| 1. |
- Abat, E., et al.
(författare)
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Study of the response of the ATLAS central calorimeter to pions of energies from 3 to 9 GeV
- 2009
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Ingår i: Nuclear Instruments & Methods in Physics Research. Section A: Accelerators, Spectrometers, Detectors, and Associated Equipment. - : Elsevier BV. - 0167-5087 .- 0168-9002 .- 1872-9576. ; 607:2, s. 372-386
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Tidskriftsartikel (refereegranskat)abstract
- A fully instrumented slice of the ATLAS central detector was exposed to test beams from the SPS (Super Proton Synchrotron) at CERN in 2004. in this paper, the response of the central calorimeters to pions with energies in the range between 3 and 9 GeV is presented. The linearity and the resolution of the combined calorimetry (electromagnetic and hadronic calorimeters) was measured and compared to the prediction of a detector simulation program using the toolkit Geant 4. (C) 2009 Elsevier B.V. All rights reserved.
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| 2. |
- Osorio, A., et al.
(författare)
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Evaluation of a candidate breast cancer associated SNP in ERCC4 as a risk modifier in BRCA1 and BRCA2 mutation carriers. Results from the consortium of investigators of modifiers of BRCA1/BRCA2 (CIMBA)
- 2009
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Ingår i: British Journal of Cancer. - : Nature Publishing Group. - 0007-0920 .- 1532-1827. ; 101:12, s. 2048-2054
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Tidskriftsartikel (refereegranskat)abstract
- Background: In this study we aimed to evaluate the role of a SNP in intron 1 of the ERCC4 gene (rs744154), previously reported to be associated with a reduced risk of breast cancer in the general population, as a breast cancer risk modifier in BRCA1 and BRCA2 mutation carriers. Methods: We have genotyped rs744154 in 9408 BRCA1 and 5632 BRCA2 mutation carriers from the Consortium of Investigators of Modifiers of BRCA1/2 (CIMBA) and assessed its association with breast cancer risk using a retrospective weighted cohort approach. Results: We found no evidence of association with breast cancer risk for BRCA1 (per-allele HR: 0.98, 95% CI: 0.93-1.04, P0.5) or BRCA2 (per-allele HR: 0.97, 95% CI: 0.89-1.06, P0.5) mutation carriers. Conclusion: This SNP is not a significant modifier of breast cancer risk for mutation carriers, though weak associations cannot be ruled out.
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| 3. |
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| 4. |
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| 5. |
- Dekundy, A, et al.
(författare)
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Effects of group I metabotropic glutamate receptors blockade in experimental models of Parkinson's disease
- 2006
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Ingår i: Brain Research Bulletin. - : Elsevier BV. - 0361-9230. ; 69:3, s. 318-326
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Tidskriftsartikel (refereegranskat)abstract
- The present study was devoted to investigate the effects of the metabotropic glutamate receptor(mGluR)5 antagonist [(2-methyl-1,3-thiazol-4-yl)ethynyl]pyridine (MTEP) and the mGluR1 antagonist, (3-ethyl-2-methyl-quinolin-6-yl)-(4-methoxy-cyclohexyl)-methanone methanesulfonate (EMQMCM), in animal studies indicative of antiparkinsonian-like activity such as haloperidol-induced catalepsy, hypoactivity in open field following haloperidol, and rotation in rats with unilateral 6-hydroxydopamine(OHDA)-induced lesions of the midbrain dopaminergic system (alone and in combination with L-DOPA). Moreover, antidyskinetic activity of different mGluR ligands was evaluated in the rat model of L-DOPA-induced dyskinesia. Both MTEP (5 mg/kg) and EMQMCM (4 mg/kg) slightly inhibited haloperidol (0.5 mg/kg)-induced catalepsy. However, neither substance reversed the hypoactivity produced by haloperidol (0.2 mg/kg). Although MTEP and not produce significant turning, it inhibited contralateral rotations after L-DOPA (at 5 mg/kg) and alleviated L-DOPA-induced dyskinesia (at 2.5 and 5 mg/kg) in 6-OHDA-lesioned rats. In contrast, mGluR1 antagonists EMQMCM and RS-1-aminoindan-1,5-dicarboxylic acid (AIDA) failed to modify L-DOPA-induced dyskinesia. The results of the present study suggest that either subtype of group I of mGluRs may be involved in the pathologically altered circuitry in the basal ganglia. However, the equivocal results do not strongly support the hypothesis that mGluR1 and mGluR5 antagonists may be beneficial in the symptomatic treatment of Parkinson's disease. However, mGluR5 antagonists may prove useful for the symptomatic treatment Of L-DOPA-induced dyskinesia. (c) 2006 Elsevier Inc. All rights reserved.
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| 7. |
- Schaefer, D., et al.
(författare)
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Compact X-ray microscopes for EUV- and soft X-radiation with spectral imaging capabilities
- 2006
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Ingår i: Advances in X-Ray/EUV Optics, Components, and Applications. - : SPIE. - 0819463965 ; , s. 31704-31704
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Konferensbidrag (refereegranskat)abstract
- We report on a compact full-field transmission microscope (CTXM) and a scanning transmission microscope (CST'XM) developed for imaging at laboratory scale X-ray sources. The microscopes are based on zone plates for imaging in the EUV and water window region (wavelength 2.3 nm to 4.4 mn). The radiation for the full-field microscope is generated by focusing short laser pulses with an energy of 100 mJ on a 20 gm cryogenic liquid nitrogen jet. A condenser zone plate in conjunction with an aperture is used to provide monochromatic sample illumination. This allows for easy wavelength selection within the N-2,-Emission spectrum. Thus, the presented setup offers the possibility of spectral imaging. A micro zone plate generates a magnified image detected by a back illuminated TE-cooled CCD camera (1,340 x 1,300 pixel). The actual configuration provides magnifications up to 1,000x at exposure times in a range of a few ten minutes with sub-100 nm resolution. Our compact scanning microscope (CSTXM) operates with a zone plate, focusing the radiation onto a sample which is placed on a piezo driven xy-stage with 1 nm lateral resolution. Using high-harmonic radiation at 13 nm wavelength sub-micron resolution is achieved. With light at 17 nm wavelength originating from the O-VI emission line of a laser plasma source based on an ethanol jet, 500 nm structures were imaged in less than 20 minutes resulting in an 100 x 40 pixel image.
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| 8. |
- Wilms, H., et al.
(författare)
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Suppression of Map Kinases Inhibits Microglial Activation and Attenuates Neuronal Cell Death Induced by Alpha-Synuclein Protofibrils
- 2009
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Ingår i: International Journal of Immunopathology and Pharmacology. - 0394-6320. ; 22:4, s. 897-909
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Tidskriftsartikel (refereegranskat)abstract
- alpha-Synuclein (alpha-Syn) accounts, as a major component of Lewy bodies (LB), for the filamentous deposits in many cases of neurodegenerative diseases. Yet, little is known about the molecular mechanisms of neuronal loss in these diseases. The correlation between alpha-Syn oligomerization/aggregation and pathologies raises the key question of which molecular form of alpha-Syn (i.e. monomeric alpha-Syn, protofibrils or mature fibrils) represents the damage-inducing culprit in the scenario of synucleinopathies. We show that human alpha-Syn protofibrils (PFs) are potent activators of parallel proinflammatory signalling pathways (p38 and ERK1/2 MAP kinases and NF-kappa B) in microglial cells in vitro. Furthermore, stereotactic injection of alpha-Syn PFs into the substantia nigra of adult rats leads to a profound activation of microglia and adjacent neuronal cell loss, which can be attenuated by the MAP kinase inhibitor semapimod. We propose that the neurodegenerative process of alpha-synucleinopathies involves microglial activation through alpha-Syn released or extruded from cells with pathogenic alpha-Syn metabolism. Compounds that inhibit the MAPK/NF-kappa B pathways might be a promising pharmacological strategy for the treatment of the inflammatory component of synucleinopathies including PD.
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| 9. |
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