Objective To explore the role of case based learning (CBL)on Otolaryngology-Head and Neck Surgery teaching. Methods First, correct and high-quailty teaching case was selected. Then, reasonable and precise question was edited. All students needed to prepare their lessons before class and were encouraged to ask question or answer question. And some warnings should be noticed. Result After CBL being implemented, the students received higher clinical grades and more clinical skills. They were more likely to retain their initial interest in or switch their preference to careers in otolaryngology. The supervisor highly appreciated our teaching. Conclusion CBL is feasible in Otolaryngology-Head and Neck Surgery teaching and it should be applied more in future.

Objective In order to improve the medical education on otolaryngology,a teaching innovation was implemented.Methods Teaching model was innovated,which included redesigning teaching plan,augmenting study activeness,establishing a teaching system to raise clinic and creative ability.A series of teaching innovation methods was used including optimizing the theoretical and clinic course,adding case course and discussing course,combining lecture and discuss and traditional and modern teaching methods.Results After the teaching innovation being implemented,the students received higher clinical grades and more clinical skills.They were more likely to retain their initial interest in or switch their preference to careers in otolaryngology.The supervisor highly appreciated our teaching.Conclusion The teaching innovation is successful and it's a good reference for deepening teaching reform in future.

Objective To investigate the possible pathogenic mechanisms of narrow pharynx in obstructive sleep apnea syndrome (OSAS) induced by neurogenic inflammation Methods The levels of nitric oxide (NO) and calcitonin gene related peptide (CGRP) in fasting plasma and pharyngeal soft tissue homogenate from mild, moderate, and severe OSAS patients, the normal controls, and patients undergoing uvulopalatopharyngoplasty (UPPP) were detected by immunoradioassay and enzyme reduction Results Plasma NO level in serious OSAS patients was the lowest in the five groups and that in the control group was the highest [severe OSAS=(53 33?7 83) mmol/L, controls=(74 30?6 40) mmol/L, UPPP group=(68 12?7 46) mmol/L, moderate OSAS=(60 45?7 51) mmol/L, mild OSAS=(69 24?6 32) mmol/L, P 0 05) [severe OSAS =(44 18?5 80) mmol/L, moderate OSAS=(48 04?6 66), mild OSAS=(50 72?5 33) mmol/L, controls =(54 37?4 43) mmol/L, UPPP group =(54 10?3 70) mmol/L] NO level in pharyngeal tissue of OSAS increased significantly [OSAS =(0 748?0 053) ?mol/g, controls=(0 382?0 031) ?mol/g, P

Although human telomerase catalytic subunit (TERT) has several cellular functions including telomere homeostasis, genomic stability, cell proliferation, and tumorigenesis, the molecular mechanism underlying anti-apoptosis regulated by TERT remains to be elucidated. Here, we show that ectopic expression of TERT in spontaneously immortalized human fetal fibroblast (HFFS) cells, which are a telomerase- and p53-positive, leads to increases of cell proliferation and transformation, as well as a resistance to DNA damage response and inactivation of p53 function. We found that TERT and a mutant TERT (no telomerase activity) induce expression of basic fibroblast growth factor (bFGF), and ectopic expression of bFGF also allows cells to be resistant to DNA-damaging response and to suppress activation of p53 function under DNA-damaging induction. Furthermore, loss of TERT or bFGF markedly increases a p53 activity and DNA-damage sensitivity in HFFS, HeLa and U87MG cells. Therefore, our findings indicate that a novel TERT-bFGF axis accelerates the inactivation of p53 and consequent increase of resistance to DNA-damage response.
*Apoptosis ; *Catalytic Domain ; Cell Line, Transformed ; Cell Proliferation ; DNA Damage ; Fetus/cytology ; Fibroblast Growth Factor 2/*genetics/metabolism ; Fibroblasts/cytology/metabolism ; Gene Expression Regulation, Neoplastic ; Hela Cells ; Humans ; RNA, Messenger/genetics/metabolism ; Telomerase/deficiency/*metabolism ; Tumor Suppressor Protein p53/*metabolism