression was negatively correlated with overall survival rate in osteosarcoma patients（P < 0.01）， it was an independent prognostic factor for osteosarcoma patients（HR=1.558，95%CI：1.041-2.641，P=0.013）. Cell proliferation and colony formation ability，as well as cell migration and invasion ability in the si-CBR3-AS1 group were significantly lower than those in the si-NC group，and cell apoptosis rate in the si-CBR3-AS1 group was higher than that in the si-NC group. The expression of LncRNA CBR3-AS1 and CBR3 was positively correlated（r=0.44，P=0.036）. The expression of CBR3 protein in the si-CBR3-AS1 group was significantly lower than that in the si-NC group（P < 0.001）. Conclusion：Downregulated expression of LncRNA CBR3-AS1 inhibits cell proliferation，migration and invasion，and promotes apoptosis，which is an independent risk factor affecting the prognosis of osteosarcoma.

Abstract:Objective：To investigate the expression of androgen receptor（AR） and its correlation with molecular classifications in invasive breast cancer. Methods：The expressions of AR，estrogen receptor（ER），progesterone receptor（PR），human epidermal growth factor receptor-type2（HER2） and Ki67 in 635 cases of invasive breast cancer were detected with immunohistochemistry. The expression of AR and its correlation with molecular classifications，histologic grades and expressions of other related proteins was investigated and analyzed. Results：The positive rates of AR in luminal subtype A，luminal subtype B with negative HER2，luminal subtype B with positive HER2，HER2 over-expressing subtype，and triple negative subtype were 74.5%（137/184），56.1%（96/171），67.8%（40/59），56.0%（56/100），and 32.2%（39/121），respectively. The expression level of AR was lower in triple negative subtype than that in other subtypes（P<0.05）. The expression of AR was significantly lower in adjacent tissues compared with invasive breast cancer tissues（P<0.05）. There were no statistical difference in the expressions of AR with different age and different histologic grades（P>0.05）. The expression of AR positively correlated with the expression of ER and PR（P<0.05），while negatively correlated with the expression of Ki-67（P<0.05）. Conclusion：AR is expressed in different molecular classification of invasive breast cancer. Combined detection of AR and ER，PR，HER-2 may play an important role in predicting clinical outcomes of breast cancer.

Abstract:Objective：To investigate the level of serum soluble growth stimulating gene 2 protein（sST2）and its correlation with the severity of coronary artery lesion in patients with acute coronary syndrome（ACS） undergoing percutaneous transtuminal coronary intervention（PCI） therapy. Methods：From July 1，2018 to December 31，2018，173 patients with ACS were selected from the Department of Cardiology，the First Affiliated Hospital of Nanjing Medical University. According to the diagnostic criteria in the critical care medicine emergency rapid diagnosis and treatment guide for ACS，they were divided into the unstable angina（UA） group，the acute ST segment elevation myocardial infarction（STEMI） group and the acute non-STEMI （NSTEMI） group. A total of 85 coronary angiography negative patients were enrolled as the control group in the same period. The results of TG，TC，LDL-C，LP（a），sST2，Killip classification were collected，and the correlations between sST2 and Gensini score，proBNP and Gensini score were analyzed. Results：Compared with the control group，sST2 level in the UA group has no significant difference，but they were increased significantly in the STEMI group and the NSTEMI group. Moreover，sST2 level in the STEMI group was higher than that in the NSTEMI group. Compared with the control group，Gensini score in the patients with ACS was significantly higher，which in the NSTEMI subgroup was higher than that in the STEMI group and the UA group. Serum sST2 level was correlated with Gensini score significantly（r=0.586，P < 0.001）. The proBNP level was correlated with Gensini score significantly（r=0.680，P < 0.001）. Conclusion：Serum sST2 level was positively correlated with the number of coronary lesions and the complexity of coronary lesions.

Abstract:Objective：This study aims to investigate the effects of gestational diabetes mellitus（GDM）on the expression and methylation status of PGC-1α and PDX1 in placenta，and to explore the correlation between PGC-1α，PDX1 and fetal blood glucose. Methods：The birth weight and placental weight of 30 pregnant women with GDM were collected. The corresponding data of 30 full-term neonates without pregnancy complications and umbilical cord abnormalities were collected as control group. DNA and RNA were isolated from placental trophoblast tissue immediately after delivery. The DNA methylation levels of the PGC-1α and PDX1 genes were quantitatively detected using sodium bisulfite sequencing. PGC-1α and PDX1 mRNA levels were measured by reverse transcription quantitative PCR（qRT-PCR）. At the same time，placental insulin，blood glucose and HbA1c levels were detected. Results：Fetal birth weight and placental weight were significantly higher in the GDM group than those in the control group（P < 0.05）. Insulin，HbA1c and blood glucose levels were significantly higher in the GDM group than those in the control group（P < 0.01）. Cord blood insulin levels were positively correlated with birth weight（r=0.648，P < 0.001），placental weight（r=0.795，P < 0.001），blood glucose（r=0.862，P < 0.001），and HbA1c（r=0.927，P < 0.001）. The levels of PGC-1α and PDX1 mRNA were lower in the GDM group compared with the control group，and the PGC-1α gene methylation level was higher in the GDM group than that in the control group（P < 0.05）. There was a negative correlation between blood glucose and mRNA expression of PGC-1α （r=-0.438，P=0.002） and PDX1（r=-0.373，P=0.007） in the placenta. Conclusion：The changes of epigenetic modification of PGC-1α gene in pregnant women with GDM may be one of the causes of abnormal glucose metabolism in their offspring.

Abstract:Objective：To investigate the application value of chronic obstructive pulmonary disease（COPD）assessment test（CAT）and monitoring pulse oxygen saturation（SpO2）in management of patients with COPD. Methods：The correlations of CAT，SpO2 during walking，CAT and SpO2（CATS）with pulmonary function were analyzed respectively. The difference of SpO2 was also analyzed between the two groups which were defined as CAT＜10 and CAT≥10. Results：CAT total score，respiratory CAT score，non-respiratory CAT score，SpO2B，SpO2L，ΔSpO2，CATS were all associated with FEV1（forced expiratory volume in 1 second）% predicted. CATS was also associated with non-respiratory CAT score. In CAT＜10 group，non-respiratory CAT score and SpO2B were associated with FEV1%pred. In CAT ≥10 group，CAT total score，non-respiratory CAT score，SpO2L and ΔSpO2 were associated with FEV1%pred. The SpO2B and SpO2L in CAT≥10 group were higher，and ΔSpO2 was lower than those in CAT＜10 group. Conclusion：Monitoring oxygen saturation may be helpful in diagnosis of acute exacerbation of COPD patients. Non-respiratory CAT score contributes more to CAT total score than respiratory CAT score. CATS，the combination of oxygen saturation and CAT，will improve the management of COPD and precision medicine treatment.

Abstract:In developmental biology，chimera refers to the mixed state that cells or tissues with different genotypes contact and coexist in the same individual. If the cells come from different species，the individual is called interspecies-chimera，whereas the chimera composed of cells coming from the same species is called the intraspecies-chimera. In this paper，we review the origin of the interspecies-chimaera，and analyze the development progress of the interspecies-chimaeras from different types of stem cells and the key factors of their formation. The application of the interspecies-chimaera in research fields and their clinical development are envisaged.

Abstract:The 3D brain organoids derived from human pluripotent stem cells（hPSCs），including embryonic stem cells（ESCs）and induced pluripotent stem cells（iPSCs），provides a new research model for brain development and neurological diseases. The iPSC reprogramming technology combined with 3D brain organoids technology can help researchers obtain syngeneic stem cells from patients directly and differentiate the iPSCs into almost any cells including neurons. The 3D brain organoids have become a bridge from animal experiments to clinical trials. This article reviews the history from the emergence of pluripotent stem cell technology to the birth and development of 3D brain organoids，and introduces the classic models of brain development and neurological diseases using 3D brain organoids as tools，and briefly mentions other applications of 3D brain organoids and the research progress of the related technologies. The limitations and future directions of 3D brain organoids are also discussed.

Abstract:Hematopoietic stem cell transplantation（HSCT）is an important method to treat hematopoietic malignancies and some inherited diseases. Hematopoietic and immunological reconstitutions are the basis of successful transplantation. One significant obstacle to the success of HSCT is represented by graft failure，which severely endangers patients’ short-term survival. As human leukocyte antigen mismatched or haploidentical transplantation，and reduced intensity conditioning technology are more and more widely carried out，the incidence of implant failure increasing. With the study of the mechanism of implant failure and the clinical analysis of larger data，identifying important predictors of implant failure can help us to prevent this important complication of hematopoietic stem cell transplantation early. Here，we provide an overview on the recent advances in the concept，pathogenesis，related factors and treatment methods of hematopoietic stem cell engraftment failure.