The use of rare-earth (RE) (e.g., Eu2+/Ce3+) ions as single luminescent centers in phosphors with tailorable emission properties has been extensively studied for their potential use in white LEDs. However, significant limitations remain, in particular, for red-emitting phosphors due to the inherently broad excitation bands which result from the underlying d–f transitions and span large parts of the visible spectral region. Guided by density functional theory calculations on the ligand structure of the non-RE Bi3+ ion, we report here on an alternative class of phosphors, [(Y,Sc)­(Nb,V)­O4:Bi3+], which exhibit homogeneous Bi3+ luminescence. In these materials, adjustment of the cation fractions enables dedicated tailoring of the excitation scheme within the spectral range of ∼340–420 nm and, in the meanwhile, allows for tunable emission spanning from about 450 nm (blue) to 647 nm (orange-red). The practical absence of any overlap between the emission and excitation spectra addresses the issues of emission color purity and visible reabsorption. Tailoring through band-gap modulation is achieved by single or parallel substitution of Nb by V and Y by Sc. Such topochemical design of the ligand configuration enables modulation of the electronic band gap and thus provides a new path toward tunable phosphors, exemplarily based on Bi3+ single doping.

Background/Aims: Ischemia-reperfusion (I/R) injury is believed to be the major cause for detriments in coronary heart diseases, but few effective therapies for prevention or treatment of I/R injury are available. Gypenoside (GP) is the predominant effective component of Gynostemma pentaphyllum and possesses capacities against inflammation and oxidation. In the present study, the role of GP in ameliorating myocardial I/R injury was investigated. Methods: effect GP on the cardiac structure of I/R injured rats was assessed by H&E and TTC staining. Then the influence of GP on the cardiac function of rat model was determined by measuring hemodynamics parameters, levels of lactate dehydrogenase (LDH) and creatine kinase (CK). Thereafter, effect of GP on apoptotic process was evaluated with both rat and cell models. The production of molecules related to ER stress and apoptosis was quantified for revelation of pathways involved in the myocardial protective effect of GP. Results: Impairments in cardiac structure due to I/R injury was ameliorated by GP treatment. And it was evidently demonstrated that administration of GP not only effectively decreased the apoptotic rates in both rat and cell models but also markedly improved the cardiac function of I/R injured rats. In addition, results of western blotting revealed that the GP inhibited ER-stress and apoptosis through the blockade of CHOP pathway and activation of PI3K/Akt pathway. Conclusion: the current study showed the potential of GP to alleviate myocardial I/R injury and preliminarily uncovered the underling mechanism driving this treatment.

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