内镜揭盖术与唇齿沟径路切除术治疗鼻前庭囊肿患者的疗效及对炎性因子的影响

目的:研究内镜揭盖术(ER)与唇齿沟径路切除术(LSPR)治疗鼻前庭囊肿(NVC)患者的临床疗效及对炎性因子的影响。方法:选择2015年7月至2017年6月来我院就诊的NVC患者106例,依据随机数字表法分别纳入ER组(53例)及LSPR组(53例)。ER组行ER治疗,LSPR组行唇齿沟径路切除术。观察两组术中出血量、手术时间、术后创口愈合时间、术后24 h疼痛评分及上皮化时间,两组术前、术后7 d白细胞介素-6(IL-6)、白细胞介素-8(IL-8)、肿瘤坏死因子-α(TNF-α)、C-反应蛋白(CRP)水平,两组术后并发症及复发情况。结果:ER组术中出血量、手术时间、术后创口愈合时间、术后24h疼痛评分及上皮化时间等手术指标均低于LSPR组,差异有统计学意义(P0.05);术后7 d,两组IL-6、IL-8、TNF-α及CRP水平均低于治疗前,且ER组低于LSPR组,差异有统计学意义(P0.05);ER组术后并发症发生率7.55%、术后复发率3.77%,均低于LSPR组的22.64%、20.75%,差异均有统计学意义(P0.05)。结论:与LSPR相比较,ER治疗NVC创伤小,恢复快,可有效降低术后炎性因子水平,术后并发症及复发率低,值得临床应用。     

超声引导下Mammotome微创旋切术治疗乳腺良性肿块

目的:研究超声引导下Mammotome微创旋切术对乳腺良性肿块的治疗价值。方法:回顾性分析2014年9月至2016年9月在本院就诊的BI-RADS分级为2~3级的387例乳腺良性肿块患者,运用Mammotome对729处乳腺病灶行微创旋切术,分析术后病理、并发症、随访半年后的治疗结果。结果:387例患者的729处乳腺病灶均获一次性成功切除。病理示均为良性病灶,其中32个合并不典型增生。术后出现局部血肿共11例(2.8%),皮下瘀斑共16例(4.1%),所有患者均未发生感染及气胸等严重并发症。术后6个月18个在病灶原部位发现肿块;手术无残留率为97.5%。结论:应用超声引导下Mammotome微创旋切术治疗乳腺良性肿块临床可行。     

七氟烷与丙泊酚对腹腔镜直肠癌根治术患者认知功能、T淋巴细胞及肝功能的影响

目的:探讨七氟烷与丙泊酚对腹腔镜直肠癌根治术患者认知功能、T淋巴细胞水平及肝功能指标的影响。方法:选择2015年6月-2017年8月期间于我院进行腹腔镜直肠癌根治术的110例患者为研究对象,按随机数字表法分为观察组和对照组,每组患者55例。观察组采用丙泊酚静脉全麻方式进行术前麻醉,对照组采用七氟烷吸入全麻方式进行术前麻醉。观察两组患者不同时间点平均动脉压(MAP)、心率(HR)情况,比较两组患者手术前后认知功能、T淋巴细胞水平、肝功能各项指标及不良反应发生情况。结果:两组患者不同时间点MAP、HR组间比较差异无统计学意义(P0.05)。术后6 h、12 h观察组简易精神状态量表(MMSE)评分低于术前,术后6 h、12 h、24 h对照组MMSE评分低于术前和观察组(P0.05)。术后3d两组患者CD3~+、CD4~+、CD4~+/CD8~+水平均降低,CD8~+水平均升高,且观察组CD3~+、CD4~+、CD4~+/CD8~+水平高于对照组,CD8~+水平低于对照组(P0.05)。术后3 d两组患者谷丙转氨酶(ALT)、谷草转氨酶(AST)、总胆红素(TBILI)、直接胆红素(DBILI)水平均升高,但观察组患者各项指标水平低于对照组(P0.05)。观察组不良反应发生率为12.73%,与对照组的7.27%比较差异无统计学意义(P0.05)。结论:七氟烷与丙泊酚在腹腔镜直肠癌根治术中的麻醉效果相当,无严重不良反应发生,但应用丙泊酚进行麻醉对患者术后的认知功能、T淋巴细胞、肝功能指标的影响较小,值得临床推广应用。     

内镜黏膜切除术治疗低位直肠侧向发育型肿瘤随机对照研究

目的:探讨内镜黏膜切除术治疗低位直肠侧向发育型肿瘤的临床效果。方法:收集我院收治的低位直肠侧向发育型肿瘤患者40例,随机分为对照组和实验组,每组各20例,对照组患者给予常规内镜下粘膜切除术,实验组患者给予内镜反转黏膜切除术,治疗结束后,对所有患者的病变残留例数、手术时间以及住院时间、并发症发生情况、手术切除效果进行检测并比较。结果:与对照组患者相比,实验组患者复发率较低(P0.05),手术时间以及住院时间、并发症发生率较低(P0.05);两组患者切除效果相比较,实验组分次切除、肿瘤残留例数患者较少,完全切除患者例数较多(P0.05),两组患者的整块切除例数无差异(P0.05)。结论:内镜反转黏膜切除术对于低位直肠侧向发育型肿瘤患者的临床疗效优于常规内镜下粘膜切除术,对临床有指导意义。     

The role of activated NLRP3 inflammatory body in acute kidney injury in rats caused by sepsis and NLRP3-TXNIP signaling pathway

ObjectiveThe model of acute renal injury (AKI) induced by sepsis in rats was established by abdominal resection through surgical suture. The activation mechanism of nod-like receptor with pyrin domain containing 3 (NLRP3) inflammatory corpuscle in AKI induced by sepsis was analyzed.MethodsHere, 60 male rats were selected and divided into two groups, including sham-operated group (NO-OPs group, n = 15) and sepsis group (CELP group, n = 45). In order to examine each index of CELP group, four time points (10, 20, 30, and 40 h) were set as control. In NO-OPs group, only abdominal resection through surgical suture was carried out. The expression levels of NLRP3, apoptosis-associated speck-like protein containing a C-terminal caspase recruitment domain (ASC), caspase-1, and the expression level of NLRP3-TXNIP signaling pathway were measured by immunohistochemistry, Western blotting, immunoprecipitation, and mito-TEMPO (a mitochondria-targeted antioxidant) 40 h after operation and 10, 20, 30, and 40 h post-operation in CELP group. Herein, 40 h post-operation in NO-OPs group and 10, 20, 30, and 40 h post-operation in CELP group, peripheral blood samples were collected.ResultsCompared with NO-OPs group, the levels of serum creatinine (Scr) and blood urea nitrogen (BUN) in CELP group were increased (P < 0.05). Compared with NO-OPs group, the expression levels of interleukin-1β (IL-1β), NLRP3, ASC, and caspase-1 in CELP group were increased (P < 0.05). The expression level of TXNIP in renal tubular epithelial cells in rats was up-regulated. There was a positive correlation between TXNIP and NLRP3. The binding of NLRP3-TXNIP signaling pathway could be inhibited by siRNA transfection or mito-TMPO, and the activity of NLRP3 inflammatory bodies could be inhibited as well.ConclusionActivation of NLRP3 inflammatory corpuscles could promote AKI induced by sepsis. Simultaneously, renal injury may lead to the production of mitochondrial reactive oxygen species (mROS), which may induce the binding of TXNIP to NLRP3.     

DNA End Resection: Nucleases Team Up with the Right Partners to Initiate Homologous Recombination

The repair of DNA double-strand breaks by homologous recombination commences by nucleolytic degradation of the 5′-terminated strand of the DNA break. This leads to the formation of 3′-tailed DNA, which serves as a substrate for the strand exchange protein Rad51. The nucleoprotein filament then invades homologous DNA to drive template-directed repair. In this review, I discuss mainly the mechanisms of DNA end resection in Saccharomyces cerevisiae, which includes short-range resection by Mre11-Rad50-Xrs2 and Sae2, as well as processive long-range resection by Sgs1-Dna2 or Exo1 pathways. Resection mechanisms are highly conserved between yeast and humans, and analogous machineries are found in prokaryotes as well.     

The dystonia gene THAP1 controls DNA double-strand break repair choice

1. Download : Download high-res image (50KB)
2. Download : Download full-size image

     

Control of DNA end resection by yeast Hmo1p affects efficiency of DNA end-joining

The primary pathways for DNA double strand break (DSB) repair are homologous recombination (HR) and non-homologous end–joining (NHEJ). The choice between HR and NHEJ is influenced by the extent of DNA end resection, as extensive resection is required for HR but repressive to NHEJ. Conversely, association of the DNA end-binding protein Ku, which is integral to classical NHEJ, inhibits resection. In absence of key NHEJ components, a third repair pathway is exposed; this alternative-end joining (A-EJ) is a highly error-prone process that uses micro-homologies at the breakpoints and is initiated by DNA end resection. In Saccharomyces cerevisiae, the high mobility group protein Hmo1p has been implicated in controlling DNA end resection, suggesting its potential role in repair pathway choice. Using a plasmid end-joining assay, we show here that absence of Hmo1p results in reduced repair efficiency and accuracy, indicating that Hmo1p promotes end-joining; this effect is only observed on DNA with protruding ends. Notably, inhibition of DNA end resection in an hmo1Δ strain restores repair efficiency to the levels observed in wild-type cells. In absence of Ku, HMO1 deletion also reduces repair efficiency further, while inhibition of resection restores repair efficiency to the levels observed in kuΔ. We suggest that Hmo1p functions to control DNA end resection, thereby preventing error-prone A-EJ repair and directing repairs towards classical NHEJ. The very low efficiency of DSB repair in kuΔhmo1Δ cells further suggests that excessive DNA resection is inhibitory for A-EJ.     

Changes in DNA double-strand break repair during aging correlate with an increase in genomic mutations

A double -strand break (DSB) is one of the most deleterious forms of DNA damage. In eukaryotic cells, two main repair pathways have evolved to repair DSBs, homologous recombination (HR) and non-homologous end-joining (NHEJ). HR is the predominant pathway of repair in the unicellular eukaryotic organism, S. cerevisiae. However, during replicative aging the relative use of HR and NHEJ shifts in favor of end-joining repair. By monitoring repair events in the HO-DSB system, we find that early in replicative aging there is a decrease in the association of long-range resection factors, Dna2-Sgs1 and Exo1 at the break site and a decrease in DNA resection. Subsequently, as aging progressed, the recovery of Ku70 at DSBs decreased and the break site associated with the nuclear pore complex at the nuclear periphery, which is the location where DSB repair occurs through alternative pathways that are more mutagenic. End-bridging remained intact as HR and NHEJ declined, but eventually it too became disrupted in cells at advanced replicative age. In all, our work provides insight into the molecular changes in DSB repair pathway during replicative aging. HR first declined, resulting in a transient increase in the NHEJ. However, with increased cellular divisions, Ku70 recovery at DSBs and NHEJ subsequently declined. In wild type cells of advanced replicative age, there was a high frequency of repair products with genomic deletions and microhomologies at the break junction, events not observed in young cells which repaired primarily by HR.     

右美托咪定联合依托咪酯对老年直肠癌根治术患者术后炎症反应、胃肠功能恢复和认知功能的影响

摘要 目的：探讨右美托咪定联合依托咪酯对老年直肠癌根治术患者术后炎症反应、胃肠功能恢复和认知功能的影响。方法：选择2019年3月~2021年5月南京鼓楼医院收治的180例老年直肠癌患者,均接受腹腔镜下直肠癌根治术治疗。根据随机数字表法将患者分为对照组和研究组,各为90例。对照组患者麻醉选用依托咪酯,研究组患者麻醉选用右美托咪定联合依托咪酯,对比两组术中血流动力学、术后炎症反应、胃肠功能恢复和认知功能,同时记录两组围麻醉期不良反应发生情况。结果：插管即刻（T2）~拔管即刻（T4）时间点,两组心率（HR）、平均动脉压（MAP）先下降后升高,且研究组的波动幅度小于对照组（P<0.05）。两组进食时间组间对比无统计学差异（P>0.05）,研究组的肠鸣音恢复时间、首次排气时间短于对照组（P<0.05）。两组气管拔管时间、呼吸恢复时间、麻醉苏醒时间对比无统计学差异（P>0.05）。两组术后3 d白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）和C反应蛋白（CRP）水平均升高,且研究组的变化幅度小于对照组（P<0.05）。两组术后1 d、术后3 d简明智能状态量表（MMSE）评分先下降后升高,且研究组的波动幅度小于对照组（P<0.05）。两组不良反应发生率组间对比无差异（P>0.05）。结论：老年直肠癌根治术患者麻醉方案选用右美托咪定联合依托咪酯,可减轻机体炎性应激,稳定机体血流动力学,有利于胃肠功能恢复,同时还可减轻对机体认知功能的损害。