Jiaqi Tang

Surface plasmon-enhanced electroluminescence in organic light-emitting diodes incorporating Au nanoparticles

Surface plasmon-enhanced electroluminescence (EL) in an organic light-emitting diode is demonstrated by incorporating the synthesized Au nanoparticles (NPs) in the hole injection layer of poly(3,4-ethylene dioxythiophene):polystyrene sulfonic acid. An increase of ∼25% in the EL intensity and efficiency are achieved for devices with Au NPs, whereas the spectral and electrical properties remain almost identical to the control device. Time-resolved photoluminescence spectroscopy reveals that the EL enhancement is ascribed to the increase in spontaneous emission rate due to the plasmonic near-field effect induced by Au NPs.

Mechanism of Cs2CO3 as an n-type dopant in organic electron-transport film

The electronic structures of cesium carbonate (Cs2CO3) doped 4,7-diphenyl-1,10-phenanthroline (BPhen) films with various doping concentration are characterized by in situ ultraviolet and x-ray photoelectron spectroscopies, in an attempt to understand the mechanism of electron-transport enhancement in Cs2CO3-doped organic electron-transport layer for organic optoelectronic devices. The n-type electrical doping effect is evidenced by the Fermi level shift in the Cs2CO3-doped BPhen films toward unoccupied molecular states with increasing doping concentration, leading to increase in electron concentration in the electron-transport layer and reduction in electron injection barrier height. These findings originate from energetically favorable electron transfer from Cs2CO3 to BPhen.

Enhanced performance in polymer photovoltaic cells with chloroform treated indium tin oxide anode modification

Enhanced performance of a poly(3-hexylthiophene):(6,6)-phenyl C61 butyric acid methyl ester bulk heterojunction polymer photovoltaic cell is reported by modifying the indium tin oxide (ITO) anode with chloroform solution. Instead of the traditional UV-ozone treatment, the optimized chloroform modification on ITO anode can result in an enhancement in the power conversion efficiency of an identical device, originating from an increase in the photocurrent with negligible change in the open-circuit voltage. The performance enhancement is attributed to the work function modification of the ITO substrate through the surface incorporation of the chlorine, and thus improved charge collection efficiency.

Thermal annealing-induced vertical phase separation of copper phthalocyanine: Fullerene bulk heterojunction in organic photovoltaic cells

The effect of thermal annealing treatment on the morphology change in bulk heterojunction (BHJ) in organic photovoltaic cells was studied by photoemission spectroscopy. The results reveal that vertical phase separation upon annealing occurs in typical BHJ layer formed between planar molecule CuPc and spherical C60 with inhomogeneous concentration distribution in profile, varying from CuPc-rich near the air surface to C60-rich adjacent to the substrate interface. The morphology variation is associated with the difference in surface energy of CuPc and C60, leading to the accumulation of CuPc to the interface with air to lower the overall energy of the free surface.

Chronic hypoxia in pregnancy affected vascular tone of renal interlobar arteries in the offspring

Hypoxia during pregnancy could affect development of fetuses as well as cardiovascular systems in the offspring. This study was the first to demonstrate the influence and related mechanisms of prenatal hypoxia (PH) on renal interlobar arteries (RIA) in the 5-month-old male rat offspring. Following chronic hypoxia during pregnancy, phenylephrine induced significantly higher pressor responses and greater vasoconstrictions in the offspring. Nitric oxide mediated vessel relaxation was altered in the RIA. Phenylephrine-stimulated free intracellular calcium was significantly higher in the RIA of the PH group. The activity and expression of L-type calcium channel (Cav1.2), not T-type calcium channel (Cav3.2), was up-regulated. The whole-cell currents of calcium channels and the currents of Cav1.2 were increased compared with the control. In addition, the whole-cell K+ currents were decreased in the offspring exposed to prenatal hypoxia. Activity of large-conductance Ca2+-activated K+ channels and the expression of MaxiKα was decreased in the PH group. The results provide new information regarding the influence of prenatal hypoxia on the development of the renal vascular system, and possible underlying cellular and ion channel mechanisms involved.

Epigenetic code and potential epigenetic-based therapies against chronic diseases in developmental origins.

Accumulated findings have demonstrated that the epigenetic code provides a potential link between prenatal stress and changes in gene expression that could be involved in the developmental programming of various chronic diseases in later life. Meanwhile, based on the fact that epigenetic modifications are reversible and can be manipulated, this provides a unique chance to develop multiple novel epigenetic-based therapeutic strategies against many chronic diseases in early developmental periods. This article will give a short review of recent findings of prenatal insult-induced epigenetic changes in developmental origins of several chronic diseases, and will attempt to provide an overview of the current epigenetic-based strategies applied in the early prevention, diagnosis and possible therapies for human chronic diseases.

Exposure to Nicotine During Pregnancy and Altered Learning and Memory in the Rat Offspring

INTRODUCTION Prenatal exposure to nicotine can cause many fetal developmental problems. This study determined the influence of nicotine during pregnancy on the development of cognitive behavior in the offspring. METHODS Nicotine was administered to pregnant rats through implanted osmotic mini-pumps at 6mg/kg/day and flow rate of 60 μl/day for whole pregnancy from gestational day 4. Fetal and offspring body and brain weight was measured. Learning and memory were tested in adult offspring with Morris water maze; Learning and memory-related receptors were measured. RESULTS The results showed that exposure to prenatal nicotine (PN) not only caused fetal growth restriction, but also had long-term effects on learning and memory in the offspring. The PN offspring exhibited longer escape latency regardless of sex. The number of passing the platform was significantly less in the PN offspring than that of the control. The expression of messenger RNA (mRNA) and protein of N-methyl-D-aspartic acid receptor (NMDAR) in the hippocampus was significantly increased, whereas alpha7 nicotinic acetylcholine receptor (α7 nAChR) protein was decreased with unchanged α7 nAChR mRNA in the PN offspring. CONCLUSION The data provided novel information on the PN-affected development in learning and memory in the offspring, suggesting that α7 nAChR and NMDAR1 in the hippocampus might be the targets for actions of PN in association with memory impairment.

Maternal high‐salt diet altered PKC/MLC20 pathway and increased ANG II receptor‐mediated vasoconstriction in adult male rat offspring

SCOPE High-salt diet (HSD) is associated with cardiovascular diseases. This study aims at ascertaining the influence of maternal HSD on offsprings angiotensin II (ANG II)-mediated vasoconstriction and the underlying mechanisms. METHODS AND RESULTS In comparison to a normal-salt diet, HSD used in pregnancy in rats changed the ultrastructures of the coronary artery (CA) in 5-month-old male offspring, and increased ANG II-mediated CA contractility. Measurement of [Ca(2+) ]i in CA using fluorescent fura-2, a Ca(2+) indicator, showed that ANG II-mediated increases in [Ca(2+) ]i were the same between HSD and normal-salt diet groups, but the ratio of diameter change/[Ca(2+) ]i induced by ANG II were significantly higher in HSD groups. Angiotensin II receptor type 1, not angiotensin II receptor type 2, caused ANG II-mediated vasoconstriction. Protein kinase C (PKC) inhibitor GF109203X attenuated the ANG II-mediated vasoconstriction, PKC agonist phorbol12,13-dibutyrate produced a greater contraction. There was an increase in PKCβ mRNA and the corresponding protein abundance in the offspring, whereas other PKC subunits PKCα, PKCδ, and PKCε did not change. Moreover, 20 kDa myosin light chain phosphorylation levels were increased in HSD group. CONCLUSION Maternal HSD affected the developmental programing for the offspring CA, with increased ANG II-mediated vasoconstrictions. The angiotensin II receptor type 1-PKC-20 kDa myosin light chain phosphorylation pathway was the possible mediated cellular mechanism.

Chronic fetal exposure to caffeine altered resistance vessel functions via RyRs-BKCa down-regulation in rat offspring

Caffeine modifies vascular/cardiac contractility. Embryonic exposure to caffeine altered cardiac functions in offspring. This study determined chronic influence of prenatal caffeine on vessel functions in offspring. Pregnant Sprague-Dawley rats (5-month-old) were exposed to high dose of caffeine, their offspring (5-month-old) were tested for vascular functions in mesenteric arteries (MA) and ion channel activities in smooth muscle cells. Prenatal exposure to caffeine increased pressor responses and vasoconstrictions to phenylephrine, accompanied by enhanced membrane depolarization. Large conductance Ca2+-activated K+ (BKCa) channels in buffering phenylephrine-induced vasoconstrictions was decreased, whole cell BKCa currents and spontaneous transient outward currents (STOCs) were decreased. Single channel recordings revealed reduced voltage/Ca2+ sensitivity of BKCa channels. BKCa α-subunit expression was unchanged, BKCa β1-subunit and sensitivity of BKCa to tamoxifen were reduced in the caffeine offspring as altered biophysical properties of BKCa in the MA. Simultaneous [Ca2+]i fluorescence and vasoconstriction testing showed reduced Ca2+, leading to diminished BKCa activation via ryanodine receptor Ca2+ release channels (RyRs), causing enhanced vascular tone. Reduced RyR1 was greater than that of RyR3. The results suggest that the altered STOCs activity in the caffeine offspring could attribute to down-regulation of RyRs-BKCa, providing new information for further understanding increased risks of hypertension in developmental origins.

A novel mechanism of angiotensin II-regulated placental vascular tone in the development of hypertension in preeclampsia

The present study tested the hypothesis that angiotensin II plays a role in the regulation of placental vascular tone, which contributes to hypertension in preeclampsia. Functional and molecular assays were performed in large and micro placental and non-placental vessels from humans and animals. In human placental vessels, angiotensin II induced vasoconstrictions in 78.7% vessels in 155 tests, as referenced to KCl-induced contractions. In contrast, phenylephrine only produced contractions in 3.0% of 133 tests. In non-placental vessels, phenylephrine induced contractions in 76.0% of 67 tests, whereas angiotensin II failed to produce contractions in 75 tests. Similar results were obtained in animal placental and non-placental vessels. Compared with non-placental vessels, angiotensin II receptors and β -adrenoceptors were significantly increased in placental vessels. Compared to the vessels from normal pregnancy, angiotensin II-induced vasoconstrictions were significantly reduced in preeclamptic placentas, which was associated with a decrease in angiotensin II receptors. In addition, angiotensin II and angiotensin converting enzyme in the maternal-placenta circulation in preeclampsia were increased, whereas angiotensin I and angiotensin1-7 concentrations were unchanged. The study demonstrates a selective effect of angiotensin II in maintaining placental vessel tension, which may play an important role in development of hypertension in preeclampsia.