1.Effects of Periodontal Ligament Cells on Alveolar Bone Metabolism under the Action of Force and Inflammatory Factors and Its Molecular Mechanisms.
Acta Academiae Medicinae Sinicae 2017;39(3):432-437
Periodontal ligament may have independent response to orthodontic stimulation and thus initiate alveolar bone osteogenesis and osteoclasts. Orthodontic-induced alveolar bone remodeling has no bone loss,while inflammation can lead to alveolar bone loss,suggesting that force signal and inflammatory factors may induce the differentiation of undifferentiated cells in the periodontal ligament via different pathways. The strength of the force and the nature of the force (basal tension and fluid shear force) may affect the differentiation of periodontal ligament cells,and may produce antagonistic or synergistic effect with the inflammatory factors through complex autocrine and paracrine regulation,resulting in local bone reconstruction,which is manifested as bone deposition and bone absorption. Studies have shown that Wnt signaling is an important regulatory pathway for osteoblast differentiation. Inflammatory factors can block the differentiation of stem cells into osteoblasts. The Wnt pathway is closely related to the effects of force and inflammatory factors on the differentiation of periodontal ligament cells.
4.Influence of factors on long-term survival of stage Ⅰ NSCLC by detection of micrometastatic tumor cells in pNO lymph nodes
Cancer Research and Clinic 2009;21(6):386-389
Objective To explore the influence of some factors on long-term survival of postoperative stage Ⅰ NSCLC patients. Methods 91 patients of NSCLC who underwent radical surgery of the primary tumor with dissection of the hilar and mediastinal lymph nodes were diagnosed as stage Ⅰ NSCLC postoperatively by pathology and followed up for 5 years. Its hilar and subcarinal lymph nodes were detected occult micrometastastic tumor cells by immunohistochemistry (SP method) by using the binoclonal antibody multicytokeratin (AE1/AE3) as a micrometastatic marker. To analyse the influence of micrometastasis and the clinicopathologic characteristics on long-term survivals. Results The rate of micromatastasis of stage Ⅰ NSCLC was 49 %. The five-year overall survival rate was 70.3 %. The median of survival time was 48.5months. The rate of metastasis was 32 % and the meantime of relapse and metastasis was 36.6months. Tumor size, differentiation, stage, and micrometastasis were significantly associated with relapse and metastasis (P <0.05). The tumor differentiation, stage, and micrometastasis were found to be significant independent factor on survival in multivariate analysis (P<0.05). Conclusion There was nodal micrometastasis in completely resected stage Ⅰ NSCLC, and the tumor differentiation, stage, and micrometastasis were found to be significant independent factor on survival.
5.Interferons 50 years and liver diseases.
Chinese Journal of Hepatology 2007;15(11):801-803
6.Strategies for the treatment of hepatic fibrosis.
Chinese Journal of Hepatology 2007;15(10):721-724
7.Challenges regarding the treatment of viral hepatitis B.
Chinese Journal of Hepatology 2005;13(7):481-482
9.A Novel Model for DNA Replication and Transcription
Progress in Biochemistry and Biophysics 2001;28(2):148-151
In two models for DNA replication and transcription, tra ditional one known as sliding model postulates that proteins involving replicati on and transcription track on the DNA template as a locomotive. In factory model proposed recently, those proteins are immobilized on nuclear structure, to pull the template. Growing evidence from biochemistry, biophysics, and cell biology suggests that the factory model is an actual fact in vivo.
10.Oncogenic mechanism and biological effect of Evi-1 gene
Journal of International Oncology 2013;(3):170-173
Ecotropic viral integration site-1 (Evi-1) gene is first identified as a binding site for retrovirus in murine myeloid leukemia.The human homologue with the murine in leukemia oncogene Evi-1 is about 91% of nuclear sequence and 94% of amino acid.Evi-1 gene is high expressed in myeloid malignancies and other tumors.The main tumorigenic mechanisms of Evi-1 gene include inhibiting TGF-β signal path by depressing Smad3,adjusting cell cycle,promoting angiogenesis,inhibiting JNK.activating AP-1,and so on.