MONTAGE RAMAN DE HAUTES PERFORMANCES ADAPTÉ A LA CARACTÉRISATION DE LA PHASE GAZEUSE DANS DES OPÉRATIONS DE DÉPÔT CHIMIQUE EN PHASE VAPEUR. RÉSULTATS PRÉLIMINAIRES

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Chemical Vapor Deposition of Thick Tungsten Coatings: Mass Transport Modelling and Experiments

Thick tungsten coatings have been produced by chemical vapor deposition (CVD) from H$_2$-WF$_6$ at a temperature in the range 773-1073 K under a reduced pressure. The experimental set-up was designed for $in$ $situ$ Raman analysis of the gas phase (temperature and WF$_6$ concentration) during the growth of tungsten coatings. A two dimensional mass transport model was proposed. It assumes a simple chemical pathway. Only the H$_2$ reduction of WF$_6$ on the substrate was taken into account. The major objective of the present paper is to report on (i) the experimental deposition rates and the rate values calculated by the model, (ii) the values of temperature and gas phase composition deduced from Raman spectroscopy measurements and the values of these quantities obtained by numerical calculations. Within the range of process parameters investigated, the predictive capabilities of the numerical modelling are demonstrated; in addition the temperature and WF$_6$ partial pressure measurements can be recorded by a Raman equipment during the deposition process

Chemical Vapour Deposition of Thick Tungsten Coatings : Raman Measurements and Mass Transport Modelling

Thick tungsten coatings have been produced by chemical vapour deposition (CVD) from H2-WF6 at a temperature in the range 773- 1073 K under a reduced pressure. The experimental set-up is designed for in situ Raman analysis of the gas phase (temperature and WF6 concentration) during the growth of tungsten coatings. A two dimensional mass transport model was proposed. It assumes a simple chemical pathway. Only the H2 reduction of WF6 has been taken into account. The major objective of the paper is to report on the comparison between (i) the experimental deposition rate and the deposition rate predicted by the model, (ii) the values of temperature and gas phase composition deduced from Raman spectroscopy measurements and the values of these quantities obtained by numerical calculations. These comparisons have shown the predictive capabilities of the numerical modelling and that the temperature and WF6 partial pressures can be recorded by a Raman equipment during the deposition process

UV damage causes uncontrolled DNA breakage in cells from patients with combined features of XP-D and Cockayne syndrome

Nucleotide excision repair (NER) removes damage from DNA in a tightly regulated multiprotein process. Defects in NER result in three different human disorders, xeroderma pigmentosum (XP), trichothiodystrophy (TTD) and Cockayne syndrome (CS). Two cases with the combined features of XP and CS have been assigned to the XP–D complementation group. Despite their extreme UV sensitivity, these cells appeared to incise their DNA as efficiently as normal cells in response to UV damage. These incisions were, however, uncoupled from the rest of the repair process. Using cell-free extracts, we were unable to detect any incision activity in the neighbourhood of the damage. When irradiated plasmids were introduced into unirradiated XP–D/CS cells, the ectopically introduced damage triggered the induction of breaks in the undamaged genomic DNA. XP–D/CS cells thus have a unique response to sensing UV damage, which results in the introduction of breaks into the DNA at sites distant from the damage. We propose that it is these spurious breaks that are responsible for the extreme UV sensitivity of these cells

Slowly Progressing Nucleotide Excision Repair in Trichothiodystrophy Group A Patient Fibroblasts ▿

Trichothiodystrophy (TTD) is a rare autosomal premature-ageing and neuroectodermal disease. The photohypersensitive form of TTD is caused by inherited mutations in three of the 10 subunits of the basal transcription factor TFIIH. TFIIH is an essential transcription initiation factor that is also pivotal for nucleotide excision repair (NER). Photosensitive TTD is explained by deficient NER, dedicated to removing UV-induced DNA lesions. TTD group A (TTD-A) patients carry mutations in the smallest TFIIH subunit, TTDA, which is an 8-kDa protein that dynamically interacts with TFIIH. TTD-A patients display a relatively mild TTD phenotype, and TTD-A primary fibroblasts exhibit moderate UV sensitivity despite a rather low level of UV-induced unscheduled DNA synthesis (UDS). To investigate the rationale of this seeming discrepancy, we studied the repair kinetics and the binding kinetics of TFIIH downstream NER factors to damaged sites in TTD-A cells. Our results show that TTD-A cells do repair UV lesions, although with reduced efficiency, and that the binding of downstream NER factors on damaged DNA is not completely abolished but only retarded. We conclude that in TTD-A cells repair is not fully compromised but only delayed, and we present a model that explains the relatively mild photosensitive phenotype observed in TTD-A patients