Cerebral dominance and speech acquisition in deaf children.

In examining the prediction that left cerebral dominance, as indexed by hand and sighting preference, should be a positive accompaniment of speech learning in individuals whose cerebral speech areas are likely to be in the left hemisphere, it was found that over a 10-12 year period of formal education right-handed-right-sighting deaf students consistently earned higher speech grades than their right-handed-left sighting and right-handed-mixed-sighting counterparts matched on the basis of hearing loss. This finding supports the hypothesis that the cerebral mechanisms relevant to speech acquisition are simplified, facilitated, and/or less prone to interference when control of speech, hand, and eye is localized primarily in 1 hemisphere of the brain. (PsycINFO Database Record (c) 2010 APA, all rights reserved)     

姜黄素对大鼠局灶性脑缺血再灌注损伤的神经保护作用

目的：探讨姜黄素对大鼠局灶性脑缺血再灌注损伤的保护作用及其可能机制。方法：采用线栓法制备大鼠大脑中动脉缺血再灌注模型,随机分成假手术组、对照组、100mg/kg姜黄素组及300mg/kg姜黄素组及300mg/kg姜黄素组,分别在脑缺血再灌注后24h处死,观察大鼠神经功能缺失的评分,应用TTC染色观察梗死体积,尼氏染色观察神经元形态结构特征,TUNEL染色计数凋亡神经元,荧光免疫组化及Western-blot检测caspase-3蛋白的表达变化。结果：姜黄素能明显改善大鼠缺血再灌注后的神经功能缺损,缩小梗死体积,明显减少TUNEL染色阳性细胞数,下调caspase-3蛋白的表达。结论：姜黄素对大鼠局灶性脑缺血再灌注损伤具有良好的神经保护作用,这可能与其减少caspase-3的表达,抑制缺钱神经元的凋亡密切相关。     

大鼠中脑水管室管膜上皮的超微结构观察

应用扫描和透射电子显微镜观察研究大鼠中脑水管室管膜的超微结构特征。发现中脑水管壁具有平行走向的纵嵴,腔面被覆单层立方或柱状上皮;上皮细胞游离面可见大量纤毛、微绒毛及分泌泡;细胞核圆形,位于细胞中央;胞浆内细胞器分布具有明显的极性特点。通过超微结构研究,认为大鼠中脑水管不仅单纯是脑脊液引流的通路,而且还具有主动参与脑脊液分泌的功能。     

氦氖激光血管外照射治疗脑缺血

目的:观察氦氖激光血管外照射治疗脑缺血的效果,讨论其可能机制.方法:对12例脑缺血进行氦氖激光血管外照射治疗,并与非血管激光照射治疗的16例进行对比.结果:血管外激光照射治疗组效果明显好于对照组.结论:氦氖激光血管外照射治疗能够提高临床脑缺血的疗效,提倡它作为脑缺血的治疗方法之一.     

核桃中血清素的提取分离与抗心肌缺血活性研究

核桃破碎后经体积分数为70%乙醇提取,乙酸乙酯萃取、浓缩后,经大孔树脂、MCI、ODS等不同层析柱分离。采用MTT法和试剂盒法,以乳鼠心肌细胞缺血/再灌注损伤模型检测各分离组分抗心肌缺血活性。结果从核桃中分离得到5,10-二羟色胺和Shepherdine化合物,其中5,10-二羟色胺能显著提高心肌细胞存活率,减少受损细胞心肌酶(LDH、CK)的释放,对心肌细胞具有保护作用。     

Protective Role of Glutathione in the Hippocampus after Brain Ischemia

Stroke is a major cause of death worldwide, leading to serious disability. Post-ischemic injury, especially in the cerebral ischemia-prone hippocampus, is a serious problem, as it contributes to vascular dementia. Many studies have shown that in the hippocampus, ischemia/reperfusion induces neuronal death through oxidative stress and neuronal zinc (Zn²⁺) dyshomeostasis. Glutathione (GSH) plays an important role in protecting neurons against oxidative stress as a major intracellular antioxidant. In addition, the thiol group of GSH can function as a principal Zn²⁺ chelator for the maintenance of Zn²⁺ homeostasis in neurons. These lines of evidence suggest that neuronal GSH levels could be a key factor in post-stroke neuronal survival. In neurons, excitatory amino acid carrier 1 (EAAC1) is involved in the influx of cysteine, and intracellular cysteine is the rate-limiting substrate for the synthesis of GSH. Recently, several studies have indicated that cysteine uptake through EAAC1 suppresses ischemia-induced neuronal death via the promotion of hippocampal GSH synthesis in ischemic animal models. In this article, we aimed to review and describe the role of GSH in hippocampal neuroprotection after ischemia/reperfusion, focusing on EAAC1.     

脑血流动力学及脑氧饱和度变化与感染性休克患者预后的相关性:前瞻性队列研究

目的探讨大脑中动脉血流动力学相关指标及脑氧饱和度变化与感染性休克患者预后的相关性。方法前瞻性收集2018年5月至2019年3月在中南大学湘雅医院重症医学科住院治疗的感染性休克患者临床资料,根据28 d内是否死亡,将患者分为死亡组和存活组。比较两组患者一般资料,入重症监护室即刻和初始复苏治疗6 h后动脉和中心静脉血气指标,重症心脏超声指标,器官功能指标,Sepsis生物标志物指标,液体复苏治疗6 h后大脑中动脉血流速度、灌注指数、动态脑血管自动调节功能[瞬时脑充血反应率(transient hyperemic response ratio,THRR)]以及脑氧饱和度变化。采用多因素Logistic回归,分析影响感染性休克患者预后的危险因素。结果 51例符合纳入和排除标准的感染休克患者入选本研究,男性31例,女性20例,年龄(53±13)岁,28 d死亡率为43%。死亡组的序贯性器官衰竭评分(sequential organ failure assessment,SOFA)(P=0. 007)、入室急性生理和慢性健康状况评估(acute physiology and chronic health evaluationⅡ,APACHEⅡ)评分(P=0. 026)以及高峰APACHEⅡ评分(P<0. 001)均高于存活组。初始复苏治疗6 h后,死亡组的氧合指数低于存活组(P=0. 047),而中心静脉-动脉二氧化碳分压差(central venous-to-arterial carbon dioxide difference,Pcva CO_2)则高于存活组(P=0. 044)。死亡组动态脑血管自动调节功能受损者(THRR<1. 09)多于存活组(P=0. 025),脑氧饱和度(regional cerebral oxygen saturation,rSO_2)均值低于存活组(P=0. 031)且rSO_2均值<60%者多于存活组(P=0. 010)。多因素Logistic回归分析显示,高峰APACHEⅡ评分(OR=1. 099,95%CI:1. 009～1. 196,P=0. 030)、液体复苏治疗6 h后的Pcv-aCO_2(OR=1. 320,95%CI:1. 001～1. 742,P=0. 050)、THRR<1. 09 (OR=4. 952,95%CI:1. 130～21. 70,P=0. 034)和rSO_2均值<60%(OR=4. 817,95%CI:1. 392～16. 663,P=0. 013)是预测感染性休克患者28 d内死亡的独立危险因素。结论感染性休克患者死亡率高,脑血流动力学和rSO_2指标中动态脑血管自动调节功能障碍(THRR<1. 09)与rSO_2均值<60%是28 d死亡率增加的独立预测因素。     

NLRP3 Inflammasome Activation Is Involved in LPA1-Mediated Brain Injury after Transient Focal Cerebral Ischemia

Lysophosphatidic acid receptor 1 (LPA₁) contributes to brain injury following transient focal cerebral ischemia. However, the mechanism remains unclear. Here, we investigated whether nucleotide-binding oligomerization domain-like receptor family pyrin domain containing 3 (NLRP3) inflammasome activation might be an underlying mechanism involved in the pathogenesis of brain injury associated with LPA₁ following ischemic challenge with transient middle cerebral artery occlusion (tMCAO). Suppressing LPA₁ activity by its antagonist attenuated NLRP3 upregulation in the penumbra and ischemic core regions, particularly in ionized calcium-binding adapter molecule 1 (Iba1)-expressing cells like macrophages of mouse after tMCAO challenge. It also suppressed NLRP3 inflammasome activation, such as caspase-1 activation, interleukin 1β (IL-1β) maturation, and apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC) speck formation, in a post-ischemic brain. The role of LPA₁ in NLRP3 inflammasome activation was confirmed in vitro using lipopolysaccharide-primed bone marrow-derived macrophages, followed by LPA exposure. Suppressing LPA₁ activity by either pharmacological antagonism or genetic knockdown attenuated NLRP3 upregulation, caspase-1 activation, IL-1β maturation, and IL-1β secretion in these cells. Furthermore, nuclear factor-κB (NF-κB), extracellular signal-regulated kinase 1/2 (ERK1/2), and p38 were found to be LPA₁-dependent effector pathways in these cells. Collectively, results of the current study first demonstrate that LPA₁ could contribute to ischemic brain injury by activating NLRP3 inflammasome with underlying effector mechanisms.     

Tissue-Specific Ferritin- and GFP-Based Genetic Vectors Visualize Neurons by MRI in the Intact and Post-Ischemic Rat Brain

(1) Background: Neurogenesis is considered to be a potential brain repair mechanism and is enhanced in stroke. It is difficult to reconstruct the neurogenesis process only from the histological sections taken from different animals at different stages of brain damage and restoration. Study of neurogenesis would greatly benefit from development of tissue-specific visualization probes. (2) Purpose: The study aimed to explore if overexpression of ferritin, a nontoxic iron-binding protein, under a doublecortin promoter can be used for non-invasive visualization of neurogenesis using magnetic resonance imaging (MRI). (3) Methods: Ferritin heavy chain (FerrH) was expressed in the adeno-associated viral backbone (AAV) under the doublecortin promoter (pDCX), specific for young neurons, in the viral construct AAV-pDCX-FerrH. Expression of the enhanced green fluorescent protein (eGFP) was used as an expression control (AAV-pDCX-eGFP). The viral vectors or phosphate-buffered saline (PBS) were injected intracerebrally into 18 adult male Sprague–Dawley rats. Three days before injection, rats underwent transient middle-cerebral-artery occlusion or sham operation. Animals were subjected to In vivo MRI study before surgery and on days 7, 14, 21, and 28 days after injection using a Bruker BioSpec 11.7 T scanner. Brain sections obtained on day 28 after injection were immunostained for ferritin, young (DCX) and mature (NeuN) neurons, and activated microglia/macrophages (CD68). Additionally, RT-PCR was performed to confirm ferritin expression. (4) Results: T2* images in post-ischemic brains of animals injected with AAV-pDCX-FerrH showed two distinct zones of MRI signal hypointensity in the ipsilesioned hemisphere starting from 14 days after viral injection—in the ischemic lesion and near the lateral ventricle and subventricular zone (SVZ). In sham-operated animals, only one zone of hypointensity near the lateral ventricle and SVZ was revealed. Immunochemistry showed that ferritin-expressing cells in ischemic lesions were macrophages (88.1%), while ferritin-expressing cells near the lateral ventricle in animals both after ischemia and sham operation were mostly mature (55.7% and 61.8%, respectively) and young (30.6% and 7.1%, respectively) neurons. RT-PCR confirmed upregulated expression of ferritin in the caudoputamen and corpus callosum. Surprisingly, in animals injected with AAV-pDCX-eGFP we similarly observed two zones of hypointensity on T2* images. Cellular studies also showed the presence of mature (81.5%) and young neurons (6.1%) near the lateral ventricle in both postischemic and sham-operated animals, while macrophages in ischemic lesions were ferritin-positive (98.2%). (5) Conclusion: Ferritin overexpression induced by injection of AAV-pDCX-FerrH was detected by MRI using T2*-weighted images, which was confirmed by immunochemistry showing ferritin in young and mature neurons. Expression of eGFP also caused a comparable reduced MR signal intensity in T2*-weighted images. Additional studies are needed to investigate the potential and tissue-specific features of the use of eGFP and ferritin expression in MRI studies.