肥胖对14岁以上扁桃体切除术患者术后出血的影响

目的探讨年龄>14岁患者扁桃体切除术后出血的发生率,评价与术后再出血相关的危险因素。方法选取2012年8月—2018年8月中南大学湘雅二医院840例住院行扁桃体切除术的成年患者(年龄>14岁)的临床资料,同时采用Logistic回归模型评估其危险因素。结果扁桃体切除术后出血发生率为3.21%(27/840),扁桃体切除术后出血最常发生在手术后的5或6 d,分别有11和8例患者。男性、慢性阻塞性呼吸暂停综合征、BMI≥30 kg/m2患者扁桃体切除术后出血发生率更高(P<0.05)。多因素Logistic回归分析提示,肥胖[■=3.914,(95%CI=1.473,10.401),P=0.006)]和男性[■=10.331,(95%CI=2.981,35.8041),P=0.000)]是扁桃体切除术后出血发生的独立危险因素。结论肥胖和男性是成人扁桃体切除术后出血的独立危险因素,在扁桃体切除术前以减轻体重为目的营养方法对于预防术后并发症的发生很有必要。

Imaging assessment of profound sensorineural deafness with inner ear anatomical abnormalities

Objective: : To explore the value of a combined computed tomography(CT) and magnetic resonance imaging(MRI) in evaluating profound sensorineural deafness patients before cochlear implant(CI) surgery.Methods: A retrospective analysis of 1012 cases of profound sensorineural deafness that received CI was performed.Results: A total of 96 cases were diagnosed with inner ear abnormalities including large vestibular aqueduct syndrome(LVAS, n ? 61), Michel deformity(n ? 3), cochlear incomplete partition I(n ? 2), cochlear incomplete partition II(n ? 6), cochlear hypoplasia with vestibular malformation(n ? 3), cochlear ossification(n ? 3), bilateral internal auditory canal obstruction(n ? 5) and internal auditory canal stenosis(n ? 2).Conclusion: High resolution CT(HRCT) can display bony structures while MRI can image the membranous labyrinth in preoperative evaluation for cochlear implantation. The combination of these two modalities provides reliable anatomical information regarding the bony and membranous labyrinths, as well as the auditory nerve.

Curcumin Inhibits Lipopolysaccharide-lnduced Mucin 5AC Hypersecretion and Airway Inflammation via Nuclear Factor Erythroid 2-Related Factor 2

Background： Excess mucus production is an important pathophysiological feature of chronic inflammatory airway diseases. Effective therapies are currently lacking. The aim of the study was to evaluate the effects ofcurcumin （CUR） on lipopolysaccharide （LPS）-induced mucus secretion and inflammation, and explored the underlying mechanism in vivo and in vitro. Methods： For the in vitro study, human bronchial epithelial （NCI-H292） cells were pretreated with CUR or vehicle for 30 min, and then exposed to LPS for 24 h. Next, nuclear factor erythroid 2-related factor 2 （Nrf2） was knocked down with Nrf2 small interfering RNA （siRNA） to confirm the specific role of Nrf2 in mucin regulation of CUR in NCI-H292 cells. In vivo, C57BL/6 mice were randomly assigned to three groups （n = 7 for each group）： control group, LPS group, and LPS ＋ CUR group. Mice in LPS and LPS ＋ CUR group were injected with saline or CUR （50 mg/kg） intraperitoneally 2 h before intratracheal instillation with LPS （ 100 μg/ml） for 7 days. Cell lysate and lung tissue were obtained to measured Mucin 5AC （MUC5AC） and Nrf2 mRNA and protein expression by a real-time polymerase chain reaction and Western blotting. Bronchoalveolar lavage fluid （BALF） was collected to enumerate total cells and neutrophils. HistopathologicaI changes of the lung were observed. Data were analyzed by one-way analysis of variance. Student＇s t-test was used when two groups were compared. Results： CUR significantly decreased the expression ofMUC5AC mRNA and protein in NCI-H292 cells exposed to LPS. This effect was dose dependent （2.424 ± 0.318 vs. 7.169 ± 1.785, t = 4.534, and 1.060 ± 0.197 vs. 2.340 ± 0.209, t = 7.716; both P 〈 0.05, respectively） and accompanied by increased mRNA and protein expression of Nrf2 （1.952 ± 0.340 vs. 1.142 ± 0.176, t = -3.661, and 2.010 ± 0.209 vs. 1.089 ±0. 132, t = -6.453; both P 〈 0.05, respectively）. Furthermore, knockdown of Nrf2 with siRNA increased MUC5A C mRN A expression by 47.7%, compared with levels observed in the siRNA-negative group （6.845 ± 1.478 vs. 3.391 ± 0.517, t = -3.821, P 〈 0.05）. Knockdown of Nrf2 with siRNA also markedly increased MUC5A C protein expression in NCI-H292 cells. CUR also significantly decreased LPS-induced mRNA and protein expression of MUC5A C in mouse lung （ 1.672 ± 0.721 vs. 5.961 ± 2.452, t = 2.906, and 0.480 ± 0.191 vs. 2.290 ± 0.834, t = 3.665, respectively; both P 〈 0.05）. Alcian blue/periodic acid-Schiff staining also showed that CUR suppressed mucin production. Compared with the LPS group, the numbers of inflammatory cells （247 ± 30 vs. 334 ± 24, t = 3.901, P 〈 0.05） and neutrophils （185 ± 22 vs. 246 ± 20, t = 3.566, P 〈 0.05） in BALF decreased in the LPS ＋ CUR group, as well as reduced inflammatory cell infiltration in lung tissue. Conclusion： CUR inhibits LPS-induced airway mucus hypersecretion and inflammation through activation of Nrf2 possibly.