Enhanced fluorescence from CdTe quantum dots self-assembled on the surface of silver nanoparticles.

This paper presents an investigation on the fluorescent properties of semiconductor CdTe quantum dots (QDs) self-assembled on the surface of PVP (polyvinylpyrrolidone)-capped silver nanoparticles (NPs) by the ligand field effect. A significant 2.5-fold enhancement in the integrated fluorescence intensities, red shift of fluorescence peak, and obvious decrease of lifetime were observed in the CdTe QDs assembled on the Ag NPs in comparison with the pure CdTe QDs. The fluorescence enhancement factor and red shift were found to depend on the Ag NP concentration. The fluorescence enhancement was attributed to a highly localized electromagnetic field on the Ag NPs generated by the surface plasma and the change in the surface trap state of the CdTe QDs originating from plasma oscillations in the Ag NPs. It is first proposed that the surface passivation of CdTe QDs is also an important factor for metal-enhanced fluorescence. The surface defects of CdTe QDs can be modified by the Cd-O coordination interaction between the CdTe QDs and PVP molecules, which will cause the trap state density and luminescence lifetime to decrease. The surface passivation of CdTe QDs can also improve fluorescence quantum yield and lead to the red shift of the fluorescence peak. Compared with previous reports, the occurrence of the self-assembly of CdTe QDs on the surface of PVP-capped Ag NPs is fairly simple and easy. From a practical point of view, the combination of CdTe QDs with Ag NPs may lead to the fluorescence enhancement, which could be utilized in a variety of chemical and biological detection applications.

Blockade of interleukin 6 accelerates acinar cell apoptosis and attenuates experimental acute pancreatitis in vivo.

BACKGROUND: It remains unclear whether interleukin (IL) 6 plays a role in initiating either the inflammatory or antiapoptotic responses in severe acute pancreatitis. This study examined the effect of neutralizing antibody against IL-6 on the induction of pancreatic acinar cell apoptosis and attenuation of the severity of severe acute pancreatitis. METHODS: Experiments were conducted on laboratory mice with severe acute pancreatitis induced by lipopolysaccharide injection following six injections of caerulein at intervals of 6 h. Neutralizing monoclonal anti-IL-6 antibody was administered either 5 min or 2 h after the first caerulein injection. Apoptosis in pancreatic sections was determined by the terminal deoxynucleotidyltransferase-mediated dUTP-biotin nick-end labelling method. RESULTS: Administration of caerulein and LPS induced an increase in serum amylase and IL-6 levels, severe acute pancreatitis, pancreatitis-associated lung injury, and phosphorylation of signal transducer and activator of transcription (STAT) 3 in the pancreas. A neutralizing antibody against IL-6 effectively suppressed these responses. Application of IL-6 neutralizing antibody caused the induction of apoptosis in the pancreatic acinar cells of mice with acute pancreatitis. CONCLUSION: Blocking IL-6 suppresses STAT-3 activation in the pancreas and consequently attenuates the severity of severe acute pancreatitis by promotion of pancreatic acinar cell apoptosis.

Suppression of potassium currents by cyanide on the mouse motor nerve terminals.

NaCN at low concentrations markedly depressed the potassium currents in the motor nerve terminal of mouse triangularis sterni neuromuscular junction pretreated with potassium channel blockers 4-aminopyridine (4-AP), tetraethylammonium (TEA) or glucose-free medium. Neither azide nor dinitrophenol nor ouabain mimicked the effect of cyanide. This inhibitory effect of cyanide on nerve terminal spikes was correlated to its dramatic increase in spontaneous transmitter release under glucose-free condition. These results suggest that the effect of cyanide on the electrogenesis of nerve terminals is due to the direct suppression of ATP-sensitive K+ current since the effect was antagonized by ATP-sensitive K+ channels opener diazoxide and this may modulate the transmitter release.

Enhancement of a slow potassium current component by uranyl nitrate and its relation to the antagonism on beta-bungarotoxin in the mouse motor nerve terminal.

Uranyl nitrate (UO2(NO3)2) has been shown to be capable of increasing transmitter release from the motor nerve accompanied by the potentiation of nerve evoked muscle contraction. In this paper, we have demonstrated that UO2(2+) induced an initial twitch depression followed by a later twitch potentiation in low (0.35 mM) Ca2+ medium. Although UO2(2+) has been identified as a K(+)-channel blocker, we have found it only partially blocked the fast K(+)-current (IK(f) as recorded in the perineurial sheath of the mouse triangularis sterni preparation. Increasing the concentration of UO2(2+) to a high concentration of 0.4 mM did not further inhibit IK(f) but markedly prolonged the duration of the outward current of the nerve terminals. From the time course of its appearance together with the specific inhibition by 4-aminopyridine, dendrotoxin and beta-bungarotoxin, which has been shown to be capable of blocking the K(+)-current of the motor nerve terminal, it was proposed that UO2(2+) prolonged the duration of the nerve terminal spikes by an enhancement of an IK(s)-like current, which was further characterized by its susceptibility to be enhanced by low K+, low Ca2+ and Cd2+ but attenuated by high K+ and high Ca2+. These cation effects not only supported UO2(2+)-induced IK(s) current but also excluded the possibility of an enhancement of Ca(2+)-activated K(+)-current induced by UO2(2+) plus TEA. The significance of this enhancement of IK(s) induced by UO2(2+) has been elucidated by the finding that dendrotoxin inhibited but tetraethylammonium potentiated not only UO2(2+)-induced IK(s) but also UO2(2+)-induced twitch depression.(ABSTRACT TRUNCATED AT 250 WORDS)