Carbon budget and carbon chemistry in Photon Dominated Regions

We present a study of small carbon chains and rings in Photon Dominated Regions (PDRs) performed at millimetre wavelengths. Our sample consists of the Horsehead nebula (B33), the rho,Oph L1688 cloud interface, and the cometary-shaped cloud IC63. Using the IRAM 30-m telescope, the SEST and the Effelsberg 100-m teles cope at Effelsberg., we mapped the emission of \cch, c-C3H2 and C4H, and searched for heavy hydrocarbons such as c-C3H, l-C3H, l-C3H2, l-C4H2 and C6H. The large scale maps show that small hydrocarbons are present until the edge of all PDRs, which is surprising as they are expected to be easily destroyed by UV radiation. Their spatial distribution reasonably agrees with the aromatic emission mapped in mid-IR wavelength bands. Their abundances relative to H2 are relatively high and comparable to the ones derived in dark clouds such as L134N or TMC-1, known as efficient carbon factories. In particular, we report the first detection of C6H in a PDR. We have run steady-state PDR models using several gas-phase chemical networks (UMIST95 and the New Standard Model) and conclude that both networks fail in reproducing the high abundances of some of these hydrocarbons by an order of magnitude. The high abundance of hydrocarbons in the PDR may suggest that the photo-erosion of UV-irradiated large carbonaceous compounds could efficiently feed the ISM with small carbon clusters or molecules. This new production mechanism of carbon chains and rings could overcome their destruction by the UV radiation field. Dedicated theoretical and laboratory measurements are required in order to understand and implement these additional chemical routes.Comment: 18 pages, 12 figure

Ellipticine cytotoxicity to cancer cell lines — a comparative study

Ellipticine is a potent antineoplastic agent exhibiting multiple mechanisms of action. This anticancer agent should be considered a pro-drug, whose pharmacological efficiency and/or genotoxic side effects are dependent on its cytochrome P450 (CYP)- and/or peroxidase-mediated activation to species forming covalent DNA adducts. Ellipticine can also act as an inhibitor or inducer of biotransformation enzymes, thereby modulating its own metabolism leading to its genotoxic and pharmacological effects. Here, a comparison of the toxicity of ellipticine to human breast adenocarcinoma MCF-7 cells, leukemia HL-60 and CCRF-CEM cells, neuroblastoma IMR-32, UKF-NB-3 and UKF-NB-4 cells and U87MG glioblastoma cells and mechanisms of its action to these cells were evaluated. Treatment of all cells tested with ellipticine resulted in inhibition of cell growth and proliferation. This effect was associated with formation of two covalent ellipticine-derived DNA adducts, identical to those formed by 13-hydroxy- and 12-hydroxyellipticine, the ellipticine metabolites generated by CYP and peroxidase enzymes, in MCF-7, HL-60, CCRF-CEM, UKF-NB-3, UKF-NB-4 and U87MG cells, but not in neuroblastoma UKF-NB-3 cells. Therefore, DNA adduct formation in most cancer cell lines tested in this comparative study might be the predominant cause of their sensitivity to ellipticine treatment, whereas other mechanisms of ellipticine action also contribute to its cytotoxicity to neuroblastoma UKF-NB-3 cells

DNA and histone deacetylases as targets for neuroblastoma treatment

Neuroblastoma, a tumor of the peripheral sympathetic nervous system, is the most frequent solid extra cranial tumor in children and is a major cause of death from neoplasia in infancy. Still little improvement in therapeutic options has been made, requiring a need for the development of new therapies. In our laboratory, we address still unsettled questions, which of mechanisms of action of DNA-damaging drugs both currently use for treatment of human neuroblastomas (doxorubicin, cis-platin, cyclophosphamide and etoposide) and another anticancer agent decreasing growth of neuroblastomas in vitro, ellipticine, are predominant mechanism(s) responsible for their antitumor action in neuroblastoma cell lines in vitro. Because hypoxia frequently occurs in tumors and strongly correlates with advanced disease and poor outcome caused by chemoresistance, the effects of hypoxia on efficiencies and mechanisms of actions of these drugs in neuroblastomas are also investigated. Since the epigenetic structure of DNA and its lesions play a role in the origin of human neuroblastomas, pharmaceutical manipulation of the epigenome may offer other treatment options also for neuroblastomas. Therefore, the effects of histone deacetylase inhibitors on growth of neuroblastoma and combination of these compounds with doxorubicin, cis-platin, etoposide and ellipticine as well as mechanisms of such effects in human neuroblastona cell lines in vitro are also investigated. Such a study will increase our knowledge to explain the proper function of these drugs on the molecular level, which should be utilized for the development of new therapies for neuroblastomas

Multi-ionization cross-sections of small ionic carbon clusters by particle impact as a tool to investigate their shapes

Single, double and triple ionization cross-sections of C$_{{n}}^{+}$ clusters in collisions with helium atoms at intermediate velocity (2.6 a.u.) have been measured ($n=1 \rightarrow 5$). The relative multi-ionization cross-sections (double over single and triple over single) are first increasing with n, then decreasing when going from n=4 to n=5. We show, on the basis of an independent atom and electron collisional treatment, that this effect is attributable to a change in the cluster shape. The role of the cluster compactness on relative multi-ionization cross-sections is pointed out here for the first time