Comparison of olfactory function between neuromyelitis optica and multiple sclerosis

Objectives: Olfactory dysfunction (ODF) has been reported in patients with neuromyelitis optica (NMO) and multiple sclerosis (MS). However, the comparison of olfactory function and olfactory-related gray matter (GM) between patients with NMO and MS needed to be further elucidated.

Materials and methods: Thirty-seven patients with NMO and 37 with MS were enrolled. Olfactory function was evaluated with a Japanese T&T olfactometer test kit, and the neuroanatomical features of olfactory-related GM were assessed using voxel-based morphometry.

Results: Olfactory deficits were found in 51.4% of patients with NMO and 40.5% of patients with MS. Patients with NMO with ODF had significantly smaller olfactory bulbs than patients with MS with ODF (p = 0.031). Olfactory-related GM atrophy was found in patients with NMO in several regions of the right orbitofrontal cortex and right superior frontal gyrus; in patients with MS, reduced GM volume was found in the right parahippocampal gyrus and piriform cortex (p < 0.05, cluster size > 200 voxels).

Conclusions: Olfactory deficits are common in both NMO and MS. However, the neuroanatomical features related to olfactory deficits differ greatly between the two diseases.     

Guillain Barre Syndrome in the elderly: Experience from a tertiary-care hospital in India

Age influences incidence and prognosis of Guillain Barre Syndrome (GBS), common cause of ascending areflexic quadriparesis. Dedicated studies on elderly GBS are infrequent. This study aimed to describe clinical features and outcome at hospital-discharge in patients aged ≥ 60 years with GBS. Medical records of 70 elderly GBS over 15 years were analysed. Mean symptom-duration was 5.78 ± 4.5 days and onset-to-peak 5.14 ± 4.4 days. Antecedent events preceded GBS by 8.07 ± 9.9 days and included: fever (n = 19), respiratory infection (n = 6), and gastroenteritis (n = 5). Clinical features were weakness of facial (n = 34), bulbar (n = 13), extraocular (n = 4) and respiratory (n = 20) muscles and recurrence (n = 4). Nine had Hughes disability score (HDS) of three or less. Sensory symptoms and signs included paresthesias (n = 40), pain (n = 24), and impaired kinaesthetic sensation (n = 14). Laboratory abnormalities included albumino-cytological dissociation (n = 50), hyponatremia (n = 36) and elevated creatine kinase (n = 18). Electrophysiological subtypes were: primary demyelinating (n = 52), inexcitable (n = 3), equivocal (n = 2) and axonal (n = 1). Fifty-seven patients treated with plasmapheresis (n = 48) or intravenous immunoglobulin (n = 9) had mean HDS of 3.53 ± 0.7 at discharge. Twenty-one were ambulant (HDS ≥ 3), one had persisting respiratory weakness and one died. Striking differences between the ‘elderly’ and 100 ‘adults’ seen over 20 months were shorter symptom-duration, higher frequency of facial palsy and hyponatremia, lower frequency of pain, lower mean MRC sum score and worse HDS at study-entry and discharge (p < 0.05). Requirement for mechanical ventilation and cardiac autonomic dysfunction was higher among elderly (p:0.02). In conclusion, in this cohort of elderly GBS, there was a higher frequency severe GBS and demyelinating electrophysiology.     

Climate change transformation: A definition and typology to guide decision making in urban environments

Climate change presents a threat to the sustainability of cities and their societies, and must be adequately addressed. Urban environments (cities) are responsible for the creation of a significant amount of greenhouse gas emissions which are the source of climate change. Cities have been increasingly the focus of action to address climate change, yet emissions are not significantly reducing. Additionally, there a lack of integration between adaptation and mitigation. This prevents responses adequate to limit global warming to 1.5^OC, and to be well adapted to anticipated changes. This paper critically analyses existing definitions and typologies of climate change actions. A definition of ‘climate change transformation’ is proposed which includes the integration of adaptation and mitigation goals to enable a new regime in which global warming is limited to 1.5^OC. A new three-part typology: ‘coping, malaction and transformation,’ is presented for categorising climate change actions by the extent to which they integrate adaptation and mitigation, and define a new regime. The typology is accompanied by illustrations to demonstrate the relationship between adaptation and mitigation. The definition, typology and illustration serve to guide effective climate change decision making, and provides principles to guide application in urban environments.     

立体定向移植骨髓间充质干细胞改善血管性大鼠的学习记忆能力

背景:大量的实验证明将骨髓间充质干细胞移植到复制的中枢神经系统疾病大鼠模型后,能迁移到损伤部位,表达神经细胞的潜在特性并且提高神经功能。目的:验证骨髓间充质干细胞对拟人类血管性痴呆模型大鼠学习记忆障碍的改善作用。方法:分离SD大鼠骨髓间充质干细胞,于细胞移植前掺入10mg/L的BrdU进行标记。建立Wistar大鼠血管性痴呆样学习记忆障碍动物模型,随机分为模型组、假手术组与移植组。移植组致伤后第14天,通过立体定向途径移植骨髓间充质干细胞到大鼠海马,假手术组给予等量生理盐水,模型组大鼠不做处理。采用Morris水迷宫检测大鼠空间学习记忆能力。损伤后第90天处死大鼠,观察海马组织有无Brdu+神经元特异性烯醇化酶、Brdu+胶质纤维酸性蛋白免疫组织化学双染阳性细胞,并且观察从侧脑室到海马是否存在神经元前体细胞的标志Doublecortin(DCX)吻侧迁移流。结果与结论:①移植组大鼠采用Morris水迷宫检测大鼠空间学习记忆能力逃避潜伏期及跨越平台次数优于模型组及假手术组(P<0.05)。②移植组大鼠海马组织及其周围可见免疫组织化学双染阳性细胞,但未见从侧脑室到海马关于神经元前体细胞的标志Doublecortin(DCX)吻侧迁移流。结果提示,骨髓间充质干细胞移植可以促进脑损伤大鼠的神经功能的恢复,其机制可能与移植细胞分化为神经元样和神经胶质细胞样细胞,并分泌或促进宿主分泌神经营养因子有关。     

Effects of nerve growth factor and Noggin-modified bone marrow stromal cells on stroke in rats

Treatment with bone marrow stromal cells (BMSCs) ameliorates neurological functional deficits after stroke. Nerve growth factor (NGF) is a neurotrophic factor that supports the survival and growth of neural cells. Noggin, an antagonist of bone morphogenetic protein (BMP), promotes the differentiation of stem cells into neurons. In this study, we hypothesize that transfection of NGF and Noggin in BMSC treatment of stroke promotes BMSC neuronal differentiation and improves functional outcome after stroke. Adenovirus was used to trasfect NGF and Noggin and the transfection efficiency was measured by Western blot and immunostaining in vitro. The transfected BMSCs with NGF and/or Noggin were administered intravenously at 5 days after middle cerebral artery occlusion (MCAo) in rats. The neurological functional outcome and BMSC migration and differentiation in the ischemic brain were measured. The transplantation of BMSCs with NGF or Noggin elicited neurological functional improvement, promoted BMSCs present in the ischemic brain, and also up-regulated neuro-like cell differentiation as well as increased synaptophysin expression in the ischemic brain compared with nontreatment control animals (P< 0.05). Treatment of stroke with a combination of transfection of NGF and Noggin in BMSCs induced a synergistic effect on improved neurological functional outcome, BMSCs present in the ischemic brain, and synaptophysin expression in the ischemic brain compared with BMSCs transfected with an NGF- or Noggin-alone group (P < 0.05). These data demonstrate that increasing NGF or Noggin expression in BMSCs contributes to brain plasticity after stroke and that a synergistic effect is induced on the coexistence of NGF and Noggin in BMSCs treatment of stroke.     

外周血内皮祖细胞数量变化与颅内动脉瘤的生成

背景：动脉内膜损伤是动脉瘤发生的始动因素,内皮祖细胞能修复受损的动脉内膜。 目的：建立大鼠颅内动脉瘤模型,探讨动脉瘤大鼠内皮祖细胞数量变化及意义。 方法：40只SD大鼠随机分为两组,正常组作为正常对照,不给予任何干预。模型组大鼠手术结扎双侧肾动脉后支以及左侧颈总动脉,术后喂食含8%氯化钠鼠粮。于2周,1,2,3个月末测量大鼠内皮祖细胞变化,并与3个月末测量各组大鼠血压及动脉瘤大小,RT-PCR检测willis环相关基因表达。 结果与结论：模型组大鼠内皮祖细胞数目于2周后就开始下降,与正常组比较差异有显著性意义(P < 0.05),一直持续到3个月末(P < 0.01)。模型组大鼠动脉瘤壁基质金属蛋白酶9表达明显高于正常组正常大鼠(P < 0.01),而内皮型一氧化氮合酶明显低于正常(P < 0.05)。结果提示循环内皮祖细胞数量降低可能是动脉瘤生成的一个重要因素。     

Hes1在成年小鼠脑中表达的免疫组织化学分析****◆

背景：近年来的研究显示,在胚胎神经系统发育过程中,Hes1的表达调控对保持神经干细胞的数量、调控其分化至关重要。此外,成年个体内处于静止期的纤维母细胞重新获得分裂增殖的能力需要Hes1表达的上调。这表明Hes1在成体中也与某些潜在干细胞的增殖具有密切的关系。因此研究Hes1在成体神经干细胞中的表达及其与成体神经细胞生成的关系也就被提上日程。但Hes1在成年个体神经系统的表达至今未明。 目的：观察和分析小鼠脑中不同部位Hes1的表达及Hes1阳性细胞的细胞类型。 方法：12只成年雄性C57BL/6小鼠随机数字表法分为单染组和双染组,每组6只。单染组直接取材,采用免疫组织化学技术检测Hes1在小鼠脑中各部位的表达。双染组小鼠以200 mg/kg Brdu的剂量每天腹腔注射1次,连续注射3 d,第4天取材,采用双标记物染色观察分析海马区Hes1阳性细胞的细胞类型。 结果与结论：在所有观察的解剖部位中,Hes1表达于所有存在神经细胞的部位,Brdu阳性细胞几乎全部表达Hes1,NeuN阳性细胞全部表达Hes1,而神经胶质原纤维酸性蛋白阳性细胞则完全不表达Hes1。由此可知,Hes1表达于神经细胞和神经干细胞中,胶质细胞不表达Hes1。