Hydrogen-assisted fabrication of spherical gold nanoparticles through sonochemical reduction of tetrachloride gold(III) ions in water

Spherical gold nanoparticles (AuNPs) were selectively synthesized through sonochemical reduction of tetrachloride gold(III) ions ([AuCl4](-)) in an aqueous solution of hydrogen tetrachloroaurate(III) tetrahydrate (HAuCl4.H2O) with the aid of hydrogen (H-2) gas in the absence of any additional capping agents. On the other hand, various shaped-AuNPs such as spherical nanoparticles, triangular and hexagonal plates were formed from sonochemical reduction of [AuCl4](-) in argon (Ar)-, nitrogen (N-2)- or oxygen (O-2)-purged aqueous [AuCl4](-) solutions. The selective fabrication of spherical AuNPs assisted by H-2 gas is most likely attributed to the generation of hydrogen radicals (H center dot) promoted by the reaction of H-2 introduced and hydrogen oxide radicals (center dot OH) produced by sonolysis of water.ArticleULTRASONICS SONOCHEMISTRY. 21(3):946-950 (2014)journal articl

Surfactant- and reducer-free synthesis of gold nanoparticles in aqueous solutions

We report here the surfactant- and reducer-free synthesis of gold nanoparticles from an aqueous hydrogen tetrachloroaurate (III) tetrahydrate (HAuCl(4)center dot 4H(2)O) solution using a high-frequency (950 kHz) ultrasound (in the absence of any stabilizing, capping and reducing agents). In particular, size, shape and stability of gold nanoparticles prepared by the 950 kHz ultrasound irradiation (sonication) for 8 min in the surfactant-free aqueous solutions were examined in terms of AuCl(4)(-) concentration (in the range of 0.01-0.1 mM), additional salts (NaCl, HCl and NaOH) and temperature (in the range of 4-60 degrees C). We found that higher AuCl(4)(-) concentration promoted particle growth (size increase) and plate formation. In addition, the plate formation was enhanced with the addition of NaCl or HCl (but not NaOH). This is most likely due to the AuCl(4)(-) reduction on a certain crystal facets (e.g. (1 1 0) facets) caused by the adsorption of Cl(-) ions on specific crystal facets (e.g. (1 1 1) facets). Furthermore, we revealed that the temperature elevated above 50 degrees C led to the formation of spherical gold nanoparticles with the diameter of 20-60 nm from a 0.1 mM AuCl(4)(-) aqueous solution while triangular plates formed coexisting with spherical nanoparticles below 50 degrees C.ArticleCOLLOIDS AND SURFACES A-PHYSICOCHEMICAL AND ENGINEERING ASPECTS. 347(1-3):18-26 (2009)journal articl

A reduced brain and liver FDG uptake

Purpose : To investigate whether or not the physiological brain and liver FDG uptake are decreased in patients with highly accelerated glycolysis lesions. Methods : We retrospectively analyzed 51 patients with malignant lymphoma. We compared the FDG uptake in the brain and liver of the patients with that in a control group. In 24 patients with a complete response (CR) or partial response (PR) to treatment, we compared the brain and liver uptake before and after treatment. Results : The maximum standardized uptake value (SUVmax) and total glycolytic volume (TGV) of the brain as well as the SUVmax and mean standardized uptake value (SUVmean) of the liver in malignant lymphoma patients were 13.1 ± 2.3, 7386.3 ± 1918.4, 3.2 ± 0.5, and 2.3 ± 0.4, respectively ; in the control group, these values were 14.9 ± 2.4, 8566.2 ± 1659.5, 3.4 ± 0.4, and 2.5 ± 0.3, respectively. The SUVmax and TGV of the brain and the SUVmean of the liver in malignant lymphoma patients were significantly lower than the control group. The SUVmax and TGV of the brain after treatment were significantly higher than before treatment. Both the SUVmax and SUVmean of liver after treatment were higher than before treatment, but not significant. Conclusion : A decreased physiological brain and liver FDG uptake is caused by highly accelerated lesion glycolysis

Artemin, a Novel Member of the GDNF Ligand Family, Supports Peripheral and Central Neurons and Signals through the GFRα3–RET Receptor Complex

AbstractThe glial cell line–derived neurotrophic factor (GDNF) ligands (GDNF, Neurturin [NTN], and Persephin [PSP]) signal through a multicomponent receptor system composed of a high-affinity binding component (GFRα1–GFRα4) and a common signaling component (RET). Here, we report the identification of Artemin, a novel member of the GDNF family, and demonstrate that it is the ligand for the former orphan receptor GFRα3–RET. Artemin is a survival factor for sensory and sympathetic neurons in culture, and its expression pattern suggests that it also influences these neurons in vivo. Artemin can also activate the GFRα1–RET complex and supports the survival of dopaminergic midbrain neurons in culture, indicating that like GDNF (GFRα1–RET) and NTN (GFRα2–RET), Artemin has a preferred receptor (GFRα3–RET) but that alternative receptor interactions also occur

Regulation of cargo-selective endocytosis by dynamin 2 GTPase-activating protein girdin.

In clathrin-mediated endocytosis (CME), specificity and selectivity for cargoes are thought to be tightly regulated by cargo-specific adaptors for distinct cellular functions. Here, we show that the actin-binding protein girdin is a regulator of cargo-selective CME. Girdin interacts with dynamin 2, a GTPase that excises endocytic vesicles from the plasma membrane, and functions as its GTPase-activating protein. Interestingly, girdin depletion leads to the defect in clathrin-coated pit formation in the center of cells. Also, we find that girdin differentially interacts with some cargoes, which competitively prevents girdin from interacting with dynamin 2 and confers the cargo selectivity for CME. Therefore, girdin regulates transferrin and E-cadherin endocytosis in the center of cells and their subsequent polarized intracellular localization, but has no effect on integrin and epidermal growth factor receptor endocytosis that occurs at the cell periphery. Our results reveal that girdin regulates selective CME via a mechanism involving dynamin 2, but not by operating as a cargo-specific adaptor