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Träfflista för sökning "WFRF:(Fredriksson Henrik) srt2:(2010-2014)"

Sökning: WFRF:(Fredriksson Henrik) > (2010-2014)

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1.
  • Nilsson, Magnus, et al. (författare)
  • A 9-band WCDMA/EDGE transceiver supporting HSPA evolution
  • 2011
  • Ingår i: [Host publication title missing]. - 0193-6530. ; , s. 366-368
  • Konferensbidrag (refereegranskat)abstract
    • The future of cellular radio ICs lies in the integration of an ever-increasing number of bands and channel bandwidths. This paper presents a transceiver together with the associated discrete front-end components. The transceiver supports 4 EDGE bands and 9 WCDMA bands (l-VI and Vlll-X), while the radio can be configured to simultaneously support the 4 EDGE bands and up to 5 WCDMA bands: 3 high bands (HB) and 2 low bands (LB). The RX is a SAW-less homodyne composed of a main RX and a diversity RX. To reduce package complexity with so many bands, we chose to minimize the number of ports by using single-ended RF interfaces for both RX and TX. This saves seve ral package pins, but requires careful attention to grounding. The main RX has 8 LNA ports and the diversity RX has 5, with some LNAs supporting multiple bands. On the TX side, 2 ports are used for all EDGE bands and 4 for the WCDMA bands.
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2.
  • Andersen, Sören M., et al. (författare)
  • A scalable route to 5-substituted 3-isoxazolol fibrinolysis inhibitor AZD6564
  • 2014
  • Ingår i: Organic Process Research & Development. - : American Chemical Society (ACS). - 1083-6160 .- 1520-586X. ; 18:8, s. 952-959
  • Tidskriftsartikel (refereegranskat)abstract
    • A practical and chromatography-free multikilogram synthesis of a 3-isoxazolol containing antifibrinolytic agent, AZD6564, has been developed in eight steps and 7% overall yield starting from methyl 2-chloroisonicotinate. Highlights in the synthesis are a Negishi coupling and an enzymatic resolution of a racemic ester. 
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3.
  • Andershed, Henrik, 1975-, et al. (författare)
  • Initial test of the new risk-need assessment instrument for youths with or at risk for conduct problems : ESTER-assessment
  • 2010
  • Ingår i: Procedia - Social and Behavioral Sciences. - : Elsevier BV. - 1877-0428. ; 5, s. 488-492
  • Tidskriftsartikel (refereegranskat)abstract
    • ESTER-assessment is a new assessment instrument for youths (0-18 years), and includes 19 empirically-derived risk and protective factors for conduct problems. This study tests the inter-rater reliability of the five-point rating scale used to assess the 19 factors in ESTER-assessment on 30 institutionalized girls and their file information. Exact agreement between raters varied from 38 to 72 percent on the 19 individual factors, a result much better than chance. Intra-class correlations of the two independent raters on the majority of the 19 individual factors were fair to good. In conclusion, the results lend support to the inter-rater reliability of ESTER-assessment.
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4.
  • Buratovic, Sonja, et al. (författare)
  • Comparison of single and repeated exposure to low doses of pyrethroids, permethrin and bioallethrin, during neonatal brain development on adult spontaneous behaviour
  • 2012
  • Konferensbidrag (refereegranskat)abstract
    • Permethrin and bioallethrin belong to the Type 1 class of pyrethroid pesticides. The primary mechanism of action is interference with nerve membrane sodium channels that results in increased neuronal activity. We have earlier reported on developmental neurotoxic effects after repeated, PND 10 to PND16, neonatal exposure to pyrethroids. The effects were manifested as altered spontaneous behavior, hyperactivity and reduced cognitive function and changes in cholinergic muscarinic/nicotinic receptors in the cerebral cortex of neonatal and adult mice. The present study was undertaken to compare repeated and single exposure to permethrin and bioallethrin during the neonatal brain growth spurt (BGS) on adult spontaneous behavior in a novel home environment. Neonatal NMRI male mice were given permethrin, orally (0.55; 3.3; 6.6 mg/kg bw/day) on PND 10-14, or just a single oral dose of 6.6 mg/kg bw on PND 10. Bioallethrin was given as a single oral dose of 0.7 mg/kg bw on PND 10, and compared to earlier published data on repeated exposure. Mice serving as controls received the 20 % fat emulsion vehicle. Spontaneous behavior test (locomotion, rearing, total activity) in 2-month-old mice revealed a significant higher activity in mice exposed to repeated doses of 6.6 mg permethrin, as well in mice just receiving a single 6.6 mg dose of permethrin. No significant difference was observed between repeated and single exposure.  A single dose of 0.7 mg bioallethrin on PND 10 caused the same effects as a repeated dose of 0.7 mg between PND 10 to PND 16. This demonstrates that a single dose of these pyrethroids can cause the same developmental neurotoxic effects as that seen following repeated doses over one week during the neonatal BGS period in mouse. This research provides is consistent with previous findings that exposure during the BGS can result in persistent behavioral defects.
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5.
  • Buratovic, Sonja, et al. (författare)
  • Developmental exposure to PBDE 209 : sex, neuroprotein and neurobehavioural analyses
  • 2012
  • Ingår i: Toxicology Letters. - 0378-4274 .- 1879-3169. ; 211:supplement, s. S90-
  • Tidskriftsartikel (refereegranskat)abstract
    • Polybrominated diphenyl ethers (PBDEs) are used in large quantities as flame-retardants in polymers products.Newborns and toddlers can be indirectly and directly exposed to PBDEs during a period of critical rapid brain development. The present study was undertaken to investigate neurotoxic effects after neonatal exposure to PBDE 209 on sex differences, cognitive function, neuroproteins and altered susceptibility to toxicants in adults. 3-day-old NMRI mice were exposed to PBDE 209 (2,2´,3,3´,4,4´,5,5´,6,6´-decaBDE at 0, 1.4, 6.0 and 14 µmol/kg bw). At 2 months of age male mice were exposed to paraoxon (0.25 mg/kg bw, every 2nd day for 7 days) and female mice exposed to nicotine (80 µg nicotine base/kg bw). At the age of 2 and 4 months mice were observed for spontaneous behaviour, before and after adult exposure to paraoxon (male) and nicotine (female). Male mice aged 5 and 7 months were observed for memory and learning. Neuroproteins CaMKII, GAP-43, synaptophysin and tau in cerebral cortex and hippocampus from 7-months old male and female mice were analyzed. The present study shows that neonatal exposure to PBDE 209 can induce developmental neurobehavioural defects in both male and female mice. Neonatal exposure to PBDE 209 also caused increased susceptibility in adult mice to paraoxon and nicotine. All these effects were dose response related. Further, neonatal exposure to PBDE 209 caused persistent defects in memory and learning in adult male mice and increased levels of important neuroproteins e.g. tau in adult male and female mice.
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6.
  • Buratovic, Sonja, et al. (författare)
  • Developmental exposure to PBDE 209 alters adult susceptibility to paraoxon and nicotine : gender and neurobehavioural analysis
  • 2011
  • Konferensbidrag (refereegranskat)abstract
    • Newborns, infants and children can be indirectly and directly exposed to PBDEs. This exposure coincides with a period of rapid brain development. Polybrominated diphenyl ethers (PBDEs) are used in large quantities as flame-retardants in polymers, especially in electric appliances.A concern is that these compounds are present at a higher level in newborns and toddlers than in the average adult individual, especially the highly brominated PBDEs. We have earlier reported that neonatal exposure to toxicants can lead to an increased susceptibility of the cholinergic system at adult age. The present study was undertaken to investigate whether neonatal exposure of male and female mice to PBDE 209 alters the adult susceptibility to the organophosphorous compound, paraoxon, and to nicotine, respectively.. Neonatal, 3-day-old, NMRI mice were exposed to PBDE 209 (2,2´,3,3´,4,4´,5,5´,6,6´-decaBDE at 1.4, 6.0 and 14 µmol/kg bw). At two months of age male mice were exposed to paraoxon (0.25 mg/kg bw, every 2nd day for 7 days) and female mice exposed to nicotine. At the age of 2 months male and female mice were observed for spontaneous behaviour in a novel home environment, before and after adult exposure to paraoxon and nicotine, respectively. Adult male and female mice neonatally exposed to PBDE 209 showed significant impaired spontaneous behaviour. Male mice neonatally exposed to PBDE 209 and to paraoxon as adults developed additional defect spontaneous behaviour and lack of habituation. Female mice neonatally exposed to PBDE 209 showed an increased susceptibility to nicotine, where PBDE 209 exposed mice responded with a decrease in activity to nicotine whereas control mice responded with increased activity. The present study shows that PBDE 209 can induce developmental neurobehavioural defects in both male and female mice. Neonatal exposure to PBDE 209 caused also increased susceptibility in adult mice to paraoxon and nicotine. All these effects were dose response related.
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7.
  • Buratovic, Sonja, et al. (författare)
  • Developmental exposure to the polybrominated diphenyl ether PBDE 209 : Neurobehavioural and neuroprotein analysis in adult male and female mice
  • 2014
  • Ingår i: Environmental Toxicology and Pharmacology. - : Elsevier BV. - 1382-6689 .- 1872-7077. ; 38:2, s. 570-585
  • Tidskriftsartikel (refereegranskat)abstract
    • Polybrominated diphenyl ethers (PBDEs), used as flame retardants in polymer products, are reported to cause developmental neurotoxic effects in mammals. The present study have investigated neurotoxic effects arising from neonatal exposure to PBDE 209, including alterations in sex differences, spontaneous behaviour, learning and memory, neuroproteins and altered susceptibility of the cholinergic system in adults. Three-day-old NMRI mice, of both sexes, were exposed to PBDE 209 (2,2',3,3',4,4',5,5',6,6'-decaBDE at 0, 1.4, 6.0 and 14.0 mu mol/kg b.w.). At adult age (2-7 months) a similar developmental neurotoxic effects in both male and female mice were seen, including lack of or reduced habituation to a novel home environment, learning and memory defects, modified response to the cholinergic agent's paraoxon (males) and nicotine (females) indicating increased susceptibility of the cholinergic system. The behavioural defects were dose-response related and persistent. In mice of both sexes and showing behavioural defects, neuroprotein tau was increased. (C) 2014 Elsevier B.V. All rights reserved.
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8.
  • Buratovic, Sonja, et al. (författare)
  • Neonatal exposure to a moderate dose of ionizing radiation causes behavioural defects and altered levels of tau protein in mice
  • 2014
  • Ingår i: Neurotoxicology. - : Elsevier BV. - 0161-813X .- 1872-9711. ; 45, s. 48-55
  • Tidskriftsartikel (refereegranskat)abstract
    • Medical use of ionizing radiation (IR) has great benefits for treatment and diagnostic imaging, butprocedures as computerized tomography (CT) may deliver a significant radiation dose to the patient.Recently, awareness has been raised about possible non-cancer consequences from low dose exposure toIR during critical phases of perinatal and/or neonatal brain development.In the present study neonatal NMRI mice were whole body irradiated with a single dose of gammaradiation (0; 350 and 500 mGy) on postnatal day 10 (PND 10). At 2 and 4 months of age, mice of bothsexes were observed for spontaneous behaviour in a novel home environment. The neuroproteinsCaMKII, GAP-43, synaptophysin and total tau in male mouse cerebral cortex and hippocampus wereanalysed 24 h post-irradiation and in adults at 6 months of age exposed to 0 or 500 mGy on PND 10.A significantly dose-response related deranged spontaneous behaviour in 2- and 4-month-old micewas observed, where both males and females displayed a modified habituation, indicating reducedcognitive function. The dose of 350 mGy seems to be a tentative threshold. Six-month-old male miceshowed a significantly increased level of total tau in cerebral cortex after irradiation to 500 mGy compared to controls. This demonstrates that a single moderate dose of IR, given during a defined criticalperiod of brain development, is sufficient to cause persistently reduced cognitive function. Moreover, anelevation of tau protein was observed in male mice displaying reduced cognitive function.
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9.
  • Buratovic, Sonja, et al. (författare)
  • Neonatal exposure to a single low dose of ionising radiation causes persistent disruptions in cognitive abilities and increased levels of tau in mice
  • 2013
  • Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
    • Ionising radiation (IR) is extensively used in the medical field for treatment and diagnostics. Concern has been raised about possible negative consequences from low dose exposure to IR during critical phases of perinatal and/or neonatal brain development. The brain growth spurt, which is characterized by maturation of axonal and dendritic outgrowth, establishment of neural connections and acquisition of new motor and sensory abilities, occurs perinatally in humans and neonatally in mice. By using the neonatal mouse as an animal model we are able to study the effect of IR during early periods of brain development and which consequences it has for the adult animal.Neonatal NMRI mice were irradiated (0; 0.35 and 0.5 Gy) at one single occasion on postnatal day 10. At 2- and 4-months of age, spontaneous behaviour was tested in a novel home environment and parameters observed were locomotion, rearing and total activity. Analyses of important neuroproteins in cerebral cortex were performed 24h following irradiation (0 and 0.5 Gy) and at 6-months of age.Observations of spontaneous behaviour revealed a significantly deranged behaviour in 2- and 4-month old mice of both sexes irradiated with 0.35 or 0.5 Gy in a dose response related manner. The observed reduced activity during the beginning of the test period and increased activity at the end of the test period indicates a lack of habituation capacity and disrupted cognitive functions. Neuroprotein analyses of cerebral cortex 24h after irradiation and at 6-months of age showed a significantly increased level of tau in mice irradiated with 0.5 Gy compared to controls. This demonstrates that a single dose of IR, given at a defined critical period during brain development, is sufficient to cause persistently reduced cognitive functions and increased levels of tau in mice. 
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10.
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