Synthesis of N-doped graphene quantum dots by pulsed laser ablation with diethylenetriamine (DETA) and their photoluminescence.

We report a facile, fast, and one-step approach to prepare N-doped graphene quantum dots (GQDs) using pulsed laser ablation with diethylenetriamine (DETA). The synthesized N-doped GQDs with an average size of about 3.4 nm and an N/C atomic ratio of 26% have been demonstrated. Compared to pristine GQDs, the N-doped GQDs emit enhanced photoluminescence (PL) with a factor as high as 66, originated from the enhanced densities of pyridinic and graphitic N. The temperature-dependent PL of the N-doped GQDs was studied from cryogenic to room temperature. An anomalous temperature dependence of PL intensity was observed for the N-doped GQDs, which was ascribed to a carrier transfer mechanism from a dopant-induced state to the quantum-dot emitting state.

Eco-friendly luminescent solar concentrators with low reabsorption losses and resistance to concentration quenching based on aqueous-solution-processed thiolate-gold nanoclusters.

Heavy-metal-containing quantum dots (QDs) with engineered electronic states have been served as luminophores in luminescent solar concentrators (LSCs) with impressive optical efficiency. Unfortunately, those QDs involve toxic elements and need to be synthesized in a hazardous solvent. Recently, biocompatible, eco-friendly gold nanoclusters (AuNCs), which can be directly synthesized in an aqueous solution, have gained much attention for promising applications in 'green photonics'. Here, we explored the solid-state photophysical properties of aqueous-solution-processed, glutathione-stabilized gold nanoclusters (GSH-AuNCs) with a ligand-to-metal charge-transfer (LMCT) state for developing 'green' LSCs. We found that such GSH-AuNCs exhibit a large Stokes shift with almost no spectral overlap between the optical absorption and PL emission due to the LMCT states, thus, suppressing reabsorption losses. Compared with GSH-AuNCs in solution, the photoluminescence quantum yields (PL-QYs) of the LSCs can be enhanced, accompanied with a lengthened PL lifetime owing to the suppression of non-radiative recombination rates. In addition, the LSCs do not suffer from severe concentration-induced PL quenching, which is a common weakness for conventional luminophores. As a result, a common trade-off between light-harvesting efficiency and solid-state PL-QYs can be bypassed due to nearly-zero spectral overlap integral between the optical absorption and PL emission. We expect that GSH-AuNCs hold great promise for serving as luminophores for 'green' LSCs by further enhancing solid-state PL-QYs.

Origin of tunable photoluminescence from graphene quantum dots synthesized via pulsed laser ablation.

A one-step synthesis of graphene quantum dots (GQDs) has been implemented using pulsed laser ablation (PLA) with carboxyl-functionalized multiwalled carbon nanotubes (MWCNTs). The synthesized GQDs with an average size smaller than 3 nm were obtained by the fragmentation of MWCNTs via oxidative cutting. The GQDs can generate tunable photoluminescence (PL) ranging from green to blue by controlling the PLA time. The PL spectrum (decay time) of the green GQDs remains unchanged under different excitation energies (emission energies), while that of the blue GQDs correlates with the excitation energy (emission energy). On the basis of the pH and temperature dependence of PL, we suggest that the localized intrinsic states associated with the sp(2) nanodomains and delocalized extrinsic states embedded on the GQD surface are responsible for blue and green emission in GQDs, respectively.

Solid-state, ambient-operation thermally activated delayed fluorescence from flexible, non-toxic gold-nanocluster thin films: towards the development of biocompatible light-emitting devices.

Luminescent gold nanoclusters (AuNCs) with good biocompatibility have gained much attention in bio-photonics. In addition, they also exhibit a unique photo-physical property, namely thermally activated delayed fluorescence (TADF), by which both singlet and triplet excitons can be harvested. The combination of their non-toxic material property and unique TADF behavior makes AuNCs biocompatible nano-emitters for bio-related light-emitting devices. Unfortunately, the TADF emission is quenched when colloidal AuNCs are transferred to solid states under ambient environment. Here, a facile, low-cost and effective method was used to generate efficient and stable TADF emissions from solid AuNCs under ambient environment using polyvinyl alcohol as a solid matrix. To unravel the underlying mechanism, temperature-dependent static and transient photoluminescence measurements were performed and we found that two factors are crucial for solid TADF emission: small energy splitting between singlet and triplet states and the stabilization of the triplet states. Solid TADF films were also deposited on the flexible plastic substrate with patterned structures, thus mitigating the waveguide-mode losses. In addition, we also demonstrated that warm white light can be generated based on a co-doped single emissive layer, consisting of non-toxic, solution-processed TADF AuNCs and fluorescent carbon dots under UV excitation.

Photo-induced Doping in GaN Epilayers with Graphene Quantum Dots.

We demonstrate a new doping scheme where photo-induced carriers from graphene quantum dots (GQDs) can be injected into GaN and greatly enhance photoluminescence (PL) in GaN epilayers. An 8.3-fold enhancement of PL in GaN is observed after the doping. On the basis of time-resolved PL studies, the PL enhancement is attributed to the carrier transfer from GQDs to GaN. Such a carrier transfer process is caused by the work function difference between GQDs and GaN, which is verified by Kelvin probe measurements. We have also observed that photocurrent in GaN can be enhanced by 23-fold due to photo-induced doping with GQDs. The improved optical and transport properties from photo-induced doping are promising for applications in GaN-based optoelectronic devices.

A Facile and Low-Cost Method to Enhance the Internal Quantum Yield and External Light-Extraction Efficiency for Flexible Light-Emitting Carbon-Dot Films.

Solution-processed, non-toxic carbon dots (CDs) have attracted much attention due to their unique photoluminescence (PL) properties. They are promising emissive layers for flexible light-emitting devices. To this end, the CDs in pristine aqueous solutions need to be transferred to form solid-state thin films without sacrificing their original PL characteristics. Unfortunately, solid-state PL quenching induced by extra non-radiative (NR) energy transfer among CDs would significantly hinder their practical applications in optoelectronics. Here, a facile, low-cost and effective method has been utilized to fabricate high-performance CD/polymer light-emitting flexible films with submicron-structured patterns. The patterned polymers can serve as a solid matrix to disperse and passivate CDs, thus achieving high internal quantum yields of 61%. In addition, they can act as an out-coupler to mitigate the waveguide-mode losses, approximately doubling the external light-extraction efficiency. Such CD/polymer composites also exhibit good photo-stability, and thus can be used as eco-friendly, low-cost phosphors for solid-state lighting.

Laser-ablation production of graphene oxide nanostructures: from ribbons to quantum dots.

A new one-step method for the preparation of graphene oxide (GO) nanostructures has been developed by pulsed laser ablation in GO solution. The formation of different shapes of GO nanostructures, such as ribbons, nanoflakes (including nano-squares, nano-rectangles, nano-triangles, nano-hexagons, and nano-disks) and quantum dots, has been demonstrated by scanning electron microscopy and transmission electron microscopy. Photoreduction for the GO occurred during irradiation by the pulsed laser. The GO quantum dots exhibit a blue photoluminescence, originating from recombination of the localized carriers in the zigzag-edge states.

Probing the photoluminescence properties of gold nanoclusters by fluorescence lifetime correlation spectroscopy.

Gold nanoclusters (Au NCs) have attracted much attention for promising applications in biological imaging owing to their tiny sizes and biocompatibility. So far, most efforts have been focused on the strategies for fabricating high-quality Au NCs and then characterized by conventional ensemble measurement. Here, a fusion single-molecule technique combining fluorescence correlation spectroscopy and time-correlated single-photon counting can be successfully applied to probe the photoluminescence (PL) properties for sparse Au NCs. In this case, the triplet-state dynamics and diffusion process can be observed simultaneously and the relevant time constants can be derived. This work provides a complementary insight into the PL mechanism at the molecular levels for Au NCs in solution.

Distance dependence of energy transfer from InGaN quantum wells to graphene oxide.

We report the distance-dependent energy transfer from an InGaN quantum well to graphene oxide (GO) by time-resolved photoluminescence (PL). A pronounced shortening of the PL decay time in the InGaN quantum well was observed when interacting with GO. The nature of the energy-transfer process has been analyzed, and we find the energy-transfer efficiency depends on the 1/d² separation distance, which is dominated by the layer-to-layer dipole coupling.

Efficient energy transfer from InGaN quantum wells to Ag nanoparticles.

Nonradiative energy transfer from an InGaN quantum well to Ag nanoparticles is unambiguously demonstrated by the time-resolved photoluminescence. The distance dependence of the energy transfer rate is found to be proportional to 1/d(3), in good agreement with the prediction of the dipole interaction calculated from the Joule losses in acceptors. The maximum energy-transfer efficiency of this energy transfer system can be as high as 83%.

Energy transfer from InGaN quantum wells to Au nanoclusters via optical waveguiding.

We present the first observation of resonance energy transfer from InGaN quantum wells to Au nanoclusters via optical waveguiding. Steady-state and time-resolved photoluminescence measurements provide conclusive evidence of resonance energy transfer and obtain an optimum transfer efficiency of ~72%. A set of rate equations is successfully used to model the kinetics of resonance energy transfer.

Clinical manifestation of esophageal carcinosarcoma: a Taiwan experience.

Carcinosarcoma of the esophagus is a rare neoplasm with both carcinomatous and sarcomatous components. This study aimed to investigate its clinicopathologic features and endoscopic characteristics. The data of patients diagnosed to have esophageal carcinosarcoma pathologically in the past 30 years (January 1976-December 2007) were reviewed. Of 3318 cases of esophageal malignancy, 12 were diagnosed as esophageal carcinosarcoma, with an incidence of 0.36%. All of the cases were male with a mean age of 62.3 years. Of the 12 tumors, 8 were polypoid type, and 4 were ulcerative type. In the endoscopic ultrasonography examination, the tumors show heterogeneous hypoechoic lesions with irregular outer margins and internal multicystic components. Four patients (33.3%) had previous head and neck squamous cell carcinoma that occurred metachronously. This is the first report about the characteristics of esophageal carcinosarcoma under endoscopic ultrasonography examination. The relationship between esophageal carcinosarcomas and head and neck cancer needs further investigation.

Hyperbaric oxygen treatment decreases post-ischemic neurotrophin-3 mRNA down-regulation in the rat hippocampus.

The therapeutic effect of hyperbaric oxygen (HBO) on ischemic injury was investigated using in situ hybridization to detect the mRNA expression of neurotrophin-3 (NT-3), which is thought to play a crucial role in protecting against neuronal death induced by brain ischemia. The rats under investigation were subjected to 10 min transient forebrain ischemia, and subsequently exposed to HBO (100% oxygen, 2.5 atm absolute) for 2 h. Levels of NT-3 mRNA in the CA1, CA2 and CA3 regions, and the dentate gyrus of the hippocampus were measured after various reperfusion periods. Neuronal death in the hippocampal CA1 region was also measured by Nissl staining, seven days post ischemia. The results demonstrated that HBO treatment significantly reduced the ischemia-induced down-regulation of the NT-3 mRNA level at 4 h post ischemia, and significantly increased cell survival 7 days after reperfusion. The findings suggest that an HBO treatment maintaining the NT-3 mRNA level in the hippocampus can be beneficial to the ischemic brain within a certain time frame.

Induction of Tie-1 and Tie-2 receptor protein expression after cerebral ischemia-reperfusion.

Tie-1 and Tie-2 are receptor tyrosine kinases (RTKs) that are exclusively expressed in endothelial cells and play important roles in endothelial cell biology. The authors have reported previously the temporal profiles of Tie-1 and Tie-2 mRNA expression after focal cerebral ischemia-reperfusion. In the current study, the localization of Tie-1/Tie-2 mRNA and proteins were further investigated in the same focal ischemia model. In situ hybridization showed that, after 60-minute ischemia and 72-hour reperfusion, both Tie-1 and Tie-2 mRNA appeared as capillary-like structures in the ischemic middle cerebral artery (MCA) cortex. Western blot analysis showed a biphasic expression of Tie-1 protein in the same region. The first peak, spanning the ischemic and early reperfusion period. was of low intensity and short-lived. The second peak was of greater intensity and spanning the period from 72 to 168 hours after reperfusion. Similarly, Tie-2 expression at the protein level also exhibited a biphasic pattern. Immunohistochemical studies, after 72 hours of reperfusion, showed that although Tie-1 and Tie-2 were detected within the ischemic cortex, they actually were expressed in different populations of endothelial cells in different regions. In agreement with the in situ hybridization study, Tie-1 immunoreactivity appeared as capillary-like structures in cortical layers 2 to 4. Similar capillary-like appearance of Tie-2 immunoreactivity was noted in the outer cortical layers. In addition, Tie-2 immunoreactivity also was observed in cortical layer 6b, where de novo large vessel formation was noted. Cellular colocalization experiments revealed that Tie-2 is expressed in proximity to its antagonist, Angpo-2, as well as basic fibroblast growth factor (bFGF) and vascular endothelial growth factor (VEGF) in cortical layer 1, where active vessel remodeling was noted. Interestingly, bFGF only partially colocalized with VEGF, suggesting differential roles for these angiogenic factors during vessel remodeling. Tie-1 protein, to a lesser degree, also colocalized with Angpo-2, bFGF, and VEGF in cortical layer 1. Magnetic resonance imaging (MRI) showed increased regional cerebral blood flow (CBF) corresponding to the expression of these angiogenesis gene products. Together, these findings suggest that the evolving expression of angiogenesis genes underlie the robust vascular remodeling after ischemia and reperfusion.

Ethanol effects on nitric oxide production in cerebral pial cultures.

BACKGROUND: Although alcohol abusers are known to have higher incidences of hemorrhagic cerebrovascular diseases, it is not known whether these changes are associated with ethanol (EtOH) action on nitric oxide (NO) production in the cerebrovascular cells. The purpose of this study was to examine the effects of EtOH treatment on basal and cytokine-induced NO production in cortical pial cultures. METHODS: Cell cultures for this study included murine primary pial vascular cells, primary glial cells and cortical neurons. These cells were exposed to cytokines or EtOH for 24 to 48 hr. The culture media were used for measurement of nitrite, as an indication for NO release, and lactate dehydrogenase (LDH), as an index of cell membrane integrity. In addition, immunocytochemical determinations were carried out to identify cell types and to assess inducible nitric oxide synthase (iNOS). RESULTS: Exposure of primary pial vascular cultures to cytokines that consisted of interleukin-1 beta (IL-1 beta; 250 pg/mL) and interferon-gamma (IFNgamma; 2 ng/mL) or to EtOH (50 to 100 mM) for 24 to 48 hr significantly elevated NO production. NO production could be attenuated by N-nitro-L-arginine (N-arg), a nonspecific NOS inhibitor, or aminoguanidine (AG), an iNOS inhibitor. Increased iNOS immunoreactivity was observed in cytokines- or EtOH-treated pial cells. When pial cells were cocultured with cortical neurons, prolonged EtOH exposure led to a large increase in NO production as well as LDH release. However, this increase was not observed in pial culture alone or in mixed cortical culture. Nevertheless, inhibition of NO production with N-arg or AG did not alter the EtOH-induced LDH release in the pial cells cocultured with cortical neurons. CONCLUSION: These results show that EtOH exposure led to increased production of NO in primary pial cell culture. In mixed culture that contained cortical neurons and pial cells, EtOH induced increase in NO as well as LDH release, which is an indication of loss of cell membrane integrity. However, EtOH-mediated LDH release in mixed cortical pial cultures was not a consequence of the increase in NO production by these cells. Studies that use mixed cortical-pial cultures may provide a unique in vitro system for examining the interactions among glial cells, neurons, and cerebrovascular cells.

Differential regulation of H- and L-ferritin messenger RNA subunits, ferritin protein and iron following focal cerebral ischemia-reperfusion.

Iron may catalyse the production of reactive oxygen species during post-ischemic reoxygenation and subsequently lead to brain damage. Ferritin, an iron sequestering and storage protein, can also be a source of iron after ischemic insult. However, its role in ischemia-reperfusion has not been carefully investigated. In the present study, we examined the temporal and spatial induction profiles of both H- and L-ferritin messenger RNA and protein in a well-defined focal cerebral ischemia model. Results of northern blot analysis showed a delayed and prolonged induction of both H- and L-ferritin messenger RNA in the ischemic cortex of rats subjected to 60min ischemic insult. A significant induction of both H- and L-ferritin messenger RNA was observed at 12h and remained elevated for up to 336h after the onset of reperfusion. At the peak level, quantitative analysis of the blot indicated a 2.5-fold and a six-fold increase in H- and L-ferritin messenger RNA, respectively, compared with the sham-operated controls. No apparent change in the levels of either messenger RNA was observed in the contralateral side. Results of in situ hybridization studies revealed constitutive expression of both H- and L-ferritin messenger RNA throughout the brain in sham-operated animals, in particular the hippocampus and the piriform cortex. Nevertheless, the signal intensity of H-ferritin messenger RNA was much higher than that of L-ferritin messenger RNA. Seventy-two hours after 60min ischemia, marked expression of H-ferritin messenger RNA was observed in the area surrounding the middle cerebral artery irrigated cortex, the medial part of the caudoputamen and in the subfield of the CA1 hippocampal region of the ipsilateral hemisphere. Similarly, a large induction of L-ferritin messenger RNA was also noted in several areas, including the middle cerebral artery irrigated cortex, the lateral part of the caudoputamen and the stratum pyramidale of the CA1 hippocampal region, which were totally different from areas where H-ferritin messenger RNA was found. At 336h after ischemia, increased expression of H-ferritin messenger RNA was observed in the peri-necrosis and ipsilateral thalamus regions, while L-ferritin messenger RNA was noted exclusively at the edge within the necrosis. Results of immunohistochemical study further revealed that ferritin immunoreactivity was present in the same areas where increased ferritin messenger RNA was found. Sixty-minute ischemia also led to iron deposition in discrete areas. Iron deposition was highly associated with the induction of ferritin, particularly in the macrophage- and microglia-positive areas where cell death or tissue necrosis was noted.In summary, our initial findings indicate that ischemic insult leads to induction of both H- and L-ferritin messenger RNA. In the present study, although the temporal induction profiles were similar, the major expression areas for these two genes were totally different. Ferritin immunoreactivity was observed in the same areas where increased ferritin messenger RNA was found. Ischemia also resulted in iron deposition, which highly associated with the ferritin immunoreactivity. The exact regulatory mechanism and pathological significance for the differential expression of H- and L-ferritin genes following ischemia/reperfusion remain to be clarified.

Induction of angiogenesis related genes in the contralateral cortex with a rat three-vessel occlusion model.

The bFGF/FGFR, VEGF/VEGFR and Angiopoietin/Tie receptor system are crucial for angiogenesis and vascular remodeling. With a rat focal cerebral ischemia model, we previously reported dramatic changes in the vascular density and angiogenesis related genes in the ipsilateral cortex after 60 minutes severe ischemia. While only a small increase in the capillary density was noted in the contralateral cortex with very mild ischemia. In the present study we further reported that only Tie-1 and VEGFR-2 mRNA were significantly changed in the contralateral cortex with a p value of 0.0001 and 0.0168, respectively, and the degree of changes were very small. Interestingly, in contrast to a huge increase in the ipsilateral cortex, Tie-1 mRNA was slowly decreased after the onset of ischemia and stayed below the basal level throughout the remaining periods studied. The mechanism and significance for this decrease is not presently clear. In contrast to the ipsilateral cortex, the Angpo-1/Angpo-2 mRNA ratio was also slightly dropped below the basal level in the contralateral side in most of the ischemia-reperfusion periods studied, which is in line with the notion that small decrease in Angpo-1/Angpo-2 mRNA ratio implied small vascular remodeling activity. It is very likely that increase in this Angpo-1/Angpo-2 ratio is crucial for remodeling into large vessels and increase in Tie-1 may be crucial for capillary density increasing. Nevertheless, the detailed mechanisms and significance of differential expression of these genes and relationship to vascular remodeling remain to be characterized.

Induction of angiopoietin and Tie receptor mRNA expression after cerebral ischemia-reperfusion.

The angiopoietin/Tie receptor system may contribute to angiogenesis and vascular remodeling by mediating interactions of endothelial cells with smooth muscle cells and pericytes. The temporal expression of angiopoietin-1 (Angpo-1), angiopoietin-2 (Angpo-2), Tie-1, and Tie-2 mRNA was studied in a focal cerebral ischemia model in rats. The cDNA fragments obtained from reverse transcription polymerase chain reaction amplification were cloned and used as a probe to detect individual genes. Northern blot analysis showed a delayed increase of a 4.4-kb Angpo-1 transcript for up to 2 weeks after ischemia, eightfold higher than the values of the sham-operated controls. A biphasic expression of a 2.4-kb Angpo-2 transcript was noted, peaking at 24 hours (6.4-fold) and 2 weeks (4.6-fold) after ischemia. The expression of Tie-2 mRNA (4.3 kb), a receptor for Angpo-1, and Tie-1 mRNA (4.3 kb) also increased starting 24 hours after reperfusion and remained elevated for up to 2 weeks after ischemia. The temporal profiles of the expression of these genes were different from those of other angiogenic genes such as basic fibrobast growth factor/fibroblast growth factor receptor and vascular endothelial growth factor/vascular endothelial growth factor receptor and proteolytic enzymes (tissue-type plasminogen activator and urokinase plasminogen activator) and their inhibitors (plasminogen activator inhibitor-1). The expression patterns of these genes could be related to progressive tissue liquefaction and neovascularization after ischemia in this stroke model. Differential expression of these angiogenesis genes suggests the involvement of complex regulatory mechanisms that remain to be characterized.

ATP-stimulated c-fos and zif268 mRNA expression is inhibited by chemical hypoxia in a rat brain-derived type 2 astrocyte cell line, RBA-2.

The stimulus-transcriptional coupling during ischemia/hypoxia was examined for ATP-stimulated expression of immediate early genes (IEGs; c-fos, zif268, c-myc and nur77) in a rat brain-derived type 2 astrocyte cell line, RBA-2. Incubation of cells with 1 mM of extracellular ATP stimulated time-dependent expression of c-fos and zif268. ATP induced the largest increases in zif268 mRNA and a lesser one in c-fos mRNA. ATP also induced a slight increase in nur77 mRNA but was ineffective in inducing c-myc expression in these cells. Brief exposure of cells to potassium cyanide to simulate chemical hypoxia induced 9-fold and 7-fold transient increases in c-fos and zif268 expression, respectively, but did not affect c-myc or nur77 expression. When cyanide and ATP were added together, the expression of c-fos and zif268 expression was inhibited, and the effect was mimicked by simulating chemical hypoxia with sodium azide. To elucidate the mechanism involved, the effect of cyanide on ATP-stimulated increases in intracellular Ca(2+) concentrations, [Ca(2+)](i), and phospholipase D (PLD) activities were measured. Cyanide induced an increase in [Ca(2&plus);](i) and further enhanced the ATP-stimulated increases in [Ca(2+)](i) and PLD activities. Nevertheless, metabolic inhibitor, iodoacetate, blocked the ATP-induced c-fos and partially inhibited zif268 expression, and deprivation of cells with glucose also inhibited the ATP-induced c-fos expression. Taken together, these results demonstrate that both extracellular ATP and chemical hypoxia induce c-fos and zif268 expression in RBA-2 type 2 astrocytes. The chemical hypoxia inhibited ATP-stimulated c-fos and zif268 expression is not due to alterations in Ca(2+) and PLD signaling, and is at least partially related to metabolic disturbance in these cells.

[Research of compound cyclosporin A mouthwash in the treatment of oral lichen planus].

Thirty patients of oral lichen planus(OLP) were treated with compound CyA mouthwash, while the control group was treated with KouTai. The results showed that the rate of success and total rate of success of patients treated with compound CyA mouthwash were 63 percent and 97 percent respectively, but those of the control group treated with kouTai were 10 percent and 63 percent respectively. There was a statistically significant difference(P < 0.01). No side-effects were found. The mouthwash is an effective, safe and local drug used in the treatment of OLP.