Zobrazeno 1 - 9
of 9
pro vyhledávání: '"R. W. Kuncl"'
Publikováno v:
Arthritis and rheumatism. 44(8)
Amyloid myopathy is a well-described, increasingly recognized clinical entity. Similar to inflammatory myopathies, amyloid myopathy presents with proximal muscle weakness and can be associated with elevated levels of muscle enzymes. We report the cas
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::7467f7097dcbbda0c04e223c9aa6e16c
https://pubmed.ncbi.nlm.nih.gov/11508448
https://pubmed.ncbi.nlm.nih.gov/11508448
Publikováno v:
Developmental medicine and child neurology. 36(8)
Twenty-five Tc/tw5 and 12 control mice were killed at different ages and radiographically and histologically examined. In addition, histochemical analysis was performed on muscles from four mutant and one control mouse. All Tc/tw5 mice were tailless
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::0e68ec86af60dac88ee45fc5e1367ec6
https://pubmed.ncbi.nlm.nih.gov/8050623
https://pubmed.ncbi.nlm.nih.gov/8050623
Autor:
D. B. Drachman, R. W. Kuncl
Publikováno v:
Immunology of Neuromuscular Disease ISBN: 9789401046220
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_________::b789dafb6057a48feaf5b67494536130
https://doi.org/10.1007/978-94-011-1422-6_7
https://doi.org/10.1007/978-94-011-1422-6_7
Publikováno v:
The Journal of pharmacology and experimental therapeutics. 267(2)
The basic abnormality in myasthenia gravis is the depletion of acetylcholine receptors (AChRs) at neuromuscular junctions, which is due in part to excessive endocytosis brought about by the action of pathogenic antibodies. We asked whether 3-deazaade
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::126b6780f4f198b0da37c939f7559858
https://pubmed.ncbi.nlm.nih.gov/8246131
https://pubmed.ncbi.nlm.nih.gov/8246131
Publikováno v:
Journal of neurology, neurosurgery, and psychiatry. 55(2)
Amyloidosis is a rare cause of myopathy. Its prominent or presenting feature may be respiratory failure. Physiological measurement of transdiaphragmatic pressure and biopsy specimens of muscle show the pathological mechanism to be diaphragm weakness
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=doi_dedup___::3b8ce638dabc41f0ab1f32f57a07bd9c
https://pubmed.ncbi.nlm.nih.gov/1538226
https://pubmed.ncbi.nlm.nih.gov/1538226
Publikováno v:
The Journal of rheumatology. 18(2)
In order to establish the degree of renal malfunction necessary for colchicine toxicity in patients receiving it daily for the prevention of recurrent acute gout, we obtained serum creatinine levels and measured or estimated creatinine clearances in
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::8d48ac5cccc5b5dba8a0a4ac10857604
https://pubmed.ncbi.nlm.nih.gov/1819267
https://pubmed.ncbi.nlm.nih.gov/1819267
Publikováno v:
Musclenerve. 10(4)
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::7549fc7818ba0bbeb124c073179a9442
https://pubmed.ncbi.nlm.nih.gov/2953971
https://pubmed.ncbi.nlm.nih.gov/2953971
Autor:
R W, Kuncl, W W, Wiggins
Publikováno v:
Neurologic clinics. 6(3)
Toxic myopathies are commonly unrecognized. An understanding of the mechanism by which toxins produce disease, identification of risk factors that predispose patients to myopathy, and recognition of a few special clinical syndromes will greatly enhan
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::0bf36b27d3d1e5058d13b31eea4f6ada
https://pubmed.ncbi.nlm.nih.gov/3065603
https://pubmed.ncbi.nlm.nih.gov/3065603
Publikováno v:
Annals of neurology. 25(1)
We studied the incidence and clinical correlates of serum antibodies to GM1 and GD1a gangliosides in patients with classical amyotrophic lateral sclerosis (ALS) and other "motor nerve" syndromes. Serum antibodies to GM1 and GD1a gangliosides were mea
Externí odkaz:
https://explore.openaire.eu/search/publication?articleId=pmid________::1542f56716414cbb237788b203eec91d
https://pubmed.ncbi.nlm.nih.gov/2913936
https://pubmed.ncbi.nlm.nih.gov/2913936