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SLT lowered (P<0.007) IOP in 5 eyes of 7 patients with steroid-induced increased IOP from 3 weeks to 6 months postoperative. Two patients required additional surgical procedures. Repeat SLT treatments may be necessary. SLT is a temporizing procedure to consider in patients with steroid-induced elevated IOP.

We have examined rDNA magnification in Drosophila melanogaster males carrying one of 11 recombination-or repair-defective mutations representing seven loci. We show that mutations defined by a defect in postreplication repair (mus-101, mei-41, and mus-108) are also defective in rDNA magnification, whereas mutations that do not affect postreplication repair have little or no effect on magnification.mei-41 inhibits only premeiotic magnification events, while mus-108 blocks both premeiotic and meiotic events. This suggests that meiotic and premeiotic events share some but not all functions. A molecular analysis of rDNA magnification reveals that in mus-108 males, changes in the rDNA restriction pattern can occur within one or a few generations under magnifying conditions. We interpret these data in terms of the role ofDNA repair systems in rDNA magnification and in terms of stable maintenance of tandemly repeated genes.In Drosophila males there are two clusters of tandemly repeated rRNA genes (rDNA), each with -250 copies. One of these arrays is located in the proximal heterochromatin of the X chromosome, and the other, on the Y chromosome (1, 2). Each array comprises a number of distinct classes of rRNA genes that differ by the presence or absence of transposon-like insertions and by variations in the spacer length (3, 4). Different wild-type strains of D. melanogaster show extraordinary differences in the degree to which various repeat classes are represented in their rDNA (5, 6). Individuals with partial deficiencies at either cluster, known as bobbed (bb) mutants, are also found in wild-type populations and in laboratory stock collections (1). However, within individual laboratory stocks, changes in rDNA redundancy or repeat class composition are rare (5). This suggests that there are events or processes that can change the copy number of the rDNA or the representation of various repeat classes.Alterations in X chromosomal rDNA redundancy occur in males carrying a Ybb-chromosome or its derivatives (7-9). Ybb-is a Y chromosome from which >80% of the rDNA is deleted (8). These changes in rDNA redundancy may be observed as either stable reversions (magnification) from bb to bb+ or as mutations (reduction) from bb+ to bb or from bb to bbl (bobbed lethal). Several lines of evidence demonstrate that magnification can occur both meiotically and premeiotically (8, 9). Considerable evidence suggests that meiotic magnification and reduction are reciprocal results of unequal sister-chromatid exchange occurring within the X chromosome rDNA (8-10).We have examined rDNA magnification in males carrying repair-and/or recombination-defective mutations (11-13) at one of seven X chromosomal loci. Previous experiments showed that two alleles of mei41 strongly inhibit magnification (14). We now have extended those observations by further testing one of these alleles and by demonstrating a magnification defect for three other alleles of mei-4. Alleles of two other loci required for postreplication repair, mus-101 and mus-108...

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rDNA magnification in Drosophila melanogaster is defined experimentally as the ability of bb/Ybb  - males to produce exceptional progeny that are wild type with respect to rDNA associated phenotypes. Here, we show that some of these bobbed-plus progeny result not from genetic reversion at the bb locus but rather from variants at two or more autosomal loci that ameliorate the bobbed phenotype of rDNA deficient males in Drosophila. In doing so we resolve several aspects of a long-standing paradox concerning the phenomenon of rDNA magnification. This problem arose from the use of two genetic assays, which were presumed to be identical, but paradoxically, produced conflicting data on both the kinetics of reversion and the stability of magnified bb  + chromosomes. We resolve this problem by demonstrating that in one assay bobbed-plus progeny arise primarily by genetic reversion at the bobbed locus, whereas in the other assay bobbed-plus progeny arise both by reversion and by an epistatic effect of autosomal modifiers on the bobbed phenotype. We further show that such modifiers can facilitate the appearance of phenotypically bobbed-plus progeny even under conditions where genetic reversion is blocked by magnification defective mutants. Finally, we present a speculative model relating the action of these modifiers to the large increases in rDNA content observed in males undergoing magnification.