ABSTRACT
Hypoxia-inducible factor-1 (HIF-1) is a critical nuclear transcriptional factor mediating cell adaptive response to hypoxia in mammalian and human .It is the key mediator which modulates oxygen homeostasis exclusively .In the one hand , HIF-1 can protect and promote kinds of physiological processes , such as embryo normal development , cartilage and bone formation .In the other hand, it is also involved in lots of human deceases which is caused by ischemia and hypoxia , such as tumor, diabetes and its complica-tions.The molecular mechanisms of HIF-1 involved in these diseases have become a research hotspot and such studies will provide the new therapeutic means for these diseases , recent new drug researches have been focused on HIF-1 related signal pathway inhibitors , HIF-1 activity inhibitors, HIF-1 targeted therapy, etc.
ABSTRACT
Embryonic stem (ES) cells have the unique capacity to proliferate extensively and maintain the potential to differentiate into advanced derivatives of all three primary germ layers. ES cell lines can also be generated from human blastocyst embryos and are considered promising donor sources for cell transplantation therapies for diseases such as juvenile diabetes, Parkinson's disease, and heart failure. However, as for organ transplants, tissue rejection remains a significant concern for ES cell transplantation. Another concern is the use of human embryos. One possible means to avoid these issues is by reprogramming the nuclei of differentiated cells to ES cell-like, pluripotent cells. This review discusses the potential of these strategies to generate tailor-made pluripotent stem cells and the role of transcription factors in the reprogramming process.
Subject(s)
Humans , Cell Culture Techniques , Cell Differentiation , Physiology , Cells, Cultured , Cellular Reprogramming , Nuclear Transfer Techniques , Pluripotent Stem Cells , Cell BiologyABSTRACT
Objective:To screen for simulation peptide binding specifically to the first and the second extra-cellular domain of CC chemokine receptor 5(CCR5),and to observe their therapeutic effect on mice with experimental autoimmune encephalomyelitis(EAE).Methods:Phage display peptide library was used to screen for peptide sequence binding specifically to CCR5;ELISA was used to identify its binding activity and analyze its DNA sequence.The simulation peptide was synthesized and was injected into abdominal cavity of the EAE mice.Spinal cord tissues were obtained and the pathologic changes were studied by H-E staining in EAE control group and simulation peptide group.Results:Twenty phage clones were randomly chosen for identification and ELISA showed that there were eighteen clones had a strong binding activity with CCR5.The positive clones were sequenced and four peptides of high frequency were obtained:STFTTTL,TPIPQLL,SLPLPKP,and QTSSAAL.Mean clinical score of mice in the EAE model group was 3 and that of the simulation peptide group was 1.H-E staining found that the spinal cord tissues in EAE model group had great number of inflammatory cells and evident demyelination changes;the simulation peptide group had less inflammatory cells and no demyelination changes.The four short peptides had an effect of suppressing and delaying the development of EAE,with the average inhibition rate being 43%(P
ABSTRACT
Objective:To study the expression of chemokine receptor CCR5 in follicular thyroid carcinoma and the serum level of CCR5 ligand,so as to assess the role of CCR5 in progression and metastasis of follicular thyroid carcinoma.Methods:Fifteen samples of follicular thyroid carcinoma,17 samples of follicular thyroid adenoma and 12 adjacent normal samples were analyzed immunohistochemically for CCR5 expression.The sera concentrations of CCL3,CCL4 and CCL5 were measured by ELISA in all patients.Results:CCR5 was positive in follicular thyroid carcinoma samples,with the positive rate being 73.33%,and was not detected in the follicular thyroid adenoma and the normal samples(P