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Search Results: 1 - 10 of 332415 matches for " Hans S. Keirstead "
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Ascending central canal dilation and progressive ependymal disruption in a contusion model of rodent chronic spinal cord injury
Milan Radojicic, Gabriel Nistor, Hans S Keirstead
BMC Neurology , 2007, DOI: 10.1186/1471-2377-7-30
Abstract: Adult female Sprague-Dawley rats were anesthetized laminectomized at T10 and received spinal cord contusion injuries with a force of 250 kilodynes using an Infinite Horizon Impactor. Animals were randomly distributed into 5 groups and killed 1 (n = 4), 28 (n = 4), 120 (n = 4), 450 (n = 5), or 540 (n = 5) days after injury. Morphometric and immunohistochemical studies were then performed on 1 mm block sections, 6 mm cranial and 6 mm caudal to the lesion epicenter. The SPSS 11.5 t test was used to determine differences between quantitative measures.Here, we document the first report of an ascending central canal dilation and progressive ependymal disruption cranial to the epicenter of injury in a contusion model of chronic SCI, which was characterized by extensive dural fibrosis and intraparenchymal cystic cavitation. Expansion of the central canal lumen beyond a critical diameter corresponded with ependymal cell ciliary loss, an empirically predictable thinning of the ependymal region, and a decrease in cell proliferation in the ependymal region. Large, aneurysmal dilations of the central canal were accompanied by disruptions in the ependymal layer, periependymal edema and gliosis, and destruction of the adjacent neuropil.Cells of the ependymal region play an important role in CSF homeostasis, cellular signaling and wound repair in the spinal cord. The possible effects of this ascending pathology on ependymal function are discussed. Our studies suggest central canal dilation and ependymal region disruption as steps in the pathogenesis of chronic SCI, identify central canal dilation as a marker of chronic SCI and provide novel targets for therapeutic intervention.By the end of the next decade, 300,000 people will be living with chronic spinal cord injury in the US alone [1]. Advances in medical and rehabilitative care have improved survival rates for these individuals, but many experience clinical decline even years after the initial injury. Clinical decline is often
Immunological Demyelination Triggers Macrophage/Microglial Cells Activation without Inducing Astrogliosis
Frank Cloutier,Ilse Sears-Kraxberger,Krista Keachie,Hans S. Keirstead
Journal of Immunology Research , 2013, DOI: 10.1155/2013/812456
Abstract: The glial scar formed by reactive astrocytes and axon growth inhibitors associated with myelin play important roles in the failure of axonal regeneration following central nervous system (CNS) injury. Our laboratory has previously demonstrated that immunological demyelination of the CNS facilitates regeneration of severed axons following spinal cord injury. In the present study, we evaluate whether immunological demyelination is accompanied with astrogliosis. We compared the astrogliosis and macrophage/microglial cell responses 7 days after either immunological demyelination or a stab injury to the dorsal funiculus. Both lesions induced a strong activated macrophage/microglial cells response which was significantly higher within regions of immunological demyelination. However, immunological demyelination regions were not accompanied by astrogliosis compared to stab injury that induced astrogliosis which extended several millimeters above and below the lesions, evidenced by astroglial hypertrophy, formation of a glial scar, and upregulation of intermediate filaments glial fibrillary acidic protein (GFAP). Moreover, a stab or a hemisection lesion directly within immunological demyelination regions did not induced astrogliosis within the immunological demyelination region. These results suggest that immunological demyelination creates a unique environment in which astrocytes do not form a glial scar and provides a unique model to understand the putative interaction between astrocytes and activated macrophage/microglial cells. 1. Introduction Myelin represents a nonpermissive substrate for neuronal adhesion, sprouting, and neurite growth [1, 2], and several myelin-associated inhibitor proteins have been identified including the myelin-associated glycoprotein (MAG) [3, 4], oligodendrocyte myelin glycoprotein (OMgp) [5, 6] and Nogo-A [7–9]. Since then, numerous studies have been dedicated to understand the mechanisms underlying the action of these inhibitory molecules [10–12]. Previous studies in our laboratory and others have used immunological demyelination to address myelin-associated inhibition and provide a permissive environment for axonal regeneration. Immunological demyelination involves the intraspinal injection of antibodies to galactocerebroside (GalC), the major sphingolipid in myelin, plus complement proteins, and results in a well-defined region of complete demyelination that spares oligodendrocytes. This treatment paradigm has been shown to promote axonal regeneration following spinal cord injury in embryonic chicks [13], hatchling chicks [14],
Human Motor Neuron Progenitor Transplantation Leads to Endogenous Neuronal Sparing in 3 Models of Motor Neuron Loss
Tanya J. Wyatt,Sharyn L. Rossi,Monica M. Siegenthaler,Jennifer Frame,Rockelle Robles,Gabriel Nistor,Hans S. Keirstead
Stem Cells International , 2011, DOI: 10.4061/2011/207230
Abstract: Motor neuron loss is characteristic of many neurodegenerative disorders and results in rapid loss of muscle control, paralysis, and eventual death in severe cases. In order to investigate the neurotrophic effects of a motor neuron lineage graft, we transplanted human embryonic stem cell-derived motor neuron progenitors (hMNPs) and examined their histopathological effect in three animal models of motor neuron loss. Specifically, we transplanted hMNPs into rodent models of SMA (Δ7SMN), ALS (SOD1 G93A), and spinal cord injury (SCI). The transplanted cells survived and differentiated in all models. In addition, we have also found that hMNPs secrete physiologically active growth factors in vivo, including NGF and NT-3, which significantly enhanced the number of spared endogenous neurons in all three animal models. The ability to maintain dying motor neurons by delivering motor neuron-specific neurotrophic support represents a powerful treatment strategy for diseases characterized by motor neuron loss. 1. Introduction Human embryonic stem cells (hESCs) can differentiate into any cell type, are amenable to genetic manipulation, and readily self-renew in vitro. Directed differentiation of hESCs into high purity populations of a defined cell type can be used to design effective treatments that are both cell and site specific. Stem cell-based transplantation is an inherently combinatorial therapeutic approach, in that it not only replaces dead or dying cells, but also provides a substrate for endogenous growth, bridges gaps where tissue is lost to injury or disease, and provides neurotrophic support for the endogenous environment. Amyotrophic lateral sclerosis (ALS), spinal muscular atrophy (SMA), and spinal cord injury (SCI) are all diseases of motor neuron loss that could potentially benefit from transplantation of hESC-derived cells. ALS is the most common form of motor neuron disease [1] and can be either sporadic or familial [2–5]. Approximately 5–10% of those diagnosed have a positive family history of the disease [1, 6]. Although the etiology of the sporadic form of ALS is largely unknown [5], the familial form has a strong genetic linkage to point mutations in either TAR DNA-binding protein 43 (TDP-43), FUS/TLS, or the Cu/Zn superoxide dismutase 1 (SOD1) genes [7]. The average age of onset is between 40 and 60 years, and the disease is generally fatal within 1–5 years of onset [1, 6]. SMA is also characterized by motor neuron loss and is the leading genetic cause of infantile death [8, 9]. The disease manifests by roughly 6 months of age in the most
Equivalence of Conventionally-Derived and Parthenote-Derived Human Embryonic Stem Cells
Julie V. Harness,Nikolay A. Turovets,Magdalene J. Seiler,Gabriel Nistor,Gulsah Altun,Larissa S. Agapova,David Ferguson,Louise C. Laurent,Jeanne F. Loring,Hans S. Keirstead
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0014499
Abstract: As human embryonic stem cell (hESC) lines can be derived via multiple means, it is important to determine particular characteristics of individual lines that may dictate the applications to which they are best suited. The objective of this work was to determine points of equivalence and differences between conventionally-derived hESC and parthenote-derived hESC lines (phESC) in the undifferentiated state and during neural differentiation.
Histological and Functional Benefit Following Transplantation of Motor Neuron Progenitors to the Injured Rat Spinal Cord
Sharyn L. Rossi,Gabriel Nistor,Tanya Wyatt,Hong Zhen Yin,Aleksandra J. Poole,John H. Weiss,Matthew J. Gardener,Sipke Dijkstra,David F. Fischer,Hans S. Keirstead
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0011852
Abstract: Motor neuron loss is characteristic of cervical spinal cord injury (SCI) and contributes to functional deficit.
Derivation of High Purity Neuronal Progenitors from Human Embryonic Stem Cells
Gabriel Nistor, Monica M. Siegenthaler, Stephane N. Poirier, Sharyn Rossi, Aleksandra J. Poole, Maura E. Charlton, John D. McNeish, Chris N. Airriess, Hans S. Keirstead
PLOS ONE , 2011, DOI: 10.1371/journal.pone.0020692
Abstract: The availability of human neuronal progenitors (hNPs) in high purity would greatly facilitate neuronal drug discovery and developmental studies, as well as cell replacement strategies for neurodegenerative diseases and conditions, such as spinal cord injury, stroke, Parkinson's disease, Alzheimer's disease, and Huntington's disease. Here we describe for the first time a method for producing hNPs in large quantity and high purity from human embryonic stem cells (hESCs) in feeder-free conditions, without the use of exogenous noggin, sonic hedgehog or analogs, rendering the process clinically compliant. The resulting population displays characteristic neuronal-specific markers. When allowed to spontaneously differentiate into neuronal subtypes in vitro, cholinergic, serotonergic, dopaminergic and/or noradrenergic, and medium spiny striatal neurons were observed. When transplanted into the injured spinal cord the hNPs survived, integrated into host tissue, and matured into a variety of neuronal subtypes. Our method of deriving neuronal progenitors from hESCs renders the process amenable to therapeutic and commercial use.
Towards universal systems for recombinant gene expression
Hans S?rensen
Microbial Cell Factories , 2010, DOI: 10.1186/1475-2859-9-27
Abstract: Escherichia coli was the first host to be used for recombinant gene expression almost 40 years ago [1]. Within the past 15 years, Pichia pastoris has successfully entered the scene and is now the second most-used host for recombinant gene expression. Based on searches of the PubMed citation database, the use of P. pastoris as an expression host has increased from 4% to 17% of the total recombinant genes reported on from 1995 to 2009 (Fig. 1). Within the same time period, the usage of E. coli as an expression host remained constant, with approximately 60% of the recombinant genes reported on in journals indexed in PubMed being expressed in E. coli. Similar trends prevailed when analyzing publications in the journal Microbial Cell Factories during the period from 2005 to 2009 (Fig. 1). Several other expression systems are widely used, but to a lesser extent than E. coli and P. pastoris. So, why are E. coli and P. pastoris particularly suited for recombinant gene expression?Protein produced from a recombinant gene in E. coli as a soluble and functional product with high yield is the ideal situation for most research and industrial protein production purposes [2-4]. However, this situation is far from realistic for all recombinant gene products. In particular, proteins derived from eukaryotes are prone to inclusion body formation and low yields. This outcome can be explained by the fact that the rate of gene translation in E. coli is 4- to 10-fold higher than in eukaryotes [5]. Correct formation of disulfide bonds, protein folding, and protein function must be carefully assessed both when the proteins have been recombinantly produced in E. coli in a soluble form, when they have been refolded in vitro, or obtained from any other source [6]. Further, E. coli should not be used as the expression system if posttranslational modifications (PTMs) are of importance for the study or purpose of the protein because these microbes are unable to incorporate PTMs, including N-linked
Analysis of Motion in Single-Point Mooring Systems
Hans R. S?rheim
Modeling, Identification and Control , 1980, DOI: 10.4173/mic.1980.3.2
Abstract: A mathematical model of the slow motions of ships in single-point moorings is described. The model is used for analysis of stability of equilibrium positions. An analytical criterion for stability relating main system parameters is derived under simplifying assumptions. A numerical example with a 100 000 dwt tanker showed that the effect of wind and current are of equal importance with respect to system stability, and astern propulsion is generally required to avoid stable oscillations. Stability problems in waves have not been found. The effects of time varying excitations are discussed and illustrated by simulation.
The work environment, critical incidents, debriefing and psychological functioning—a study of trade union members in Sweden
Hans Peter S?ndergaard
SJWEH Supplements , 2008,
Abstract: OBJECTIVES: This study explored the associations between critical incidents, the psychosocial work environment, debriefing, and poor psychological health, including posttraumatic stress disorder (PTSD), among shop attendants. METHODS: Questionnaires were administered to members of the Swedish trade union and to persons who had had brief treatment after a robbery. RESULTS: Of the respondents, 6.6% reported robbery in their workplace. Those who were repeatedly exposed to robberies and scored above the cut-off for PTSD comprised 14.2–16.4% of the total number of PTSD cases. The workers exposed to a robbery felt less safe at work, without differing from others regarding other measures of psychosocial factors, namely, social support, influence, and job strain. The participants with PTSD reported significantly worse social support at work, but did not differ as to influence or demand–control. Debriefing (yes, no) had no statistical relationship with the prevalence of PTSD among robbery victims, but, in the whole group, including other traumatic events, debriefing showed a weak, albeit significant association with self-rated psychological function. The debriefed (after any negative work- or nonwork-related event) participants did not differ as regards symptoms of PTSD, but they reported less depression and better psychological functioning, even after adjustment for social support at work. A long sick leave after a robbery was associated with poor support from managers and colleagues. CONCLUSIONS: Social support, including support from managers, was associated with few symptoms, good psychological function, and shorter sick leave. People with PTSD have poorer general work conditions and social support, but similar influence or demand–control at work.
Open access publishing: a girder in the success of the Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine
Hans Lossius, Kjetil S?reide
Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine , 2011, DOI: 10.1186/1757-7241-19-7
Abstract: SJTREM converted into open access (OA) online publishing in July 2008 [2]. The decision was based on the importance of making research accessible for all, regardless of financial status or capabilities. This conversion resulted in a substantial rise in submissions, and not least citations. In line with the visions of saving more lives, the Norwegian Air Ambulance Foundation and the Laerdal Foundation for Acute Medicine have supported SJTREM by covering the article processing charges for the first and critical 2 years of establishing an independent scientific, open access journal of trauma, resuscitation and emergency medicine [3-5].The OA conversion was timely. Scandinavian research founders have for the last two years been steadily moving from a supportive attitude for the OA principles, to making policy decisions that have a direct guidance to authors to publish OA. The Norwegian Research Council declared in 2009 that all public founded research should be published OA [6], and in Denmark the Open Access Committee has, on behalf of the Ministry of Science, Technology and Innovation, made clear recommendations for OA publishing [7]. But the most significant step till now was the decision of the Swedish Research Council and other major Swedish research founders to include an OA mandate for all its research grants from 2010 [8-10]. In line with this, universities in Scandinavia are moving towards OA publishing, and national libraries are following closely. Chalmers University of Technology was in 2010 the first Swedish university to take a strong Open Access mandate [11], and there is probably just a question of time before this is the common policy within most Scandinavian Universities.The Scandinavian move is part of the wider global picture where mandates and funding mechanisms, constituting the equivalent of library budgets at many universities, are springing into life. With the support of European Commission, OA are evolving all over Europe http://www.openaire.eu
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