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Sökning: WFRF:(Liljeroth E)

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  • Bengtsson, Therese, et al. (författare)
  • Proteomics and transcriptomics of the BABA-induced resistance response in potato using a novel functional annotation approach
  • 2014
  • Ingår i: BMC Genomics. - : Springer Science and Business Media LLC. - 1471-2164. ; 15
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Induced resistance (IR) can be part of a sustainable plant protection strategy against important plant diseases. beta-aminobutyric acid (BABA) can induce resistance in a wide range of plants against several types of pathogens, including potato infected with Phytophthora infestans. However, the molecular mechanisms behind this are unclear and seem to be dependent on the system studied. To elucidate the defence responses activated by BABA in potato, a genome-wide transcript microarray analysis in combination with label-free quantitative proteomics analysis of the apoplast secretome were performed two days after treatment of the leaf canopy with BABA at two concentrations, 1 and 10 mM. Results: Over 5000 transcripts were differentially expressed and over 90 secretome proteins changed in abundance indicating a massive activation of defence mechanisms with 10 mM BABA, the concentration effective against late blight disease. To aid analysis, we present a more comprehensive functional annotation of the microarray probes and gene models by retrieving information from orthologous gene families across 26 sequenced plant genomes. The new annotation provided GO terms to 8616 previously un-annotated probes. Conclusions: BABA at 10 mM affected several processes related to plant hormones and amino acid metabolism. A major accumulation of PR proteins was also evident, and in the mevalonate pathway, genes involved in sterol biosynthesis were down-regulated, whereas several enzymes involved in the sesquiterpene phytoalexin biosynthesis were up-regulated. Interestingly, abscisic acid (ABA) responsive genes were not as clearly regulated by BABA in potato as previously reported in Arabidopsis. Together these findings provide candidates and markers for improved resistance in potato, one of the most important crops in the world.
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  • Burra, Dharani, et al. (författare)
  • Phosphite-induced changes of the transcriptome and secretome in Solanum tuberosum leading to resistance against Phytophthora infestans
  • 2014
  • Ingår i: BMC Plant Biology. - : Springer Science and Business Media LLC. - 1471-2229. ; 14
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Potato late blight caused by the oomycete pathogen Phytophthora infestans can lead to immense yield loss. We investigated the transcriptome of Solanum tubersoum (cv. Desiree) and characterized the secretome by quantitative proteomics after foliar application of the protective agent phosphite. We also studied the distribution of phosphite in planta after application and tested transgenic potato lines with impaired in salicylic and jasmonic acid signaling. Results: Phosphite had a rapid and transient effect on the transcriptome, with a clear response 3 h after treatment. Strikingly this effect lasted less than 24 h, whereas protection was observed throughout all time points tested. In contrast, 67 secretome proteins predominantly associated with cell-wall processes and defense changed in abundance at 48 h after treatment. Transcripts associated with defense, wounding, and oxidative stress constituted the core of the phosphite response. We also observed changes in primary metabolism and cell wall-related processes. These changes were shown not to be due to phosphate depletion or acidification caused by phosphite treatment. Of the phosphite-regulated transcripts 40% also changed with beta-aminobutyric acid (BABA) as an elicitor, while the defence gene PR1 was only up-regulated by BABA. Although phosphite was shown to be distributed in planta to parts not directly exposed to phosphite, no protection in leaves without direct foliar application was observed. Furthermore, the analysis of transgenic potato lines indicated that the phosphite-mediated resistance was independent of the plant hormones salicylic and jasmonic acid. Conclusions: Our study suggests that a rapid phosphite-triggered response is important to confer long-lasting resistance against P. infestans and gives molecular understanding of its successful field applications.
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  • Liljeroth, E., et al. (författare)
  • Low-dose propofol reduces the incidence of moderate to severe local pain induced by the main dose
  • 2007
  • Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172 .- 1399-6576. ; 51:4, s. 460-463
  • Tidskriftsartikel (refereegranskat)abstract
    • Background Local pain on injection of propofol remains a considerable problem in clinical anaesthesiology. As slow infusion of a low dose of propofol induces little or no pain at the site of injection, and as propofol-induced pain fades during prolonged exposure, this randomized, double-blind, clinical cross-over study was designed to test whether pain on injection of propofol is attenuated by initial slow injection of a low dose of propofol by the same intravenous line. Methods Seventy-seven adult surgical patients were cannulated in a dorsal vein on each hand. In each cannula, a 0.5-ml priming dose of either propofol 10 mg/ml dissolved in an emulsion of medium- and long-chain triglycerides or aqueous sodium chloride 9.0 mg/ml was injected over 30 s, and followed 120 s later by a main dose of 2.0 ml of the same propofol formula over 6 s. After each injection, the patients were asked by a blind investigator to score the maximal pain intensity on a visual analogue scale (VAS). Results Although the decrease in maximal pain intensity did not reach statistical significance (P = 0.070), significantly fewer patients reported moderate or severe pain intensity (corresponding to 3.0 VAS units or more) after the main dose of propofol was preceded by a priming dose of propofol than by sodium chloride (P = 0.041). Conclusions The incidence of moderate to severe local pain induced by intravenous propofol can be decreased by a readily applicable technique in which a low dose of propofol emulsion is slowly administered by the same intravenous route 2 min in advance.
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  • Liljeroth, E, et al. (författare)
  • Pain on injection of propofol with or without infusion of carrier fluid
  • 2001
  • Ingår i: Acta Anaesthesiologica Scandinavica. - : Wiley. - 0001-5172. ; 45:7, s. 839-841
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: Propofol, a popular intravenous (iv) anaesthetic induction agent for brief cases or day surgery, is associated with smooth induction, pleasant sleep, rapid recovery and little postoperative nausea. A major disadvantage is pain at the site of injection. The aim of the present study was to examine the influence of simultaneous iv infusion of carrier fluid on propofol-induced local pain. METHODS: Thirty patients, scheduled for ear-nose-throat or plastic surgery under general anaesthesia, were randomly allocated into two groups. Each patient had two 2 ml iv bolus injections of propofol given at two minutes' interval. In group I (n=15) the first bolus injection was given with no iv carrier fluid and the second one given with a 10 ml iv carrier fluid infused over 10 s. Correspondingly, the patients in group II (n=15) had their first injection with and their second one without the iv carrier fluid. Following each injection of propofol the patients were asked by a blinded investigator to score their pain on a 10-point visual analogue scale, and to report the appearance, maximum and disappearance of pain. After the second assessment of pain, general anaesthesia was induced with more propofol. RESULTS: Pain intensity at the site of propofol injection was found not to be influenced by simultaneous iv infusion of carrier fluid. CONCLUSION: It seems, from the results obtained here, that simultaneous iv infusion of carrier fluid has no particular effect on local pain following iv administration of propofol.
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  • Tarkowski, E, et al. (författare)
  • Cerebral pattern of pro- and anti-inflammatory cytokines in dementias
  • 2003
  • Ingår i: Brain Research Bulletin. - 0361-9230. ; 61:3, s. 255-260
  • Tidskriftsartikel (refereegranskat)abstract
    • The knowledge regarding putative inflammatory component(s) participating in Alzheimer's disease (AD) and vascular dementia (VAD) is scarce. Recently, we have demonstrated the presence of certain inflammatory cytokines in the cerebrospinal fluid (CSF) of demented patients. Although the initial event(s) triggering the neurodegenerative processes in AD versus VAD may be different and lead to different neuropathological changes, it may initiate a similar cascade of cytokine production in response to neuronal injury. The cytokines released in the central nervous system (CNS) may, in turn, act in a similar manner in both diseases, amplifying some pathological changes such as amyloidogenesis and white matter lesions or on the contrary acting as neuroprotective molecules. This review will focus on the intracerebral production of the pro- and anti-inflammatory cytokines interleukin IL-1beta, IL-1 receptor antagonist (IL-1ra), IL-6 and TNF-alpha in dementia, and their relation to gene polymorphism, to cerebral neuronal damage, apoptosis, and to clinical variables of dementia. Our results, which show for the first time strikingly increased CSF levels of TNF-alpha but not of TNF-beta, IL-1beta or IL-6 in AD and VAD, may form a conceptual framework for further studies of neuroprotective mechanisms in dementias. (C) 2003 Elsevier Science Inc. All rights reserved.
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  • Tarkowski, E, et al. (författare)
  • Decreased levels of intrathecal interleukin 1 receptor antagonist in Alzheimer's disease
  • 2001
  • Ingår i: Dementia and Geriatric Cognitive Disorders. - : S. Karger AG. - 1420-8008 .- 1421-9824. ; 12:5, s. 314-317
  • Tidskriftsartikel (refereegranskat)abstract
    • A growing body of evidence points out the potential role of inflammatory mechanisms in the pathophysiology of brain damage in dementia. In previous studies, we have demonstrated intrathecal production of the proinflammatory cytokine tumor necrosis factor (TNF)alpha in patients with Alzheimer's disease (AD). The aim of the present study was to investigate the downstream products of TNF-alpha expression including interleukin (IL)1beta and its naturally occurring antagonist IL-1 receptor agonist (ra) in patients with AD. The cytokine levels were related to neuronal damage, as measured by intrathecal tau and beta-amyloid concentration and certain clinical features of the disease. Fifty-two patients with AD and 25 healthy controls were analyzed with respect to cerebrospinal fluid (CSF) levels of IL-1beta and IL-1ra. CSF IL-1beta was neither detectable in CSF of AD nor in control CSF. In contrast, a significantly lower (p < 0.01) number of patients (24 of 49) than of controls (20 of 24) showed detectable levels of IL-1ra in the CSF. The intrathecal levels of IL-1ra were significantly lower in patients with AD than in the controls. Our study demonstrates a decreased production of the anti-inflammatory compound IL-1ra, suggesting a propensity towards inflammation in patients with AD.
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  • Tarkowski, E, et al. (författare)
  • TNF gene polymorphism and its relation to intracerebral production of TNFalpha and TNFbeta in AD
  • 2000
  • Ingår i: Neurology. - 1526-632X. ; 54:11, s. 2077-2081
  • Tidskriftsartikel (refereegranskat)abstract
    • OBJECTIVE: To analyze the extent of tumor necrosis factor-alpha (TNFalpha) and TNFbeta gene polymorphism in patients with AD and to relate it to intrathecal levels of these cytokines. METHODS: Analyses of TNFalpha and TNFbeta gene polymorphism were performed using PCR in 52 patients with AD and in 25 control subjects, and the levels of corresponding cytokines were analyzed using ELISA. RESULTS: Patients with AD displayed significantly higher intrathecal levels of TNFalpha, but not TNFbeta, compared with the control subjects. The levels of these cytokines did not differ significantly in patients displaying different alleles of the TNF gene. CONCLUSIONS: Results indicate that increased intrathecal production of TNFalpha in AD is preferentially controlled by environmental stimuli rather than genetic makeup.
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