The two neutral His that coordinate the BChls appeared to have th

The two neutral His that coordinate the BChls appeared to have the NMR signatures of a double-protonated, i.e. positively charged His (Alia et al. 2001, 2004). This was explained by a charge selleck chemicals llc transfer in the ground state between the His and their coordinating BChl, resulting in a partial positive charge on the His imidazoles. In density functional theory (DFT) modeling, the effect would disappear if the BChl-His geometry was optimized beforehand, but was clearly present when the coordinates were taken directly from the X-ray structure (Wawrzyniak et al. 2008). Running a geometry optimization would increase the distance between the His and the BChl from 2.12 to 2.31 Å.

One could argue that this moderate change falls within the error of the X-ray spatial resolution, and indeed the sensitivity of the NMR chemical shifts to electronic effects, which might be induced by small spatial PD0332991 solubility dmso re-arrangements, exceeds the resolution LY2109761 clinical trial of the X-ray crystallographic structures. The LH2 His model explained the electronic effects of charge transfer by mechanical stress, induced by

the protein conformational constraints in the LH2 oligomer packing. It was speculated that the His-BChl charge transfer could have an effect on the light-harvesting properties. A more clear example how a coordinating His may control the chromophore function was found for the special pair of photosystem II. Here, the inverted electronic charge of the Chl nitrogens in the special pair was explained by a hinge model, in which the coordinating His imidazole ring hangs over the Chl macrocycle, altering its electronic structure in the ground state and its oxidation state compared to PSI (Diller et

al. 2007). The light-harvesting complex 2 as an NMR model; the BChl pigments In addition to the protein chemical shifts, NMR assignments were obtained for the BChl-conjugated macrocycles of the three types of BChl in LH2: the α- and β-bound BChls that build a ring of BChl dimers, called the B850 GPCR & G Protein inhibitor band, and the so-called B800 BChls that form a ring of monomers (van Gammeren et al. 2005a). To discriminate between the B850 and B800 signals, a sample was prepared from unlabeled LH2 of which the B800 BChls were extracted and substituted with uniformly labeled BChls. The three types of BChls have a distinctive set of chemical shifts, reflecting their conformational structures and variation in the local protein environment. The differences between the NMR signals in the protein-bound BChls and free BChl in organic solvent Δσ determine the electronic structures in the ground state. Recently, the data set was expanded with the BChl assignments of the acidophila LH1 complex, the core antenna that forms a ring-shaped oligomer of dimer αβ subunits surrounding the photosynthetic reaction center (RC) (Pandit et al. 2010a).

siamensis sequences, similar results were observed This tree sho

siamensis sequences, similar results were observed. This tree showed high congruence to hsp70 tree since all taxa were concordantly clustered into the same species complex and placed L. selleck chemicals siamensis at the basal branch of Leishmania in Euleishmania section. Figure 1 The unrooted phylogenetic tree inferred from DNA sequences of four markers using Neighbor Joining method. The bootstrapping values less than 50 are omitted. The bootstrapping and posterior probability values estimated by Maximum parsimony and Bayesian inference methods are shown in parenthesis at each node, respectively. Asterisks indicate

bootstrapping and posterior probability values that are below 50 or 0.5 or are not calculated by the analyses. Dense lines indicate Leishmania species complexes as described by Lainson and Shaw [30]. The species complex of L. adleri, L. turanica, L. gerbilli, JAK inhibitor and L. arabica are unclassified. Dot lines indicate the lineage sections suggested by Cupolillo et al. [35]. (a) SSU-rRNA, (b) ITS1, (c) hsp70, (d) cyt b. In addition, the L. siamensis lineage TR was closely related to L. enrietti whereas lineage PG was furcated into a sister clade (Figure 1d). For sequence alignments of the ITS1, hsp70, and cyt b regions, see

Additional files 1, 2, 3. Discussion This study characterized L. siamensis isolated from autochthonous VL Thai patients based on sequencing of four genetic loci.

The construction of molecular evolutionary trees of Leishmania species has been extensively studied on various genetic markers both in conserved and variable regions [10–17]. The results of these studies allow us to view evolutionary processes, classify and discriminate species among Leishmania isolates. One of the widely used genetic markers for phylogenetic studies is the ribosomal RNA gene. This gene has proved to be useful for inferring the relationships of a wide range of organisms, including Leishmania[7, 27]. Even though the phylogenetic study based on the complete SSU-rRNA has shown that the variation of this gene limits the classification of this parasite at the subgenus level, studying the phylogenetic position using this gene is fundamentally required for a novel species, Reverse transcriptase like L. siamensis[28, 29]. In this study, L. siamensis was grouped in the monophyletic branch of subgenus Leishmania (Leishmania) at a long distance in a unique subclade, primarily suggesting that this novel species is closely related to the members of L. (Leishmania) but evolved rapidly and nonrelative to the members in this subgenus. The incapability to discriminate between two lineages of L. siamensis proposed from the genetic distance analysis was not selleck chemicals llc beyond our expectation since the studied region of this gene was remarkably conserved.

218 0 069 <0 01 Adjusted for age, body mass index, calcium intake

218 0.069 <0.01 Adjusted for age, body mass index, calcium intake, physical activity level, smoking status, education level, and metabolic syndrome AF autofluorescence, OSI osteo-sono assessment index, SE standard error Table 4 Relationship of the tertile of skin autofluorescence (AF) with log-transformed

OSI among adult Japanese men   Tertiles of skin AF Range (unit, AU) Low Middle High (1.28–1.82) (1.82–2.05) (2.05–2.88) Number of participants 65 64 64 Crude 2.83 (2.76–2.90) 2.78 (2.71–2.85) learn more 2.68 (2.61–2.74)* Adjusteda 2.81 (2.75–2.87) 2.81 (2.74–2.87) 2.66(2.61–2.73)*,** Data are geometric means (95% confidence interval). Unit of leg extension power is watts per kilogram Analysis of variance or analysis of covariance * P < 0.01; significantly different from lowest skin autofluorescence tertile (Bonferroni correction) ** P < 0.01; significantly different from middle skin autofluorescence tertile (Bonferroni correction) aAdjusted for age, body mass index, calcium intake, physical activity level, smoking status, education level, and metabolic syndrome Discussion The present study examined the relationship between skin AF associated with AGE accumulation and OSI, a quantitative ultrasound measure, among

non-diabetic adult Japanese men. Consistent with our hypothesis, our results showed that levels of skin AF were independently associated with OSI, suggesting that participants

with higher skin AF had lower OSI. In previous population studies, the relationship between AGE accumulation A-1155463 cost and fracture risk has been controversial. Some studies reported that there was no association between urinary pentosidine and fracture risk after adjustment in non-diabetic older Caucasian [14] Glutathione peroxidase and among postmenopausal Caucasian women [27]. On the other hand, in elderly Japanese women, a high level of urinary pentosidine was an independent risk factor for osteoporotic vertebral fractures [13]. Possibly in line with these findings, we found a negative association between skin AF with OSI among adult Japanese men after adjustment for potential confounders, given that lower OSI may lead to higher fracture risk. Although the reasons for this discrepancy are unknown, racial differences may potentially explain the inconsistent results of the studies. While Japanese have twice the incidence of the methylenetetrahydrofolate Stem Cells inhibitor reductase polymorphism (C677T) compared with Caucasians, Japanese subjects are predisposed to mild hyperhomocysteinemia [28–30]. Indeed, hyperhomocysteinemia caused a reduction in bone toughness through the accumulation of pentosidine in bone in rabbit models [31]. Other explanation could be diet, which is a major source of exogenous AGEs [32].

For this purpose, we investigated ARH77 cells that had shown the

For this purpose, we investigated ARH77 cells that had shown the highest TXNIP VX-809 cell line RNA level response compared to the unresponsive MC/CAR cells (Figure 1A). As expected, phloretin blocked the hyperglycemia effect on TXNIP RNA level (1.5 ± 0.05 vs. 1.03 ± 0.03, p < 0.01) (Figure 4A) and significantly reduced ROS (2.1 ± 0.08 vs 1.84 ± 0.14, p < 0.05) in ARH77 cells (Figure 4B). The addition of phloretin had no effect on either TXNIP or ROS levels in the MC/CAR cells (Figure 4A, B). This confirmed that glucose played a major role in the TXNIP RNA regulation in responsive

cells ARH77. Figure 4 A. Blocking glucose transport blocks the hyperglycemia effect oon thioredoxin-interacting protein (TXNIP) RNA levels. Cells were grown in 5 mM glucose or 20 XL184 research buy mM chronically.. For glucose uptake inhibition, phlor (200 μM) was added to 20 mM media and cells harvested after 24 hours. Fold change is based on comparison to 5 mM glucose. B. Reactive oxygen species (ROS)-levels in response to phlor pre-treatment. Cells were treated as in A. ROS levels were measured as mean fluorescence

of 50,000 cells and compared to 5 mM as baseline. Hyperglycemia increases the DEX-IC50 in MM cells At this point our data were suggesting that DEX and glucose together reduced ROS production in ARH77, NCIH929 and MC/CAR cells independently from the TXNIP-TRX regulation. Paradoxically, DEX + glucose further decreased ROS level by increasing TRX activity in MC/CAR cells. It seemed that DEX was mitigating the oxidative stress and ROS production

induced by glucose in those cells independently from TXNIP expression. We then decided to test the hypothesis of TXNIP-independent effect by assessing the cytotoxicity of DEX in TXNIP-glucose/DEX responsive cells ARH77 and TXNIP-glucose/DEX unresponsive cells MC/CAR. When the dose response effect to DEX was evaluated in ARH77 and MC/CAR cells in 20 mM glucose, we found that hyperglycemia increased the IC50 for both cell lines by a factor of Sulfite dehydrogenase 10 (ARH77: 48 μM to 510 μM; MC/CAR 36 μM to 303 μM) (Figure 5). These data selleck inhibitor suggest that MM cells were more resistant to DEX in conditions of hyperglycemia, probably because of the hampering effect of DEX on ROS production as shown in Figure 2. Figure 5 Hyperglycemia increase the DEX-IC 50 in MM cells . Cells were grown in 5 or 20 mM glucose chronically. Dexamethasone, in varying concentrations, was added for 24 hour after which cells were harvested. IC50 was calculated using Calcusyn software and represented as median dose response. A. ARH77 response B. MC/CAR response. Discussion Our study addresses the response of cancerous cells in conditions of hyperglycemia either related to drug induction or underlining diabetes.

Mol Microbiol 1999,31(3):893–902 PubMedCrossRef 9 Outten FW, Out

Mol Microbiol 1999,31(3):893–902.PubMedCrossRef 9. Outten FW, Outten CE, Hale J, selleck screening library O’Halloran TV: Transcriptional activation of an Escherichia coli copper efflux regulon by the chromosomal MerR homologue, cueR. J Biol Chem 2000,275(40):31024–31029.PubMedCrossRef 10. Blindauer CA, Harrison MD, Parkinson JA, Robinson AK, Cavet JS, Robinson NJ, Sadler PJ: A metallothionein containing a zinc finger within a four-metal cluster protects a bacterium from zinc toxicity. Proc Natl Acad Sci U S A 2001,98(17):9593–9598.PubMedCentralPubMedCrossRef 11. Pulliainen AT, Kauko A, Haataja S, Papageorgiou AC, Finne J: Dps/Dpr ferritin-like protein: insights into the

mechanism of iron incorporation and evidence for a central

role in cellular iron homeostasis in Streptococcus suis . Mol Microbiol 2005,57(4):1086–1100.PubMedCrossRef 12. Hantke K: Bacterial zinc uptake and regulators. Curr Opin Microbiol 2005,8(2):196–202.PubMedCrossRef MX69 datasheet 13. Moore CM, Helmann JD: Metal ion homeostasis in Bacillus subtilis . Curr Opin Microbiol 2005,8(2):188–195.PubMedCrossRef 14. Carpenter BM, Whitmire JM, Merrell DS: This is not your mother’s repressor: the complex role of fur in pathogenesis. Infect Immun 2009,77(7):2590–2601.PubMedCentralPubMedCrossRef 15. Horsburgh MJ, Ingham E, Foster SJ: In Staphylococcus aureus , Fur is an interactive regulator with PerR, contributes to virulence, and Is necessary for oxidative stress resistance through positive regulation of catalase and iron homeostasis. J Bacteriol 2001,183(2):468–475.PubMedCentralPubMedCrossRef 16. Wösten MM, Kox LF, Chamnongpol S, Soncini FC, Groisman EA: A signal transduction

system that responds to extracellular iron. Cell 2000,103(1):113–125.PubMedCrossRef 17. Gunn JS: The Salmonella PmrAB regulon: lipopolysaccharide modifications, antimicrobial peptide resistance and more. Trends Microbiol 2008,16(6):284–290.PubMedCrossRef 18. Nishino K, Hsu FF, Turk J, Cromie MJ, Wosten MM, Groisman EA: Identification of the lipopolysaccharide modifications controlled by the Salmonella PmrA/PmrB system mediating resistance to Fe(III) and Al(III). Mol Microbiol 2006,61(3):645–654.PubMedCentralPubMedCrossRef 19. Kato A, Chen HD, Latifi T, Groisman Decitabine EA: Reciprocal control between a bacterium’s regulatory system and the modification status of its lipopolysaccharide. Mol Cell 2012,47(6):897–908.PubMedCentralPubMedCrossRef 20. Ogasawara H, Shinohara S, Yamamoto K, Ishihama A: Novel regulation targets of the metal-response BasS-BasR HDAC assay two-component system of Escherichia coli . Microbiology 2012,158(Pt 6):1482–1492.PubMedCrossRef 21. Leonhartsberger S, Huber A, Lottspeich F, Bock A: The hydH/G Genes from Escherichia coli code for a zinc and lead responsive two-component regulatory system. J Mol Biol 2001,307(1):93–105.PubMedCrossRef 22.

J Bone Miner Res 15:2019–2025PubMedCrossRef 19 Tsai K, Twu S, Ch

J Bone Miner Res 15:2019–2025PubMedCrossRef 19. Tsai K, Twu S, Chieng P et al (1996) Prevalence of vertebral fractures in Chinese men and women in urban Taiwanese communities. Calcif Tissue Int 59:249–253PubMedCrossRef 20. Kung AW, Luk KD, Chu LW et al (1999) Quantitative ultrasound and symptomatic vertebral fracture risk in Chinese women. Osteoporos Int 10:456–461PubMedCrossRef 21. Lau HH, Ho AY, Luk KD et al (2002)

Estrogen receptor beta gene polymorphisms are associated with higher bone mineral density in premenopausal, but not postmenopausal southern Chinese GSK2118436 chemical structure women. Bone 31:276–281PubMedCrossRef 22. Black DM, Cummings SR, Stone K et al (1991) A new approach to defining normal vertebral dimensions. J Bone Miner Res 6:883–892PubMedCrossRef 23. Cauley JA, Palermo L, Vogt M et al Nirogacestat order (2008) Prevalent vertebral fractures in black women and white women. J Bone Miner Res 23:1458–1467PubMedCrossRef 24. Delmas PD, Genant HK, Crans GG et al (2003) Severity of prevalent vertebral fractures and the risk of subsequent vertebral and nonvertebral fractures: results from the MORE trial. Bone 33:522–532PubMedCrossRef 25. Ismail AA, Cooper C, Felsenberg D et al (1999) Number

and type of vertebral deformities: epidemiological characteristics and relation to back pain and height loss. European Vertebral Osteoporosis Study Group. Osteoporos Int 9:206–213PubMedCrossRef 26. Melton LJ III, Kan SH, Frye MA et al (1989) Epidemiology of vertebral fractures in women. Am J Epidemiol 129:1000–1011PubMed 27. O’Neill TW, Felsenberg D, Etofibrate Varlow

J et al (1996) The prevalence of vertebral deformity in European men and women: the European Vertebral Osteoporosis Study. J Bone Miner Res 11:1010–1018PubMedCrossRef 28. Pluijm SM, Tromp AM, Smit JH et al (2000) Consequences of vertebral deformities in older men and women. J Bone Miner Res 15:1564–1572PubMedCrossRef 29. Spector TD, McCloskey EV, Doyle DV et al (1993) Prevalence of vertebral fracture in women and the relationship with bone density and symptoms: the Chingford Study. J Bone Miner Res 8:817–822PubMedCrossRef 30. Melton LJ III, Lane AW, Cooper C et al (1993) Prevalence and incidence of vertebral deformities. Osteoporos Int 3:113–119PubMedCrossRef 31. Finkelstein JS, Lee ML, Sowers M et al (2002) Ethnic variation in bone density in premenopausal and early perimenopausal women: effects of anthropometric and lifestyle factors. J Clin Endocrinol Metab 87:3057–Vactosertib concentration 3067PubMedCrossRef 32. Johansson H, Kanis JA, Oden A et al (2009) BMD, clinical risk factors and their combination for hip fracture prevention. Osteoporos Int 20:1675–1682PubMedCrossRef 33. Kanis JA, Johnell O, Oden A et al (2008) FRAX and the assessment of fracture probability in men and women from the UK. Osteoporos Int 19:385–397PubMedCrossRef 34. Kanis JA, Oden A, Johnell O et al (2007) The use of clinical risk factors enhances the performance of BMD in the prediction of hip and osteoporotic fractures in men and women.

thermophilus fitness in response to sudden increased of the tempe

thermophilus fitness in response to sudden increased of the temperature. As observed in other streptococcal strains [24, 25], the deletion of the rgg 0182 gene is not associated with a drastic modification of the survival to stress suggesting that this regulator is not essential but selleck kinase inhibitor important for heat stress adaptation. Furthermore, our results showed that cspB and clpE genes were 2-fold lower and 3-fold higher, respectively, in the mutant compared to the wild-type strain after the heat stress. Data from literature indicate that most

Csp proteins are required when cells are grown at low growth temperature [2, 3]. Thus, the Rgg0182 would learn more negatively control the production of CspB when the latter is not required. Moreover, in S. pneumoniae, the clpE gene has been demonstrated to be required for thermo-tolerance [33], therefore we hypothesize that the heat sensitivity of the S. thermophilus Δrgg

0182 mutant would result, at least partially, from a reduced level of ClpE expression. Alternatively, it is also conceivable that Rgg0182 regulates the transcription of other genes encoding proteins involved in the S. thermophilus heat stress Vorinostat supplier response. A transcriptomic analysis would identify all targets of this regulator within S. thermophilus LMG18311. Conclusions In conclusion, our study gave a better understanding of the thermal adaptation of the important dairy starter, S. thermophilus. These data showed the importance of the Rgg0182 transcriptional regulator on the survival of S. thermophilus during industrial processes and more specifically during changes in temperature. Methods

Bacterial strains, media and reagents Streptococcus thermophilus LMG18311 and its derivatives are presented in Table 1. S. thermophilus strains were grown at 30 or 42°C in M17 medium with lactose (10 g/l) (LM17, a classical Resminostat medium for S. thermophilus growth) [34] or in a chemically defined medium (CDM, a peptide free-medium) [35]. Pre-cultures were incubated at 42°C in milk medium except for the luciferase assays as mentioned below. For numeration, agar was added to the medium (15 g/l) and cells were incubated under anaerobic conditions using GENbox anaer in Generbox jars (bioMérieux SA, Marcy-l’Etoile, France). S. thermophilus strains containing the pG+host9 vector [36] were cultivated in the presence of erythromycin (final concentration 2 μg/ml) at 30°C when plasmid self-maintenance was required and at 42°C for selection of clones with the chromosome’s integrated plasmid. Table 1 Bacterial strains and plasmids used in this study Strains and plasmids Genotype/phenotype/source Origin or reference Streptococcus thermophilus LMG18311 Wild-type; isolated from yogurt.

All samples were diluted serially from 106 CFU/ml to 10 CFU/ml in

All samples were diluted serially from 106 CFU/ml to 10 CFU/ml in a sterile round bottom 96-well plate (Corning). Optical density was recorded at 600 nm using a PowerWave XS (BioTek) selleckchem spectrometer operated in an anaerobic chamber. The plate was incubated at 55°C for the duration of the experiment, and was shaken every 30 seconds. OD600 was measured every three minutes. The duration of lag phase was evaluated based on the time needed to reach an OD600 of 0.1. Acknowledgments We would like to thank Dan Olson for his suggestions and input on the eFT508 ic50 manuscript. This research was supported by a grant from the BioEnergy Science Center (BESC), Oak Ridge National Laboratory,

a U.S. Department of Energy (DOE) BioEnergy Research Center supported by the Office of Biological and Environmental Research in the DOE Office of Science. References 1. Lynd LR, Weimer PJ, van Zyl WH, Pretorius IS: Microbial cellulose utilization: fundamentals and biotechnology. Microbiol Mol Biol Rev 2002,66(3):506–577. table of contentsPubMedCrossRef 2. Barer MR: Physiological and molecular aspects of growth, non-growth,

culturability and viability in bacteria. GS-1101 concentration Cambridge University Press, Cambridge; 2003. 3. Dawes IW, Mandelstam J: Sporulation of Bacillus subtilis in continuous culture. J Bacteriol 1970,103(3):529–535.PubMed 4. Schaeffer P: Sporulation and the production of antibiotics, exoenzymes, and exotonins. Bacteriol Rev 1969,33(1):48–71.PubMed 5. Li J, Chen J, Vidal JE, McClane BA: The Agr-like quorum-sensing system regulates sporulation and production PAK5 of enterotoxin and beta2 toxin by Clostridium perfringens type A non-food-borne human gastrointestinal disease strain F5603. Infect Immun 2011,79(6):2451–2459.PubMedCrossRef 6. Philippe VA, Mendez MB, Huang IH, Orsaria LM, Sarker MR, Grau RR: Inorganic phosphate induces spore morphogenesis and enterotoxin production in the intestinal pathogen Clostridium perfringens. Infect Immun 2006,74(6):3651–3656.PubMedCrossRef 7. Long SJ DT, Woods DR: Initiation of solvent production, clostridial sage and endospore formation in Clostridium acetobutylicum P262. Appl Microbiol Biotechnol 1984, 20:256–261. 8. Gehin A, Gelhaye E, Raval G, Petitdemange

H: Clostridium cellulolyticum Viability and Sporulation under Cellobiose Starvation Conditions. Appl Environ Microbiol 1995,61(3):868–871.PubMed 9. Payot S, Guedon E, Desvaux M, Gelhaye E, Petitdemange E: Effect of dilution rate, cellobiose and ammonium availabilities on Clostridium cellulolyticum sporulation. Appl Microbiol Biotechnol 1999,52(5):670–674.PubMedCrossRef 10. Desvaux M, Petitdemange H: Sporulation of Clostridium cellulolyticum while grown in cellulose-batch and cellulose-fed continuous cultures on a mineral-salt based medium. Microb Ecol 2002,43(2):271–279.PubMedCrossRef 11. Weigel JW, Dykstra M: Clostridium thermocellum: Adhesion and sporulation while adhered to cellulose and hemicellulose. Appl Microbiol Biotechnol 1984, 20:59–65.

51 Egly JM: The 14th Datta Lecture TFIIH: from transcription to

51. Egly JM: The 14th Datta Lecture. TFIIH: from transcription to clinic. FEBS Lett 2001, 498: 124–128.CrossRefPubMed 52. Friedberg EC: How nucleotide excision repair protects against cancer. PF-04929113 mw Nat Rev Cancer 2001,

1: 22–33.CrossRefPubMed 53. Leadon SA, Cooper PK: Preferential repair of ionizing radiation-induced damage in the transcribed strand of an active human gene is defective in Cockayne syndrome. Proc Natl Acad Sci USA 1993, 90: 10499–10503.CrossRefPubMed 54. Satoh MS, Jones CJ, Wood RD, Lindahl T: DNA excision-repair defect of xeroderma pigmentosum prevents removal of a class of oxygen free radical-induced base lesions. Proc Natl Acad Sci USA 1993, 90: 6335–6339.CrossRefPubMed 55. Coin F, Marinoni JC, Rodolfo C, Fribourg S, Pedrini AM, Egly JM: Mutations in the XPD helicase gene result in XP and TTD phenotypes, preventing interaction between XPD and the p44 subunit of TFIIH. Nat Genet 1998, 20: 184–188.CrossRefPubMed 56. Brewster AM, Jorgensen TJ, Ruczinski I, Huang HY, Hoffman S, Thuita L, Newschaffer C, Lunn RM, Bell D, Helzlsouer KJ: Polymorphisms of the DNA repair genes XPD (Lys751Gln) and XRCC1 (Arg399Gln and Arg194Trp): relationship to breast cancer risk and familial predisposition to breast cancer. Breast Cancer Res Treat 2006, 95: 73–80.CrossRefPubMed 57. Dufloth RM, Costa S, Schmitt F, Zeferino LC: DNA repair gene polymorphisms

MK-4827 ic50 and susceptibility to familial breast cancer in a group of patients from Campinas, Brazil. Genet Mol Res 2005, 4: 771–782.PubMed 58. Metsola K, Kataja V, Sillanpaa P, Siivola P, Heikinheimo L, Eskelinen M, Kosma VM, Uusitupa M, Hirvonen A: XRCC1 and XPD genetic polymorphisms, smoking and breast cancer risk in a Finnish case-control study. Breast Cancer

Res 2005, 7: R987-R997.CrossRefPubMed ever 59. Shi Q, Wang LE, Bondy ML, Brewster A, Singletary SE, Wei Q: Reduced DNA repair of benzo[a]pyrene diol epoxide-induced adducts and common XPD polymorphisms in breast cancer patients. Carcinogenesis 2004, 25: 1695–1700.CrossRefPubMed 60. Bernard-Gallon D, Bosviel R, Delort L, Fontana L, Chamoux A, Rabiau N, Kwiatkowski F, Chalabi N, Satih S, Bignon YJ: DNA repair gene ERCC2 polymorphisms and associations with breast and ovarian cancer risk. Mol Cancer 2008, 7: 36.CrossRefPubMed 61. Terry MB, Gammon MD, Zhang FF, Eng SM, Sagiv SK, Paykin AB, Wang Q, Hayes S, Teitelbaum SL, Neugut AI, Santella RM: Polymorphism in the DNA repair gene XPD, polycyclic aromatic hydrocarbon-DNA adducts, cigarette smoking, and breast cancer risk. Cancer selleck screening library Epidemiol Biomarkers Prev 2004, 13: 2053–2058.PubMed 62. Ramachandran S, Ramadas K, Hariharan R, Rejnish KR, Radhakrishna PM: Single nucleotide polymorphisms of DNA repair genes XRCC1 and XPD and its molecular mapping in Indian oral cancer. Oral Oncol 2006, 42: 350–362.CrossRefPubMed Competing interests The authors declare that they have no competing interests.

For pump-probe measurements, a commercial Ti:sapphire laser syste

For pump-probe measurements, a commercial Ti:sapphire laser system providing short pulses (approximately 30 fs) with repetition rate of 75 MHz and wavelength of 800 nm (hv = 1.55 eV) was used. The pump beam was focused at a diameter of about 50 μm with pump fluence ranging from 15.2 to 45.7 μJ/cm2, while the probe fluence was fixed at approximately 1 μJ/cm2 at spot diameter of 20 μm. The pump pulses were modulated at 2 KHz with a chopper. A mechanical delay stage was used to vary the time delay between the pump and probe NCT-501 pulses. The transient reflectivity change ΔR/R of the probe beam was measured as a function of the pump-probe delay time. The small reflected signals were detected

and fed into a lock-in amplifier. Results and discussion Figure  1a,b shows the laser-produced plasmas (LPP) at the surface of the CIGS GM6001 order target by ns and fs laser, respectively. It exhibits substantial dissimilarities in LPPs that can be explained by the various laser-target interactions. For the ns-PLD process (Figure  1a), there is much residual heat, which is caused by the longer duration of laser pulse, as the pulse laser hits the target. The residual

heat is due to the picosecond order of both the heat conduction time and ion energy transfer time, which is much faster than the pulse width of the excimer laser. It leads to the mixing of the melted CIGS (gray color) debris with the direct-transferred undesirable Cu2Se secondary phases (yellow color) from the target as

clusters were ejected along with the plasma in expansive directions. The effect of residual heat can spread to a wider range in the target, thus leading to an enlarged heat-affected zone (HAZ) (red region) that brings the plasma and debris with variation in energy and random transportation directions. This is why the expansive plasma was observed as shown in the inset of Figure  1a. Nonetheless, these large clusters can re-crystallize into a preferred orientation directed by the flow of the remaining residual energy of the laser pulses and the thermal energy from the heated substrate. Figure 1 Schematic selleck inhibitor illustrations and photos of laser-produced plasmas on CIGS target. (a) ns-PLD and (b) Lck fs-PLD. On the contrary, the highly localized interactions with target minimize the HAZ by the fs pulse laser. This is because the duration of laser pulse is shorter than the heat conduction time, so the residual energy can be eliminated. The main mechanism of producing plasma by fs pulse laser is coulomb explosion, a process that ionizes atoms in a solid-state target through an extremely intensive electric field, rather than conventional evaporation. With the absence of residual heat, concentrated plasma was generated by fs laser pulses (Figure  1b), which consists of the mixture of atoms and nanometer particles.