Occurrence of proteinaceous moieties in S-and O-rich Late Tithonian kerogen (Kashpir oil Shales, Russia)

Abstract The polar fraction, isolated from the o-line pyrolysate at 400 C of a Late Tithonian, sulphur-and oxygen-rich, kerogen was examined via Raney Nickel desulphurization and TMAH thermochemolysis. Important information on this kerogen, not accessible via conventional pyrolysis, was thus obtained: (i) its structure is not simply based on alkyl skeletons cross-linked by ether and (poly)sulphide bridges, (ii) TMAH thermochemolysis aorded direct evidence of the survival of proteinaceous moieties in this 140 million years old kerogen and (iii) encapsulation within an aliphatic organic matrix was probably the main pathway reponsible for such a conspicuous preservation, also possibly favoured by the presence of numerous sulphur links.

Solar-like oscillations in distant stars as seen by CoRoT : the special case of HD 42618, a solar sister

We report the observations of a main-sequence star, HD 42618 (T[SUB]eff[/SUB] = 5765 K, G3V) by the space telescope CoRoT. This is the closest star to the Sun ever observed by CoRoT in term of its fundamental parameters. Using a preliminary version of CoRoT light curves of HD 42618, p modes are detected around 3.2 mHz associated to l = 0, 1 and 2 modes with a large spacing of 142 μHz. Various methods are then used to derive the mass and radius of this star (scaling relations from solar values as well as comparison between theoretical and observationnal frequencies) giving values in the range of (0.80 - 1.02)M[SUB]solar[/SUB] and (0.91 - 1.01)R[SUB]solar[/SUB]. A preliminary analysis of l = 0 and 1 modes allows us also to study the amount of penetrative convection at the base of the convective envelope

MRE11 Function in Response to Topoisomerase Poisons Is Independent of its Function in Double-Strand Break Repair in Saccharomyces cerevisiae

Camptothecin (CPT) and etoposide (ETP) trap topoisomerase-DNA covalent intermediates, resulting in formation of DNA damage that can be cytotoxic if unrepaired. CPT and ETP are prototypes for molecules widely used in chemotherapy of cancer, so defining the mechanisms for repair of damage induced by treatment with these compounds is of great interest. In S. cerevisiae, deficiency in MRE11, which encodes a highly conserved factor, greatly enhances sensitivity to treatment with CPT or ETP. This has been thought to reflect the importance of double-strand break (DSB) repair pathways in the response to these to agents. Here we report that an S. cerevisiae strain expressing the mre11-H59A allele, mutant at a conserved active site histidine, is sensitive to hydroxyurea and also to ionizing radiation, which induces DSBs, but not to CPT or ETP. We show that TDP1, which encodes a tyrosyl-DNA phosphodiesterase activity able to release both 5′- and 3′-covalent topoisomerase-DNA complexes in vitro, contributes to ETP-resistance but not CPT-resistance in the mre11-H59A background. We further show that CPT- and ETP-resistance mediated by MRE11 is independent of SAE2, and thus independent of the coordinated functions of MRE11 and SAE2 in homology-directed repair and removal of Spo11 from DNA ends in meiosis. These results identify a function for MRE11 in the response to topoisomerase poisons that is distinct from its functions in DSB repair or meiotic DNA processing. They also establish that cellular proficiency in repair of DSBs may not correlate with resistance to topoisomerase poisons, a finding with potential implications for stratification of tumors with specific DNA repair deficiencies for treatment with these compounds

Genetic polymorphisms of the RAS-cytokine pathway and chronic kidney disease

Chronic kidney disease (CKD) in children is irreversible. It is associated with renal failure progression and atherosclerotic cardiovascular (CV) abnormalities. Nearly 60% of children with CKD are affected since birth with congenital or inherited kidney disorders. Preliminary evidence primarily from adult CKD studies indicates common genetic risk factors for CKD and atherosclerotic CV disease. Although multiple physiologic pathways share common genes for CKD and CV disease, substantial evidence supports our attention to the renin angiotensin system (RAS) and the interlinked inflammatory cascade because they modulate the progressions of renal and CV disease. Gene polymorphisms in the RAS-cytokine pathway, through altered gene expression of inflammatory cytokines, are potential factors that modulate the rate of CKD progression and CV abnormalities in patients with CKD. For studying such hypotheses, the cooperative efforts among scientific groups and the availability of robust and affordable technologies to genotype thousands of single nucleotide polymorphisms (SNPs) across the genome make genome-wide association studies an attractive paradigm for studying polygenic diseases such as CKD. Although attractive, such studies should be interpreted carefully, with a fundamental understanding of their potential weaknesses. Nevertheless, whole-genome association studies for diabetic nephropathy and future studies pertaining to other types of CKD will offer further insight for the development of targeted interventions to treat CKD and associated atherosclerotic CV abnormalities in the pediatric CKD population

3D modeling and kinematics of the External Zone of the French Western Alps (Belledonne and Grand Châtelard Massifs, Maurienne valley, Savoie).

International audienc

Prévision des contraintes macroscopiques obtenues au cours d'essais de traction-torsion simultanées. Relation avec la texture.

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