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Fu X.,Chengdu Womens and Childrens Central Hospital | Fu X.,University of California at San Diego | Xu Y.,University of California at San Diego
Regenerative Medicine | Year: 2011

Human embryonic stem cells (hESCs) can undergo unlimited self-renewal and retain the pluripotency to differentiate into all cell types in the body. Therefore, as a renewable source of various cell types, hESCs hold great promise for human cell replacement therapy. While significant progress has been made in establishing the culture conditions for the long-term self-renewal of hESCs, several challenges remain to be overcome for the clinical application of hESCs. One such challenge is to develop strategies to scale-up the production of clinic-grade hESCs in xeno-free and chemically defined medium without inducing genomic instability. To achieve this goal, it is critical to elucidate the molecular pathways required to maintain the self-renewal, survival and genomic stability of hESCs. This article describes recent progress in addressing this challenge and discusses the strategies to improve the scalability of the production of hESCs by inhibiting their apoptosis. © 2011 Future Medicine Ltd.

Huang J.,Chengdu Womens and Childrens Central Hospital | Ni S.,Tianjin Central Hospital of Gynecology Obstetrics | Li D.,University of Sichuan | He Y.,University of Sichuan
Genetic Testing and Molecular Biomarkers | Year: 2015

Objective: Previous studies have shown that miRNA plays a key role in cervical carcinogenesis. Interleukin (IL)-1α can promote tumor growth, invasion, migration, and angiogenesis. An insertion/deletion polymorphism (rs3783553) in the IL1A 3′ untranslated region may disrupt a binding site for miR-122 and miR-378 and thus change the transcription of IL-1α. The purpose of this study was to evaluate the association between the rs3783553 polymorphism and the risk of cervical squamous cell carcinoma (CSCC). Methods: Polymerase chain reaction was used to genotype the IL1A rs3783553 polymorphism in 235 patients with CSCC and 326 controls. Results: We found that the ins/ins genotype had a decreased risk to develop CSCC (odds ratio [OR]=0.48, 95% confidence interval [CI], 0.25-0.95). However, no significant association was observed between the IL1A rs3783553 genotype and clinical features. Conclusion: These findings indicate that the IL1A rs3783553 polymorphism may be associated with the etiology of CSCC. © 2015, Mary Ann Liebert, Inc.

Fu X.,Chengdu Womens and Childrens Central Hospital | Fu X.,University of California at San Diego | Xu Y.,University of California at San Diego
Genome Medicine | Year: 2012

Human embryonic stem cells (hESCs) can undergo unlimited self-renewal and are pluripotent, retaining the ability to differentiate into all cell types in the body. As a renewable source of various types of human cells, hESCs hold great therapeutic potential. Although significant advances have been achieved in defining the conditions needed to differentiate hESCs into various types of biologically active cells, many challenges remain in the clinical development of hESC-based cell therapy, such as the immune rejection of allogeneic hESC-derived cells by recipients. Breakthroughs in the generation of induced pluripotent stem cells (iPSCs), which are reprogrammed from somatic cells with defined factors, raise the hope that autologous cells derived from patient-specific iPSCs can be transplanted without immune rejection. However, recent genomic studies have revealed epigenetic and genetic abnormalities associated with induced pluripotency, a risk of teratomas, and immunogenicity of some iPSC derivatives. These findings have raised safety concerns for iPSC-based therapy. Here, we review recent advances in understanding the genomic and functional stability of human pluripotent stem cells, current challenges to their clinical application and the progress that has been made to overcome these challenges. © 2012 BioMed Central Ltd.

Li F.,Shanghai JiaoTong University | Wu T.,Shanghai JiaoTong University | Lei X.,Shanghai JiaoTong University | Zhang H.,Shanghai JiaoTong University | And 2 more authors.
PLoS ONE | Year: 2013

Objective:To evaluate if the Apgar score remains pertinent in contemporary practice after more than 50 years of wide use, and to assess the value of the Apgar score in predicting infant survival, expanding from the neonatal to the post-neonatal period.Methods:The U.S. linked live birth and infant death dataset was used, which included 25,168,052 singleton births and 768,305 twin births. The outcome of interest was infant death within 1 year after birth. Cox proportional hazard-model was used to estimate risk ratio of infant mortality with different Apgar scores.Results:Among births with a very low Apgar score at five minutes (1-3), the neonatal and post-neonatal mortality rates remained high until term (≥ 37 weeks). On the other hand, among births with a high Apgar score (≥7), neonatal and post-neonatal mortality rate decreased progressively with gestational age. Non-Hispanic White had a consistently higher neonatal mortality than non-Hispanic Black in both preterm and term births. However, for post-neonatal mortality, Black had significantly higher rate than White. The pattern of changes in neonatal and post-neonatal mortality by Apgar score in twin births is essentially the same as that in singleton births.Conclusions:The Apgar score system has continuing value for predicting neonatal and post-neonatal adverse outcomes in term as well as preterm infants, and is applicable to twins and in various race/ethnic groups. © 2013 Li et al.

Wang X.-Q.,University of Sichuan | Wang X.-M.,Chengdu Womens and Childrens Central Hospital | Zhou T.-F.,University of Sichuan | Dong L.-Q.,University of Sichuan
European Review for Medical and Pharmacological Sciences | Year: 2012

BACKGROUND: Asthma is a disease resulting from a complex interaction of multiple genetic and environmental factors. More than 200 asthma candidate genes have been identified in the past decades by using genetic association studies, positional cloning and knockout mouse approaches. AIM: This study was to identify differentially expressed genes and provide direction for medicine design related to pediatric allergic asthma with DNA microarray. MATERIALS AND METHODS: The gene expression profile of pediatric allergic asthma GSE18965 was downloaded from Gene Expression Omnibus database which includes 16 samples, 7 normal and 9 pediatric allergic asthma samples. The differentially expressed genes between normal and disease samples were identified by using R language. The co-expression coefficient was calculated among the differentially expressed genes to construct co-expression networks with String Software. Software DAVID and FuncAssociate were used to analyze the functions of genes in the co-expression networks. RESULTS: A total of 133 genes were identified as differentially expressed genes between normal and disease samples, and 8 related small medicine molecules were also obtained (penbutolol, felbinac, iodixanol, josamycin, oxolamine, 3-nitropropionic acid, scriptaid, and sanguinarine) from database CMAP. The differentially expressed genes were enriched in several biological processes, in which viral transcription and lysosome were the most significant GO term of up-or down-regulated genes. CONCLUSIONS: Our present findings shed new light on the molecular mechanism of allergic asthma and provide three small molecular medicines (3-nitropropionic acid, scriptaid, and sanguinarine) which have the potential to use in clinic for treatment of allergic asthma in future.

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