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Bone morphogenetic proteins inhibit the tumorigenic potential of human brain tumour-initiating cells.
Piccirillo SG, Reynolds BA, Zanetti N, Lamorte G, Binda E, Broggi G, Brem H, Olivi A, Dimeco F, Vescovi AL.
Nature. 2006 Dec 7;444(7120):761-5.
Transformed, oncogenic precursors, possessing both defining neural-stem-cell properties and the ability to initiate intracerebral tumours, have been identified in human brain cancers. Here we report that bone morphogenetic proteins (BMPs), amongst which BMP4 elicits the strongest effect, trigger a significant reduction in the stem-like, tumour-initiating precursors of human glioblastomas (GBMs).
Transient in vitro exposure to BMP4 abolishes the capacity of transplanted GBM cells to establish intracerebral GBMs. Most importantly, in vivo delivery of BMP4 effectively blocks the tumour growth and associated mortality that occur in 100% of mice after intracerebral grafting of human GBM cells. We demonstrate that BMPs activate their cognate receptors (BMPRs) and trigger the Smad signalling cascade in cells isolated from human glioblastomas (GBMs). This is followed by a reduction in proliferation, and increased expression of markers of neural differentiation, with no effect on cell viability. The concomitant reduction in clonogenic ability, in the size of the CD133+ population and in the growth kinetics of GBM cells indicates that BMP4 reduces the tumour-initiating cell pool of GBMs.
These findings show that the BMP-BMPR signalling system--which controls the activity of normal brain stem cells--may also act as a key inhibitory regulator of tumour-initiating, stem-like cells from GBMs and the results also identify BMP4 as a novel, non-cytotoxic therapeutic effector, which may be used to prevent growth and recurrence of GBMs in humans.
PMID: 17151667 [PubMed - in process]
Surgical management of jugular foramen schwannomas with hearing and facial nerve function preservation: A series of 23 cases and review of the literat
Sanna M, Bacciu A, Falcioni M, Taibah A.
Laryngoscope. 2006 Dec;116(12):2191-204.
OBJECTIVE: Schwannomas of the jugular foramen are rare lesions and controversy regarding their management still exists. The objective of this retrospective study was to analyze the management and outcome in a series of 23 cases collected at a single center.
SETTING: This study was conducted at a quaternary private otology and skull base center.
METHODS: Charts belonging to patients with a diagnosis of jugular foramen schwannoma attending our center between May 1988 and April 2006 were examined retrospectively.
RESULTS: The study group consisted of 23 patients. One patient (a 73-year-old woman) with normal lower cranial nerves function was managed with watchful expectancy and regular clinical and radiologic follow ups. The infratemporal fossa approach-type A (IFTA-A) was performed in 3 cases. One patient underwent a transcochlear-transjugular approach. Of the 22 patients surgically treated, 12 patients were operated on by the petrooccipital transsigmoid approach (POTS). In one patient with a preoperative dead ear, a combined POTS-translabyrinthine approach was adopted. Two patients were operated on through the POTS approach combined with the transotic approach. In another case (a 67-year-old woman), a subtotal tumor removal through a transcervical approach was planned to resect a 10-cm mass in the neck. One patient underwent a first-stage combined transcervical-subtotal petrosectomy approach to remove a huge tumor in the neck; the second-stage intradural removal of the tumor was accomplished through a translabyrinthine-transsigmoid-transjugular approach. The last patient underwent a first-stage combined transcervical-subtotal petrosectomy approach to remove the neck tumor component; this patient is now waiting for the second-stage intradural removal of the tumor. Complete tumor removal was accomplished in 21 cases and in one case, a residual schwannoma was left in place in the area of the jugular foramen. The 3 patients who were operated on by IFTA-A underwent permanent anterior transposition of the facial nerve. At 1-year follow up, 2 of these patients had House-Brackmann grade I and 1 reached grade IV. The patient who underwent a transcochlear-transjugular approach had a permanent posterior transposition of the facial nerve. At 1-year follow up, he had grade III facial nerve function. Postoperative facial nerve function was normal (House-Brackmann grade I) in all patients operated on by the POTS approach. Twelve patients had hearing-preserving surgery using the POTS approach. Good hearing was preserved in 10 cases (83.3%), the majority of whom (58.3%) maintained their preoperative hearing level. There was no perioperative mortality. One patient (4.5%) experienced a postoperative cerebrospinal fluid leak. After surgery, all patients did not recover the function of the preoperatively paralyzed lower cranial nerves. A new deficit of one or more of the lower cranial nerves was recorded in 50% of cases. So far, no patient has experienced recurrence during the follow-up period as ascertained by computed tomography or magnetic resonance imaging.
CONCLUSIONS: Surgical resection is the treatment of choice for jugular foramen schwannomas. The POTS approach allowed single-stage, total tumor removal with preservation of the facial nerve and of the middle and inner ear functions in the majority of cases. Despite the advances in skull base surgery, new postoperative lower cranial nerve deficits still represent a challenge.
Regulation of angiogenesis and invasion by human Pituitary tumor transforming gene (PTTG) through increased expression and secretion of matrix metalloproteinase-2 (MMP-2).
Malik MT, Kakar SS.
Mol Cancer. 2006 Nov 10;5:61.
BACKGROUND: Pituitary tumor transforming gene (PTTG) is a novel oncogene that is expressed at higher level in most of the tumors analyzed to date compared to normal tissues. Existence of a relationship between PTTG levels and tumor angiogenesis and metastasis has been reported. However, the mechanisms by which PTTG achieve these functions remain unknown. In the present study, we investigated the effect of overexpression of PTTG on secretion and expression of metastasis-related metalloproteinase-2 (MMP-2) in HEK293 cells, cell migration, invasion and tubule formation.
RESULTS: Transient or stable transfection of HEK293 cells with PTTG cDNA showed a significant increase in secretion and expression of MMP-2 measured by zymography, reverse transcriptase (RT/PCR), ELISA, and MMP-2 gene promoter activity. Furthermore, in our studies, we showed that tumor developed in nude mice on injection of HEK293 cells that constitutively express PTTG expressed high levels of both MMP-2 mRNA and protein, and MMP-2 activity. Conditioned medium collected from the HEK293 cells overexpressing PTTG showed a significant increase in cell migration, invasion and tubule formation of human umbilical vein endothelial cells (HUVEC). Pretreatment of conditioned medium with MMP-2-specific antibody significantly decreased these effects, suggesting that PTTG may contribute to tumor angiogenesis and metastasis via activation of proteolysis and increase in invasion through modulation of MMP-2 activity and expression.
CONCLUSION: Our results provide novel information that PTTG contributes to cell migration, invasion and angiogenesis by induction of MMP-2 secretion and expression. Furthermore, we showed that tumors developed in nude mice on injection of HEK293 cells that constitutively express PTTG induce expression of MMP-2 and significantly increase its functional activity, suggesting a relationship between PTTG levels and MMP-2 which may play a critical role in regulation of tumor growth, angiogenesis and metastasis. Blocking of function of PTTG or down regulation of its expression in tumors may result in suppression of tumor growth and metastasis, through the down regulation of MMP-2 expression and activity. To our knowledge, this study is the first study demonstrating the modulation of MMP-2 expression and biological activity by PTTG.
Bone morphogenetic proteins inhibit the tumorigenic potential of human brain tumour-initiating cells.
骨形成蛋白能抑制人类脑部肿瘤起始细胞的致瘤潜能。
作者Piccirillo SG, Reynolds BA, Zanetti N, Lamorte G, Binda E, Broggi G, Brem H, Olivi A, Dimeco F, Vescovi AL.
发表于Nature. 2006 Dec 7;444(7120):761-5.
Transformed, oncogenic precursors, possessing both defining neural-stem-cell properties and the ability to initiate intracerebral tumours, have been identified in human brain cancers. Here we report that bone morphogenetic proteins (BMPs), amongst which BMP4 elicits the strongest effect, trigger a significant reduction in the stem-like, tumour-initiating precursors of human glioblastomas (GBMs).
人类脑部肿瘤中已经证实，突变的致瘤前体细胞不仅具有神经干细胞性能并且能致脑部肿瘤发生的潜能。本研究我们报告骨形成蛋白4最大程度的降低人类恶性胶质瘤干细胞样致瘤前体细胞的致瘤作用。
Transient in vitro exposure to BMP4 abolishes the capacity of transplanted GBM cells to establish intracerebral GBMs. Most importantly, in vivo delivery of BMP4 effectively blocks the tumour growth and associated mortality that occur in 100% of mice after intracerebral grafting of human GBM cells. We demonstrate that BMPs activate their cognate receptors (BMPRs) and trigger the Smad signalling cascade in cells isolated from human glioblastomas (GBMs). This is followed by a reduction in proliferation, and increased expression of markers of neural differentiation, with no effect on cell viability. The concomitant reduction in clonogenic ability, in the size of the CD133+ population and in the growth kinetics of GBM cells indicates that BMP4 reduces the tumour-initiating cell pool of GBMs.
骨形成蛋白4在体外很快就可停止移植的恶性胶质瘤细胞构建瘤体的能力。更为重要的是，在移植人类恶性胶质瘤细胞的小鼠体内，骨形成蛋白4能有效阻止肿瘤生长并且降低移植恶其性胶质瘤细胞后100%死亡的概率。我们发现骨形成蛋白激活其同源受体并触发Smad信号级联发生，从而使人类恶性胶质瘤细胞增殖能力下降，尽管其分化能力表达上调。无性系能力、CD133+总数和恶性胶质瘤细胞生长动力等均随之降低，都说明骨形成蛋白4能降低恶性胶质瘤细胞前体细胞库数量。
These findings show that the BMP-BMPR signalling system--which controls the activity of normal brain stem cells--may also act as a key inhibitory regulator of tumour-initiating, stem-like cells from GBMs and the results also identify BMP4 as a novel, non-cytotoxic therapeutic effector, which may be used to prevent growth and recurrence of GBMs in humans.
本研究发现控制正常大脑干细胞活性的骨形成蛋白-骨形成蛋白受体信号系统，可能在恶性胶质瘤干细胞样致瘤前体细胞致瘤调控中起关键作用，其中骨形成蛋白4作为一种新的无细胞毒作用效应器，可以用来有效阻止恶性胶质瘤生长和复发。
PMID: 17151667 [PubMed - in process]
颈静脉孔斯(雪)旺细胞瘤的外科处理及面听神经功能保护：23例报告及文献回顾（复习）
作者Sanna M, Bacciu A, Falcioni M, Taibah A.
发表于Laryngoscope. 2006 Dec;116(12):2191-204.
目的：颈静脉孔斯（雪）旺细胞瘤是一种少见疾病，对于其治疗的争议一直存在。本文通过回顾性研究对某一中心的23例该病例的治疗以及预后进行分析。
背景：本研究在一（四人组）私立的耳和颅底中心进行。
结果：研究组共23例病人。一例73岁的妇女，颅神经功能较差（后组颅神经功能正常），对其密切关注（其进行了谨慎处理），并进行了正规的临床及放射学检查随访。3例病人行颞下窝A型入路，一例病人行经耳蜗－颈静脉孔联合入路，12例行岩枕经矢（乙）状窦入路（POTS），一例病人术前一耳已失聪，予以联合POTS和经迷路入路。两例病人行联合POTS－经耳入路，另一例67岁的妇女通过经颈入路对颈部10cm大小的肿瘤予以部分切除。一例病人一期行联合经颈－部分岩骨切除入路切除了颈部的巨大肿瘤，二期通过联合经迷路－经矢状窦－经颈静脉孔入路予以硬膜下肿瘤全切。最后一例病人一期行联合经颈－部分岩骨切除入路切除颈部部分肿瘤，现等待二期硬膜下肿瘤全切。21例病人肿瘤得以全切，一例病人颈静脉孔处残留少许肿瘤。3例行颞下窝A型入路的病人伴有永久的面神经前移位。一年后随访，两例病人面神经功能House-Brackmann分级一级，一例四级。经耳蜗－颈静脉孔的病人伴有永久的面神经后移位。一年后随访，病人面神经功能三级，经POTS入路的病人术后面神经功能全都正常（House-Brackmann分级一级）。12例病人行POTS入路手术的病人都获得了听功能保存。10例（83.3％）病人听力保存良好，其中大多数（58.3％）恢复了术前听力水平。术中无死亡，一例术后伴有脑脊液漏。所有术前存有后组颅神经麻痹的病人术后神经功能均未恢复。50％的病人术后有新发的一处或多处后组颅神经障碍。迄今随访期间CT和MRI尚无发现有病人复发。
结论：手术切除是颈静脉孔斯（雪）旺细胞瘤的治疗方法。POTS入路对大多数病人可以一次肿瘤全切，并保存面神经、内耳和中耳功能。尽管颅底外科手术发展，术后后组颅神经新发功能障碍问题仍旧是个挑战。
谢谢larrylmh的精心翻译！
颈静脉孔区肿瘤在耳鼻咽喉头颈外科属于侧颅底的范畴，现代颅底外科的许多经典手术入路多数亦由原耳科或鼻科手术入路演绎而来。复杂颈静脉孔颅内外沟通性肿瘤的有效治疗，需要综合运用侧颅底和显微神经外科颅底的知识和技术。
选择此文献的目的是了解耳科医生在处理此类病变的做法和思路，以期对神经外科医生处理复杂颈静脉孔区肿瘤有所启迪。
leuking
Regulation of angiogenesis and invasion by human Pituitary tumor transforming gene (PTTG) through increased expression and secretion of matrix metalloproteinase-2 (MMP-2).
垂体瘤转化基因(PTTG)通过促进基质金属蛋白酶（MMP-2）表达和分泌来实现对血管生成和肿瘤侵袭性的调节
Malik MT, Kakar SS.
Mol Cancer. 2006 Nov 10;5:61.
背景：垂体瘤转化基因是一个新发现的癌基因，在迄今已研究的肿瘤中，大多数都有PTTG高表达。PTTG表达水平与肿瘤血管生成和转移的关系已有文献报道。然而，PTTG通过何种机制行使功能仍然未知。在本项研究中，我们探讨了PTTG高表达对于转移相关MMP-2在HEK293细胞中的表达和分泌、细胞移行、侵袭性和小血管形成的作用。
结果：通过酶谱、逆转录酶（RT/PCR）、ELISA和MMP-2基因启动子活性的检测, PTTG cDNA瞬时转染或稳定转染HEK293细胞均显示出MMP-2分泌和表达的增加。而且在研究中，我们证实了在注射HEK293细胞的裸鼠体内生长的肿瘤，PTTG的表达均导致MMP-2 mRNA和蛋白的表达以及MMP-2活性的显著增加。PTTG高表达的HEK293细胞条件培养液中也显示在细胞移行、侵袭性和人脐静脉内皮细胞(HUVEC)的血管生成方面有明显增强。对条件培养液进行MMP-2特异性抗体预处理，这些效应则明显减弱，结果表明，通过促进蛋白水解与调节MMP-2活性和表达增强肿瘤侵袭性，PTTG能够促进肿瘤血管生成和转移。
结论：我们的研究结果提供了一个新信息：PTTG通过对MMP-2分泌和表达的调节来促进细胞移行、侵袭和血管生成。而且，我们证实了在注射HEK293细胞的裸鼠体内生长的肿瘤，PTTG的表达均导致MMP-2表达以及MMP-2功能活性的显著增加。这表明PTTG水平与MMP-2的关系可能在肿瘤生长、肿瘤血管生成和转移中具有关键作用。对肿瘤的PTTG功能阻断或者使其表达下调使MMP-2表达和活性降低，从而可能抑制肿瘤生长和转移。迄今为止，这项研究是首次研究证实PTTG能够调节MMP-2的表达和生物活性。
Nature Medicine - 13, 84 - 88 (2006)
Published online: 10 December 2006; | doi:10.1038/nm1517
Loss of tumor suppressor PTEN function increases B7-H1 expression and immunoresistance in glioma
Andrew T Parsa1, James S Waldron1, Amith Panner1, Courtney A Crane1, Ian F Parney1, Jeffrey J Barry1, Kristine E Cachola1, Joseph C Murray1, Tarik Tihan1, Michael C Jensen2, Paul S Mischel3, David Stokoe1 & Russell O Pieper1
Department of Neurological Surgery, University of California San Francisco, 505 Parnassus Avenue, M-779, San Francisco, California 94143, USA.
Cancer immunoresistance and immune escape may play important roles in tumor progression and pose obstacles for immunotherapy. Expression of the immunosuppressive protein B7 homolog 1 (B7-H1), also known as programmed death ligand-1 (PD-L1), is increased in many pathological conditions, including cancer.
Here we show that expression of the gene encoding B7-H1 increases post transcriptionally in human glioma after loss of phosphatase and tensin homolog (PTEN) and activation of the phosphatidylinositol-3-OH kinase (PI(3)K) pathway. Tumor specimens from individuals with glioblastoma multiforme (GBM) had levels of B7-H1 protein that correlated with PTEN loss, and tumor-specific T cells lysed human glioma targets expressing wild-type PTEN more effectively than those expressing mutant PTEN.
These data identify a previously unrecognized mechanism linking loss of the tumor suppressor PTEN with immunoresistance, mediated in part by B7-H1.
肿瘤抑制基因PTEN功能丢失可增加神经胶质瘤B7-H1的表达和免疫抵抗
肿瘤免疫抵抗和免疫逃逸也许在肿瘤发展过程中起着重要的作用，并给肿瘤的免疫疗法带来障碍。免疫抑制蛋白B7同系物1 （B7-H1），也被称为程序性死亡配体- 1（PD-L1），在许多病理条件下表达增加，包括癌症。
研究结果显示，当神经胶质瘤患者磷脂酸-张力蛋白基因（PTEN）丢失、磷脂酰肌醇3激酶（PI（3）K）途径激活时，基因编码的B7-H1转录增加。多形性胶质母细胞瘤（GBM）个体的肿瘤样本中B7-H1蛋白水平与PTEN丢失相关，肿瘤特异性T细胞溶解人类神经胶质瘤时表达的野生PTEN较变异PTEN更有效。
研究数据表明了先前没有意识到的一种机制，即肿瘤抑制基因PTEN丢失与免疫抵抗相关，部分由于B7-H1介导。
不好意思,发晚了.请斧正.
Nature Medicine - 13, 84 - 88 (2006)
Published online: 10 December 2006; | doi:10.1038/nm1517
Loss of tumor suppressor PTEN function increases B7-H1 expression and immunoresistance in glioma肿瘤抑制基因PTEN功能丢失可能强化神经胶质瘤B7-H1的表达及免疫耐受
Andrew T Parsa1, James S Waldron1, Amith Panner1, Courtney A Crane1, Ian F Parney1, Jeffrey J Barry1, Kristine E Cachola1, Joseph C Murray1, Tarik Tihan1, Michael C Jensen2, Paul S Mischel3, David Stokoe1 & Russell O Pieper1
Department of Neurological Surgery, University of California San Francisco, 505 Parnassus Avenue, M-779, San Francisco, California 94143, USA.
Cancer immunoresistance and immune escape may play important roles in tumor progression and pose obstacles for immunotherapy. Expression of the immunosuppressive protein B7 homolog 1 (B7-H1), also known as programmed death ligand-1 (PD-L1), is increased in many pathological conditions, including cancer.癌瘤的免疫耐受和免疫逃避可能在其发展进程中起重要作用，同时也妨碍其免疫治疗。免疫抑制蛋白B7同系物1(B7-H1)，亦称程序性死亡配体1(PD-L1)在包括癌症等许多病变中表达增高。
Here we show that expression of the gene encoding B7-H1 increases post transcriptionally in human glioma after loss of phosphatase and tensin homolog (PTEN) and activation of the phosphatidylinositol-3-OH kinase (PI(3)K) pathway. Tumor specimens from individuals with glioblastoma multiforme (GBM) had levels of B7-H1 protein that correlated with PTEN loss, and tumor-specific T cells lysed human glioma targets expressing wild-type PTEN more effectively than those expressing mutant PTEN. 本实验结果显示，当胶质瘤患者磷酸酯酶和张力蛋白同系物(PTEN)缺失以及磷脂酰肌醇3激酶(PI(3)K)途径激活时，编码B7-H1的基因转录增加。多形性成胶质细胞瘤(GBM)患者的肿瘤标本中显示B7-H1蛋白水平与肿瘤抑制基因PTEN功能的丢失具有相关性， 肿瘤特异T细胞在溶解人类胶质瘤时表达的野生型PTEN较突变的PTEN更有效。
These data identify a previously unrecognized mechanism linking loss of the tumor suppressor PTEN with immunoresistance, mediated in part by B7-H1.这些结果明确了先前没有被人认识的机制，既肿瘤抑制基因PTEN功能丢失与免疫抵抗相关部分性可由B7-H1介导。
衷心感谢大家支持！！请最好以中英对照发布。
Eur J Radiol. 2006 Dec;60(3):367-78. Epub 2006 Sep 11
Contrast-enhanced MR 3D angiography in the assessment of brain AVMs.
Unlu E, Temizoz O, Albayram S, Genchellac H, Hamamcioglu MK, Kurt I, Demir MK.
BACKGROUND AND PURPOSE: Digital subtraction angiography (DSA) is the current reference standard for the diagnosis, assessment, and management of brain arteriovenous malformations (AVMs). The purpose of this study was to compare the diagnostic utility of three-dimensional (3D) time-of-flight (TOF) magnetic resonance angiography (MRA) and contrast-enhanced 3D MRA in patients with intracranial arteriovenous malformations (AVMs) in different sizes and locations. The AVM diagnosis was proved via DSA and almost half of the patients had also hematoma.
MATERIALS AND METHODS: Two radiologists, experienced on neurovascular imaging and independent from each other, retrospectively reviewed two MRA techniques and DSA with regard to the assessment of feeding arteries, AVM nidus, and venous drainage patterns on 20 patients with 23 examinations by scoring system. Disagreements were resolved by consensus.
RESULTS: An excellent agreement between contrast-enhanced MRA and DSA was found in order to assess the numbers of arterial feeders and draining veins (Spearman r=0.913, P<0.001). The average scores in contrast-enhanced MRA for feeders, nidi, and drainers were respectively 2.26, 2.69, and 2.48, while in TOF-MRA they are 1.96, 1.35, and 0.89, respectively.
CONCLUSION: Compared to TOF-MRA, 3D contrast-enhanced MRA is useful for visualization by subtraction technique of malformation components presented by hematoma or by haem product. On the other hand, for the cases presented by slow or complex flow that is especially in around or nidi or around the venous portion is also advantageous because of the independence from flow-related enhancement. Therapeutic effects were clearly demonstrated in three follow-up patients. A major limitation of this technique is the low spatial resolution. Since there is such a limitation, arterial feeder of a case with micro-AVM is not detected by contrast-enhanced MRA and nidus for the same case was observed retrospectively. In this respect, we believe that 3D contrast-enhanced MRA is a less invasive and inexpensive angiographic tool, but not a safe substitute for DSA. Yet, it can be a beneficial supplement to DSA in patients with cerebral AVMs at both initial diagnosis and at follow-up processes after therapy.
PMID: 16965882 [PubMed - in process]
Int J Mol Med. 2006 Nov;18(5):813-9
Endothelial cells from human cerebral aneurysm and arteriovenous malformation release ET-1 in response to vessel rupture.
Boscolo E, Pavesi G, Zampieri P, Conconi MT, Calore C, Scienza R, Parnigotto PP, Folin M.
Cerebral aneurysms and arteriovenous malformations (AVM) are a common cause of stroke and cerebral hemorrage. Both are often discovered when they rupture, causing subarachnoid hemorrhage (SAH). SAH-induced vasospasm is mediated by enhanced vasoconstriction due to endothelin-1 (ET-1). We investigated whether endothelial cells (ECs) obtained from aneurysm and AVM express phenotypic and genotypic alterations contributing to the development of vasospasm after SAH.
We isolated ECs from human AVM and aneurysm and then confirmed their EC origin by polymerase chain reaction and immunocytochemistry with endothelial markers. Experiments were also carried out with human cerebral microvascular and umbilical vein ECs (HCECs and HUVECs respectively) for comparison. We tested EC proliferation ability and microtubule formation in Matrigel at different cell passages. Five aneurysm (3 ruptured, 2 unruptured) and 3 AVM (2 ruptured, 1 unruptured) ECs were tested for ET-1 release in the culture medium. Aneurysm and AVM ECs expressed von Willebrand factor, Adrenomedullin, and exhibited a progressive reduction of proliferation and in vitro angiogenic ability after the V passage. Significantly higher levels of ET-1 have been detected in ECs from ruptured aneurysms and AVMs.
We report the first successful isolation and characterization of primary EC lines from human cerebral vascular lesions. Augmented release of ET-1 is correlated with the rupture of the abnormal vessel confirming its role in vasospasm after SAH. Furthermore, ECs obtained from these vascular malformations can be used as an experimental model to study SAH-induced vasoconstriction.
PMID: 17016610 [PubMed - in process]
Neurosurgery. 2006 Nov;59(5):1044-51;
Early and intermediate-term outcomes with drug-eluting stents in high-risk patients with symptomatic intracranial stenosis.
Qureshi AI, Kirmani JF, Hussein HM, Harris-Lane P, Divani AA, Suri MF, Janjua N, Alkawi A.
OBJECTIVE: To report the 1-month and intermediate-term results of treatment of symptomatic intracranial stenosis using drug-eluting stents.
BACKGROUND: Patients with intracranial stenosis who are at high risk because of either high-grade stenosis or medication failure may have an annual risk of recurrent ischemic events in excess of 40%. Drug-eluting stents may reduce the rate of ischemic events in patients with a low restenosis rate.
METHODS: We determined rates of technical success (defined as reduction of target lesion to stenosis <30%) and 1-month major stroke or death in patients with symptomatic intracranial stenosis (> or =70% and/or medication failure). Patients' clinical and follow-up information during a mean period of 14.3 +/- 7 months were obtained. Kaplan-Meier analysis was performed to determine the rate of major stroke-free survival during 12 months. RESULTS: There were 18 patients (mean age, 58 +/- 16 yr; 12 were men) treated with either a sirolimus-eluting stent (n = 14) or a paclitaxel-eluting stent (n = 4) for stenosis located in the: intracranial internal carotid artery (n = 6), proximal middle cerebral artery (n = 4), intracranial vertebral artery (n = 4), vertebrobasilar junction (n = 2), or basilar artery (n = 2). There was one major stroke and no death observed in the 1-month follow-up. At the 6-month follow-up examination, no major stroke or death was observed. Major stroke-free survival was 86% (+/-standard error of 9%) at 12 months after the procedure. One symptomatic angiographic restenosis was observed during the follow-up period.
CONCLUSION: A low rate of major stroke or death was observed after treatment of symptomatic intracranial stenosis using drug-eluting stents in high-risk patients.
PMID: 17143239 [PubMed - indexed for MEDLINE]
Eur J Radiol. 2006 Dec;60(3):367-78. Epub 2006 Sep 11
Contrast-enhanced MR 3D angiography in the assessment of brain AVMs.
三维对比增强磁共振血管造影在评估脑动静脉血管畸形（AVMs）中的应用
作者：Unlu E, Temizoz O, Albayram S, Genchellac H, Hamamcioglu MK, Kurt I, Demir MK.
BACKGROUND AND PURPOSE: Digital subtraction angiography (DSA) is the current reference standard for the diagnosis, assessment, and management of brain arteriovenous malformations (AVMs). The purpose of this study was to compare the diagnostic utility of three-dimensional (3D) time-of-flight (TOF) magnetic resonance angiography (MRA) and contrast-enhanced 3D MRA in patients with intracranial arteriovenous malformations (AVMs) in different sizes and locations. The AVM diagnosis was proved via DSA and almost half of the patients had also hematoma.
背景与目的：数字减影血管造影(DSA)是现代诊断、评估和治疗脑动静脉畸形（AVMs）的参考标准。此次研究旨在比较三维（3D）时间飞跃法（TOF）磁共振血管造影（MRA）和三维对比增强磁共振血管造影在不同位置和不同大小的颅内动静脉畸形（AVMs）患者中的诊断效果。AVM由DSA确诊且约有半数患者同时伴有血肿。
MATERIALS AND METHODS: Two radiologists, experienced on neurovascular imaging and independent from each other, retrospectively reviewed two MRA techniques and DSA with regard to the assessment of feeding arteries, AVM nidus, and venous drainage patterns on 20 patients with 23 examinations by scoring system. Disagreements were resolved by consensus.
材料与方法：两个放射科医师，均有各自独立的、丰富的神经血管影像经验。回顾性调查了两项MRA技术与DSA旨在评估供血动脉、AVM病灶和静脉引流方式，该项调查在通过评分系统接受过23项检查的20位患者中进行。意见不一致性部分通过意见一致性部分折中。
RESULTS: An excellent agreement between contrast-enhanced MRA and DSA was found in order to assess the numbers of arterial feeders and draining veins (Spearman r=0.913, P<0.001). The average scores in contrast-enhanced MRA for feeders, nidi, and drainers were respectively 2.26, 2.69, and 2.48, while in TOF-MRA they are 1.96, 1.35, and 0.89, respectively.
结果：在评估动脉供血与引流静脉的数目方面，对比增强MRA与DSA之间之间具有高度一致性（Spearman 统计分析，r=0.913, P＜0.001）。在对比增强MRA评估中，供血、病灶、引流的平均分分别为2.26、2.69、2.48，而在TOF-MRA中分别为1.96、 1.35、 0.89。
CONCLUSION: Compared to TOF-MRA, 3D contrast-enhanced MRA is useful for visualization by subtraction technique of malformation components presented by hematoma or by haem product. On the other hand, for the cases presented by slow or complex flow that is especially in around or nidi or around the venous portion is also advantageous because of the independence from flow-related enhancement. Therapeutic effects were clearly demonstrated in three follow-up patients. A major limitation of this technique is the low spatial resolution. Since there is such a limitation, arterial feeder of a case with micro-AVM is not detected by contrast-enhanced MRA and nidus for the same case was observed retrospectively. In this respect, we believe that 3D contrast-enhanced MRA is a less invasive and inexpensive angiographic tool, but not a safe substitute for DSA. Yet, it can be a beneficial supplement to DSA in patients with cerebral AVMs at both initial diagnosis and at follow-up processes after therapy.
结论：与TOF-MRA相比，三维对比增强磁共振血管造影通过减影技术将由血肿或血红素形成的伪畸形病灶消除，因而更益于显影。此外，对于呈现血流缓慢、复杂血流，尤其是出现在病灶周围、病灶或者静脉段部分的病例也有益，这是由于该技术与流动相关增强效应无关。治疗效果在3个被随访的患者中清楚的证实。空间分辨率低是该项技术的主要缺陷，由于此限制，一例患有微小AVM的患者没有被三维对比增强磁共振血管造影检测出，而是之后被回顾性的检测到。基于此，我们相信三维对比增强磁共振血管造影是一项侵入性小且价廉的血管造影工具，但是不能够可靠地替代DSA。然而，在大脑AVMs患者的初次诊断及治疗后的随访中，可以为DSA提供有利的补充。
Int J Mol Med. 2006 Nov;18(5):813-9
Endothelial cells from human cerebral aneurysm and arteriovenous malformation release ET-1 in response to vessel rupture. 来源于人大脑动脉瘤和动静脉血管畸形中的内皮细胞可伴随血管破裂释放内皮素-1
Boscolo E, Pavesi G, Zampieri P, Conconi MT, Calore C, Scienza R, Parnigotto PP, Folin M.
Cerebral aneurysms and arteriovenous malformations (AVM) are a common cause of stroke and cerebral hemorrage. Both are often discovered when they rupture, causing subarachnoid hemorrhage (SAH). SAH-induced vasospasm is mediated by enhanced vasoconstriction due to endothelin-1 (ET-1). We investigated whether endothelial cells (ECs) obtained from aneurysm and AVM express phenotypic and genotypic alterations contributing to the development of vasospasm after SAH. 大脑动脉瘤和动静脉型血管畸形(AVM)是中风及脑出血的常见原因。两者均常由于血管破裂导致蛛网膜下腔出血而被发现。蛛网膜下腔出血后血管痉挛是由能增强血管收缩的作用内皮素-1(ET-1)所介导。本实验我们探讨在蛛网膜下腔出血后促进血管痉挛进展过程中，来源于大脑动脉瘤和动静脉型血管畸形的内皮细胞(ECs)是发生了表型改变还是基因型改变。
We isolated ECs from human AVM and aneurysm and then confirmed their EC origin by polymerase chain reaction and immunocytochemistry with endothelial markers. Experiments were also carried out with human cerebral microvascular and umbilical vein ECs (HCECs and HUVECs respectively) for comparison. We tested EC proliferation ability and microtubule formation in Matrigel at different cell passages. Five aneurysm (3 ruptured, 2 unruptured) and 3 AVM (2 ruptured, 1 unruptured) ECs were tested for ET-1 release in the culture medium. Aneurysm and AVM ECs expressed von Willebrand factor, Adrenomedullin, and exhibited a progressive reduction of proliferation and in vitro angiogenic ability after the V passage. Significantly higher levels of ET-1 have been detected in ECs from ruptured aneurysms and AVMs. 我们将人脑动脉瘤和动静脉血管畸形中的内皮细胞分离出来，并用内皮标志物结合多聚酶链反应和免疫组化等方法确认其内皮来源性。同时选用人脑微血管中及脐静脉中的内皮细胞（分别是HCECs和HUVECs）作对照。我们测定了基质胶中内皮细胞各代的增殖能力及微管形成情况。也测定了5例动脉瘤（3例破裂，2例未破裂）和3例AVM（2例破裂，1例未破裂）中的内皮细胞在培养基里内皮素-1的释放量。来源于动脉瘤和动静脉型血管畸形的内皮细胞培养5代以后表达血管假性血友病因子、肾上腺髓质素，同时在活体外增殖及生成血管的能力方面呈顺行性退化。内皮素-1在破裂的动脉瘤和动静脉型血管畸形的内皮细胞中呈现引人注目的高水平。
We report the first successful isolation and characterization of primary EC lines from human cerebral vascular lesions. Augmented release of ET-1 is correlated with the rupture of the abnormal vessel confirming its role in vasospasm after SAH. Furthermore, ECs obtained from these vascular malformations can be used as an experimental model to study SAH-induced vasoconstriction.我们首次报告了人脑病变血管中初级内皮细胞系成功分离及其特征，确定了在蛛网膜下腔出血后血管痉挛过程中内皮素-1的增强释放与异常血管破裂相关联，并证实了其在蛛网膜下腔出血后血管痉挛中起的作用。 此外，这些来源于畸形血管的内皮细胞可作为研究蛛网膜下腔出血引发血管收缩的实验模型。
PMID: 17016610 [PubMed - in process]
Int J Mol Med. 2006 Nov;18(5):813-9
Endothelial cells from human cerebral aneurysm and arteriovenous malformation release ET-1 in response to vessel rupture. 来源于人大脑动脉瘤和动静脉血管畸形中的内皮细胞可伴随血管破裂释放内皮素-1
Boscolo E, Pavesi G, Zampieri P, Conconi MT, Calore C, Scienza R, Parnigotto PP, Folin M.
Cerebral aneurysms and arteriovenous malformations (AVM) are a common cause of stroke and cerebral hemorrage. Both are often discovered when they rupture, causing subarachnoid hemorrhage (SAH). SAH-induced vasospasm is mediated by enhanced vasoconstriction due to endothelin-1 (ET-1). We investigated whether endothelial cells (ECs) obtained from aneurysm and AVM express phenotypic and genotypic alterations contributing to the development of vasospasm after SAH. 大脑动脉瘤和动静脉型血管畸形(AVM)是中风及脑出血的常见原因。两者均常由于血管破裂导致蛛网膜下腔出血而被发现。蛛网膜下腔出血后血管痉挛是由能增强血管收缩的作用内皮素-1(ET-1)所介导。本实验我们探讨在蛛网膜下腔出血后促进血管痉挛进展过程中，来源于大脑动脉瘤和动静脉型血管畸形的内皮细胞(ECs)是发生了表型改变还是基因型改变。
We isolated ECs from human AVM and aneurysm and then confirmed their EC origin by polymerase chain reaction and immunocytochemistry with endothelial markers. Experiments were also carried out with human cerebral microvascular and umbilical vein ECs (HCECs and HUVECs respectively) for comparison. We tested EC proliferation ability and microtubule formation in Matrigel at different cell passages. Five aneurysm (3 ruptured, 2 unruptured) and 3 AVM (2 ruptured, 1 unruptured) ECs were tested for ET-1 release in the culture medium. Aneurysm and AVM ECs expressed von Willebrand factor, Adrenomedullin, and exhibited a progressive reduction of proliferation and in vitro angiogenic ability after the V passage. Significantly higher levels of ET-1 have been detected in ECs from ruptured aneurysms and AVMs. 我们将人脑动脉瘤和动静脉血管畸形中的内皮细胞分离出来，并用内皮标志物结合多聚酶链反应和免疫组化等方法确认其内皮来源性。同时选用人脑微血管中及脐静脉中的内皮细胞（分别是HCECs和HUVECs）作对照。我们测定了基质胶中内皮细胞各代的增殖能力及微管形成情况。也测定了5例动脉瘤（3例破裂，2例未破裂）和3例AVM（2例破裂，1例未破裂）中的内皮细胞在培养基里内皮素-1的释放量。来源于动脉瘤和动静脉型血管畸形的内皮细胞培养5代以后表达血管假性血友病因子、肾上腺髓质素，同时在活体外增殖及生成血管的能力方面呈顺行性退化。内皮素-1在破裂的动脉瘤和动静脉型血管畸形的内皮细胞中呈现引人注目的高水平。
We report the first successful isolation and characterization of primary EC lines from human cerebral vascular lesions. Augmented release of ET-1 is correlated with the rupture of the abnormal vessel confirming its role in vasospasm after SAH. Furthermore, ECs obtained from these vascular malformations can be used as an experimental model to study SAH-induced vasoconstriction.我们首次报告了人脑病变血管中初级内皮细胞系成功分离及其特征，确定了在蛛网膜下腔出血后血管痉挛过程中内皮素-1的增强释放与异常血管破裂相关联，并证实了其在蛛网膜下腔出血后血管痉挛中起的作用。 此外，这些来源于畸形血管的内皮细胞可作为研究蛛网膜下腔出血引发血管收缩的实验模型。
PMID: 17016610 [PubMed - in process]
Int J Mol Med. 2006 Nov;18(5):813-9
Endothelial cells from human cerebral aneurysm and arteriovenous malformation release ET-1 in response to vessel rupture.
来自人类脑动脉瘤和动静脉畸形的内皮细胞在血管破裂时释放ET-1
作者：Boscolo E, Pavesi G, Zampieri P, Conconi MT, Calore C, Scienza R, Parnigotto PP, Folin M.
Cerebral aneurysms and arteriovenous malformations (AVM) are a common cause of stroke and cerebral hemorrage. Both are often discovered when they rupture, causing subarachnoid hemorrhage (SAH). SAH-induced vasospasm is mediated by enhanced vasoconstriction due to endothelin-1 (ET-1). We investigated whether endothelial cells (ECs) obtained from aneurysm and AVM express phenotypic and genotypic alterations contributing to the development of vasospasm after SAH.
脑动脉瘤与动静脉畸形(AVM)是卒中和脑出血的常见原因。二者皆经常在破裂，导致蛛网膜下腔出血（SAH）时被发现。SAH诱导的血管痉挛是通过增强血管收缩介导的，而增强血管收缩归因于内皮素-1（ET-1）。我们旨在研究来自于动脉瘤和AVM的内皮细胞（ECs）是否表现出表型或基因型的变更，进而导致SAH.后血管痉挛的发展。
We isolated ECs from human AVM and aneurysm and then confirmed their EC origin by polymerase chain reaction and immunocytochemistry with endothelial markers. Experiments were also carried out with human cerebral microvascular and umbilical vein ECs (HCECs and HUVECs respectively) for comparison. We tested EC proliferation ability and microtubule formation in Matrigel at different cell passages. Five aneurysm (3 ruptured, 2 unruptured) and 3 AVM (2 ruptured, 1 unruptured) ECs were tested for ET-1 release in the culture medium. Aneurysm and AVM ECs expressed von Willebrand factor, Adrenomedullin, and exhibited a progressive reduction of proliferation and in vitro angiogenic ability after the V passage. Significantly higher levels of ET-1 have been detected in ECs from ruptured aneurysms and AVMs.
我们从人类AVM和动脉瘤中分离ECs，然后应用聚合酶链反应和免疫细胞化学法通过内皮标志物证实EC起源。实验同时也在人类大脑微血管和脐静脉的ECs中进行(HCECs、 HUVECs分别进行)，以便比较。我们在基底膜基质（Matrigel）中检测EC在各代的增值能力以及微血管的形成情况。在培养基中检测到5个动脉瘤（3个破裂，2个未破裂）和3个动静脉畸形（2个破裂，1个未破裂）的ECs释放ET-1。动脉瘤与动静脉畸形的ECs表达血管性血友病因子、肾上腺髓质素并显示培养五代后EC的增值能力和活体外血管增生能力进行性下降。ET-1在源于破裂的血管瘤和AVMs的ECs中水平明显较高。
We report the first successful isolation and characterization of primary EC lines from human cerebral vascular lesions. Augmented release of ET-1 is correlated with the rupture of the abnormal vessel confirming its role in vasospasm after SAH. Furthermore, ECs obtained from these vascular malformations can be used as an experimental model to study SAH-induced vasoconstriction.
我们报道了人类脑血管病变的基本EC普的首次成功分离与鉴定。ET-1释放增加与异常血管破裂有关，这证实了其在SAH.后血管痉挛中的作用。此外，从这些血管畸形中获得的ECs可以用作实验模型来研究SAH诱导的血管收缩。
Neurosurgery. 2006 Nov;59(5):1044-51;
Early and intermediate-term outcomes with drug-eluting stents in high-risk patients with symptomatic intracranial stenosis.
药物洗脱支架治疗高危症状性颅内动脉狭窄的早期及中期结果
Qureshi AI, Kirmani JF, Hussein HM, Harris-Lane P, Divani AA, Suri MF, Janjua N, Alkawi A.
OBJECTIVE: To report the 1-month and intermediate-term results of treatment of symptomatic intracranial stenosis using drug-eluting stents.
目的：本研究旨在报道使用药物洗脱支架治疗症状性颅内动脉狭窄的1个月及中期结果。
BACKGROUND: Patients with intracranial stenosis who are at high risk because of either high-grade stenosis or medication failure may have an annual risk of recurrent ischemic events in excess of 40%. Drug-eluting stents may reduce the rate of ischemic events in patients with a low restenosis rate.
背景：因动脉高度狭窄或药物治疗无效而处于高风险之中的颅内动脉狭窄患者，每年缺血事件的再发风险超过40%。药物洗脱支架可降低缺血事件发生频率，且再狭窄率低。
METHODS: We determined rates of technical success (defined as reduction of target lesion to stenosis <30%) and 1-month major stroke or death in patients with symptomatic intracranial stenosis (> or =70% and/or medication failure). Patients' clinical and follow-up information during a mean period of 14.3 +/- 7 months were obtained. Kaplan-Meier analysis was performed to determine the rate of major stroke-free survival during 12 months.
方法：确定症状性颅内动脉狭窄患者（狭窄≥70%和/或药物治疗无效）支架术的成功率（将病灶处狭窄率降至30%以下定义为治疗成功），以及1个月时大卒中和死亡的发生率。采集平均14.3±7个月中患者的临床及随访结果。通过Kaplan-Meier分析确定12个月内无大卒中的患者生存率。
RESULTS: There were 18 patients (mean age, 58 +/- 16 yr; 12 were men) treated with either a sirolimus-eluting stent (n = 14) or a paclitaxel-eluting stent (n = 4) for stenosis located in the: intracranial internal carotid artery (n = 6), proximal middle cerebral artery (n = 4), intracranial vertebral artery (n = 4), vertebrobasilar junction (n = 2), or basilar artery (n = 2). There was one major stroke and no death observed in the 1-month follow-up. At the 6-month follow-up examination, no major stroke or death was observed. Major stroke-free survival was 86% (+/-standard error of 9%) at 12 months after the procedure. One symptomatic angiographic restenosis was observed during the follow-up period.
结果：研究共纳入18名患者（平均年龄58±16岁；男性12名），狭窄灶分别位于颈内动脉颅内段（n=6），大脑中动脉近端（n=4），椎动脉颅内段（n=4），椎－基底动脉环（n=2）及基底动脉（n=2）。14名患者使用西罗莫司洗脱支架，4名使用紫杉醇洗脱支架。１个月随访时发生１例大卒中，未见死亡病例。６个月随访时未发现大卒中及死亡。支架术后12个月时，无大卒中的生存率为86%（标准误±9%）。整个随访期间血管造影发现1例再狭窄。
CONCLUSION: A low rate of major stroke or death was observed after treatment of symptomatic intracranial stenosis using drug-eluting stents in high-risk patients.
结论：采用药物洗脱支架可降低高危症状性颅内动脉狭窄患者大卒中的发生率或死亡率。
已拜读gaoshanwater的翻译，更改了几处不妥之处，谢谢指点。
DXY高手入云，我要更加努力才是。
Neurosurgery. 2006 Nov;59(5):1044-51;
Early and intermediate-term outcomes with drug-eluting stents in high-risk patients with symptomatic intracranial stenosis.药物洗脱支架治疗高危症状性颅内动脉狭窄患者的早期和中期结果
Qureshi AI, Kirmani JF, Hussein HM, Harris-Lane P, Divani AA, Suri MF, Janjua N, Alkawi A.
OBJECTIVE: To report the 1-month and intermediate-term results of treatment of symptomatic intracranial stenosis using drug-eluting stents. 目的：本研究旨在报告药物洗脱支架在治疗症状性颅内动脉狭窄患者一个月及中期结果。
BACKGROUND: Patients with intracranial stenosis who are at high risk because of either high-grade stenosis or medication failure may have an annual risk of recurrent ischemic events in excess of 40%. Drug-eluting stents may reduce the rate of ischemic events in patients with a low restenosis rate. 背景：鉴于高度狭窄和药物治疗失败使得颅内动脉狭窄的高危患者每年缺血性事件再发率高于40﹪。药物洗脱支架可以减少患者缺血事件的发生率并且具有低的再狭窄率。
METHODS: We determined rates of technical success (defined as reduction of target lesion to stenosis <30%) and 1-month major stroke or death in patients with symptomatic intracranial stenosis (> or =70% and/or medication failure). Patients' clinical and follow-up information during a mean period of 14.3 +/- 7 months were obtained. Kaplan-Meier analysis was performed to determine the rate of major stroke-free survival during 12 months. RESULTS: There were 18 patients (mean age, 58 +/- 16 yr; 12 were men) treated with either a sirolimus-eluting stent (n = 14) or a paclitaxel-eluting stent (n = 4) for stenosis located in the: intracranial internal carotid artery (n = 6), proximal middle cerebral artery (n = 4), intracranial vertebral artery (n = 4), vertebrobasilar junction (n = 2), or basilar artery (n = 2). There was one major stroke and no death observed in the 1-month follow-up. At the 6-month follow-up examination, no major stroke or death was observed. Major stroke-free survival was 86% (+/-standard error of 9%) at 12 months after the procedure. One symptomatic angiographic restenosis was observed during the follow-up period. 方法：我们选定颅内动脉狭窄患者（大于或等于70% 和/或药物治疗失败）、技术成功率（降低靶目标损害狭窄率达到<30%定义为成功）以及一个月时大卒中发生率和死亡率。同时获取患者平均14.3 +/- 7月的临床和随访资料。应用Kaplan-Meier分析确定12个月期间内患者患大卒中率及存活率。结果：对18名患者（平均年龄58 +/- 16岁；男性12名），14例应用西罗莫司（免疫抑制药）洗脱支架4例应用紫杉醇(抗肿瘤药)洗脱支架。狭窄灶分别位于：颈内动脉颅内段(n = 6)，大脑中动脉近心端(n = 4)，椎动脉颅内段(n = 4)，脊椎基底动脉结合部(n = 2)及基底动脉(n = 2)。一个月内的随访发现一例大的卒中但无死亡。在6个月时的随访检查没有发现大的卒中和死亡。支架术后12个月时患者无大卒中生存率为86%（标准误+/- 9%）。随访期间血管造影发现一例再狭窄。
CONCLUSION: A low rate of major stroke or death was observed after treatment of symptomatic intracranial stenosis using drug-eluting stents in high-risk patients.结论：采用药物洗脱支架治疗可降低高危症状性颅内动脉狭窄患者发生大卒中和死亡的几率。
PMID: 17143239 [PubMed - indexed for MEDLINE]
Lancet Neurol. 2006 Jul;5(7):578-88
Cognitive sequelae of subthalamic nucleus deep brain stimulation in Parkinson's disease: a meta-analysis.
Parsons TD, Rogers SA, Braaten AJ, Woods SP, Troster AI.
BACKGROUND: Deep brain stimulation of the subthalamic nucleus (STN DBS) is an increasingly common treatment for Parkinson's disease. Qualitative reviews have concluded that diminished verbal fluency is common after STN DBS, but that changes in global cognitive abilities, attention, executive functions, and memory are only inconsistently observed and, when present, often nominal or transient. We did a quantitative meta-analysis to improve understanding of the variability and clinical significance of cognitive dysfunction after STN DBS.
METHODS: We searched MedLine, PsycLIT, and ISI Web of Science electronic databases for articles published between 1990 and 2006, and extracted information about number of patients, exclusion criteria, confirmation of target by microelectrode recording, verification of electrode placement via radiographic means, stimulation parameters, assessment time points, assessment measures, whether patients were on levodopa or dopaminomimetics, and summary statistics needed for computation of effect sizes. We used the random-effects meta-analytical model to assess continuous outcomes before and after STN DBS.
FINDINGS: Of 40 neuropsychological studies identified, 28 cohort studies (including 612 patients) were eligible for inclusion in the meta-analysis. After adjusting for heterogeneity of variance in study effect sizes, the random effects meta-analysis revealed significant, albeit small, declines in executive functions and verbal learning and memory. Moderate declines were only reported in semantic (Cohen's d 0.73) and phonemic verbal fluency (0.51). Changes in verbal fluency were not related to patient age, disease duration, stimulation parameters, or change in dopaminomimetic dose after surgery.
INTERPRETATION: STN DBS, in selected patients, seems relatively safe from a cognitive standpoint. However, difficulty in identification of factors underlying changes in verbal fluency draws attention to the need for uniform and detailed reporting of patient selection, demographic, disease, treatment, surgical, stimulation, and clinical outcome parameters.
PMID: 16781988 [PubMed - indexed for MEDLINE]
J Neurosci. 2006 Nov 29;26(48):12497-511
Transplantation of human neural stem cells exerts neuroprotection in a rat model of Parkinson's disease.
Yasuhara T, Matsukawa N, Hara K, Yu G, Xu L, Maki M, Kim SU, Borlongan CV.
Neural stem cells (NSCs) possess high potencies of self-renewal and neuronal differentiation. We explored here whether transplantation of human NSCs cloned by v-myc gene transfer, HB1.F3 cells, is a feasible therapeutic option for Parkinson's disease.
In vivo, green fluorescent protein-labeled HB1.F3 cells (200,000 viable cells in 3 microl of PBS) when stereotaxically transplanted (same-day lesion-transplant paradigm) into the 6-hydroxydopamine-lesioned striatum of rats significantly ameliorated parkinsonian behavioral symptoms compared with controls (vehicle, single bolus, or continuous minipump infusion of trophic factor, or killed cell grafts). Such graft-derived functional effects were accompanied by preservation of tyrosine hydroxylase (TH) immunoreactivity along the nigrostriatal pathway. Grafted HB1.F3 cells survived in the lesioned brain with some labeled with neuronal marker mitogen-activated protein 2 and decorated with synaptophysin-positive terminals. Furthermore, endogenous neurogenesis was activated in the subventricular zone of transplanted rats. To further explore the neuroprotective mechanisms underlying HB1.F3 cell transplantation, we performed cell culture studies and found that a modest number of HB1.F3 cells were TH and dopamine and cAMP-regulated phosphoprotein 32 positive, although most cells were nestin positive, suggesting a mixed population of mature and immature cells. Administration of the HB1.F3 supernatant to human derived dopaminergic SH-SY5Y cells and fetal rat ventral mesencephalic dopaminergic neurons protected against 6-hydroxydopamine neurotoxicity by suppressing apoptosis through Bcl-2 upregulation, which was blocked by anti-stem cell factor antibody alone, the phosphatidylinositol 3-kinase/Akt inhibitor LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one] alone, or a combination of both.
These results suggest that HB1.F3 cell transplantation exerts neuroprotective effects against dopaminergic depletion in vitro and in vivo because of trophic factor secretion and neuronal differentiation.
PMID: 17135412 [PubMed - indexed for MEDLINE]
Brain. 2007 Jan 5;
Surgical outcome and prognostic factors of frontal lobe epilepsy surgery.
Jeha LE, Najm I, Bingaman W, Dinner D, Widdess-Walsh P, Luders H.
Department of Neurology, Section of Epilepsy, Cleveland Clinic, Cleveland, OH, USA.
Frontal lobe epilepsy (FLE) surgery is the second most common surgery performed to treat pharmacoresistant epilepsy. Yet, little is known about long-term seizure outcome following frontal lobectomy. The aim of this study is to investigate the trends in longitudinal outcome and identify potential prognostic indicators in a cohort of FLE patients investigated using modern diagnostic techniques.
We reviewed 70 patients who underwent a frontal lobectomy between 1995 and 2003 (mean follow-up 4.1 +/- 3 years). Data were analysed using survival analysis and multivariate regression with Cox proportional hazard models.
A favourable outcome was defined as complete seizure-freedom, allowing for auras and seizures restricted to the first post-operative week. The estimated probability of complete seizure-freedom was 55.7% [95% confidence interval (CI) = 50-62] at 1 post-operative year, 45.1% (95% CI = 39-51) at 3 years, and 30.1% (95% CI = 21-39) at 5 years. Eighty per cent of seizure recurrences occurred within the first 6 post-operative months. Late remissions and relapses occurred, but were rare. After multivariate analysis, the following variables retained their significance as independent predictors of seizure recurrence: MRI-negative malformation of cortical development as disease aetiology [risk ratio (RR) = 2.22, 95% CI = 1.40-3.47], any extrafrontal MRI abnormality (RR = 1.75, 95% CI = 1.12-2.69), generalized/non-localized ictal EEG patterns (RR = 1.83, 95% CI = 1.15-2.87), occurrence of acute post-operative seizures (RR = 2.17, 95% CI = 1.50-3.14) and incomplete surgical resection (RR = 2.56, 95% CI = 1.66-4.05) (log likelihood-ratio test P-value < 0.0001). More than half of patients in favourable prognostic categories were seizure-free at 3 years, and up to 40% were seizure-free at 5 years, compared to <15% in those with unfavourable outcome predictors.
These data underscore the importance of appropriate selection of potential surgical candidates.
PMID: 17209228 [PubMed - as supplied by publisher]
对这篇文章理解的不是很好，请高手斧正。谢谢！
Lancet Neurol. 2006 Jul;5(7):578-88
Cognitive sequelae of subthalamic nucleus deep brain stimulation in Parkinson's disease: a meta-analysis.
丘脑下（底）核深部脑刺激治疗帕金森（病）的认知后遗症：一项meta分析
作者：Parsons TD, Rogers SA, Braaten AJ, Woods SP, Troster AI.
BACKGROUND: Deep brain stimulation of the subthalamic nucleus (STN DBS) is an increasingly common treatment for Parkinson's disease. Qualitative reviews have concluded that diminished verbal fluency is common after STN DBS, but that changes in global cognitive abilities, attention, executive functions, and memory are only inconsistently observed and, when present, often nominal or transient. We did a quantitative meta-analysis to improve understanding of the variability and clinical significance of cognitive dysfunction after STN DBS.
背景：丘脑下（底）核深部脑刺激(STN DBS)是一种日渐增加的治疗帕金森（病）的常用方法。定性的观察回顾分析（已）发现STN DBS后经常出现言语流畅度下降，（而）大脑认知能力、注意力、执行功能和记忆的改变（仅）间或地被观察到，当这些症状出现时表现较轻或是一过性的。我们做了一个定量的meta分析以便更好的了解STN DBS后认知功能障碍的差别和临床意义。
METHODS: We searched MedLine, PsycLIT, and ISI Web of Science electronic databases for articles published between 1990 and 2006, and extracted information about number of patients, exclusion criteria, confirmation of target by microelectrode recording, verification of electrode placement via radiographic means, stimulation parameters, assessment time points, assessment measures, whether patients were on levodopa or dopaminemimetics, and summary statistics needed for computation of effect sizes. We used the random-effects meta-analytical model to assess continuous outcomes before and after STN DBS.
方法：我们检索了于1990～2006年发表在MedLine、PsycLIT和ISI 网络电子期刊数据库上的文章，并提取如下信息：患者数量、淘汰标准、微电极记录确证病例、X 线照相技术确定电极所在的位置、刺激参数、评估时间点、评估测量方法、患者是否在服用左旋多巴或dopaminemimetics、对计算机计算的作用范围进行简要的统计学分析。我们应用随机效应meta-分析模型评估STN DBS治疗前后的连续病情变化。
FINDINGS: Of 40 neuropsychological studies identified, 28 cohort studies (including 612 patients) were eligible for inclusion in the meta-analysis. After adjusting for heterogeneity of variance in study effect sizes, the random effects meta-analysis revealed significant, albeit small, declines in executive functions and verbal learning and memory. Moderate declines were only reported in semantic (Cohen's d 0.73) and phonemic verbal fluency (0.51). Changes in verbal fluency were not related to patient age, disease duration, stimulation parameters, or change in dopaminomimetic dose after surgery.
结果：共分析了40个神经心理学研究，28个队列研究（612位患者）适合进行meta-分析。校正研究作用范围后，随机效应meta-分析显示执行功能、言语学习和记忆有所下降，下降幅度较小但有显著意义。语义（Cohen， d= 0.73）和语音（0.51）的流畅性中度下降。言语流畅度的改变与患者年龄、疾病持续时间、刺激参数或术后dopaminomimetic剂量改变无关。
INTERPRETATION: STN DBS, in selected patients, seems relatively safe from a cognitive standpoint. However, difficulty in identification of factors underlying changes in verbal fluency draws attention to the need for uniform and detailed reporting of patient selection, demographic, disease, treatment, surgical, stimulation, and clinical outcome parameters.
结论：STN DBS，在选择性人群中，从认知观点来讲相对安全。但是辨别语言流畅度有哪些方面改变很难，这需要对患者的选择、人口统计学、疾病、治疗、外科手术、刺激以及临床结果等一些列参数进行详细的了解。
哈哈 wlntcm战友过谦了,我认为你的功力强于啊.感谢\斑竹提供的相互交流学习提高的平台.
请高手指点斧正.谢谢!
J Neurosci. 2006 Nov 29;26(48):12497-511
Transplantation of human neural stem cells exerts neuroprotection in a rat model of Parkinson's disease.人类神经干细胞移植对帕金森大鼠模型的神经保护作用
Yasuhara T, Matsukawa N, Hara K, Yu G, Xu L, Maki M, Kim SU, Borlongan CV.
Neural stem cells (NSCs) possess high potencies of self-renewal and neuronal differentiation. We explored here whether transplantation of human NSCs cloned by v-myc gene transfer, HB1.F3 cells, is a feasible therapeutic option for Parkinson's disease. 神经干细胞(NSCs) 具有高效能的自我更新和神经分化能力。本实验旨在探究移植HB1.F3细胞（ 由v-myc基因转入人类神经干细胞克隆而来）能否成为治疗帕金森病的可行方法。
In vivo, green fluorescent protein-labeled HB1.F3 cells (200,000 viable cells in 3 microl of PBS) when stereotaxically transplanted (same-day lesion-transplant paradigm) into the 6-hydroxydopamine-lesioned striatum of rats significantly ameliorated parkinsonian behavioral symptoms compared with controls (vehicle, single bolus, or continuous minipump infusion of trophic factor, or killed cell grafts). Such graft-derived functional effects were accompanied by preservation of tyrosine hydroxylase (TH) immunoreactivity along the nigrostriatal pathway. Grafted HB1.F3 cells survived in the lesioned brain with some labeled with neuronal marker mitogen-activated protein 2 and decorated with synaptophysin-positive terminals. Furthermore, endogenous neurogenesis was activated in the subventricular zone of transplanted rats. To further explore the neuroprotective mechanisms underlying HB1.F3 cell transplantation, we performed cell culture studies and found that a modest number of HB1.F3 cells were TH and dopamine and cAMP-regulated phosphoprotein 32 positive, although most cells were nestin positive, suggesting a mixed population of mature and immature cells. Administration of the HB1.F3 supernatant to human derived dopaminergic SH-SY5Y cells and fetal rat ventral mesencephalic dopaminergic neurons protected against 6-hydroxydopamine neurotoxicity by suppressing apoptosis through Bcl-2 upregulation, which was blocked by anti-stem cell factor antibody alone, the phosphatidylinositol 3-kinase/Akt inhibitor LY294002 [2-(4-morpholinyl)-8-phenyl-1(4H)-benzopyran-4-one] alone, or a combination of both.应用立体定向术向当天损伤移植大鼠模型6-羟基多巴胺受损的纹状体中移植绿色荧光蛋白标记的HB1.F3细胞（3微升PBS液中含200,000个活性细胞），与对照组（快速灌注方式，连续微泵注射营养因子或死亡的细胞移植物）相比，可显著地改善帕金森大鼠的症状行为。黑质纹状体通路上酪氨酸羟化酶免疫活性可随移植衍生物机能效应得以保存。移植后在受损脑组织存活的HB1.F3细胞中有一些是示踪标记的细胞，有一些具有神经元标记物促分裂原活化蛋白2的细胞，并且均被突触素阳性反应终产物所修饰。此外，被移植大鼠脑室下区内源性神经发生的过程被激活。为进一步探究移植细胞后的神经保护机制，我们将HB1.F3细胞进行培养后发现尽管绝大多数是巢蛋白阳性反应细胞，但其中有适量细胞呈现酪氨酸羟化酶、多巴胺及cAMP调节的磷蛋白32阳性反应，这提示其中混合有成熟细胞和未成熟细胞。将HB1.F3细胞上清液给予人多巴胺能SH-SY5Y细胞及胎鼠中脑腹侧多巴胺能神经元时可抵御6-羟基多巴胺的神经毒性作用。该作用是通过上调Bcl-2表达而抑制凋亡实现的，并可被抗干细胞因子及磷脂酰肌醇3位羟基激酶LY294002（Akt抑制剂）单独或合并阻断。
These results suggest that HB1.F3 cell transplantation exerts neuroprotective effects against dopaminergic depletion in vitro and in vivo because of trophic factor secretion and neuronal differentiation.这些结果提示移植的HB1.F3细胞由于分泌营养因子和神经元分化可在体内外通过对抗多巴胺能的耗竭发挥神经保护作用。
PMID: 17135412 [PubMed - indexed for MEDLINE]
请高手斧正，谢谢！
Brain. 2007 Jan 5;
Surgical outcome and prognostic factors of frontal lobe epilepsy surgery.
额叶癫痫术后转归和预测因子(预后因素)
作者：Jeha LE, Najm I, Bingaman W, Dinner D, Widdess-Walsh P, Luders H.
Department of Neurology, Section of Epilepsy, Cleveland Clinic, Cleveland, OH, USA.
Frontal lobe epilepsy (FLE) surgery is the second most common surgery performed to treat pharmacoresistant epilepsy. Yet, little is known about long-term seizure outcome following frontal lobectomy. The aim of this study is to investigate the trends in longitudinal outcome and identify potential prognostic indicators in a cohort of FLE patients investigated using modern diagnostic techniques.
额叶癫痫（FLE）手术是治疗耐药癫痫的第二大常用外科手术。然而，人们对额叶切除后长期的癫痫发作情况知之甚少。此次研究旨在调查一组应用现代诊断技术诊断的FLE患者术后的纵向（长期的）转归趋势，并识别潜在的预测因子
We reviewed 70 patients who underwent a frontal lobectomy between 1995 and 2003 (mean follow-up 4.1 +/- 3 years). Data were analysed using survival analysis and multivariate regression with Cox proportional hazard models.
我们回顾性调查了70位患者，皆在1995～2003年间接受过额叶切除术（平均随访4.1±3年）。应用生存分析和多变量回归协同Cox比例风险模型对研究数据进行分析。
A favourable outcome was defined as complete seizure-freedom, allowing for auras and seizures restricted to the first post-operative week. The estimated probability of complete seizure-freedom was 55.7% [95% confidence interval (CI) = 50-62] at 1 post-operative year, 45.1% (95% CI = 39-51) at 3 years, and 30.1% (95% CI = 21-39) at 5 years. Eighty per cent of seizure recurrences occurred within the first 6 post-operative months. Late remissions and relapses occurred, but were rare. After multivariate analysis, the following variables retained their significance as independent predictors of seizure recurrence: MRI-negative malformation of cortical development as disease aetiology [risk ratio (RR) = 2.22, 95% CI = 1.40-3.47], any extrafrontal MRI abnormality (RR = 1.75, 95% CI = 1.12-2.69), generalized/non-localized ictal EEG patterns (RR = 1.83, 95% CI = 1.15-2.87), occurrence of acute post-operative seizures (RR = 2.17, 95% CI = 1.50-3.14) and incomplete surgical resection (RR = 2.56, 95% CI = 1.66-4.05) (log likelihood-ratio test P-value < 0.0001). More than half of patients in favourable prognostic categories were seizure-free at 3 years, and up to 40% were seizure-free at 5 years, compared to <15% in those with unfavourable outcome predictors.
考虑到预测和癫痫发作在术后第一周被限制，良性转归被定义为癫痫发作完全缓解。癫痫发作完全缓解的概率在术1年为55.7% （95%CI=50～62），术后3年为45.1%（95%CI=39～51），术后5年为30.1% (95% CI= 21～39)。术后6个月内80%癫痫发作再发。之后会出现缓解、复发，但是比较少见。多变量分析后，下述变量保持着独立预测癫痫发作再发的显著意义：疾病病原学为皮质发育畸形MRI阴性（RR = 2.22，95% CI = 1.40～3.47），额叶边缘（任何额叶以外）MRI异常（RR = 1.75，95% CI=1.12～2.69），广泛的或非局灶性的发作脑电图（RR=1.83，95% CI =1.15～2.87），急性术后癫痫发作发生（RR = 2.17，95% CI=1.50-3.14)，外科切除不完全（RR=2.17，95% CI =1.50～3.14)，（对数似然比检验，P＜0.0001）。与含不良转归预测因子的癫痫发作的完全缓解率<15%相比，超过半数患者在术后3年达到良性转归范畴即癫痫发作完全缓解，术后5年缓解率为40%。
These data underscore the importance of appropriate selection of potential surgical candidates.
这些数据（资料）着重强调对拟手术患者的适宜选择（合理选择潜在手术病人的重要性）。
已经学习了leuking版主的斧正之处，非常感谢。通过对斧正之处中英文对照的学习，我了解了我的欠缺之处，我会更加努力。感谢给我一个学习英语的平台，期待以后向更多的战友学习。
本人感觉该文章内容属于神经内科，但文章选自 Neurosurgery，所以我把它放入神经外科进展栏。对于文章的翻译还请高手斧正、指导。谢谢！
THREE-DAY PHENYTOIN PROPHYLAXIS IS ADEQUATE AFTER SUBARACHNOID HEMORRHAGE.
蛛网膜下腔出血后应用苯妥英钠预防性治疗３天即可
CLINICAL STUDIES
Neurosurgery. 60(1):99-103, January 2007.
Chumnanvej, Sorayouth M.D.; Dunn, Ian F. M.D.; Kim, Dong H. M.D.
Abstract:
OBJECTIVE: Phenytoin (PHT) is widely administered after subarachnoid hemorrhage, often for several weeks or months. In addition to known side effects, PHT use has been correlated with cognitive disability and poor outcome. To reduce the rate of PHT complications, we converted from a multi-week prophylactic regimen to a 3-day course of treatment. This study evaluates the changes in seizure rates and adverse events
背景：苯妥英钠（PHT）在蛛网膜下腔出血后被广泛地应用，经常应用数周或数月。由于其药物副作用，被认为与认知功能障碍和不良转归相关。为了降低PHT并发症的发病率，我们把预防性治疗疗程由数周改为3天，并评估了癫痫发作的发病率和负性事件的改变情况。
METHODS: From July 1998 to June 2002, 453 patients with spontaneous subarachnoid hemorrhage were treated. In the first 9 months, 79 patients were administered PHT until discharged from the hospital, unless a drug reaction occurred first. In the last 39 months, PHT was discontinued 3 days after admission (370 patients), unless there was a history of epilepsy (four patients). This study represents a retrospective analysis of prospectively collected data, with follow-up periods of 3 to 12 months after discharge.
方法：研究纳入1998年7月～2002年6月，453位接受治疗的自发性蛛网膜下腔出血患者。前9个月内，79位患者接受了PHT预防性治疗直至出院，首先排除了一例发生药物反应的患者。后39个月内，PHT在入院后3天停止应用（370位患者），排除了有癫痫病史的患者（4位）。该研究对前瞻性收集的数据进行了回顾性分析，并在出院后随访3～12个月。
RESULTS: The 3-day PHT regimen produced a statistically significant reduction (P = 0.002) in the rate of PHT complications. In the first period, seven (8.8%) out of 79 patients experienced a hypersensitivity reaction, compared with two (0.5%) out of 370 patients in the second period. The percentage of patients having seizures, both short- and long-term, did not change significantly. In the first period, the seizure rate during hospitalization was 1.3%; in the second period, it was 1.9% (P = 0.603). At an average follow-up period of 6.7 months, three (5.7%) out of 53 survivors in the first period experienced a seizure (including those who had a seizure during hospitalization). In the second period, 12 (4.6%) out of 261 survivors experienced a seizure at an average follow-up period of 5.4 months (P = 0.573).
结果：PHT治疗3天可显著减少PHT并发症的发病率，且有统计学意义（P=0.002）。第一个时间段（前９个月），79位患者中有7位（8.8%）发生过敏反应；第二个时间段（后39个月），370位患者中有2位（0.5%）发生过敏反应。第一个时间段，住院期间癫痫发作的发病率为1.3%；第二个时间段为1.9% (P = 0.603)。第一时间段，平均随访6.7个月， 53位生存者中有3位（5.7%）发生过一次癫痫发作（包括在住院期间发生的癫痫发作）；第二个时间段，平均随访5.4个月，261位生存者中有12位（4.6% ）发生过一次癫痫发作（P=0.573）。
CONCLUSION: A 3-day regimen of PHT prophylaxis is adequate to prevent seizures in subarachnoid hemorrhage patients. Drug reactions are significantly reduced, but seizure rates do not change. Short-term PHT administration may be a superior treatment paradigm.
结论：PHT 3天疗程法可以充分地预防蛛网膜下腔出血患者癫痫发作，且药物反应显著下降。但是癫痫发作的发病率未改变。短期PHT治疗也许是一个比较好的治疗方法。
Copyright (C) by the Congress of Neurological Surgeons
The Lancet Neurology---Volume 6, Number 1, January 2007
Magnesium sulfate for neuroprotection after traumatic brain injury: a randomised controlled trial
脑外伤后使用硫酸镁进行神经保护：一项随机对照试验
Background
Traumatic brain injuries represent an important and costly health problem. Supplemental magnesium positively affects many of the processes involved in secondary injury after traumatic brain injury and consistently improves outcome in animal models. We aimed to test whether treatment with magnesium favourably affects outcome in head-injured patients.
背景：脑外伤是一严重的健康问题，治疗费用高。动物实验中，补充镁可对脑外伤后继发损伤的许多环节产生积极影响，并持续改善预后。本研究旨在探讨使用镁治疗能否对脑外伤患者的预后产生积极影响。
Methods
In a double-blind trial, 499 patients aged 14 years or older admitted to a level 1 regional trauma centre between August, 1998, and October, 2004, with moderate or severe traumatic brain injury were randomly assigned one of two doses of magnesium or placebo within 8 h of injury and continuing for 5 days. Magnesium doses were targeted to achieve serum magnesium ranges of 1•0–1•85 mmol/L or 1•25–2•5 mmol/L. The primary outcome was a composite of mortality, seizures, functional measures, and neuropsychological tests assessed up to 6 months after injury. Analyses were done according to the intention-to-treat principle. This trial is registered with Clinicaltrials.gov, number NCT00004730.
方法：此项双盲试验的研究对象为1998年8月~2004年10月，在地区一级外伤中心住院治疗的499名中或重度脑外伤患者，年龄≥14岁。受试者受伤8 h内随机接受一种剂量的硫酸镁（共两种剂量）或安慰剂治疗，持续5 d。硫酸镁给予剂量以血清镁浓度达到1.0~1.85 mmol/L或1.25~2.5 mmol/L为准。主要终点指标为伤后6个月时死亡率、癫痫发作情况、功能指标和神经生理测试的复合结果。根据意向性分析原则分析数据。此项试验在Clinicaltrials.gov注册，编号为NCT00004730。
Findings
Magnesium showed no significant positive effect on the composite primary outcome measure at the higher dose (mean=55 average percentile ranking on magnesium vs 52 on placebo, 95% CI for difference −7 to 14; p=0•70). Those randomly assigned magnesium at the lower dose did significantly worse than those assigned placebo (48 vs 54, 95% CI −10•5 to −2; p=0•007). Furthermore, there was higher mortality with the higher magnesium dose than with placebo. Other major medical complications were similar between groups, except for a slight excess of pulmonary oedema and respiratory failure in the lower magnesium target group. No subgroups were identified in which magnesium had a significantly positive effect.
结果：较高剂量的硫酸镁对主要终点的各项指标未产生显著的正向影响（百分位数全距平均值 镁55 vs 安慰剂52，差异95%CI：−7~14；P=0.70）。而随机分配接受较低剂量硫酸镁的患者结果较安慰剂组差（48 vs 54，95%CI：−10.5~−2；P=0.007）。此外，高剂量硫酸镁组死亡率较安慰剂组高。除低剂量硫酸镁组肺水肿和呼吸衰竭的发生率轻微升高外，各组间其他主要并发症情况相似。亚族分析未发现硫酸镁可产生积极影响。
Interpretation
Continuous infusions of magnesium for 5 days given to patients within 8 h of moderate or severe traumatic brain injury were not neuroprotective and might even have a negative effect in the treatment of significant head injury.
结论：中重度脑外伤患者8 h内开始连续输注硫酸镁5 d并无神经保护作用，甚至可能对重度脑外伤的治疗不利。
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请高手指点、斧正。谢谢！
DELAYED CEREBRAL VASOSPASM SECONDARY TO BACTERIAL MENINGITIS AFTER LUMBOSACRAL SPINAL SURGERY: CASE REPORT.
继发于腰骶段脊柱术后细菌性脑膜炎的迟发性脑血管痉挛：病历报道
Neurosurgery. 60(1):E206,E207, January 2007.
Chaichana, Kaisorn B.S.; Riley, Lee H. III M.D.; Tamargo, Rafael J. M.D.
Abstract: [color=yellow][/color]
OBJECTIVE: Delayed cerebral vasospasm is an under-recognized complication of meningitis. This case report is important because it is the first to definitively associate vasospasm with meningitis using catheter angiography. Furthermore, it is the first to correlate the time course of delayed cerebral vasospasm with meningitis.
背景：迟发性脑血管痉挛是一个未被认识的脑膜炎并发症。此病例报道非常重要，因为这是第一次应用导管血管造影证实了血管痉挛与脑膜炎的相关性。此外，也第一次证实了迟发性脑血管痉挛的时程与脑膜炎之间的关系。
CLINICAL PRESENTATION: We present a patient who developed a partial expressive aphasia 9 days after developing meningitis, consistent with cerebral vasospasm, after lumbosacral spinal surgery.
临床表现：我们接诊了一个腰骶段脊柱术后脑膜炎患者，脑膜炎9天后出现部分表达性失语症，这与脑血管痉挛的症状相一致。
INTERVENTION: Vasospasm was confirmed by angiography and transcranial Doppler sonography, and symptoms responded to hypervolemia, hypertension, and hemodilution therapy.
干涉: 血管痉挛通过血管造影和经颅多普勒超声证实，针对血容量过多、高血压和血液稀释等症状进行治疗。
CONCLUSION: If a patient develops neurological symptoms consistent with a timeline of delayed cerebral vasospasm in the setting of meningitis, angiographic evaluation and appropriate therapy should be pursued.
结论：如果一个患者出现神经系统症状，并且在脑膜炎后发生迟发性脑血管痉挛的时间线内，则应用血管造影评估血管痉挛情况并进行适当的治疗。
Copyright (C) by the Congress of Neurological Surgeons
BMC Genomics. 2007 Jan 12;8(1):16
Comprehensive genetic and epigenetic analysis of sporadic meningioma for macro-mutations on 22q and micro-mutations within the NF2 locus.
Hansson CM, Buckley PG, Grigelioniene G, Piotrowski A, Hellstrom AR, Mantripragada KK, Jarbo C, Mathiesen T, Dumanski JP.
BACKGROUND: Meningiomas are the most common intracranial neoplasias, representing a clinically and histopathologically heterogeneous group of tumors. The neurofibromatosis type 2 (NF2) tumor suppressor is the only gene known to be frequently involved in early development of meningiomas.
The objective of this study was to identify genetic and/or epigenetic factors contributing to the development of these tumors.
A large set of sporadic meningiomas were analyzed for presence of 22q macro-mutations using array-CGH in order to identify tumors carrying gene dosage aberrations not encompassing NF2. The NF2 locus was also comprehensively studied for point mutations within coding and conserved non-coding sequences. Furthermore, CpG methylation within the NF2 promoter region was thoroughly analyzed.
RESULTS: Monosomy 22 was the predominant finding, detected in 47% of meningiomas. Thirteen percent of the tumors contained interstitial/terminal deletions and gains, present singly or in combinations. We defined at least two minimal overlapping regions outside the NF2 locus that are small enough (~550 kb and ~250 kb) to allow analysis of a limited number of candidate genes. Biallelic inactivation of the NF2 gene was detected in 36% of meningiomas. Among the monosomy 22 cases, no additional NF2 mutations could be identified in 35% (17 out of 49) of tumors. Furthermore, the majority of tumors (9 out of 12) with interstitial/terminal deletions did not have any detectable NF2 mutations. Methylation within the NF2 promoter region was only identified at a single CpG site in one tumor sample. CONCLUSIONS: We confirmed previous findings of pronounced differences in mutation frequency between different histopathological subtypes. There is a higher frequency of biallelic NF2 inactivation in fibroblastic (52%) compared to meningothelial (18%) tumors. The presence of macro-mutations on 22q also shows marked differences between fibroblastic (86%) and meningothelial (39%) subtypes. Thus, inactivation of NF2, often combined with the presence of macro-mutation on 22q, is likely not as important for the development of the meningothelial subtype, as opposed to the fibroblastic form.
Analysis of 40 CpG sites distributed within 750 bp of the promoter region suggests that NF2 promoter methylation does not play a major role in meningioma development.
PMID: 17222329 [PubMed - as supplied by publisher]
Acta Neurochir (Wien). 2006 Dec 21;
Olfactory groove meningiomas: functional outcome in a series treated microsurgically.
Bassiouni H, Asgari S, Stolke D.
Background. A systematic investigation of long-term follow-up results after microsurgical treatment of patients harbouring an olfactory groove meningioma, particularly with regard to postoperative olfactory and mental function, has rarely been performed. We reassessed a series of patients treated microsurgically for an olfactory groove meningioma in regard to clinical presentation, surgical approaches and long-term functional outcome.
Method. Clinical, radiological and surgical data in a consecutive series of 56 patients suffering from olfactory groove meningioma were retrospectively reviewed.
Findings. Presenting symptoms of the 41 women and 15 men (mean age 51 years) were mental changes in 39.3%, visual impairment in 16.1% and anosmia in 14.3% of the patients. Preoperative neurological examination revealed deficits in olfaction in 71.7%, mental disturbances in 55.4% and reduced vision in 21.4% of the cases. The tumour was resected via a bifrontal craniotomy in 36, a pterional route in 13, a unilateral frontal approach in 4 and via a supraorbital approach in 3 patients. Extent of tumour resection according to Simpson's classification system was grade I in 42.9% and grade II in 57.1% of the cases. After a mean follow-up period of 5.6 years (range 1-13 years) by clinical examination and magnetic resonance imaging (MRI), 86.8% of the patients resumed normal life activity. Olfaction was preserved in 24.4% of patients in whom pre- and postoperative data were available. Mental and visual disturbances improved in 88 and 83.3% of cases, respectively. Five recurrences (8.9%) were observed and had to be reoperated.
Conclusions. Frontal approaches allowed better resection of tumours with gross infiltration of the anterior cranial base, tumours extending into the ethmoids or nasal cavity and in cases with deep olfactory grooves. Preservation of olfaction should be attempted in patients with normal or reduced smelling preoperatively.
PMID: 17180303 [PubMed - as supplied by publisher]
1 Cancer Cell. 2007 Jan;11(1):69-82.
A Perivascular Niche for Brain Tumor Stem Cells.
Calabrese C, Poppleton H, Kocak M, Hogg TL, Fuller C, Hamner B, Oh EY, Gaber MW, Finklestein D, Allen M, Frank A, Bayazitov IT, Zakharenko SS, Gajjar A, Davidoff A, Gilbertson RJ.
Department of Developmental Neurobiology, St. Jude Children's Research Hospital, 332 North Lauderdale Street, Memphis, TN 38105, USA.
Cancers are believed to arise from cancer stem cells (CSCs), but it is not known if these cells remain dependent upon the niche microenvironments that regulate normal stem cells. We show that endothelial cells interact closely with self-renewing brain tumor cells and secrete factors that maintain these cells in a stem cell-like state. Increasing the number of endothelial cells or blood vessels in orthotopic brain tumor xenografts expanded the fraction of self-renewing cells and accelerated the initiation and growth of tumors. Conversely, depletion of blood vessels from xenografts ablated self-renewing cells from tumors and arrested tumor growth. We propose that brain CSCs are maintained within vascular niches that are important targets for therapeutic approaches.
PMID: 17222791 [PubMed - as supplied by publisher]
2 Neurobiol Dis. 2007 Jan 11;
Modified expression of Mts1/S100A4 protein in C6 glioma cells or surrounding astrocytes affects migration of tumor cells in vitro and in vivo.
Takenaga K, Nygren J, Zelenina M, Ohira M, Iuchi T, Lukanidin E, Sjoquist M, Kozlova EN.
Department of Neuroscience, Biomedical Center, Box 587, Uppsala University, 751 23 Uppsala, Sweden; Division of Chemotherapy, Chiba Cancer Center Research Institute, 666-2 Nitona, Chuoh-ku, Chiba, 260-8717 Chiba, Japan.
The calcium-binding Mts1/S100A4 protein plays an important role in motility and metastatic activity of tumor cells. Recently we showed that Mts1/S100A4 is expressed in white matter astrocytes and influences their migration in vitro and in vivo. Here, we have investigated the role of Mts1/S100A4 expression in C6 glioma cells or surrounding astrocytes for migration of C6 cells on astrocytes, using short interference (si) RNA to silence Mts1/S100A4 expression. We find that in vitro, the migration of Mts1/S100A4 expressing and silenced C6 cells on astrocytes is predominantly dependent on the expression of Mts1/S100A4 in astrocytes, i.e. C6 cells preferably migrate on Mts1/S100A4-silenced astrocytes. In vivo, Mts1/S100A4-positive C6 cells preferably migrate in white matter. In contrast Mts1/S100A4-silenced C6 cells avoid white matter and migrate in gray matter and meninges. Thus, the migration pattern of C6 cells is affected by their intrinsic Mts1/S100A4 expression as well as Mts1/S100A4 expression in astrocytes. To investigate if Mts1/S100A4 has a significant role on brain tumor progression, we made quantitative RT-PCR analysis for the expression of S100A4/Mts1 in various grades of astrocytic tumors. Our data showed that high-grade glioblastomas express higher amount of S100A4/Mts1 than low-grade astrocytic tumors.
PMID: 17223348 [PubMed - as supplied by publisher]
请高手斧正,谢谢!
BMC Genomics. 2007 Jan 12;8(1):16
Comprehensive genetic and epigenetic analysis of sporadic meningioma for macro-mutations on 22q and micro-mutations within the NF2 locus.散发脑膜瘤22q巨突变和NF2基因座内微突变的遗传和后天因素综合分析
Hansson CM, Buckley PG, Grigelioniene G, Piotrowski A, Hellstrom AR, Mantripragada KK, Jarbo C, Mathiesen T, Dumanski JP.
BACKGROUND: Meningiomas are the most common intracranial neoplasias, representing a clinically and histopathologically heterogeneous group of tumors. The neurofibromatosis type 2 (NF2) tumor suppressor is the only gene known to be frequently involved in early development of meningiomas. 背景：脑膜瘤是最常见的颅内原发肿瘤，是在临床上和组织病理学上不同的一组肿瘤。多发性神经纤维瘤2型(NF2) 肿瘤抑制基因是已知唯一的经常出现在脑膜瘤早期发展过程中基因。
The objective of this study was to identify genetic and/or epigenetic factors contributing to the development of these tumors. 本研究目的是鉴别遗传因素和/或后天因素在促进肿瘤形成过程中的作用。
A large set of sporadic meningiomas were analyzed for presence of 22q macro-mutations using array-CGH in order to identify tumors carrying gene dosage aberrations not encompassing NF2. The NF2 locus was also comprehensively studied for point mutations within coding and conserved non-coding sequences. Furthermore, CpG methylation within the NF2 promoter region was thoroughly analyzed.应用绒(毛)膜促性腺激素（CGH）芯片分析一组散发脑膜瘤中22q巨突变的存在度，从而鉴别NF2不是基因剂量失常的肿瘤，同时综合研究NF2 基因座在编码和保守非编码序列中的(基因)点突变。此外，充分分析了NF2启动子区域内的CpG甲基化。
RESULTS: Monosomy 22 was the predominant finding, detected in 47% of meningiomas. Thirteen percent of the tumors contained interstitial/terminal deletions and gains, present singly or in combinations. We defined at least two minimal overlapping regions outside the NF2 locus that are small enough (~550 kb and ~250 kb) to allow analysis of a limited number of candidate genes. Biallelic inactivation of the NF2 gene was detected in 36% of meningiomas. Among the monosomy 22 cases, no additional NF2 mutations could be identified in 35% (17 out of 49) of tumors. Furthermore, the majority of tumors (9 out of 12) with interstitial/terminal deletions did not have any detectable NF2 mutations. Methylation within the NF2 promoter region was only identified at a single CpG site in one tumor sample. CONCLUSIONS: We confirmed previous findings of pronounced differences in mutation frequency between different histopathological subtypes. There is a higher frequency of biallelic NF2 inactivation in fibroblastic (52%) compared to meningothelial (18%) tumors. The presence of macro-mutations on 22q also shows marked differences between fibroblastic (86%) and meningothelial (39%) subtypes. Thus, inactivation of NF2, often combined with the presence of macro-mutation on 22q, is likely not as important for the development of the meningothelial subtype, as opposed to the fibroblastic form. 结果：突出的发现是单体22可在47%的脑膜瘤中检测出来。13%的肿瘤包含染色体中间/终端单独或联合地缺失和获得。我们确定了NF2基因座外至少有两个微小的重叠区域，该区域足够小(~550 kb 和~250 kb)因而可进行候补基因有限数量分析。NF2双等位基因钝化可在36%的脑膜瘤中检测到。在单体22病例中，35%的肿瘤中（49例中有17例）没有检测到多余的NF2突变。而且，带有中间和终端缺失的绝大多数肿瘤没有检测到NF2突变。NF2启动子区域甲基化只在一例肿瘤样品中单个CpG位点中检测到。结论：我们证实了原先发现的结论，即不同组织病理学亚型之间突变频率存在显著的差异。成纤维细胞瘤（52%）与脑膜瘤（18%）比较有更高的NF 2双等位基因钝化频率。22q巨突变的存在度在成纤维细胞瘤（86%）和脑膜瘤亚型（ 39%）之间也有显著的差异。因此，与成纤维细胞瘤形成不同，NF2的钝化和经常伴随的22q巨突变 ，在脑膜瘤亚型的发展中或许并非同等重要。
Analysis of 40 CpG sites distributed within 750 bp of the promoter region suggests that NF2 promoter methylation does not play a major role in meningioma development.通过分析分布在启动子区域750 硷基中40 CpG部位表明NF2启动子甲基化在脑膜瘤发展中不占主要作用。
PMID: 17222329 [PubMed - as supplied by publisher]
Acta Neurochir (Wien). 2006 Dec 21;
Olfactory groove meningiomas: functional outcome in a series treated microsurgically.
Bassiouni H, Asgari S, Stolke D.
Background. A systematic investigation of long-term follow-up results after microsurgical treatment of patients harbouring an olfactory groove meningioma, particularly with regard to postoperative olfactory and mental function, has rarely been performed. We reassessed a series of patients treated microsurgically for an olfactory groove meningioma in regard to clinical presentation, surgical approaches and long-term functional outcome.
Method. Clinical, radiological and surgical data in a consecutive series of 56 patients suffering from olfactory groove meningioma were retrospectively reviewed.
Findings. Presenting symptoms of the 41 women and 15 men (mean age 51 years) were mental changes in 39.3%, visual impairment in 16.1% and anosmia in 14.3% of the patients. Preoperative neurological examination revealed deficits in olfaction in 71.7%, mental disturbances in 55.4% and reduced vision in 21.4% of the cases. The tumour was resected via a bifrontal craniotomy in 36, a pterional route in 13, a unilateral frontal approach in 4 and via a supraorbital approach in 3 patients. Extent of tumour resection according to Simpson's classification system was grade I in 42.9% and grade II in 57.1% of the cases. After a mean follow-up period of 5.6 years (range 1-13 years) by clinical examination and magnetic resonance imaging (MRI), 86.8% of the patients resumed normal life activity. Olfaction was preserved in 24.4% of patients in whom pre- and postoperative data were available. Mental and visual disturbances improved in 88 and 83.3% of cases, respectively. Five recurrences (8.9%) were observed and had to be reoperated.
Conclusions. Frontal approaches allowed better resection of tumours with gross infiltration of the anterior cranial base, tumours extending into the ethmoids or nasal cavity and in cases with deep olfactory grooves. Preservation of olfaction should be attempted in patients with normal or reduced smelling preoperatively
嗅沟脑膜瘤：嗅沟脑膜瘤微创术后患者的随访分析
Bassiouni H, Asgari S, Stolke D.
背景：一个关于嗅沟脑膜瘤微创术后患者的系统长期的随访分析 关于独立观测嗅觉精神状况的试验并不多.我们通过其临床表现 入路 远期的功能状况 进行评估
方法 回顾性的对嗅沟脑膜瘤微创术后患者进行 包括临床 影像 外科医生的评定进行综合再评估
结果：41女15男性患者的主述中 性格改变是39.3% 视觉缺损是16.1% 嗅觉丧失14.3%
术前检查性格改变是55.4% 视觉缺损是21.4% 嗅觉丧失71.7%, 纵裂入路36例 翼点13 单额侧4 框上1例。 用Simpson's 分级法 一级42.9%二级57.1%
.在平均5。6（平均1-13）年的回访中
通过临床症状和mri的检查86.8%的患者恢复正常生活术前术后均保留嗅觉的为24.4% 分别精神和视力障碍改善的共为88例 即83.3%。5例复发(8.9%)再次手术
结论：额部入路能更好的前颅窝的肉眼可及的肿瘤 及那些侵犯筛骨 鼻腔 和深入筛沟,嗅沟的肿瘤 术前嗅觉正常和稍减退的病人保留可能性更大
