The Global Star Formation Rate from the 1.4 GHz Luminosity Function

The decimetric luminosity of many galaxies appears to be dominated by synchrotron emission excited by supernova explosions. Simple models suggest that the luminosity is directly proportional to the rate of supernova explosions of massive stars averaged over the past 30 Myr. The proportionality may be used together with models of the evolving 1.4 GHz luminosity function to estimate the global star formation rate density in the era z < 1. The local value is estimated to be 0.026 solar masses per year per cubic megaparsec, some 50% larger than the value inferred from the Halpha luminosity density. The value at z ~ 1 is found to be 0.30 solar masses per year per cubic megaparsec. The 10-fold increase in star formation rate density is consistent with the increase inferred from mm-wave, far-infrared, ultra-violet and Halpha observations.Comment: 10 pages, 2 figures, Astrophysical Journal Letters (in press); new PS version has improved figure placemen

Optically Faint Microjansky Radio Sources

We report on the identifications of radio sources from our survey of the Hubble Deep Field and the SSA13 fields, both of which comprise the deepest radio surveys to date at 1.4 GHz and 8.5 GHz respectively. About 80% of the microjansky radio sources are associated with moderate redshift starburst galaxies or AGNs within the I magnitude range of 17 to 24 with a median of I = 22 mag. Thirty-one (20%) of the radio sources are: 1) fainter than $I>$25 mag, with two objects in the HDF $I_{AB}>$28.5, 2) often identified with very red objects $I-K>$4, and 3) not significantly different in radio properties than the brighter objects. We suggest that most of these objects are associated with heavily obscured starburst galaxies with redshifts between 1 and 3. However, other mechanisms are discussed and cannot be ruled out with the present observations.Comment: to appear in Astrophysical Journal Letters, 3 figures, 1 tabl

Measurement of radiotherapy x-ray skin dose on a chest wall phantom

Sufficient skin dose needs to be delivered by a radiotherapy chest wall treatment regimen to ensure the probability of a near surface tumor recurrence is minimized. To simulate a chest wall treatment a hemicylindrical solid water phantom of 7.5 cm radius was irradiated with 6 MV x-rays using 20×20 cm2 and 10×20 cm2 fields at 100 cm source surface distance (SSD) to the base of the phantom. A surface dose profile was obtained from 0 to 180°, in 10° increments around the circumference of the phantom. Dosimetry results obtained from radiochromic film (effective depth of 0.17 mm) were used in the investigation, the superficial doses were found to be 28% (of Dmax) at the 0° beam entry position and 58% at the 90° oblique beam position. Superficial dose results were also obtained using extra thin thermoluminescent dosimeters (TLD) (effective depth 0.14 mm) of 30% at 0°, 57% at 90°, and a metal oxide semiconductor field effect transistor (MOSFET) detector (effective depth 0.5 mm) of 43% at 0°, 62% at 90°. Because the differences in measured superficial doses were significant and beyond those related to experimental error, these differences are assumed to be mostly attributable to the effective depth of measurement of each detector. We numerically simulated a bolus on/bolus off technique and found we could increase the coverage to the skin. Using an alternate “bolus on,” “bolus off” regimen, the skin would receive 36.8 Gy at 0° incidence and 46.4 Gy at 90° incidence for a prescribed midpoint dose of 50 Gy. From this work it is evident that, as the circumference of the phantom is traversed the SSD increases and hence there is an inverse square fluence fall-off, this is more than offset by the increase in skin dose due to surface curvature to a plateau at about 90°. Beyond this angle it is assumed that beam attenuation through the phantom and inverse square fall-off is causing the surface dose to reduce

Reinitiation of compensatory lung growth after subsequent lung resection

ObjectiveIn experimental animals, pneumonectomy results in rapid, hyperplastic compensatory growth of the remaining lung. The limits of this induced growth are unknown. We tested the hypothesis that compensatory growth can be reinitiated in the same lung after subsequent lung resection.MethodsA left thoracotomy (Sham group) or left pneumonectomy (PNX group) was performed in Sprague–Dawley rats. A third group underwent left pneumonectomy followed 4 weeks later by a bilobectomy of the right upper and middle lobes (PNX+LBX group). Four weeks after bilobectomy in the PNX+LBX group (8 weeks in the Sham and PNX groups), right ventricular pressures were measured by using the open chest technique, and total lung weight and lower plus cardiac lobe weight indices were measured. Lungs were inflation fixed at 25 cm H2O to measure lobe volume index and to perform morphometric measurements on lung sections. Right ventricle/left ventricle plus septum weight index was measured as another index of pulmonary hypertension.ResultsTotal lung weight index was similar in all groups. Pneumonectomy resulted in increased lower plus cardiac lobe weight and volume indices, which were significantly augmented in the PNX+LBX group. The PNX+LBX group underwent a significant increase in total volume of respiratory region, airspace, and tissue and a decrease in alveolar surface density versus the PNX group. The PNX+LBX group also had significantly increased right ventricular systolic pressure and right ventricle/left ventricle plus septum index.ConclusionThese results demonstrate that compensatory growth can be reinitiated in lungs that had previously undergone postpneumonectomy compensatory growth. This subsequent growth, however, is more hypertrophic, and pulmonary hypertension develops despite subsequent compensatory growth

Adenosine A1 receptor activation attenuates lung ischemia–reperfusion injury

ObjectivesIschemia–reperfusion injury contributes significantly to morbidity and mortality in lung transplant patients. Currently, no therapeutic agents are clinically available to prevent ischemia–reperfusion injury, and treatment strategies are limited to maintaining oxygenation and lung function. Adenosine can modulate inflammatory activity and injury by binding to various adenosine receptors; however, the role of the adenosine A1 receptor in ischemia–reperfusion injury and inflammation is not well understood. The present study tested the hypothesis that selective, exogenous activation of the A1 receptor would be anti-inflammatory and attenuate lung ischemia–reperfusion injury.MethodsWild-type and A1 receptor knockout mice underwent 1 hour of left lung ischemia and 2 hours of reperfusion using an in vivo hilar clamp model. An A1 receptor agonist, 2-chloro-N6-cyclopentyladenosine, was administered 5 minutes before ischemia. After reperfusion, lung function was evaluated by measuring airway resistance, pulmonary compliance, and pulmonary artery pressure. The wet/dry weight ratio was used to assess edema. The myeloperoxidase and cytokine levels in bronchoalveolar lavage fluid were measured to determine the presence of neutrophil infiltration and inflammation.ResultsIn the wild-type mice, 2-chloro-N6-cyclopentyladenosine significantly improved lung function and attenuated edema, cytokine expression, and myeloperoxidase levels compared with the vehicle-treated mice after ischemia–reperfusion. The incidence of lung ischemia–reperfusion injury was similar in the A1 receptor knockout and wild-type mice; and 2-chloro-N6-cyclopentyladenosine had no effects in the A1 receptor knockout mice. In vitro treatment of neutrophils with 2-chloro-N6-cyclopentyladenosine significantly reduced chemotaxis.ConclusionsExogenous A1 receptor activation improves lung function and decreases inflammation, edema, and neutrophil chemotaxis after ischemia and reperfusion. These results suggest a potential therapeutic application for A1 receptor agonists for the prevention of lung ischemia–reperfusion injury after transplantation

Radio Continuum Emission at 1.4 GHz from KISS Emission-Line Galaxies

We have searched the Faint Images of the Radio Sky at Twenty centimeters (FIRST) and the NRAO VLA Sky Survey (NVSS) 1.4 GHz radio surveys for sources that are coincident with emission-line galaxy (ELG) candidates from the KPNO International Spectroscopic Survey (KISS). A total of 207 of the 2157 KISS ELGs (~10%) in the first two H-alpha-selected survey lists were found to possess radio detections in FIRST and/or NVSS. Follow-up spectra exist for all of the radio detections, allowing us to determine the activity type (star-forming vs. AGN) for the entire sample. We explore the properties of the radio-detected KISS galaxies in order to gain a better insight into the nature of radio-emitting galaxies in the local universe (z < 0.1). No dwarf galaxies were detected, despite the large numbers of low-luminosity galaxies present in KISS, suggesting that lower mass, lower luminosity objects do not possess strong galaxian-scale magnetic fields. Due to the selection technique used for KISS, our radio ELGs represent a quasi-volume-limited sample, which allows us to develop a clearer picture of the radio galaxy population at low redshift. Nearly 2/3rds of the KISS radio galaxies are starburst/star-forming galaxies, which is in stark contrast to the results of flux-limited radio surveys that are dominated by AGNs and elliptical galaxies (i.e., classic radio galaxies). While there are many AGNs among the KISS radio galaxies, there are no objects with large radio powers in our local volume. We derive a radio luminosity function (RLF) for the KISS ELGs that agrees very well with previous RLFs that adequately sample the lower-luminosity radio population.Comment: Accepted for publication in the Astronomical Journal (April 2004); 23 pages, 16 figure

Tissue-derived proinflammatory effect of adenosine A2B receptor in lung ischemia–reperfusion injury

ObjectiveIschemia–reperfusion injury after lung transplantation remains a major source of morbidity and mortality. Adenosine receptors have been implicated in both pro- and anti-inflammatory roles in ischemia–reperfusion injury. This study tests the hypothesis that the adenosine A2B receptor exacerbates the proinflammatory response to lung ischemia–reperfusion injury.MethodsAn in vivo left lung hilar clamp model of ischemia–reperfusion was used in wild-type C57BL6 and adenosine A2B receptor knockout mice, and in chimeras created by bone marrow transplantation between wild-type and adenosine A2B receptor knockout mice. Mice underwent sham surgery or lung ischemia–reperfusion (1 hour ischemia and 2 hours reperfusion). At the end of reperfusion, lung function was assessed using an isolated buffer-perfused lung system. Lung inflammation was assessed by measuring proinflammatory cytokine levels in bronchoalveolar lavage fluid, and neutrophil infiltration was assessed via myeloperoxidase levels in lung tissue.ResultsCompared with wild-type mice, lungs of adenosine A2B receptor knockout mice were significantly protected after ischemia–reperfusion, as evidenced by significantly reduced pulmonary artery pressure, increased lung compliance, decreased myeloperoxidase, and reduced proinflammatory cytokine levels (tumor necrosis factor-α; interleukin-6; keratinocyte chemoattractant; regulated on activation, normal T-cell expressed and secreted; and monocyte chemotactic protein-1). Adenosine A2B receptor knockout→adenosine A2B receptor knockout (donor→recipient) and wild-type→ adenosine A2B receptor knockout, but not adenosine A2B receptor knockout→wild-type, chimeras showed significantly improved lung function after ischemia–reperfusion.ConclusionsThese results suggest that the adenosine A2B receptor plays an important role in mediating lung inflammation after ischemia–reperfusion by stimulating cytokine production and neutrophil chemotaxis. The proinflammatory effects of adenosine A2B receptor seem to be derived by adenosine A2B receptor activation primarily on resident pulmonary cells and not bone marrow-derived cells. Adenosine A2B receptor may provide a therapeutic target for prevention of ischemia–reperfusion-related graft dysfunction in lung transplant recipients