Improved normalization of lesioned brains via cohort‐specific templates

In MRI studies, spatial normalization is required to infer results at the group level. In the presence of a brain lesion, such as in stroke patients, the normalization process can be affected by tissue loss, spatial deformations, signal intensity changes, and other stroke sequelae that introduce confounds into the group analysis results. Previously, most neuroimaging studies with lesioned brains have used normalization methods optimized for intact brains, raising potential concerns about the accuracy of the resulting transformations and, in turn, their reported group level results. In this study, we demonstrate the benefits of creating an intermediate, cohort‐specific template in conjunction with diffeomorphism‐based methods to normalize structural MRI images in stroke patients. We show that including this cohort‐specific template improves accuracy compared to standard methods for normalizing lesioned brains. Critically, this method reduces overall differences in normalization accuracy between stroke patients and healthy controls, and may improve the localization and connectivity of BOLD signal in functional neuroimaging data.     

Bone lesions: Role of sediment cytology

This study was conducted to evaluate the role of sediment cytology of biopsy specimen fixatives, which is usually discarded, in early diagnosis of bone lesions. Cytological smears prepared from sediments of biopsy specimen fixatives (sediment cytology) were used to study 65 bone specimens biopsied with suspicion of malignancy. The cytological diagnosis was then compared with histological diagnosis, taking the latter as gold standard. Smears were adequately cellular and showed good preservation of cellular morphology. Some of the smears showed microfragments of tissue. Cytology labeled 29 lesions as malignant, 26 lesions as benign, 3 as inflammatory, and 7 smears as inconclusive because of low cell yield. Sediment cytology was able to correctly diagnose 58 of 65 lesions. There was no false‐positive or false‐negative case. The sediment cytology could be considered as an easy and effective diagnostic tool that can provide early diagnosis for the lesion of bone. Diagn. Cytopathol. 2009. © 2009 Wiley‐Liss, Inc.     

Mitochondrial Complex I Subunits are Altered in Rats with Neonatal Ventral Hippocampal Damage but not in Rats Exposed to Oxygen Restriction at Neonatal Age

Several independent lines of evidence suggest mitochondrial dysfunction in schizophrenia in brain and periphery, including mitochondrial hypoplasia, dysfunction of the oxidative phosphorylation system, and altered mitochondrial-related gene expression. In an attempt to decipher whether mitochondrial complex I abnormality in schizophrenia is a core pathophysiological process or is attributable to medication, we studied two animal models of schizophrenia related to the neurodevelopmental hypothesis of this disorder. Protein levels of complex I subunits, 24, 51, and 75 kDa, were assessed in neonatal ventral hippocampal lesion rat model and in rats exposed to hypoxia at a neonatal age. In the prefrontal cortex, a major anatomical substrate of schizophrenia, neonatal ventral hippocampal lesion induced a significant prepubertal increase and postpubertal decrease in all three subunits of complex I as compared to sham-treated rats, while no change was observed in the cingulate cortex. Neonatal exposure to hypoxia did not affect protein levels of any of the three subunits in the prefrontal cortex. An age-dependent increase in the expression of complex I subunits was observed, which was distorted in the prefrontal cortex by the neonatal ventral hippocampal lesion. Complex I alterations in schizophrenia-related neurodevelopmental rat models appear to be brain region and animal model dependent. The results of this study support previous findings suggesting abnormal complex I expression as a pathological characteristic of schizophrenia rather than an effect of medication.     

A brainstem inflammatory lesion causing REM sleep behavior disorder and sleepwalking (parasomnia overlap disorder)

A 40-year-old woman with no prior parasomnia developed an acute inflammatory rhombencephalitis with multiple cranial nerve palsies and cerebellar ataxia, followed by myelitis 6 months later, and by an intracranial thrombophlebitis 1 month after. Between and after these episodes, she had a persistent, mild right internuclear ophtalmoplegia, a mild cerebellar ataxia, and a severe REM sleep behavior disorder (RBD) lasting for 2 years. She talked, sang and moved nightly while asleep, and injured her son (cosleeping with her) while asleep. In addition, she walked asleep nightly. During video-polysomnography, there were two arousals during slow wave sleep without abnormal behavior, while 44% of REM sleep was without chin muscle atonia with bilateral arm and leg movements. There were small hypointensities in the right pontine tegmentum and in the right dorsal medulla on T1-weighted magnetic resonance imaging, suggesting post-inflammatory lesions that persisted between acute episodes. The RBD and sleepwalking did not improve with clonazepam, but improved with melatonin 9 mg/d. The unilateral small lesion of the pontine tegmentum could be responsible for the parasomnia overlap disorder as in other rare lesional cases.     

Are drawing perseverations part of the neglect syndrome?

Unilateral neglect patients typically omit to cancel contralesional targets. Moreover, they can repeatedly cancel ipsilesional stimuli exhibiting what is termed ‘perseverative behavior’. Two alternative accounts of this behavior have been proposed. According to one of them, it is considered as integral to neglect and due either to a perceptual (allochiria), or a premotor (directional hypokinesia) pathological mechanism leading to the ipsilesional displacement of contralesional responses. According to the other one, perseverations are interpreted as the consequence of motor-control-disinhibition co-occurring with, although independent of, spatial neglect. We compared some crucial predictions of these two hypotheses on a group of 10 right-brain-damaged patients, eight with neglect and two without neglect, showing a perseverative behavior in both conventional and experimental cancellation tasks. In our experiment, the spatial location and the numerosity of targets were manipulated to obtain different degrees of horizontal alignment between targets on the left and on the right of the central vertical axis of the sheet. We found that ipsilesional perseverations were not influenced by left neglected targets and were not correlated to neglect severity. Additionally, perseverative errors were associated with right basal ganglia lesions rather than with presence of neglect. These findings support the view that two different pathological mechanisms might be involved in left spatial neglect and ipsilesional perseverative behavior.     

IGF-I gene delivery promotes corticospinal neuronal survival but not regeneration after adult CNS injury

An unmet challenge of spinal cord injury research is the identification of mechanisms that promote regeneration of corticospinal motor axons. Recently it was reported that IGF-I promotes corticospinal axon growth during nervous system development. We therefore investigated whether IGF-I also promotes regeneration or survival of adult lesioned corticospinal neurons. Adult Fischer 344 rats underwent C3 dorsal column transections followed by grafts of IGF-I-secreting marrow stromal cell grafts into the lesion cavity. IGF-I secreting cell grafts promoted growth of raphespinal and cerulospinal axons, but not corticospinal axons, into the lesion/graft site. We then examined whether IGF-I-secreting cell grafts promote corticospinal motor neuron survival or axon growth in a subcortical axotomy model. IGF-I expression coupled with infusion of the IGF binding protein inhibitor NBI-31772 significantly prevented corticospinal motor neuron death (93% cell survival compared to 49% in controls, P < 0.05), but did not promote corticospinal axon regeneration. Coincident with observed effects of IGF-I on corticospinal survival but not growth, expression of IGF-I receptors was restricted to the somal compartment and not the axon of adult corticospinal motor neurons. Thus, whereas IGF-I influences corticospinal axonal growth during development, its application to sites of adult spinal cord injury or subcortical axotomy fails to promote corticospinal axonal regeneration under conditions that are sufficient to prevent corticospinal cell death and promote the growth of other supraspinal axons. We conclude that developmental patterns of growth factor responsiveness are not simply recapitulated after adult injury, potentially due to post-natal shifts in patterns of IGF-I receptor expression.     

细针穿刺检测乳腺癌原发灶和转移灶ER、PR及C-erbB-2受体表达差异的意义

目的 探讨细针穿刺检测乳腺癌原发灶和转移灶雌激素受体(ER)、孕激素受体(PR)及C-erbB-2受体表达差异的意义.方法用细针穿刺检测60例乳腺癌原发灶和转移灶ER、PR及C-erbB-2受体表达情况,同时对其中28例乳腺癌原发灶ER、PR及CerbB-2受体表达的术后检测结果进行了对照分析.结果28例乳腺癌原发灶的...     

甘草酸二铵肠溶胶囊治疗甲巯咪唑所致的肝功能异常的疗效观察

目的:评价甘草酸二铵肠溶胶囊治疗甲巯咪唑所致的肝功能异常的临床疗效。方法:因甲巯咪唑所致肝功能异常的患者分为治疗组29例及对照组28例,治疗组给予甘草酸二铵肠溶胶囊口服,对照组组予护肝片口服,观察比较2周后2组患者治疗肝损害的疗效。结果:2组治疗后丙氨酸氨基转移酶(ALT)、碱性磷酸酶(ALP)及总胆红素较治疗前均明显下降(P<0.05),2组之间差异无显著性(P>0.05)。治疗组总有效率(89.66%)明显高于对照组(75.00%)(P<0.05)。结论:甘草酸二铵肠溶胶囊治疗甲巯咪唑所致的肝功能异常有较好的治疗效果。     

内窥镜手术治疗脑积水及颅内囊性占位病灶的临床分析

目的探讨神经内窥镜治疗梗阻性脑积水及颅内囊性占位病灶的临床特点。方法回顾性分析该院2005年2月~2008年2月应用神经内窥镜技术治疗颅内病变患者48例临床资料,其中梗阻性脑积水26例,蛛网膜囊肿12例,透明隔囊肿6例,鞍上巨大囊肿3例,鞍上囊性颅咽管瘤1例。术后随访24个月,观察患者并发症及治疗效果。结果并发症:发热3例,硬膜下积液2例,脑室出血1例,并发症发生率仅12.5%;疗效:42例有效,有效率高达87.5%,6例无效(脑积水5例,鞍上巨大囊肿1例)。结论神经内窥镜治疗颅内病变具有创伤小、直观、并发症少、有效率高等优点,但要严格掌握手术适应证。     

温针灸减低阿司匹林抗风湿致胃肠道副作用的研究

目的:探讨温针灸减低阿司匹林致胃肠道副作用的疗效及机制。方法:用随机数字表法将SD大鼠分为空白组、模型组、温针灸组与奥美拉唑组,每组10只。阿司匹林灌胃造模。灌胃后温针灸组取"中脘"下脘"、双侧"足三里"与双侧"内关",平补平泻手法针刺穴位后用温针灸架进行温针灸30 min,每日1次,连续治疗7 d。参照Guth标准测量大鼠胃溃疡指数,黄嘌呤氧化酶法(羟氨法)测血清和胃黏膜的超氧化物歧化酶(SOD)活力,硫代巴比妥酸法测其丙二醛(MDA)含量。结果:与空白组比较,模型组各指标均有明显变化(P<0.01);温针灸组的血清和胃黏膜SOD活力均提高,MDA含量均降低,溃疡指数减小,与模型组比较差异有统计学意义(P<0.01);奥美拉唑组的溃疡抑制率优于温针灸组(P<0.05),但是温针灸组在提高血清和胃黏膜SOD活力和降低胃黏膜MDA含量方面优于奥美拉唑组(P<0.05)。结论:温针灸能明显减低阿司匹林所致的胃肠道副作用,其机制可能与抗氧自由基损伤有关。