A One-sided, Highly Relativistic Jet from Cygnus X-3

Very Long Baseline Array images of the X-ray binary, Cygnus X-3, were obtained 2, 4 and 7 days after the peak of a 10 Jy flare on 4 February 1997. The first two images show a curved one-sided jet, the third a scatter-broadened disc, presumably at the position of the core. The jet curvature changes from the first to the second epoch, which strongly suggests a precessing jet. The ratio of the flux density in the approaching to that in the (undetected) receding jet is > 330; if this asymmetry is due to Doppler boosting, the implied jet speed is > 0.81c. Precessing jet model fits, together with the assumptions that the jet is intrinsically symmetric and was ejected during or after the major flare, yield the following constraints: the jet inclination to the line of sight must be < 14 degrees; the cone opening angle must be < 12 degrees; and the precession period must be > 60 days.Comment: 12 pages 7 figures, accepted by Ap

Gamma-Ray and Radio Observations of PSR B1509-58

Abstract : We report concurrent radio and gamma-ray observations of PSR B1509-58 carried out by the Parkes Radio Telescope and by the Burst and Transient Source Experiment (BATSE) and the Oriented Scintillation Spectrometer Experiment (OSSE) on the Compton Gamma Ray Observatory (CGRO-Gamma-ray light curves fitted at several energies between ~ 20-500 keV yield a phase offset with respect to the radio pulse that is independent of energy, with an average value 0.32 plus or minus 0.02. Although this value is larger by 0.07 than that reported by Kawai et al., the difference is not statistically significant (only~2 sigma) when account is taken of the uncertainty associated with their result. We briefly discuss the possibility that the energy-independence of the gamma-ray pulse phase is a signature of non-thermal radiation in the X-ray/gamma-ray range and the suggestion of a dependence of pulsar radio-gamma-ray phase offset on pulse period

Voltage-gated calcium channel subunits from platyhelminths : potential role in praziquantel action

Author Posting. © The Author(s), 2006. This is the author's version of the work. It is posted here by permission of Elsevier B.V. for personal use, not for redistribution. The definitive version was published in International Journal for Parasitology 36 (2006): 625-632, doi:10.1016/j.ijpara.2006.02.002.Voltage-gated calcium (Ca2+) channels provide the pathway for Ca2+ influxes that underlie Ca2+-dependent responses in muscles, nerves, and other excitable cells. They are also targets of a wide variety of drugs and toxins. Ca2+ channels are multisubunit protein complexes consisting of a pore-forming α1 subunit and other modulatory subunits, including the β subunit. Here, we review the structure and function of schistosome Ca2+ channel subunits, with particular emphasis on variant Ca2+ channel β subunits (Cavβvar) found in these parasites. In particular, we examine the role these β subunits may play in the action of praziquantel, the current drug of choice against schistosomiasis. We also present evidence that Cavβvar homologs are found in other praziquantel-sensitive platyhelminths such as the pork tapeworm, Taenia solium, and that these variant β subunits may thus represent a platyhelminth-specific gene family.This work was supported by PAPIIT grant IN-221702 to MCJ. RMG is supported by NIH grant AI 40522 and by the Neal Cornell Research Fund at the Marine Biological Laboratory

Microangiopathy in the cerebellum of patients with mitochondrial DNA disease

Neuropathological findings in mitochondrial DNA disease vary and are often dependent on the type of mitochondrial DNA defect. Many reports document neuronal cell loss, demyelination, gliosis and necrotic lesions in post-mortem material. However, previous studies highlight vascular abnormalities in patients harbouring mitochondrial DNA defects, particularly in those with the m.3243A>G mutation in whom stroke-like events are part of the mitochondrial encephalopathy lactic acidosis and stroke-like episodes syndrome. We investigated microangiopathic changes in the cerebellum of 16 genetically and clinically well-defined patients. Respiratory chain deficiency, high levels of mutated mitochondrial DNA and increased mitochondrial mass were present within the smooth muscle cells and endothelial cells comprising the vessel wall in patients. These changes were not limited to those harbouring the m.3243A>G mutation frequently associated with mitochondrial encephalopathy, lactic acidosis and stroke-like episodes, but were documented in patients harbouring m.8344A>G and autosomal recessive polymerase (DNA directed), gamma (POLG) mutations. In 8 of the 16 patients, multiple ischaemic-like lesions occurred in the cerebellar cortex suggestive of vascular smooth muscle cell dysfunction. Indeed, changes in vascular smooth muscle and endothelium distribution and cell size are indicative of vascular cell loss. We found evidence of blood–brain barrier breakdown characterized by plasma protein extravasation following fibrinogen and IgG immunohistochemistry. Reduced immunofluorescence was also observed using markers for endothelial tight junctions providing further evidence in support of blood–brain barrier breakdown. Understanding the structural and functional changes occurring in central nervous system microvessels in patients harbouring mitochondrial DNA defects will provide an important insight into mechanisms of neurodegeneration in mitochondrial DNA disease. Since therapeutic strategies targeting the central nervous system are limited, modulating vascular function presents an exciting opportunity to lessen the burden of disease in these patients

Enabling and Enhancing Science Exploration Across the Solar System: Aerocapture Technology for SmallSat to Flagship Missions

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Biofilm Development on Caenorhabditis elegans by Yersinia Is Facilitated by Quorum Sensing-Dependent Repression of Type III Secretion

Yersinia pseudotuberculosis forms biofilms on Caenorhabditis elegans which block nematode feeding. This genetically amenable host-pathogen model has important implications for biofilm development on living, motile surfaces. Here we show that Y. pseudotuberculosis biofilm development on C. elegans is governed by N-acylhomoserine lactone (AHL)-mediated quorum sensing (QS) since (i) AHLs are produced in nematode associated biofilms and (ii) Y. pseudotuberculosis strains expressing an AHL-degrading enzyme or in which the AHL synthase (ypsI and ytbI) or response regulator (ypsR and ytbR) genes have been mutated, are attenuated. Although biofilm formation is also attenuated in Y. pseudotuberculosis strains carrying mutations in the QS-controlled motility regulator genes, flhDC and fliA, and the flagellin export gene, flhA, flagella are not required since fliC mutants form normal biofilms. However, in contrast to the parent and fliC mutant, Yop virulon proteins are up-regulated in flhDC, fliA and flhA mutants in a temperature and calcium independent manner. Similar observations were found for the Y. pseudotuberculosis QS mutants, indicating that the Yop virulon is repressed by QS via the master motility regulator, flhDC. By curing the pYV virulence plasmid from the ypsI/ytbI mutant, by growing YpIII under conditions permissive for type III needle formation but not Yop secretion and by mutating the type III secretion apparatus gene, yscJ, we show that biofilm formation can be restored in flhDC and ypsI/ytbI mutants. These data demonstrate that type III secretion blocks biofilm formation and is reciprocally regulated with motility via QS