非编码RNA与胸主动脉瘤的研究进展

摘要：非编码RNA是一类缺乏编码蛋白能力的RNA,在机体发育和疾病发生发展过程中发挥着复杂而精确的调控功能。目前认为胸主动脉瘤（Thoracic aortic aneurysm, TAA）的发病涉及遗传因素、动脉内血流动力学变化、透壁炎症反应及细胞外基质降解和重构等。研究发现胸主动脉瘤病理进展过程中,易累及主动脉中膜平滑肌细胞,从而发生平滑肌细胞的丢失以及表型转化,而这些改变受到众多非编码RNA的调节。因此本文针对非编码RNA与胸主动脉瘤发病机制的密切关联做详细阐述。     

A disorder of collagen biosynthesis in patients with cerebral artery aneurysm

12 patients with subarachnoid hemorraghe due to rupture of a cerebral aneurysm were examined clinically for symptoms and signs of a connective tissue disorder and biochemically for details of the biosynthesis of collagen. No uniform clinical pattern of any connective tissue disorder was seen in these patients, although selected signs were observed. Skin fibroblast cultures were then established. The rate of procollagen production in two cell lines was reduced by 40% and 50%, respectively, and the intracellular accumulation of hydroxyl[¹⁴C]proline (as a percentage of total hydroxy[¹⁴C]proline) was increased by 70% in each relative to eight control cell lines. No difference was found in the degree of intracellular degradation of procollagen. After pulse-labelling, however, the radioactive procollagen was secreted into the medium in 1 h in the control cells, but required at least 3 h in the two aneursym patient cell lines. The results, thus, suggest that delayed secretion of procollagen rather than increased intracellular degradation led to the reduction in the rate of procollagen synthesis in these two fibroblast lines from patients with cerebral artery aneurysm.     

Synthesis of structurally unstable type III procollagen in patients with cerebral artery aneurysm

The biosynthesis of collagen was studied in skin fibroblast cultures established from 11 patients with cerebral artery aneurysms. Six patients had familial subarachnoid hemorrhage (SAH), while five patients were considered as sporadic cases. The structural stability of the triplet-helical medium procollagen was studied by measuring the thermal denaturation temperature (T_m) of type I and type II procollagen molecules. Structural instability of type III procollagen was demonstrated in two patients with familial SAH. Te T_m of type III procollagen was 39.0°C and 39.5°C in two of the cell lines, while the control value was 40.3°C. The stability of type I procollagen did not differ from that of the controls, and the main features of the biosynthesis of collagen were similar in the aneurysm patient cell lines and in the controls. The results suggest that a structural defect of type III procollagen may serve as an etiological factor in the formation of cerebral artery aneurysms.     

多层螺旋CT 血管造影在脑动脉瘤中应用

目的:观察多层螺旋CT血管造影对脑动脉瘤的诊断价值.方法:对16例脑动脉瘤患者的多层螺旋CT血管造影结果进行总结分析.结果:多层螺旋CT血管造影的诊断准确性与DSA无明显差异;多层螺旋CT血管造影显示动脉瘤的部位、大小、动脉瘤颈结构及其与周围血管的关系等与手术结果基本符合.结论:多层螺旋CT血管造影对脑动脉瘤的诊断准确率高,具备十分重要的临床应用价值.     

不同时机行血管介入栓塞术治疗颅内动脉瘤的疗效及对患者预后、神经功能和血清炎性因子的影响

摘要 目的：探讨不同时机行血管介入栓塞术治疗颅内动脉瘤的疗效及对患者预后、神经功能和血清炎性因子的影响。方法：选择2019年3月到2020年12月期间我院收治的80例颅内动脉瘤患者,按手术时间的不同将其分为早期组、延期组,其中早期组36例,发病至手术时间≤72 h;延期组44例,发病至手术时间＞72 h,对比两组疗效、预后、神经功能、血清炎性因子及并发症发生率。结果：早期组的完全栓塞率高于延期组,基本栓塞率低于延期组（P<0.05）。两组术后3个月美国国立卫生研究院卒中量表（NIHSS）、改良Rankin量表评分均较术前下降,且早期组低于延期组（P<0.05）。早期组的预后良好率高于延期组（P<0.05）。两组术后3 d血清白介素-6（IL-6）、肿瘤坏死因子-α（TNF-α）水平下降,且早期组低于延期组（P<0.05）,白介素-10（IL-10）水平升高,且早期组高于延期组（P<0.05）。早期组的并发症发生率低于延期组（P<0.05）。结论：早期行血管介入栓塞术治疗颅内动脉瘤患者,可提高完全栓塞率,减轻神经功能损伤及炎性应激,降低并发症的发生风险,促进预后和生活质量改善。     

Flow dynamics in Models of Intracranial Terminal Aneurysms

Flow dynamics play an important role in the pathogenesis and treatment of intracranial aneurysms. The evaluation of the velocity field in the aneurysm dome and neck is important for the correct placement of endovascular coils, and the temporal and spatial variations of wall shear stress in the aneurysm are correlated with its growth and rupture. This numerical investigation describes the hemodynamic in two models of terminal aneurysm of the basilar artery. Aneurysm models with a aspect ratio of 1.0 and 1.67 were studied. Each model was subject to physiological representative waveform of inflow for a mean Reynolds number of 560. The effects of symmetric and asymmetric outflow conditions in the branches were studied.     

瑞芬太尼复合七氟醚在颅内动脉瘤栓塞术中的临床观察

目的：探讨瑞芬太尼复合七氟醚在颅内动脉瘤栓塞术中的临床效果。方法：回顾性分析在我院行择期颅脑动脉瘤栓塞术的70例患者的临床资料,按照随机序号的方式将其分为观察组和对照组各35例,观察组患者采用瑞芬太尼复合七氟醚麻醉,对照组采用瑞芬太尼复合异丙酚麻醉,对两组麻醉诱导前1min（T1）、麻醉诱导后1min（T2）、插管时（T3）、手术开始后30min（T4）以及拔管时（T5）患者的血压、心率变化及清醒后拔管时间进行记录和分析。结果：两组患者在T2时收缩压（Systolic blood pressure,SBP）、舒张压（Diastolic blood pressure,DBP）和心率（HeartRate,HR）均较T1明显下降,比较差异均有统计学意义（P〈0．05）;观察组患者的清醒时间（5．1±1．5）min及拔管时间（15．5±7．5）min均明显短于对照组,两组比较差异有统计学意义（P〈0．05o结论：在进行颅内动脉瘤栓塞术时,选择使用瑞芬太尼复合七氟醚的麻醉方式,可使患者血流动力学较为稳定,术后苏醒较快,值得在临床推广应用。     

Anatomically specific reactive oxygen species production participates in Marfan syndrome aneurysm formation

Marfan syndrome (MFS) is a connective tissue disorder that results in aortic root aneurysm formation. Reactive oxygen species (ROS) seem to play a role in aortic wall remodelling in MFS, although the mechanism remains unknown. MFS Fbn1^C1039G/+ mouse root/ascending (AS) and descending (DES) aortic samples were examined using DHE staining, lucigenin‐enhanced chemiluminescence (LGCL), Verhoeff's elastin‐Van Gieson staining (elastin breakdown) and in situ zymography for protease activity. Fbn1^C1039G/+ AS‐ or DES‐derived smooth muscle cells (SMC) were treated with anti‐TGF‐β antibody, angiotensin II (AngII), anti‐TGF‐β antibody + AngII, or isotype control. ROS were detected during early aneurysm formation in the Fbn1^C1039G/+ AS aorta, but absent in normal‐sized DES aorta. Fbn1^C1039G/+ mice treated with the unspecific NADPH oxidase inhibitor, apocynin reduced AS aneurysm formation, with attenuated elastin fragmentation. In situ zymography revealed apocynin treatment decreased protease activity. In vitro SMC studies showed Fbn1^C1039G/+‐derived AS SMC had increased NADPH activity compared to DES‐derived SMC. AS SMC NADPH activity increased with AngII treatment and appeared TGF‐β dependent. In conclusion, ROS play a role in MFS aneurysm development and correspond anatomically with aneurysmal aortic segments. ROS inhibition via apocynin treatment attenuates MFS aneurysm progression. AngII enhances ROS production in MFS AS SMCs and is likely TGF‐β dependent.