Flavones provide resistance to DUX4-induced toxicity via an mTor-independent mechanism.

Facioscapulohumeral muscular dystrophy (FSHD) is among the most common of the muscular dystrophies, affecting nearly 1 in 8000 individuals, and is a cause of profound disability. Genetically, FSHD is linked to the contraction and/or epigenetic de-repression of the D4Z4 repeat array on chromosome 4, thereby allowing expression of the DUX4 gene in skeletal muscle. If the DUX4 transcript incorporates a stabilizing polyadenylation site the myotoxic DUX4 protein will be synthesized, resulting in muscle wasting. The mechanism of toxicity remains unclear, as many DUX4-induced cytopathologies have been described, however cell death does primarily occur through caspase 3/7-dependent apoptosis. To date, most FSHD therapeutic development has focused on molecular methods targeting DUX4 expression or the DUX4 transcript, while therapies targeting processes downstream of DUX4 activity have received less attention. Several studies have demonstrated that inhibition of multiple signal transduction pathways can ameliorate DUX4-induced toxicity, and thus compounds targeting these pathways have the potential to be developed into FSHD therapeutics. To this end, we have screened a group of small molecules curated based on their reported activity in relevant pathways and/or structural relationships with known toxicity-modulating molecules. We have identified a panel of five compounds that function downstream of DUX4 activity to inhibit DUX4-induced toxicity. Unexpectedly, this effect was mediated through an mTor-independent mechanism that preserved expression of ULK1 and correlated with an increase in a marker of active cellular autophagy. This identifies these flavones as compounds of interest for therapeutic development, and potentially identifies the autophagy pathway as a target for therapeutics.

Deep Mutational Scanning in Disease-related Genes with Saturation Mutagenesis-Reinforced Functional Assays (SMuRF).

Interpretation of disease-causing genetic variants remains a challenge in human genetics. Current costs and complexity of deep mutational scanning methods hamper crowd-sourcing approaches toward genome-wide resolution of variants in disease-related genes. Our framework, Saturation Mutagenesis-Reinforced Functional assays (SMuRF), addresses these issues by offering simple and cost-effective saturation mutagenesis, as well as streamlining functional assays to enhance the interpretation of unresolved variants. Applying SMuRF to neuromuscular disease genes FKRP and LARGE1, we generated functional scores for over 99.8% of all possible coding single nucleotide variants and resolved 310 clinically reported variants of uncertain significance with high confidence, enhancing clinical variant interpretation in dystroglycanopathies. SMuRF also demonstrates utility in predicting disease severity, resolving critical structural regions, and providing training datasets for the development of computational predictors. Our approach opens new directions for enabling variant-to-function insights for disease genes in a manner that is broadly useful for crowd-sourcing implementation across standard research laboratories.

Death after High-Dose rAAV9 Gene Therapy in a Patient with Duchenne's Muscular Dystrophy.

We treated a 27-year-old patient with Duchenne's muscular dystrophy (DMD) with recombinant adeno-associated virus (rAAV) serotype 9 containing dSaCas9 (i.e., "dead" Staphylococcus aureus Cas9, in which the Cas9 nuclease activity has been inactivated) fused to VP64; this transgene was designed to up-regulate cortical dystrophin as a custom CRISPR-transactivator therapy. The dose of rAAV used was 1×1014 vector genomes per kilogram of body weight. Mild cardiac dysfunction and pericardial effusion developed, followed by acute respiratory distress syndrome (ARDS) and cardiac arrest 6 days after transgene treatment; the patient died 2 days later. A postmortem examination showed severe diffuse alveolar damage. Expression of transgene in the liver was minimal, and there was no evidence of AAV serotype 9 antibodies or effector T-cell reactivity in the organs. These findings indicate that an innate immune reaction caused ARDS in a patient with advanced DMD treated with high-dose rAAV gene therapy. (Funded by Cure Rare Disease.).

Functional Characterization of MC4R Variants in Chinese Morbid Obese Patients and Weight Loss after Bariatric Surgery.

Mutations in MC4R are the most common genetic cause of obesity. In the reported Chinese morbid obesity cohort, 10 out of 59 harbor six MC4R variants, including Y35C, T53I, V103I, R165W, G233S, and C277X, among which V103I has a relatively high frequency, while other five variants are rare in the population. The prevalence of MC4R carriers in Chinese morbid obese patients (body mass index ≥ 45 kg m-2 ) is detected as 16.9% in this study. R165W and C277X are loss-of-function variants. The patient with R165W achieves excess weight loss (%EWL) as high as 20.6% and 50.3% at 1 and 8 months after surgery, respectively. G233S is reported for the first time in Asia obese population. The patient harboring G233S has a %EWL as 23.3% one month postsurgery. It is concluded that morbid obese patients with rare MC4R variants can benefit from metabolic surgery. More importantly, the choice of surgery procedure and MC4R variant should be taken into consideration for personalized treatment. In the future, a larger size cohort, accompanied with regular and longer follow-up, would be helpful.

Flavones provide resistance to DUX4-induced toxicity via an mTor-independent mechanism.

Facioscapulohumeral muscular dystrophy (FSHD) is among the most common of the muscular dystrophies, affecting nearly 1 in 8000 individuals, and is a cause of profound disability. Genetically, FSHD is linked to the contraction and/or epigenetic de-repression of the D4Z4 repeat array on chromosome 4, thereby allowing expression of the DUX4 gene in skeletal muscle. If the DUX4 transcript incorporates a stabilizing polyadenylation site the myotoxic DUX4 protein will be synthesized, resulting in muscle wasting. The mechanism of toxicity remains unclear, as many DUX4-induced cytopathologies have been described, however cell death does primarily occur through caspase 3/7-dependent apoptosis. To date, most FSHD therapeutic development has focused on molecular methods targeting DUX4 expression or the DUX4 transcript, while therapies targeting processes downstream of DUX4 activity have received less attention. Several studies have demonstrated that inhibition of multiple signal transduction pathways can ameliorate DUX4-induced toxicity, and thus compounds targeting these pathways have the potential to be developed into FSHD therapeutics. To this end, we have screened a group of small molecules curated based on their reported activity in relevant pathways and/or structural relationships with known toxicity-modulating molecules. We have identified a panel of five compounds that function downstream of DUX4 activity to inhibit DUX4-induced toxicity. Unexpectedly, this effect was mediated through an mTor-independent mechanism that preserved expression of ULK1 and correlated with an increase in a marker of active cellular autophagy. This identifies these flavones as compounds of interest for therapeutic development, and potentially identifies the autophagy pathway as a target for therapeutics.

A new phenotype of syndromic retinitis pigmentosa with myopathy is caused by mutations in retinol dehydrogenase 11.

Retinol dehydrogenase 11 (RDH11) is an 11-cis-retinol dehydrogenase that has a well-characterized, albeit auxiliary role in the retinoid cycle. Diseases caused by mutations in the RDH11 gene are very rare, and only one affected family with eye and intelligence involvement has been reported. In the present study, we describe the clinical and genetic findings in a Chinese patient with retinitis pigmentosa (RP), juvenile cataracts, intellectual disability, and myopathy. Trio-based whole-exome sequencing and whole genomic copy number variation detection were performed in this family, and compound heterozygous mutations were identified in RDH11 of the patient: c.938T>C (p.Leu313Pro) derived from the father and c.75-3C>A derived from the mother. Variant c.75-3C>A was confirmed to be a splice-site mutation by cDNA sequencing. It caused exon 2 skipping, resulting in a frameshift mutation and premature translation termination (p.Lys26Serfs*38). Moreover, we found mislocalization of RDH11 protein in muscle cells of the patient by using immunofluorescence staining. This is the first case reported in the Chinese population harboring mutations in RDH11 and revealing a new phenotype of syndromic RP with myopathy.

Phosphorus- and fluorine-co-doped carbon nitride: modulated visible light absorption, charge carrier kinetics and boosted photocatalytic hydrogen evolution.

A phosphorus and fluorine co-doped carbon nitride (PF-CN) photocatalyst was synthesized to modulate the band gap structure, visible light response ability and photocatalytic H2 evolution activity. Experimental results demonstrated that the electronic structure of g-C3N4 was regulated by phosphorus replacing the C site and fluorine substituting the N site in the g-C3N4 framework to form P-N species and C-F bonds, respectively. P- and F-co-doped carbon nitride gave rise to a more negative conduction band potential, larger surface area, efficient separation of photogenerated charge carriers and a faster charge transfer rate, contributing to an enhancement of photocatalytic H2 production activity. PF-CN achieved an optimal H2 evolution activity of 1690.56 µmol g-1 which was 17.83 times higher with respect to that of pristine g-C3N4 (94.81 µmol g-1). Meanwhile, PF-CN achieved the highest apparent quantum efficiency of 3.76% at 435 nm.

Effectiveness of companion-intensive multi-aspect weight management in Chinese adults with obesity: a 6-month multicenter randomized clinical trial.

BACKGROUND: Obesity is a globally increasing health epidemic requiring early lifestyle intervention. Our main objective was to examine the effectiveness of companion-intensive multi-aspect weight management (CIMWM) in Chinese adults with obesity. METHODS: In this 6-month, prospective, open-label, multicenter, randomized controlled clinical trial, we recruited 272 obese adults aged 18-50 years with a body mass index (BMI) ≥ 28.0 kg/m2 and capable of using smartphones. CIMWM (n = 136) offered both daily online instructions and monthly face-to-face guidance by physicians, dietitians, and health managers along with the provision of meal replacements in the first 3 months. Traditional multi-aspect weight management (TMWM, n = 136) provided monthly face-to-face guidance by the same panel of professionals and the same meal replacements as CIMWM group, but required subjects to complete daily self-monitoring instead of offering daily online instructions. Body composition and metabolic parameters were assessed at baseline, 1, 2, 3, and 6 months by physicians. The primary outcomes were clinically-significant weight loss and changes in BMI and body composition. RESULTS: Participants in both groups showed significantly reduced BMI, body fat mass (BFM), visceral fat area (VFA), and HOMA-IR (p < 0.05). CIMWM was shown to be superior to TMWM in the improvement of clinically-significant weight loss, BMI, total cholesterol (TC), the body composition parameters BFM and the skeletal muscle mass-to-visceral fat area ratio (S/V) (p < 0.05). The non-alcoholic fatty liver disease score (NFS) was negatively related to S/V at baseline. After weight management, NFS was lowered among individuals with levels in the highest tertile (p < 0.05). Metabolic memory in terms of the continuous reduction of BMI, BFM, and TC was retained up to 6 months in spite of participants transferring to self-monitoring assessment in the final 3 months. CONCLUSIONS: The CIMWM strategy in obese Chinese adults is proved to be more effective than TMWM in weight loss, and motivates greater adherence to intervention and lifestyle reprogramming. Trial registration Chinese Clinical Trial Registry, ChiCTR1800017463, Registered July 31, 2018. http://www.chictr.org.cn/showproj.aspx?proj=29649 .

Exome sequencing in paediatric patients with movement disorders.

BACKGROUND: Movement disorders are a group of heterogeneous neurological diseases including hyperkinetic disorders with unwanted excess movements and hypokinetic disorders with reduction in the degree of movements. The objective of our study is to investigate the genetic etiology of a cohort of paediatric patients with movement disorders by whole exome sequencing and to review the potential treatment implications after a genetic diagnosis. RESULTS: We studied a cohort of 31 patients who have paediatric-onset movement disorders with unrevealing etiologies. Whole exome sequencing was performed and rare variants were interrogated for pathogenicity. Genetic diagnoses have been confirmed in 10 patients with disease-causing variants in CTNNB1, SPAST, ATP1A3, PURA, SLC2A1, KMT2B, ACTB, GNAO1 and SPG11. 80% (8/10) of patients with genetic diagnosis have potential treatment implications and treatments have been offered to them. One patient with KMT2B dystonia showed clinical improvement with decrease in dystonia after receiving globus pallidus interna deep brain stimulation. CONCLUSIONS: A diagnostic yield of 32% (10/31) was reported in our cohort and this allows a better prediction of prognosis and contributes to a more effective clinical management. The study highlights the potential of implementing precision medicine in the patients.

A three-year follow-up study evaluating clinical utility of exome sequencing and diagnostic potential of reanalysis.

Exome sequencing (ES) has become one of the important diagnostic tools in clinical genetics with a reported diagnostic rate of 25-58%. Many studies have illustrated the diagnostic and immediate clinical impact of ES. However, up to 75% of individuals remain undiagnosed and there is scarce evidence supporting clinical utility beyond a follow-up period of >1 year. This is a 3-year follow-up analysis to our previous publication by Mak et al. (NPJ Genom. Med. 3:19, 2018), to evaluate the long-term clinical utility of ES and the diagnostic potential of exome reanalysis. The diagnostic yield of the initial study was 41% (43/104). Exome reanalysis in 46 undiagnosed individuals has achieved 12 new diagnoses. The additional yield compared with the initial analysis was at least 12% (increased from 41% to at least 53%). After a median follow-up period of 3.4 years, change in clinical management was observed in 72.2% of the individuals (26/36), leading to positive change in clinical outcome in four individuals (11%). There was a minimum healthcare cost saving of HKD$152,078 (USD$19,497; €17,282) annually for these four individuals. There were a total of six pregnancies from five families within the period. Prenatal diagnosis was performed in four pregnancies; one fetus was affected and resulted in termination. None of the parents underwent preimplantation genetic diagnosis. This 3-year follow-up study demonstrated the long-term clinical utility of ES at individual, familial and health system level, and the promising diagnostic potential of subsequent reanalysis. This highlights the benefits of implementing ES and regular reanalysis in the clinical setting.

Double defective group modified nitrogen-deficient carbon nitride with bimetallic PtSn as a cocatalyst for efficient photocatalytic hydrogen evolution up to 765 nm.

Cyano- and urea-defective group co-modified nitrogen-deficient carbon nitride with PtSn as a cocatalyst was constructed to optimize the optical and electronic structure as well as the photocatalytic activity. Defective engineering over carbon nitride gave rise to a stronger light absorption in the visible and near-infrared regions, more negative conduction band edge potential and more efficient separation behavior of photogenerated charge carriers. The optimal photocatalyst exhibited a high hydrogen yield of 2.96 mmol g-1 h-1 with an apparent quantum yield of 8.42% at 435 nm. Moreover, the photocatalytic hydrogen generation capability was maintained under illumination up to 765 nm with an apparent quantum yield of 0.076%.

Applying genome-wide CRISPR-Cas9 screens for therapeutic discovery in facioscapulohumeral muscular dystrophy.

The emergence of CRISPR-Cas9 gene-editing technologies and genome-wide CRISPR-Cas9 libraries enables efficient unbiased genetic screening that can accelerate the process of therapeutic discovery for genetic disorders. Here, we demonstrate the utility of a genome-wide CRISPR-Cas9 loss-of-function library to identify therapeutic targets for facioscapulohumeral muscular dystrophy (FSHD), a genetically complex type of muscular dystrophy for which there is currently no treatment. In FSHD, both genetic and epigenetic changes lead to misexpression of DUX4, the FSHD causal gene that encodes the highly cytotoxic DUX4 protein. We performed a genome-wide CRISPR-Cas9 screen to identify genes whose loss-of-function conferred survival when DUX4 was expressed in muscle cells. Genes emerging from our screen illuminated a pathogenic link to the cellular hypoxia response, which was revealed to be the main driver of DUX4-induced cell death. Application of hypoxia signaling inhibitors resulted in increased DUX4 protein turnover and subsequent reduction of the cellular hypoxia response and cell death. In addition, these compounds proved successful in reducing FSHD disease biomarkers in patient myogenic lines, as well as improving structural and functional properties in two zebrafish models of FSHD. Our genome-wide perturbation of pathways affecting DUX4 expression has provided insight into key drivers of DUX4-induced pathogenesis and has identified existing compounds with potential therapeutic benefit for FSHD. Our experimental approach presents an accelerated paradigm toward mechanistic understanding and therapeutic discovery of a complex genetic disease, which may be translatable to other diseases with well-established phenotypic selection assays.

Steering Charge Kinetics of Tin Niobate Photocatalysts: Key Roles of Phase Structure and Electronic Structure.

Tin niobate photocatalysts with the phase structures of froodite (SnNb2O6) and pyrochlore (Sn2Nb2O7) were obtained by a facile solvothermal method in order to explore the impact of phase structure and electronic structure on the charge kinetics and photocatalytic performance. By employing tin niobate as a model compound, the effects of phase structure over electronic structure, photocatalytic activity toward methyl orange solution and hydrogen evolution were systematically investigated. It is found that the variation of phase structure from SnNb2O6 to Sn2Nb2O7 accompanied with modulation of particle size and band edge potentials that has great consequences on photocatalytic performance. In combination with the electrochemical impedance spectroscopy (EIS), transient photocurrent responses, transient absorption spectroscopy (TAS), and the analysis of the charge-carrier dynamics suggested that variation of electronic structure has great impacts on the charge separation and transfer rate of tin niobate photocatalysts and the subsequent photocatalytic performance. Moreover, the results of the X-ray photoelectron spectroscopy (XPS) indicated that the existent of Sn4+ species in Sn2Nb2O7 could result in a decrease in photocatalytic activity. Photocatalytic test demonstrated that the SnNb2O6 (froodite) catalyst possesses a higher photocatalytic activity toward MO degradation and H2 evolution compared with the sample of Sn2Nb2O7 (pyrochlore). On the basis of spin resonance measurement and trapping experiment, it is expected that photogenerated holes, O2-•, and OH• active species dominate the photodegradation of methyl orange.

Validation of the simplified Chinese version of the quality of life questionnaire of the European foundation for osteoporosis (QUALEFFO-31).

PURPOSE: To translate quality of life questionnaire of the European foundation for osteoporosis (QUALEFFO-31) into a simplified Chinese version, and test its reliability and validity in osteoporosis patients from mainland Chinese population. METHODS: Postmenopausal osteoporosis women with history of vertebral fracture were included as cases, and age-matched healthy female were included as controls. All subjects were from mainland China. The simplified Chinese version of QUALEFFO-31 and SF-36 were assigned to the two groups. Reliability was assessed using kappa statistics of agreement for each item and the intra-class correlation coefficient (ICC). The internal consistency was assessed with Cronbach's α. Pearson's correlation was used to assess convergent and discriminant validity. RESULTS: Overall, 66 cases and 66 age-matched controls were included. The ICC for the test-retest reliability ranged from 0.76 to 0.91. Cronbach's α for pain, physical function, and mental function domains were 0.94, 0.87, and 0.79, respectively. Convergent validity and discriminant validity showed that each correlation coefficient between score of each item with total score of related domain was higher than that with total score of unrelated domain. Pearson's correlation coefficients indicated significantly high correlations between corresponding domains of QUALEFFO-31 and SF-36. CONCLUSIONS: The simplified Chinese version of the QUALEFFO-31 is a reliable and valid outcome measure of functional status in patients with osteoporosis. This Chinese version of the QUALEFFO-31 can be utilized for future clinical studies in mainland China.

Defect-meditated efficient catalytic activity toward p-nitrophenol reduction: A case study of nitrogen doped calcium niobate system.

This work reported on the synthesis of a series of nitrogen doped Ca2Nb2O7 with tunable nitrogen content that were found to be efficient and green noble-metal-free catalysts toward catalytic reduction of p-nitrophenol. XPS and ESR results indicated that the introduction of nitrogen in Ca2Nb2O7 gave rise to a large number of defective nitrogen and oxygen species. Defective nitrogen and oxygen species were found to play synergetic roles in the reduction of p-nitrophenol. The underlying mechanism is completely different from those reported for metallic nanoparticles. Moreover, the more negative conduction band edge potential enabled nitrogen doped Ca2Nb2O7 to show photo-synergistic effects that could accelerate the reduction rate toward p-nitrophenol under UV light irradiation. This work may provide a strategy for tuning the catalytic performance by modulating the chemical composition, electronic structure as well as surface defect chemistry.

Investigation of the 53 Markers in a DNA-Based Prognostic Test Revealing New Predisposition Genes for Adolescent Idiopathic Scoliosis.

STUDY DESIGN: A genetic association study of 53 single nucleotide polymorphisms (SNPs) with adolescent idiopathic scoliosis (AIS). OBJECTIVE: To explore new predisposition genes of AIS in Chinese Han population SUMMARY OF BACKGROUND DATA.: A panel of 53 SNPs were reported to be associated with curve severity of AIS. However, there is still a lack of knowledge concerning the association of these SNPs with the susceptibility of AIS in the Chinese Han population. METHODS: A gene-based association study was conducted by genotyping the 53 SNPs of a prognostic test. DNA samples of 990 female patients with AIS and 1188 age-matched healthy controls were analyzed using the polymerase chain reaction-based Invader assay. The χ test was carried out to compare the differences of genotype and allele distributions between patients with AIS and healthy controls. RESULTS: A total of 4 SNPs were found to present significant differences in allele or genotype frequencies between the 2 groups. Compared with normal controls, patients were found to have significantly higher allele G of rs12618119 and allele A of rs9945359. Besides, patients were found to have significantly lower allele T of rs4661748 and allele C of rs4782809 than the normal controls. BIN1, CDH13, SETBP1, and SPATA21 genes could be associated with the susceptibility of AIS. CONCLUSION: Four new predisposition genes of AIS were identified on the basis of a large-scale case-control study. Putting all these findings together, it suggests that AIS is a multifactorial disease possibly involving different pathways such as development of central neural system and bone formation. Further studies exploring more predisposition gene are essential to illustrate the etiology of AIS and to guide the prevention or prognosis of the disease. LEVEL OF EVIDENCE: 3.

Relationship between sagittal spinal alignment and the incidence of vertebral fracture in menopausal women with osteoporosis: a multicenter longitudinal follow-up study.

PURPOSE: To investigate the relationship between sagittal spinal alignment and the incidence of vertebral fracture in patients with osteoporosis. METHODS: A cohort of 1,044 postmenopausal women with osteoporosis were prospectively observed for the incidence of lumbar vertebral fracture. Baseline characteristics of the subjects were recorded, including age, year post-menopause, body height and weight, lumbar spine BMD (LSBMD) and femoral neck BMD (FNBMD). Patients with radiologically diagnosed lumbar vertebral fractures were assigned to the fracture group, and 150 randomly selected participants were assigned to the non-fracture group. Parameters depicting sagittal spinal alignment, including sacral slope (SS), pelvic tilt, pelvic incidence (PI), thoracic kyphpsis, lumbar lordosis (LL), lumbar lordosis index (LLI) and sagittal vertical axis, were measured for both groups. Comparison between the two groups was carried out by Student's t test. Variables showing significant differences were entered into a logistic regression analysis to determine the independent risk factors. RESULTS: Patients with fracture events had significantly lower LSBMD as well as a significantly longer year post-menopause. Besides, patients with vertebral fracture were found to have significantly lower LL, LLI, SS and PI. Regression analysis showed that LSBMD (OR = 0.27), LL (OR = 0.3), LLI (OR = 0.43) and PI (OR = 0.67) had significant associations with the risk of vertebral fracture. CONCLUSIONS: Osteoporosis patients with low LL, LLI, and PI could be at high risk of lumbar vertebral fracture. In addition to BMD, the abnormal sagittal spinal profile should also be taken into consideration when predicting the incidence of vertebral fracture in such patients.

Zoledronic acid increases bone mineral density and improves health-related quality of life over two years of treatment in Chinese women with postmenopausal osteoporosis.

INTRODUCTION: Osteoporosis is characterised by decreased bone mass and weakened bones, with an increased risk of fractures. Osteoporotic fracture, the most serious complication of osteoporosis, is related not only to lower bone mineral density (BMD), but also falls. Osteoporosis and fractures are associated with a decreased health-related quality of life (HRQL). Zoledronic acid (ZOL) is an intravenous once-yearly bisphosphonate that has been shown to be effective and safe in improving BMD and reducing fracture risk in controlled clinical trials. MATERIAL AND METHODS: In this self-controlled, prospective trial, 220 postmenopausal women with osteoporosis (mean age 67 years) received a single infusion of ZOL 5 mg at baseline and month 12. BMD, HRQL and Fall Index (FI) were measured at baseline, and months 12 and 24 (before each use of ZOL). The main outcome measures were the changes in lumbar spine and hip BMD and the changes in HRQL, the Short Form-36 questionnaire (SF-36). Additional comparisons were based on the FI. LSD multiple comparisons were used in the comparisons of BMD, SF-36 domain scores and FI. RESULTS: The patients had significantly higher L1-4, total hip, femoral neck and trochanter BMD (P < 0.05) with improved HRQL (P < 0.05) over two years of treatment of once-yearly ZOL 5mg. FI was reduced (P < 0.05) with oral daily elemental calcium and vitamin D in the treatment course. CONCLUSIONS: ZOL improves BMD and HRQL, especially in the physical aspects, over two years of treatment in women with postmenopausal osteoporosis, and can help improve balance ability.

Microwave-assisted synthesis and luminescence properties of Cd(1-x)Eu(x)MoO4 red phosphor.

Cd(1-x)Eu(x)MoO4 nanoparticles were prepared by a microwave-assisted method. X-ray diffraction (XRD), scanning electron microscopy (SEM), transmission electron microscopy (TEM) and photoluminescence (PL) spectra were used to characterize the structures, morphologies and the luminescent properties of as-prepared products. Emission and excitation spectra showed that the phosphor exhibits a dominant red emission at 612 nm with excitation wavelength of 330 nm at room temperature. The optimized concentration of Eu3+ is 5 mol.% for the highest emission intensity at 612 nm. The concentration quenching mechanism can be interpreted by the nearest-neighbor ions interaction of Eu3+ ions. It is found that Eu3+ concentration has great impact on the luminescent intensity which is attributed to the variation of the local symmetry. The red emission is visible to naked eyes, indicating that CdMoO4 may act as a promising host material for Eu3+ doped red phosphors.