scispace - formally typeset
W

William M. Bourne

Researcher at Mayo Clinic

Publications -  220
Citations -  14198

William M. Bourne is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Corneal endothelium & Cornea. The author has an hindex of 62, co-authored 219 publications receiving 13507 citations. Previous affiliations of William M. Bourne include University of Florida.

Papers
More filters
Journal ArticleDOI

A 48-Year Clinical and Epidemiologic Study of Keratoconus

TL;DR: From 1935 through 1982, keratoconus was newly diagnosed in a total of 64 residents of Olmsted County, Minnesota; there were no significant trends in incidence rates over time; the overall average annual rate was 2.0 per 100,000 population.
Journal ArticleDOI

The Corneal Endothelium: Normal and Pathologic Structure and Function

TL;DR: A summary of normal and abnormal endothelial structure and function is presented in this paper, where a leaky barrier formed by the apical gap and macula occludens junctions that keep some water out of the stroma but allow nutrients to pass, and an ATPase-dependent metabolic pump that is located in the lateral plasma membranes.
Journal ArticleDOI

Central corneal endothelial cell changes over a ten-year period.

TL;DR: In this paper, the authors rephotographed the central corneal endothelium of 52 normal subjects with the same contact specular microscope and found that the mean endothelial cell density decreased during the 10.6-year interval from 2715 +/- 301 cells/mm2 to 2539 +/- 284 cells/m2 (P < 0.001).
Journal Article

Central corneal endothelial cell changes over a ten-year period.

TL;DR: Human central endothelial cell density decreases at an average rate of approximately 0.6% per year in normal corneas throughout adult life, with gradual increases in polymegethism and pleomorphism.
Journal ArticleDOI

Ten-year postoperative results of penetrating keratoplasty.

TL;DR: From 5 to 10 years after penetrating keratoplasty, the annual rate of endothelial cell loss was seven times the normal rate, indicating continued endothelial instability and dysfunction, resulting in an increasing rate of late endothelial failure.