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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Science Ltd
    Journal of neurochemistry 66 (1996), S. 0 
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: The time dependence of N-acetyl-aspartate (NAA) concentrations relative to lactate and pyruvate in the injured rat spinal cord was investigated. Segments of spinal cord from regions rostral, caudal, and at the epicenter of the injury were analyzed. NAA concentrations were determined by gas chromatography-mass spectrometry and lactate and pyruvate concentrations were determined by UV spectroscopy at 20 min, 60 min, 2 h, 8 h, 24 h, 3 days, and 1 week after injury. NAA levels fell most significantly at the epicenter of the injury, reaching 30% of basal levels within 24 h. In all segments, lactate levels increased significantly shortly after injury, peaking at two to five times normal basal levels between 20 and 60 min after injury. Rostral and caudal to the injury site, lactate elevations and NAA reductions were less dramatic. Pyruvate concentrations were not significantly altered in any of the sections after injury. The temporal and spatial relationships of NAA and lactate changes indicated that ischemic conditions due to injury in the upper thoracic rat spinal cord were distributed asymmetrically. Acute ischemia was more severe caudal to the injury site, and NAA concentrations were more severely impaired in the rostral direction. The results suggest that the extent of neuronal degeneration due to spinal cord injury does not correlate directly with acute ischemic severity as measured by the lactate/pyruvate ratio, and may be more closely related to secondary changes in the neuronal environment.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Increasing evidence suggests that excessive activation of the calcium-activated neutral protease μ-calpain could play a major role in calcium-mediated neuronal degeneration after acute brain injuries. To further investigate the changes of the in vivo activity of μ-calpain after unilateral cortical impact injury in vivo, the ratio of the 76-kDa activated isoform of μ-calpain to its 80-kDa precursor was measured by western blotting. This μ-calpain activation ratio increased to threefold in the pellet of cortical samples ipsilateral to the injury site at 15 min, 1 h, 3 h, and 6 h after injury and returned to control levels at 24–48 h after injury. We also investigated the effect of μ-calpain activation on proteolysis of the neuronal cytoskeletal protein α-spectrin. Immunoreactivity for α-spectrin breakdown products was detectable within 15 min after injury in cortical samples ipsilateral to the injury site. The levels of α-spectrin breakdown products increased in a biphasic manner, with a large increase between 15 min and 6 h after injury, followed by a smaller increase between 6 and 24 h after the insult. No further accumulation of α-spectrin breakdown products was observed between 24 and 48 h after injury. Histopathological examinations using hematoxylin and eosin staining demonstrated dark, shrunken neurons within 15 min after traumatic brain injury. No evidence of μ-calpain autolysis, calpain-mediated α-spectrin degradation, or hematoxylin and eosin neuronal pathology was detected in the contralateral cortex. Although μ-calpain autolysis and cytoskeletal proteolysis occurred concurrently with early morphological alterations, evidence of calpain-mediated proteolysis preceded the full expression of evolutionary histopathological changes. Our results indicate that rapid and persistent μ-calpain activation plays an important role in cortical neuronal degeneration after traumatic brain injury. Our data also suggest that specific inhibitors of calpain could be potential therapeutic agents for the treatment of traumatic brain injury in vivo.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Woodbury, NY : American Institute of Physics (AIP)
    Applied Physics Letters 80 (2002), S. 3295-3297 
    ISSN: 1077-3118
    Source: AIP Digital Archive
    Topics: Physics
    Notes: The Schwoebel-Ehrlich barrier—the additional barrier for an adatom to diffuse down a surface step—dictates the growth modes of thin films. The conventional concept of this barrier is two dimensional (2D), with the surface step being one monolayer. We propose the concept of a three-dimensional (3D) Schwoebel-Ehrlich barrier, and identify the 2D to 3D transition, taking aluminum as a prototype and using the molecular statics method. Our results show that: (1) substantial differences exist between the 2D and 3D barriers; (2) the transition completes in four monolayers; and (3) there is a major disparity in the 3D barriers between two facets; further, alteration of this disparity using surfactants can lead to the dominance of surface facet against thermodynamics. © 2002 American Institute of Physics.
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Physics Letters A 189 (1994), S. 479 
    ISSN: 0375-9601
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Physics Letters A 195 (1994), S. 135-143 
    ISSN: 0375-9601
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Physics Letters A 184 (1994), S. 347-351 
    ISSN: 0375-9601
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Physics
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Polyhedron 11 (1992), S. 2427-2430 
    ISSN: 0277-5387
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 0277-5387
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1432-0614
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Process Engineering, Biotechnology, Nutrition Technology
    Notes: Abstract Active butyrate kinase (Buk) and phosphotransbutyrylase (Ptb) were purified in three steps: ammonium sulfate precipitation, hydrophobic chromatography on phenyl-Sepharose and affinity chromatography on Matrex Red A from recombinant Escherichia coli K2006 (pJC7). They were then successfully exploited for in vitro synthesis of 3-hydroxybutyryl-CoA (3HBCoA), 4-hydroxybutyryl-CoA (4HBCoA), 4-hydroxyvaleryl-CoA (4HVCoA) and poly(hydroxyalkanoic acid) (PHA). In addition, the ability of the PHA synthase of Chromatium vinosum, PhaECCv, to use these CoA thioesters was evaluated. Combination of Buk and Ptb with PhaECCv established a new system for in vitro synthesis of poly(3-hydroxybutyric acid) [poly(3HB)]. In this system, 3-hydroxybutyric acid was converted to 3HBCoA by Buk and Ptb at the expense of ATP. Formation of 3HBCoA was further driven by the polymerization of 3HBCoA molecules to poly(3HB) by PHA synthase, and the released CoA was recycled by Ptb. This system therefore also ensured the regeneration of CoA. With ATP as the energy supply, which was hydrolyzed to ADP and phosphate, 2.6 mg poly(3HB) was obtained from a 1-ml reaction mixture containing 7.6 mg 3-hydroxybutyrate at the beginning. Studies showed that Ptb and PHA synthase were the rate-limiting steps in this system, and initial CoA concentrations ranging from 1 to 7 mM did not inhibit poly(3HB) synthesis. Synthesis of various polyesters of 3HB and 4HB with this system was also tested, and copolyesters containing 4HB of 1–46 mol % were obtained.
    Type of Medium: Electronic Resource
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  • 10
    Electronic Resource
    Electronic Resource
    Springer
    Archives of toxicology 25 (1969), S. 238-253 
    ISSN: 1432-0738
    Keywords: Parathion ; Parathion Toxicity ; Pesticides ; Pesticide Toxicity ; Protein Deficiency ; Parathion ; Toxicität von Parathion ; Schädlingsbekämpfungsmittel ; Toxicität der Schädlingsbekämpfungsmittel ; Eiweißmangel
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Zusammenfassung Die akute perorale Toxizität von Parathion (98,5% technisch) wurde an jungen, männlichen Albino-Ratten bestimmt. Die Tiere in Gruppe I erhielten eine gereinigte Diät, in der Eiweiß als Casein in sehr geringen Mengen (3,5%) enthalten war, in Gruppe II die gleiche Nahrung wie Gruppe I, jedoch mit Casein in normaler Menge (26%), und in Gruppe III die übliche gepreßte Trockennahrung (Chow). Die LD50±S.F. betrug in Gruppe I 4,86±0,31 mg/kg Körpergewicht, 37,1±4,9 mg/kg in Gruppe II, und 23,4±5,4 mg/kg in Gruppe III. Das klinisch-pathologische Vergiftungssyndrom war im wesentlichen in allen 3 Gruppen gleich. Die klinischen Manifestationen umfaßten: Haaraufrichtung, Diarrhöe, Sialarrhoe, Dakryorrhoe, Hemodakryorrhoe, Nasenbluten, Exophthalmus, Zittern, Hyporeflexie, Lustlosigkeit, Ataxie, Anorexie, Oligodipsie, Körpergewichtsverlust, Oligurie, Albuminurie, Hematurie, und Glykosurie. Die meisten Todesfälle traten nach 10–35 Std ein. Bei der Autopsie fanden sich geringe akute Enteritis, ausgedehnte Erweiterung der venösen Capillaren, degenerative Veränderungen in Leber und Nieren und Wasserverlust und Gewichtsverlust der Körperorgane. Die Überlebenden schienen nach 4 Tagen wieder normal zu sein, die Organgewichte sowie der Wassergehalt lagen nach 2 Wochen und nach 1 Monat in den Normbereichen.
    Notes: Summary The clinicopathological syndrome of acute oral toxicity to parathion (98.5% technical) was determined in male albino rats fed for 28 days from weaning on a diet containing 3.5% protein as casein (group I), normal amounts of protein as casein (26% group II), and normal amounts of mixed natural protein as laboratory chow. The LD50±S.E. was found to be 4.86±0.31 mg/kg in group I, 37.1±4.9 mg /kg in group II and 23.4±5.4 mg/kg in group III. The LD50 in group I was significantly lower than that in group II which, in turn, was significantly higher than that in group III. Most deaths occurred at 10–35 hours in all three groups. The clinical syndrome of intoxication was essentially the same in all three groups and included signs of cholinergic stimulation such as diarrhea, sialarrhea and dacryorrhea, of stimulation of the central nervous system such as piloerection, tremors, and exophthalmos, alternating with signs of depression of the central nervous system such as hyporeflexia, drowsiness, ataxia, prostration and pallor. These signs were accompanied by anorexia, oligodipsia, hypothermia, loss of body weight, oliguria, proteinuria, hematuria and glucosuria. At autopsy there were found a very mild local irritant gastroenteritis, vascular congestion of many organs, a contracted spleen and, when death was delayed, gastric ulcers and degenerative changes in organs such as the liver and kidneys. Most organs were dehydrated and had lost weight. The survivors appeared normal by the 4th day but there was a persistent hematuria, glucosuria and proteinuria. Organ weights and water contents were mostly within normal limits at 2 weeks and 1 month but autopsy at these intervals occasionally disclosed healed or healing abscesses, indicating that resistance to infection had been lowered by parathion, and other residual changes such as a megacolon and hydrated muscle.
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