ABSTRACT
@#【Objective】To investigate the clinical efficacy of endoscopic tympanoplasty for chronic suppurative otitis with large tympanic membrane perforation.【Methods】A total of 110 cases（115 ears）which were diagnosed as chronic suppurative otitis with large tympanic membrane perforation were retrospectively collected from May 2017 to Jan 2019. All cases were performed endoscopic tympanoplasty；including removing tympanic lesions，reconstruction of ossicular chain， and myringoplasty with cartilage and perichondrium complex by underlay technique. At the same time of tympanoplasty ， balloon eustachian tuboplasty（BET）was performed in patients who were diagnosed with eustachian tube dysfunction. The graft success rate，pure tone threshold average（PTA）of speech frequency and the air-bone gap（ABG）were assessed at 3 months after surgery.【Results】The primary graft success rate was 95.7%，and the PTA and ABG were（25.7±11.8）dB HL and（13.8 ± 6.9）dB HL，respectively，which showed significant differences compared with pre- operation conditions （P < 0.001）. Furthermore，29 ears which were diagnosed with eustachian tube dysfunction were treated with BET at the same time of tympanoplasty. Compared with simply tympanoplasty （86 ears），no difference was found in primary graft success rate ，PTA and ABG post-operation（P > 0.05）.【Conclusions】 Endoscopic tympanoplasty is an effective surgery，and the cartilage and perichondrium complex is a reliable repair material for large tympanic membrane perforation ，which are both worthy of clinical promotion. Furthermore ，BET at the same time of tympanoplasty could ensure clinical efficacy for the patients with eustachian tube dysfunction.
ABSTRACT
Squamous cell carcinoma(SCC) is a significant cause of cancer morbidity and mortality worldwide, with an incidence of up to 166 cases per 100 000 population. It arises in the skin, upper aerodigestive tract, lung, and cervix and affects more than 200 000 Americans each year. We report here that a microarray experiment comparing 41 SCC and 13 normal tissue specimens showed that Id2, a gene that controls the cell cycle, was significantly up-regulated in SCC. Enforced expression of Id2 in vitro stimulated the proliferation of SCC cells and up-regulated the transcription of nuclear factor kappa B (NF-κB) and cyclin D1. Enhancement of the NF-κB activity with p65 significantly increased the cell proliferation and the transcription of cyclin D1, whereas inhibition of the NF-κB activity with I kappa B alpha mutant (IκBαM) and pyrroline dithiocarbamate (PDTC) abrogated cell proliferation and transcription of cyclin D1. Furthermore, a mutated NF-κB binding site in the cyclin D1 promoter fully abrogated the Id2-induced transcription of cyclin D1. Taken together, these data indicate that Id2 induces SCC tumor growth and proliferation through the NF-κB/cyclin D1 pathway.