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  • S. Karger AG  (2)
  • 1
    Online Resource
    Online Resource
    S. Karger AG ; 2006
    In:  Pathophysiology of Haemostasis and Thrombosis Vol. 35, No. 3-4 ( 2006), p. 322-345
    In: Pathophysiology of Haemostasis and Thrombosis, S. Karger AG, Vol. 35, No. 3-4 ( 2006), p. 322-345
    Abstract: It has long been known that the oxidative state of the various plasma lipoproteins modulates platelet aggregability, thereby contributing to atherogenesis. Low-density lipoprotein (LDL), occurring in vivo both in the native and oxidised forms, interacts directly with platelets, by binding to specific receptors. While the identity of the receptors for native LDL and some subfractions of high-density lipoproteins (HDL) remains disputed, apoE-containing HDL 〈 sub 〉 2 〈 /sub 〉 binds to LRP8. The nature of these interactions as well as the distinction between candidate receptor proteins was elucidated using covalently modified apolipoproteins, which pointed to the participation of apolipoproteins in high affinity binding. However, the platelet effects initiated by binding of native lipoproteins remain controversial. Some of this ambiguity can be traced to the fact that native LDL inevitably undergoes substantial oxidisation upon modification, including by radiolabelling. The platelet-activating effects provoked by oxidised LDL are irrefutable, but many details remain unknown. The role of CD36 in platelet binding by oxidised LDL is well established, although additional receptors may exist. Much less is known about the interaction of oxidised HDL with platelets, since platelet activation was observed in some, but not all studies. Various frequently applied in vitro oxidation methods produce modified lipoprotein species that may not be relevant in vivo. Based on the reported modifications obtained by in vitro oxidation of LDL, early investigations focused mainly on the formation and the eventual effects of oxidised lipids. More recently, alterations to lipoproteins performed using hypochloric acid and myeloperoxidase redirected the attention to the role of modified apoproteins in triggering platelet responses.
    Type of Medium: Online Resource
    ISSN: 1424-8832 , 1424-8840
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2006
    detail.hit.zdb_id: 2081182-2
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  • 2
    In: Neuropsychobiology, S. Karger AG, Vol. 81, No. 1 ( 2022), p. 69-79
    Abstract: 〈 b 〉 〈 i 〉 Introduction: 〈 /i 〉 〈 /b 〉 Asymmetrical alpha and frontal theta activity have been discussed as neurobiological markers for antidepressant treatment response. While most studies focus on resting-state EEG, there is evidence that task-related activity assessed at multiple time points might be superior in detecting subtle early differences. 〈 b 〉 〈 i 〉 Methods: 〈 /i 〉 〈 /b 〉 This was a naturalistic study design assessing participants in a psychiatric in- and outpatient hospital setting. We investigated stimulus-related EEG asymmetry (frontal and occipital alpha-1 and alpha-2) and power (frontal midline theta) assessed at baseline and 1 week after initiation of pharmacological depression treatment while presenting affective stimuli. We then compared week 4 responders and nonresponders to antidepressant treatment. 〈 b 〉 〈 i 〉 Results: 〈 /i 〉 〈 /b 〉 Follow-up analyses of a significant group × emotion × time interaction ( 〈 i 〉 p 〈 /i 〉 & #x3c; 0.04) for alpha-1 asymmetry showed that responders differed significantly at baseline in their asymmetry scores in response to sad compared to happy faces with a change in this pattern 1 week later. Nonresponders did not show this pattern. No significant results were found for alpha-2, occipital alpha-1, and occipital alpha-2 asymmetry or frontal midline theta power. 〈 b 〉 〈 i 〉 Discussion: 〈 /i 〉 〈 /b 〉 Our study addresses the gap in comparisons of task-related EEG activity changes measured at two time points and supports the potential value of this approach in detecting early differences in responders versus nonresponders to pharmacological treatment. Important limitations include the small sample size and the noncontrolled study design.
    Type of Medium: Online Resource
    ISSN: 0302-282X , 1423-0224
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2022
    detail.hit.zdb_id: 1483094-2
    SSG: 5,2
    SSG: 15,3
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