慢传输型便秘对结直肠癌术后吻合口瘘发生的影响及原因探讨

目的:分析慢传输型便秘对结直肠癌术后吻合口瘘发生的影响及原因。方法:回顾性分析我院普外科2010年10月1日—2017年10月1日收治的1307例行手术治疗的结直肠癌患者,其中无便秘组患者1128例,伴慢传输型便秘组179例;术后发生吻合口瘘患者109例,其中无便秘组92例,伴慢传输型便秘组17例。通过比较两组术后吻合口瘘的发生率、发生时间、发生瘘的级别等来分析慢传输型便秘对结直肠癌术后吻合口瘘发生的影响;在伴慢传输便秘组中根据术后吻合口近和(或)远端肠壁是否存在神经节细胞减少(或缺失)分为两组,通过比较两组术后吻合口瘘的发生率、发生时间及瘘的级别等进一步从病理学方面研究慢传输型便秘对结直肠癌术后吻合口瘘发生的影响。结果:伴慢传输型便秘组术后吻合口瘘的发生率为9.50%,高于无便秘组8.16%(P0.05);但术后吻合口瘘发生时间(7.34±3.17)天,晚于无便秘组(6.08±2.55)天(P0.05);在179例伴慢传输型便秘组中,神经节细胞正常组吻合口瘘的发生率7.89%,低于神经节细胞减少或缺失组12.31%(P0.05);且瘘的发生时间短于神经节细胞减少或缺失组[(6.12±3.29)天vs(8.71±4.36)]天(P0.05)。结论:慢传输型便秘增加结直肠癌术后吻合口瘘的发生率,且延长术后吻合口瘘发生时间;慢传输型便秘增加术后吻合口瘘发生率可能与结直肠切除范围不够,导致吻合口近和(或)远端肠壁存在神经节细胞的减少或缺失有关。     

地氯雷他定联合雷公藤多苷片对慢性特发性荨麻疹患者的临床疗效及情绪的影响

目的 探讨分析地氯雷他定联合雷公藤多苷片对慢性特发性荨麻疹(CIU)患者的临床疗效及负面情绪的影响.方法 选取本院2018年2月～2020年6月住院治疗的80例CIU患者作为主要研究对象,按随机数字表法将研究对象随机分为观察组和对照组,对照组40例患者予以地氯雷他定治疗,观察组40例患者予以地氯雷他定联合雷公藤多苷片治疗.观察比较两组的临床疗效、不良反应发生率、复发率,及治疗前后的风团数目、风团大小、瘙痒评分、汉密尔顿焦虑量表(Hamilton anxiety scale,HAMA)评分和汉密尔顿抑郁量表(Hamilton depression scale,HAMD)评分.结果 (1)观察组患者临床总有效率(95.00％)高于对照组(72.50％)(P＜0.05).(2)观察组患者的风团数目减少、风团变小、瘙痒评分降低,改善优于对照组(P＜0.05).(3)观察组患者的不良反应发生率(5.00％)低于对照组(7.50％)(P＜0.05),观察组患者的复发率(2.50％)低于对照组(15.00％)(P＜0.05).(4)观察组患者的HAMA评分和HAMD评分低于对照组(P＜0.05).结论 地氯雷他定联合雷公藤多苷片可有效缓解CIU患者的瘙痒症状,减少风团数目,缓解患者负面情绪,且不良反应较少,患者复发率较低,临床疗效确切,值得临床推广应用.     

Endodontic treatment of a hypertaurodontic mandibular left second molar in a patient with many taurodonts combined with multiple pulp stones

Taurodontism is a rare embryologic anomaly of teeth, defined by an apical displacement of the furcation of roots and enlarged pulp chambers. Taurodontism has been classified as hypo‐, meso‐ or hypertaurodontism according to the severity of the anomaly. The aim of this case report was to illustrate a clinical case with multiple bilateral taurodonts and to describe the endodontic management of the hypertaurodontic mandibular left second molar with a C‐shaped canal and extensive dental pulp calcifications. A healthy 20‐year‐old male patient was referred for the endodontic treatment of his lower left second molar. Cone beam computed tomography revealed a C‐shaped root canal configuration and several dental pulp calcifications in this tooth. The endodontic treatment was performed in two appointments under an operating dental microscope. A panoramic radiograph, made during the 18 months follow‐up appointment, revealed nine other taurodontic molars, most of them associated with dental pulp calcifications.     

Protein kinase Cδ mediates trimethyltin-induced neurotoxicity in mice in vivo via inhibition of glutathione defense mechanism

We investigated whether protein kinase C (PKC) is involved in trimethyltin (TMT)-induced neurotoxicity. TMT treatment (2.8 mg/kg, i.p.) significantly increased PKCδ expression out of PKC isozymes (i.e., α, βI, βII, δ, and ?) in the hippocampus of wild-type (WT) mice. Consistently, treatment with TMT resulted in significant increases in cleaved PKCδ expression. Genetic or pharmacological inhibition (PKCδ knockout or rottlerin) was less susceptible to TMT-induced seizures than WT mice. TMT treatment increased glutathione oxidation, lipid peroxidation, protein oxidation, and levels of reactive oxygen species. These effects were more pronounced in the WT mice than in PKCδ knockout mice. In addition, the ability of TMT to induce nuclear translocation of Nrf2, Nrf2 DNA-binding activity, and upregulation of γ-glutamylcysteine ligase was significantly increased in the PKCδ knockout mice and rottlerin (10 or 20 mg/kg, p.o. × 6)-treated WT mice. Furthermore, neuronal degeneration (as shown by nuclear chromatin clumping and TUNEL staining) in WT mice was most pronounced 2 days after TMT. At the same time, TMT-induced inhibition of phosphoinositol 3-kinase (PI3K)/Akt signaling was evident, thereby decreasing phospho-Bad, expression of Bcl-xL and Bcl-2, and the interaction between phospho-Bad and 14-3-3 protein, and increasing Bax expression and caspase-3 cleavage were observed. Rottlerin or PKCδ knockout significantly protected these changes in anti- and pro-apoptotic factors. Importantly, treatment of the PI3K inhibitor LY294002 (0.8 or 1.6 µg, i.c.v.) 4 h before TMT counteracted protective effects (i.e., Nrf-2-dependent glutathione induction and pro-survival phenomenon) of rottlerin. Therefore, our results suggest that down-regulation of PKCδ and up-regulations of Nrf2-dependent glutathione defense mechanism and PI3K/Akt signaling are critical for attenuating TMT neurotoxicity.     

A Stable Q Compensated Reverse Time Migration Method Based on Excitation Amplitude Imaging Condition

The stability and efficiency, especially the stability, are generally concerned issues in Q compensated reverse time migration (Q-RTM). The instability occurs because of the exponentially boosted high frequency ambient noise during the forward or backward seismic wavefield propagation. The regularization and low-pass filtering methods are two effective strategies to control the instability of the wave propagation in Q-RTM. However, the regularization parameters are determined experimentally, and the wavefield cannot be recovered accurately. The low-pass filtering method cannot balance the selection of cutoff frequency for varying Q values, and may damage the effective signals, especially when the signal-to-noise ratio (SNR) of the seismic data is low, the Q-RTM will be a highly unstable process. In order to achieve the purpose of stability, the selection of cutoff frequency will be small enough, which can cause great damage to the effective high frequency signals. In this paper, we present a stable Q-RTM algorithm based on the excitation amplitude imaging condition, which can compensate both the amplitude attenuation and phase dispersion. Unlike the existing Q-RTM algorithms enlarging the amplitude, the exponentially attenuated seismic wavefield will be used during both the forward and backward wavefield propagation of Q-RTM. Therefore, the new Q-RTM algorithm is relative stable, even for the low SNR seismic data. In order to show the accuracy and stability of our stable Q-RTM algorithm clearly, an example based on Graben model will be illustrated. Then, a realistic BP gas chimney model further demonstrates that the proposed method enjoys good stability and anti-noise performance compared with the traditional Q-RTM with amplitude amplification. Compare the Q-RTM images of these two models to the reference images obtained by the acoustic RTM with acoustic seismic data, the new Q-RTM results match the reference images quite well. The proposed method is also tested using a field seismic data, the result shows the effectiveness of our proposed method.     

以肺动脉高压为首发表现的先天性中枢性低通气综合征临床特征和基因分析

目的探讨先天性中枢性低通气综合征(CCHS)的临床和基因变异特征。方法分析1例首发表现为不明原因肺动脉高压的CCHS患儿的临床资料,并总结国内外文献中CCHS病例的临床特点、致病机制和基因变异情况。结果11月龄女婴,主要表现为浮肿、尿少、低血压、嗜睡、发绀、抽搐及颅内压增高。B型脑利钠肽、丙氨酸氨基转移酶升高,凝血酶原时间延长。颅脑磁共振示右侧额叶出血;超声心动图示中重度肺动脉高压。靶向捕获二代测序未发现可能的致病基因。采用Sanger法验证示患儿PHOX 2 B基因第3外显子存在多聚丙氨酸重复扩展变异,基因型为20/25。患儿入院后采用无创通气,睡眠时呼吸浅慢、微弱,伴血氧下降;血气分析提示二氧化碳潴留。随后改用夜间无创通气、降肺压药物治疗。复查肺动脉压力明显下降,生命体征稳定。随访至24月龄,夜间只需较低压力水平的无创通气,生长发育无异常。结论对于不明原因的肺动脉高压伴撤机困难患儿,需警惕CCHS。疑诊者应尽早针对CCHS相关基因进行靶向捕获二代测序及PHOX 2 B基因Sanger法验证。早期给予无创通气有望改善预后。     

ELAM-1在鼻咽癌裸鼠移植瘤中的表达及其与转移的关系

目的 建立裸鼠鼻咽癌转移模型并探讨 E-选择素（ELAM-1）与鼻咽癌转移的相关性。方法 将鼻咽癌5-8F细胞悬液注射于裸鼠左后肢爪垫，观察裸鼠状态、成瘤情况并测量裸鼠体重及移植瘤长短径；采用连续病理切片苏木精-伊红染色观察移植瘤及转移情况，将16只人鼻咽癌荷瘤裸鼠分为转移组和非转移组；采用免疫组织化学法检测两组移植瘤组织中ELAM-1的表达。 结果 16只裸鼠均成瘤，成瘤率为100.0%，其中10只裸鼠出现转移瘤，转移率为62.5%。建模前，两组裸鼠体重差异无统计学意义［（13.83±0.56）g vs （14.62±0.30） g，t=1.026，P=0.071］。建模后4~7周，裸鼠瘤体体积呈指数增长，且转移组移植瘤增长速度较非转移组快，非转移组裸鼠瘤体体积小于转移组［（198.91 ± 163.29） mm³ vs （268.76 ±174.31） mm³，t=4.376，P=0.005］。ELAM-1在鼻咽癌裸鼠移植瘤、淋巴结转移灶及远处转移灶中的表达均为阳性，主要表达于细胞膜。转移组移植瘤光密度值高于非转移组（0.4497±0.0705 vs 0.0435±0.0082，t=4.388，P＝0.001）。结论 本研究成功构建稳定性好、转移率高的鼻咽癌裸鼠移植瘤转移模型，且ELAM-1在裸鼠移植瘤中高表达，可促进鼻咽癌裸鼠移植瘤生长和转移。