SCI分析工具在干细胞移植研究中的应用

背景：对干细胞移植研究的文献计量分析报告目前较少。 目的：通过干细胞移植研究文献的计量分析总结概括目前研究的状况和前沿。 方法：以美国科学情报研究所(ISI)开发的Web of Science网络数据库为数据源基础,对2001-01/2010-12 SCI收录的干细胞移植研究论文的情况,从论文的发表时间分布、国家地区分布、机构分布、期刊分布和被引频次分布等方面进行统计与分析。 结果与结论：2001-01/2010-12共有干细胞移植研究文献22 437篇,文献呈年度递增。中国2010年在SCI收录期刊上发表的论文数(406篇)少于美国2001年发表的论文数(486篇)。以美国发表论文最多,有11家核心研究机构和13种核心期刊和12篇经典文献。得出了干细胞移植研究这一领域的研究动态和发展趋势,为中国深入研究干细胞移植提供可供借鉴的参考建议。     

RSF-1在胶质瘤组织中的表达及其与病人预后的关系

目的 探讨染色质重塑因子1（RSF-1）在人脑胶质瘤中的表达及其与病人预后的关系。方法 采用免疫组织化学染色法和免疫印迹法检测2010年1月~2013年4月手术切除的121例胶质瘤组织和2017年6月~2018年9月颅脑损伤内减压术中切取的50例正常脑组织RSF-1的表达水平。胶质瘤病人随访时间截止至2019年4月。多因素Cox比例回归风险模型分析影响胶质瘤病人生存预后的因素。结果 免疫组化染色结果显示胶质瘤组织RSF-1高表达率（66.12%,80/121）明显高于正常脑组织（0%;P<0.001）。免疫印迹法检测结果显示,胶质瘤组织RSF-1蛋白表达水平明显高于正常脑组织（P<0.05）,而且,随胶质瘤级别增高,RSF-1蛋白表达水平明显增高（P<0.05）。多因素Cox比例回归风险模型分析结果显示,术前KPS评分<80分、WHO分级为Ⅲ~Ⅳ级、术后未化疗和RSF-1高表达是胶质瘤病人总生存期和无进展生存期缩短的独立影响因素（P<0.05）。RSF-1高表达病人总体生存期[中位数（M）:13个月;四分位间距（IQR）:11~26个月]较低表达者（M:26个月;IQR:20~36个月）明显缩短（P<0.05）。 RSF-1高表达病人无进展生存期（M:11个月;IQR:7~23个月）较低表达者（M:21个月;IQR:16~28个月）明显缩短（P<0.05）。结论 RSF-1高表达可能预示着胶质瘤病人的不良生存预后     

人脑胶质瘤lncRNA PIK3CD-AS2表达及临床意义

目的 探讨lncRNA PIK3CD-AS2 在人脑胶质瘤中的表达及临床意义。方法 计算机检索TCGA和GTEx数据库关于PIK3CD-AS2在胶质瘤和正常脑组织中表达的RNA数据，应用生物信息学方法分析PIK3CD-AS2表达与胶质瘤病人预后的关系。收集2010年9月至2015年6月我院手术切除的胶质瘤组织127例以及2018年1月至2019年10月颅脑损伤内减压术中切除的正常脑组织38例，qRT-PCR检测PIK3CD-AS2表达量。127例胶质瘤病人随访至2020年6月或病人死亡，分析PIK3CD-AS2表达与胶质瘤病人预后的关系。结果 生信分析和临床病例分析结果显示，与正常脑组织相比，胶质瘤组织PIK3CD-AS2表达显著升高（P<0.05）；胶质瘤WHO分级越高，PIK3CD-AS2的表达水平也越高（P<0.05）；PIK3CD-AS2高表达是胶质瘤病人预后不佳的独立预测因子（P<0.05），PIK3CD-AS2高表达病人总生存期显著低于PIK3CD-AS2低表达病人（P<0.05）。结论 PIK3CD-AS2在胶质瘤中高表达，可作为胶质瘤病人的预后标志物。     

Divergent Findings in Brain Reorganization After Spinal Cord Injury: A Review

Spinal cord injury (SCI) leads to a general lack of sensory and motor functions below the level of injury and may promote deafferentation‐induced brain reorganization. Functional magnetic resonance imaging (fMRI) has been established as an essential tool in neuroscience research and can precisely map the spatiotemporal distribution of brain activity. Task‐based fMRI experiments associated with the tongue, upper limbs, or lower limbs have been used as the primary paradigms to study brain reorganization following SCI. A review of the current literature on the subject shows one common trait: while most articles agree that brain networks are usually preserved after SCI, and that is not the case as some articles describe possible alterations in brain activation after the lesion. There is no consensus if those alterations indeed occur. In articles that show alterations, there is no agreement if they are transient or permanent. Besides, there is no consensus on which areas are most prone to activation changes, or on the intensity and direction (increase vs. decrease) of those possible changes. In this article, we present a critical review of the literature and trace possible reasons for those contradictory findings on brain reorganization following SCI. fMRI studies based on the ankle dorsiflexion, upper‐limb, and tongue paradigms are used as case studies for the analyses.     

Contusive spinal cord injury up regulates mu-opioid receptor (mor) gene expression in the brain and down regulates its expression in the spinal cord: possible implications in spinal cord injury research

Abstract

Traumatic spinal cord injury (SCI) is one of the dreaded neurological conditions and finding a cure for it has been a hot area of research. Naloxone – a mu-opiate receptor (mor) antagonist was considered for SCI treatment based on its positive effects under shock conditions. In contrary to animal studies based reports about the potential benefits of naloxone in treating SCI, a large scale clinical trial [National Acute Spinal Cord Injury Study II (NASCIS II)] conducted in USA failed to witness any effectiveness. The inconsistency noticed was intriguing. Therefore, the objective of the present study was to re-examine the role of naloxone in treating SCI using a highly standardised Multicenter Animal Spinal Cord Injury Study (MASCIS) animal model of contusive SCI. Results indicated that naloxone produced negligible and insignificant neuroprotection. In an attempt to understand the cause for the failure, it was found that mu-opioid receptor (mor) gene expression was upregulated in the brain but was down regulated in the spinal cord after contusive SCI. Given that the beneficial effects of naloxone are through its action on the mor, the results indicate that unlike the brain, spinal cord might not be bracing to utilise the opiate system in the repair process. This could possibly explain the failure of naloxone treatment in NASCIS II. To conclude, opiate antagonists like naloxone may be neuroprotective for treating traumatic brain injuries, but not for traumatic/contusive spinal cord injuries.     

The top cited articles on glioma stem cells in Web of Science

BACKGROUND: Glioma is the most common intracranial tumor and has a poor patient prognosis. The presence of brain tumor stem cells was gradually being understood and recognized, which might be beneficial for the treatment of glioma. OBJECTIVE: To use bibliometric indexes to track study focuses on glioma stem cell, and to investigate the relationships among geographic origin, impact factors, and highly cited articles indexed in Web of Science. METHODS: A list of citation classics for glioma stem cells was generated by searching the database of Web of Science-Expanded using the terms "glioma stem cell" or "glioma, stem cell’" or "brain tumor stem cell". The top 63 cited research articles which were cited more than 100 times were retrieved by reading the abstract or full text if needed. Each eligible article was reviewed for basic information on subject categories, country of origin, journals, authors, and source of journals. Inclusive criteria: (1) articles in the field of glioma stem cells which was cited more than 100 times; (2) fundamental research on humans or animals, clinical trials and case reports; (3) research article; (4) year of publication: 1899-2012; and (5) citation database: Science Citation Index-Expanded. Exclusive criteria: (1) articles needing to be manually searched or accessed only by telephone; (2) unpublished articles; and (3) reviews, conference proceedings, as well as corrected papers. RESULTS: Of 2 040 articles published, the 63 top-cited articles were published between 1992 and 2010. The number of citations ranged from 100 to 1 754, with a mean of 280 citations per article. These citation classics came from nineteen countries, of which 46 articles came from the United States. Duke University and University of California, San Francisco led the list of classics with seven papers each. The 63 top-cited articles were published in 28 journals, predominantly Cancer Research and Cancer Cell, followed by Cell Stem Cell and Nature. CONCLUSION: Our bibliometric analysis provides a historical perspective on the progress of glioma stem cell research. Articles originating from outstanding institutions of the United States and published in high-impact journals are most likely to be cited.     

Disruption of transient receptor potential canonical channel 1 causes incomplete cytokinesis and slows the growth of human malignant gliomas

Despite decades of research, primary brain tumors, gliomas, lack effective treatment options and present a huge clinical challenge. Particularly, the most malignant subtype, Glioblastoma multiforme, proliferates extensively and cells often undergo incomplete cell divisions, resulting in multinucleated cells. We now present evidence that multinucleated glioma cells result from the functional loss of transient receptor potential canonical 1 (TRPC1) channels, plasma membrane proteins involved in agonist‐induced calcium entry and reloading of intracellular Ca²⁺ stores. Pharmacological inhibition or shRNA mediated suppression of TRPC1 causes loss of functional channels and store‐operated calcium entry in D54MG glioma cells. This is associated with reduced cell proliferation and, frequently, with incomplete cell division. The resulting multinucleated cells are reminiscent of those found in patient biopsies. In a flank tumor model, tumor size was significantly decreased when TRPC1 expression was disrupted using a doxycycline inducible shRNA knockdown approach. These results suggest that TRPC1 channels play an important role in glioma cell division most likely by regulating calcium signaling during cytokinesis. © 2010 Wiley‐Liss, Inc.     

The ketogenic diet for the treatment of glioma: insights from genetic profiling

Seizures, particularly first onset seizures in adults, are a diagnostic hallmark of brain tumors (Giglio and Villano, 2010). Unfortunately, malignant brain tumors are almost uniformly fatal due, in part, to the limitations of available therapies. Improvement in the survival of brain cancer patients requires the design of new therapeutic modalities including those that enhance currently available therapies. One potential strategy is to exploit differences in metabolic regulation between normal cells and tumor cells through dietary approaches. Previous studies have shown that a high-fat, low-carbohydrate ketogenic diet (KD) extends survival in animal models of glioma; however, the mechanism for this effect is not entirely known. We examined the effects of an experimental KD on a mouse model of glioma, and compared patterns of gene expression in tumors versus contralateral non-tumor containing brain from animals fed either a KD or a standard diet. We found that the KD reduced reactive oxygen species (ROS) production in tumor cells. Gene expression profiling demonstrated that the KD induces an overall reversion to expression patterns seen in non-tumor specimens, and a number of genes involved in modulating ROS levels and oxidative stress were altered in tumor cells. In addition, there was reduced expression of genes involved in signal transduction from growth factors known to be involved in glioma growth. These results suggest that the anti-tumor effect of the KD is multifactorial, and elucidation of genes whose expression is altered will help identify mechanisms through which ketones inhibit tumor growth, reduce seizure activity and provide neuroprotection.     

Brain gliomas,hydrocephalus and idiopathic aqueduct stenosis in children with neurofibromatosis type 1

PurposeTo evaluate the incidence and clinical importance of brain gliomas – optic pathway gliomas (OPGs) and especially gliomas outside the optic pathway (GOOP) for children with neurofibromatosis type 1 (NF1), additionally, to assess the causes of obstructive hydrocephalus in NF1 children with an emphasis on cases caused by idiopathic aqueduct stenosis.Subjects and methodsWe analysed data from 285 NF1 children followed up on our department from 1990 to 2010 by the same examination battery.ResultsWe have found OPGs in 77/285 (27%) children and GOOPs in 29/285 (10,2%) of NF1 children, of who 19 had OPG and GOOP together, so the total number of brain glioma was 87/285 (30,5%). GOOPs were significantly more often treated than OPGs (p > 0.01). OPGs contain clinically important subgroup of 14/285 (4.9%) spreading to hypothalamus. Spontaneous regression was documented in 4/285 (1.4%) gliomas and the same number of NF1 children died due to gliomas.Obstructive hydrocephalus was found in 22/285 (7.7%) patients and 14/22 cases were due to glioma. Idiopathic aqueduct stenosis caused hydrocephalus in 6/22 cases and was found in 2.1% of NF1 children. Two had other cause.ConclusionsThe total brain glioma number (OPGs and only GOOPs together) better reflected the overall brain tumour risk for NF1 children. However, GOOPs occur less frequently than OPGs, they are more clinically relevant. The obstructive hydrocephalus was severe and featuring frequent complication, especially those with GOOP. Idiopathic aqueduct stenosis shows an unpredictable cause of hydrocephalus in comparison with glioma and is another reason for careful neurologic follow up.     

Experiment and observation on invasion of brain glioma in vivo.

Research on invasion and metastasis of glioma in vivo was performed by implanting C6 glioma cells transfected with enhanced green fluorescent protein (EGFP) gene into the brain of SD rats. Firstly, C6 glioma cells were transfected with a plasmid vector (pEGFP-N3) containing the EGFP gene. Stable EGFP-expressing clones were isolated and examination for these cells by flow cytometry and electron microscope was done. Secondly, EGFP-expressing cells were stereotactically injected into the brain parenchyma of SD rats to establish xenotransplanted tumor. Four weeks later rats were killed and continuous brain sections were examined using fluorescence microscopy after adjacent sections were examined by immunohistochemistry or routine hematoxylin and eosin staining for the visualization and detection of tumor cell invasion. Xenotransplanted tumor was primarily cultured to determine the storage of EGFP gene in vivo. The results showed that EGFP-transfected C6 glioma cells maintained stable high-level EGFP expression in the central nervous system during their growth in vivo. EGFP fluorescence clearly demarcated the primary tumor margin and readily allowed for the visualization of distant micrometastasis and invasion on the single-cell level. Small locally invasive foci, including those immediately adjacent to the leading invasive edge of the tumor, were virtually undetectable by routine hematoxylin and eosin staining and immunohistochemistry. These results suggested that EGFP-transfected C6 cells can be visualized by fluorescence microscopy after intracranial implantation. This model is an excellent experimental animal model in research on invasion and metastasis of brain glioma in vivo.     

脾酪氨酸激酶在不同等级胶质瘤中的表达及其与周期素1水平的相关性

目的 探讨人脑胶质瘤中脾酪氨酸激酶(Syk)的表达及其与周期索1(CyclinDl)水平的相关性.方法 收集贵州航天医院神经外科自2005年1月至2010年1月间手术切除并经病理证实的脑胶质瘤标本46例,其中Ⅰ级13例,Ⅱ级9例,Ⅲ级5例,Ⅳ级胶质母细胞瘤19例.另取5例因脑创伤行内减压术患者的正常脑组织标本作为对照,RT-PCR检测脑组织标本Syk mRNA、CyclinD1 mRNA的表达并分析二者的相关性.结果 与正常脑组织比较,Ⅰ、Ⅱ、Ⅲ、Ⅳ级脑胶质细胞瘤标本Syk mRNA表达较低,CyclinDl mRNA表达较高,差异有统计学意义(P＜0.05),而且胶质瘤的病理级别越高,Syk mRNA的表达越低,CyclinDl mRNA表达较高,差异均有统计学意义(P＜0.05);胶质瘤中Syk与CyclinDl的表达呈负相关关系(r=-0.832,P=0.000).结论 Syk在脑胶质瘤中表达较低或缺失,提示其可能具有抑癌基因功能,其机制可能与下调胶质瘤中CyclinD1的表达有关.     

黑色素瘤抗原-1,-3基因在脑胶质瘤中的表达及意义

目的 探讨肿瘤特异性黑色素瘤抗原（MAGE）-1、-3基因作为胶质瘤的免疫检测和治疗、基因治疗分子标志物的可行性。方法 采用逆转录-聚合酶链反应（RT-PCR）检测52例胶质瘤、6例正常脑组织、5例脑脓肿、10例脑膜瘤组移标本中MAGE-1、MAGE-3mRNA的表达。结果 脑胶质瘤中MAGE-1、MAGE-3mRNA阳性表达率分别为64．5％、55．8％，MAGE-1及MAGE-3mRNA同时表达22例（42.3％）。正常脑组织、脑脓肿和脑膜瘤均不表达MAGE-1和MAGE-3mRNA。在胶质瘤组织中MAGE-1、MAGE-3mRNA的表达均与病理级别和病人生存时间有关（P＜0．05），而与性别、年龄、肿瘤部位及肿瘤直径无关（P＞0．05）MAGE-1的表达与MAGE-3的表达有关（P＜0．05）。结论 基于MAGE-1和MAGE-3在胶质瘤中的高表达率，可利用这两种蛋白作为靶分子进行免疫治疗，同时也可作为一种临床有用的随访指标。     

Preserved somatosensory conduction in complete spinal cord injury: Discomplete SCI

ObjectiveSpinal cord injury (SCI) disrupts the communication between brain and body parts innervated from below-injury spinal segments, but rarely results in complete anatomical transection of the spinal cord. The aim of this study was to investigate residual somatosensory conduction in clinically complete SCI, to corroborate the concept of sensory discomplete SCI.MethodsWe used fMRI with a somatosensory protocol in which blinded and randomized tactile and nociceptive stimulation was applied on both legs (below-injury level) and one arm (above-injury level) in eleven participants with chronic complete SCI. The experimental design accounts for possible confounding mechanical (e.g. vibration) and cortico-cortical top-down mechanisms (e.g. attention/expectation).ResultsSomatosensory stimulation on below-level insensate body regions activated the somatotopically corresponding part of the contralateral primary somatosensory cortex in six out of eleven participants.ConclusionsOur results represent afferent-driven cortical activation through preserved somatosensory connections to the brain in a subgroup of participants with clinically complete SCI, i.e. sensory discomplete SCI.SignificanceIdentifying patients with residual somatosensory connections might open the door for new rehabilitative and restorative strategies as well as inform research on SCI-related conditions such as neuropathic pain and spasticity.     

A potential entanglement between the spinal cord and hippocampus: Theta rhythm correlates with neurogenesis deficiency following spinal cord injury in male rats

Cognitive deficits due to spinal cord injury (SCI) have been elucidated in both animals and humans with SCI. Such disorders may cause concomitant oscillatory changes in regions of the brain involving in cognition; a subject that has not been directed mechanistically. One of the crucial oscillations, having a prominent role in cognition, particularly spatial memory, is hippocampal theta rhythm. Our research revealed that SCI could induce changes not only in the neurogenesis and apoptosis rate of the hippocampus but also in theta power as well as receptors involving in the generation of this rhythm. Herein we used 24 male Wistar rats (Sham/SCI = 12) and examined the effect of spinal cord contusion on hippocampal theta rhythm, spatial memory, and neurodegeneration. We proved that SCI eliminates hippocampus-dependent theta power through spatial working memory, and correlates significantly with neurodegeneration and expression of receptors (NMDA, GABAA, Muscarinic1/M1), which are in turn essential in generation of theta rhythm. The immunohistochemistry analysis also demonstrated a significant decrease in DCX+ and BrdU+ cells; however, according to TUNEL assay, apoptosis is significantly higher in SCI-induced animals. The western blotting analysis further showed a significant reduction of the abovementioned receptors in the hippocampus. We also verified that SCI impairs the spatial memory, proved by poor performance in the Y-maze task. As well as, based on the local field potential recordings analysis, SCI decreases the power of theta rhythm. Eventually, this study demonstrated that chronic brain neurodegeneration occurs after SCI accompanied by theta rhythm and cognitive deficiency.     

CDCA7L在人脑胶质瘤组织中的表达及意义

目的 探讨细胞分裂周期相关7样蛋白（CDCA7L）在胶质瘤组织中的表达及其与病人预后的关系。方法 免疫组织化学染色法检测2012年1月至2013年5月手术切除的112例胶质瘤组织和2018年1~12月颅脑损伤内减压术中切除的45例正常脑组织中CDCA7L的表达水平,根据染色情况将胶质瘤病人分为高表达组和低表达组。胶质瘤病人随访截止2019年6月,记录总生存期（OS）和无进展生存期（PFS）。结果 胶质瘤组织CDCA7L高表达率（66.96%,75/112）明显高于正常脑组织（17.78%,8/45;P<0.05）。高级别胶质瘤组织CDCA7L高表达率（79.41%,54/68）明显高于低级别胶质瘤（47.73%,21/44;P<0.05）。多因素Cox比例风险回归模型分析结果显示,CDCA7L高表达是胶质瘤病人OS和PFS较短的独立影响因素（P<0.05）。生存曲线分析显示,高表达组中位OS（21个月,四分位区间16~41个月）和中位PFS（18个月,四分位区间13~38个月）均明显低于低表达组[分别为60个月（48~65个月）和45个月（41~52个月）;P<0.05]。结论 胶质瘤组织CDCA7L呈高表达,而且与胶质瘤不良生存预后和肿瘤进展有关。     

ERH在人脑胶质瘤中的表达及其与病人预后的关系

目的 探讨未成熟同源蛋白增强子（ERH）在人脑胶质瘤组织中的表达及其与病人生存预后的关系。方法 免疫组织化学染色法检测2012年5月至2017年5月手术切除的121例胶质瘤组织和2012年5月~2017年5月颅脑损伤内减压术中切除的40例正常脑组织中ERH的表达水平。根据染色结果将胶质瘤分为高表达组和低表达组。采用多因素Cox比例回归风险模型分析胶质瘤病人总生存期（OS）和无进展生存期（PFS）的影响因素。结果 正常脑组织ERH高表达率（15.00%,6/40）明显低于胶质瘤组织（61.16%,74/121;P<0.05）。多因素Cox比例回归风险模型分析结果显示,WHO分级Ⅲ~Ⅳ级和ERH高表达是胶质瘤病人OS和PFS较短的独立影响因素（P<0.05）。生存曲线分析显示低表达组OS和PFS均明显高于高表达组（P<0.05）。结论 ERH在胶质瘤组织中高表达,并且与病人不良生存预后和肿瘤进展有关。     

Interleukin-2 and lymphokine activated killer (LAK) cells in the treatment of malignant glioma: clinical and experimental studies

The phenomenon of glioma killing by lymphokine activated killer cells (LAK) was studied. We demonstrate that LAK cells generated by culturing the lymphokine interleukin-2 (IL-2) with peripheral blood lymphocytes from brain tumour patients destroys autologous glioma. The rat 9L glioma model was used to show that LAK killing was tumour-selective as glioma but not syngeneic normal brain tissue was destroyed. The susceptibility of both human and 9L rat glioma to LAK cell killing was markedly diminished by pretreating glioma cells with trypsin or chymotrypsin, but was unaffected by pretreatment with neuraminidase, glycosidases, sodium periodate or hydrocortisone. These results suggest that the cell surface determinant on glioma cells responsible for its tumour selective lysis by LAK is a protein sensitive to trypsin and chymotrypsin.

The tumour-selective killing of glioma by LAK in vitro prompted the initiation of a Phase I study in which ten patients with malignant glioma have been treated with direct intracerebral injection of IL-2 or LAK without evidence of systemic or brain toxicity.     

Cognitive dysfunction in patients with amyotrophic lateral sclerosis is associated with spherical or crescent-shaped ubiquitinated intraneuronal inclusions in the parahippocampal gyrus and amygdala, but not in the neostriatum

Skeins or skein-like inclusions, one of the two types of ubiquitinated intraneuronal inclusions in amyotrophic lateral sclerosis (ALS), in the neostriatum are not specific to the disease, but it has not yet been determined whether the other, spherical or crescent-shaped inclusions (SCI) are pathognomonic. To clarify this and also to investigate whether the distribution of SCI in particular brain regions is associated with clinical parameters, we examined the occurrence of SCI in the brains of 24 patients with ALS and 94 controls. SCI in the neostriatum were specifically detected in 54% of the ALS cases, but not in any of the controls. No apparent phenotypic denominator, such as disease duration or the occurrence of dementia, correlated to the distribution of SCI in the neostriatum in ALS cases. On the other hand, the occurrence of SCI in both the second and third layers of the parahippocampal gyrus and amygdala was significantly correlated to the presence of dementia in ALS cases. SCI were distributed in association with each other among the parahippocampal gyrus, dentate gyrus of the hippocampus and amygdala, but not between the spinal anterior horn and any non-motor-associated brain regions. These findings suggest that these particular brain regions might be significantly involved in the neurodegenerative process associated with ALS. The relationship of SCI to either ALS pathogenesis or cognitive dysfunction depends on the brain regions in which they are distributed, and this indicates that the neurodegenerative processes in ALS proceed differentially in particular motor-associated and nonmotor-associated brain regions.     

无症状脑梗塞MRI、MRA及TCD的临床对比研究

目的 探讨无症状脑梗塞(SCI)的临床特征与头颅MRI、MRA、TCD改变。方法 对50例病人进行临床分析，并进行头颅MRI、MRA和TCD检测，加以对比分析。结果 MRI检出梗塞灶的病人行MRA检查，异常检出率为93.02％，TCD异常检出率为94.87％。结论 MRI是确诊SCI重要条件之一，并能清晰、准确显示小脑、脑干梗塞；MRA能显示病变血管；TCD对SCI有早期辅助诊断价值，对治诊及预后有很好指导作用。     

立体定向技术建立大鼠脑胶质瘤激光间质热疗模型

目的 利用立体定向技术接种SD大鼠C6脑胶质瘤,并建立脑胶质瘤激光间质热疗(LITT)模型.方法 采用立体定向技术,将体外培养并调制的C6胶质瘤细胞悬液20μl(浓度1×10~(11)/L)接种于SD大鼠右侧尾状核区.分时段MRI检查;做组织病理学和Ⅷ因子相关抗原(FⅧR),胶质纤维酸性蛋白(GFAP)和S-100蛋白免疫组化检查.根据MRI扫描监测,校正肿瘤定位,按2～10 W不同功率和热疗时间分组,插入半导体激光光纤进行间质热疗,同时使用ThermaCAM S65型红外热像仪测量肿瘤的中心靶点皮层温度和(或)热电偶仪间质测量靶区周边的深部温度.结果 优化的立体定向接种技术使本组大鼠脑胶质瘤动物模型具有颅内生长稳定,成瘤率高,未见颅外转移病灶,实验周期短,可重复性好,可插入热疗光纤热疗,组织学上接近人类特征.LITT各组靶区温度高于假手术组(P<0.05);在同一治疗组内中心靶点皮层温度和靶区周边的深部温度之间有近似性,差异无统计学意义(P>0.05).结论 利用立体定向技术可成功建立SD大鼠脑尾状核C6胶质瘤模型,其肿瘤MRI影像及病理特征与人脑胶质瘤相似.红外热像测温技术在大鼠实验性LITT研究中的应用具有可行性,可联合热电偶深部测温技术应用于脑肿瘤LITT治疗.