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Julie A. Vrana

Researcher at Mayo Clinic

Publications -  99
Citations -  5583

Julie A. Vrana is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Amyloidosis & Amyloid. The author has an hindex of 41, co-authored 88 publications receiving 4709 citations. Previous affiliations of Julie A. Vrana include University of Rochester.

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Classification of amyloidosis by laser microdissection and mass spectrometry-based proteomic analysis in clinical biopsy specimens.

TL;DR: The development of a highly specific and sensitive novel test for the typing of amyloidosis in routine clinical biopsy specimens that combines specific sampling by laser microdissection (LMD) and analytical power of tandem mass spectrometry (MS)-based proteomic analysis.
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C3 glomerulonephritis: Clinicopathological findings, complement abnormalities, glomerular proteomic profile, treatment, and follow-up

TL;DR: The clinical features, kidney biopsy findings, alternative pathway abnormalities, glomerular proteomic profile, and follow-up in 12 cases of C3GN are described, finding that renal function remained stable in the majority of patients with native kidney disease.
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TLE1 expression is not specific for synovial sarcoma: a whole section study of 163 soft tissue and bone neoplasms.

TL;DR: Morphology, ancillary immunohistochemistry for traditional markers such as cytokeratins and CD34, and molecular confirmation of synovial sarcoma-associated fusion genes should remain the ‘gold standards’ for this diagnosis.
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Renal Amyloidosis: Origin and Clinicopathologic Correlations of 474 Recent Cases

TL;DR: The newly identified leukocyte chemotactic factor 2 amyloidosis form was the most common of the rarer causes of renal amyloidalosis and was associated with lower serum creatinine, higher degree of proteinuria, and amyloids spicules.
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Glomeruli of Dense Deposit Disease contain components of the alternative and terminal complement pathway

TL;DR: This study shows that in addition to fluid-phase dysregulation of the alternative pathway, soluble components of the terminal complement complex contribute to glomerular lesions found in DDD.