Gold nanoparticles have potential applications in biomedicine, but one of the important concerns is about their safety. Most toxicology data are derived from in vitro studies and may not reflect in vivo responses. Here, an animal toxicity study of 13.5 nm gold nanoparticles in mice is presented. Animal survival, weight, hematology, morphology, and organ index are characterized at different concentrations (137.5-2200 µg/kg) over 14-28 days. The results show that low concentrations of gold nanoparticles do not cause an obvious decrease in body weight or appreciable toxicity, even after their breakdown in vivo. High concentrations of gold nanoparticles induced decreases in body weight, red blood cells, and hematocrit. It was also found that gold nanoparticles administered orally caused significant decreases in body weight, spleen index, and red blood cells. Of the three administration routes, the oral and intraperitoneal routes showed the highest toxicity, and the tail vein injection showed the lowest toxicity. Combining the results of all of these studies, we suggest that targeted gold nanopartices by tail vein injection may be suitable for enhancement of radiotherapy, photothermal therapy, and related medical diagnostic procedures.

The four α-cobalt hydroxides (green or blue) with different intercalated anions were synthesized by a chemical precipitation route in which polyethylene glycol was used as the structure-directing reagent for application in the electrode materials of electrochemical capacitors. Every one among the four samples displays an interesting and distinctive morphology although the synthesis conditions were the same except for the anions. The intercalated anions have a critical effect on the basal plane spacing, morphologies, and capacitive properties of the products. Structural and morphological characterizations were performed by using power X-ray diffraction (XRD) and field emission scanning electron microscopy (FESEM). The component and thermal stability of the sample were respectively measured by FT-IR and thermal analyses, including thermogravimetry (TG) and differential thermogravimetry (DTG). The electrochemical behaviors were measured by cyclic voltammogram and galvanostatic charge−discharge. The specific capacitance is up to 697 F g−1 at a charge−discharge current density of 1 A g−1 for the sample with intercalated chlorine. But the sample with intercalated sulfate, which has small crystalline size, more disordered structure, and almost perfect alveolate nanostructure with a large surface area, exhibits relatively poor specific capacitance (420 F g−1). The exceptive phenomena caused by intercalated anions were explained by hydrogen bonding and electrostatic forces. Moreover, the relationships between the specific capacitance, basal plane spacing, as well as the content of the interlayer water were discussed in detail for the four as-synthesized samples.

ZnO/reduced graphite oxide composites were synthesized using a two-step method in which KOH reacts with Zn(NO3)2 in the aqueous dispersions of graphite oxide (GO) to form a Zn(OH)2/graphite oxide precursor, followed by thermal treatment in air. It was found that the dispersion of reduced graphene oxide (rGO) sheets within composites was key for achieving an excellent capacitive performance of the samples. However, the mass ratio of ZnO to rGO determined whether rGO sheets within composites were dispersed or agglomerated. The composite achieved homogeneous incorporation of rGO sheets within the ZnO matrix when the mass ratio of ZnO to rGO was equal to 93.3:6.7. This composite, in which the weight percent of rGO was only 6.7%, appeared in the SEM images to be almost entirely filled with rGO sheets coated by ZnO and exhibited high specific capacitance and excellent cycling ability. Furthermore, the sheets overlapped to form a three-dimensional network structure, through which electrolyte ions easily access the surface of the rGO or electrochemical active sites. The homogeneously incorporated rGO sheets were shown to provide 128% enhancement in specific capacitance compared with 135 F g−1 for pure zinc oxide samples. Also, the unexpected phenomena involved in the experimental processes are discussed in detail.

AIDS (acquired immune deficient syndrome) is a deadly human viral infectious disease caused by HIV (human immune-deficient virus) infection. Almost every AIDS patient losses his/her life before mid 1990s. AIDS was once the 1st disease killer in US (1993). After one decade hard work, antiviral drug cocktails-high active anti-retroviral therapy (HAART) have been invented for almost all HIV infection treatments. Due to the invention of HAART, 80-90% HIV/AIDS patients still effectively response to HAART for deadly AIDS episode controls and life saving. Yet, this type of HIV therapeutics is incurable. HIV/AIDS patients need to take HAART medications regularly and even life-long. To counteract this therapeutic drawback, more revolutionary efforts (different angles of therapeutic modes/attempts) are urgently needed. In this article, the major progresses and drawbacks of HIV/AIDS chemotherapy (HAART) to HIV/AIDS patients have been discussed. Future trends (updating pathogenesis study, next generations of drug developments, new drug target discovery, different scientific disciplinary and so on) are highlighted.

Our recent studies showed that total body irradiation (TBI) induces long-term bone marrow (BM) suppression in part by induction of hematopoietic stem cell (HSC) senescence through NADPH oxidase 4 (NOX4)-derived reactive oxygen species (ROS). Therefore, in the present study we examined if resveratrol (3,5,4’-trihydroxy-trans-stilbene), a potent antioxidant and a putative activator of Sirtuin 1 (Sirt1), can ameliorate TBI-induced long-term BM injury by inhibiting radiation-induced chronic oxidative stress and senescence in HSCs. Our results showed that pretreatment with resveratrol not only protected mice from TBI-induced acute BM syndrome and lethality but also ameliorated TBI-induced long-term BM injury. This later effect is likely attributed to resveratrol-mediated reduction of chronic oxidative stress in HSCs, because resveratrol treatment significantly inhibited TBI-induced increase in ROS production in HSCs and prevented mouse BM HSCs from TBI-induced senescence, leading to a significant improvement of HSC clonogenic function and long-term engraftment after transplantation. The inhibition of TBI-induced ROS production in HSCs is likely attributable to resveratrol-mediated down-regulation of NOX4 expression and up-regulation of Sirt1, superoxide dismutase 2 (SOD2), and glutathione peroxidase 1 (GPX1) expression. Furthermore, we showed that resveratrol increased Sirt1 deacetylase activity in BM hematopoietic cells; and Ex527, a potent Sirt1 inhibitor, can attenuate resveratrol-induced SOD2 expression and the radioprotective effect of resveratrol on HSCs. These findings demonstrate that resveratrol can protect HSCs from radiation at least in part via activation of Sirt1. Therefore, resveratrol has the potential to be used as an effective therapeutic agent to ameliorate TBI-induced long-term BM injury.