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  • 1
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/General Subjects 882 (1986), S. 305-310 
    ISSN: 0304-4165
    Keywords: (Rat liver) ; Fatty-acid activation ; Ingensin ; Proteinase
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Amsterdam : Elsevier
    Biochimica et Biophysica Acta (BBA)/General Subjects 882 (1986), S. 297-304 
    ISSN: 0304-4165
    Keywords: (Rat liver) ; Fatty acid ; Ingensin ; Proteinase isoenzyme ; SDS activation
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Medicine , Physics
    Type of Medium: Electronic Resource
    Library Location Call Number Volume/Issue/Year Availability
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  • 3
    ISSN: 0014-5793
    Keywords: Ingensin ; Proteinase ; RNA ; RNA-degradation
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Chemistry and Pharmacology , Physics
    Type of Medium: Electronic Resource
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  • 4
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 60 (1983), S. 167-174 
    ISSN: 1432-0533
    Keywords: Muscle necrosis ; Regeneration ; Local anesthetic ; Bupivacaine ; Leupeptin ; Protease inhibitor ; Skinned fibers
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary A single direct injection of a local anesthetic, 0.5% bupivacaine hydrochloride (BPVC) (Marcaine), into rat soleus and extensor digitorum longus (EDL) muscles produced massive fiber necrosis with extensive phagocytosis followed by rapid regeneration, predominantly in the soleus. Since the sarcoplasmic reticulum (SR) was functionally disturbed by BPVC administration as confirmed by an in vitro study, the sarcolemmal lysis seen in the early phase of degeneration was not assumed to simply results from direct damage to the plasma membrane caused by BPVC. The extracellular fluid containing a high concentration of calcium (Ca) ions then permeated into the sarcoplasm through the defective membrane resulting in hypercontracted myofibrils. Selective damage to the Z-line, an early sign of muscle degeneration, was shown by electron microscopy and SDS gel electrophoresis (preferential loss of α-actinin). Administration of leupeptin, a thiol protease inhibitor, proved to be ineffective in inhibiting the necrotic process, because the BPVC induced muscle fiber breakdown was probably too acute and fulminant to demonstrate the inhibitory effect upon the degenerative process. Well preserved satellite cells, peripheral nerves, and acetylcholinesterase activity, and the absence of fibrous tissue proliferation in this system may be responsible for the extremely rapid regeneration with complete muscle fiber type differentiation. Since the sequence of fiber breakdown induced by BPVC administration was similar to that of progressive muscular dystrophy, this chemical will be one of the most useful tools for studying the pathophysiology of fiber necrosis and regeneration in diseased muscle.
    Type of Medium: Electronic Resource
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  • 5
    ISSN: 1432-0533
    Keywords: Acid maltase deficiency ; Japanese quail ; Early morphological change ; Membrane-bound glycogen
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The skeletal muscle of Japanese quails with acid maltase deficiency (AMD) was studied morphologically at various developmental stages, from the 16th embryonal day up to 3 months after hatching. Membrane-bound glycogen particles began to appear in the affected skeletal muscle at the 16th embryonal day. In normal embryonic muscles, a certain amount of free glycogen particles was observed but they were not membrane-bound. Therefore, this is the earliest morphological event in the muscle of Japanese quails with AMD. In muscle at 3 weeks after hatching, the initial focal degeneration of myofibrils was recognizable but it was not associated with autophagic vacuoles. Quails with AMD developed muscle weakness and difficulty in lifting their wings at about 3 months after hatching: then numerous autophagic vacuoles were present. The formation of large autophagic vacuoles followed by fiber loss and fatty replacement seemed ot contribute to the progressive muscle weakness. The study of Japanese quail with AMD will greatly facilitate the elucidation of the pathogenetic mechanism and is also a useful model for therapeutic trials in human AMD.
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Springer
    Acta neuropathologica 58 (1982), S. 279-285 
    ISSN: 1432-0533
    Keywords: Protease inhibitor ; Leupeptin ; Muscular dystrophy ; Dystrophic chicken
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary For the purpose of observing the therapeutic benefit of protease inhibitors for progressive muscular dystrophy, a large quantity of doses of leupeptin of 10 mg/kg/day and 50 mg/kg/day were administered i.p. to male chickens afflicted with hereditary muscular dystrophy (line 413) for 4 months starting on the 7th day ex ovo. No clinical improvement was identified in physical ability as a result of the examination by flip test, and creatine kinase (CK) values. The number of necrotic fibers in the pectoralis superficialis (PS) muscle which is known to be preferentially damaged in dystrophic chicken, did not decrease significantly in the birds treated with 10 mg leupeptin/kg/day (number of necrotic fibers; 47.7/mm2) and 50 mg/kg/day (46.4/mm2) as compared to that of the untreated ones (43.2/mm2). A morphometric analysis of fiber diameter distribution also showed no statistical difference between the treated and untreated birds. In the second group, 10 mg leupeptin/kg and a combination of leupeptin and bestatin of 10 mg/kg each were injected directly into the left lower half of the PS muscle three times a week for 4 months. Necrotic fibers were still present in the injected site, remote area of the left upper PS muscle treated with leupeptin (52.7/mm2), leupeptin and bestatin (52.2/mm2), and contralateral right upper PS muscle (41.6 and 53.5/mm2, respectively). The number of necrotic fibers in treated muscles was again not significantly different from that in untreated dystrophic ones (39.6/mm2). In fiber diameter analysis, no statistical difference was recognized between the treated and untreated dystrophic muscles.
    Type of Medium: Electronic Resource
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