Am J Phys Anthropol 141:452-462, 2010. (C) 2009 Wiley-Liss, Inc.”
“Rationale: NFATc1 ( nuclear factor of activated T-cells cytoplasmic 1) activity in endocardial cushion (ECC) endothelial cells is required for normal ECC growth and extracellular matrix (ECM) remodeling during heart valve development.\n\nObjective: The mechanisms of NFATc1 activation and downstream effects on cell proliferation and ECM-remodeling enzyme gene expression were examined in NFATc1 mutant mice and chick ECC explants.\n\nMethods
and Results: NFATc1(-/-) mice display reduced proliferation of ECC endothelial and mesenchymal cells at embryonic day 10.5, whereas myocardial cells are unaffected. Vascular endothelial growth factor A ( VEGF) activates NFATc1 and promotes ECC cell proliferation via the regulatory selleck products phosphatase, calcineurin, and mitogen-activated protein kinase-extracellular signal-regulated YH25448 Protein Tyrosine Kinase inhibitor kinase 1-extracellular signal-regulated kinase 1/2 (MEK1-ERK1/2)-dependent signaling. As ECCs mature, RANKL ( receptor activator of nuclear factor kappa B ligand) and the ECM-remodeling enzyme cathepsin K (CtsK) are expressed by ECC endothelial cells. RANKL inhibits VEGF-induced cell proliferation while causing increased expression of CtsK via calcineurin/NFATc1 and c-Jun N-terminal kinase (JNK) 1/2-dependent signaling.\n\nConclusion: These data support a novel mechanism
for the transition from ECC growth to remodeling in which NFATc1 promotes a sequential pattern of gene expression via cooperation with ligand-specific cofactors such as MEK1-ERK1/2 or JNK1/2. ( Circ Res. 2009; 105: 565-574.)”
“Objective: Estimation of the glomerular filtration rate (GFR) is essential for the evaluation of patients with kidney disease, and for correct dosage of drugs that are eliminated from the circulation by the kidneys. In most cases GFR
is estimated based on serum creatinine and the Modification of Diet in Renal Disease (MDRD) formula. As both cystatin C and creatinine are used for the determination of GFR it is important to investigate if estimated GFR by the two methods differ in various patient groups.\n\nDesign and methods: We have compared cystatin C and MDRD estimated NU7441 GFR calculated from the same request from primary care units (n=488), a cardiology ward (n=826), the cardiointensive care unit (n=1026), two oncology wards (n=919 and 1021), and the neurosurgical intensive care unit (n = 1515) in an observational cross-sectional study.\n\nResults: We found better agreement between the two GFR estimates in samples from primary care patients and patients in the cardiology wards, than in samples from oncology wards or the neurosurgical intensive care unit. In the latter settings there was a pronounced difference between the two GFR estimates.