Characterizing the Conformational Distribution in an Amorphous Film of an Organic Emitter and Its Application in a "Self-Doping" Organic Light-Emitting Diode.

The conformational distribution and mutual interconversion of thermally activated delayed fluorescence (TADF) emitters significantly affect the exciton utilization. However, their influence on the photophysics in amorphous film states is still not known due to the lack of a suitable quantitative analysis method. Herein, we used temperature-dependent time-resolved photoluminescence spectroscopy to quantitatively measure the relative populations of the conformations of a TADF emitter for the first time. We further propose a new concept of "self-doping" for realizing high-efficiency nondoped OLEDs. Interestingly, this "compositionally" pure film actually behaves as a film with a dopant (quasi-equatorial form) in a matrix (quasi-axial form). The concentration-induced quenching that may occur at high concentrations is thus expected to be effectively relieved. The "self-doping" OLED prepared with the newly developed TADF emitter TP2P-PXZ as a neat emitting layer realizes a high maximum external quantum efficiency of 25.4 % and neglectable efficiency roll-off.

Using fluorene to lock electronically active moieties in thermally activated delayed fluorescence emitters for high-performance non-doped organic light-emitting diodes with suppressed roll-off.

Thermally activated delayed fluorescence (TADF) emitters with aggregation-induced emission (AIE) features are hot candidates for non-doped organic light-emitting diodes (OLEDs), as they are highly emissive in solid states upon photoexcitation. Nevertheless, not every AIE-TADF emitter in the past had guaranteed decent efficiencies in non-doped devices, indicating that the AIE character alone does not necessarily afford ideal non-doped TADF emitters. As intermolecular electron-exchange interaction that involves long-lived triplet excitons plays a dominant role in the whole quenching process of TADF, we anticipate that it is the main reason for the different electroluminescence performances of AIE-TADF emitters. Therefore, in this work, we designed two TADF emitters SPBP-DPAC and SPBP-SPAC by modifying a reported less successful emitter BP-DPAC with extra fluorenes to increase intermolecular distances and attenuate this electron-exchange interaction. With the fluorene lock as steric hindrance, SPBP-DPAC and SPBP-SPAC exhibit significantly higher exciton utilization in non-doped films due to the suppressed concentration quenching. The non-doped OLEDs based on SPBP-DPAC and SPBP-SPAC show an excellent maximum external quantum efficiency (EQE) of 22.8% and 21.3% respectively, and what's even more promising is that ignorable roll-offs at practical brightness (e.g., 1000 and 5000 cd m-2) were realized. These results reveal that locking the phenyl rings as steric hindrance can not only enhance the molecular rigidity, but also cause immediate relief of concentration quenching, and result in significant performance improvement under non-doped conditions. Our approach proposes a feasible molecular modification strategy for AIE-TADF emitters, potentially increasing their applicability in OLEDs.

Cadmium toxicity induces ER stress and apoptosis via impairing energy homoeostasis in cardiomyocytes.

Cadmium, a highly toxic environmental pollutant, is reported to induce toxicity and apoptosis in multiple organs and cells, all possibly contributing to apoptosis in certain pathophysiologic situations. Previous studies have described that cadmium toxicity induces biochemical and physiological changes in the heart and finally leads to cardiac dysfunctions, such as decreasing contractile tension, rate of tension development, heart rate, coronary flow rate and atrioventricular node conductivity. Although many progresses have been made, the mechanism responsible for cadmium-induced cellular alternations and cardiac toxicity is still not fully understood. In the present study, we demonstrated that cadmium toxicity induced dramatic endoplasmic reticulum (ER) stress and impaired energy homoeostasis in cultured cardiomyocytes. Moreover, cadmium toxicity may inhibit protein kinase B (AKT)/mTOR (mammalian target of rapamycin) pathway to reduce energy productions, by either disrupting the glucose metabolism or inhibiting mitochondrial respiratory gene expressions. Our work will help to reveal a novel mechanism to clarify the role of cadmium toxicity to cardiomyocytes and provide new possibilities for the treatment of cardiovascular diseases related to cadmium toxicity.

Upregulated microRNA-214 enhances cardiac injury by targeting ITCH during coxsackievirus infection.

Viral myocarditis (VM), a severe clinical condition characterized by cardiac inflammation, is most frequently induced as a result of coxsackievirus infection. Evidence suggests that microRNAs may have significant roles in the progression of cardiac injury during coxsackievirus infection. Concurrently, microRNA (miR)-214 was found to be upregulated in the plasma and myocardial cells during this process. In the present study, eight candidate miRNAs, the functions of which are associated with myocarditis, were selected and their expression levels were evaluated by reverse transcription-quantitative polymerase chain reaction. miR-146b and miR-214 were found to have significantly upregulated expression levels in the heart tissues of patients with VM compared with those of the control subjects. Predictions via the use of online bioinformatics tools and confirmed by dual-luciferase assay and western blot analysis, revealed that ITCH, an NF-κB signaling suppressor, was a target gene of miR-214. To investigate the biological function of miR-214, tumor necrosis factor-α and interleukin-6 expression levels were evaluated in HeLa cell culture supernatant. The results revealed that miR-214 overexpression enhanced the expression of the two cytokines. In addition, the function of miR-214 was partially rescued by ITCH overexpression. Subsequently, concurrent results were obtained following experiments in murine cardiac myocytes. In conclusion, the results of the present study demonstrated that miR-214 contributed to the adverse inflammatory response to viral infection of the heart during coxsackievirus infection and is therefore a potential therapeutic target for the treatment of viral myocarditis.

[Complete genome sequencing of enterovirus 71 (EV71) HENAN08 strain isolated in Henan province].

OBJECTIVE: To sequence the whole-genome of enterovirus 71 (EV71) srtain isolated from patient with hand, foot and mouth in Henan province in 2008. METHODS: Eight overlapping clones covering the whole viral genome were obtained by RT-PCR and the sequences were determined by Sanger dideoxg-mediated chain termination method. RESULTS: Data it showed that the full length of enterovirus 71 (EV71) HENAN08 genome (not including Poly A tail) is 7405 bp. No deletion or insertion was detected in the coding region. There were several deletions and insertions in 5'UTR and 3'UTR regions. In P1 region, HENAN08 strain shared high homology with AnhuiFY08 strain, Zhejiang08 strain and SHZH strains (SHZH98, SHZH03) but low homology with Cox. A16. In P2 and P3 regions, HENAN08 strain shared higher nucleotide homology with Cox. A16 (81.7% and 83.7%) than that with BrCr and TW2086 strains. The phylogenetic analysis based on P1 region demonstrates that HENAN08 strain had the nearest genetic relationship with AnhuiFY and Zhejiang strains (isolated in 2008). CONCLUSION: The HENAN08 strain might belong to the same genogroup with AnhuiFY08 and Zhejiang08 strains as C4 gene subtypes.