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  • 1
    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.
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  • 2
    ISSN: 1433-8491
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 3
    ISSN: 1433-8491
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
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  • 4
    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.
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  • 5
    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.
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  • 6
    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.
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  • 7
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Stimuli that evoke seizure are capable of inducing structural changes in the hippocampus. However, late-acting genes related to these changes have not been described. Administration of pentylenetetrazole (PTZ; 50 mg/kg) to rats of various ages evoked tonic-clonic seizures. Using RNA gel blot analysis we found that the level of the mRNA for microtubule-associated protein 1B (MAP1B) was robustly increased in the hippocampus of 3-month-old rats. The levels of MAP1B mRNA in hippocampus peaked at 40 h and began to decline by 72 h following PTZ treatment. Immunoblotting with anti-MAP1B antibody demonstrates the increase in content of immunoreactive proteins 40–72 h after seizure onset in the hippocampus of PTZ-treated rats. These results indicate that MAP1B is a sensitive indicator of hippocampal structural changes occurring in response to PTZ-induced seizure activity.
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  • 8
    ISSN: 1617-4623
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Heteroduplex DNA molecules were prepared in vitro using one strand of DNA carrying a point mutation and one strand of the corresponding wild-type DNA. The heteroduplex DNA was transfected into competent bacteria and the progeny genotypes in the resulting infective centers were determined. From the results were conclude that about 80% of all transfected DNA molecules are repaired before DNA replication starts. This fraction of repaired DNA is independent of the location of the mismatched nucleotide pair. However, mismatch correction occurs preferentially on the H strand of the heteroduplex DNA. The repair does not depend on a known phage coded function but requires the active bacterial genes mut U, mut H, mut S and probably mut L.
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  • 9
    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.
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  • 10
    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.
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