Central corneal thickness of Caucasians and African Americans in glaucomatous and nonglaucomatous populations.

OBJECTIVE: To determine whether there is a difference in central corneal thickness between African American and Caucasian patients. If present, a difference might alter the measurement of intraocular pressure and potentially the assessment and management of glaucoma in these populations. METHODS: Central corneal thickness was measured by means of ultrasound pachymetry in African American (n = 56) and Caucasian (n = 32) patients with suspected or confirmed glaucoma and control populations of African American (n = 26) and Caucasian (n = 51) subjects in whom there was no evidence of elevated intraocular pressure or glaucomatous optic nerve damage. Measurements of central corneal thickness were then compared between different subpopulations by means and population distribution analysis. RESULTS: A statistically significant difference was noted between the mean (+/-SD) central corneal thickness of all African American (including those with and without glaucoma) (right eye, 531.0 +/- 36.3 microm; left eye, 530.0 +/- 34.6 microm) and all Caucasian (including those with and without glaucoma) (right eye, 558.0 +/- 34.5 microm; left eye, 557.6 +/- 34.5 microm) patients. Similar results were found when subpopulations were tested. Distribution analysis of central corneal thickness measurements noted the largest cluster of African American patients around 520 to 540 microm, whereas the largest cluster of Caucasian patients was between 580 and 600 microm. CONCLUSIONS: African Americans were found to have thinner central cornea thickness measurements than Caucasians. This finding in African Americans may lead to lower applanation intraocular pressure readings compared with those of Caucasians, potentially resulting in an underestimation of the actual level of intraocular pressure.

Collagen degradation in glaucoma: will it gain a therapeutic value?

The extracellular matrix is in a constant state of turnover, and several studies suggest that this homeostasis is out of balance in open-angle glaucoma. Recent evidence suggests that matrix metalloproteinases, which are the enzymes primarily responsible for degradation, play a role in numerous modern glaucoma therapies, including topical prostaglandin analogues, topical steroids, and argon laser trabeculoplasty. Additionally, direct and indirect regulation of this system has been shown to increase aqueous humor outflow facility. It is possible that therapies directed at modulating specific enzymes represent the next generation of glaucoma therapy.

Comparison of changes in manifest refraction and corneal power after photorefractive keratectomy.

PURPOSE: To determine which corneal curvature values most closely correlate to change in manifest refraction after excimer laser photorefractive keratectomy. METHODS: In a prospective study at the Cullen Eye Institute, excimer laser photorefractive keratectomy was performed on 27 eyes of 27 patients (mean age, 38.07+/-6.65 years). Preoperative refractive errors ranged from -2.25 diopters to -8.75 diopters (mean, -5.74+/-2.09 diopters). Preoperatively and 1 month postoperatively, we determined the spherical equivalent of the subjective manifest refraction (corrected for a 12-mm vertex distance) and measured corneal power using standard keratometry (Bausch & Lomb Keratometer; Rochester, New York) and computerized videokeratography (EyeSys Corneal Analysis System; Premier Laser Systems Inc, Houston, Texas). We collected 15 corneal values: standard keratometry and 14 computerized videokeratography values calculated using the axial, instantaneous, and refractive formulas. All calculations were performed with 1.3375 and 1.376 for the refractive index of the cornea. For each of the corneal values, we subtracted the change in corneal power from the change in manifest refraction and calculated for this difference the means, SDs, correlations, and regressions. RESULTS: Mean differences between change in refraction and change in corneal power were lower when for a refractive index of 1.376 than for 1.3375, were lowest for the most central measurement points, and displayed a high SD. A value of 1.408 for the refractive index would be required to optimize the correlation between change in manifest refraction and effective refractive power of the central 3 mm of the cornea. CONCLUSIONS: For individual patients who have undergone photorefractive keratectomy, changes in corneal values determined by computerized videokeratography or by standard keratometry do not reliably predict change in manifest refraction.

Differential regulation of the c-myc oncogene promoter by the NF-kappa B rel family of transcription factors.

The murine c-myc gene contains two elements responsive to the rel-oncogene-related family of NF-kappa B factors. Previously we have shown that factor binding to these two NF-kappa B elements mediates induction of transcription of the c-myc promoter upon interleukin-1 treatment of human dermal fibroblasts and human T-cell leukemia virus type I tax gene expression in T cells (D. J. Kessler, M. P. Duyao, D. B. Spicer, and G. E. Sonenshein, J. Exp. Med. 176:787-792, 1992; M. P. Duyao, D. J. Kessler, D. B. Spicer, C. Bartholomew, J. L. Cleveland, M. Siekevitz, and G. E. Sonenshein, J. Biol. Chem. 267:16288-16291, 1992). To begin to delineate the specific roles of the individual members of the NF-kappa B family, here we have tested their effects on activation of a c-myc promoter/exon 1-CAT construct in NIH 3T3 cells. Classical NF-kappa B (p65/p50) was a potent transcriptional activator of the c-myc promoter. Cotransfection with either p65 alone or p65 in combination with p50 mediated significant induction. In contrast, expression of either v-rel or chicken c-rel failed to transactivate, while murine c-rel induced c-myc promoter activity only slightly. Furthermore, induction by classical NF-kappa B was inhibited by coexpression of either v-rel or chicken c-rel. Thus, individual members of the rel family have differential effects of the c-myc promoter, which can modulate overall transcriptional activity and allow for precise regulation of this oncogene under diverse physiologic conditions.

A novel NF-kappa B element within exon 1 of the murine c-myc gene.

We have mapped a site within exon 1 of the murine c-myc gene that forms a variety of complexes with nuclear proteins derived from the murine WEHI 231 B-lymphoma cell line in exponential growth that are altered following treatment with phorbol ester, when transcription of this gene is reduced [Levine, R.A., McCormack, J.E., Buckler, A.J. & Sonenshein, G.E. (1986). Mol. Cell Biol., 6, 4112-4116]. This site, located at +440 to +459 bp relative to the P1 promoter, contains an NK-kappa B-like binding element. The sequence of this element, AGGGAATTTTT, is unusual in that the stretch of pyrimidines is entirely T residues. Binding of NF-kappa B protein was demonstrated by oligonucleotide competition, induction of binding upon 70Z/3 pre-B- to B-cell differentiation, response to GTP in the binding reaction, reduction of binding upon addition of I kappa B protein and uv cross-linking analysis. Functional activity of this internal regulatory element (IRE) was demonstrated in transfection assays using chloramphenicol acetyl transferase (CAT) reporter constructs containing multimerized copies of the IRE driving a heterologous promoter. Mutation of the IRE within the context of the c-myc promoter prevented NF-kappa B-mediated induction of transcription of this oncogene. Thus additional NF-kappa B elements may be defined by this new sequence.