Dynamic 3D phase-shifting profilometry based on a corner optical flow algorithm.

Real-time 3D reconstruction has been applied in many fields, calling for many ongoing efforts to improve the speed and accuracy of the used algorithms. Phase shifting profilometry based on the Lucas-Kanade optical flow method is a fast and highly precise method to construct and display the three-dimensional shape of objects. However, in this method, a dense optical flow calculation is required for the modulation image corresponding to the acquired deformed fringe pattern, which consumes a lot of time and affects the real-time performance of 3D reconstruction and display. Therefore, this paper proposes a dynamic 3D phase shifting profilometry based on a corner optical flow algorithm to mitigate this issue. Therein, the Harris corner algorithm is utilized to locate the feature points of the measured object, so that the optical flow needs to calculate for only the feature points which, greatly reduces the amount of calculation time. Both our experiments and simulations show that our method improves the efficiency of pixel matching by four times and 3D reconstruction by two times.

CO2 laser thermal reflow shaped convex glass microlens array after Bessel picosecond laser inscribing and hydrofluoric acid processing.

In this paper, a convex micro-glass lens array fabrication process that utilizes ${{\rm CO}_2}$CO2 laser thermal reflow in the Bessel picosecond laser inscribing and hydrofluoric acid processed micro-glass pillars array is presented. The Bessel picosecond laser permits high tolerance and precise micro-pillar fabrication. In the thermal reshape process, the ${{\rm CO}_2}$CO2 laser power, relative defocus length, and scanning velocity are three crucial parameters to the microlens array's focal length. By using this method, microlens arrays with focal length ranging from several tens of micrometers to several hundred micrometers can be created. This research provides another way to fabricate convex micro-glass lens arrays with several hundred micrometers focal length in good utility.

Defect-Induced Enhancement Emission Intensity of Ca4.85(BO3)3F(C4.85BF):0.15Bi3+ by Introducing Cation (Na+, Sr2+, Ba2+) or Anion (Cl-).

Generally, the emission intensity of phosphors can be enhanced by introducing a proper number of defects. To enhance the emission intensity of Ca4.85(BO3)3F(C4.85BF):0.15Bi3+, more Frenkel defects were introduced by Na+, Sr2+, and Ba2+. It is found that the number of Frenkel defects is related to volume and covalence of the crystal, in which the covalence has a greater effect than the volume. Furthermore, the larger the volume of the crystal is, the stronger the covalence of the crystal is, the more Frenkel defects will be produced. The volume of Ca4.85- xSr x(BO3)3F(C4.85- xSr xBF):0.15Bi3+ is larger than that of Ca4.85- xNa x(BO3)3F(C4.85- xNa xBF):0.15Bi3+; however, the covalence of Na+ is similar to that of Sr2+, which leads to the same trap depth ( Eα) and defect density (µg) in the quenching concentration. The results also confirmed that the number of Frenkel defects is mainly influenced by the covalence of crystal. Furthermore, crystal distortion also affects the number of Frenkel defects. C4.85- xSr xBF:0.15Bi3+ and C4.85- xNa xBF:0.15Bi3+ have the same distortion at quenching concentration, which results in the same emission intensity in the quenching concentration. Ca4.85- xBa x(BO3)3F (C4.85- xBa xBF):0.15Bi3+ has a larger volume and stronger covalence; meanwhile, it has deeper trap depth ( Eα) and larger defect density (µg) at the quenching concentration, comparing with C4.85- xSr xBF:0.15Bi3+ and C4.85- xNa xBF:0.15Bi3+. However, the distortion of C4.85- xBa xBF:0.15Bi3+ is in agreement with C4.85- xNa xBF:0.15Bi3+ and C4.85- xSr xBF:0.15Bi3+, which leads to the emission intensity of C4.85- xBa xBF:0.15Bi3+ basically the same as that of C4.85- xNa xBF:0.15Bi3+ and C4.85- xSr xBF:0.15Bi3+ in quenching concentration. And the different rates of distortion result in the different quenching concentrations of C4.85- xNa xBF:0.15Bi3+, C4.85- xSr xBF:0.15Bi3+, and C4.85- xBa xBF:0.15Bi3+. Moreover, for Ca4.85- xMg x(BO3)3F(C4.85- xMg xBF):0.15Bi3+ and Ca4.85(BO3)3F1- yCl y(C4.85BF1- yCl y):0.15Bi3+, there are no Frenkel defects due to weaker covalence and smaller volume of the crystal in C4.85- xMg xBF:0.15Bi3+. However, Frenkel defects can be observed in C4.85BF1- yCl y:0.15Bi3+ due to stronger covalence and larger volume of the crystal, furthermore, and the emission spectra and thermoluminescence spectra of C4.85BF1- yCl y:0.15Bi3+ are similar to those of 0.15Bi3+ doped C4.85- xNa xBF:0.15Bi3+, C4.85- xSr xBF:0.15Bi3+, and C4.85- xBa xBF:0.15Bi3+.

Mechanism of Crystal Structure Transformation and Abnormal Reduction in Ca5- y(BO3)3- x(PO4) xF (CBP xF): yBi3.

Tricoordinated planar triangle (PO4)3- may be formed due to the structural differences between planar triangular (BO3)3- and tetrahedral (PO4)3- when (BO3)3- is gradually substituted by (PO4)3-. This transformation of structure may affect the luminescence properties of phosphor. Therefore, a series of Ca5- y(BO3)3- x(PO4) xF (CBP xF): yBi3+ ( y = 0.05, 0.15; x = 0-3), Ca5- y(PO4)3- X(BO3) XF (CPB XF): yBi3+ ( y = 0.05, 0.15; X = 0-1), Ca4.9(PO4)3F (CPF):0.1Eu3+, Ca4.95(PO4)3F (CPF):0.05Bi3+, and nCaF2/CaCl2 ( n = 0-0.1) are synthesized to explore transformation of the crystal structure on luminescence properties. In CBP xF:0.15Bi3+ ( x = 0-3), (PO4)3- is doped to substitute for (BO3)3-, the position of emission spectra remains unchanged and the emission intensity decreases rapidly with increasing x. The underlying main reason for that is formation of the triangular plane (PO4)3-, which has been verified by performing a series of verification experiments of CPB XF: yBi3+ ( y = 0.5, 0.15; X = 0-1). In CPB XF: yBi3+ ( y = 0.5, 0.15; X = 0-1), (BO3)3- is doped to substitute for (PO4)3-, P-O2 bond breaks and the coordination of (PO4)3- varies from four to three when 0.5 < X < 1; meanwhile, the crystal structure transforms from Ca5(PO4)3F (ICSD-9444) to Ca5(PO4)3F (ISCD-30261), which impedes abnormal reduction from Bi3+ to Bi2+. Furthermore, Bi3+ should non-luminance in the plane triangular (PO4)3-, but luminescence in (BO3)3-. Therefore, the emission intensity starts to increase and the emission position suddenly changes from 553 to 474 nm in CPB XF: yBi3+ ( y = 0.05, 0.15; 0.5 < X < 1). From this, the crystal structures of CBP xF: yBi3+ ( y = 0.05, 0.15; x = 0-3) has been inferred to transform from Ca5(BO3)3F (ISCD-65763) to Ca5(PO4)3F (ISCD-30261), and then to Ca5(PO4)3F (ISCD-9444) with x increasing. Emission position remains unchanged and the emission intensity decreases rapidly in CBP xF: yBi3+ ( y = 0.05, 0.15; x = 0-3) do to formation of the triangular plane (PO4)3-. In addition, the rate of abnormal reduction from Bi3+ to Bi2+ can be improved by reducing the electronegativity of the environment around the activator or increasing the ionization energy of the activator, which has been confirmed by verification experiments of CPF:0.05Bi3+, nCaF2/CaCl2 ( n = 0-0.1), and CPF:0.1Eu3+.

Kanamycin Resistance Cassette for Genetic Manipulation of Treponema denticola.

Treponema denticola has been recognized as an important oral pathogen of the "red complex" bacterial consortium that is associated with the pathogenesis of endodontal and periodontal diseases. However, little is known about the virulence of T. denticola due to its recalcitrant genetic system. The difficulty in genetically manipulating oral spirochetes is partially due to the lack of antibiotic resistance cassettes that are useful for gene complementation following allelic replacement mutagenesis. In this study, a kanamycin resistance cassette was identified and developed for the genetic manipulation of T. denticola ATCC 35405. Compared to the widely used ermF-ermAM cassette, the kanamycin cassette used in the transformation experiments gave rise to additional antibiotic-resistant T. denticola colonies. The kanamycin cassette is effective for allelic replacement mutagenesis as demonstrated by inactivation of two open reading frames of T. denticola, TDE1430 and TDE0911. In addition, the cassette is also functional in trans-chromosomal complementation. This was determined by functional rescue of a periplasmic flagellum (PF)-deficient mutant that had the flgE gene coding for PF hook protein inactivated. The integration of the full-length flgE gene into the genome of the flgE mutant rescued all of the defects associated with the flgE mutant that included the lack of PF filament and spirochetal motility. Taken together, we demonstrate that the kanamycin resistance gene is a suitable cassette for the genetic manipulation of T. denticola that will facilitate the characterization of virulence factors attributed to this important oral pathogen.

A Comprehensive Pyrolysis Mechanism of Binuclear Chromium-Based Complexes for Superior OER Activity.

Transition metal oxides are widely pursued as potent electrocatalysts for the oxygen evolution reaction (OER). However, single-metal chromium catalysts remain underexplored due to their intrinsic activity limitations. Herein, we successfully synthesize mixed-valence, nitrogen-doped Cr2O3/CrO3/CrN@NC nanoelectrocatalysts via one-step targeted pyrolysis techniques from a binuclear Cr-based complex (Cr2(Salophen)2(CH3OH)2), which is strategically designed as a precursor. Comprehensive pyrolysis mechanisms were thoroughly delineated by using coupled thermogravimetric analysis and mass spectrometry (TG-MS) alongside X-ray diffraction. Below 800 °C, the generation of a reducing atmosphere was noted, while continuous pyrolysis at temperatures exceeding 800 °C promoted highly oxidized CrO3 species with an elevated +6 oxidation state. The optimized catalyst pyrolyzed at 1000 °C (Cr2O3/CrO3/CrN@NCs-1000) demonstrated remarkable OER activity with a low overpotential of 290 mV in 1 M KOH and excellent stability. Further density functional theory (DFT) calculations revealed a much smaller reaction energy barrier of CrO3 than the low oxidation state species for OER reactivity. This work reveals fresh strategies for rationally engineering chromium-based electrocatalysts and overcoming intrinsic roadblocks to enable efficient OER catalysis through a deliberate oxidation state and compositional tuning.

Endogenous Protease-Activatable Nanosensor Based on PNA-Peptide-DNA Engineering for AND-Gated and Dual-Model Detection of MicroRNA in Single Living Tumor Cells.

The in situ detection of low-content cancer biomarkers by an endogenous activator instead of an exogenous initiator in vitro remains a great challenge, leaving a gap in the development of a tumor-specific nanosensor with an endogenous protease-activatable manner. Herein, we proposed an endogenous protease-activatable nanosensor (PA-NS) guided by peptide nucleic acid-peptide-DNA copolymers to realize AND-gated and dual-model sensing of miRNA-21 (miR-21) by combining electrochemical detection with optical imaging in living tumor cells, without an additional introduction of an exogenous activator or nanomaterials. Moreover, the PA-NS can only be activated by "dual keys" (overexpressed miR-21 and cathepsin B protease in tumor cells) simultaneously, which enables effective improvement of the tumor-to-healthy cells ratio. The fluorescence intensity measured in single tumor cells was ∼3.5-fold higher than that in single healthy cells, and the electrochemical response decreased ∼30% in the presence of target miRNA. Furthermore, studies on regulation of the protease activity and miR-21 fluctuation under external stimulation have contributed to our understanding of the biological processes and drug screenings underlying disease development. This specific endogenous protease-mediated manner for dual-model detection of miRNA guarantees excellent tumor-selective capability, which offers new opportunities to study cell heterogeneity and provides more reliable fundamentals for the diagnosis and treatment of cancer down to the single-cell level.

Calmodulin mediates Fas-induced FADD-independent survival signaling in pancreatic cancer cells via activation of Src-extracellular signal-regulated kinase (ERK).

Pancreatic cancer remains a devastating malignancy with a poor prognosis and is largely resistant to current therapies. To understand the resistance of pancreatic tumors to Fas death receptor-induced apoptosis, we investigated the molecular mechanisms of Fas-activated survival signaling in pancreatic cancer cells. We found that knockdown of the Fas-associated protein with death domain (FADD), the adaptor that mediates downstream signaling upon Fas activation, rendered Fas-sensitive MiaPaCa-2 and BxPC-3 pancreatic cells resistant to Fas-induced apoptosis. By contrast, Fas activation promoted the survival of the FADD knockdown MiaPaCa-2 and BxPC-3 cells in a concentration-dependent manner. The pharmacological inhibitor of ERK, PD98059, abrogated Fas-promoted cell survival in FADD knockdown MiaPaCa-2 and BxPC-3 cells. Furthermore, increased phosphorylation of Src was demonstrated to mediate Fas-induced ERK activation and cell survival. Immunoprecipitation of Fas in the FADD knockdown cells identified the presence of increased calmodulin, Src, and phosphorylated Src in the Fas-associated protein complex upon Fas activation. Trifluoperazine, a calmodulin antagonist, inhibited Fas-induced recruitment of calmodulin, Src, and phosphorylated Src. Consistently, trifluoperazine blocked Fas-promoted cell survival. A direct interaction of calmodulin and Src and their binding site were identified with recombinant proteins. These results support an essential role of calmodulin in mediating Fas-induced FADD-independent activation of Src-ERK signaling pathways, which promote survival signaling in pancreatic cancer cells. Understanding the molecular mechanisms responsible for the resistance of pancreatic cells to apoptosis induced by Fas-death receptor signaling may provide molecular insights into designing novel therapies to treat pancreatic tumors.

The effect of high concentration and exposure duration of nanoceria on human lens epithelial cells.

Nanotechnology has the potential for treating diseases and conditions of ageing. The eye is particularly vulnerable, because chronic pathologies can lead to sight loss. Human lens epithelial cells were exposed to 10, 20, and 100 µg/mL of negatively charged nanoceria for 48 and 72 hours; DNA damage and cell growth were assessed. Concentrations up to 100 µg/mL for 48 hours did not cause measurable genotoxic effects. For exposures of 72 hours, concentrations above 10 µg/mL showed small but statistically significant differences in DNA damage from negative controls. All treated samples were less damaged than positive controls. Cell growth, monitored for up to 7 days, did not show deviations in cell morphology or growth between treated and untreated samples. Whereas time of exposure may have greater effect than dosage, indicating potential for genotoxicity at higher exposures, human lens epithelial cells can sustain normal growth when exposed to concentrations of nanoceria of up to 100 µg/mL. From the Clinical Editor: Human lens epithelial cells were exposed to various concentrations of negatively charged nanoceria for 48 and 72 hours to assess DNA damage and cell growth. The authors demonstrate that epithelial cells can sustain normal growth when exposed to concentrations of up to 100 µg/mL, with time of exposure having a greater effect than dosage, indicating potential genotoxicity at higher exposures.

Cost-Effectiveness of Life Cycle Cost Theory-Based Large Medical Equipment.

The purpose of this study is to use the life cycle cost theory to analyze the efficiency of large medical equipment in hospitals, so as to implement life cycle cost (LCC) management and solve the current problems in hospitals. The analysis model of cost benefit of large medical equipment is established, and the cost-effectiveness of 4 large medical equipment between 2019 and 2021 is investigated and analyzed. In terms of the data in each information system of hospitals, the utilization of large medical equipment is quantitatively evaluated and analyzed by life cycle theory. The results show that the Revolution 256 row has the highest revenue of 113.29%. The annual depreciation of Signa 3.0 T HDxt is the highest, amounting to 4,160,000 yuan. However, there is lack of quality control and preventive maintenance of most equipment during use. The cost and benefit of large medical equipment in hospitals are analyzed, which demonstrates that Signa 3.0 T HDxt shows better effectiveness. Too high hospital warranty cost reflects the weak maintenance strength of hospital engineering technicians. The fundamental point of the maintenance and management of large medical equipment is to strengthen the performance evaluation of medical engineering technicians.

All-Inorganic Perovskite Solar Cells with Tetrabutylammonium Acetate as the Buffer Layer between the SnO2 Electron Transport Film and CsPbI3.

All-inorganic CsPbI3 perovskites have great potential in tandem cells in combination with other photovoltaic devices. However, CsPbI3 perovskite solar cells (PSCs) still face a huge challenge, resulting in a low power conversion efficiency (PCE) relative to organic-inorganic PSCs. In this work, we introduced tetrabutylammonium acetate (TBAAc) as a buffer layer between the SnO2 electron-transport layer (ETL) and CsPbI3 all-inorganic perovskite film interface for the first time. TBAAc not only improved the conductivity of SnO2 ETL but also formed a 1D TBAPbI3 layer between the SnO2 ETL and the 3D CsPbI3 all-inorganic perovskite film, thereby enhancing the stability and passivating the surface defects of the CsPbI3 perovskite to fabricate high-efficiency carbon-counter electrode (CE)-based CsPbI3 solar cells. We fabricated carbon-CE-based hole-transporting layer ( HTL)-free PSCs with an FTO/SnO2/TBAAc/CsPbI3/C structure. The open-circuit voltage (Voc), short circuit current density (Jsc), PCE, and fill factor of the champion CsPbI3 PSCs simultaneously enhanced to 1.08 V, 17.48 mA/cm2, 12.79, and 67.8%, respectively. This PCE is currently one of the high efficiencies reported for the above planar-structured carbon-CE-based CsPbI3 PSCs to date. Moreover, the optimized device exhibits excellent stability, which retained over 83% of its initial PCE after 350 h. This work provides a facile way of simultaneous optimization of the SnO2 ETL and the CsPbI3 perovskite layer to fabricate stable and high-efficiency carbon-CE-based CsPbI3 PSCs.

Selective suppression of melanoma lacking IFN-γ pathway by JAK inhibition depends on T cells and host TNF signaling.

Therapeutic resistance to immune checkpoint blockers (ICBs) in melanoma patients is a pressing issue, of which tumor loss of IFN-γ signaling genes is a major underlying mechanism. However, strategies of overcoming this resistance mechanism have been largely elusive. Moreover, given the indispensable role of tumor-infiltrating T cells (TILs) in ICBs, little is known about how tumor-intrinsic loss of IFN-γ signaling (IFNγR1KO) impacts TILs. Here, we report that IFNγR1KO melanomas have reduced infiltration and function of TILs. IFNγR1KO melanomas harbor a network of constitutively active protein tyrosine kinases centered on activated JAK1/2. Mechanistically, JAK1/2 activation is mediated by augmented mTOR. Importantly, JAK1/2 inhibition with Ruxolitinib selectively suppresses the growth of IFNγR1KO but not scrambled control melanomas, depending on T cells and host TNF. Together, our results reveal an important role of tumor-intrinsic IFN-γ signaling in shaping TILs and manifest a targeted therapy to bypass ICB resistance of melanomas defective of IFN-γ signaling.

Structural insights into serine-rich fimbriae from Gram-positive bacteria.

The serine-rich repeat family of fimbriae play important roles in the pathogenesis of streptococci and staphylococci. Despite recent attention, their finer structural details and precise adhesion mechanisms have yet to be determined. Fap1 (Fimbriae-associated protein 1) is the major structural subunit of serine-rich repeat fimbriae from Streptococcus parasanguinis and plays an essential role in fimbrial biogenesis, adhesion, and the early stages of dental plaque formation. Combining multidisciplinary, high resolution structural studies with biological assays, we provide new structural insight into adhesion by Fap1. We propose a model in which the serine-rich repeats of Fap1 subunits form an extended structure that projects the N-terminal globular domains away from the bacterial surface for adhesion to the salivary pellicle. We also uncover a novel pH-dependent conformational change that modulates adhesion and likely plays a role in survival in acidic environments.

A novel red-emitting phosphor Mg2Y2Al2Si2O12:Ce3+/Mn2+ for blue chip-based white LEDs.

Traditional white light-emitting diodes (LEDs) (blue chip + YAG:Ce3+ yellow phosphor) have the limitation of red deficiency, which limits their application in the illumination field. The single cation/anion substitution or co-doping of activators can increase the red component; however, the large energy loss is attributed to the ultra-long Stokes shift and energy transfer. This work attempts to utilize the short-distance Stokes shift and a small amount of energy transfer to increase the red component in two steps. First, based on a large number of previous research results, the Mg2Y2Al2Si2O12:Ce3+ phosphor is selected. Second, additional enhancement of the red component in the emission spectrum was achieved by ion co-doping Mn2+ into Mg2Y2Al2Si2O12:Ce3+. The emission peaks for samples Mg2Y2Al2Si2O12:Ce3+,Mn2+ shift from 600 to 635 nm with increase in the concentration of Mn2+, and the emission spectra intensity of Mg1.97Y1.93Al2Si2O12:0.07 Ce3+,0.03 Mn2+ anomalously increased by ∼37%, which was attributed to the increase in the distance between Ce3+ ions because of the doping of Mn2+ ions, and reduction in the concentration of defects in the crystal, resulting in the energy loss decreases of Ce3+. The emission peak of Mg1.97Y1.93Al2Si2O12:0.07 Ce3+,0.03 Mn2+ shifts to 618 nm and the quantum efficiency was as high as 83.07%. Furthermore, this sample has high thermal stability and the emission intensity was still 80.14% at 120 °C. As such, it has great potential in the application of white LEDs.

Nanoceria have no genotoxic effect on human lens epithelial cells.

There are no treatments for reversing or halting cataract, a disease of the structural proteins in the eye lens, that has associations with other age-related degenerative conditions such as Alzheimer's disease. The incidence of cataract and associated conditions is increasing as the average age of the population rises. Protein folding diseases are difficult to assess in vivo as proteins and their age-related changes are assessed after extraction. Nanotechnology can be used to investigate protein changes in the intact lens as well as for a potential means of drug delivery. Nanoparticles, such as cerium oxide (CeO(2)) which have antioxidant properties, may even be used as a means of treating cataract directly. Prior to use in treatments, nanoparticle genotoxicity must be tested to assess the extent of any DNA or chromosomal damage. Sister chromatid exchanges were measured and DNA damage investigated using the alkaline COMET assay on cultured human lens epithelial cells, exposed to 5 and 10 microg ml(-1) of CeO(2) nanoparticles (nanoceria). Nanoceria at these dosages did not cause any DNA damage or significant increases in the number of sister chromatid exchanges. The absence of genotoxic effects on lens cells suggests that nanoceria, in the doses and exposures tested in this study, are not deleterious to the eye lens and have the potential for use in studying structural alterations, in developing non-surgical cataract treatments and in investigating other protein folding diseases.

Synthesis and luminescence of CePO4:Tb/LaPO4 core/sheath nanowires.

CePO(4):Tb/LaPO(4) nanowires with a core/sheath architecture have been successful synthesized by a facile aqueous chemical method mediated by original CePO(4):Tb aggregation seeds. The seed crystals serve as both a luminescence center and a nucleation site for epitaxial growth. The seed nanocrystals have an irregular sphere-like shape with an average size of around 6.8 nm and a narrow size distribution. When the seed crystals are coated with LaPO(4), the resulting core/sheath CePO(4):Tb/LaPO(4) nanowires have mean diameters of about 7.6 nm and lengths up to 331 nm. Both photo- and x-ray luminescence demonstrate that the LaPO(4) coating increases the luminescence efficiency. These core/sheath structured nanowires may find potential applications in solid state lighting, medical imaging and radiation detection.

Luminescence and energy transfer in water soluble CeF3 and CeF3:Tb3+ nanoparticles.

CeF3 and CeF3:Tb3+ water soluble nanoparticles (NPs) were prepared by wet chemistry, and their structure and luminescence properties were studied systematically. The results of XRD indicate that the obtained CeF3 and CeF3:Tb3+ NPs have a hexagonal structure with the P 6(3)/mcm space group. The average size of CeF3 NPs is about 10 nm, and that of CeF3:Tb3+ NPs is about 5.5 nm as measured from transmission electron microscope (TEM). The aqueous solution sample of CeF3 NPs has an emission peaking at 325.5 nm, which is from the 5d-->4f transition of Ce3+, and CeF3:Tb3+ NPs have a broad emission at 355.5 nm, which is from the 5d--4f transition of Ce3+ (325.5 nm), and several sharp emissions in the visible ranges that are from the (5)D4-->7F(J) transition of Tb3+. As the concentration of Tb3+ increases, the emission intensity of Ce3+ decreases gradually, while the emission intensity of Tb3+ first increases and then decreases. Our observations indicate that there is an energy transfer from Ce3+ to Tb3+ in the CeF3:Tb3+ nanoparticles, and the maximal energy transfer rate is estimated to be 93.2% at the Tb3+ concentration of 25%.

Determination of luminescence and occupy sites of Ce3+ in Zn3(BO3)(PO4) by introducing Ca2+ and Mg2+ ions.

Series of (Zn, M)3(BO3)(PO4) (M = Ca, Mg):Ce3+ were synthesized by a high temperature solid state method, and the luminescence properties were investigated. Zn3(BO3)(PO4):Ce3+ presents two emission bands, which shows the different changing trends with increasing Ce3+ concentration. When introduced Mg2+ and Ca2+ into Zn3(BO3)(PO4), (Zn, M)3(BO3)(PO4) (M = Ca, Mg):Ce3+ also shows two emission bands because Ce3+ occupies three kinds of Zn sites and transits from 5d energy level to double ground state. Therefore, the two emission bands of Zn3(BO3)(PO4):Ce3+ should be assigned to the different occupancy sites of Ce3+. Moreover, the selective emission was realized and the emission intensity of Ce3+ was enhanced by the cationic substitution.

Trap distribution and mechanism for near infrared long-afterglow material AlMgGaO4:Cr3.

Near infrared (NIR) long-afterglow materials have attracted much attention due to their high penetration and low destruction in biological tissues. Here, a series of deep red and near infrared materials, AlMgGaO4:xCr3+, were successfully synthesized by a high temperature solid state method. AlMgGaO4 was selected as the host considering its rich antisite defects, which can effectively capture electrons. The emission spectra of AlMgGaO4:xCr3+ range from 680 nm to 1100 nm, which can be nicely decomposed into four Gaussian bands with peaks centered at 706 nm, 723 nm, 916 nm, and 938 nm, respectively. At low temperature (10 K), the emission spectra show there are four emission peaks: a sharp line (peak 1) and broad emission band (peak 2) come from Cr3+ substituting for the regular octahedron [AlO6], and two broad emission bands (peaks 3 and 4) which originate from the spin-allowed transition 4T2(4F) → 4A2(4F) of Cr3+ in the disordered [GaO6] and [MgO6] octahedra, respectively. Remarkably, after removing the excitation source, it exhibited more than 10 hours of afterglow emission which decreased sharply in the first 30 min and then decreased slowly. With an increase in the Cr3+ concentration, the trap depth became shallower due to the generation of the electronic trap centers . The distribution of trap centers and the mechanism of the persistent luminescence have been carefully analyzed and are also discussed.