Highly stable and luminescent InP/GaP/ZnS QDs with a maximum quantum yield of 85% were synthesized by in situ method. The GaP shell rendered passivation of the surface and removed the traps. TCSPC data showed an evidence for the GaP shell. InP/GaP/ZnS QDs show better stability than InP/ZnS. We studied the optical properties of white QD-LEDs corresponding to various QD concentrations. Among various concentrations, the white QD-LEDs with 0.5 mL of QDs exhibited a luminous efficiency of 54.71 lm/W, Ra of 80.56, and CCT of 7864 K.

Targeting cancer: Multifunctional magnetic gold nanoshells (Mag‐GNS) are prepared by coating silica spheres with gold nanoshells embedded with Fe3O4 nanoparticles. The Fe3O4 nanoparticles allow magnetic resonance imaging (MRI) for diagnosis, and the gold nanoshells enable photothermal therapy. By attaching an antibody to the Mag‐GNS by a poly(ethylene glycol) (PEG) linker, cancer cells can be targeted.

Krebs im Visier: Multifunktionelle magnetische Gold‐Nanoschalen (Mag‐GNS) entstehen beim Beschichten von Siliciumoxid‐Kugeln mit Gold‐Nanoschalen, in die Fe3O4‐Nanopartikel eingelagert sind. Die Fe3O4‐Nanopartikel ermöglichen eine kernspintomographische Diagnose (MRI) und die Gold‐Nanoschalen eine photothermische Therapie. Nach Anbinden eines Antikörpers an die Mag‐GNS über einen Polyethylenglycol(PEG)‐Linker lassen sich Krebszellen gezielt ansteuern.

No abstract

The accumulation of uric acid, an end-product of purine metabolism, is responsible for the many deleterious effects observed in gouty arthritis, including renal injury. Here, we present evidence that under conditions of hyperuricemia (>10(-4) M uric acid) [(3)H]thymidine incorporation into primary renal proximal tubule cells (PTCs) is inhibited, and we delineate the signaling pathways involved. Elevated uric acid was observed to stimulate MAPK phosphorylation. The uric acid induced p38 MAPK phosphorylation was also blocked by H-7 (a PKC inhibitor), indicating that p38 MAPK was a downstream target of PKC. Evidence that cytoplasmic phospholipase A(2) (cPLA(2)) was involved further downstream included 1) the stimulatory effect of uric acid on [(3)H]-labeled arachidonic acid (AA) release; 2) the stimulation of AA release in response to uric acid was blocked by the PKC inhibitor H-7 as well as by the p38 MAPK inhibitor SB 203580; and 3) the uric acid-induced inhibition of [(3)H]thymidine incorporation was prevented by SB 203580, as well as by the cPLA(2) inhibitor arachidonyl trifluoromethyl ketone, and mepacrine (another PLA(2) inhibitor). Evidence of a uric acid-induced activation of NF-kappaB as well as PLA(2) was obtained. Moreover the uric acid-induced inhibition of [(3)H]thymidine incorporation was also blocked by two NF-kappaB inhibitors, pyrrolidine dithiocarbamate and SN 50. However, SN 50 did not block the uric acid induced [(3)H]AA release. Thus the inhibition of [(3)H]thymidine incorporation caused by uric acid can be explained by two distinct mechanisms, the activation of NF-kappaB as well as the activation of PLA(2).

These results concur largely with the characteristic features of IBS, visceral hypersensitivity and altered defecation pattern in the absence of detectable disease, suggesting that this animal model is a methodologically convenient and useful model for studying a subset of IBS.

Analysis of the full genome of an environmentally unique, halotolerant Streptomyces sp. strain GSL-6C, isolated from the Great Salt Lake, revealed a gene cluster encoding the biosynthesis of the salinipeptins, d-amino-acid-containing members of the rare linaridin subfamily of ribosomally synthesized and post-translationally modified peptides (RiPPs). The sequence organization of the unmodified amino acid residues in salinipeptins A–D (1–4) were suggested by genome annotation, and subsequently, their sequence and post-translational modifications were defined using a range of spectroscopic techniques and chemical derivatization approaches. The salinipeptins are unprecedented linaridins bearing nine d-amino acids, which are uncommon in RiPP natural products and are the first reported in the linaridin subfamily. Whole genome mining of GSL-6C did not reveal any homologues of the reported genes responsible for amino acid epimerization in RiPPs, inferring new epimerases may be involved in the conversion of l- to d-amino acids. In addition, the N-oxide and dimethylimidazolidin-4-one moieties in salinipeptins B and C, which are modified from N,N-dimethylalanine, are unknown in bacterial peptides. The three-dimensional structure of salinipeptin A, possessing four loops generated by significant hydrogen bonding, was established on the basis of observed nuclear Overhauser effect (NOE) correlations. This study demonstrates that integration of genomic information early in chemical analysis significantly facilitates the discovery and structure characterization of novel microbial secondary metabolites.

ABSTRACT. In two previous reports, we have demonstrated that injection of bee venom (BV) into an acupoint produces a significant antinociceptive and anti-inflammatory effect in both a mouse model of visceral nociception and a rat model of chronic arthritis. Th e present study was designed to evaluate the potential antinociceptive effect of BV pretreatment on formalin-induced pain behavior and it associated spinal cord Fos expression in rats. Adult Sprague-Dawley rats were injected with BV directly into the Zusanli (ST36) acupoint or into an arbitrary non-acupoint located on the back. BV pretreatment into the Zusanli acupoint significantly decreased paw-licking time in the late phase of the formalin test. In contrast, BV injected into a non-acupoint in the back region did not suppress the paw-licking time. In addition, BV pretreatment into the Zusanli acupoint markedly inhibited spinal cord Fos expression induced by formalin injection. These findings indicate that BV pretreatment into the Zusanli acupoint has an antinociceptive effect on formalin-induced pain behavior. Bee venom (BV) from the honeybee consists of melittin, phospholipase A 2 , apamin, adolapin, mast cell degranulating peptide and several other bioactive substances [26]. Melittin and phospholipase A 2 , two major components of BV, are generally thought to play an important role in the induction of the irritation and allergic reaction associated with the bee stings. In this regard, intradermal injection of melittin produces a local hyperthermic effect in human [23]. Phospholipase A 2 is a membrane-associated phospholipid converting enzyme that is important in the production of arachidonic acid. Arachidonic acid is further metabolized by one of two enzyme pathways into various prostaglandins (by cyclooxygenase) or leukotrienes (by lipooxygenase). Subcutaneous BV injection into plantar surface of the rat paw produces characteristic pain behaviors including paw licking and flinching [26] while BV administration in cats has been shown to produce prolonged and tonic nociceptive responses associated with changes in the firing of spinal cord neurons [7]. Chen and his colleagues have since published several reports that have elucidated some of the mechanisms underlying BV-induced nociception in rats and cats [7-13, 27, 28, 34, 35].In contrast to this recent focus on BV's nociceptive effects, Kwon and his co-workers have reported that longterm treatment with BV at a dose of 1 mg/kg/day produces a significant antinociceptive and anti-inflammatory effect on the Freund's complete adjuvant-induced arthritis in rats [24]. Although natural BV produces irritation when injected subcutaneously, injection of diluted BV, particularly into an acupoint, can reduce chronic nociception and inflammation. Thus Kwon et al. have shown that BV treatment into an acupoint can significantly reduce arthritisassociated edema and nociceptive responses [24]. In addition, BV injection into the Zhongwan acupoint significantly reduces the number of abdominal stretches induced by intraper...