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| 1 | Delayed atomoxetine or fluoxetine treatment coupled with limited voluntary running promotes motor recovery in mice after ischemic stroke显示文摘Currently, there is an unmet need for treatments promoting post-stroke functional recovery.The aim of this study was to evaluate and compare the dose-dependent effect of delayed atomoxetine or fluoxetine therapy(starting on post-stroke day 5), coupled with limited physical exercise(2 hours daily voluntary wheel running;post-stroke days 9 to 42), on motor recovery of adult male mice after photothrombotic stroke.These drugs are selective norepinephrine or serotonin reuptake inhibitors indicated for disorders unrelated to stroke.The predetermined primary end-point for this study was motor function measured in two tasks of spontaneous motor behaviors in grid-walking and cylinder tests.Additionally, we quantified the running distance and speed throughout the study, the number of parvalbumin-positive neurons in the medial agranular cortex and infarct volumes.Both sensorimotor tests revealed that neither limited physical exercise nor a drug treatment alone significantly facilitated motor recovery in mice after stroke.However, combination of physical exercise with either of the drugs promoted restoration of motor function by day 42 post-stroke, with atomoxetine being a more potent drug.This was accompanied by a significant decrease in parvalbumin-positive inhibitory interneurons in the ipsilateral medial agranular cortex of mice with recovering motor function, while infarct volumes were comparable among experimental groups.If further validated in larger studies, our observations suggest that add-on atomoxetine or fluoxetine therapy coupled with limited, structured physical rehabilitation could offer therapeutic modality for stroke survivors who have difficulty to engage in early, high-intensity physiotherapy.Furthermore, in light of the recently completed Assessment o F Fluoxet INe In s Troke recover Y(AFFINITY) and Efficacy o F Fluoxetine-a randomis Ed Controlled Trial in Stroke(EFFECTS) trials, our observations call for newly designed studies where fluoxetine or atomoxetine pharmacotherapy is evaluated in combination with structured physical rehabilitation rather than alone.This study was approved by the Texas Tech University Health Sciences Center Institutional Animal Care and Use Committee(protocol # 16019). | Faisal F.Alamri Abdullah Al Shoyaib Nausheen Syeara Anisha Paul Srinidhi Jayaraman Serob T.Karamyan Thiruma V.Arumugam Vardan T.Karamyan | 2021 | Neural Regeneration Research2021，16，7： | 2 |
| 2 | Diabetes impairs hippocampal function through glucocorticoid-mediated effects on new and mature neurons显示文摘 | Alexis M S Thiruma V A Roy G C | 2008 | Nat Neurosci2008，11，： | 1 |
| 3 | TOLL-LIKE RECEPTORS IN ISCHEMIA-REPERFUSION INJURY显示文摘 | Thiruma V. Arumugam Eitan Okun Sung-Chun Tang John Thundyil Stephen M. Taylor Trent M. Woodruff | 2009 | Shock2009，，1： | 1 |
| 4 | Toll-like receptors in ischemia- reperfusion injury 显示文摘 | Thiruma VA Eitan O Sung-Chun T | 2009 | Shock2009，32，： | 1 |
| 5 | Role of T lymphocytes and interferon in ischemic stroke显示文摘 | Gokhan Yilmaz Thiruma V | 2006 | Circulation2006，113，5： | 1 |
| 6 | Neuronal oxidative stress in acute ischemic stroke: Sources and contribution to cell injury显示文摘 | Silvia Manzanero Tomislav Santro Thiruma V. Arumugam | 2012 | Neurochemistry International2012，，： | 1 |
| 7 | Rutin Attenuates Metabolic Changes, Nonalcoholic Steatohepatitis, and Cardiovascular Remodeling in High-Carbohydrate, High-Fat Diet-Fed Rats1-3显示文摘 | Panchal Sunil K Poudyal Hemant Arumugam Thiruma V Brown Lindsay | 2011 | The Journal of Nutrition2011，，6： | 1 |
| 8 | Vascular cognitive impairment and Alzheimer’s disease: role of cerebral hypoperfusion and oxidative stress显示文摘 | Hyun Kim Alyson Miller Grant Drummond Amanda Thrift Thiruma Arumugam Thanh Phan Velandai Srikanth Christopher Sobey | 2012 | Naunyn-Schmiedeberg’s Archives of Pharmacology2012，，10： | 1 |
| 9 | CD40/CD40 Ligand Signaling in Mouse Cerebral Microvasculature After Focal Ischemia/Reperfusion显示文摘 | Mami Ishikawa Thorsten Vowinkel Karen Y. Stokes Thiruma V. Arumugam Gokhan Yilmaz Anil Nanda D Neil Granger | 2005 | Circulation2005，，13： | 1 |
| 10 | Platelet-leukocyte-endothelial cell Interactions after middle cerebral artery occlusion and reperfusion arumugam显示文摘 | Ishikawa M Cooper D Thiruma V | 2004 | J Cereb Blood Flow Metab2004，24，： | 1 |
| 11 | Evidence that collaboration between HIF-1α and Notch-1 promotes neuronal cell death in ischemic stroke显示文摘 | Yi-Lin Cheng Jong-Sung Park Silvia Manzanero Yuri Choi Sang-Ha Baik Eitan Okun Mathias Gelderblom David Yang-Wei Fann Tim Magnus Bradley S. Launikonis Mark P. Mattson Christopher G. Sobey Dong-Gyu Jo Thiruma V. Arumugam | 2014 | Neurobiology of Disease2014，，： | 1 |
| 12 | Toll-like receptors in ischemia-reperfusion injury显示文摘 | Thiruma V Arumuga M Okun E | 2009 | Shock2009，32，1： | 1 |
| 13 | Neuronal oxidative stress in acute ischemic stroke: Sources and contribution to cell injury显示文摘 | Silvia Manzanero Tomislav Santro Thiruma V. Arumugam | 2012 | Neurochemistry International2012，，： | 1 |
| 14 | PLGA nanoparticles preparation by nanoprecipitation:Drug loading and release studies of a water solution drug显示文摘 | THIRUMA G SNJEZATA S | 1999 | J of Controlled Release1999，57，： | 1 |
| 15 | THE ROLE OF THE COMPLEMENT SYSTEM IN ISCHEMIA-REPERFUSION INJURY显示文摘 | Thiruma V Arumugam Ian A Shiels Trent M Woodruff D Neil Granger Stephen M Taylor | 2004 | Shock2004，，5： | 1 |
| 16 | TLR2 activation inhibits embryonic neural progenitor cell proliferation显示文摘 | EitanOkun Kathleen J.Griffioen TaeGen Son Jong‐HwanLee Nicholas J.Roberts Mohamed R.Mughal EmmetteHutchison AiwuCheng Thiruma V.Arumugam Justin D.Lathia HenrietteVan Praag Mark P.Mattson | 2010 | Journal of Neurochemistry2010，，： | 1 |
| 17 | Diabetes impairs hippocampal function through glucocorticoid-mediated effects on new and mature neurons显示文摘 | Alexis MS Thiruma VA Roy GC | | 0，，03： | 1 |
| 18 | PLGA nanoparticles preparation by nanoprecipitation:drug loading an d release studies of a water solution drug显示文摘 | Thiruma G Snjezata S | 1999 | J Controll Release1999，57，： | 1 |
| 19 | γ分泌酶介导的Notch信号传递加重缺血性卒中后的脑损伤和功能障碍显示文摘反义Notch基因转基因小鼠和用Notch激活酶-分泌酶抑制剂处理的正常小鼠实验显示在局灶性缺血性卒中模型中脑细胞损伤减小和功能改善。Notch基因通过调节凋亡易感性信号通路、激活小胶质细胞和刺激前炎性淋巴细胞浸润使神经元损伤危险增加。这些发现表明Notch信号通路对于卒中和相关神经变性疾病治疗提供了可能的治疗靶点。 | Thiruma V Arumugam Sic L Chan Dong-Gyu Jol 徐蔚海(编译) | 2006 | 国际内科双语杂志(中英文)2006，6，8： | 0 |
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