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BACKGROUND: Monosaccharide transporter (MST) family, as a carrier for monosaccharide transport, plays an important role in carbon partitioning and widely involves in plant growth and development, stress response, and signaling transduction. However, little information on the MST family genes is reported in maize (Zea mays), especially in response to abiotic stresses. In this study, the genome-wide identification of MST family genes was performed in maize. RESULT: A total of sixty-six putative members of MST gene family were identified and divided into seven subfamilies (including SPT, PMT, VGT, INT, pGlcT, TMT, and ERD) using bioinformatics approaches, and gene information, phylogenetic tree, chromosomal location, gene structure, motif composition, and cis-acting elements were investigated. Eight tandem and twelve segmental duplication events were identified, which played an important role in the expansion of the ZmMST family. Synteny analysis revealed the evolutionary features of MST genes in three gramineous crop species. The expression analysis indicated that most of the PMT, VGT, and ERD subfamilies members responded to osmotic and cadmium stresses, and some of them were regulated by ABA signaling, while only a few members of other subfamilies responded to stresses. In addition, only five genes were induced by NaCl stress in MST family. CONCLUSION: These results serve to understand the evolutionary relationships of the ZmMST family genes and supply some insight into the processes of monosaccharide transport and carbon partitioning on the balance between plant growth and development and stress response in maize.
Assuntos
Proteínas de Transporte de Monossacarídeos , Família Multigênica , Filogenia , Proteínas de Plantas , Estresse Fisiológico , Zea mays , Zea mays/genética , Zea mays/fisiologia , Estresse Fisiológico/genética , Proteínas de Transporte de Monossacarídeos/genética , Proteínas de Transporte de Monossacarídeos/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Evolução Molecular , Reguladores de Crescimento de Plantas/farmacologia , Reguladores de Crescimento de Plantas/metabolismo , Regulação da Expressão Gênica de Plantas , Genoma de Planta , Genes de PlantasRESUMO
Cadmium (Cd) pollution in soil poses a global concern due to its serious impacts on human health and ecological security. In plants, tremendous efforts have been made to identify some key genes and pathways in Cd stress responses. However, studies on the roles of epigenetic factors in response to Cd stress were still limited. In the study, we first gain insight into the gene expression dynamics for maize seedlings under 0â¯h, 12â¯h, and 72â¯hâ¯Cd stress. As a result, six distinct groups of genes were identified by hierarchical clustering and principal component analysis. The key pathways associated with 12â¯hâ¯Cd stress were protein modifications including protein ubiquitination, signal transduction by protein phosphorylation, and histone modification. Whereas, under 72â¯h stress, main pathways were involved in biological processes including phenylalanine metabolism, response to oxygen-containing compounds and metal ions. Then to be noted, one of the most highly expressed genes at 12â¯h under Cd treatment is annotated as histone demethylases (ZmJMJ20). The evolutionary tree analysis and domain analysis showed that ZmJMJ20 belonged to the JmjC-only subfamily of the Jumonji-C (JmjC) family, and ZmJMJ20 was conserved in rice and Arabidopsis. After 72â¯h of Cd treatment, the zmjmj20 mutant created by EMS treatment manifested less severe chlorosis/leaf yellowing symptoms compared with wild-type plants, and there was no significant difference in Fv/Fm and φPSII value before and after Cd treatment. Moreover, the expression levels of several photosynthesis-related down-regulated genes in EMS mutant plants were dramatically increased compared with those in wild-type plants at 12â¯h under Cd treatment. Our results suggested that ZmJMJ20 plays an important role in the Cd tolerance response pathway and will facilitate the development of cultivars with improved Cd stress tolerance.
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Cádmio , Perfilação da Expressão Gênica , Regulação da Expressão Gênica de Plantas , Poluentes do Solo , Estresse Fisiológico , Zea mays , Zea mays/genética , Zea mays/efeitos dos fármacos , Cádmio/toxicidade , Poluentes do Solo/toxicidade , Estresse Fisiológico/efeitos dos fármacos , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Histona Desmetilases/genética , Histona Desmetilases/metabolismo , Proteínas de Plantas/genética , Proteínas de Plantas/metabolismo , Plântula/efeitos dos fármacos , Plântula/genéticaRESUMO
Advancing electronics to interact with tissue necessitates meeting material constraints in electrochemical, electrical, and mechanical domains simultaneously. Clinical bioelectrodes with established electrochemical functionalities are rigid and mechanically mismatched with tissue. Whereas conductive materials with tissue-like softness and stretchability are demonstrated, when applied to electrochemically probe tissue, their performance is distorted by strain and corrosion. We devise a layered architectural composite design that couples strain-induced cracked films with a strain-isolated out-of-plane conductive pathway and in-plane nanowire networks to eliminate strain effects on device electrochemical performance. Accordingly, we developed a library of stretchable, highly conductive, and strain-insensitive bioelectrodes featuring clinically established brittle interfacial materials (iridium-oxide, gold, platinum, and carbon). We paired these bioelectrodes with different electrochemical probing methods (amperometry, voltammetry, and potentiometry) and demonstrated strain-insensitive sensing of multiple biomarkers and in vivo neuromodulation.
Assuntos
Materiais Biocompatíveis , Elastômeros , Neuroestimuladores Implantáveis , Condutividade Elétrica , Eletrônica , Animais , CamundongosRESUMO
The sugar will eventually be exported transporters (SWEET) family is an important group of transport carriers for carbon partitioning in plants and has important functions in growth, development, and abiotic stress tolerance. Although the SWEET family is an important sugar transporter, little is known of the functions of the SWEET family in maize (Zea mays), especially in response to abiotic stresses. To further explore the response pattern of maize SWEET to abiotic stress, a bioinformatics-based approach was used to predict and identify the maize SWEET gene (ZmSWEET) family. Twenty-four ZmSWEET genes were identified using the MaizeGDB database. Phylogenetic analysis resolved these twenty-four genes into four clades. One tandem and five segmental duplication events were identified, which played a major role in ZmSWEET family expansion. Synteny analysis provided insight into the evolutionary characteristics of the ZmSWEET genes with those of three graminaceous crop species. A heatmap showed that most ZmSWEET genes responded to at least one type of abiotic stress. By an abscisic acid signaling pathway, among which five genes were significantly induced under NaCl treatment, eight were obviously up-regulated under PEG treatment and five were up-regulated under Cd stress, revealing their potential functions in response to abiotic stress. These findings will help to explain the evolutionary links of the ZmSWEET family and contribute to future studies on the functional characteristics of ZmSWEET genes, and then improve abiotic stress tolerance in maize through molecular breeding.
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Regulação da Expressão Gênica de Plantas , Zea mays , Zea mays/genética , Zea mays/metabolismo , Regulação da Expressão Gênica de Plantas/genética , Ácido Abscísico/farmacologia , Ácido Abscísico/metabolismo , Cloreto de Sódio/metabolismo , Proteínas de Plantas/metabolismo , Filogenia , Família Multigênica , Cádmio/metabolismo , Estresse Fisiológico/genética , Proteínas de Membrana Transportadoras/genética , Hormônios , Carbono/metabolismo , Açúcares/metabolismoRESUMO
Therapeutic drug monitoring is essential for dosing pharmaceuticals with narrow therapeutic windows. Nevertheless, standard methods are imprecise and involve invasive/resource-intensive procedures with long turnaround times. Overcoming these limitations, we present a microneedle-based electrochemical aptamer biosensing patch (µNEAB-patch) that minimally invasively probes the interstitial fluid (ISF) and renders correlated, continuous, and real-time measurements of the circulating drugs' pharmacokinetics. The µNEAB-patch is created following an introduced low-cost fabrication scheme, which transforms a shortened clinical-grade needle into a high-quality gold nanoparticle-based substrate for robust aptamer immobilization and efficient electrochemical signal retrieval. This enables the reliable in vivo detection of a wide library of ISF analytes-especially those with nonexistent natural recognition elements. Accordingly, we developed µNEABs targeting various drugs, including antibiotics with narrow therapeutic windows (tobramycin and vancomycin). Through in vivo animal studies, we demonstrated the strong correlation between the ISF/circulating drug levels and the device's potential clinical use for timely prediction of total drug exposure.
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The awareness of individuals' biological status is critical for creating interactive and adaptive environments that can actively assist the users to achieve optimal outcomes. Accordingly, specialized humanmachine interfacesequipped with bioperception and interpretation capabilitiesare required. To this end, we devised a multimodal cryptographic bio-humanmachine interface (CB-HMI), which seamlessly translates the user's touch-based entries into encrypted biochemical, biophysical, and biometric indices. As its central component, the CB-HMI features thin hydrogel-coated chemical sensors and inference algorithms to noninvasively and inconspicuously acquire biochemical indices such as circulating molecules that partition onto the skin (here, ethanol and acetaminophen). Additionally, the CB-HMI hosts physical sensors and associated algorithms to simultaneously acquire the user's heart rate, blood oxygen level, and fingerprint minutiae pattern. Supported by human subject studies, we demonstrated the CB-HMI's capability in terms of acquiring physiologically relevant readouts of target bioindices, as well as user-identifying and biometrically encrypting/decrypting these indices in situ (leveraging the fingerprint feature). By upgrading the common surrounding objects with the CB-HMI, we created interactive solutions for driving safety and medication use. Specifically, we demonstrated a vehicle-activation system and a medication-dispensing system, where the integrated CB-HMI uniquely enabled user bioauthentication (on the basis of the user's biological state and identity) prior to rendering the intended services. Harnessing the levels of bioperception achieved by the CB-HMI and other intelligent HMIs, we can equip our surroundings with a comprehensive and deep awareness of individuals' psychophysiological state and needs.
Assuntos
Condução de Veículo , Percepção do Tato , Interface Usuário-Computador , Humanos , TatoRESUMO
Objective: To analyze the factors influencing the distribution of 131-I in the liver of patients with advanced hepatic carcinoma treated with the combination of Licartin (131I Metuximab) and transcatheter arterial chemoembolization (TACE). This study provides a reference and basis for the clinic on how to choose the best time for the treatment of Licartin and how to reduce other possible factors affecting the role of Licartin. Methods: Data from 41 patients with advanced hepatic carcinoma treated with the combination of Licartin and TACE in the Interventional Department of our hospital from March 2014 to December 2020 were collected. This included general characteristics, history of open and interventional surgery, interval between the last interventional surgery and the Licartin treatment, selected arteries in the Licartin perfusion, and 131-I distribution in the liver. Regression analysis was conducted to investigate the factors affecting the distribution of 131I in the liver. Results: In 14 cases (34.1%), 131-I was evenly distributed in the liver, and there was no correlation between the cause of even distribution with age(OR=0.961, P = 0.939), previous open surgery history(OR=3.547,P= 0.128), previous history of interventional therapy(OR=0.140,P = 0.072), the interval between the last interventional surgery and the Licartin treatment(OR=0.858,P = 0.883), or the choice of the perfusion artery in the Licartin treatment (OR=1.489,P = 0.419). In 14 cases (34.1%), there was higher aggregation in the tumor than in the normal liver, which was related to previous interventional surgery (OR=7.443,P = 0.043). In 13 cases (31.7%), there was lower aggregation in the tumor than in the normal liver, which was related to the selected vessels in the Licartin perfusion (OR=0.23,P = 0.013). Conclusion: The effective aggregation of 131-I in the liver, even in tumors, the previous history of TACE, and the choice of vessels in the Licartin infusion might be the factors influencing the distribution of 131-I in the liver during hepatic artery infusion of Licartin in combination with TACE therapy.
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Papillary thyroid cancer (PTC) is a common tumor malignancy of the endocrine system worldwide. Recently, circular RNAs (circRNAs) have been reported to participate in diverse pathological processes, especially in tumorigenesis. However, the functional role and mechanism of circRNA pleckstrin and Sec7 domain containing 3 (circ-PSD3) in PTC are still unclear. In this study, qRT-PCR results showed that circ-PSD3 was significantly upregulated in PTC tissues and cell lines. Meanwhile, circ-PSD3 overexpression was positively associated with larger tumor size, TNM stage, and lymph node metastasis. Knockdown of circ-PSD3 suppressed the proliferation and invasion of PTC cells. Besides, circ-PSD3 interacted with miR-7-5p to reduce its expression, and methyltransferase like 7B (METTL7B) was verified as a target gene of miR-7-5p. Functionally, inhibition of circ-PSD3 impeded PTC cell proliferation and invasion via targeting miR-7-5p to downregulate METTL7B expression. Taken together, silencing of circ-PSD3 hampered the proliferation and invasion of PTC cells via upregulating the inhibitory effect of miR-7-5p on METTL7B expression. Therefore, circ-PSD3 could be a potential diagnostic biomarker or molecular treatment target for PTC.
Assuntos
MicroRNAs , Neoplasias da Glândula Tireoide , Proteínas de Transporte , Linhagem Celular Tumoral , Proliferação de Células/genética , Humanos , MicroRNAs/genética , MicroRNAs/metabolismo , RNA Circular/genética , Câncer Papilífero da Tireoide/genética , Câncer Papilífero da Tireoide/metabolismo , Câncer Papilífero da Tireoide/patologia , Neoplasias da Glândula Tireoide/genética , Neoplasias da Glândula Tireoide/patologiaRESUMO
Active biofluid management is central to the realization of wearable bioanalytical platforms that are poised to autonomously provide frequent, real-time, and accurate measures of biomarkers in epidermally-retrievable biofluids (e.g., sweat). Accordingly, here, a programmable epidermal microfluidic valving system is devised, which is capable of biofluid sampling, routing, and compartmentalization for biomarker analysis. At its core, the system is a network of individually-addressable microheater-controlled thermo-responsive hydrogel valves, augmented with a pressure regulation mechanism to accommodate pressure built-up, when interfacing sweat glands. The active biofluid control achieved by this system is harnessed to create unprecedented wearable bioanalytical capabilities at both the sensor level (decoupling the confounding influence of flow rate variability on sensor response) and the system level (facilitating context-based sensor selection/protection). Through integration with a wireless flexible printed circuit board and seamless bilateral communication with consumer electronics (e.g., smartwatch), contextually-relevant (scheduled/on-demand) on-body biomarker data acquisition/display was achieved.
Assuntos
Biomarcadores/análise , Técnicas Analíticas Microfluídicas/métodos , Microfluídica , Técnicas Biossensoriais , Epiderme/química , Humanos , Suor/química , Dispositivos Eletrônicos VestíveisRESUMO
To achieve the mission of personalized medicine, centering on delivering the right drug to the right patient at the right dose, therapeutic drug monitoring solutions are necessary. In that regard, wearable biosensing technologies, capable of tracking drug pharmacokinetics in noninvasively retrievable biofluids (e.g., sweat), play a critical role, because they can be deployed at a large scale to monitor the individuals' drug transcourse profiles (semi)continuously and longitudinally. To this end, voltammetry-based sensing modalities are suitable, as in principle they can detect and quantify electroactive drugs on the basis of the target's redox signature. However, the target's redox signature in complex biofluid matrices can be confounded by the immediate biofouling effects and distorted/buried by the interfering voltammetric responses of endogenous electroactive species. Here, we devise a wearable voltammetric sensor development strategy-centering on engineering the molecule-surface interactions-to simultaneously mitigate biofouling and create an "undistorted potential window" within which the target drug's voltammetric response is dominant and interference is eliminated. To inform its clinical utility, our strategy was adopted to track the temporal profile of circulating acetaminophen (a widely used analgesic and antipyretic) in saliva and sweat, using a surface-modified boron-doped diamond sensing interface (cross-validated with laboratory-based assays, R2 â¼ 0.94). Through integration of the engineered sensing interface within a custom-developed smartwatch, and augmentation with a dedicated analytical framework (for redox peak extraction), we realized a wearable solution to seamlessly render drug readouts with minute-level temporal resolution. Leveraging this solution, we demonstrated the pharmacokinetic correlation and significance of sweat readings.
Assuntos
Acetaminofen/análise , Monitoramento de Medicamentos/métodos , Saliva/química , Suor/química , Acetaminofen/administração & dosagem , Técnicas Biossensoriais/instrumentação , Técnicas Biossensoriais/métodos , Monitoramento de Medicamentos/instrumentação , Humanos , Medicina de Precisão , Dispositivos Eletrônicos VestíveisRESUMO
A vast amount of evidence indicates that long non-coding RNAs (lncRNAs) are involved in cancer. Previous studies have indicated that lncRNA DiGeorge syndrome critical region gene 5 (DGCR5) is aberrantly expressed in lung cancer, pancreatic ductal adenocarcinoma and hepatocellular carcinoma. However, the role of DGCR5 in papillary thyroid carcinoma (PTC) has remained elusive. In the present study, it was revealed that DGCR5 was significantly downregulated in PTC tissues compared with that in adjacent normal tissues. Through functional experiments, it was demonstrated that ectopic overexpression of DGCR5 markedly suppressed PTC cell growth and invasion. A bioinformatics analysis suggested that DGCR5 binds to microRNA (miR)-2861. A total of 5 putative binding sites for miR-2861 were identified in DGCR5, and a luciferase reporter assay confirmed the direct interaction between DGCR5 and miR-2861. Furthermore, reverse transcription-quantitative polymerase chain reaction analysis indicated that ectopic overexpression of DGCR5 led to a decreased expression of miR-2861 in PTC cells and miR-2861 mimic transfection caused a downregulation of DGCR5. miR-2861 level was upregulated in PTC tissues compared with adjacent tissues and negatively correlated with DGCR5 level. In addition, rescue experiments indicated that ectopic expression of miR-2861 reversed the effects of DGCR5 overexpression on PTC cell proliferation and invasion. Taken together, the present results demonstrated that DGCR5 inhibits PTC progression via sponging miR-2861, indicating DGCR5 may serve as a therapeutic target.
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Considering the resistance of papillary thyroid cancer (PTC) 131I therapy, this study was designed to find a solution at molecular respect. By probing into lncRNA-NEAT1/miR-101-3p/FN1 axis and PI3K/AKT signaling pathway, this study provided a potential target for PTC therapy. 131I-resistant cell lines were established by continuous treatment with median-lethal 131I. Bioinformatic analysis was applied to filtrate possible lncRNA/miRNA/mRNA and related signaling pathway. Luciferase reporter assay was employed in the verification of the targeting relationship between lncRNA and miRNA as well as miRNA and mRNA. MTT assay and flow cytometry assay were performed to observe the impact of NEAT1/miR-101-3p/FN1 on cell viability and apoptosis in radioactivity iodine (RAI)-resistant PTC cell lines, respectively. Western blot and qRT-PCR were conducted to measure the expression of proteins and mRNAs in RAI-resistant PTC tissues and cells. Meanwhile, endogenous PTC mice model were constructed, in order to verify the relation between NEAT1 and RAI-resistance in vivo. NEAT1 was over-expressed in RAI-resistant PTC tissues and cell lines and could resist RAI by accelerating proliferation accompanied by suppressing apoptosis. It indicated that overexpressed NEAT1 restrained the damage of RAI to tumor in both macroscopic and microcosmic. Besides, NEAT1/miR-101-3p exhibited a negative correlation by directly targeting each other. The expression of FN1, an overexpressed downstream protein in RAI-resistance PTC tissues, could be tuned down by miR-101-3p, while the decrease could be restored by NEAT1. In conclusion, both in vitro and in vivo, NEAT1 suppression could inhibit 131I resistance of PTC by upregulating miR-101-3p/FN1 expression and inactivated PI3K/AKT signaling pathway both in vitro and in vivo.
Assuntos
Resistencia a Medicamentos Antineoplásicos/genética , Fibronectinas/metabolismo , Radioisótopos do Iodo/farmacologia , MicroRNAs/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , RNA Longo não Codificante/metabolismo , Câncer Papilífero da Tireoide/metabolismo , Neoplasias da Glândula Tireoide/metabolismo , Animais , Apoptose/genética , Linhagem Celular Tumoral , Sobrevivência Celular/genética , Modelos Animais de Doenças , Técnicas de Silenciamento de Genes , Humanos , Camundongos , Camundongos Nus , Camundongos Transgênicos , RNA Longo não Codificante/genética , TransfecçãoRESUMO
OBJECTIVE: To identify the significantly altered circRNAs and mRNAs in thyroid cancer, investigate their target miRNAs and determine their biological functions. METHODS: The differentially expressed circRNAs, mRNAs and pathways in thyroid cancer were identified by microarray analysis and gene set enrichment analysis (GSEA). The correlative circRNAs and mRNAs were found out through Pearson correlative analysis. The common target miRNAs of circNEK6 and FZD8 related to thyroid cancer was screened out through Targetscan, miRanda and HMDD analysis. The mRNA and protein expressions in thyroid cancer tissues and cells were detected by qRT-PCR and western blot. CircRNA was confirmed by the RNase R digestion and nucleic acid electrophoresis. The target relationships were verified by the dual luciferase reporter assay. Cell viability, invasion and apoptosis were determined by MTT assay, Transwell assay and flow cytometry, respectively. RESULTS: CircNEK6 and FZD8 were significantly up-regulated in thyroid cancer, with strong correlations. The Wnt signaling pathway was activated in thyroid cancer. MiR-370-3p was the common target miRNA of circNEK6 and FZD8, and it was down-regulated in thyroid cancer. Overexpression of circNEK6 and FZD8 could promote the growth and invasion of thyroid cancer cells, while up-regulation of miR-370-3p could suppress thyroid cancer progression and inhibit the Wnt signaling pathway. MiR-370-3p's effect on thyroid cancer cells could be rescued by circNEK6 or FZD8. CONCLUSION: CircNEK6 promoted the progression of thyroid cancer through up-regulating FZD8 and activating Wnt signaling pathway by targeting miR-370-3p.
Assuntos
MicroRNAs/genética , Interferência de RNA , RNA/genética , Neoplasias da Glândula Tireoide/genética , Neoplasias da Glândula Tireoide/metabolismo , Via de Sinalização Wnt , Sítios de Ligação , Linhagem Celular Tumoral , Movimento Celular/genética , Proliferação de Células/genética , Sobrevivência Celular/genética , Perfilação da Expressão Gênica , Regulação Neoplásica da Expressão Gênica , Redes Reguladoras de Genes , Humanos , Modelos Biológicos , Quinases Relacionadas a NIMA/genética , RNA Circular , Neoplasias da Glândula Tireoide/patologiaRESUMO
Thyroid carcinoma is primarily treated by surgery combined with radioactive 131iodine (131I) treatment; however, certain patients exhibit resistance to 131I treatment. Previous research indicated that nuclear factorκB (NFκB) was associated with resistance to 131I in cancer cells. The present study aimed to investigate the effects of NFκB on 131I uptake and apoptosis in thyroid carcinoma cells. TPC1 and BCPAP cell lines were employed as research models in the present study, and the expression of NFκB was inhibited by RNA interference (RNAi). The ability of TPC1 and BCPAP cells to uptake 131I was measured and the cell viability was detected by an MTT assay. Finally, the expression of the apoptosisassociated proteins Xlinked inhibitor of apoptosis (XIAP), cellular inhibitor of apoptosis protein 1 (cIAP1) and caspase3 in TCP1 and BCPAP cells was determined by western blotting. Western blotting results demonstrated that the expression levels of NFκB in TPC1 and BCPAP cells were successfully downregulated by RNAi (P<0.05), while analysis of 131I uptake revealed no significant alterations in the 131I uptake ability of cells following RNAi (P>0.05). MTT experiments demonstrated that the inhibition of NFκB expression in combination with radiation (131I treatment) led to a marked reduction in cell viability (P<0.05). Furthermore, western blot analysis revealed that the inhibition of NFκB expression downregulated the expression levels of XIAP and cIAP1 (P<0.05), while the expression levels of caspase3 were upregulated, indicating that the observed reduction in cell viability following NFκB inhibition may be due to an increased level of apoptosis. Although NFκB inhibition did not affect the 131I uptake of thyroid cancer cells, this inhibition may increase the apoptotic effects of radioactive 131I.
Assuntos
Apoptose , Radioisótopos do Iodo/metabolismo , NF-kappa B/metabolismo , Neoplasias da Glândula Tireoide/metabolismo , Proteínas Reguladoras de Apoptose/metabolismo , Linhagem Celular Tumoral , Sobrevivência Celular , Expressão Gênica , Humanos , NF-kappa B/genética , Interferência de RNA , Neoplasias da Glândula Tireoide/genética , Neoplasias da Glândula Tireoide/patologiaRESUMO
Yb, Er co-doped Y2SiO5 inverse opal photonic crystals with three-dimensionally ordered macroporous were fabricated using polystyrene colloidal crystals as the template. Under 980 nm excitation, the effect of the photonic stopband on the upconversion luminescence of Er3+ ions has been investigated in the Y2SiO5:Yb, Er inverse opals. Significant suppression of the green or red UC emissions was detected if the photonic band-gap overlaps with the Er3+ ions emission band.
RESUMO
Upconversion luminescence properties of Yb-Tb codoped Bi4Ti3O12 inverse opals have been investigated. The results show that the upconversion emission can be modulated by the photonic band gap. More significantly, in the upconversion inverse opals, the excited-state absorption of Tb3+ is greatly enhanced by the suppression of upconversion spontaneous emissions of the intermediate excited state, and thus the short wavelength upconversion emission from Tb3+ is considerably improved. We believe that the present work will be valuable for not only the foundational study of upconversion emission modifications but also new optical devices in upconversion displays and short wavelength upconversion lasers.