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Intranasal Delivery of lincRNA-Cox2 siRNA Loaded Extracellular Vesicles Decreases Lipopolysaccharide-Induced Microglial Proliferation in Mice 经鼻递送lincRNA-Coox2-siRNA负载的细胞外小泡降低脂多糖诱导的小鼠微胶质细胞增殖
IF 6.2 3区 医学 Q1 NEUROSCIENCES Pub Date : 2019-07-20 DOI: 10.1007/s11481-019-09864-z
K. Liao, F. Niu, R. Dagur, Meng He, C. Tian, Guoku Hu
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引用次数: 30
Neuroprotective Effects of Genistein in a SOD1-G93A Transgenic Mouse Model of Amyotrophic Lateral Sclerosis 染料木素在SOD1-G93A转基因肌萎缩性侧索硬化症小鼠模型中的神经保护作用
IF 6.2 3区 医学 Q1 NEUROSCIENCES Pub Date : 2019-07-18 DOI: 10.1007/s11481-019-09866-x
Zichun Zhao, Jin-Sheng Fu, Shiping Li, Zhenzhong Li
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引用次数: 23
Modulation of Binge-like Ethanol Consumption by IL-10 Signaling in the Basolateral Amygdala. 基底外侧杏仁核中IL-10信号对狂饮样乙醇消耗的调节
IF 6.2 3区 医学 Q1 NEUROSCIENCES Pub Date : 2017-06-01 Epub Date: 2016-09-17 DOI: 10.1007/s11481-016-9709-2
S Alex Marshall, Kyle H McKnight, Allyson K Blose, Donald T Lysle, Todd E Thiele

Excessive ethanol consumption alters the neuroimmune system and particularly impacts the cytokine milieu of the CNS. Cytokine dysregulation has been shown to underlie addictive-like behaviors including alcohol abuse; however, many studies focus primarily on the proinflammatory cytokine profile during alcohol dependence. The current study furthers this research by determining the impact of excessive ethanol consumption on interleukin-10 (IL-10) and interleukin-4 (IL-4) activity in a model of non-dependent binge consumption called the "drinking in the dark" (DID) paradigm. Furthermore, the ability of IL-10 to modulate ethanol consumption was tested using site-directed pharmacology. Immunohistochemistry analyses determined that ethanol decreased IL-10 by 50 % in the basolateral amygdala (BLA) but had no effect on IL-4. Neither IL-10 nor IL-4, however, were altered in the central amygdala (CEA). Enzyme linked immunosorbent assays confirmed that IL-10 was decreased in the amygdala but not in the serum, suggesting changes of this cytokine with the DID paradigm are restricted to the central nervous system. Finally, bilateral infusions of IL-10 into the BLA, but not CeA, reduced binge-like drinking and corresponding blood ethanol concentrations without impacting either locomotor activity or anxiety-like behavioral correlates. Together, these data support the idea that alcohol abuse dysregulates specific anti-inflammatory cytokines; however, ameliorating alcohol-induced effects on cytokines, like IL-10, may prove to be an effective therapy in curbing excessive consumption.

过量摄入乙醇会改变神经免疫系统,尤其会影响中枢神经系统的细胞因子环境。细胞因子失调已被证明是包括酗酒在内的成瘾性行为的基础;然而,许多研究主要侧重于酒精依赖期间的促炎细胞因子谱。目前的研究通过确定过量摄入乙醇对白细胞介素-10(IL-10)和白细胞介素-4(IL-4)活性的影响,在一种被称为 "黑暗中饮酒"(DID)范例的非依赖性暴饮暴食模型中推进了这项研究。此外,还利用定点药理学测试了IL-10调节乙醇消耗的能力。免疫组化分析表明,乙醇使杏仁基底外侧(BLA)的IL-10减少了50%,但对IL-4没有影响。然而,IL-10和IL-4在杏仁核中央(CEA)均未发生变化。酶联免疫吸附试验证实,杏仁核中的IL-10减少了,但血清中的IL-4没有减少,这表明DID范式引起的这种细胞因子的变化仅限于中枢神经系统。最后,向BLA(而非CeA)双侧输注IL-10可减少狂饮和相应的血液乙醇浓度,但不会影响运动活动或焦虑行为相关性。总之,这些数据支持了酗酒会导致特定抗炎细胞因子失调的观点;然而,改善酒精对细胞因子(如 IL-10)的影响可能会被证明是抑制过度饮酒的一种有效疗法。
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引用次数: 0
Reply to Letter to the Editor 回复给编辑的信
IF 6.2 3区 医学 Q1 NEUROSCIENCES Pub Date : 2017-05-04 DOI: 10.1080/10428194.2016.1233544
Qingsheng Li, Woong-Ki Kim
We thank Sahu et al. for their comments on our paper ‘Pregnancy: part of life in chronic myelogenous leukemia.’[1] The issues highlighted in their submission are highly relevant and important to a setting where resources are constrained and optimal standards of care may be difficult to achieve. This situation is commonly encountered in developing countries where access to drugs and the ability to closely monitor disease by advanced molecular diagnostics is limited. Management of chronic myelogenous leukemia (CML) in unusual clinical situations such as pregnancy requires an individualized approach directed toward optimizing care to ensure favorable outcomes for both the parent and the fetus wherever possible. As shown in our paper, close monitoring of disease status by quantitative polymerase chain reaction (PCR)based testing and judicious use of available therapies can be used effectively to manage such patients. Although both the hydroxyurea and leukocyte apheresis are useful adjuncts to therapy in some conditions, there is little evidence to recommend these as the mainstay of management in all cases. Despite emerging data describing favorable outcomes in the fetuses of patients exposed to Imatinib and some other tyrosine kinase inhibitors (TKIs) in the early stages of pregnancy, it is important to consider that these agents were immediately withdrawn at the time pregnancy was detected thereby minimizing exposure where possible.[2–4] Adverse fetal outcomes were documented in cases where Imatinib was not discontinued early.[5] In this respect, interferon-based therapy appears to be the least likely to result in adverse maternal or fetal outcomes and can also provide some measure of disease control beyond cytoreduction alone. We recognize that there are likely to be differences in practice in resource-constrained settings and appreciate the difficulties that may be associated in managing complex issues such as pregnancy in CML, particularly in a younger patient population. This scenario effectively demonstrates the premise of our article that with the life expectancy of CML patients now being nearly the same as that of normal individuals. Efforts are necessary to ensure that pregnancy and childbirth can also be an achievable milestone without compromising disease control.
我们感谢Sahu等人对我们的论文《妊娠:慢性粒细胞白血病生活的一部分》的评论[1] 他们提交的材料中强调的问题与资源有限、可能难以达到最佳护理标准的环境高度相关和重要。这种情况在发展中国家很常见,因为发展中国家获得药物的机会和通过先进分子诊断密切监测疾病的能力有限。在妊娠等不寻常的临床情况下治疗慢性粒细胞白血病(CML)需要一种个性化的方法,旨在优化护理,以确保尽可能为父母和胎儿带来有利的结果。如我们的论文所示,通过基于定量聚合酶链式反应(PCR)的检测来密切监测疾病状态,并明智地使用可用的治疗方法,可以有效地管理这些患者。尽管羟基脲和白细胞单采在某些情况下都是有用的辅助治疗药物,但几乎没有证据表明这些药物是所有病例的主要治疗方法。尽管新出现的数据描述了在妊娠早期接触伊马替尼和其他一些酪氨酸激酶抑制剂(TKIs)的患者胎儿的良好结果,但重要的是要考虑到,在检测到妊娠时立即停用这些药物,从而尽可能减少接触。[2-4]在未提前停用伊马替尼的情况下,记录了不良的胎儿结局。[5] 在这方面,基于干扰素的治疗似乎最不可能导致不良的母体或胎儿结局,并且除了单独的细胞减少外,还可以提供一些疾病控制措施。我们认识到,在资源受限的环境中,实践中可能存在差异,并认识到在管理复杂问题(如慢性粒细胞白血病患者的妊娠)方面可能存在的困难,特别是在年轻患者群体中。这种情况有效地证明了我们文章的前提,即CML患者的预期寿命现在与正常人的预期寿命几乎相同。必须努力确保怀孕和分娩也能成为一个可实现的里程碑,而不影响疾病控制。
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引用次数: 0
A Gap in Time: Extending our Knowledge of Temporal Processing Deficits in the HIV-1 Transgenic Rat. 时间上的差距:扩展我们对HIV-1转基因大鼠时间加工缺陷的认识
IF 6.2 3区 医学 Q1 NEUROSCIENCES Pub Date : 2017-03-01 Epub Date: 2016-10-03 DOI: 10.1007/s11481-016-9711-8
Kristen A McLaurin, Landhing M Moran, Hailong Li, Rosemarie M Booze, Charles F Mactutus

Approximately 50 % of HIV-1 seropositive individuals develop HIV-1 associated neurocognitive disorders (HAND), which commonly include alterations in executive functions, such as inhibition, set shifting, and complex problem solving. Executive function deficits in HIV-1 are fairly well characterized, however, relatively few studies have explored the elemental dimensions of neurocognitive impairment in HIV-1. Deficits in temporal processing, caused by HIV-1, may underlie the symptoms of impairment in higher level cognitive processes. Translational measures of temporal processing, including cross-modal prepulse inhibition (PPI), gap-prepulse inhibition (gap-PPI), and gap threshold detection, were studied in mature (ovariectomized) female HIV-1 transgenic (Tg) rats, which express 7 of the 9 HIV-1 genes constitutively throughout development. Cross-modal PPI revealed a relative insensitivity to the manipulation of interstimulus interval (ISI) in HIV-1 Tg animals in comparison to control animals, extending previously reported temporal processing deficits in HIV-1 Tg rats to a more advanced age, suggesting the permanence of temporal processing deficits. In gap-PPI, HIV-1 Tg animals exhibited a relative insensitivity to the manipulation of ISI in comparison to control animals. In gap-threshold detection, HIV-1 Tg animals displayed a profound differential sensitivity to the manipulation of gap duration. Presence of the HIV-1 transgene was diagnosed with 91.1 % accuracy using gap threshold detection measures. Understanding the generality and permanence of temporal processing deficits in the HIV-1 Tg rat is vital to modeling neurocognitive deficits observed in HAND and provides a key target for the development of a diagnostic screening tool.

大约50%的HIV-1血清阳性个体发展为HIV-1相关的神经认知障碍(HAND),通常包括执行功能的改变,如抑制、集合转移和复杂问题解决能力。HIV-1的执行功能缺陷已经被很好地表征,然而,相对较少的研究探索了HIV-1神经认知障碍的基本维度。由HIV-1引起的时间加工缺陷可能是高级认知过程受损症状的基础。在成熟(去卵巢)雌性HIV-1转基因(Tg)大鼠中研究了时间加工的翻译措施,包括跨模态预脉冲抑制(PPI)、间隙-预脉冲抑制(gap-PPI)和间隙阈值检测,这些大鼠在整个发育过程中组成性地表达9个HIV-1基因中的7个。跨模态PPI显示,与对照动物相比,HIV-1 Tg动物对间刺激间隔(ISI)的操纵相对不敏感,将先前报道的HIV-1 Tg大鼠的时间加工缺陷延长到更大的年龄,表明时间加工缺陷是永久性的。在gap-PPI中,与对照动物相比,HIV-1 Tg动物对ISI的操纵表现出相对不敏感。在间隙阈值检测中,HIV-1 Tg动物对间隙持续时间的操纵表现出深刻的差异敏感性。使用间隙阈值检测方法诊断HIV-1转基因的准确率为91.1%。了解HIV-1 Tg大鼠时间加工缺陷的普遍性和持久性对于模拟HAND中观察到的神经认知缺陷至关重要,并为开发诊断筛查工具提供了关键目标。
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引用次数: 19
Destination Brain: the Past, Present, and Future of Therapeutic Gene Delivery 目的脑:治疗性基因传递的过去、现在和未来
IF 6.2 3区 医学 Q1 NEUROSCIENCES Pub Date : 2017-02-03 DOI: 10.1007/s11481-016-9724-3
Chaitanya Joshi, V. Labhasetwar, A. Ghorpade
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引用次数: 41
Galectin-1 Reduces Neuroinflammation via Modulation of Nitric Oxide-Arginase Signaling in HIV-1 Transfected Microglia: a Gold Nanoparticle-Galectin-1 “Nanoplex” a Possible Neurotherapeutic? 半乳糖凝集素-1通过调节一氧化氮-精氨酸酶信号减少HIV-1转染的小胶质细胞中的神经炎症:金纳米颗粒-半乳糖凝集素-1“纳米复合物”可能是神经治疗药物?
IF 6.2 3区 医学 Q1 NEUROSCIENCES Pub Date : 2016-12-27 DOI: 10.1007/s11481-016-9723-4
R. Aalinkeel, Courtney S. Mangum, E. Abou-Jaoude, J. Reynolds, Maixian Liu, K. Sundquist, Neil U. Parikh, L. Chaves, M. Mammen, S. Schwartz, S. Mahajan
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引用次数: 24
Safety and Efficacy of Anti-Amyloid-β Immunotherapy in Alzheimer’s Disease: A Systematic Review and Meta-Analysis 抗β淀粉样蛋白免疫疗法治疗阿尔茨海默病的安全性和有效性:一项系统综述和荟萃分析
IF 6.2 3区 医学 Q1 NEUROSCIENCES Pub Date : 2016-12-26 DOI: 10.1007/s11481-016-9722-5
Ross Penninkilampi, Holly M. Brothers, G. Eslick
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引用次数: 52
HIV-1 Glycoprotein 120 Enhancement of N-Methyl-D-Aspartate NMDA Receptor-Mediated Excitatory Postsynaptic Currents: Implications for HIV-1-Associated Neural Injury HIV-1糖蛋白120增强N-甲基-D-天冬氨酸NMDA受体介导的兴奋性突触后电流:对HIV-1相关神经损伤的意义
IF 6.2 3区 医学 Q1 NEUROSCIENCES Pub Date : 2016-12-22 DOI: 10.1007/s11481-016-9719-0
Yan Zhou, Jianuo Liu, H. Xiong
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引用次数: 25
Vitamin D Treatment Attenuates Neuroinflammation and Dopaminergic Neurodegeneration in an Animal Model of Parkinson’s Disease, Shifting M1 to M2 Microglia Responses 维生素D治疗减轻帕金森病动物模型中的神经炎症和多巴胺能神经变性,将M1小胶质细胞反应转移到M2
IF 6.2 3区 医学 Q1 NEUROSCIENCES Pub Date : 2016-12-16 DOI: 10.1007/s11481-016-9720-7
R. Calvello, A. Cianciulli, G. Nicolardi, F. De Nuccio, L. Giannotti, Rosaria Salvatore, C. Porro, T. Trotta, M. Panaro, D. Lofrumento
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引用次数: 4
期刊
Journal of Neuroimmune Pharmacology
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