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21.
脑部胶质瘤是临床中常见的一种原发性脑肿瘤,具有复发率高、死亡率高以及治愈率低的特点。常规临床诊断主要依靠计算机断层扫描(CT)和磁共振成像(MRI)检查技术进行鉴别。随着成像技术和机器学习方法的不断发展,多模态影像智能分析技术已经逐步成为研究热点,在脑胶质瘤的病灶分割测量、肿瘤分级、预后生存周期预测和基因型辨别等方面具有重要的应用前景。本文重点介绍基于机器学习和多模态影像在脑胶质瘤临床辅助诊断和预后评估中的应用进展。  相似文献   
22.
IntroductionThe choroid plexuses, blood vessels, and brain barriers are closely related both in terms of morphology and function. Hypertension causes changes in cerebral blood flow and in small vessels and capillaries of the brain. This review studies the effects of high blood pressure (HBP) on the choroid plexuses and brain barriers.DevelopmentThe choroid plexuses (ChP) are structures located in the cerebral ventricles, and are highly conserved both phylogenetically and ontogenetically. The ChPs develop during embryogenesis, forming a functional barrier during the first weeks of gestation. They are composed of highly vascularised epithelial tissue covered by microvilli, and their main function is cerebrospinal fluid (CSF) production. The central nervous system (CNS) is protected by the blood-brain barrier (BBB) and the blood–CSF barrier (BCSFB). While the BBB is formed by endothelial cells of the microvasculature of the CNS, the BCSFB is formed by epithelial cells of the choroid plexuses. Chronic hypertension induces vascular remodelling. This prevents hyperperfusion at HBPs, but increases the risk of ischaemia at low blood pressures. In normotensive individuals, in contrast, cerebral circulation is self-regulated, blood flow remains constant, and the integrity of the BBB is preserved.ConclusionsHBP induces changes in the choroid plexuses that affect the stroma, blood vessels, and CSF production. HBP also exacerbates age-related ChP dysfunction and causes alterations in the brain barriers, which are more marked in the BCSFB than in the BBB. Brain barrier damage may be determined by quantifying blood S-100β and TTRm levels.  相似文献   
23.
《Journal of endodontics》2019,45(10):1228-1236
IntroductionThe balance between the host proinflammatory immune response and the counteracting anti-inflammatory and reparative responses supposedly determine the outcome of periapical lesions. In this scenario, the vasoactive intestinal peptide (VIP) may exert a protective role because of its prominent immunoregulatory capacity. In this study, we investigated (in a cause-and-effect manner) the potential involvement of VIP in the development of human and experimental periapical lesions.MethodsPeriapical granulomas (n = 124) and control samples (n = 48) were comparatively assessed for VIP and multiple immunologic/activity marker expression through real-time polymerase chain reaction. Experimental periapical lesions (C57Bl/6 wild-type mice) were evaluated regarding endogenous VIP expression correlation with lesion development and the effect of recombinant VIP therapy in lesion outcome. CCR4KO and IL4KO strains and anti-glucocorticoid-induced TNFR-related protein inhibition were used to test the involvement of Treg and Th2 cells in VIP-mediated effects.ResultsVIP expression was more prevalent in periapical granulomas than in controls, presenting a positive association with immunoregulatory factors and an inverse association/correlation with proinflammatory mediators and the receptor activator of nuclear factor kappa B ligand/osteoprotegerin ratio. Endogenous VIP expression up-regulation was temporally associated with lesion immunoregulation and a decline of bone loss. VIP therapy in mice prompted the arrest of lesion development, being associated with an anti-inflammatory and proreparative response that limits the proinflammatory, Th1, Th17, and osteoclastogenic response in the periapex. The VIP protective effect was dependent of Treg migration and activity and independent of interleukin 4.ConclusionsOur results show that VIP overexpression in human and experimental periapical lesions is associated with lesion inactivity and that VIP therapy results in the attenuation of experimental lesion progression associated with the immunosuppressive response involving Treg cells.  相似文献   
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25.
《Brain stimulation》2020,13(6):1668-1677
BackgroundEndovascular delivery of current using ‘stentrodes’ – electrode bearing stents – constitutes a potential alternative to conventional deep brain stimulation (DBS). The precise neuroanatomical relationships between DBS targets and the vascular system, however, are poorly characterized to date.ObjectiveTo establish the relationships between cerebrovascular system and DBS targets and investigate the feasibility of endovascular stimulation as an alternative to DBS.MethodsNeuroanatomical targets as employed during deep brain stimulation (anterior limb of the internal capsule, dentatorubrothalamic tract, fornix, globus pallidus pars interna, medial forebrain bundle, nucleus accumbens, pedunculopontine nucleus, subcallosal cingulate cortex, subthalamic nucleus, and ventral intermediate nucleus) were superimposed onto probabilistic vascular atlases obtained from 42 healthy individuals. Euclidian distances between targets and associated vessels were measured. To determine the electrical currents necessary to encapsulate the predefined neurosurgical targets and identify potentially side-effect inducing substrates, a preliminary volume of tissue activated (VTA) analysis was performed.ResultsSix out of ten DBS targets were deemed suitable for endovascular stimulation: medial forebrain bundle (vascular site: P1 segment of posterior cerebral artery), nucleus accumbens (vascular site: A1 segment of anterior cerebral artery), dentatorubrothalamic tract (vascular site: s2 segment of superior cerebellar artery), fornix (vascular site: internal cerebral vein), pedunculopontine nucleus (vascular site: lateral mesencephalic vein), and subcallosal cingulate cortex (vascular site: A2 segment of anterior cerebral artery). While VTAs effectively encapsulated mfb and NA at current thresholds of 3.5 V and 4.5 V respectively, incremental amplitude increases were required to effectively cover fornix, PPN and SCC target (mean voltage: 8.2 ± 4.8 V, range: 3.0–17.0 V). The side-effect profile associated with endovascular stimulation seems to be comparable to conventional lead implantation. Tailoring of targets towards vascular sites, however, may allow to reduce adverse effects, while maintaining the efficacy of neural entrainment within the target tissue.ConclusionsWhile several challenges remain at present, endovascular stimulation of select DBS targets seems feasible offering novel and exciting opportunities in the neuromodulation armamentarium.  相似文献   
26.
Central illustration: geographic distribution of the 49 centres participating in the FRENSHOCK registry (35 academic hospitals, 10 general hospitals and four private clinics). Inclusion per centre varied from 1 to 72 patients.
  相似文献   
27.
目的 分析脑胶质瘤的氢质子磁共振波谱(proton magnetic resonance spectroscopy,^1H—MRS)表现及其临床意义;探讨脑胶质瘤的^1H—MRS特点与其病理级别相关性。资料与方法 搜集经临床手术、病理证实的脑胶质瘤36例,按照WHO诊断标准分成两组:低级别脑胶质瘤组、高级别脑胶质瘤组。所有患者在术前行^1H—MRS检查。均在MR非增强成像的基础上获得。使用Siemens Sonata 1.5T超导磁共振扫描仪,多体素扫描,点分辨表面线圈法,检测不同区域代谢物变化。结果 脑胶质瘤的^1H—MRS表现:肌酸(Cr)轻度下降,N-乙酰天门冬氨酸(NAA)显著下降。胆碱(Cho)显著增高。低级别、高级别脑胶质瘤的肿瘤组织分别和对侧正常脑组织的NAA/Cr、Cho/Cr、NAA/Cho比值存在非常显著性差异(P〈0.01);低级别脑胶质瘤和高级别脑胶质瘤的肿瘤组织的NAA/Cr、Cho/Cr、NAA/Cho比值存在显著性差异(P〈0.05)。脑胶质瘤的NAA/Cho、Cho/Cr、NAA/Cr比值与病理级别相关,其中NAA/Cho和Cho/cr比值反映肿瘤级别较稳定;NAA/Cr、NAA/Cho比值存在负相关关系(相关系数rs分别为-0.663,-0.851),Cho/Cr比值存在正相关关系(相关系数rs为0.858)。结论 ^1H—MRS与MRI相结合能提高脑胶质瘤术前诊断的准确性。^1H-MRS可评价脑胶质瘤的分级,反映脑胶质瘤代谢特性以及肿瘤生长潜能。  相似文献   
28.
脑静脉畸形的MRI表现及其诊断价值   总被引:7,自引:0,他引:7  
目的 探讨脑静脉畸形的MRI表现,评价各成像序列的诊断价值。资料与方法 搜集经临床手术证实的脑静脉畸形8例进行回顾性分析,所有患者均进行了常规MRI平扫及3D-MOTSA MRA检查。6例行Gd-DTPA增强T1WI,其中3例行3D-MOTSA增强MRA检查。结果 小脑4例,额叶、顶叶、枕叶共4例。5例MRI平扫引流静脉为长T1短T2流空信号,3例呈长T1低信号、长T2高信号。扩张的髓静脉为网状及条状长T1低信号、长T2高信号,增强扫描呈“海蛇头”样改变,即多条髓静脉呈辐射状汇入粗大的引流静脉。3D-MOTSA MRA检查显示部分引流静脉,髓静脉显示较少。3D-MOTSA增强MRA检查引流静脉全程显示,髓静脉显示数目多。结论 MRI能明确诊断脑静脉畸形的合并症,弥补脑血管造影的不足,3D-MOTSA增强MRA检查可取代脑血管造影。  相似文献   
29.
不同强度运动对大鼠心脏降钙素基因相关肽的影响   总被引:5,自引:0,他引:5  
目的:探讨不同强度运动训练对降钙素基因相关肽(CGRP)在心脏组织中表达的影响及其作用机制。方法:将60只SD大鼠随机分为对照组(C组)、小强度运动组(LE组)、中等强度运动组(ME组)和大强度运动组(HE组),每组15只。建立8周不同强度运动训练动物模型,采用免疫组织化学法和计算机图像分析技术,对大鼠心脏形态结构进行观察,并进行心脏CGRP免疫组化分析。结果:8周小强度运动后,大鼠心脏CGRP表达较对照组变化不明显;8周中等强度运动后,大鼠心脏CGRP表达较对照组显著增加(P<0.05),HE染色、HBFP染色和变色酸2R亮绿染色显示心肌组织形态结构无明显改变,仅心肌纤维有轻度缺血缺氧改变;8周大强度运动后,大鼠心脏CGRP表达较对照组显著减少(P<0.05),HE染色、HBFP染色和变色酸2R亮绿染色显示心肌形态结构发生改变并存在明显的缺血缺氧损伤。结果表明,长期中等强度运动使心脏CGRP表达增加,改善了冠状循环和心肌血液供应,对心肌细胞具有保护作用;长期大强度运动使心脏CGRP对心肌细胞的保护作用减弱,可能是导致心肌发生缺血缺氧性损伤的重要原因之一。  相似文献   
30.
重型颅脑损伤的手术治疗   总被引:5,自引:1,他引:4  
目的探讨重型颅脑损伤梯度减压的手术方法对预防术中脑膨出、降低死亡率及致残率的效果。方法对100例重型颅脑损伤患者采用分次减压手术方式及去骨瓣后,硬膜与颞肌筋膜瓣减张缝闭硬膜切口方法。结果40例脑肿胀患者术中脑嘭出6例占15.0%,死亡19例占47.5%;60例脑内血肿病人未发生脑膨出,死亡12例占20%。结论脑外伤后脑血管调节麻痹及血肿压迫继发脑水肿易造成脑膨出.术中分次减压降低了骨窗部位脑组织的顺应性,从而降低了局部的压力梯度,避免脑血管急性扩张,能有效防止脑膨出,降低死亡率及致残率。  相似文献   
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