Relativistic Binaries in Globular Clusters

Galactic globular clusters are old, dense star systems typically containing 10\super{4}--10\super{7} stars. As an old population of stars, globular clusters contain many collapsed and degenerate objects. As a dense population of stars, globular clusters are the scene of many interesting close dynamical interactions between stars. These dynamical interactions can alter the evolution of individual stars and can produce tight binary systems containing one or two compact objects. In this review, we discuss theoretical models of globular cluster evolution and binary evolution, techniques for simulating this evolution that leads to relativistic binaries, and current and possible future observational evidence for this population. Our discussion of globular cluster evolution will focus on the processes that boost the production of hard binary systems and the subsequent interaction of these binaries that can alter the properties of both bodies and can lead to exotic objects. Direct {\it N}-body integrations and Fokker--Planck simulations of the evolution of globular clusters that incorporate tidal interactions and lead to predictions of relativistic binary populations are also discussed. We discuss the current observational evidence for cataclysmic variables, millisecond pulsars, and low-mass X-ray binaries as well as possible future detection of relativistic binaries with gravitational radiation.Comment: 88 pages, 13 figures. Submitted update of Living Reviews articl

Kinetics and osmoregulation of Na+- and Cl--dependent betaine transporter in rat renal medulla

Betaine is one of the major organic osmolytes that accumulate in the renal medulla in response to high extracellular tonicity. Recent studies in MDCK cells have shown that betaine is taken up by an Na+- and Cl--dependent transporter located on the basolateral membrane. We demonstrate here the presence of Na+-Cl--dependent betaine transporter(s) in tubule suspensions prepared from the rat outer and inner medulla. The betaine transport activity was two to three times higher in the inner medulla compared with the outer medulla. The removal of Na+ and Cl- reduced betaine uptake in the outer medullary tubules by 86% and 82%, respectively. The betaine uptake was decreased by 39% in hypotonic buffer (189 mosmol/kgH2O) and increased by 82% in hypertonic buffer (545 mosmol/kgH2O), compared with isotonic buffer (308 mosmol/kgH2O). Kinetic studies of Na+-dependent betaine uptake in the outer medullary tubules revealed both a low- and a high-affinity component as follows: low-affinity and high-volume component with Michaelis constant (K(m1)) of 8.6 mM and maximal uptake rate (V(max1)) of 112 pmol ?? ??g protein-1 ?? h-1; and a low-volume and high-affinity component with K(m2) of 0.141 mM and V(max2) of 10 pmol ?? ??g protein-1 ?? h-1. To investigate whether the Na+-Cl--dependent betaine transporter is regulated by tonicity in vivo, we quantitated its mRNA in rat renal cortex and outer and inner medulla using both canine and rat Na+-Cl--dependent betaine transporter cDNA probes. A single band of 3.0 kb was seen in the Northern blots prepared from both outer and inner medulla, but not in the cortex. Water deprivation for 3 days increased the abundance of this mRNA in the outer and inner medulla by 140% and 170%, respectively, but did not affect its expression in the cortex. In conclusion, Na+-Cl--dependent betaine transporter(s) is present in rat outer and inner medullary tubules, and betaine transporter mRNA abundance is regulated by the hydration state in vivo.open353

ANCA-negative pauci-immune crescentic glomerulonephritis

Crescentic glomerulonephritis is a severe form of glomerular injury that is characterized by disruption of the glomerular basement membrane, cellular proliferation within Bowman space, and (often) fibrinoid necrosis. Pauci-immune crescentic glomerulonephritis, so called because it involves little or no glomerular immunoglobulin deposition, is one of the most common causes of rapidly progressive glomerulonephritis. in the majority of patients, pauci-immune crescentic glomerulonephritis is a manifestation of antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis. However, some patients with pauci-immune crescentic glomerulonephritis lack ANCAs. This review compares the prevalence, clinical manifestations, histopathology, and outcomes of ANCA-negative pauci-immune crescentic glomerulonephritis with those of ANCA-positive disease. we also discuss the possible pathogenesis of ANCA-negative pauci-immune crescentic glomerulonephritis, paying particular attention to the mechanisms and role of neutrophil activation