Novocastratm Lyophilized Mouse Monoclonal Antibody Dysferlin

Vævsfarvning er afhængig af håndteringen og behandlingen af vævet inden farvning. Forkert fiksering, frysning, optøning, vask, tørring,
opvarmning, sektionering eller kontaminering med andet væv eller andre væsker kan frembringe artefakter, indfangning af antistof
eller falske negative resultater. Inkonsistente resultater kan skyldes variationer i fikserings- og indstøbningsmetoder eller irregulariteter
indeholdt i vævet. 4
For kraftig eller ukomplet kontrastfarvning kan gøre korrekt fortolkning af resultaterne vanskelig.
Klinisk fortolkning af farvning eller mangel derpå skal suppleres med morfologiske undersøgelser under anvendelse af passende
kontroller og bør evalueres i sammenhæng med patientens kliniske historie og andre diagnostiske tests af en kvalificeret patolog.
Antistoffer fra Leica Biosystems Newcastle Ltd er som angivet beregnet til anvendelse på enten frosne eller paraffinindstøbte vævssnit
med specifikke krav til fiksering. Der kan forekomme uventet antigenekspression, navnlig i neoplasmer. Den kliniske fortolkning af alle
farvede vævssnit skal indbefatte morfologisk analyse og evaluering af passende kontroller.
Bibliografi - Generelt
1. National Committee for Clinical Laboratory Standards (NCCLS). Protection of laboratory workers from infectious diseases transmitted
by blood and tissue; proposed guideline. Villanova, P.A. 1991;7(9). Order code M29-P.
2. Battifora H. Diagnostic uses of antibodies to keratins: a review and immunohistochemical comparison of seven monoclonal and
three polyclonal antibodies. Progress in Surgical Pathology. 6:1–15. eds. Fenoglio-Preiser C, Wolff CM, Rilke F. Field & Wood, Inc.,
Philadelphia.
3. Nadji M, Morales AR. Immunoperoxidase, part I: the techniques and pitfalls. Laboratory Medicine. 1983; 14:767.
4. Omata M, Liew CT, Ashcavai M, Peters RL. Nonimmunologic binding of horseradish peroxidase to hepatitis B surface antigen: a
possible source of error in immunohistochemistry. American Journal of Clinical Pathology. 1980; 73:626.
5. Mahjneh I, Marconi G, Bushby K, et al. Dysferlinopathy (LGMD2B): a 23-year follow-up study of 10 patients homozygous for the
same frameshifting dysferlin mutations. Neuromuscular Disorders. 2001; 11:20–26.
6. Pollitt C, Anderson LVB, Pogue R et al. The phenotype of calpainopathy: diagnosis based on a multidisciplinary approach.
Neuromuscular Disorders. 2001; 11(3):287–296.
7. Anderson LVB, Harrison RM, Pogue R et al. Secondary reduction in calpain 3 expression in patients with limb girdle muscular
dystrophy type 2B and Miyoshi myopathy (primary dysferlinopathies). Neuromuscular Disorders. 2000; 10(8):553–559.
8. Bornemann A and Anderson LVB. Diagnostic protein expression in human muscle biopsies. Brain Pathology. 2000; 10:193–214.
9. Anderson LVB. Immunomarkers for molecular mass. Neuromuscular Disorders. 1999; 9(6-7):421–422.
10. Anderson LVB, Davison K, Moss JA, et al. Dysferlin is a plasma membrane protein and is expressed early in human development.
Human Molecular Genetics. 1999; 8(5):855–861.
11. Bittner RE, Anderson LVB, Burkhardt E, et al. Dysferlin deletion in SJL mice (SJL-Dysf) defines a natural model for limb girdle
muscular dystrophy 2B. Nature Genetics. 1999; 23:141–142.
12. Weiler T, Bashir R, Anderson LVB, et al. Identical mutation in patients with limb girdle muscle dystrophy type 2B or Miyoshi myopathy
suggests a role for modifier gene(s). Human Molecular Genetics. 1999; 8(5):871–877.
13. Matsuda C, Hayashi YK, Ogawa M, et al. The sarcolemmal proteins dysferlin and caveolin-3 interact in skeletal muscle. Human
Molecular Genetics. 2001; 10(17):1761–1766.
Rettelser Til Tidligere Udgave
Ingen rettelser.
Udgivelsesdato
18 Juni 2008 (NCL-Hamlet/CE/UK)
NCL-Hamlet
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