Metal nanostructures, such as nanoparticles and nanowires, have been proposed as building blocks for several applications in nanofabrication and nanoelectronics. However, even when atmospheric corrosion is common in metals, there is a lack of information about the stability of those nanostructures against such phenomenon. Therefore, we decided to study the atmospheric corrosion of silver nanowires and nanoparticles synthesized by the polyol method using poly(vinylpyrrolidone) (PVP) as the capping agent by different techniques, including transmission electron microscopy (TEM) and X-ray photoelectron spectroscopy (XPS). After synthesis and purification, the silver nanostructures were deposited on different substrates and exposed to laboratory air at ambient conditions. The structural changes in the samples were monitored by TEM as a function of time for a period of time of 24 weeks. Our results demonstrated that these silver nanostructures are susceptible to atmospheric corrosion and that, in most cases, a thin layer of silver sulfide nanocrystals is formed on their surfaces. The enhanced reactivity of regions with defects and dislocations could explain the observation that the corrosion rate of the nanowires is higher than the corrosion rate of the nanoparticles, since it is well-known that the structure of the nanowires synthesized by the polyol method is multitwinned, while most of the nanoparticles that remained after synthesis are single crystals. Additionally, part of the original sample of silver nanostructures was sulfidized using hydrogen sulfide (H 2 S) as corrodent gas. After performing XPS studies of this sample, we confirmed the presence of PVP on the surface of the sulfidized silver nanostructures. This result agrees with the observation that in the atmospherically corroded samples, even when in some cases the original silver nanostructure was completely corroded, the silver sulfide nanocrystals remained together adopting the shape of silver nanostructure. Finally, our results indicate that the corrosion at the nanoscale seems to be similar to that of the bulk silver.

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The Arabidopsis root has a unique cellular pattern in its singlelayered epidermis. Cells residing over the intercellular spaces between underlying cortical cells (H position) differentiate into hair cells, whereas those directly over cortical cells (N position) differentiate into non-hair cells. Recent studies have revealed that this cellular pattern is determined by interactions of six patterning genes CPC, ETC, GL2, GL3͞EGL3, TTG, and WER, and that the position-dependent expression of the CPC, GL2, and WER genes is essential for their appropriate interactions. However, little is known about how the expressions of the pattern genes are determined. Here we show that trichostatin A (TSA) treatment of germinating Arabidopsis seedlings alters the cellular pattern of the root epidermis to induce hair cell development at nonhair positions. The effects of TSA treatment are rapid, reversible, concentration-dependent, and position-independent. TSA inhibition of histone deacetylase activity results in hyperacetylation of the core histones H3 and H4, and alters the expression levels and cell specific expression of the patterning genes CPC, GL2 and WER. Analysis of histone deacetylase mutant cellular patterning further verified the participation of histone acetylation in cellular patterning, and revealed that HDA18 is a key component in the regulatory machinery of the Arabidopsis root epidermis. We propose a working model to suggest that histone acetylation may function in mediating a positional cue to direct expression of the patterning genes in the root epidermal cells.histone as a signaling mediator ͉ trichostatin A ͉ histone deacetylase ͉ positional cue ͉ chromatin immunoprecipitation

To identify new genetic risk factors for cervical cancer, we conducted a genome-wide association study in the Han Chinese population. The initial discovery set included 1,364 individuals with cervical cancer (cases) and 3,028 female controls, and we selected a 'stringently matched samples' subset (829 cases and 990 controls) from the discovery set on the basis of principal component analysis; the follow-up stages included two independent sample sets (1,824 cases and 3,808 controls for follow-up 1 and 2,343 cases and 3,388 controls for follow-up 2). We identified strong evidence of associations between cervical cancer and two new loci: 4q12 (rs13117307, Pcombined, stringently matched=9.69×10(-9), per-allele odds ratio (OR)stringently matched=1.26) and 17q12 (rs8067378, Pcombined, stringently matched=2.00×10(-8), per-allele ORstringently matched=1.18). We additionally replicated an association between HLA-DPB1 and HLA-DPB2 (HLA-DPB1/2) at 6p21.32 and cervical cancer (rs4282438, Pcombined, stringently matched=4.52×10(-27), per-allele ORstringently matched=0.75). Our findings provide new insights into the genetic etiology of cervical cancer.