Blue-Light Emission of Cu(I) Complexes and Singlet Harvesting

Strongly luminescent neutral copper(I) complexes of the type Cu(pop)(NN), with pop = bis(2-(diphenylphosphanyl)phenyl)ether and NN = bis(pyrazol-1-yl)borohydrate (pz2BH2), tetrakis(pyrazol-1-yl)borate (pz4B), or bis(pyrazol-1-yl)-biphenyl-borate (pz2Bph2), are readily accessible in reactions of Cu(acetonitrile)4+ with equimolar amounts of the pop and NN ligands at ambient temperature. All products were characterized by means of single crystal X-ray diffractometry. The compounds exhibit very strong blue/white luminescence with emission quantum yields of up to 90%. Investigations of spectroscopic properties and the emission decay behavior in the temperature range between 1.6 K and ambient temperature allow us to assign the emitting electronic states. Below 100 K, the emission decay times are in the order of many hundreds of microseconds. Therefore, it is concluded that the emission stems from the lowest triplet state. This state is assigned to a metal-to-ligand charge-transfer state (3MLCT) involving Cu-3d and pop-π* orbitals. With temperature increase, the emission decay time is drastically reduced to e.g. to 13 μs (Cu(pop)(pz2Bph2)) at ambient temperature. At this temperature, the complexes exhibit high emission quantum yields, as neat material or doped into poly(methyl methacrylate) (PMMA). This behavior is assigned to an efficient thermal population of a singlet state (being classified as 1MLCT), which lies only 800 to 1300 cm–1 above the triplet state, depending on the individual complex. Thus, the resulting emission at ambient temperature largely represents a fluorescence. For applications in OLEDs and LEECs, for example, this type of thermally activated delayed fluorescence (TADF) creates a new mechanism that allows to harvest both singlet and triplet excitons (excitations) in the lowest singlet state. This effect of singlet harvesting leads to drastically higher radiative rates than obtainable for emissions from triplet states of Cu(I) complexes

Tracking of Single Charge Carriers in a Conjugated Polymer Nanoparticle

The motion of individual charge carriers in organic nanostructures was tracked by fluorescence microscopy. A twinkling effect is observed in fluorescence microscopy of single conjugated polymer nanoparticles, that is, small displacements in the fluorescence spot of single nanoparticles of the conjugated polymer PFBT are observed over time. There is evidence that superquenching by the charge carrier induces a dark spot in the nanoparticle, which moves with the carrier, resulting in the observed displacements in the fluorescence. Zero-field mobilities of individual charge carriers consistent with highly trapped polarons were obtained from tracking experiments

Hydrothermal Synthesis of Single-Crystalline Antimony Telluride Nanobelts

The single-crystalline Sb2Te3 nanobelts were successfully synthesized by a novel and convenient surfactant-assisted hydrothermal approach. The ionic surfactant AOT acted as the shape controller in the synthetic process. We believe that this synthetic route could be applied to obtain other low-dimensional semiconducting telluride nanostructures

DataSheet1_N6-Methyladenosine Methyltransferase METTL3 Promotes Angiogenesis and Atherosclerosis by Upregulating the JAK2/STAT3 Pathway via m6A Reader IGF2BP1.docx

Atherosclerosis (AS) is a life-threatening vascular disease. RNA N6-methyladenosine (m6A) modification level is dysregulated in multiple pathophysiologic processes including AS. In this text, the roles and molecular mechanisms of m6A writer METTL3 in AS progression were explored in vitro and in vivo. In the present study, cell proliferative, migratory, and tube formation capacities were assessed through CCK-8, Transwell migration, and tube formation assays, respectively. RNA m6A level was examined through a commercial kit. RNA and protein levels of genes were measured through RT-qPCR and western blot assays, respectively. VEGF secretion level was tested through ELISA assay. JAK2 mRNA stability was detected through actinomycin D assay. The relationship of METTL3, IGF2BP1, and JAK2 was investigated through bioinformatics analysis, MeRIP, RIP, RNA pull-down, and luciferase reporter assays. An AS mouse model was established to examine the effect of METTL3 knockdown on AS development in vivo. The angiogenetic activity was examined through chick chorioallantoic membrane assay in vivo. The results showed that METTL3 was highly expressed in ox-LDL-induced dysregulated HUVECs. METTL3 knockdown inhibited cell proliferation, migration, tube formation, and VEGF expression/secretion in ox-LDL-treated HUVECs, hampered AS process in vivo, and prevented in vivo angiogenesis of developing embryos. METTL3 positively regulated JAK2 expression and JAK2/STAT3 pathway in an m6A dependent manner in HUVECs. IGF2BP1 positively regulated JAK2 expression through directly binding to an m6A site within JAK2 mRNA in HUVECs. METTL3 knockdown weakened the interaction of JAK2 and IGF2BP1. METTL3 exerted its functions through JAK2/STAT3 pathway. In conclusion, METTL3 knockdown prevented AS progression by inhibiting JAK2/STAT3 pathway via IGF2BP1.</p

Ultrabright Pdots with a Large Absorbance Cross Section and High Quantum Yield

Semiconducting polymer dots (Pdots) are increasingly used in biomedical applications due to their extreme single-particle brightness, which results from their large absorption cross section (σ). However, the quantum yield (Φ) of Pdots is typically below 40% due to aggregation-induced self-quenching. One approach to reducing self-quenching is to use FRET between the donor (D) and acceptor (A) groups within a Pdot; however, Φ values of FRET-based Pdots remain low. Here, we demonstrate an approach to achieve ultrabright FRET-based Pdots with simultaneously high σ and Φ. The importance of self-quenching was revealed in a non-FRET Pdot: adding 30 mol % of a nonabsorbing polyphenyl to a poly­(9,9-dioctylfluorene) (PFO) Pdot increased Φ from 13.4 to 71.2%, yielding an ultrabright blue-emitting Pdot. We optimized the brightness of FRET-based Pdots by exploring different D/A combinations and ratios with PFO and poly­[(9,9-dioctylfluorenyl-2,7-diyl)-co-(1,4-phenylene)] (PFP) as donor polymers and poly­[(9,9-dioctyl-2,7-divinylenefluorenylene)-alt-co-(1,4-phenylene)] (PFPV) and poly­[(9,9-dioctylfluorenyl-2,7-diyl)-alt-co-(1,4-benzo-{2,1′,3}-thiadiazole)] (PFBT) as acceptor polymers, with a fixed concentration of poly­(styrene-co-maleic anhydride) as surfactant polymer. Ultrabright blue-emitting Pdots possessing high Φ (73.1%) and σ (σR = σabs/σall, 97.5%) were achieved using PFP/PFPV Pdots at a low acceptor content (A/[D + A], 2.5 mol %). PFP/PFPV Pdots were 1.8 times as bright as PFO/PFPV Pdots due to greater coverage of acceptor absorbance by donor emissiona factor often overlooked in D/A pair selection. Ultrabright green-emitting PFO Pdots (Φ = 76.0%, σR = 92.5%) were obtained by selecting an acceptor (PFBT) with greater spectral overlap with PFO. Ultrabright red-emitting Pdots (Φ = 64.2%, σR = 91.0%) were achieved by blending PFO, PFBT, and PFTBT to create a cascade FRET Pdot at a D:A1:A2 molar ratio of 61:5:1. These blue, green, and red Pdots are among the brightest Pdots reported. This approach of using a small, optimized amount of FRET acceptor polymer with a large donor–acceptor spectral overlap can be generalized to produce ultrabright Pdots with emissions that span the visible spectrum

Image1_N6-Methyladenosine Methyltransferase METTL3 Promotes Angiogenesis and Atherosclerosis by Upregulating the JAK2/STAT3 Pathway via m6A Reader IGF2BP1.tif

Atherosclerosis (AS) is a life-threatening vascular disease. RNA N6-methyladenosine (m6A) modification level is dysregulated in multiple pathophysiologic processes including AS. In this text, the roles and molecular mechanisms of m6A writer METTL3 in AS progression were explored in vitro and in vivo. In the present study, cell proliferative, migratory, and tube formation capacities were assessed through CCK-8, Transwell migration, and tube formation assays, respectively. RNA m6A level was examined through a commercial kit. RNA and protein levels of genes were measured through RT-qPCR and western blot assays, respectively. VEGF secretion level was tested through ELISA assay. JAK2 mRNA stability was detected through actinomycin D assay. The relationship of METTL3, IGF2BP1, and JAK2 was investigated through bioinformatics analysis, MeRIP, RIP, RNA pull-down, and luciferase reporter assays. An AS mouse model was established to examine the effect of METTL3 knockdown on AS development in vivo. The angiogenetic activity was examined through chick chorioallantoic membrane assay in vivo. The results showed that METTL3 was highly expressed in ox-LDL-induced dysregulated HUVECs. METTL3 knockdown inhibited cell proliferation, migration, tube formation, and VEGF expression/secretion in ox-LDL-treated HUVECs, hampered AS process in vivo, and prevented in vivo angiogenesis of developing embryos. METTL3 positively regulated JAK2 expression and JAK2/STAT3 pathway in an m6A dependent manner in HUVECs. IGF2BP1 positively regulated JAK2 expression through directly binding to an m6A site within JAK2 mRNA in HUVECs. METTL3 knockdown weakened the interaction of JAK2 and IGF2BP1. METTL3 exerted its functions through JAK2/STAT3 pathway. In conclusion, METTL3 knockdown prevented AS progression by inhibiting JAK2/STAT3 pathway via IGF2BP1.</p

Table1_N6-Methyladenosine Methyltransferase METTL3 Promotes Angiogenesis and Atherosclerosis by Upregulating the JAK2/STAT3 Pathway via m6A Reader IGF2BP1.xlsx

Atherosclerosis (AS) is a life-threatening vascular disease. RNA N6-methyladenosine (m6A) modification level is dysregulated in multiple pathophysiologic processes including AS. In this text, the roles and molecular mechanisms of m6A writer METTL3 in AS progression were explored in vitro and in vivo. In the present study, cell proliferative, migratory, and tube formation capacities were assessed through CCK-8, Transwell migration, and tube formation assays, respectively. RNA m6A level was examined through a commercial kit. RNA and protein levels of genes were measured through RT-qPCR and western blot assays, respectively. VEGF secretion level was tested through ELISA assay. JAK2 mRNA stability was detected through actinomycin D assay. The relationship of METTL3, IGF2BP1, and JAK2 was investigated through bioinformatics analysis, MeRIP, RIP, RNA pull-down, and luciferase reporter assays. An AS mouse model was established to examine the effect of METTL3 knockdown on AS development in vivo. The angiogenetic activity was examined through chick chorioallantoic membrane assay in vivo. The results showed that METTL3 was highly expressed in ox-LDL-induced dysregulated HUVECs. METTL3 knockdown inhibited cell proliferation, migration, tube formation, and VEGF expression/secretion in ox-LDL-treated HUVECs, hampered AS process in vivo, and prevented in vivo angiogenesis of developing embryos. METTL3 positively regulated JAK2 expression and JAK2/STAT3 pathway in an m6A dependent manner in HUVECs. IGF2BP1 positively regulated JAK2 expression through directly binding to an m6A site within JAK2 mRNA in HUVECs. METTL3 knockdown weakened the interaction of JAK2 and IGF2BP1. METTL3 exerted its functions through JAK2/STAT3 pathway. In conclusion, METTL3 knockdown prevented AS progression by inhibiting JAK2/STAT3 pathway via IGF2BP1.</p

Table5_N6-Methyladenosine Methyltransferase METTL3 Promotes Angiogenesis and Atherosclerosis by Upregulating the JAK2/STAT3 Pathway via m6A Reader IGF2BP1.xlsx

Atherosclerosis (AS) is a life-threatening vascular disease. RNA N6-methyladenosine (m6A) modification level is dysregulated in multiple pathophysiologic processes including AS. In this text, the roles and molecular mechanisms of m6A writer METTL3 in AS progression were explored in vitro and in vivo. In the present study, cell proliferative, migratory, and tube formation capacities were assessed through CCK-8, Transwell migration, and tube formation assays, respectively. RNA m6A level was examined through a commercial kit. RNA and protein levels of genes were measured through RT-qPCR and western blot assays, respectively. VEGF secretion level was tested through ELISA assay. JAK2 mRNA stability was detected through actinomycin D assay. The relationship of METTL3, IGF2BP1, and JAK2 was investigated through bioinformatics analysis, MeRIP, RIP, RNA pull-down, and luciferase reporter assays. An AS mouse model was established to examine the effect of METTL3 knockdown on AS development in vivo. The angiogenetic activity was examined through chick chorioallantoic membrane assay in vivo. The results showed that METTL3 was highly expressed in ox-LDL-induced dysregulated HUVECs. METTL3 knockdown inhibited cell proliferation, migration, tube formation, and VEGF expression/secretion in ox-LDL-treated HUVECs, hampered AS process in vivo, and prevented in vivo angiogenesis of developing embryos. METTL3 positively regulated JAK2 expression and JAK2/STAT3 pathway in an m6A dependent manner in HUVECs. IGF2BP1 positively regulated JAK2 expression through directly binding to an m6A site within JAK2 mRNA in HUVECs. METTL3 knockdown weakened the interaction of JAK2 and IGF2BP1. METTL3 exerted its functions through JAK2/STAT3 pathway. In conclusion, METTL3 knockdown prevented AS progression by inhibiting JAK2/STAT3 pathway via IGF2BP1.</p

Purification of Semiconducting Polymer Dots by Size Exclusion Chromatography Prior to Cytotoxicity Assay and Stem Cell Labeling

Semiconducting polymer dots (Pdots) as fluorescent probes have shown promising applications because of their excellent optical properties. However, apparent differences were observed in cytotoxicity assays, which might originate from impurities introduced in polymer synthesis or nanoparticle preparation. A simple gel-filtration-based purification method was used to address this issue. Purified Pdots displayed obviously decreased cytotoxicity as compared with the same batch of unpurified Pdots. The purified Pdots were further examined in a cytotoxicity study on mesenchymal stem cells (MSCs), which are very sensitive to exogenous probes. The results indicated that purified Pdots did not affect the proliferation ability of MSCs, while unpurified Pdots could have obvious cytotoxicity. In addition, the purified Pdots did not show cytotoxicity even after 6 months of storage. Our results demonstrated that gel filtration is an effective method for obtaining Pdots with minimal cytotoxicity, which are more suitable for biological applications

Table4_N6-Methyladenosine Methyltransferase METTL3 Promotes Angiogenesis and Atherosclerosis by Upregulating the JAK2/STAT3 Pathway via m6A Reader IGF2BP1.xlsx

Atherosclerosis (AS) is a life-threatening vascular disease. RNA N6-methyladenosine (m6A) modification level is dysregulated in multiple pathophysiologic processes including AS. In this text, the roles and molecular mechanisms of m6A writer METTL3 in AS progression were explored in vitro and in vivo. In the present study, cell proliferative, migratory, and tube formation capacities were assessed through CCK-8, Transwell migration, and tube formation assays, respectively. RNA m6A level was examined through a commercial kit. RNA and protein levels of genes were measured through RT-qPCR and western blot assays, respectively. VEGF secretion level was tested through ELISA assay. JAK2 mRNA stability was detected through actinomycin D assay. The relationship of METTL3, IGF2BP1, and JAK2 was investigated through bioinformatics analysis, MeRIP, RIP, RNA pull-down, and luciferase reporter assays. An AS mouse model was established to examine the effect of METTL3 knockdown on AS development in vivo. The angiogenetic activity was examined through chick chorioallantoic membrane assay in vivo. The results showed that METTL3 was highly expressed in ox-LDL-induced dysregulated HUVECs. METTL3 knockdown inhibited cell proliferation, migration, tube formation, and VEGF expression/secretion in ox-LDL-treated HUVECs, hampered AS process in vivo, and prevented in vivo angiogenesis of developing embryos. METTL3 positively regulated JAK2 expression and JAK2/STAT3 pathway in an m6A dependent manner in HUVECs. IGF2BP1 positively regulated JAK2 expression through directly binding to an m6A site within JAK2 mRNA in HUVECs. METTL3 knockdown weakened the interaction of JAK2 and IGF2BP1. METTL3 exerted its functions through JAK2/STAT3 pathway. In conclusion, METTL3 knockdown prevented AS progression by inhibiting JAK2/STAT3 pathway via IGF2BP1.</p