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  • 1
    Online Resource
    Online Resource
    Die Versorgung Psychischer Erkrankungen in Deutschland : Aktuelle Stellungnahmen der DGPPN 2003-2004. (2004)
    Berlin, Heidelberg :Springer Berlin / Heidelberg,
    Details
    Keywords: Psychiatry -- Germany. ; Medicine. ; Electronic books.
    Type of Medium: Online Resource
    Pages: 1 online resource (173 pages)
    Edition: 1st ed.
    ISBN: 9783540268680
    URL: https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=324779
    DDC: 548.9
    Language: German
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    GEOMAR EBL
  • 2
    Electronic Resource
    Electronic Resource
    Interleukin-1β and Tumor Necrosis Factor-α Induce Expression of α1-Antichymotrypsin in Human Astrocytoma Cells by Activation of Nuclear Factor-κB (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 67 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The protease inhibitor α1-antichymotrypsin (ACT) has been suggested to be involved in the etiology of Alzheimer's disease (AD). Increased levels of ACT have been found in serum and brains of AD patients, and ACT has been proposed to regulate β-amyloid fibril formation in vitro. To gain insight into the regulation of ACT in the brain, we investigated the signal transduction pathways involved in ACT gene expression and protein synthesis in the human astrocytoma cell line U373. This cell line has previously been shown to respond with strong ACT synthesis on stimulation with interleukin-1β (IL-1β) or tumor necrosis factor-α (TNFα). Here, we describe that both IL-1β and TNFα activate the transcription factor nuclear factor-κB (NF-κB) via production of reactive oxygen intermediates resulting in ACT expression. In addition, we show that neither protein kinase C nor protein kinase A is involved in IL-1β- or TNFα-induced ACT expression. These results suggest that activation of NF-κB may be one possible cause of increased ACT levels in AD and provide a basis for the development of drugs used for the modulation of inflammatory processes occurring in AD.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.67052039.x
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Interleukin-1β Uses Common and Distinct Signaling Pathways for Induction of the Interleukin-6 and Tumor Necrosis Factor α Genes in the Human Astrocytoma Cell Line U373 (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 66 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Cytokines are involved in the etiology of different disorders of the CNS. For a better understanding of their pathogenic role, we analyzed signal transduction pathways mediating the interleukin (IL)-1β-induced synthesis of IL-6 and tumor necrosis factor α (TNFα) in the human astrocytoma cell line U373 MG. Both protein kinase C and reactive oxygen intermediates (ROIs) were involved in IL-6 and TNFα gene expression by IL-1β. In contrast, protein tyrosine kinases were only necessary for expression of the IL-6 gene. Whereas activation of protein kinase A was able to induce expression of the IL-6 gene, it did not induce TNFα gene expression and was not involved in IL-1β-induced IL-6 and TNFα gene expression. Activation of the transcription factor nuclear factor-κB by IL-1β involved ROIs, whereas the IL-1β-induced activation of the transcription factor AP-1 was mediated via protein kinase C. Our findings provide the basis for the development of specific drugs for the treatment of disorders of the CNS in which cytokines play a pathogenic role.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.66041496.x
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Adenosine A2b Receptors Mediate an Increase in Interleukin (IL)-6 mRNA and IL-6 Protein Synthesis in Human Astroglioma Cells (1996)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 66 (1996), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The cytokine interleukin (IL)-6 has recently been demonstrated to play a role in the pathology of Alzheimer's disease (AD). The mechanisms leading to increased IL-6 levels in brains of AD patients are still unknown. Because in experimental animals ischemia increases both the level of cytokines and the extracellular concentrations of adenosine in the brain, we hypothesized that these two phenomena may be functionally connected and that adenosine might increase IL-6 gene expression in the brain. Here we show that the mixed A1 and A2 agonist 5′-(N-ethylcarboxamido)adenosine (NECA) induces an increase in IL-6 mRNA levels and protein synthesis in the human astrocytoma cell line U373 MG. The A1-specific agonists R-phenylisopropyladenosine and cyclopentyladenosine are much less potent, and the A2a-specific agonist CGS-21680 shows only marginal effects. Increased levels of mRNA are already found within 30 min after NECA treatment. The A2a-selective antagonists 8-(3-chlorostyryl)caffeine and KF17837 [(E)-8-(3,4-dimethoxystyryl)-1,3-dipropyl-7-methylxanthine], which have also some antagonistic properties at A2b receptors, and the nonspecific adenosine antagonist 8-phenyltheophylline were equipotent at inhibiting the NECA-induced increase in IL-6 protein synthesis, whereas the specific A1 antagonist 8-cyclopentyl-1,3-dipropylxanthine is much less potent. The results indicate that adenosine A2b receptors participate in the regulation of the IL-6 gene in astrocytoma cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1996.66041426.x
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    Paper (German National Licenses)
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  • 5
    Electronic Resource
    Electronic Resource
    Prostaglandin E2 Induces Interleukin-6 Synthesis in Human Astrocytoma Cells (1997)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 68 (1997), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Prostaglandins (PGs) and cytokines, such as interleukin-1 (IL-1) and interleukin-6 (IL-6), have been implicated in the etiopathology of various inflammatory and degenerative disorders, including Alzheimer's disease (AD) and prion diseases. Nonsteroidal antiinflammatory drugs (NSAIDs), potent inhibitors of PG synthesis, appear to be beneficial in the treatment of AD. To assess whether PGs are able to induce IL-6 synthesis in cells of the CNS, IL-6 mRNA and protein syntheses were measured in a human astrocytoma cell line after stimulation with different PGs. PGE1 and PGE2, but not PGD2 and PGF2α, led to a rapid and transient induction of IL-6 mRNA, followed by IL-6 protein synthesis. Furthermore, PGE2 potentiated IL-1β-induced IL-6 mRNA synthesis. These results are discussed with respect to the participation of PGs in neurodegenerative diseases (and its inhibition by NSAIDs) by affecting cytokine expression.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1997.68020704.x
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    Paper (German National Licenses)
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  • 6
    Electronic Resource
    Electronic Resource
    Substance P and Histamine Induce Interleukin-6 Expression in Human Astrocytoma Cells by a Mechanism Involving Protein Kinase C and Nuclear Factor-IL-6 (1998)
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 70 (1998), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Interleukin-6 (IL-6) is a proinflammatory cytokine whose synthesis is induced by a variety of stimuli including interleukin-1 (IL-1), substance P (SP), and histamine. Because IL-6 has been implicated in the etiopathology of different human diseases including multiple myeloma, rheumatoid arthritis, multiple sclerosis, acquired immunodeficiency syndrome dementia complex, and Alzheimer's disease, its inhibition may be of therapeutic interest. A main demand on an effective inhibitor of IL-6 expression is that it inhibits IL-6 synthesis independently of the inducing stimulus. We therefore used human astrocytoma cells to search for signal transduction cascades and transcription factors whose inhibition suppresses IL-6 synthesis after stimulation with three different inductors, IL-1β, SP, and histamine. Whereas the antioxidant pyrrolidinedithiocarbamate was only able to inhibit IL-1β-induced IL-6 expression, inhibition of protein kinase C prevented IL-6 expression induced by all three substances. Promoter deletion analysis revealed that IL-1β-induced IL-6 expression required the transcription factor nuclear factor-κB (NF-κB), whereas SP- and histamine-induced IL-6 synthesis was essentially controlled by NF-IL-6. These findings suggest that inhibition of protein kinase C or a combinatory inhibition of NF-IL-6 and NF-κB binding are strategies to effectively suppress IL-6 synthesis. They therefore provide the basis for the development of antiinflammatory drugs used to treat disorders in which IL-6 is pathogenically involved.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1471-4159.1998.70041577.x
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    Paper (German National Licenses)
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  • 7
    Electronic Resource
    Electronic Resource
    Immunologische Systemerkrankungen als Differentialdiagnose in der Psychiatrie (1997)
    Springer
    Der Nervenarzt 68 (1997), S. 696-707 
    Details
    ISSN: 1433-0407
    Keywords: Schlüsselwörter Autoimmunerkrankung ; Systemischer Lupus erythematodes ; Sjögren-Syndrom ; Vaskulitis ; Depression ; Schizophrenie ; Demenz ; Hirnorganisches Psychosyndrom ; Key words Autoimmune diseases ; Systemic lupus erythematodes ; Sjögren’s syndrome ; Mental disorders ; Depressive disorders ; Schizophrenia ; Dementia ; Organic brain syndrome
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Psychiatric symptoms may be caused by systemic autoimmune diseases. Quite often, mental disorders are an early symptom during the course of an autoimmune disease and sometimes they may even be the presenting symptom. This article reviews psychiatric and neurologic symptoms in systemic lupus erythematodes, Sjögren syndrome, primary vasculitides and other immunopathies such as the primary antiphospholipid syndrome and Sneddon’s syndrome. The article also discusses diagnostic aspects and therapeutic options if an autoimmune disease as cause of a psychiatric or neurologic symptom is suspected. An increased awareness of psychiatrists and neurologists will make it possible that systemic autoimmune diseases are early identified as a possible cause of psychiatric symptoms and may then be treated adequately.
    Notes: Zusammenfassung Psychische Störungen können bei zahlreichen immunologischen Systemerkrankungen auftreten. Häufig sind sie ein frühes Krankheitssymptom, gelegentlich sogar das präsentierende Symptom. Die vorliegende Arbeit gibt eine Übersicht über das Vorkommen psychischer und neurologischer Symptome bei verschiedenen immunologischen Systemerkrankungen wie dem systemischen Lupus erythematodes, dem Sjögren-Syndrom, den primären Vaskulitiden und anderen Immunopathien wie dem Antiphospholipidsyndrom und dem Sneddon-Syndrom. Darüber hinaus werden Leitlinien zum differentialdiagnostischen Vorgehen und zur Therapie bei Verdacht auf eine immunologische Systemerkrankung als Ursache einer psychischen Störung dargelegt und diskutiert. Durch Beachtung der gegebenen Leitlinien kann es in Einzelfällen psychischer Störungen gelingen, eine immunologische Systemerkrankung als Ursache der psychischen Störung zu identifizieren und so frühzeitig eine kausale Therapie einzuleiten.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001150050184
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    Paper (German National Licenses)
    Fulltext
  • 8
    Electronic Resource
    Electronic Resource
    Interleukin-6 is present in early stages of plaque formation and is restricted to the brains of Alzheimer's disease patients (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 544-551 
    Details
    ISSN: 1432-0533
    Keywords: Senile plaques ; Primitive plaques ; Alzheimer's disease ; Interleukin-6 ; Pathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Interleukin-6 (IL-6) immunoreactivity has previously been shown in plaques in Alzheimer's disease (AD) and elevated IL-6 concentrations have been measured biochemically in brains of AD patients. In this study, we investigated the appearance of IL-6 immunoreactivity in AD plaques according to the stage of plaque formation. Using the Bielschowsky silver-staining method, we were able to differentiate between four types of plaques described earlier: diffuse, primitive, classic and compact. While diffuse plaques represent the early stage of plaque formation, primitive and classic plaques are thought to represent later stages of plaque development. We investigated serial sections of paraffin-embedded cortices of ten clinically diagnosed and histopathologically confirmed AD patients and ten patients with no clinical history of dementia. We found plaques in the brains of both nondemented and demented persons using the silver staining method or immunohistochemistry with antibodies against the amyloid precursor protein. In the group of clinically nondemented persons, diffuse plaques were the predominant plaque type, whereas primitive plaques formed the larger portion of lesions in the group of AD brains. IL-6 could not be detected in plaques of patients without dementia. Many IL-6-positive plaques were found in six of the AD brains and to a smaller extent in the other four AD cases. In the six cases with a large number of IL-6-positive plaques, IL-6 was found in a significantly higher ratio of diffuse plaques than expected from a random distribution of IL-6 in all plaque types. We conclude from these findings that IL-6 immunoreactivity correlates with clinical dementia and that in AD patients, an IL-6-related immunological event may contribute to plaque formation. IL-6 might be involved both in the transformation from diffuse to primitive plaques in AD as well as in the development of dementia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571510
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    Paper (German National Licenses)
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  • 9
    Electronic Resource
    Electronic Resource
    Interleukin-6 is present in early stages of plaque formation and is restricted to the brains of Alzheimer's disease patients (1995)
    Springer
    Acta neuropathologica 89 (1995), S. 544-551 
    Details
    ISSN: 1432-0533
    Keywords: Key words Senile plaques ; Primitive plaques ; Alzheimer's disease ; Interleukin-6 ; Pathology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Interleukin-6 (IL-6) immunoreactivity has previously been shown in plaques in Alzheimer's disease (AD) and elevated IL-6 concentrations have been measured biochemically in brains of AD patients. In this study, we investigated the appearance of IL-6 immunoreactivity in AD plaques according to the stage of plaque formation. Using the Bielschowsky silver-staining method, we were able to differentiate between four types of plaques described earlier: diffuse, primitive, classic and compact. While diffuse plaques represent the early stage of plaque formation, primitive and classic plaques are thought to represent later stages of plaque development. We investigated serial sections of paraffin-embedded cortices of ten clinically diagnosed and histopathologically confirmed AD patients and ten patients with no clinical history of dementia. We found plaques in the brains of both nondemented and demented persons using the silver staining method or immunohistochemistry with antibodies against the amyloid precursor protein. In the group of clinically nondemented persons, diffuse plaques were the predominant plaque type, whereas primitive plaques formed the larger portion of lesions in the group of AD brains. IL-6 could not be detected in plaques of patients without dementia. Many IL-6-positive plaques were found in six of the AD brains and to a smaller extent in the other four AD cases. In the six cases with a large number of IL-6-positive plaques, IL-6 was found in a significantly higher ratio of diffuse plaques than expected from a random distribution of IL-6 in all plaque types. We conclude from these findings that IL-6 immunoreactivity correlates with clinical dementia and that in AD patients, an IL-6-related immunological event may contribute to plaque formation. IL-6 might be involved both in the transformation from diffuse to primitive plaques in AD as well as in the development of dementia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00571510
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    Paper (German National Licenses)
    Fulltext
  • 10
    Electronic Resource
    Electronic Resource
    Neurobiological similarities in antidepressant sleep deprivation and psychostimulant use: a psychostimulant theory of antidepressant sleep deprivation (1998)
    Springer
    Psychopharmacology 140 (1998), S. 1-10 
    Details
    ISSN: 1432-2072
    Keywords: Key words Depression ; Sleep deprivation ; Psychostimulant ; Dopamine ; Therapy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract This paper attempts to summarize the evidence for the hypothesis that psychostimulant-like neurotransmitter processes within certain regions of the limbic system induce the positive effects of antidepressant sleep deprivation (SD). Preclinical and human studies indicate similar neurobiological effects of psychostimulants such as amphetamines, cocaine and SD. In clinical use, SD and psychostimulants have similar characteristics and behavioral effects. Furthermore, acute psychostimulant challenge decreases limbic metabolism in imaging studies, and SD decreases elevated limbic metabolism in SD responders, indicating that psychostimulant-like neurotransmitter release could decrease limbic metabolism in SD responders. Most antidepressant pharmacotherapies change the reactivity of the dopamine system, and a decrease of presynaptic dopamine or postsynaptic availability can induce depression. Sleep is accompanied by a reduction of catecholamine release and those processes which are increased by psychostimulants. It is concluded that a proposed regional postsynaptic deficit in catecholaminergic neurotransmission can be overcome either acutely by enhanced release during SD or psychostimulant use, or chronically by changes in receptor sensitivity or gene expression due to antidepressant therapies. A postsynaptic deficit in these areas becomes evident if presynaptic release is reduced in conditions such as sleep. Therefore, sleep is depressiogenic for predisposed individuals and the reduction of sleep avoids understimulation of subsensitive postsynaptic processes, which are enhanced by psychostimulants.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002130050732
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