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  • 1
    facet.materialart.
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  32. Wissenschaftliche Jahrestagung der Deutschen Gesellschaft für Phoniatrie und Pädaudiologie (DGPP); 20150924-20150927; Oldenburg; DOC26 /20150907/
    Publication Date: 2015-09-08
    Description: Hintergrund: Neben mechanischen Kräften der Zunge sind in der Literatur auch atmosphärische Druckänderungen in der Mundhöhle beschrieben, deren klinische Bedeutung für den Schluckvorgang noch unklar ist [Lit.]. In unserer Studie soll die orale Phase bei gesunden Probanden und bei Patienten mit einer amyotrophen Lateralsklerose (ALS) manometrisch untersucht werden.Material und Methoden: Es wurden 20 gesunde Probanden und 10 Patienten mit einer ALS untersucht. Bei allen Probanden und Patienten führten wir eine flexibel endoskopische Evaluation des Schluckens (FEES) (rpszene, Fa. Rehder&Partner, Hamburg) durch sowie eine manometrische Messung im Mundraum (GSOFT, Fa. Greisinger, Regenstauf). Hierbei wurden sowohl der maximale Sog als auch die Druckänderungen beim Trockenschlucken ermittelt. Die Selbstbeurteilung des Schluckvermögens durch die Probanden und Patienten erfolgte durch den Sydney Swallow Questionnaire (SSQ).Ergebnisse: Die Druckmessung wurde von allen Probanden und Patienten problemlos toleriert. Negative orale Drücke konnten bei allen Untersuchten während des Schluckvorganges nachgewiesen werden. Die Mittelwerte des maximalen Sogs beim Normkollektiv (-260,3 mmHg) und bei ALS-Patienten (-96,7 mmHg) unterschieden sich signifikant (p-Wert 〈0,001). Nicht signifikant zeigte sich der Vergleich der maximalen Drücke während des Trockenschluckens (p-Wert 0,936026). Die subjektive Einschätzung der Schluckfunktion (SSQ) insgesamt differierte in beiden Kollektiven signifikant (p-Wert 〈0,001).Diskussion: Die Betrachtung der oralen Phase verdient in der Dysphagie-Diagnostik Beachtung. Da der Mundraum für eine Untersuchung leicht zugänglich ist, würde sich ein Messverfahren auch für Screenings im Rahmen stationärer Behandlungen oder zu Kontrollen im Verlauf von Schlucktherapien oder als Biofeedback anbieten. Zuvor sind jedoch weitere Evaluationen zur klinischen Bedeutung auch an anderen Patientengruppen erforderlich.
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 2
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  84. Jahresversammlung der Deutschen Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie; 20130508-20130512; Nürnberg; DOC13hnod553 /20130415/
    Publication Date: 2013-04-16
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 3
    Keywords: RECEPTOR ; MOUSE MODEL ; CENTRAL-NERVOUS-SYSTEM ; HEMATOPOIETIC STEM-CELLS ; FAS-LIGAND ; PARKINSONS-DISEASE ; INFLAMMATORY MONOCYTES ; DOPAMINERGIC NEURODEGENERATION ; MICROGLIAL ACTIVATION ; BODY IRRADIATION
    Abstract: Neuroinflammation is increasingly recognized as a hallmark of neurodegeneration. Activated central nervous system-resident microglia and infiltrating immune cells contribute to the degeneration of dopaminergic neurons (DNs). However, how the inflammatory process leads to neuron loss and whether blocking this response would be beneficial to disease progression remains largely unknown. CD95 is a mediator of inflammation that has also been proposed as an apoptosis inducer in DNs, but previous studies using ubiquitous deletion of CD95 or CD95L in mouse models of neurodegeneration have generated conflicting results. Here we examine the role of CD95 in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP)-induced neurodegeneration using tissue-specific deletion of CD95 or CD95L. We show that DN death is not mediated by CD95-induced apoptosis because deletion of CD95 in DNs does not influence MPTP-induced neurodegeneration. In contrast, deletion of CD95L in peripheral myeloid cells significantly protects against MPTP neurotoxicity and preserves striatal dopamine levels. Systemic pharmacological inhibition of CD95L dampens the peripheral innate response, reduces the accumulation of infiltrating myeloid cells, and efficiently prevents MPTP-induced DN death. Altogether, this study emphasizes the role of the peripheral innate immune response in neurodegeneration and identifies CD95 as potential pharmacological target for neurodegenerative disease.
    Type of Publication: Journal article published
    PubMed ID: 25779632
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  • 4
    Abstract: Since cancer cells often evade apoptosis, induction of necroptosis as another mode of programmed cell death is considered a promising therapeutic alternative. Here, we identify a novel synergistic interaction of Smac mimetics that antagonize x-linked Inhibitor of Apoptosis (XIAP), cellular Inhibitor of Apoptosis (cIAP) 1 and 2 with interferon (IFN)gamma to induce necroptosis in apoptosis-resistant cancer cells in which caspase activation is blocked. This synergism is confirmed by calculation of combination indices (CIs) and found in both solid and hematological cancer cell lines as well as for different Smac mimetics (i.e. BV6, Birinapant), pointing to a broader relevance. Importantly, individual genetic knockdown of key components of necroptosis signaling, i.e. receptor-interacting protein (RIP) 1, RIP3 or mixed lineage kinase domain-like pseudokinase (MLKL), significantly protects from BV6/IFNgamma-induced cell death. Similarly, pharmacological inhibitors of RIP1 (necrostatin-1(Nec-1)), RIP3 (GSK'872) or MLKL (necrosulfonamide (NSA)) significantly reduce BV6/IFNgamma-stimulated cell death. Of note, IFN-regulatory factor (IRF)1 is required for BV6/IFNgamma-mediated necroptosis, as IRF1 silencing provides protection from cell death. By comparison, antibodies blocking tumor necrosis factor (TNF)alpha, TNF-related apoptosis-inducing ligand (TRAIL) or CD95 ligand fail to inhibit BV6/IFNgamma-induced cell death, pointing to a mechanism independently of death receptor ligands. This is the first report showing that Smac mimetics synergize with IFNgamma to trigger necroptosis in apoptosis-resistant cancer cells with important implications for Smac mimetic-based strategies for the treatment of cancer.
    Type of Publication: Journal article published
    PubMed ID: 28923396
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  • 5
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    German Medical Science; Düsseldorf, Köln
    In:  Kooperative Versorgung - Vernetzte Forschung - Ubiquitäre Information; 49. Jahrestagung der Deutschen Gesellschaft für Medizinische Informatik, Biometrie und Epidemiologie (gmds), 19. Jahrestagung der Schweizerischen Gesellschaft für Medizinische Informatik (SGMI) und Jahrestagung 2004 des Arbeitskreises Medizinische Informatik (ÖAKMI) der Österreichischen Computer Gesellschaft (OCG) und der Österreichischen Gesellschaft für Biomedizinische Technik (ÖGBMT); 20040926-20040930; Innsbruck; DOC04gmds102 /20040914/
    Publication Date: 2004-09-14
    Keywords: ddc: 610
    Language: German
    Type: conferenceObject
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  • 6
    ISSN: 1432-072X
    Keywords: Collagenase ; Alkaline protease ; Temperature control ; Oxygen control ; Regulation ; Vibrio alginolyticus ; Secretion exoproteins ; Cerulenin ; Quinacrine ; Microbial ecology
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The production of an extracellular collagenase and an alkaline protease by Vibrio alginolyticus during stationary phase was inhibited by a temperature shift from 30 to 37°C and by a lack of oxygen. The stability of the exoproteases was unaffected by incubation at 37°C and aeration. The optimum growth temperature for the V. alginolyticus strain was 33.5°C Aeration enhanced the rate of growth of exponential phase cells. Temperature and oxygen did not affect the growth of stationary phase cells when the exoproteases were being produced. Macromolecular synthesis in stationary phase cells was not affected by temperature. There was no rapid release of the exoproteases after temperature shift down and chloramphenicol inhibited the production of the enzymes when added at time of temperature shift down from 37 to 30°C. The regulation of exoprotease production by temperature and oxygen was specific and has implications regarding the ecology of V. alginolyticus. Cerulenin, quinacrine and O-phenanthroline inhibited the production of the exoproteases.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-072X
    Keywords: Vibrio alginolyticus ; Glutamine synthetase ; Metabolic regulation ; Catabolic repression
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract Glutamine synthetase (EC 6.3.1.2) has been purified from a collagenolytic Vibrio alginolyticus strain. The apparent molecular weight of the glutamine synthetase subunit was approximately 62,000. This indicates a particle weight for the undissociated enzyme of 744,000, assuming the enzyme is the typical dodecamer. The glutamine synthetase enzyme had a sedimentation coefficient of 25.9 S and seems to be regulated by a denylylation and deadenylylation. The pH profiles assayed by the γ-glutamyltransferase method were similar for NH4-shocked and unshocked cell extracts and isoactivity point was not obtained from these eurves. The optimum pH for purified and crude cell extracts was 7.9. Cell-free glutamine synthetase was inhibited by some amino acids and AMP. The transferase activity of glutamine synthetase from mid-exponential phase cells varied greatly depending on the sources of nitrogen or carbon in the growth medium. Glutamine synthetase level was regulated by nitrogen catabolite repression by (NH4)2SO4 and glutamine, but cells grown, in the presence of proline, leucine, isoleucine, tryptophan, histidine, glutamic acid, glycine and arginine had enhanced levels of transferase activity. Glutamine synthetase was not subject to glucose, sucrose, fructose, glycerol or maltose catabolite repression and these sugars had the opposite effect and markedly enhanced glutamine synthetase activity.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-1106
    Keywords: Motor control ; Speed-accuracy trade-off ; Prehension ; Human
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Earlier studies have suggested that the size of an object to be grasped influences the time taken to complete a prehensile movement. However, the use of cylindrical objects in those studies confounded the effects of object size — extent orthogonal to the reach axis — and object width — extent along the reach axis. In separating these effects, the present study demonstrates that movement time is not affected by manipulation of object size, as long as the latter does not approach the maximal object size that can be grasped. Object width, on the other hand, is shown to exert a systematic influence on movement time: Smaller object widths give rise to longer movement times through a lengthening of the deceleration phase of the movement, thus reproducing the effect of target width on the kinematics of aiming movements. As in aiming, movement amplitude also affects the movement time in prehension, influencing primarily the acceleration phase (i.e. peak velocity attained). The effects of object width and movement amplitude were found to combine in a way predicted by Fitts' law, allowing a generalisation of the latter to the transport component in prehensile actions. With respect to the grasp component, both object size and object width are shown to affect peak hand aperture. Increasing object width thus lowers the spatial accuracy demands on the transport component, permitting a faster movement to emerge. At the same time, the hand opens to a larger grip in order to compensate for eventual directional errors that result. Finally, with respect to the control mode of the grasp component, it was found that peak finger closing velocity scales to distance to be covered, defined as the peak hand aperture minus object size.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0983
    Keywords: α-amylase ; Filamentous fungi ; Gene duplication
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Using synthetic oligonucleotide probes, we cloned genomic DNA sequences encoding an α-amylase gene from Aspergillus niger var. awamori (A. awamori) on a 5.8 kb EcoRI fragment. Hybridization experiments, using a portion of this cloned fragment to probe DNA from A. awamori, suggested the presence of two α-amylase gene copies which were subsequently cloned as 7 kb (designated as amyA) and 4 kb (amyB) HindIII fragments. DNA sequence analysis of the amyA and amyB genes revealed the following: (1) Both genes are arranged as nine exons and eight introns; (2) The nucleotide sequences of amyA and amyB are identical throughout all but the last few nucleotides of their respective coding regions; (3) The amyA and amyB genes from A. awamori share extensive homology (≥98% identity) with the genes encoding Taka-amylase from A. oryzae. In order to test whether both amyA and amyB were functional in the genome, we constructed vectors containing gene fusions of either amyA and amyB to bovine prochymosin cDNA and used these vectors to transform A. awamori. Transformants which contained either the amyA- or amyB-prochymosin gene fusions produced extracellular chymosin, suggesting that both genes are functional.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1432-1211
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Five sets of cytotoxic effector cells were generated, using haploidentical, first degree relatives in five different families, against the HLA-A3; B7 serological determinants combined with different DR antigens. When tested against a panel of cells bearing combinations of the HLA-A, -B and -DR antigens it was shown that the HLA-B7 antigen was as strong a CML target determinant alone as it was in the presence of HLA-A3. The strength of the HLA-A3 antigen as target determinant varied. With effector cells primed to the HLA-A3; B7; DR2 haplotype, the A3 antigen alone behaved as a weak target determinant. When the same target cells were tested with the effector cells generated against HLA-A3; B7 without DR2, the A3 antigen behaved as a strong target determinant. A number of target cells lacking the serologically detectable HLA determinants present on the sensitizing HLA haplotype were identified as being killed by specific effector cells. These data suggest either a number of new CML target determinants controlled by different loci or the presence of a single, new locus with multiple alleles controlling CML targets.
    Type of Medium: Electronic Resource
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