原发性脑室出血型Moyamoya病21例临床分析

目的通过回顾性分析我院10年来收治的21例原发性脑室出血型Moyamoya病患者的临床资料,探讨非高血压性原发性脑室出血与Moyamoya病及其影像学特征的关系。方法对我院神经外科10年来确诊的原发性脑室出血Moyamoya病患者的CT、DSA和临床治疗进行回顾性分析。结果 25例非高血压性原发性脑室出血患者中DSA证实21例为Moyamoya病。3例合并基底动脉动脉瘤。所有患者出血侧均存在脉络膜前动脉异常扩张扭曲及异常分支。该组患者首次治疗均获得良好结果。结论 Moyamoya病是成人非高血压性原发性脑室出血的主要病因,对成人非高血压性原发性脑室出血应常规行DSA明确是否存在Moyamoya病。成人非高血压性原发性脑室出血与脉络膜前动脉的扩张扭曲或异常分支密切相关,并且后者可作为前者的预测指标。     

ADAM8 is selectively up‐regulated in endothelial cells and is associated with angiogenesis after spinal cord injury in adult mice

Endothelial cell (EC) loss and subsequent angiogenesis occur over the first week after spinal cord injury (SCI). To identify molecular mechanisms that could be targeted with intravenous (i.v.) treatments, we determined whether transmembrane “a disintegrin and metalloprotease” (ADAM) proteins are expressed in ECs of the injured spinal cord. ADAMs bind to integrins, which are important for EC survival and angiogenesis. Female adult C57Bl/6 mice with a spinal cord contusion had progressively more ADAM8 (CD156) immunostaining in blood vessels and individual ECs between 1 and 28 days following injury. Uninjured spinal cords had little ADAM8 staining. The increase in ADAM8 mRNA and protein was confirmed in spinal cord lysates, and ADAM8 mRNA was present in FACS‐enriched ECs. ADAM8 colocalized extensively and exclusively with the EC marker PECAM and also with i.v.‐injected lectins. Intravenous isolectin B4 (IB4) labels a subpopulation of blood vessels at and within the injury epicenter 3–7 days after injury, coincident with angiogenesis. Both ADAM8 and the proliferation marker Ki‐67 were present in IB4‐positive microvessels. ADAM8‐positive proliferating cells were seen at the leading end of IB4‐positive blood vessels. Angiogenesis was confirmed by BrdU incorporation, binding of i.v.‐injected nucleolin antibodies, and MT1‐MMP immunostaining in a subset of blood vessels. These data suggest that ADAM8 is vascular selective and plays a role in proliferation and/or migration of ECs during angiogenesis following SCI. J. Comp. Neurol. 512:243–255, 2009. © 2008 Wiley‐Liss, Inc.     

分化抑制因子1对创伤组织新生血管化的促进作用观察

目的 探讨分化抑制因子1(Id1)对创伤组织新生血管化的促进作用及其机制.方法 经基因鉴定的SD大鼠16只,随机分为非创伤组(即正常对照组,n=4)和创伤组(包括Id1基因敲除组、Id1诱导表达组和Id1正常表达组,n=4).采用MTT法测定Id1对血管内皮细胞Eahy026增殖的影响,实时定量RT-PCR、蛋白免疫印迹技术检测创伤1、24、48、72h后创伤组织中新生血管化标志物血管内皮细胞生长因子(VEGF)、CD105、内皮素-1(ET-1)等的mRNA和蛋白表达变化,并用报告基因技术检测Id1对VEGF、CD105、ET-1基因表达的调控作用.结果 血管内皮细胞模型实验显示转染Id1siRNA后,血管内皮细胞Eahy926增殖明显受到抑制,以72h时最显著(P<0.01);而转染pcDNAId1后,细胞增殖于48h时即增强(P<0.05),以72h时最显著(P<0.01).创伤组Id1基因敲除大鼠VEGF、CD105的mRNA及蛋白表达均受到抑制(P<0.05),且伤后各时间点表达水平无明显变化.Id1诱导表达组24h后大鼠Id1、VEGF、CD105表达均明显增强(P<0.05),于72h达高峰(P<0.01),而ET-1 mRNA水平在伤后24h升高,48h达高峰(P<0.05),72h下降.报告基因检测结果显示,Id1敲除后VEGF、CD105荧光素酶活性明显受到抑制(P<0.05),而Id1基因诱导表达后VEGF、CD105活性明显增强(P<0.01),但Id1对ET-1的表达无明显影响.结论 Id1能有效促进血管内皮细胞Eahy926增殖,调节血管内皮细胞、创伤组织中VEGF、CD105以及ET-1的表达,在组织细胞新生血管化中起重要作用.     

Glioma morphology and tumor‐induced vascular alterations revealed in seven rodent glioma models by in vivo magnetic resonance imaging and angiography

Purpose:

To evaluate the added value of non–contrast‐enhanced MR angiography (MRA) to conventional MR imaging for a detailed characterization of different rodent glioma models.

Materials and Methods:

Intracerebral tumor cell implantation and chemical induction methods were implemented to obtain rat C6, 9L/LacZ, F98, RG2, and ethyl‐nitrosourea (ENU) ‐induced glioma models, a human U87 MG tumor model as well as a mouse GL261 glioma model. MR assessments were regularly conducted on a 7 Tesla Bruker BioSpin system. The tumor border sharpness and growth characteristics of each glioma model were assessed from T₂‐weighted images. Neovascularization and vascular alterations inherent to each model were characterized by assessing absolute blood volumes, vessel density, length, and diameter using Mathematica and Amira software.

Results:

The 9L/LacZ and ENU gliomas both presented flaws that hinder their use as reliable brain tumor models. C6 gliomas were slightly invasive and induced moderate vascular alterations, whereas GL261 tumors dramatically altered the brain vessels in the glioma region. F98, RG2, and U87 are infiltrative models that produced dramatic vascular alterations.

Conclusion:

MRI and MRA provided crucial in vivo information to identify a distinctive “fingerprint” for each of our seven rodent glioma models. J. Magn. Reson. Imaging 2010;32:267–275. © 2010 Wiley‐Liss, Inc.     

骨髓内皮祖细胞在恶性肿瘤血管生成中的作用

新的血管生成是肿瘤发生和发展的重要病理生理过程。人骨髓中含有内皮祖细胞，骨髓内皮祖细胞通过不同的机制动员进入血液循环，并参与肿瘤的血管生成。深入研究骨髓内皮祖细胞参与肿瘤血管生成的机制将为肿瘤治疗提供新的措施。     

(-)-Epigallocatechin-3-gallate,reduces corneal damage secondary from experimental grade II alkali burns in mice

Background

Since recent reports have shown that (-)-Epigallocatechin-3-gallate (EGCG) could be used for treating proliferative and inflammatory disorders, we explored its use for the management of corneal chemical burns.

Fibrotic changes in the infrapatellar fat pad induce new vessel formation and sensory nerve fiber endings that associate prolonged pain

The infrapatellar fat pad (IFP) contains nerve fiber endings and is considered to play an important role in the perception of knee pain. However, it is unclear whether and to what degree prolonged pain influences the nociceptive role of the IFP. To answer this question, we established a novel rat model of knee pain in which inflammation is restricted to the IFP. Rats received a single intra-IFP injection of monoiodoacetic acid (MIA) (0.2 mg/10 µL or 1.0 mg/10 µL) in the left knee and a phosphate-buffered saline (10 µL) injection in the right knee as a control. Pain-avoidance behavior and histological changes of the knee joint were measured at multiple time points up to 28 days after MIA injection. Histological analysis showed a transient inflammatory response in the IFP body in the 0.2-mg model, whereas prolonged inflammation followed by fibrotic changes was observed in the 1.0-mg model. Subtle histological alterations were observed in the articular cartilage and IFP surface regardless of the dose. The pain-avoidance behavior test indicated the development of prolonged knee pain throughout the experimental period in the 1.0-mg group. Histological assessments showed a significant increase in calcitonin gene-related peptide (CGRP)-positive nerve fiber endings inside IFPs with fibrosis in newly vascularized surrounding regions. These data suggest that irreversible fibrotic changes in the IFP induce the formation of new vessels and CGRP-positive nerve fiber endings that associate prolonged pain in the joint.     

Minimally Invasive Achilles Tendon Stripping for the Management of Tendinopathy of the Main Body of the Achilles Tendon

Achilles tendinopathy is a common cause of disability. New nerves fibers grow from the paratenon into the Achilles tendon, and they could play a central role in the development of pain. We report the results of minimally invasive Achilles tendon stripping for Achilles tendinopathy in 47 active patients. The Victorian Institute of Sports Assessment-Achilles questionnaire score improved from 53.8 preoperatively to 85.3 postoperatively (p < .001). After a mean follow-up period of 40.5 months, 41 patients had resumed sporting activities at an average of 3.5 months postoperatively. A sural nerve injury was recorded in 5 patients (10.6%), and all 5 complications occurred during the first 12 cases. As a result, the technique was slightly modified, and no sural nerve neuropathy was observed subsequently. One superficial infection (2.1%) was recorded. Minimally invasive Achilles tendon stripping seems to be an effective, technically simple, and inexpensive treatment of Achilles tendinopathy. Further randomized controlled trials involving more patients are needed to confirm these outcomes.     

脑部脉络膜裂囊肿的MRI诊断

目的　探讨脑部脉络膜裂囊肿的MR影像学表现及其诊断价值。方法　对 16例脉络膜裂囊肿的MR影像学特征进行了回顾性分析 ,对MR影像与临床表现之间的关系进行了讨论。结果　 16例病灶均位于脉络膜裂内 ,表现为界线清楚的囊性病变 ,囊壁及其周围无软组织信号 ,内部信号均匀且在各个序列上均与脑脊液信号一致 ,平均大小为 0 9cm× 1 3cm× 1 5cm ,病灶周围均无水肿。 6例行钆喷替酸葡甲胺 (Gd DTPA)增强扫描后均未见病灶强化。结论　脑部脉络膜裂囊肿是 1种良性的先天性发育异常 ,通常与临床表现无关。由于脉络膜裂囊肿发生在特殊的位置 ,横轴面扫描易误诊为脑内病变 ,MR冠状面及矢状面扫描可做出明确诊断并能够与其他囊性病变相鉴别。     

Angiostatin基因转染对膀胱癌BIU-87细胞系生物学行为的影响

目的 探讨外源性血管抑素(angiostatin)基因在人膀胱癌BIU-87细胞中的表达及其意义。方法 将人全长angiostatin基因经脂质体包裹转染膀胱癌BIU-87细胞,行G418筛选获得转基因瘤细胞克隆,比较转基因和未转基因的瘤细胞生长特性。采用免疫荧光、免疫组化及Western blot等方法检测瘤细胞angiostatin蛋白的表达,并应用鸡胚尿囊膜血管生成实验及脐静脉内皮细胞增殖实验检测其活性。结果 外源性angiostatin基因的表达对BIU-87瘤细胞的生长并无影响。转染细胞在体外明显抑制脐静脉内皮细胞的增殖并对鸡胚尿囊膜的血管生成具有明显的抑制作用。结论Angiostatin能特异性地抑制血管内皮细胞增殖,进而抑制血管生成。