Titanium dioxide nanoparticles (nanoTiO2) have been widely used as a photocatalyst in air and water cleaning. However, these nanoparticles inhalation can induce pulmonary toxicity and its mechanism is not fully understood. In this study we investigated the pulmonary toxicity of nanoTiO2 and its molecular pathogenesis. The adult male ICR mice were exposed to intratracheal single dose of 0.1 or 0.5 mg nanoTiO2 (19-21 nm) and lung tissues were collected at 3rd day, 1st wk, and 2nd wk for morphometric, microarray gene expression, and pathway analyses. NanoTiO2 can induce pulmonary emphysema, macrophages accumulation, extensive disruption of alveolar septa, type II pneumocyte hyperplasia, and epithelial cell apoptosis. NanoTiO2 induced differential expression of hundreds of genes include activation of pathways involved in cell cycle, apoptosis, chemokines, and complement cascades. In particular, nanoTiO2 up-regulates placenta growth factor (PlGF) and other chemokines (CXCL1, CXCL5, and CCL3) expressions that may cause pulmonary emphysema and alveolar epithelial cell apoptosis. Cultured human THP-1 cell-derived macrophages treated with nanoTiO2 in vitro also resulted in up-regulations of PlGF, CXCL1, CXCL5, and CCL3. These results indicated that nanoTiO2 can induce severe pulmonary emphysema, which may be caused by activation of PlGF and related inflammatory pathways.

We demonstrate a polymer-free method that can routinely transfer relatively large-area graphene to any substrate with advanced electrical properties and superior atomic and chemical structures as compared to the graphene sheets transferred with conventional polymer-assisted methods. The graphene films that are transferred with polymer-free method show high electrical conductance and excellent optical transmittance. Raman spectroscopy and X-ray/ultraviolet photoelectron spectroscopy also confirm the presence of high quality graphene sheets with little contamination after transfer. Atom-resolved images can be obtained using scanning tunneling microscope on as-transferred graphene sheets without additional cleaning process. The mobility of the polymer-free graphene monolayer is as high as 63,000 cm(2) V(-1) s(-1), which is 50% higher than the similar sample transferred with the conventional method. More importantly, this method allows us to place graphene directly on top of devices made of soft materials, such as organic and polymeric thin films, which widens the applications of graphene in soft electronics.

Hepatitis B virus (HBV)-related hepatocellular carcinoma (HCC) occurs more often in men than in women. Male HBV carriers usually have higher viral loads, which is a well-known risk factor for HCC. Whether and how the male androgen axis regulates HBV transcription and replication is investigated here. We used HBV transgenic mice to evaluate any sex disparity of serum hepatitis B surface antigen and HBV titers as well as the castration effect on this disparity. Compared to females, HBV transgenic male mice showed higher hepatitis B surface antigen and viral titers, which were lessened by castration of the males. In a cell culture system, HepG2 cells transfected with HBV and androgen receptor (AR) constructs were used to study the effect of the androgen pathway on viral transcription and replication. H epatitis B virus (HBV) chronically infects more than 350 million people worldwide and is a major risk factor for the development of liver cirrhosis and hepatocellular carcinoma (HCC). 1 The prevalence of chronic HBV infection in children has declined (Ͼ90%) following universal immunization. 2 However, adult HBV carriers still have a significant risk for HCC, especially those in areas where HBV infection is endemic. Investigation of mechanisms of HBV infection for HCC may discover new approaches to reduce the risk.Large cohort studies have identified risk factors for HBVrelated HCC, including old age, higher viral titer, diabetes, familial history of HCC, and the male sex. 3,4 The mechanisms of male susceptibility to HCC after HBV infection have been an important topic for study. Both higher androgen levels and more active androgen receptor (AR) gene alleles correlated with an increased risk of HCC among male hepatitis B surface antigen (HBsAg) carriers. 5,6 In AR knockout mice, the development of chemically induced HCC was delayed and the mice had fewer tumors. 7 These studies indicate that the AR axis is involved in hepatocarcinogenesis, and an active AR pathway may augment HCC risk. Consistent with this, we recently showed that HBV X protein (HBx) can enhance the transcriptional activity of AR in a ligand concentration-dependent manner, which may explain the male predominance of HBV-related HCC. 8 Because of the

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