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Granulocytic sarcoma (GS) is a localized tumour of immature granulocytes that is usually associated with myelogenous leukaemia. We report an unusual case of mastoid GS with meningeal extension but no bone marrow involvement on presentation. Histological examination of the surgical specimen and the characteristic cerebrospinal fluid (CSF) cytology showing cytoplasmic granulations and Auer bodies led to the diagnosis of GS. Positive cytochemical staining of the immature CSF cells for naphtol-ASD chloroacetate esterase and myeloperoxidase confirmed their myeloid origin. Immunophenotyping did not reveal common acute lymphoblastic leukaemia antigen, cytokeratin, T or B-cell antigens. The patient underwent surgical resection of the localized tumour, followed by radiation therapy, intrathecal and systemic chemotherapy, as if he had acute myelogenous leukaemia (AML). He did not develop AML in the 21 months after the tumour resection. This case emphasizes the value of CSF cytological examination of tumour cells and the use of an immumocytochemical marker for differentiating GS from malignant lymphoma. 相似文献
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Jobst Sievers Christina von Knebel Doeberitz Fritz-Wilhelm Pehlemann Martin Berry 《Anatomy and embryology》1986,175(1):91-100
Summary We have investigated the influence of meningeal cells on the development of the cerebellum by destroying these cells with 6-hydroxydopamine in hamsters of different ages. The ensuing foliation and lamination disruption in the cerebellar vermis is attributed to a disintegration of the cerebellar surface and a disorganization of the glial scaf-fold of the cerebellar cortex due to a loss of meningeal-glial interaction in stabilizing the extracellular matrix at the glia limitans superficialis (v. Knebel Doeberitz et al. 1986, Neuroscience 17:409–426). The severity of these cerebellar defects is correlated with the ontogenetic stage at which meningeal cells are destroyed, being greatest after treatment at postnatal day 1 and decreasing thereafter until day 5 and beyond, when no abnormalities occur, although all meningeal cells are destroyed throughout. The absence of cerebellar defects after destruction of meningeal cells at day 5 or later is associated firstly with the end of the period of branching morphogenesis of the cerebellum when all folial primordia are established, and, secondly, with the maturation of the glia limitans superficialis. These findings indicate that meningeal cells stabilize the cerebellar surface and glial scaffold over a critical period that ends, when the pattern of cerebellar foliation is established, and when the glia limitans superficialis has reached a mature state. Beyond this stage glial end-feet alone are sufficient to maintain the epithelial integrity of the cerebellum. 相似文献
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Jian Sun Chengjun Wang Qingming Shu Jie Liu Gengsheng Mao 《International journal of clinical and experimental pathology》2015,8(9):11698-11703
Meningeal melanocytoma is a kind of extremely rare pigmented tumor of the central nervous system, which often occurs in the groove around the base of the brain and spinal pia mater. Age of onset is 40 to 50 years old, mostly presenting a benign course of disease and the prognosis is good. Case reports of partial invasion or metastasis from lesions are even rarer. This report described a case of 56-year-old meningeal melanoma patient with partial skull and muscle invasion at the lantooccipital transition zone. Intraoperative histological examination showed moderate malignancy and Ki-67 index was 10%. 相似文献
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Thomas Iype Ayyappan Kunjukrishna Pillai Ajith Cherian Zinia T. Nujum Chithra Pushpa Dalus Dae Vijayakumar Krishnapillai 《Annals of Indian Academy of Neurology》2014,17(3):281-286
Background:
Revised National Tuberculosis Control Programme (RNTCP) of Government of India provides intermittent thrice-a-week directly observed treatment short course (RNTCP regimen).Objective:
Assessments of all-cause mortality and nine-month morbidity outcomes of patients with tuberculous meningitis (TBM) on RNTCP regimen.Materials and Methods:
We prospectively followed up patients registered with RNTCP center, with a diagnosis of TBM from January 1st, 2010 to December 31st, 2011. Morbidity was assessed using modified Rankin Scale (mRS).Results:
We had 43 patients with median duration for follow-up of 396 days and that of survivors of 425 days. Two patients defaulted. Fourteen patients (32.5%) had mRS score of 4 to 6 and 29 had mRS of 0 to 3 after 9-month treatment. Severe disability was not related to any factor on logistic regression. Severe disability was seen in one patient (6.66%) among the 15 patients with stage 1, nine (37.5%) out of 24 patients with stage 2 and three (75%) out of 4 patients with stage 3 disease. Eight patients died (18.6%) of whom 4 died during the intensive phase and 4 during the continuation phase of RNTCP regimen. Mortality was independently related to treatment failure with adjusted Hazard ratio of 8.29 (CI: 1.38-49.78) (P = 0.02). One patient (6.66%) died out of the 15 patients with stage 1 disease, 5 (20.8%) out of 24 patients with stage 2 disease and 2 (50%) out of the 4 with stage 3 disease.Discussion and Conclusion:
RNTCP regimen was associated with good compliance, comparable mortality and morbidity. 相似文献9.
MR增强后FLAIR序列对脑膜病变诊断价值 总被引:5,自引:3,他引:5
目的分析增强后液体衰减反转恢复(FLAIR)序列对脑膜病变的显示。方法脑膜病变26例,除MR检查常规平扫和增强外,在增强后加扫FLAIR,图像由3位有经验的放射科医师评估。结果增强后FLAIR对邻近脑实质、神经和脑脊液的强化较敏感,而且可克服常规T1WI增强血管强化易与病变混淆的缺点。结论增强后FLAIR是增强后T1WI的有效补充,联合使用能提高脑膜病变诊断的准确性。 相似文献
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目的 观察转化生长因子-β1(TGF-β1)对大鼠软脑膜间皮细胞(RLMCs)结缔组织生长因子( CTCF)表达的影响.方法 体外培养RLMCs,并将其分为4组:(1)0组(正常对照组):用无血清培养基(FSM)培养细胞;(2)1组:用含TGF-β11 ng/ml培养细胞;(3)2组:用含TGF-β1 2 ng/ml培养细胞;(4)3组:用含TGF-β14 ng/ml培养细胞;各组分别在TCF-β1刺激6、12及24 b后,采用逆转录-聚合酶链反应(RT-PCR)方法测定CTCF mRNA水平;蛋白免疫印迹(Westem blot)测定CTCF蛋白表达.数据以平均值±标准差(-χ±s)表示,各个浓度点组间比较采用单因素方差分析(One-way ANOVA),两两比较采用最小显著法(LSD)检验,以P〈0.05有统计学意义.结果 在6、12及24 h分别以TCF-β1 1ng/mL、2 ng/mL、4 ng/mL处理,CTGF mRNA表达水平与对照组比较,差异有显著性(F6h=46.549、F12h= 287.098、F24h=109.202,P均〈0.001),呈剂量依赖性,以TGF-β1处理12 h组CTGF mRNA表达差异明显.western blotting:正常对照组RLMCs细胞和不同浓度的TGF-β1刺激后均表达CTGF蛋白,在TGF-β1刺激6、12及24 h后,各组均随着浓度的增加而增加,差异有显著性(F6h= 52.988、F12h= 95.331、F24h=157.107,P均〈0.001),呈剂量依赖性,以TGF-β1处理6h组CTGF蛋白表达差异明显.结论 TGF-β1能诱导RLMCs中CTGF通路激活.TGF-β1刺激RLMCs中CTGF mRNA和蛋白的表达,而且随浓度增加而显著.CTGF可能作为神经系统疾病中抑制脑膜纤维化的靶点而进一步研究. 相似文献