A visual examination of the images from the Galactic Legacy Infrared Mid-Plane Survey Extraordinaire (GLIMPSE) has revealed 322 partial and closed rings that we propose represent partially or fully enclosed three-dimensional bubbles. We argue that the bubbles are primarily formed by hot young stars in massive star formation regions. We have found an average of about 1.5 bubbles per square degree. About 25% of the bubbles coincide with known radio H ii regions, and about 13% enclose known star clusters. It appears that B4-B9 stars (too cool to produce detectable radio H ii regions) probably produce about three-quarters of the bubbles in our sample, and the remainder are produced by young O-B3 stars that produce detectable radio H ii regions. Some of the bubbles may be the outer edges of H ii regions where PAH spectral features are excited and may not be dynamically formed by stellar winds. Only three of the bubbles are identified as known SNRs. No bubbles coincide with known planetary nebulae or W-R stars in the GLIMPSE survey area. The bubbles are small. The distribution of angular diameters peaks between 1 0 and 3 0 with over 98% having angular diameters less than 10 0 and 88% less than 4 0. Almost 90% have shell thicknesses between 0.2 and 0.4 of their outer radii. Bubble shell thickness increases approximately linearly with shell radius. The eccentricities are rather large, peaking between 0.6 and 0.7; about 65% have eccentricities between 0.55 and 0.85.

Abstract. Erythropoietin (EPO) is upregulated by hypoxia and causes proliferation and differentiation of erythroid progenitors in the bone marrow through inhibition of apoptosis. EPO receptors are expressed in many tissues, including the kidney. Here it is shown that a single systemic administration of EPO either preischemia or just before reperfusion prevents ischemia-reperfusion injury in the rat kidney. Specifically, EPO (300 U/kg) reduced glomerular dysfunction and tubular injury (biochemical and histologic assessment) and prevented caspase-3, -8, and -9 activation in vivo and reduced apoptotic cell death. In human (HK-2) proximal tubule epithelial cells, EPO attenuated cell death in response to oxidative stress and serum starvation. EPO reduced DNA fragmentation and prevented caspase-3 activation, with upregulation of Bcl-X L and XIAP. The antiapoptotic effects of EPO were dependent on JAK2 signaling and the phosphorylation of Akt by phosphatidylinositol 3-kinase. These findings may have major implications in the treatment of acute renal tubular damage.Erythropoietin (EPO) is the major regulator of proliferation and differentiation of erythroid progenitor cells through its antiapoptotic actions (1). EPO gene expression is under the control of the oxygen-sensitive transcription factor hypoxiainducible factor (HIF-1), which consists of the regulatory subunit HIF-1␣ and the constitutively expressed subunit HIF-1␤. Low oxygen tension adverts enzymatic prolyl-residue hydroxylation by prolyl-4-hydroxylase, which, in normoxia, serves as a signal for polyubiquitination and proteosomal degradation, thereby preventing von-Hippel-Lindau (VHL)-dependent HIF degradation, leading to nuclear accumulation of HIF-1 (2). HIF-1 controls the expression of several cytokines that mediate the adaptive response to ischemia, including vascular endothelial growth factor and glucose metabolism. The prolyl-4-hydroxylase requires iron as a co-factor, and cobalt mimics the effect of hypoxia on HIF-1␣ activation (3). Cobalt administration to rats caused upregulation of HIF-dependent proteins, including EPO, and diminished the degree of renal injury caused by ischemia-reperfusion (I/R), suggesting the HIF/EPO pathway may play an important role in ischemic preconditioning (4). EPO is upregulated in the brain and spinal cord after hypoxic stimuli and protects neurones against ischemic or oxidative injury in vivo and in vitro (5,6). The neuroprotective effects of EPO are dependent on EPO receptormediated JAK2 phosphorylation and NF-B-dependent transcription of antiapoptotic genes, including endogenous inhibitors of apoptosis XIAP and cIAP-2 (7). In the retina, EPO upregulation is essential for hypoxic preconditioning via HIF-1␣ stabilization. The systemic administration of recombinant EPO also reduces the degree of retinal apoptosis induced by high-intensity light insult (8). EPO receptor-mediated intracellular signaling may involve nuclear translocation of the transcription factor NF-B and phosphorylation of Akt (protein kinase B) by phosph...

No abstract

No abstract

No abstract

Diabetic nephropathy is the leading cause of end-stage renal disease in the Western world. Poor glycemic control contributes to the development of diabetic nephropathy, but the mechanisms underlying high glucose-induced tissue injury are not fully understood. In the present study, the effect of high glucose on a proximal tubular epithelial cell (PTEC) line was investigated. Reactive oxygen species (ROS) were detected using the fluorescent probes dichlorofluorescein diacetate, dihydrorhodamine 123, and 2,3-diaminonapthalene. Peroxynitrite (ONOO-) generation and nitrite concentrations were increased after 24 h of high glucose treatment (P<0.05). LLC-PK1 cells exposed to high D-glucose (25 mM) for up to 48 h had increased DNA fragmentation (P<0.01), caspase-3 activity (P<0.001), and annexin-V staining (P<0.05) as well as decreased expression of XIAP when compared with controls (5 mM D-glucose). The ONOO- scavenger ebselen reduced DNA fragmentation and caspase-3 activity as well as the high glucose-induced nitrite production and DCF fluorescence. High glucose-induced DNA fragmentation was completely prevented by an inhibitor of caspase-3 (P<0.01) and a pan-caspase inhibitor (P<0.001). Caspase inhibition did not affect ROS generation. This study, in a PTEC line, demonstrates that high glucose causes the generation of ONOO-, leading to caspase-mediated apoptosis. Ebselen and a caspase-3 inhibitor provided significant protection against high glucose-mediated apoptosis, implicating ONOO- as a proapoptotic ROS in early diabetic nephropathy.

Mare than 100 symbiotic stars are now known. A catalogue of them, complete to 1984 January 1, is presented. Finding charts are given for all examples, and optical spectra for the majority. A table summarises the observational material at X-ray, ultraviolet, infrared and radio wavelengths.

No abstract