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  • Axelsson, Jimmy, et al. (författare)
  • Ejection fraction in left bundle branch block is disproportionately reduced in relation to amount of myocardial scar
  • 2018
  • Ingår i: Journal of Electrocardiology. - : Elsevier. - 0022-0736 .- 1532-8430. ; 51:6, s. 1071-1076
  • Tidskriftsartikel (refereegranskat)abstract
    • Introduction: The relationship between left ventricular (LV) ejection fraction (EF) and LV myocardial scar can identify potentially reversible causes of LV dysfunction. Left bundle branch block (LBBB) alters the electrical and mechanical activation of the LV. We hypothesized that the relationship between LVEF and scar extent is different in LBBB compared to controls. Methods: We compared the relationship between LVEF and scar burden between patients with LBBB and scar (n = 83), and patients with chronic ischemic heart disease and scar but no electrocardiographic conduction abnormality (controls, n = 90), who had undergone cardiovascular magnetic resonance (CMR) imaging at one of three centers. LVEF (%) was measured in CMR cine images. Scar burden was quantified by CMR late gadolinium enhancement (LGE) and expressed as % of LV mass (%LVM). Maximum possible LVEF (LVEFmax) was defined as the function describing the hypotenuse in the LVEF versus myocardial scar extent scatter plot. Dysfunction index was defined as LVEFmax derived from the control cohort minus the measured LVEF. Results: Compared to controls with scar, LBBB with scar had a lower LVEF (median [interquartile range] 27 [19–38] vs 36 [25–50] %, p < 0.001), smaller scar (4 [1–9] vs 11 [6–20] %LVM, p < 0.001), and greater dysfunction index (39 [30–52] vs 21 [12–35] % points, p < 0.001). Conclusions: Among LBBB patients referred for CMR, LVEF is disproportionately reduced in relation to the amount of scar. Dyssynchrony in LBBB may thus impair compensation for loss of contractile myocardium.
  • Bashkanov, M., et al. (författare)
  • Double-Pionic Fusion of Nuclear Systems and the "ABC" Effect : Approaching a Puzzle by Exclusive and Kinematically Complete Measurements
  • 2009
  • Ingår i: Physical Review Letters. - 0031-9007 .- 1079-7114. ; 102:5, s. 052301-
  • Tidskriftsartikel (refereegranskat)abstract
    • The ABC effect-a puzzling low-mass enhancement in the pi pi invariant mass spectrum, first observed by Abashian, Booth, and Crowe-is well known from inclusive measurements of two-pion production in nuclear fusion reactions. Here we report on the first exclusive and kinematically complete measurements of the most basic double-pionic fusion reaction pn -> d pi(0)pi(0) at beam energies of 1.03 and 1.35 GeV. The measurements, which have been carried out at CELSIUS-WASA, reveal the ABC effect to be a (pi pi)(I=L=0) channel phenomenon associated with both a resonancelike energy dependence in the integral cross section and the formation of a Delta Delta system in the intermediate state. A corresponding simple s-channel resonance ansatz provides a surprisingly good description of the data.
  • Bilbao, Ainhoa, et al. (författare)
  • Loss of the Ca2+/calmodulin-dependent protein kinase type IV in dopaminoceptive neurons enhances behavioral effects of cocaine
  • 2008
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : National Academy of Sciences; 1999. - 0027-8424 .- 1091-6490. ; 105:45, s. 17549-17554
  • Tidskriftsartikel (refereegranskat)abstract
    • The persistent nature of addiction has been associated with activity-induced plasticity of neurons within the striatum and nucleus accumbens (NAc). To identify the molecular processes leading to these adaptations, we performed Cre/loxP-mediated genetic ablations of two key regulators of gene expression in response to activity, the Ca2+/calmodulin-dependent protein kinase IV (CaMKIV) and its postulated main target, the cAMP-responsive element binding protein (CREB). We found that acute cocaine-induced gene expression in the striatum was largely unaffected by the loss of CaMKIV. On the behavioral level, mice lacking CaMKIV in dopaminoceptive neurons displayed increased sensitivity to cocaine as evidenced by augmented expression of locomotor sensitization and enhanced conditioned place preference and reinstatement after extinction. However, the loss of CREB in the forebrain had no effect on either of these behaviors, even though it robustly blunted acute cocaine-induced transcription. To test the relevance of these observations for addiction in humans, we performed an association study of CAMK4 and CREB promoter polymorphisms with cocaine addiction in a large sample of addicts. We found that a single nucleotide polymorphism in the CAMK4 promoter was significantly associated with cocaine addiction, whereas variations in the CREB promoter regions did not correlate with drug abuse. These findings reveal a critical role for CaMKIV in the development and persistence of cocaine-induced behaviors, through mechanisms dissociated from acute effects on gene expression and CREB-dependent transcription.
  • Chaudhry, Uzma, et al. (författare)
  • Evaluation of the ECG based Selvester scoring method to estimate myocardial scar burden and predict clinical outcome in patients with left bundle branch block, with comparison to late gadolinium enhancement CMR imaging
  • 2017
  • Ingår i: Annals of Noninvasive Electrocardiology. - : Wiley-Blackwell. - 1082-720X. ; 22:5
  • Tidskriftsartikel (refereegranskat)abstract
    • Background: Myocardial scar burden quantification is an emerging clinical parameter for risk stratification of sudden cardiac death and prediction of ventricular arrhythmias in patients with left ventricular dysfunction. We investigated the relationships among semiautomated Selvester score burden and late gadolinium enhancement-cardiovascular magnetic resonance (LGE-CMR) assessed scar burden and clinical outcome in patients with underlying heart failure, left bundle branch block (LBBB) and implantable cardioverter-defibrillator (ICD) treatment. Methods: Selvester QRS scoring was performed on all subjects with ischemic and nonischemic dilated cardiomyopathy at Skåne University Hospital Lund (2002-2013) who had undergone LGE-CMR and 12-lead ECG with strict LBBB pre-ICD implantation. Results: Sixty patients were included; 57% nonischemic dilated cardiomyopathy and 43% ischemic cardiomyopathy with mean left ventricular ejection fraction of 27.6% ± 11.7. All patients had scar by Selvester scoring. Sixty-two percent had scar by LGE-CMR (n = 37). The Spearman correlation coefficient for LGE-CMR and Selvester score derived scar was r = .35 (p = .007). In scar negative LGE-CMR, there was evidence of scar by Selvester scoring in all patients (range 3%-33%, median 15%). Fourteen patients (23%) had an event during the follow-up period; 11 (18%) deaths and six adequate therapies (10%). There was a moderate trend indicating that presence of scar increased the risk of clinical endpoints in the LGE-CMR analysis (p = .045). Conclusion: There is a modest correlation between LGE-CMR and Selvester scoring verified myocardial scar. CMR based scar burden is correlated to clinical outcome, but Selvester scoring is not. The Selvester scoring algorithm needs to be further refined in order to be clinically relevant and reliable for detailed scar evaluation in patients with LBBB.
  • Engblom, David, 1975-, et al. (författare)
  • EP3 and EP4 receptor mRNA expression in peptidergic cell groups of the rat parabrachial nucleus
  • 2004
  • Ingår i: Neuroscience. - 0306-4522 .- 1873-7544. ; 126:4, s. 989-999
  • Tidskriftsartikel (refereegranskat)abstract
    • This study examines the distribution of prostaglandin E2 receptors of subtype EP3 and EP4 among brain stem parabrachial neurons that were characterized with respect to their neuropeptide expression. By using a dual-labeling in situ hybridization method, we show that preprodynorphin mRNA expressing neurons in the dorsal and central lateral subnuclei express EP3 receptor mRNA. Such receptors are also expressed in preproenkephalin, calcitonin gene related peptide and preprotachykinin mRNA positive neurons in the external lateral subnucleus, whereas preprodynorphin mRNA expressing neurons in this subnucleus are EP receptor negative. In addition, EP3 receptor expression is seen among some enkephalinergic neurons in the Kölliker-Fuse nucleus. Neurons in the central part of the cholecystokininergic population in the regions of the superior lateral subnucleus express EP4 receptor mRNA, whereas those located more peripherally express EP3 receptors. Taken together with previous findings showing that discrete peptidergic cell groups mediate nociceptive and/or visceral afferent information to distinct brain stem and forebrain regions, the present results suggest that the processing of this information in the parabrachial nucleus is influenced by prostaglandin E2. Recent work has shown that prostaglandin E2 is released into the brain following peripheral immune challenge; hence, the parabrachial nucleus may be a region where humoral signaling of peripheral inflammatory events may interact with neuronal signaling elicited by the same peripheral processes.
  • Engblom, David, 1975-, et al. (författare)
  • Induction of microsomal prostaglandin E synthase in the rat brain endothelium and parenchyma in adjuvant-induced arthritis
  • 2002
  • Ingår i: Journal of Comparative Neurology. - 0021-9967 .- 1096-9861. ; 452:3, s. 205-214
  • Tidskriftsartikel (refereegranskat)abstract
    • Although central nervous symptoms such as hyperalgesia, fatigue, malaise, and anorexia constitute major problems in the treatment of patients suffering from chronic inflammatory disease, little has been known about the signaling mechanisms by which the brain is activated during such conditions. Here, in an animal model of rheumatoid arthritis, we show that microsomal prostaglandin E-synthase, the inducible terminal isomerase in the prostaglandin E2-synthesizing pathway, is expressed in endothelial cells along the blood-brain barrier and in the parenchyma of the paraventricular hypothalamic nucleus. The endothelial cells but not the paraventricular hypothalamic cells displayed a concomitant induction of cyclooxygenase-2 and expressed interleukin-1 type 1 receptors, which indicates that the induction is due to peripherally released cytokines. In contrast to cyclooxygenase-2, microsomal prostaglandin E synthase had very sparse constitutive expression, suggesting that it could be a target for developing drugs that will carry fewer side effects than the presently available cyclooxygenase inhibitors. These findings, thus, suggest that immune-to-brain communication during chronic inflammatory conditions involves prostaglandin E2-synthesis both along the blood-brain barrier and in the parenchyma of the hypothalamic paraventricular nucleus and point to novel avenues for the treatment of the brain-elicited disease symptoms during these conditions.
  • Engblom, David, 1975-, et al. (författare)
  • Microsomal prostaglandin E synthase-1 is the central switch during immune-induced pyresis
  • 2003
  • Ingår i: Nature Neuroscience. - 1097-6256 .- 1546-1726. ; 6:11, s. 1137-1138
  • Tidskriftsartikel (refereegranskat)abstract
    • We studied the febrile response in mice deficient in microsomal prostaglandin E synthase-1 (mPGES-1), an inducible terminal isomerase expressed in cytokine-sensitive brain endothelial cells. These animals showed no fever and no central prostaglandin (PG) E2 synthesis after peripheral injection of bacterial-wall lipopolysaccharide, but their pyretic capacity in response to centrally administered PGE2 was intact. Our findings identify mPGES-1 as the central switch during immune-induced pyresis and as a target for the treatment of fever and other PGE2-dependent acute phase reactions elicited by the brain.
  • Engblom, David, 1975-, et al. (författare)
  • Prostaglandins as inflammatory messengers across the blood-brain barrier
  • 2002
  • Ingår i: Journal of Molecular Medicine. - 0946-2716 .- 1432-1440. ; 80:1
  • Tidskriftsartikel (refereegranskat)abstract
    • Upon immune challenge the brain launches a wide range of responses, such as fever, anorexia, and hyperalgesia that serve to maintain homeostasis. While these responses are adaptive during acute infections, they may be destructive during chronic inflammatory conditions. Research performed during the last decade has given us insight into how the brain monitors the presence of a peripheral inflammation and the mechanisms underlying the brain-mediated acute-phase reactions. Here we give a brief review on this subject, with focus on the role of prostaglandin E2 produced in cells associated with the blood-brain barrier in immune-to-brain signaling. The recent advances in this field have not only elucidated the mechanisms behind the anti-pyretic and anti-hyperalgesic effects of cyclooxygenase inhibitors, but have also identified novel and more-selective potential drug targets.
  • Engblom, Henrik, et al. (författare)
  • The evaluation of an electrocardiographic myocardial ischemia acuteness score to predict the amount of myocardial salvage achieved by early percutaneous coronary intervention Clinical validation with myocardial perfusion single photon emission computed tomography and cardiac magnetic resonance.
  • 2011
  • Ingår i: Journal of Electrocardiology. - : Elsevier. - 1532-8430. ; 44, s. 525-532
  • Tidskriftsartikel (refereegranskat)abstract
    • BACKGROUND: The time from symptom onset to reperfusion in acute myocardial infarction (MI) has been shown to be a poor predictor of patient outcome. Acute electrocardiographic (ECG) changes, however, have been shown useful for estimated acuteness of myocardial ischemia using the Anderson-Wilkins ECG ischemia acuteness score (AW-acuteness score). The aim was to study whether acute ischemic ECG changes can predict the amount of salvageable myocardium in patients with acute ST-elevation MI. METHODS: Thirty-eight patients treated with primary percutaneous coronary intervention for first-time ST-elevation MI were retrospectively enrolled. Myocardium at risk (MaR) was determined by myocardial perfusion single photon emission computed tomography acutely or by T2-weighted cardiac magnetic resonance after 1 week, at the same time when final MI size was determined by late gadolinium enhancement. Myocardial salvage was calculated as (MaR - MI size)/MaR and compared with AW-acuteness score and time from symptom onset to primary percutaneous coronary intervention. RESULTS: The AW-acuteness score correlated significantly with salvageable myocardium for right coronary artery (RCA) occlusions (r = -0.57; P = .02) but not for left anterior descending artery (LAD) occlusions (r = -0.04; P = .88). Time from symptom onset did not correlate with the amount of salvageable myocardium (LAD, r = 0.04 and P = .87; RCA, r = -0.40 and P = .13). CONCLUSIONS: There is a moderate correlation between AW-acuteness score and salvageable myocardium in patients with acute RCA occlusion but not in patients with LAD occlusion.
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