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  • 1
    Electronic Resource
    Electronic Resource
    [S.l.] : American Institute of Physics (AIP)
    Review of Scientific Instruments 69 (1998), S. 2120-2126 
    ISSN: 1089-7623
    Source: AIP Digital Archive
    Topics: Physics , Electrical Engineering, Measurement and Control Technology
    Notes: A low-energy ion-beam facility for surface and materials science has been built which allows ion beam treatments of solid surfaces via single-ion impacts up to high-fluence implantations. The system offers mass-separated ion beams of 0.5–10 keV by a normal acceleration, and of 5–2000 eV by an acceleration/deceleration lens combination. Its energy spread is estimated to be as small as 2 eV in the whole range. Ion current densities are available in the range between 0.1 nA/cm2 and up to 50 μA/cm2, corresponding to a particle flux of 109–1014 ions/cm2 s. Homogeneous implantation profiles are achieved using an electrostatic x-y deflection system. First applications for ion induced defect production on highly oriented pyrolytic graphite surfaces detected via scanning tunneling microscopy are presented. Hillock shaped defect formations were detected and attributed to protusions of the atomic surface structure, which were induced by interstitials and interstitial clusters between the first atomic planes originated from recoil atoms of the collision cascade. © 1998 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 2
    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
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  • 3
    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
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  • 4
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 68 (1997), S. 0 
    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
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  • 5
    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
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  • 6
    Electronic Resource
    Electronic Resource
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 78 (1995), S. 2303-2310 
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: Antimony/aluminium films in bilayer and multilayer geometries were irradiated at liquid-nitrogen temperature with 50–900 keV ion beams ranging in mass from 20Ne to 208Pb. Depth profiling of the element concentrations was carried out via Rutherford backscattering spectroscopy. The formation of intermetallic phases and phase segregation was analyzed by means of x-ray diffraction, cross-section transmission electron microscopy, and scanning electron microscopy. From the low-dose irradiation data, the mixing rates k were obtained and found to depend linearly on the energy density FD deposited at the interface. The mixing efficiency of Sb/Al bilayers, k/FD=296(30) A(ring)5/eV, supports the local thermal spike model. After high-fluence irradiations of Sb/Al bilayers with 550 keV Xe++ ions, a reacted layer of crystalline SbAl (B3 phase) at the interface was observed. Sb/Al multilayers irradiated with 900 keV Xe++ ions were found to become amorphous. Phase formation was studied as a function of the ion fluence, irradiation energy, and ion mass, and was found to start at that fluence, where cracking and shrinking of the Sb top layer and an increase of the sputtering yield were also observed. © 1995 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    [S.l.] : American Institute of Physics (AIP)
    Journal of Applied Physics 85 (1999), S. 3120-3123 
    ISSN: 1089-7550
    Source: AIP Digital Archive
    Topics: Physics
    Notes: We report on the evaluation of ion-beam induced damage in α-quartz and its dynamic annealing behavior in the temperature range between 80 and 1050 K using Rutherford backscattering spectrometry in channeling geometry. The results illustrate that the critical temperature for inhibiting amorphization during irradiation is about Tc(approximate)940 K. The critical fluence φc for amorphization is independent of the temperature up to 550 K, but strongly increases at higher temperatures. The activation energy for the diffusion of defects in the collision cascade or at the amorphous/crystalline interface is found to be 0.28±0.02 eV. The dynamic annealing mechanism is explained by the vacancy out-diffusion model of Morehead and Crowder. © 1999 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 8
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    European journal of neuroscience 8 (1996), S. 0 
    ISSN: 1460-9568
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: In order to analyse mechanisms of sex differentiation of the hippocampus at the cellular level, the differentiation of hippocampal GABAergic neurons was studied in vitro. Serum-supplemented and serum-free dissociated cell cultures were raised from the hippocampus of embryonic day 17 male and female rat embryos for up to 14 days in vitro. This time period roughly corresponds to the critical phase for sex differentiation of the rat brain as determined in vivo. Serum-free cultures were treated with testosterone and/or 17β-oestradiol for the entire culture period. Control cultures from male donors contained twice as many GABA-immunoreactive neurons as those from female donors, while there was no sex difference in overall counts of neurons stained for microtubule-associated protein 5. Measurements of high-affinity uptake of [3H]GABA essentially confirmed this sex difference. The development of the sex difference could not be influenced by long-term treatment with androgen or oestrogen. It is concluded that sex differentiation of a specific subpopulation of hippocampal neurons may take place independently of the environment provided by gonadal steroids and in the absence of extrinsic connections with the hypothalamus or other relays of the limbic circuit.
    Type of Medium: Electronic Resource
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  • 9
    Electronic Resource
    Electronic Resource
    Springer
    Der Nervenarzt 68 (1997), S. 696-707 
    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
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  • 10
    ISSN: 1432-0878
    Keywords: Key words: Interleukin-6 ; Interleukin-1β ; Tenidap ; Astrocytes ; Alzheimer’s disease ; Therapy ; Cell culture ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Tenidap is a structurally novel antirheumatic agent with anti-inflammatory and analgesic properties. Previous studies have shown that tenidap is able to inhibit the production and action of cytokines such as interleukin-1, interleukin-6 (IL-6) and tumour necrosis factor α. However, the mechanisms by which tenidap inhibits cytokine synthesis are not yet known. We investigated in the human astrocytoma cell line U373 whether tenidap inhibits IL-6 synthesis by inhibition of certain signal transduction processes leading to IL-6 synthesis. Cells were stimulated with different substances which have previously been shown to activate protein kinase A or C, reactive oxygen intermediates as well as transcription factors such as nuclear factor kappa B and AP-1 and which all result in IL-6 synthesis. Tenidap was a very potent inhibitor of IL-6 synthesis independent of the stimuli used, suggesting an inhibitory mechanism other than inhibition of a certain signal transduction pathway. Since IL-6 has been shown to be involved in the etiopathology of Alzheimer’s disease and since the use of nonsteroidal anti-inflammatory drugs appears to be of therapeutical benefit, it is concluded that tenidap should be tested in clinical trials in order to determine whether it may be useful for the treatment of Alzheimer’s disease.
    Type of Medium: Electronic Resource
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