| 1. |
- Bereczky-Veress, Biborka, et al.
(författare)
-
Host strain-dependent difference in susceptibility in a rat model of herpes simplex type 1 encephalitis.
- 2008
-
Ingår i: Journal of neurovirology. - : Springer Science and Business Media LLC. - 1538-2443 .- 1355-0284. ; 14:2, s. 102-18
-
Tidskriftsartikel (refereegranskat)abstract
- Herpes simplex encephalitis (HSE) is characterized by severe focal brain inflammation leading to substantial loss of nervous tissue. The authors established a model of Herpes simplex virus type 1 (HSV)-1-induced acute encephalitis in the rat by injecting into the whiskers' area a virus strain isolated from a fatal human HSE case. The model might resemble natural propagation of HSV-1 in humans; spreading from the mouth and lips via the trigeminal nerve to trigeminal ganglia and subsequently entering the central nervous system (CNS). HSV-1 infected Dark Agouti (DA) rats developed a well-synchronized disease and died 5 days after inoculation. HSV-1 detection by quantitative polymerase chain reaction (qPCR), virus isolation and immunohistochemistry, magnetic resonance imaging, and histopathological examination verified dramatic encephalitis mainly in the brainstem, but also in the olfactory bulb and other segments of the brain of diseased rats. In contrast, Piebald Virol Glaxo (PVG) rats were completely resistant to disease, displaying a more rapid clearance of peripheral infection and no evidence of virus entering into neither the trigeminal ganglia nor the CNS. These results suggest a regulation of susceptibility to HSV-1-induced encephalitis at the level of peripheral infection and subsequent neuronal uptake/transport of the virus. This provides a basis for future positioning of genetic polymorphisms regulating HSE and for dissection of important pathogenetic mechanisms of this severe human disease.
|
|
| 2. |
- Blomdell, Anders, et al.
(författare)
-
Extending an Industrial Robot Controller-Implementation and Applications of a Fast Open Sensor Interface
- 2005
-
Ingår i: IEEE Robotics & Automation Magazine. - 1070-9932. ; 12:3, s. 85-94
-
Tidskriftsartikel (refereegranskat)abstract
- Many promising robotics research results were obtained during the late 1970s and early 1980s. Some examples include Cartesian force control and advanced motion planning. Now, 20 years and many research projects later, many technologies still have not reached industrial usage. An important question to consider is how this situation can be improved for future deployment of necessary technologies. Today, modern robot control systems used in industry provide highly optimized motion control that works well in a variety of standard applications. To this end, computationally intensive, model-based robot motion control techniques have become standard during the last decade. While the principles employed have been known for many years, deployment in products required affordable computing power, efficientengineering tools, customer needs for productivity/performance, and improved end-user competence in the utilization of performance features. However, applications that are considered nonstandard today motivate a variety of research efforts and system development to package results in a usable form. Actually, robots are not useful for many manufacturing tasks today, in particular those found in small and medium enterprises (SMEs). Reasonsinclude complex configuration, nonintuitive (for the shop floor) programming, and difficulties instructing robots to deal with variations in their environment. The latter challenge includes both task definitions and definition of motion control utilizing external sensors. The key word here is flexibility, and flexible motion control is particularly difficult since the user or system integrator needs to influence the core real-time software functions that are critical for the performance and safe operation of the system. We must find techniques that permit real-time motion controllers to be extended for new, demanding application areas.
|
|
| 3. |
- Andler, Sten F., et al.
(författare)
-
Information Fusion from Databases, Sensors and Simulations : A Collaborative Research Program
- 2005
-
Ingår i: Proceedings. - : IEEE Computer Society. - 0769523064 ; , s. 234-241
-
Konferensbidrag (refereegranskat)abstract
- This paper provides an overview of a collaborative research program in information fusion from databases, sensors and simulations. Information fusion entails the combination of data from multiple sources, to generate information that cannot be derived from the individual sources. This area is of strategic importance for industry and defense, as well as public administration areas such as health care, and needs to be pursued as an academic subject. A large number of industrial partners are supporting and participating in the development of the area. The paper describes the program’s general approach and main research areas, with a particular focus on the role of information fusion in systems development
|
|
| 4. |
- Björk, Per, et al.
(författare)
-
Identification of human S100A9 as a novel target for treatment of autoimmune disease via binding to quinoline-3-carboxamides.
- 2009
-
Ingår i: PLoS Biology. - : Public Library of Science (PLoS). - 1545-7885. ; 7:4, s. 800-812
-
Tidskriftsartikel (refereegranskat)abstract
- Despite more than 25 years of research, the molecular targets of quinoline-3-carboxamides have been elusive although these compounds are currently in Phase II and III development for treatment of autoimmune/inflammatory diseases in humans. Using photoaffinity cross-linking of a radioactively labelled quinoline-3-carboxamide compound, we could determine a direct association between human S100A9 and quinoline-3-carboxamides. This interaction was strictly dependent on both Zn++ and Ca++. We also show that S100A9 in the presence of Zn++ and Ca++ is an efficient ligand of receptor for advanced glycation end products (RAGE) and also an endogenous Toll ligand in that it shows a highly specific interaction with TLR4/MD2. Both these interactions are inhibited by quinoline-3-carboxamides. A clear structure-activity relationship (SAR) emerged with regard to the binding of quinoline-3-carboxamides to S100A9, as well as these compounds potency to inhibit interactions with RAGE or TLR4/MD2. The same SAR was observed when the compound's ability to inhibit acute experimental autoimmune encephalomyelitis in mice in vivo was analysed. Quinoline-3-carboxamides would also inhibit TNFalpha release in a S100A9-dependent model in vivo, as would antibodies raised against the quinoline-3-carboxamide-binding domain of S100A9. Thus, S100A9 appears to be a focal molecule in the control of autoimmune disease via its interactions with proinflammatory mediators. The specific binding of quinoline-3-carboxamides to S100A9 explains the immunomodulatory activity of this class of compounds and defines S100A9 as a novel target for treatment of human autoimmune diseases.
|
|
| 5. |
- Boström, Gustav, et al.
(författare)
-
Quality of Service Evaluation in Virtual Organizations Using SLAs
- 2006. - 1
-
Ingår i: 1st International Workshop on Interoperability Solutions to Trust, Security, Policies and QoS for Enhanced Enterprise Systems (IS-TSPQ 2006).
-
Konferensbidrag (refereegranskat)abstract
- Cooperating in Virtual organizations requires trust between the constituting organizations. SLA contracts are put in place in order to specify the quality of service of services offered. For these contracts to be effective they also need to be monitored effectively. In a Service Oriented Architecture this often means monitoring Web service invocations and evaluating if the service fulfills the obligations in its SLA. In this paper we present an implementation of a rule engine based SLA Evaluator specifically designed for the needs of a virtual organization. The evaluator fits in the context of a virtual organization through the use of open XML-based standards and a loosely coupled, event-driven architecture.
|
|
| 6. |
|
|
| 7. |
- Covacu, Ruxandra, et al.
(författare)
-
Nitric oxide exposure diverts neural stem cell fate from neurogenesis towards astrogliogenesis
- 2006
-
Ingår i: Stem Cells. - : Oxford University Press (OUP). - 1066-5099 .- 1549-4918. ; 178, s. 268-268
-
Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- Regeneration of cells in the central nervous system is a process that might be affected during neurological disease and trauma. Because nitric oxide (NO) and its derivatives are powerful mediators in the inflammatory cascade, we have investigated the effects of pathophysiological concentrations of NO on neurogenesis, gliogenesis, and the expression of proneural genes in primary adult neural stem cell cultures. After exposure to NO, neurogenesis was downregulated, and this corresponded to decreased expression of the proneural gene neurogenin-2 and beta-III-tubulin. The decreased ability to generate neurons was also found to be transmitted to the progeny of the cells. NO exposure was instead beneficial for astroglial differentiation, which was confirmed by increased activation of the Janus tyrosine kinase/signal transducer and activator of transcription transduction pathway. Our findings reveal a new role for NO during neuroinflammatory conditions, whereby its proastroglial fate-determining effect on neural stem cells might directly influence the neuroregenerative process.
|
|
| 8. |
- Danilov, Alexandre, et al.
(författare)
-
Neurogenesis in the adult spinal cord in an experimental model of multiple sclerosis
- 2006
-
Ingår i: European Journal of Neuroscience. - : Wiley. - 1460-9568 .- 0953-816X. ; 23:2, s. 394-400
-
Tidskriftsartikel (refereegranskat)abstract
- Multiple sclerosis is an inflammatory disease of the central nervous system characterized by inflammation, demyelination, axonal degeneration and accumulation of neurological disability. Previously, we demonstrated that stem cells constitute a possible endogenous source for remyelination. We now addressed the question of whether neurogenesis can occur in neuroinflammatory lesions. We demonstrated that, in experimental autoimmune encephalomyelitis, induced in rats 1,1'-dioctadecyl-6,6'-di(4sulphopentyl)-3,3,3',3'tetramethylindocarbocyani n(DiI)-labelled ependymal cells not only proliferated but descendants migrated to the area of neuroinflammation and differentiated into cells expressing the neuronal markers beta-III-tubulin and NeuN. Furthermore, these cells were immunoreactive for bromodeoxyuridine and PCNA, markers for cells undergoing cell proliferation. Using the whole-cell patch-clamp technique on freshly isolated 1, DiI-labelled cells from spinal cord lesions we demonstrated the ability of these cells to fire overshooting action potentials similar to those of immature neurones. We thus provide the first evidence for the initiation of neurogenesis in neuroinflammatory lesions in the adult spinal cord.
|
|
| 9. |
- Deierborg Olsson, Tomas, et al.
(författare)
-
Overexpression of UCP2 protects thalamic neurons following global ischemia in the mouse.
- 2008
-
Ingår i: Journal of Cerebral Blood Flow and Metabolism. - : SAGE Publications. - 1559-7016 .- 0271-678X. ; 28, s. 1186-1195
-
Tidskriftsartikel (refereegranskat)abstract
- Uncoupling protein 2 (UCP2) is upregulated in the brain after sublethal ischemia, and overexpression of UCP2 is neuroprotective in several models of neurodegenerative disease. We investigated if increased levels of UCP2 diminished neuronal damage after global brain ischemia by subjecting mice overexpressing UCP2 (UCP2/3tg) and wild-type littermates (wt) to a 12-min global ischemia. The histopathological outcome in the cortex, hippocampus, striatum, and thalamus was evaluated at 4 days of recovery, allowing maturation of the selective neuronal death. Global ischemia led to extensive cell death in the striatum, thalamus, and in the CA1 and CA2, and less-pronounced cell death in the CA3 and dentate gyrus (DG) hippocampal subfields. Histologic damage was significantly lower in the ventral posterolateral VPL and medial VPM thalamic nuclei in UCP2/3tg animals compared with wt. These thalamic regions showed a larger increase in UCP2 expression in UCP2/3tg compared with wt animals relative to the nonprotected DG. In the other regions studied, the histologic damage was lower or equal in UCP2/3tg animals compared with wt. Consequently, neuroprotection in the thalamus correlated with a high expression of UCP2, which is neuroprotective in a number of models of neurodegenerative diseases.Journal of Cerebral Blood Flow & Metabolism advance online publication, 27 February 2008; doi:10.1038/jcbfm.2008.8.
|
|
| 10. |
|
|
