Background Hemodialysis (HD) and peritoneal dialysis (PD) are both viable options for renal replacement therapy. Technique failure has been shown to be a major problem in PD therapy. Objective To examine the relationship between center size and PD technique failure. Setting ESRD Network #1 (NW1). Design Retrospective review of NW1 database. Patients and Methods 5003 incident PD patients between 2001 and 2005 in 105 PD units were included. Patients were grouped into 2 based on center size: group A, patients in units with ≤25 patients, and group B, patients in units with >25 patients. Outcome measures were analyzed for the first and second years of PD therapy. Patients were censored at transplantation, transfer to HD, or death. Outcome Measures Technique failure and mortality reported as death in Standard Information Management Systems (SIMS) database (NW1 data system). Results Technique failure rates were significantly higher in group A for year 1 (odds ratio: 1.36, p = 0.005) and for year 2 (odds ratio: 1.35, p = 0.03). Mortality rates were not statistically different between the 2 groups. Conclusion Technique failure was higher in units with ≤25 patients than in units with >25 patients. There was no difference in mortality between the 2 groups. The majority of patients in NW1 receive care in small units.
A screen for mutants of budding yeast defective in meiotic gene conversion identified a novel allele of the POL3 gene. POL3 encodes the catalytic subunit of DNA polymerase ␦, an essential DNA polymerase involved in genomic DNA replication. The new allele, pol3-ct, specifies a protein missing the last four amino acids. pol3-ct shows little or no defect in DNA replication, but displays a reduction in the length of meiotic gene conversion tracts and a decrease in crossing over. We propose a model in which DNA synthesis determines the length of strand exchange intermediates and influences their resolution toward crossing over.H OMOLOGOUS recombination plays a critical role parental origin. If the two parental duplexes are genetically different within the region of strand exchange, the in maintaining genome integrity throughout cell division. In meiosis, homologous recombination is esresulting hDNA contains mismatched base pairs and is referred to as heteroduplex DNA. sential for proper homolog pairing and for the correct segregation of chromosomes at the first meiotic division.Single-end invasion intermediates can be channeled toward either of two repair pathways. In the first pathIn vegetative cells, recombination plays an important role during DNA replication by providing a mechanism way, described by the DSB repair model (Szostak et al. 1983;Sun et al. 1989), DNA synthesis, capture of the to bypass DNA lesions and other obstacles that block replication fork progression. Homologous recombinasecond end, and ligation generate a double Holliday junction intermediate with asymmetric hDNA (i.e., hDNA on tion also provides a means to generate new combinations of genetic markers through gene conversion and only one of the two duplexes) on each side of the DSB and on each chromatid (Figure 1, left). If a Holliday crossing over, thereby generating genetic diversity among different individuals in the same population. junction undergoes branch migration, then hDNA will be formed on both duplexes (symmetric hDNA). EvenNumerous insights into the mechanism of homologous recombination have been obtained from meiotic studies tually, double Holliday junction intermediates are resolved by cutting, at each junction, either both outside using the convenient model organism, Saccharomyces cerevisstrands or both inside strands. Cutting of the two junciae (Paques and Haber 1999). Meiotic recombination in tions in opposite directions generates crossovers, while budding yeast is initiated by the formation of DNA doublecutting in the same direction generates noncrossovers. strand breaks (DSBs) at recombination hotspots. The The second pathway is described by the synthesisstrands with 5Ј ends at the site of the break are processed dependent strand annealing (SDSA) model (Paques to expose single-stranded tails with 3Ј termini (Figure and Haber 1999) and supported by recent meiotic stud-1). DSB formation and 5Ј-end resection are followed by ies (
We examined whether endothelial cells (ECs) inhibit smooth muscle cell (SMC) transforming growth factor-β1 (TGF-β1) activation in bilayer coculture. Western analysis showed that SMCs cocultured with ECs as a bilayer had lower amounts of active TGF-β1 protein compared with SMCs cultured alone and SMCs cocultured with ECs as a monolayer. EC inhibition of TGF-β1 activation could be blocked with plasminogen activator inhibitor-1 (PAI-1) antibody. Similarly, SMC hill-and-valley growth, a marker for TGF-β1 activity, was present in SMCs cultured alone and SMCs cocultured with ECs as a monolayer but was absent in SMCs cocultured as a bilayer. SMCs cocultured with ECs as a bilayer migrated at a greater rate than SMCs cultured either alone or cocultured as a monolayer. The EC effect on SMC migration was inhibited by the addition of 5 ng/ml TGF-β1. ECs had no effect on SMC RNA levels of TGF-β1. PAI-1 levels were increased in ECs and ECs cocultured with SMCs compared with SMCs cultured alone. ECs inhibit TGF-β1 activation in bilayer coculture. This appears to be mediated through an increase in EC PAI-1 release. Alterations in coculture conditions, in particular the degree of EC-SMC cell contact, have profound effects on this process.
Endothelin-1 (ET-1) is a potent mitogen secreted by endothelial cells (ECs) in culture and is a putative factor in vascular lesion development. The purpose of this study was to examine whether smooth muscle cells (SMCs) inhibit EC secretion of ET-1. The effect of SMCs on EC ET-1 and constitutively expressed nitric oxide (NO) synthase activity was examined by using a bilayer co-culture model. SMCs inhibited both EC ET-1 protein and RNA levels, compared with ECs cultured alone. SMCs increased EC NO production when compared with ECs cultured alone. In addition, SMC inhibition of EC ET-1 production could be blocked by the NO synthase inhibitor N(G)-nitro-L-arginine-methyl ester. ECs stimulated SMC proliferation, and the ET-1 AB and B receptor blockers inhibited EC stimulation of SMC proliferation. The ET-1 A blocker had no effect on SMC proliferation. We conclude that SMCs regulate EC ET-1 and ecNOS synthase transcript levels and protein levels. SMC inhibition of ET-1 production by ECs may be mediated through SMC-modulated changes in EC NO activity. Finally, EC stimulation of SMC proliferation in bilayer co-culture is mediated by ET-1 through the ET-1 B receptor.
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