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  • 1
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    Cham : Springer International Publishing
    Keywords: Medicine ; Neurosciences ; Neurology ; Biomedicine ; Neurosciences ; Neurology ; Springer eBooks
    Description / Table of Contents: Part I: Clinical and Genetic Considerations of LRRK2 Associated Parkinson’s Disease -- Leucine-rich repeat kinase (LRRK2) genetics and Parkinson’s disease -- Clinical features of LRRK2 carriers with Parkinson’s disease -- Part II: Fundamentals of LRRK2 Biology -- LRRK2 phosphorylation -- Understanding the GTPase activity of LRRK2: regulation, function and neurotoxicity -- LRRK2 and autophagy -- Molecular insights and functional implication of LRRK2 dimerization -- LRRK2 and the immune system -- Regulation of LRRK2 by phosphatases -- Part III: LRRK2 Neurodegeneration, Modeling, and Therapeutic Options -- Animal models of LRRK2-associated Parkinson’s disease -- LRRK2 and the “LRRKtosome” at the crossroads of programmed cell death: Clues from RIP kinase relatives -- Interaction of LRRK2 and α-synuclein in Parkinson’s disease -- Mechanisms of mutant LRRK2 neurodegeneration -- Small molecule inhibitors of LRRK2
    Abstract: This is the first book to assemble the leading researchers in the field of LRRK2 biology and neurology and provide a snapshot of the current state of knowledge, encompassing all major aspects of its function and dysfunction. The contributors are experts in cell biology and physiology, neurobiology, and medicinal chemistry, bringing a multidisciplinary perspective on the gene and its role in disease. The book covers the identification of LRRK2 as a major contributor to the pathogenesis of Parkinson's Disease. It also discusses the current state of the field after a decade of research, putative normal physiological roles of LRRK2, and the various pathways that have been identified in the search for the mechanism(s) of its induction of neurodegeneration
    Pages: XVII, 271 p. 27 illus., 17 illus. in color. : online resource.
    ISBN: 9783319499697
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  • 2
    ISSN: 0260-8774
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 0260-8774
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 0260-8774
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Process Engineering, Biotechnology, Nutrition Technology
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0975
    Keywords: Key words Coral ; Remote sensing ; Optical spectra ; Pigments
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Geosciences
    Notes: Abstract  Coastal reef degradation and widespread bleaching of corals, i.e. loss of pigments and/or symbiotic zooxanthellae, is increasing globally. Remote sensing from boats, aircraft or satellites has great potential for assessing the extent of reef change, but will require ground-verified spectral algorithims characteristic of healthy and degraded reef populations. We collected seven species of Caribbean reef corals and also representative macroalgae from reefs near Lee Stocking Island, Bahamas and quantified their pigments using high performance liquid chromatography. We also measured the fluorescence and reflectance spectra of corals and macroalgae using an in situ benthic spectrofluorometer. In visibly pigmented (unbleached) coral from 4 to 5 m depth, the mean (±SD) surface density of pigments (3.0±1.3 μg chlorophyll-a cm-2 and 2.1±0.7 μg peridinin cm-2) was similar between colonies of the same species, but differed among species. The mean quantity of pigment per zooxanthella (1.8±0.9 pg chl-a cell-1 and 1.4±0.7 pg peridinin cell-1) also differed among species and sometimes between colonies of the same species. Chl-a and peridinin densities per surface area of coral were positively correlated. When excited with blue light (480 nm), macroalgae and corals had typical chlorophyll fluorescence with a peak at 680 nm and a smaller shoulder peak at 730 to 740 nm. Most corals, unlike macroalgae, also had distinct fluorescence peaks between 500 and 530 nm. In visibly bleached corals 680 nm fluorescence was greatly reduced in amplitude. Pigmented coral, under natural lighting conditions, had a reflected light peak at about 570 nm. Reflectance increased over all wavelengths in bleached corals, with the greatest increase at the wavelengths where chlorophyll and accessory pigments absorb light, i.e. 670 and 450 to 550 nm. Both fluorescence and reflectance spectra appear promising to remotely differentiate between pigmented and bleached coral and between coral and macroalgae.
    Type of Medium: Electronic Resource
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  • 6
    ISSN: 1432-8798
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary.  Liver samples from rabbits killed by RHDV, collected from five States in Australia in 1996 and 1997 were analysed by RT-PCR. A 398 bp fragment of the capsid protein (VP60) gene was amplified by PCR and directly sequenced. The alignment of the nucleotide and amino acid sequences and their comparison with the original strain of the virus released in Australia indicated genetic changes after two years have been small with 98.2% to 100% identity. The constructed phylogenetic tree suggests slight differences in nucleotide substitutions in various States but there is no clear evidence of clustering of sequences according to their geographic origin. In practical terms, sequencing of viral RNA provides a means of testing the efficacy of further releases and subsequent spread of the virus if such a strategy is employed as a means of enhancing RHD as a biological control of the wild rabbit in Australia.
    Type of Medium: Electronic Resource
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  • 7
    ISSN: 1432-069X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die Verhornung der Epidermis im Mäuseschwanz verläuft in unterschiedlicher Weise. In der Umgebung der Haarfollikeln ist eine granuläre Schicht, die Keratohyalin-Körnchen enthält; die Zellkerne fehlen in der verhornten Schicht. In der Schuppenregion wird kein Keratohyalin gebildet, und Kernreste bleiben in den verhornten Zellen, wie allgemein in der Parakeratose. Die Befunde des Lichtmikroskops konnten durch Transmission-Elektronmikroskopie bestätigt werden. Der vollständige Zusammenbruch der Organelle in der Region der Follikeln stand in Gegensatz zu dem Weiterbestehen der alten Zellkerne in den Schuppen. Manche dieser Kernreste waren pyknotisch wie in anormaler Parakeratose des Menschen, aber die meisten waren mehr degeneriert und hatten die Kernmembranen verloren. Die Epidermiszellen in der Grenzzone zwischen der Follikel und Schuppenregion enthielten ein paar Keratohyalin-Körnchen, und der Verfall der Nuklearreste in den verhornten Zellen war unvollkommen. Der Übergang zwischen lebenden Epidermiszellen und toten verhornten Zellen war scharf abgegrenzt sowohl in der Follikel als in der Schuppenregion. Die Plasmamembrane der Hornzellen waren in beiden Lagen verdickt, und die Zellen enthielten ein cytoplasmisches Netzwerk von Mikrofibrillen.
    Notes: Summary The mouse tail epidermis undergoes contrasting forms of keratinization. Around the hair follicle there is a granular layer containing keratohyalin granules, and nuclei are absent from the horny layer. In the scale regions keratohyalin is not formed and nuclear remnants are retained in the horny cells as in parakeratosis generally. These findings from light microscopy were confirmed by transmission electron microscopy. The complete breakdown of organelles in the follicular regions contrasted with the retention of effete nuclei in the scales. Some of these nuclear remnants were pyknotic as in abnormal human parakeratosis, but most were further degraded with loss of nuclear membranes. In the boundary zone between the follicular and scale regions the epidermal cells had a few small keratohyalin granules and also showed incomplete degradation of nuclear remnants in the horny cells. The change from living epidermal cells to dead keratinized cells was abrupt in both the follicular and scale regions. In both sites the plasma membranes of the horny cells were thickened and there was a cytoplasmic meshwork of microfibrils in the cells.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1432-0533
    Keywords: Key words Dementia ; Lewy body ; Neuropathology ; Synuclein ; Western blotting
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The identification of the α-synuclein gene on chromosome 4q as a locus for familial Lewy-body parkinsonism and of α-synuclein as a component of Lewy bodies has heralded a new era in the study of Parkinson’s disease. We have identified a large family with Lewy body parkinsonism linked to a novel locus on chromosome 4p15 that does not have a mutation in the α-synuclein gene. Here we report the clinical and neuropathological findings in an individual from this family and describe unusual high molecular weight α-synuclein-immunoreactive proteins in brain homogenates from brain regions with the most marked neuropathology. Distinctive histopathology was revealed with α-synuclein immunostaining, including pleomorphic Lewy bodies, synuclein-positive glial inclusions and widespread, severe neuritic dystrophy. We also discuss the relationship of this familial disorder to a Lewy body disease clinical spectrum, ranging from Parkinson’s disease to dementia with psychosis.
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: 1-Methyl-4-phenylpyridinium (MPP+) was taken up into human and rat striatal synaptosomes by a saturable system, similar to that for dopamine, with Km values of 0.24 and 0.17 μM, respectively, and similar Vmax values. Uptake of MPP+ and dopamine into both rat and human synaptosomes was inhibited by cocaine and amfonelic acid, with the latter being five to 10 times more potent than the former. MPP+ uptake was potently inhibited by dopamine in preparations from both species. In general, the characteristics of human and rat synaptosomal MPP+ uptake were very similar. It seems unlikely that species differences in toxicity to 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine or reaction to dopamine uptake blockers stem from this system.
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Slices of rat cerebral cortex, preloaded with [14C]γ-aminobutyric acid (GABA) and either [3H]5-hy-droxytryptamine (5-HT) or [3H]noradrenaline, were super-fused with media in which varying concentrations of Cl−had been replaced with other monovalent anions. Rapid reduction of [Cl″], by superfusion with media containing instead the impermeant anions propionate, isethionate, glu-conate, or methyl sulphate, caused increases in the efflux of tritiated biogenic amines, but the increase in that of [14C]-GABA was not significant. The increased efflux of [3H]5-HT evoked by superfusion with low Cl− levels when propionate was the replacement anion, was transient and was linearly related to the log[Cl−]−1. It was not affected by removal of Ca2+ or by addition of 10 mM Mg2+ and was delayed but not abolished by tetrodotoxin. The low C1–-evoked efflux of [3H]5-HT was not affected by pretreatment with neuronal reuptake blockers but was inhibited by picrotoxin, strychnine, and 4-acetamido-4-isothiocyanostilbene-2,2-disul-phonic acid and was enhanced by glycine. Muscimol and GABA were without effect. These observations are taken to indicate that the efflux of biogenic amines is brought about by terminal depolarisation due to outward movement of Cl−in low chloride-containing media. They are of relevance to other physiological and pharmacological studies in which anion concentrations are manipulated and suggest that the anion-evoked release phenomenon may provide a model for the analysis of Cl−-dependent mechanisms in nerve terminals.
    Type of Medium: Electronic Resource
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