We have successfully synthesized cluster/shell Fe 3 O 4 /Au nanoparticles using a pH-sensitive polyethyleneimine (PEI) linker. We propose that PEI binds gold seeds, prevents the formation of large aggregates, and changes the spatial structure in an alkaline environment to bundle several Fe 3 O 4 /Au seed nanoparticles together through a bridging flocculation function, thereby producing cluster/shell Fe 3 O 4 /Au nanoparticles. We successfully applied the synthesized cluster/shell Fe 3 O 4 /Au nanoparticles to free-PSA detection via a surface-enhanced Raman scattering (SERS) method, presenting a convenient way for preconcentrating, purifying, and detecting target proteins in complex biosamples. The synthesis strategy demonstrated here can be extended to the fabrication of a wide range of cluster/shell nanocomposites for biomedical applications.

By taking advantage of the anisotropy of AuNRs, we design different bifunctional PEG molecules to selectively bind to either the end or side face and simultaneously protect other faces of individual AuNRs. In this way, we successfully achieve orientation-controllable assemblies of AuNRs into side-by-side (SS), end-to-end (EE) and end-to-side (ES) orientations based on the electrostatic interaction between carboxylic PEG and CTAB capping on AuNRs. Furthermore, we find that the different orientations of assembledmotifs in these three types of AuNRs assemblies exhibited different near field coupling between the surface plasma of the neighboring AuNRs, leading to different surface-enhanced Raman signals. Undoubtedly, the current rational design of oriented assembly can be potentially useful for directing anisotropic nanoparticles into well-defined orientations, which provides a powerful route in designing families of novel nanodevices and nanomaterials with programmable electrical and optical properties.National Natural Science Foundation of China[20725310, 90923042]; Research Fund for the Doctoral Program of Higher Education of China[20100121120038]; Natural Science Foundation of Fujian Province of China[2010J01046]; Fundamental Research Funds for the Central Universities[2010121023]; key laboratory of Biomedical Material of Tianji

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Epidemiological evidence suggests that fine particulate matter (PM 2.5 ) in air pollution promotes the formation of deep venous thrombosis. However, no evidence is available on the effects of PM 2.5 lead to disseminated intravascular coagulation (DIC). For the first time, this study explored the effects of PM 2.5 on DIC via coagulation disorders in vivo . SD rats received intratracheal instillation of PM 2.5 once every three days for one month. Doppler ultrasound showed that the pulmonary valve (PV) and aortic valve (AV) peak flow were decreased after exposure to PM 2.5 . Fibrin deposition and bleeding were observed in lung tissue and vascular endothelial injury was found after exposure to PM 2.5 . Expression of thrombomodulin (TM) in vessel was downregulated after PM 2.5 -treated, whereas the levels of proinflammatory factors and adhesion molecules (IL-6, IL-1β, CRP, ICAM-1 and VCAM-1) were markedly elevated after exposure to PM 2.5 . Tissue factor (TF) and the coagulation factor of FXa were increased, while vWF was significantly lowered induced by PM 2.5 . Thrombin-antithrombin complex (TAT) and fibrinolytic factor (t-PA) were elevated, while there was no significantly change in the expression of anticoagulant factors (TFPI and AT-III). To clarify the relationship between PM 2.5 and DIC, we examined the general diagnostic indices of DIC: PM 2.5 prolonged PT and increased the expression of D-dimer but decreased platelet count and fibrinogen. In addition, the gene levels of JAK1 and STAT3 showed an upward trend, whereas there was little effect on JAK2 expression. And inflammatory factors (IL-6, IL-1β and TNF) in blood vessels of were up-reglated in PM 2.5 -treated rats. In summary, our results found that PM 2.5 could induce inflammatory response, vascular endothelial injury and prothrombotic state, eventually resulted in DIC. It will provide new evidence for a link between PM 2.5 and cardiovascular disease.

There is compelling evidence that exposure to particulate matter (PM) is linked to lung tumorigenesis. However, there is not enough experimental evidence to support the specific mechanisms of PM-induced DNA damage and cell cycle arrest in lung tumorigenesis. In this study, we investigated the toxic effects and molecular mechanisms of PM on bronchial epithelial (BEAS-2B) cells. PM exposure reduced cell viability and enhanced LDH activity. The cell growth curves of BEAS-2B cells decreased gradually with the increase in PM dosage. A significant increase in MDA content and a decrease in GSH-Px activity were observed. The generation of ROS was enhanced obviously, while apoptosis increased in BEAS-2B cells exposed to PM for 24 h. DNA damage was found to be more severe in the exposed groups compared with the control. For in-depth study, we have demonstrated that PM stimulated the activation of HER2/ErbB2 while significantly upregulating the expression of Ras/GADPH, p-BRAF/BRAF, p-MEK/MEK, p-ERK/ERK, and c-Myc/GADPH in a dose-dependent manner. In summary, we suggested that exposure to PM sustained the activation of HER2/ErbB2, which in turn promoted the activation of the Ras/Raf/MAPK pathway and the expression of the downstream target c-Myc. The overexpression of c-Myc may lead to G2/M arrest and aggravate the DNA damage and apoptosis in BEAS-2B after exposure to PM.