| 1. |
- Yurganov, L.N., et al.
(författare)
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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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Ingår i: Journal of Geophysical Research. - 0148-0227 .- 2156-2202. ; 109:15, s. D15305-
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Tidskriftsartikel (refereegranskat)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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| 2. |
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| 3. |
- Kuznetsov, A. Y., et al.
(författare)
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Dynamic annealing in ion implanted SiC : Flux versus temperature dependence
- 2003
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Ingår i: Journal of Applied Physics. - : AIP Publishing. - 0021-8979 .- 1089-7550. ; 94:11, s. 7112-7115
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Tidskriftsartikel (refereegranskat)abstract
- A strong influence of ion implantation flux on the accumulation of radiation damage, the so-called dose rate effect, is observed and systematically studied in SiC. 100 keV Si+ ions were implanted into bulk 4H-SiC wafers using different ion fluxes (1.9x10(10)-4.9x10(13) ions/cm(2) s) and keeping the implantation dose constant at 5x10(14) Si+/cm(2). The implants were performed both at room and elevated temperatures, up to 220 degreesC. Rutherford backscattering spectrometry in the channelling mode using 2 MeV He+ ions was employed to measure ion implantation damage profiles in the samples. For the flux interval used the most, pronounced dynamic annealing effect was detected at 80-160degreesC, having an activation energy of 1.3 eV. For example, at 100degreesC the amount of disordered Si atoms at the projected ion range is reduced by a factor of 4 by decreasing the ion flux from 4.9x10(13) to 1.9x10(10) ions/cm(2) s. The results are discussed in terms of migration and annihilation of intrinsic type defects for both the Si- and C-sublattices. In addition, two regions for the damage accumulation - at the surface and at the damage peak for 100 keV Si+ ions - are observed.
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| 4. |
- Leong, Gary M, et al.
(författare)
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Estrogen up-regulates hepatic expression of suppressors of cytokine signaling-2 and -3 in vivo and in vitro.
- 2004
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Ingår i: Endocrinology. - : The Endocrine Society. - 0013-7227 .- 1945-7170. ; 145:12, s. 5525-31
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Tidskriftsartikel (refereegranskat)abstract
- Suppressors of cytokine signaling (SOCS) are important negative regulators of cytokine action. We recently reported that estrogen stimulates SOCS-2 expression and inhibits GH signaling in kidney cells. The effects of estrogen on SOCS expression in other tissues are unclear. The aim of this study was to investigate in vivo and in vitro whether estrogen affected SOCS expression in the liver, a major target organ of GH. The in vivo hepatic effects of estrogen on ovariectomized mice lacking estrogen receptor (ER)-alpha, ERbeta, or both and their wild-type littermates were examined by DNA microarray analysis. In vitro, the effects of estrogen on SOCS expression in human hepatoma cells were examined by reverse transcription quantitative PCR. Long-term (3 wk) estrogen treatment induced a 2- to 3-fold increase in hepatic expression of SOCS-2 and -3 in wild-type and ERbeta knockout mice but not in those lacking ERalpha or both ER subtypes. Short-term treatment (at 24 h) increased the mRNA level of SOCS-3 but not SOCS-2. In cultured hepatoma cells, estrogen increased SOCS-2 and -3 mRNA levels by 2-fold in a time- and dose-dependent manner (P < 0.05). Estrogen induced murine SOCS-3 promoter activity by 2-fold (P < 0.05) in constructs containing a region between nucleotides -1862 and -855. Moreover, estrogen and GH had additive effects on the SOCS-3 promoter activity. In summary, estrogen, via ERalpha, up-regulated hepatic expression of SOCS-2 and -3, probably through transcriptional activation. This indicates a novel mechanism of estrogen regulation of cytokine action.
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| 5. |
- Leung, K C, et al.
(författare)
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Estrogen inhibits GH signaling by suppressing GH-induced JAK2 phosphorylation, an effect mediated by SOCS-2.
- 2003
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Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 100:3, s. 1016-21
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Tidskriftsartikel (refereegranskat)abstract
- Oral estrogen administration attenuates the metabolic action of growth hormone (GH) in humans. To investigate the mechanism involved, we studied the effects of estrogen on GH signaling through Janus kinase (JAK)2 and the signal transducers and activators of transcription (STATs) in HEK293 cells stably expressing the GH receptor (293GHR), HuH7 (hepatoma) and T-47D (breast cancer) cells. 293GHR cells were transiently transfected with an estrogen receptor-alpha expression plasmid and luciferase reporters with binding elements for STAT3 and STAT5 or the beta-casein promoter. GH stimulated the reporter activities by four- to sixfold. Cotreatment with 17beta-estradiol (E(2)) resulted in a dose-dependent reduction in the response of all three reporters to GH to a maximum of 49-66% of control at 100 nM (P < 0.05). No reduction was seen when E(2) was added 1-2 h after GH treatment. Similar inhibitory effects were observed in HuH7 and T-47D cells. E(2) suppressed GH-induced JAK2 phosphorylation, an effect attenuated by actinomycin D, suggesting a requirement for gene expression. Next, we investigated the role of the suppressors of cytokine signaling (SOCS) in E(2) inhibition. E(2) increased the mRNA abundance of SOCS-2 but not SOCS-1 and SOCS-3 in HEK293 cells. The inhibitory effect of E(2) was absent in cells lacking SOCS-2 but not in those lacking SOCS-1 and SOCS-3. In conclusion, estrogen inhibits GH signaling, an action mediated by SOCS-2. This paper provides evidence for regulatory interaction between a sex steroid and the GHJAKSTAT pathway, in which SOCS-2 plays a central mechanistic role.
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| 6. |
- Leung, Kin-Chuen, et al.
(författare)
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Estrogen regulation of growth hormone action.
- 2004
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Ingår i: Endocrine reviews. - : The Endocrine Society. - 0163-769X .- 1945-7189. ; 25:5, s. 693-721
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Tidskriftsartikel (refereegranskat)abstract
- GH plays a pivotal role in regulating body growth and development, which is modulated by sex steroids. A close interplay between estrogen and GH leads to attainment of gender-specific body composition during puberty. The physiological basis of the interaction is not well understood. Most previous studies have focused on the effects of estrogen on GH secretion. There is also strong evidence that estrogen modulates GH action independent of secretion. Oral but not transdermal administration of estrogen impairs the metabolic action of GH in the liver, causing a fall in IGF-I production and fat oxidation. This results in a loss of lean tissue and a gain of body fat in postmenopausal women and an impairment of GH effect in hypopituitary women on GH replacement. The negative metabolic sequelae are potentially important because of the widespread use of oral estrogen and estrogen-related compounds. Estrogen affects GH action at the level of receptor expression and signaling. More recently, estrogen has been shown to inhibit Janus kinase/signal transducer and activator of transcription signaling by GH via the induction of suppressor of cytokine signaling-2, a protein inhibitor for cytokine signaling. This represents a novel paradigm of steroid regulation of cytokine receptors and is likely to have significance for a diverse range of cytokine function.
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| 7. |
- Leveque, Patrick, et al.
(författare)
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Vacancy and interstitial depth profiles in ion-implanted silicon.
- 2003
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Ingår i: Journal of Applied Physics. - : AIP Publishing. - 0021-8979 .- 1089-7550. ; 93:2, s. 871-877
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Tidskriftsartikel (refereegranskat)abstract
- An experimental method of studying shifts between concentration-versus-depth profiles of vacancy- and interstitial-type defects in ion-implanted silicon is demonstrated. The concept is based on deep level transient spectroscopy measurements utilizing the filling pulse variation technique. The vacancy profile, represented by the vacancy-oxygen center, and the interstitial profile, represented by the interstitial carbon-substitutional carbon pair, are obtained at the same sample temperature by varying the duration of the filling pulse. The effect of the capture in the Debye tail has been extensively studied and taken into account. Thus, the two profiles can be recorded with a high relative depth resolution. Using low doses, point defects have been introduced in lightly doped float zone n-type silicon by implantation with 6.8 MeV boron ions and 680 keV and 1.3 MeV protons at room temperature. The effect of the angle of ion incidence has also been investigated. For all implantation conditions the peak of the interstitial profile is displaced towards larger depths compared to that of the vacancy profile. The amplitude of this displacement increases as the width of the initial point defect distribution increases. This behavior is explained by a simple model where the preferential forward momentum of recoiling silicon atoms and the highly efficient direct recombination of primary point defects are taken into account.
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