ABSTRACT
Objective:To investigate risk factors of nerve injury after carotid body tumor resection.Methods:From 1991 to 2016, the clinical data of patients with neurologic complications after resection of carotid body tumor was retrospectively analyzed. Logistic regression analysis was used to investigate the risk factors of nerve injury.Results:A total of 132 patients with 142 tumors underwent surgery. 45 patients (46 sides) suffered nerve injury, including 4 strokes and 44 nerve injuries. After active rehabilitation, 18 cases were left with permanent nerve injury, and the 4 patients with strokes regained self-care ability. By multivariate regression analysis, high-lying tumors ( OR=4.345, P=0.005), Shamblin Ⅲ tumor ( OR=4.382, P=0.047) increase the risks of postoperative nerve injury. Resection of high-lying tumors carried a higher risk of developing permanent nerve injury ( OR=7.290, P=0.001). Conclusions:Neurologic complication could be alleviated by rehabilitation. Intraoperative abrupt rupture of carotid artery is the leading cause of stroke. Shamblin Ⅲ and high-lying tumor are the predictors of postoperative nerve injury.
ABSTRACT
Objective To investigate the expression characteristics of epidermal growth factor-like domain 7 ( egfl 7 ) in arteriosclerosis obliterans ( ASO) tissues and abdominal aortic aneurysm ( AAA ) tissues, and it's role in atherosclerosis (AS).Methods In this study, 8 normal artery, 11 lower extremity ASO and 34 AAA samples were collected.Immunohistochemistry and in situ hybridization were performed in artery sections to investigate the expression characteristics of egfl 7 at protein and mRNA levels.The relative quantitative detection of egfl 7 mRNA was detected by qRT-PCR.The effect of egfl 7 was examined by RNA interference.Results In ASO and AAA samples, the expression of egfl 7 protein was mainly in the tunica media; The expression site of egfl 7 mRNA was the same as that of egfl 7 protein.Compared with normal artery samples, the expression of egfl 7 mRNA was significantly upregulated in the early stage of ASO samples and AAA samples (325 ± 120 vs.100 ± 36, P ＜ 0.01, 216 ± 133 vs.100 ± 36, P ＜ 0.05 ).Compared with the control group, the proliferative ability of smooth muscle cells was significantly down regulated after egfl 7 interference (0.85 ± 0.05 vs.1.34 ± 0.04, P ＜ 0.01).Conclusions egfl 7 might be a gene that regulates the pathogenic process of atherosclerosis through promoting vascular smooth muscle cell proliferation.