AGAPE, an experiment to detect MACHO's in the direction of the Andromeda galaxy

The status of the Agape experiment to detect Machos in the direction of the andromeda galaxy is presented.Comment: 4 pages, 1 figure in a separate compressed, tarred, uuencoded uufile. In case ofproblem contact [email protected]

Spitzer/IRS Imaging and Spectroscopy of the luminous infrared galaxy NGC 6052 (Mrk 297)

We present photometric and spectroscopic data of the interacting starburst galaxy NGC 6052 obtained with the Spitzer Space Telescope. The mid-infrared (MIR) spectra of the three brightest spatially resolved regions in the galaxy are remarkably similar and are consistent with dust emission from young nearly coeval stellar populations. Analysis of the brightest infrared region of the system, which contributes ~18.5 % of the total 16\micron flux, indicates that unlike similar off-nuclear infrared-bright regions found in Arp 299 or NGC 4038/9, its MIR spectrum is inconsistent with an enshrouded hot dust (T > 300K) component. Instead, the three brightest MIR regions all display dust continua of temperatures less than ~ 200K. These low dust temperatures indicate the dust is likely in the form of a patchy screen of relatively cold material situated along the line of sight. We also find that emission from polycyclic aromatic hydrocarbons (PAHs) and the forbidden atomic lines is very similar for each region. We conclude that the ionization regions are self-similar and come from young (about 6 Myr) stellar populations. A fourth region, for which we have no MIR spectra, exhibits MIR emission similar to tidal tail features in other interacting galaxies.Comment: 20 pages in preprint form, estimated 7 pages in ApJ Aeptember 10, 2007, v666n 2 issue, six encapsulated postscript figure

AgapeZ1: a Large Amplification Microlensing Event or an Odd Variable Star Towards the Inner Bulge of M31

AgapeZ1 is the brightest and the shortest duration microlensing candidate event found in the Agape data. It occured only 42" from the center of M31. Our photometry shows that the half intensity duration of the event6 is 4.8 days and at maximum brightness we measure a stellar magnitude of R=18.0 with B-R=0.80 mag color. A search on HST archives produced a single resolved star within the projected event position error box. Its magnitude is R=22.Comment: 4 pages with 5 figure

AGAPE: a microlensing search in the direction of M31

A status report of the microlensing search by the pixel method in the direction of M31, on the 2 meter telescope at Pic du Midi is given. Pixels are stable to a level better than 0.5%. Pixel variations as small as 0.02 magnitude can clearly be detected

Variable stars towards the bulge of M31: the AGAPE catalogue

We present the AGAPE astrometric and photometric catalogue of 1579 variable stars in a 14'x10' field centred on M31. This work is the first survey devoted to variable stars in the bulge of M31. The R magnitudes of the objects and the B-R colours suggest that our sample is dominated by red long-period variable stars (LPV), with a possible overlap with Cepheid-like type II stars. Twelve nova candidates are identified. Correlations with other catalogues suggest that 2 novae could be recurrent novae and provide possible optical counterparts for 2 supersoft X-ray sources candidates observed with Chandra.Comment: 11 pages, Latex, accepted for publication in A&

Poly(ADP-ribose)glycohydrolase is an upstream regulator of Ca2+ fluxes in oxidative cell death

Oxidative DNA damage to cells activates poly(ADP-ribose)polymerase-1 (PARP-1) and the poly(ADP-ribose) formed is rapidly degraded to ADP-ribose by poly(ADP-ribose)glycohydrolase (PARG). Here we show that PARP-1 and PARG control extracellular Ca2+ fluxes through melastatin-like transient receptor potential 2 channels (TRPM2) in a cell death signaling pathway. TRPM2 activation accounts for essentially the entire Ca2+ influx into the cytosol, activating caspases and causing the translocation of apoptosis inducing factor (AIF) from the inner mitochondrial membrane to the nucleus followed by cell death. Abrogation of PARP-1 or PARG function disrupts these signals and reduces cell death. ADP-ribose-loading of cells induces Ca2+ fluxes in the absence of oxidative damage, suggesting that ADP-ribose is the key metabolite of the PARP-1/PARG system regulating TRPM2. We conclude that PARP-1/PARG control a cell death signal pathway that operates between five different cell compartments and communicates via three types of chemical messengers: a nucleotide, a cation, and proteins

Signalling mechanisms mediating Zn2+-induced TRPM2 channel activation and death cell in microglial cells

Excessive Zn2+ causes brain damage via promoting ROS generation. Here we investigated the role of ROS-sensitive TRPM2 channel in H2O2/Zn2+-induced Ca2+ signalling and cell death in microglial cells. H2O2/Zn2+ induced concentration-dependent increases in cytosolic Ca2+ concentration ([Ca2+]c), which was inhibited by PJ34, a PARP inhibitor, and abolished by TRPM2 knockout (TRPM2-KO). Pathological concentrations of H2O2/Zn2+ induced substantial cell death that was inhibited by PJ34 and DPQ, PARP inhibitors, 2-APB, a TRPM2 channel inhibitor, and prevented by TRPM2-KO. Further analysis indicate that Zn2+ induced ROS production, PARP-1 stimulation, increase in the [Ca2+]c and cell death, which were suppressed by chelerythrine, a protein kinase C inhibitor, DPI, a NADPH-dependent oxidase (NOX) inhibitor, GKT137831, a NOX1/4 inhibitor, and Phox-I2, a NOX2 inhibitor. Furthermore, Zn2+-induced PARP-1 stimulation, increase in the [Ca2+]c and cell death were inhibited by PF431396, a Ca2+-sensitive PYK2 inhibitor, and U0126, a MEK/ERK inhibitor. Taken together, our study shows PKC/NOX-mediated ROS generation and PARP-1 activation as an important mechanism in Zn2+-induced TRPM2 channel activation and, TRPM2-mediated increase in the [Ca2+]c to trigger the PYK2/MEK/ERK signalling pathway as a positive feedback mechanism that amplifies the TRPM2 channel activation. Activation of these TRPM2-depenent signalling mechanisms ultimately drives Zn2+-induced Ca2+ overloading and cell death

Cisplatin-DNA adduct formation in patients treated with cisplatin-based chemoradiation: lack of correlation between normal tissues and primary tumor

Contains fulltext : 69595.pdf (publisher's version ) (Closed access)PURPOSE: In this study, the formation of cisplatin-DNA adducts after concurrent cisplatin-radiation and the relationship between adduct-formation in primary tumor tissue and normal tissue were investigated. METHODS: Three intravenous cisplatin-regimens, given concurrently with radiation, were studied: daily low-dose (6 mg/m(2)) cisplatin, weekly 40 mg/m(2), three-weekly 100 mg/m(2). A (32)P-postlabeling technique was used to quantify adducts in normal tissue [white blood cells (WBC) and buccal cells] and tumor. RESULTS: Normal tissue samples for adduct determination were obtained from 63 patients and tumor biopsies from 23 of these patients. Linear relationships and high correlations were observed between the levels of two guanosine- and adenosine-guanosine-adducts in normal and tumor tissue. Adduct levels in tumors were two to five times higher than those in WBC (P<0.001). No significant correlations were found between adduct levels in normal tissues and primary tumor biopsies, nor between WBC and buccal cells. CONCLUSIONS: In concurrent chemoradiotherapy schedules, cisplatin adduct levels in tumors were significantly higher than in normal tissues (WBC). No evidence of a correlation was found between adduct levels in normal tissues and primary tumor biopsies. This lack of correlation may, to some extent, explain the inconsistencies in the literature regarding whether or not cisplatin-DNA adducts can be used as a predictive test in anticancer platinum therapy