Theory of sub-10 fs Generation in Kerr-lens Mode-locked Solid-State Lasers with a Coherent Semiconductor Absorber

The results of the study of ultra-short pulse generation in continuous-wave Kerr-lens mode-locked (KLM) solid-state lasers with semiconductor saturable absorbers are presented. The issues of extremely short pulse generation are addressed in the frames of the theory that accounts for the coherent nature of the absorber-pulse interaction. We developed an analytical model that bases on the coupled generalized Landau-Ginzburg laser equation and Bloch equations for a coherent absorber. We showed, that in the absence of KLM semiconductor absorber produces 2pi - non-sech-pulses of self-induced transparency, while the KLM provides an extremely short sech-shaped pulse generation. 2pi- and pi-sech-shaped solutions and variable-area chirped pulses have been found. It was shown, that the presence of KLM removes the limitation on the minimal modulation depth in absorber. An automudulational stability and self-starting ability were analyzed, too.Comment: revised version, 18 pages, 6 figures, LaTeX, Maple program is available on http://www.geocities.com/optomaple

Assessing associations between the AURKAHMMR-TPX2-TUBG1 functional module and breast cancer risk in BRCA1/2 mutation carriers

While interplay between BRCA1 and AURKA-RHAMM-TPX2-TUBG1 regulates mammary epithelial polarization, common genetic variation in HMMR (gene product RHAMM) may be associated with risk of breast cancer in BRCA1 mutation carriers. Following on these observations, we further assessed the link between the AURKA-HMMR-TPX2-TUBG1 functional module and risk of breast cancer in BRCA1 or BRCA2 mutation carriers. Forty-one single nucleotide polymorphisms (SNPs) were genotyped in 15,252 BRCA1 and 8,211 BRCA2 mutation carriers and subsequently analyzed using a retrospective likelihood appr

Genome-Wide Association Study in BRCA1 Mutation Carriers Identifies Novel Loci Associated with Breast and Ovarian Cancer Risk

BRCA1-associated breast and ovarian cancer risks can be modified by common genetic variants. To identify further cancer risk-modifying loci, we performed a multi-stage GWAS of 11,705 BRCA1 carriers (of whom 5,920 were diagnosed with breast and 1,839 were diagnosed with ovarian cancer), with a further replication in an additional sample of 2,646 BRCA1 carriers. We identified a novel breast cancer risk modifier locus at 1q32 for BRCA1 carriers (rs2290854, P = 2.7×10-8, HR = 1.14, 95% CI: 1.09-1.20). In addition, we identified two novel ovarian cancer risk modifier loci: 17q21.31 (rs17631303, P = 1.4×10-8, HR = 1.27, 95% CI: 1.17-1.38) and 4q32.3 (rs4691139, P = 3.4×10-8, HR = 1.20, 95% CI: 1.17-1.38). The 4q32.3 locus was not associated with ovarian cancer risk in the general population or BRCA2 carriers, suggesting a BRCA1-specific associat