Intracellular chloride: a regulator of transepithelial transport in the distal nephron.

Purpose Of Review: This review focuses on the role of intracellular chloride in regulating transepithelial ion transport in the distal convoluted tubule (DCT) in response to perturbations in plasma potassium homeostasis.

Recent Findings: Low dietary potassium increases the phosphorylation and activity of the sodium chloride cotransporter (NCC) in the DCT, and vice versa, affecting sodium-dependent potassium secretion in the downstream aldosterone-sensitive distal nephron. In cells, NCC phosphorylation is increased by lowering of intracellular chloride, via activation of the chloride-sensitive with no lysine (WNK)-SPAK/OSR1 (Ste20-related proline/alanine-rich kinase/oxidative stress response) kinase cascade.

β-Thalassemia due to intronic LINE-1 insertion in the β-globin gene (HBB): molecular mechanisms underlying reduced transcript levels of the β-globin(L1) allele.

We describe the molecular etiology of β(+)-thalassemia that is caused by the insertion of the full-length transposable element LINE-1 (L1) into the intron-2 of the β-globin gene (HBB). The transcript level of the affected β-globin gene was severely reduced. The remaining transcripts consisted of full-length, correctly processed β-globin mRNA and a minute amount of three aberrantly spliced transcripts with a decreased half-life due to activation of the nonsense-mediated decay pathway.

Evaluation of histological techniques for quantifying haemodialysis arteriovenous (AV) graft hyperplasia.

Background: Assessing treatment efficacies for preventing haemodialysis arteriovenous (AV) graft stenosis requires a reproducible method for quantifying intimal hyperplasia. We identified sources of variability in three histological methods for assessing hyperplasia in a porcine AV graft model.

Methods: Carotid-jugular synthetic grafts were placed in pigs.