119 resultados para NSC


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El presente estudio se realizó basándose en los registros de un hato pardo suizo. Ubicado a 12 grados 15 minutos de latitud, 86 grados 25 minutos de longitud y una elevación de 49 m.s.n.m, con temperatura y humedad relativa promedio en los últimos 12 años de 27 grados Celcius y 70.8% respectivamente y 1250m anuales de precipitación en los últimos 10 años. Las variables en estudio fueron; EPS; EPP; EPPI; PS; IPP: PL;NSC: ML con promedio de 671+/-99 días, 965+/-132 días, 105+/-44dias, 185+/-113 días, 419+/57 días 3445+/-697kg, 1.08+/-1.2ser, 9.6+/-1.6 meses respectivamente. En el ANDEVA para EPS resulto significativo el AM y MN; para la EPP resulto significativo el AN y no significativo el MN; para el IPPI resulto Significativo el AP, no significativo el MP y la variable EP; para el PS e IPP, resulto significativo AP, MP y las variables ML. EP. Las correlaciones lineales entre Ep y NSC; IPPI y ISC, IPPI Y PS, PS y IPPI e IPP, PS e IPP, ML e IPPI, PS IPP, PL y PS, IPP; Il, EP; resultaron significativas con un coeficiente de +0.2815, -067, +0.327, +0.458, +0879, +0.146, +0275, +0.71, +0.247, +0.208, +0.7102, +0.227, respectivamente, las regresiones de NSC con Ep; IPP con EP, PS con IPP con PS; PL con ML y EP; resultaron significativas con valores de coeficiente de +0.327 ser ./año, +5.9 días/año, +0.227 día/días, +0.967 días/días, +430.86 kg/mes de lactancia y +238.3 kg./año respectivamente.

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:探索以Lentivirus为载体,构建同时表达绿色荧光蛋白(GFP)和神经营养因子一3(NT一3)的基因工程化鼠胚神经于细胞(NSC)的可行性。方法:体外分离培养鼠胚NSC,用同时携带NT一3和GFP的lentivirus转染构建工程化NSC;用荧光显微镜、鼠胚背根神经结培养(Dorsal Root Ganglion,DRG)、Westem blot等方法检测基因工程NSC 的转基因表达。结果:荧光显微镜观察到几乎100%的工程化NSC表达GFP:DRG培养和Westem blot检测到基因工程化NSC能高效分泌NT一3蛋白。结论:以IJentivirus为载体,构建同时携带并稳定表达GFP和N‘r_3的基因工程化鼠胚NSC是可行的,可为脊髓损伤基础研究提供有价值的细胞资源。

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神经干细胞(NSC)是中枢神经系统中具有自我更新能力和多种分化潜能的细胞,是脊髓损伤(SCI)后再生修复的理想材料和基因载体。我们探讨了Lentivirus介导分泌神经营养因子-3(NT-3)的基因工程NSC移植治疗SCI的可行性,以期为SCI后功能恢复的实验研究以及进一步临床研究提供基础资料。材料与方法一、实验材料1.试剂与来源:DMEM/F12、B27、N2(Gibco公司),bFGF(Sigma公司),Nestin抗体、NF-200抗体、GFAP抗体(武汉博士德公司),羊抗鼠NT-3抗体(USB公司),超信号West Pico化学发光底物试剂盒(Pierce34079ZZ)、人胚肾293T细胞购自武汉大学保藏中心,携带NT-3和绿色荧光蛋白(GFP)的Lentivirus的各种质粒由美国迈阿密大学Oudega M教授提供。2.实验动物:Wistar大鼠由成都军区昆明总医院实验动物中心提供。二、实验方法1.NSC的分离培养:取孕14d的Wistar胎鼠皮层组织,分离筋膜和血管,反复剪碎,再用200目细胞筛过滤,转入DMEM/F12,加B27添加剂、bFGF(20ng/ml);6~7d传代。

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An augmented immersed interface method (IIM) is proposed for simulating one-phase moving contact line problems in which a liquid drop spreads or recoils on a solid substrate. While the present two-dimensional mathematical model is a free boundary problem, in our new numerical method, the fluid domain enclosed by the free boundary is embedded into a rectangular one so that the problem can be solved by a regular Cartesian grid method. We introduce an augmented variable along the free boundary so that the stress balancing boundary condition is satisfied. A hybrid time discretization is used in the projection method for better stability. The resultant Helmholtz/Poisson equations with interfaces then are solved by the IIM in an efficient way. Several numerical tests including an accuracy check, and the spreading and recoiling processes of a liquid drop are presented in detail. (C) 2010 Elsevier Ltd. All rights reserved.

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通常认为,随着林木不断接近其海拔分布极限,光合作用产量不断下降,导致碳水化合物供应不足(碳供应限制),或者低温限制了碳投资(生长限制)。植物组织内非结构性碳水化合物(Nonstructural carbohydrates,NSC)的含量反映了植物碳供应与碳吸收的平衡。为了检验"碳供应限制"和"生长抑制"假说,我们对长白山海拔1700~2050m的自然生境下生长的岳桦(Betula ermanii)的叶片和枝条组织的NSC含量进行了比较。结果表明:岳桦叶片的NSC含量随海拔升高变化不显著,枝条的NSC含量随海拔升高显著增加;叶片和枝条中淀粉含量与可溶性总糖含量的比值均随海拔的升高而减小;林线附近的岳桦林木不存在碳水化合物供应不足的问题,这在一定程度上表明生长限制导致长白山岳桦林线的形成。

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In the present study, we examined the possible utility of a three-dimensional culture system using a thermo-reversible gelation polymer to isolate and expand neural stem cells (NSCs). The polymer is a synthetic biologically inert polymer and gelates at temperatures higher than the gel-sol transition point ( approximately 20 degrees C). When fetal mouse brain cells were inoculated into the gel, spherical colonies were formed ( approximately 1% in primary culture and approximately 9% in passage cultures). The spheroid-forming cells were positive for expression of the NSC markers nestin and Musashi. Under conditions facilitating spontaneous neural differentiation, the spheroid-forming cells expressed genes characteristic to astrocytes, oligodendrocytes, and neurons. The cells could be successively propagated at least to 80 poly-D-lysines over a period of 20 weeks in the gel culture with a growth rate higher than that observed in suspension culture. The spheroids formed by fetal mouse brain cells in the gel were shown to be of clonal origin. These results indicate that the spheroid culture system is a convenient and powerful tool for isolation and clonal expansion of NSCs in vitro.

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PURPOSE: To describe the prevalence of different types of cataract and their association with visual acuity in a Tanzanian population aged 40 years and older. METHODS: A prevalence survey for lens opacity, glaucoma, and visual impairment was carried out on all residents age 40 and older of six villages in Kongwa, Tanzania. One examiner graded the lens for presence of nuclear (NSC), posterior subcapsular (PSC), and cortical cataract (CC), using the new WHO Simplified Cataract Grading System. Visual acuity was measured in each eye, both presenting and best corrected, using an illiterate E chart. RESULTS: The proportion of eligible subjects participating was 90% (3268/3641). The prevalence of cataract was as follows: NSC, 15.6%; CC, 8.8%; and PSC, 1.9%. All types of cataract increased with age, from NSC, 1.7%; CC, 2.4%; and PSC, 0.4% for those aged 40 to 49 years to NSC, 59.2%; CC, 23.5%; and PSC, 5.9% for those aged 70 years and older (P < 0.0001 for all cataract types, chi(2) test for trend). Cataract prevalence was higher among women than men for NSC (P = 0.0001), but not for CC (P = 0.15) or PSC (P = 0.25), after adjusting for age. Prevalence rates of visual impairment (BCVA < 6/12), US blindness (< or = 6/60) and WHO blindness (< 6/120) for this population were 13.3%, 2.1%, and 1.3%, respectively. Older age and each of the major types of pure and mixed cataract were independently associated with worse vision in regression modeling. CONCLUSIONS: Unlike African-derived populations in Salisbury and Barbados, NSC rather than CC was most prevalent in this African population. The seeming lower prevalence of CC may to some extent be explained by different grading schemes, differential availability of cataract surgery, the younger mean age of the Tanzanian subjects, and a higher prevalence of NSC in this population.

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The fact that the adult brain is able to produce new neurons or glial cells from neural stem cells (NSC) became one of the most interesting and challenging fields of research in neuroscience. Endogenous adult neurogenesis occurs in two main regions of the brain: the subventricular zone (SVZ) of the lateral ventricles and the subgranular zone (SGZ) in the dentate gyrus. Brain injury may be accompanied by increased neurogenesis, although neuroinflammation promotes the activation of microglial cells that can be detrimental to the neurogenic process. Nitric oxide (NO) is one of the factors released by microglia that can be proneurogenic. The mechanism by which NO promotes the proliferation of NSCs has been intensively studied. However, little is known about the role of NO in migration, survival and differentiation of the newborn cells. The aim of this work was to investigate the role of NO from inflammatory origin in proliferation, migration, differentiation and survival of NSCs from the dentate gyrus in a mouse model of status epilepticus. We also assessed neuroinflammation in the same injury model. Our work showed that NO increased proliferation of the early-born cells after seizures, but is detrimental for their survival. NO also increased migration of neuroblasts. Moreover, NO was important to maintain long-term neuroinflammation. Taken together, these results show that NO may be a good target to promote proliferation and migration of NSCs following seizures, but compromises survival of early-born cells.

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Tese de doutoramento, Farmácia (Bioquímica), Universidade de Lisboa, Faculdade de Farmácia, 2014

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Tese de mestrado, Ciências do Sono, Faculdade de Medicina, Universidade de Lisboa, 2015

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We analyse the relationship between the privatization of a public firm and government preferences for tax revenue in a Stackelberg duopoly with the public firm as the leader. We assume that the government payoff is given by a weighted sum of tax revenue and the sum of consumer and producer surplus. We get that if the government puts a sufficiently larger weight on tax revenue than on the sum of both surpluses, it will not privatize the public firm. In contrast, if the government puts a moderately larger weight on tax revenue than on the sum of both surpluses, it will privatize the public firm.

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We study whether privatization of a public firm improves (or deteriorates) the environment in a mixed Stackelberg duopoly with the public firm as the leader. We assume that each firm can prevent pollution by undertaking abatement measures. We get that, since in the mixed market the industry output is higher than in the private market, the abatement levels are also higher in the mixed market, and, thus, environmental tax rate in the mixed duopoly is higher than that in the privatized duopoly. Furthermore, the environment is more damaged in the mixed than in the private market. The overall effect on the social welfare is that it will becomes higher in the private than in the mixed market.

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In the present paper we consider a differentiated Stackelberg model, when the leader firm engages in an R&D process that gives an endogenous cost-reducing innovation. The aim is to study the licensing of the cost-reduction by a per-unit royalty and a fixed-fee. We analyse the implications of these types of licensing contracts over the R&D effort, the profits of the firms, the consumer surplus and the social welfare. By using comparative static analysis, we conclude that the degree of the differentiation of the goods plays an important role in the results.

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NMDA receptors (NMDARs) mediate ischemic brain damage, for which interactions between the C termini of NR2 subunits and PDZ domain proteins within the NMDAR signaling complex (NSC) are emerging therapeutic targets. However, expression of NMDARs in a non-neuronal context, lacking many NSC components, can still induce cell death. Moreover, it is unclear whether targeting the NSC will impair NMDAR-dependent prosurvival and plasticity signaling. We show that the NMDAR can promote death signaling independently of the NR2 PDZ ligand, when expressed in non-neuronal cells lacking PSD-95 and neuronal nitric oxide synthase (nNOS), key PDZ proteins that mediate neuronal NMDAR excitotoxicity. However, in a non-neuronal context, the NMDAR promotes cell death solely via c-Jun N-terminal protein kinase (JNK), whereas NMDAR-dependent cortical neuronal death is promoted by both JNK and p38. NMDAR-dependent pro-death signaling via p38 relies on neuronal context, although death signaling by JNK, triggered by mitochondrial reactive oxygen species production, does not. NMDAR-dependent p38 activation in neurons is triggered by submembranous Ca(2+), and is disrupted by NOS inhibitors and also a peptide mimicking the NR2B PDZ ligand (TAT-NR2B9c). TAT-NR2B9c reduced excitotoxic neuronal death and p38-mediated ischemic damage, without impairing an NMDAR-dependent plasticity model or prosurvival signaling to CREB or Akt. TAT-NR2B9c did not inhibit JNK activation, and synergized with JNK inhibitors to ameliorate severe excitotoxic neuronal loss in vitro and ischemic cortical damage in vivo. Thus, NMDAR-activated signals comprise pro-death pathways with differing requirements for PDZ protein interactions. These signals are amenable to selective inhibition, while sparing synaptic plasticity and prosurvival signaling.

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Nous avons précédemment montré que l’activation du récepteur natriurétique de type C (NPR-C) par son agoniste spécifique, le C-ANP4-23, atténue l’augmentation de la prolifération des cellules du muscle lisse vasculaire (CMLV) induite par les peptides vasoactifs (Ang II, ET-1 et l’AVP). Puisque les CMLV provenant de rats spontanément hypertendus (SHR) montrent elles aussi un taux de prolifération plus élevé que leur contrôle, les CMLV de rats Wystar-Kyoto (WKY), nous avons entrepris cette étude dans le but de déterminer si C-ANP4-23 peut également diminuer le taux élevé de prolifération des CMLV de SHR et, le cas échéant déterminer les mécanismes responsables de cette réponse. Nos résultats montrent que le taux de prolifération des CMLV de SHR est significativement plus élevé que celui des CMLV de WKY et que la présence de C-ANP4-23 diminue de manière-dose dépendante le taux de prolifération des CMLV de SHR. En plus, l’expression des protéines de la phase G1 du cycle cellulaire, la cycline D1, la kinase dépendante des cyclines 2 (cdk2) et la forme phosphorylée de la protéine du rétinoblastome (pRb) est augmentée dans les CMLV de SHR comparativement aux CMLV de WKY et est atténué par C-ANP4-23. De plus, nos résultats montrent que les inhibiteurs du complexe cycline D1/cdk4 (NSC 625987) et cdk2 (NU2058) diminue le taux de prolifération élevé des CMLV de SHR. Les CMLV de SHR montrent également un taux de phosphorylation de ERK1/2 et d’AKT et est atténué par C-ANP4-23. De plus, le taux d’expression élevé des protéines cycline D1, cdk2 et pRb des CMLV de SHR est diminué par la toxine pertussis qui inactive la protéine Giα, le PD 98095, un inhibiteur de MEK de la voie des MAPK, du wortmannin, un inhibiteur de la PI3-K et finalement du losartan, un antagoniste du récepteur AT1. Ces résultats suggèrent que l’activation du récepteur NPR-C par C-ANP4-23 diminue le taux de prolifération élevé des CMLV de SHR par une régulation à la baisse des composantes du cycle cellulaire via l’inhibition de la protéine Giα et des voies signalétique MAP kinase/PI3-K.