0.05).The relative bioavailability of the lecithin-bound iodine capsules was 117.4%.CONCLUSION: The test and reference preparations of iodized lecithin were bioequivalent.

OBJECTIVE To drew the map of distribution of concealed sites in epistaxis and optimize the mode of diagnosis and treatment. METHODS We have searched 117 references on intractable/refractory/latent epistaxis treated under nasal endoscopy in the last decade, including 11 708 cases with epistaxis. There were total 11 860 cases in this study plus 152 cases in our hospital. We summed up the experiences of the optimized treatment mode performed on concealed epistaxis, which was searching the accurate bleeding areas by nasal endoscopy and performing minimally invasive radiofrequency treatment without nasal packing. RESULTS We had found that the offending arteries about epistaxis are mainly sphenopalatine artery and anterior or posterior ethmoid artery. The frequency of bleeding areas came as follows: the vault of inferior nasal meatus in 3783 cases(31.90%), the olfactory sulcus of middle turbinate in 3522 cases(29.70%), the posterior regions of middle meatus in 1349 cases(11.37%), the regions of deviation of nasal septum in 1065 cases(8.98%), the foremost regions of nasal cavity in 738 cases(6.22%), and the others or uncertain in 1403 cases(11.83%). Finally, we drew a concise map of distribution about epistaxis on the basis of the concealed bleeding areas and offending vessels. 151 of 152 patients(99.34%) could find out the bleeding sites accurately and stop the bleeding through minimally invasive radiofrequency ablation. CONCLUSION We drew a map of distribution about epistaxis in concealed areas so that it is convenient for us to seek out the bleeding sites. Rational use of nasal endoscopy to explore the sites of intractable epistaxis and minimally invasive radiofrequency are optimized mode of treatment.

Background and objective Activating mutations in epidermal growth factor receptor (EGFR) and KARS are important markers in non-small cell lung cancer. However, EGFR and KARS gene mutations in lung squamous cell carcinoma are rarely reported. hTe aim of this study was to analyze EGFR and KARS gene mutation rate and their relationship with clinical features in patients with lung squamous cell carcinomas. Methods A total of 139 patients undergoing treatment for na?ve lung squamous cell carcinomas with tumor tissue samples available for testing were recruited. EGFR and KARS mutation statuses of the tumor samples were detected using a mutant enriched liquid chip. Results Of the 139 cases of lung squamous cell carcinoma, EGFR mutations were detected in 25 cases (18%), KARS mutations were detected in 7 cases (5%), and the pres-ence of both EGFR and KARS mutations was detected in 1 case (0.7%). EGFR mutations occurred more otfen in females than in males (33.3%vs 16.5%) and in patients that never smoked than in those who smoke (29.6%vs 16.1%). However, the differ-ence did not reach statistical signiifcance (P>0.05). No signiifcant differences were observed in age, stage, and different biopsy type. KARS mutations occurred more otfen in males than in females (5.5%vs 0%), but the difference did not reach statistical signiifcance (P>0.05). No signiifcant differences were observed in age, stage, different biopsy type, and smoking status (P>0.05). Conclusion EGFR and KARS mutations were low in lung squamous cell carcinomas, and had no signiifcant correlation with clinical features. Before using tyrosine kinase inhibitor targeted therapy, EGFR and KARS mutations should be detected in pa-tients with lung squamous cell carcinomas.

Background and objectiveMutations in epidermal growth factor receptor (EGFR) andKARS are im-portant markers in non-small cell lung cancer, which are closely related to the clinical therapeutic effect. To analysis theEGFR andKARS gene mutation rate and its relationship with clinical features in patients with lung adenocarcinoma.Methods395 patients with treatment na?ve lung adenocarcinoma, tumor tissue samples were available for testing. Tumor sampleEGFR and KARS mutation status were detected using mutant enriched liquidchip.Results 395 cases of lung adenocarcinoma,EGFR mutations were detected in 192 cases (48.9%),KARS mutations were detected in 29 cases (7.8%), and the presence ofEGFR andKARS mutation were detected in 1 case (0.3%).EGFR mutations were found to occur signiifcantly more otfen in female than in male patients (62.0%vs 37.1%,P<0.001) and in never smokers than in smokers (61.9%vs 30.3%,P<0.001), no sig-niifcant differences were observed in age, stage and different biopsy type.KARS mutations were not found to have statistical signiifcance (P>0.05) in each clinical factors, only occurred in the wild typeEGFR gene in patients (13.5%, 27/200) was sig-niifcantly higher than that of patients withEGFR mutation (1.0%, 2/192), the difference was statistically signiifcant (P<0.001). ConclusionIn lung adenocarcinomas,EGFR mutation was higher in female and non-smoking patients,KARS mutation only in patients with wild-typeEGFR gene was higher. Before using TKI targeted therapy,EGFR andKARS mutations should be detected.