This allows us to conclude that the band with the fine structure is due to the P-donor-B-acceptor pair recombination. This identification was confirmed by the observation of As-donor-B-acceptor pair luminescence in an As-doped sample. The present findings indicate that P and B impurities with concentrations on the order

of 10(16) cm(-3) are unlikely to form complexes and that their ionization energies are not changed from those in the low concentration range. (C) 2011 American Institute of Physics. [doi:10.1063/1.3622560]“
“As nanomaterials might enter into cells and have high reactivity with intracellular structures, it is necessary to assay possible genotoxic risk of them. One of these approaches, we investigated possible genotoxic potential of gold nanoparticle (AuNP) using L5178Y cells. Four different sizes of AuNP (4, 15, 100 or 200 nm) were GDC 0032 chemical structure 4-Hydroxytamoxifen synthesized and the sizes and structures of AuNP were analyzed using transmission electron microscopy (TEM), scanning electron microscopy (SEM) and stability was analyzed by a UV/Vis. Spectrophotometer. Cytotoxicity was assessed by direct cell counting, and cellular location was detected by dark field microscope at 6, 24 and 48 h after treatment of AuNP. Comet assay was conducted to examine DNA damage and,tumor necrosis factor (TNF)-alpha mRNA level was assay by real-time reverse

transcription polymerase chain reaction. Synthetic AuNP (4, 50, 100 and 200 nm size) had constant characteristics and stability confirmed by TEM, SEM and spectrophotometer for 10 days, respectively. Dark field microscope revealed the location of AuNP in the cytoplasm at 6, 24 and 48 h. Treatment of 4 nm AuNP induced dose and time dependent cytotoxicity, while other sizes of AuNP did not. However, Comet assay represented that treatment of 100 nm and 200 nm AuNP significantly increased DNA damage

compared to vehicle control (p < 0.01). Treatment of 100 nm and 200 nm AuNP significantly increased TNF-alpha mRNA expression Birinapant solubility dmso compared to vehicle control (p<0.05, p<0.01, respectively). Taken together, AuNP induced DNA damage in L5178Y cell, associated with induction of oxidative stress.”
“The cause of striae gravidarum is still unclear. The study objective was to test the hypothesis that relaxin is involved in the process of striae gravidarum appearance during pregnancy.

A prospective observational study in 32 pregnant women. Participants were observed at 12th, 24th and 36th gestational week. During each session, striae scoring was assessed and blood for relaxin estimation was withdrawn. The striae assessment was done according to Davey score. Serum relaxin was estimated using Relaxin ELISA kit (Immunodiagnostic AG, Bensheim, Germany).

Serum relaxin levels decreased as the pregnancy advanced (585.9 +/- A 295.1, 424.2 +/- A 253.8, 402.1 +/- A 221.2 pg/ml, respectively) but this decrease did not attain statistical significance.