Anomalous organic magnetoresistance from competing carrier-spin-dependent interactions with localized electronic and nuclear spins

We describe a new regime for low-field magnetoresistance in organic semiconductors, in which the spin-relaxing effects of localized nuclear spins and electronic spins interfere. The regime is studied by the controlled addition of localized electronic spins to a material that exhibits substantial room-temperature magnetoresistance ($\sim 20$\%). Although initially the magnetoresistance is suppressed by the doping, at intermediate doping there is a regime where the magnetoresistance is insensitive to the doping level. For much greater doping concentrations the magnetoresistance is fully suppressed. The behavior is described within a theoretical model describing the effect of carrier spin dynamics on the current

A Search for Hard X-Ray Emission from Globular Clusters - Constraints from BATSE

We have monitored a sample of 27 nearby globular clusters in the hard X-ray band (20-120 keV) for approximately 1400 days using the BATSE instrument on board the Compton Gamma-Ray Observatory. Globular clusters may contain a large number of compact objects (e.g., pulsars or X-ray binaries containing neutron stars) which can produce hard X-ray emission. Our search provides a sensitive (~50 mCrab) monitor for hard X-ray transient events on time scales of >1 day and a means for observing persistent hard X-ray emission. We have discovered no transient events from any of the clusters and no persistent emission. Our observations include a sensitive search of four nearby clusters containing dim X-ray sources: 47 Tucanae, NGC 5139, NGC 6397, and NGC 6752. The non-detection in these clusters implies a lower limit for the recurrence time of transients of 2 to 6 years for events with luminosities >10^36 erg s^-1 (20-120 keV) and ~20 years if the sources in these clusters are taken collectively. This suggests that the dim X-ray sources in these clusters are not transients similar to Aql~X-1. We also place upper limits on the persistent emission in the range 2-10*10^34 erg s^-1 (2 sigma, 20-120 keV) for these four clusters. For 47 Tuc the upper limit is more sensitive than previous measurements by a factor of 3. We find a model dependent upper limit of 19 isolated millisecond pulsars (MSPs) producing gamma-rays in 47 Tuc, compared to the 11 observed radio MSPs in this cluster.Comment: 20 pages; accepted, ApJ; uu encoded tar file; 7 figure

β-adrenergic receptor activation in immortalized human urothelial cells stimulates inflammatory responses by PKA-independent mechanisms

BACKGROUND: Interstitial cystitis (IC) is a debilitating disease characterized by chronic inflammation of the urinary bladder, yet specific cellular mechanisms of inflammation in IC are largely unknown. Multiple lines of evidence suggest that β-adrenergic receptor (AR) signaling is increased in the inflamed urothelium, however the precise effects of these urothelial cell signals have not been studied. In order to better elucidate the AR signaling mechanisms of inflammation associated with IC, we have examined the effects of β-AR stimulation in an immortalized human urothelial cell line (UROtsa). For these studies, UROtsa cells were treated with effective concentrations of the selective β-AR agonist isoproterenol, in the absence or presence of selective inhibitors of protein kinase A (PKA). Cell lysates were analyzed by radioimmunoassay for generation of cAMP or by Western blotting for induction of protein products associated with inflammatory responses. RESULTS: Radioligand binding demonstrated the presence of β-ARs on human urothelial UROtsa cell membranes. Stimulating UROtsa cells with isoproterenol led to concentration-dependent increases of cAMP production that could be inhibited by pretreatment with a blocking concentration of the selective β-AR antagonist propranolol. In addition, isoproterenol activation of these same cells led to significant increases in the amount of phosphorylated extracellular signal-regulated kinase (pERK), inducible nitric oxide synthase (iNOS) and the induced form of cyclooxygenase (COX-2) when compared to control. Moreover, preincubation of UROtsa cells with the selective PKA inhibitors H-89 or Rp-cAMPs did not diminish this isoproterenol mediated phosphorylation of ERK or production of iNOS and COX-2. CONCLUSION: Functional β-ARs expressed on human urothelial UROtsa cell membranes increase the generation of cAMP and production of protein products associated with inflammation when activated by the selective β-AR agonist isoproterenol. However, the increased production of iNOS and COX-2 by isoproterenol is not blocked when UROtsa cells are preincubated with inhibitors of PKA. Therefore, UROtsa cell β-AR activation significantly increases the amount of iNOS and COX-2 produced by a PKA-independent mechanism. Consequently, this immortalized human urothelial cell line can be useful in characterizing potential AR signaling mechanisms associated with chronic inflammatory diseases of the bladder