Helen K Smith

Louisiana State University Health Sciences Center Shreveport, Shreveport, Louisiana, United States

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Publications (5)29.08 Total impact

  • Felicity Ne Gavins · Helen K Smith
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    ABSTRACT: Stem cell therapy has showed considerable potential in the treatment of stroke over the last decade. In order that these therapies may be optimized, the relative benefits of growth factor release, immunomodulation, and direct tissue replacement by therapeutic stem cells are widely under investigation. Fundamental to the progress of this research are effective imaging techniques that enable cell tracking in vivo. Direct analysis of the benefit of cell therapy includes the study of cell migration, localization, division and/or differentiation, and survival. This review explores the various imaging tools currently used in clinics and laboratories, addressing image resolution, long-term cell monitoring, imaging agents/isotopes, as well as safety and costs associated with each technique. Finally, burgeoning tracking techniques are discussed, with emphasis on multimodal imaging.Journal of Cerebral Blood Flow & Metabolism advance online publication, 13 May 2015; doi:10.1038/jcbfm.2015.93.
    Journal of cerebral blood flow and metabolism: official journal of the International Society of Cerebral Blood Flow and Metabolism 05/2015; 35(7). DOI:10.1038/jcbfm.2015.93 · 5.41 Impact Factor
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    ABSTRACT: Stroke is the third leading cause of death and the leading cause of long-term disability in North America. On average, someone in the US has a stroke every 45seconds, and worldwide, stroke claims 15 million lives each year. Therefore, reliable stroke models are vital to the production of effective new therapies for the treatment of this devastating cerebral vascular accident. Middle cerebral artery occlusion (MCAo) is considered to be the most clinically relevant surgical model of ischemic stroke, in which a variety of methods may be employed to block the MCA (the most common being through insertion of a monofilament). In this study, we have compared two different approaches that are currently used arbitrarily in various laboratories worldwide: one involving insertion of a monofilament via the common carotid artery (Koizumi et al.) and one via the external carotid artery (Longa et al.). We assessed various parameters, including: mortality rates, neurological scores, inflammation levels, cellular trafficking (using intravital microscopy) and infarct volumes in mice after using each of the two approaches. We found that the Longa method produced a greater, and robust, inflammatory response, versus the Koizumi method. In conclusion, we suggest that the Longa method is superior for the study of both short and long-term outcomes of ischemic stroke. These results have considerable implications on stroke model selection for researchers. Copyright © 2015. Published by Elsevier B.V.
    Journal of Neuroscience Methods 04/2015; 249. DOI:10.1016/j.jneumeth.2015.04.008 · 2.05 Impact Factor
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    ABSTRACT: Ischemia/reperfusion (I/R) injury following stroke can worsen patient outcome through excess inflammation. This study investigated the pharmacologic potential of targeting an endogenous anti-inflammatory circuit via formyl peptide receptor (FPR) 2/lipoxin receptor (ALX) (Fpr2/3 in mouse) in global cerebral I/R. Mice (C57BL/6 and Fpr2/3(-/-)) were subjected to bilateral common carotid artery occlusion, followed by reperfusion and treatment with FPR agonists: AnxA1Ac2-26 [Annexin A1 mimetic peptide (Ac-AMVSEFLKQAWFIENEEQEYVQTVK), 2.5 μg/kg] and 15-epimer-lipoxin A4 (15-epi-LXA4; FPR2/ALX specific, 12.5 and 100 ng/kg). Leukocyte-endothelial (L-E) interactions in the cerebral microvasculature were then quantified in vivo using intravital fluorescence microscopy. 15-epi-LXA4 administration at the start of reperfusion reduced L-E interactions after 40 min (which was sustained at 2 h with high-dose 15-epi-LXA4) to levels seen in sham-operated animals. AnxA1Ac2-26 treatment decreased leukocyte adhesion at 40 min and all L-E interactions at 2 h (up to 95%). Combined treatment with AnxA1Ac2-26 plus FPR antagonists t-Boc-FLFLF (250 ng/kg) or WRW4 (FPR2/ALX selective, 1.4 μg/kg) abrogated the effects of AnxA1Ac2-26 fully at 40 min. Antagonists were less effective at 2 h, which we demonstrate is likely because of their impact on early L-E interactions. Our findings indicate that FPR2/ALX activity elicits considerable control over vascular inflammatory responses during cerebral I/R and, therefore, provide evidence that targeting FPR2/ALX may be beneficial for patients who suffered from stroke.-Smith, H. K., Gil, C. D., Oliani, S. M., and Gavins, F. N. E. Targeting formyl peptide receptor 2 reduces leukocyte-endothelial interactions in a murine model of stroke. © FASEB.
    The FASEB Journal 02/2015; 29(5). DOI:10.1096/fj.14-263160 · 5.04 Impact Factor
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    Helen K Smith · Felicity N E Gavins
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    ABSTRACT: Substantial developments in the field of stem cell research point toward novel therapies for the treatment of diseases such as stroke. This review covers the establishment of tissue damage in stroke and the status of current therapies. We evaluate stem cell therapy with respect to other treatments, including clinical, preclinical, and failed, and provide a comprehensive account of stem cell clinical trials for stroke therapy currently underway. Finally, we describe mechanisms through which stem cells improve outcome in experimental stroke as well as potential pitfalls this basic research has identified.
    The FASEB Journal 03/2012; 26(6):2239-52. DOI:10.1096/fj.11-195719 · 5.04 Impact Factor
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    ABSTRACT: The melanocortin receptors are a subfamily of G-protein-coupled, rhodopsin-like receptors that are rapidly being acknowledged as an extremely promising target for pharmacological intervention in a variety of different inflammatory pathologies, including stroke. Stroke continues to be a leading cause of death worldwide, with risk factors including smoking, diabetes, hypertension and obesity. The pathophysiology of stroke is highly complex: reintroduction of blood flow to the infarcted brain region is paramount in limiting ischaemic damage caused by stroke, yet a concomitant inflammatory response can compound tissue damage. The possibilities of pro-resolving treatments that target this inflammatory response have only recently begun to be explored. This review discusses the endogenous roles of the melanocortin system in reducing characterized aspects of inflammation, and how these, together with potent neuroprotective actions, suggest its potential as a therapeutic target in stroke.
    Trends in Pharmacological Sciences 02/2011; 32(2):90-8. DOI:10.1016/j.tips.2010.11.010 · 11.54 Impact Factor