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- R. Feifel, K. Ueda, A. De Fanis, K. Okada, S. Tanimoto, T. Furuta, H. Shindo, M. Kitajima, H. Tanaka, O. Björneholm, L. Karlsson, S. Svensson and S. L. Sorensen
(author)
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Probing doubly excited ionic states of N2+ via a triple excitation above the N1s threshold in the N2 moecule
- 2003
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In: Phys. Rev.. ; A:67, s. 32504-
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Journal article (peer-reviewed)
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| 2. |
- Feifel, R, et al.
(author)
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Probing doubly excited ionic states of N-2(+) via a triple excitation above the N 1s threshold in the N-2 molecule
- 2003
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In: Physical Review A (Atomic, Molecular and Optical Physics). - 1050-2947. ; 67:3: 032504
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Journal article (peer-reviewed)abstract
- Angle-resolved resonant Auger-electron spectroscopy has been carried out on the nitrogen molecule at selected photon energies around 419 eV, where a 1s core electron and two valence electrons are promoted into the lowest unoccupied molecular orbital 1pi(g). Significant enhancement of a specific band, which cannot be disentangled in direct photoionization, is observed at a binding energy of 37.6 eV, with a value of the anisotropy parameter beta much smaller than 2. We assign this new band to the transition to a doubly excited cationic state of N-2, in which two of the excited valence electrons remain in the 1pi(g) orbital, proposing a "double spectator" type decay mechanism. This observation shows how to preferentially probe multiply excited configurations of cations using multiple resonant excitation.
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| 3. |
- Bujakowska, Kinga, et al.
(author)
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Study of Gene-Targeted Mouse Models of Splicing Factor Gene Prpf31 Implicated in Human Autosomal Dominant Retinitis Pigmentosa (RP)
- 2009
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In: Investigative Ophthalmology & Visual Science. - : Association for Research in Vision and Ophthalmology (ARVO). - 1552-5783. ; 50:12, s. 5927-5933
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Journal article (peer-reviewed)abstract
- PURPOSE. Pre-mRNA processing factor 31 (PRPF31) is a ubiquitous protein needed for the assembly of the pre-mRNA splicing machinery. It has been shown that mutations in this gene cause autosomal dominant retinitis pigmentosa 11 (RP11), which is characterized by rod-cell degeneration. Interestingly, mutations in this ubiquitously expressed gene do not lead to phenotypes other than retinal malfunction. Furthermore, the dominant inheritance pattern has shown incomplete penetrance, which poses interesting questions about the disease mechanism of RP11. METHODS. To characterize PRPF31 function in the rod cells, two animal models have been generated. One was a heterozygous knock-in mouse (Prpf31(A216P/+)) carrying a point mutation p.A216P, which has previously been identified in RP11 patients. The second was a heterozygous knockout mouse (Prpf31(+/-)). Retinal degeneration in RP11 mouse models was monitored by electroretinography and histology. RESULTS. Generation of the mouse models is presented, as are results of ERGs and retinal morphology. No degenerative phenotype on fundus examination was found in Prpf31(A216P/+) and Prpf31(+/-) mice. Prpf31(A216P/A216P) and Prpf31(-/-) genotypes were embryonic lethal. CONCLUSIONS. The results imply that Prpf31 is necessary for survival, and there is no compensation mechanism in mouse for the lack of this splicing factor. The authors suggest that p.A216P mutation in Prpf31 does not exert a dominant negative effect and that one Prpf31 wild-type allele is sufficient for maintenance of the healthy retina in mice.
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| 4. |
- Sahaboglu, A, et al.
(author)
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Knockout of PARG110 confers resistance to cGMP-induced toxicity in mammalian photoreceptors.
- 2014
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In: Cell Death & Disease. - : Springer Science and Business Media LLC. - 2041-4889. ; 5:May 22
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Journal article (peer-reviewed)abstract
- Hereditary retinal degeneration (RD) relates to a heterogeneous group of blinding human diseases in which the light sensitive neurons of the retina, the photoreceptors, die. RD is currently untreatable and the underlying cellular mechanisms remain poorly understood. However, the activity of the enzyme poly-ADP-ribose polymerase-1 (PARP1) and excessive generation of poly-ADP-ribose (PAR) polymers in photoreceptor nuclei have been shown to be causally involved in RD. The activity of PARP1 is to a large extent governed by its functional antagonist, poly-ADP-glycohydrolase (PARG), which thus also may have a role in RD. To investigate this, we analyzed PARG expression in the retina of wild-type (wt) mice and in the rd1 mouse model for human RD, and detected increased PARG protein in a subset of degenerating rd1 photoreceptors. Knockout (KO) animals lacking the 110 kDa nuclear PARG isoform were furthermore analyzed, and their retinal morphology and function were indistinguishable from wild-type animals. Organotypic wt retinal explants can be experimentally treated to induce rd1-like photoreceptor death, but PARG110 KO retinal explants were unexpectedly highly resistant to such treatment. The resistance was associated with decreased PAR accumulation and low PARP activity, indicating that PARG110 may positively regulate PARP1, an event that therefore is absent in PARG110 KO tissue. Our study demonstrates a causal involvement of PARG110 in the process of photoreceptor degeneration. Contrasting its anticipated role as a functional antagonist, absence of PARG110 correlated with low PARP activity, suggesting that PARG110 and PARP1 act in a positive feedback loop, which is especially active under pathologic conditions. This in turn highlights both PARG110 and PARP1 as potential targets for neuroprotective treatments for RD.
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| 5. |
- Ueda, K, et al.
(author)
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Nuclear motion and symmetry breaking of the B 1s-excited BF3 molecule
- 2003
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In: Chemical Physics. - 0301-0104. ; 289:1, s. 135-147
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Journal article (peer-reviewed)abstract
- Out-of-plane nuclear motion stimulated in the core-excited state and symmetry breaking due to this nuclear motion have been investigated for B Is excitation in the BF3 molecule by a combination of three different experimental methods: angle-resolved ion-yield spectroscopy, vibrationally resolved resonant Auger electron spectroscopy and quadruple-ion coincidence momentum-imaging technique. (C) 2002 Elsevier Science B.V. All rights reserved.
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| 7. |
- Yurganov, L.N., et al.
(author)
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A Quantitative Assessment of the 1998 Carbon Monoxide Emission Anomaly in the Northern Hemisphere Based on Total Column and Surface Concentration Measurements
- 2004
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In: Journal of Geophysical Research. - 0148-0227 .- 2156-2202. ; 109:15, s. D15305-
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Journal article (peer-reviewed)abstract
- Carbon monoxide abundances in the atmosphere have been measured between January 1996 and December 2001 in the high Northern Hemisphere (HNH) (30degrees-90degreesN) using two different approaches: total column amounts of CO retrieved from infrared solar spectra and CO mixing ratios measured in situ at ground-based stations. The data were averaged, and anomalies of the CO HNH burden ( deviations of the total tropospheric mass between 30degreesN and 90degreesN from the mean seasonal profile, determined as the 5 year average) were analyzed. The anomalies obtained from in situ and total column data agree well and both show two maxima, by far the largest in October 1998 and a lower one in August 1996. A noticeable decrease of the positive 1998 summer anomaly with increasing height was found. A box model was applied, and anomalies in source rates were obtained under the assumption of insignificant interannual sink variations. In August 1998 the HNH emission anomaly was estimated to be 38 Tg month(-1). The annual 1998 emission positive anomaly was 96 Tg yr(-1). Nearly all excess CO may be attributed to the emissions from boreal forest fires. According to available inventories, biomass burning emits around 52 Tg yr(-1) during the "normal'' years; therefore total biomass emissions in 1998 were as large as 148 Tg yr(-1). In August 1998, CO contribution from the biomass burning was twice as large as that from fossil fuel combustion. The results were compared to available emission inventories.
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