28 research outputs found
Dna replication and cell-cycle progression of cultured mouse fm3a cells after treatment with 8-methoxypsoralen plus near-uv radiation.
Use of the synthetic superoxide dismutase/catalase mimetic EUK-134 to compensate for seasonal antioxidant deficiency by reducing pre-existing lipid peroxides at the human skin surface
Supplementary Material for: L-Type Voltage-Dependent Calcium Channel Alpha Subunit 1C Is a Novel Candidate Gene Associated with Secondary Hyperparathyroidism: An Application of Haplotype-Based Analysis for Multiple Linked Single Nucleotide Polymorphisms
<p><i>Background and Methods:</i> We conducted a large-scale
case-control study that explored the association of 358 single
nucleotide polymorphisms (SNPs) in 185 patients with end-stage renal
disease. A variety of SNPs were recognized as significant in simple
association studies. In addition, haplotype analysis identified the gene
for the alpha 1C subunit of the voltage-dependent L-type calcium
channel (CACNA1C) as having a significant association with secondary
hyperparathyroidism (intact parathyroid hormone level >200 pg/ml)
among 61 haplotypes. Since CACNA1C is a relatively large molecule, we
examined 84 SNP markers from the CACNA1C region located on chromosome 12
by haplotype case-control association analysis. <i>Results:</i> Sixteen
SNPs of 14 genes were significant according to allelic and/or genotypic
studies (p < 0.05 by Fisher’s exact test). Three different SNPs were
from the CACNA1C gene. Next, we performed haplotype-based association
testing with a focus on the CACNA1C region, revealing an odds ratio (OR)
of 1.63 and 95% confidence interval (CI) of 1.05–2.52. The second major
haplotype with a frequency of 27% was also significant and acted as a
protective haplotype (p = 0.022 by Fisher’s exact test, with an OR of
0.55 and 95% CI of 0.33–0.90). <i>Conclusion:</i> These results suggest
that CACNA1C may be associated with secondary hyperparathyroidism. In
addition, the haplotype-based approach may be useful to screen for key
molecules associated with complex traits.</p
A possible role for squalene in the pathogenesis of acne. II. In vivo study of squalene oxides in skin surface and intra-comedonal lipids of acne patients
Acute parathyroid hormone differentially regulates renal brush border membrane phosphate cotransporters
Renal phosphate reabsorption across the brush border membrane (BBM) in the proximal tubule is mediated by at least three transporters, NaPi-IIa (SLC34A1), NaPi-IIc (SLC34A3), and Pit-2 (SLC20A2). Parathyroid hormone (PTH) is a potent phosphaturic factor exerting an acute and chronic reduction in proximal tubule phosphate reabsorption. PTH acutely induces NaPi-IIa internalization from the BBM and lysosomal degradation, but its effects on NaPi-IIc and Pit-2 are unknown. In rats adapted to low phosphate diet, acute (30 and 60 min) application of PTH decreased BBM phosphate transport rates both in the absence and the presence of phosphonoformic acid, an inhibitor of SLC34 but not SLC20 transporters. Immunohistochemistry showed NaPi-IIa expression in the S1 to the S3 segment of superficial and juxtamedullary nephrons; NaPi-IIc was only detectable in S1 segments and Pit-2 in S1 and weakly in S2 segments of superficial and juxtamedullary nephrons. PTH reduced NaPi-IIa staining in the BBM with increased intracellular and lysosomal appearance. NaPi-IIa internalization was most prominent in S1 segments of superficial nephrons. We did not detect changes in NaPi-IIc and Pit-2 staining over this time period. Blockade of lysosomal protein degradation with leupeptin revealed NaPi-IIa accumulation in lysosomes, but no lysosomal staining for NaPi-IIc or Pit-2 could be detected. Immunoblotting of BBM confirmed the reduction in NaPi-IIa abundance and the absence of any effect on NaPi-IIc expression. Pit-2 protein abundance was also significantly reduced by PTH. Thus, function and expression of BBM phosphate cotransporters are differentially regulated allowing for fine-tuning of renal phosphate reabsorption