Charge-Compensated Doping Extends Carrier Lifetimes in SrTiO₃ by Passivating Oxygen Vacancy Defects

Experiments reported that oxygen vacancies shorten the charge carrier lifetime of SrTiO3 but that it is greatly improved upon Al and Na doping. Using nonadiabatic (NA) molecular dynamics, we demonstrate that the in-gap hole trap state created by an oxygen vacancy can be eliminated by charge-compensated doping when two Ti4+ ions or two Sr2+ ions are equally replaced by Al3+ or Na+ ions. Nevertheless, Al3+ and Na+ reduce the strength of NA coupling to a different extent, resulting in increased charge carrier lifetimes of 4.6 and 1.3 ns. The lifetimes are several times longer than that of the pristine system and 3 orders of magnitude longer than that of defective SrTiO3, which is within 50 ps due to strong NA coupling. The weakly correlated electron and hole wave functions in doped systems accelerate decoherence, further delaying charge recombination. Our study rationalizes the complex charge-phonon dynamics in SrTiO3 and proposes charge-compensated doping for the design of advanced visible-light photocatalysts

A Sensitive and Specific Genomic RNA Sensor for Point-of-Care Screening of Zika Virus from Serum

This work presents a sensitive and specific single-step RNA sensor for Zika virus (ZIKV) in serum. Using AC electrokinetics (ACEK)-enhanced capacitive sensing technology, ZIKV genomic RNA (gRNA) can be directly detected from serum. The sensors are interdigitated electrodes modified with oligonucleotide probes complementary to the conserved regions of ZIKV gRNA. The ACEK capacitive sensing applies an optimized AC excitation signal over the sensor, which induces ACEK microfluidic enrichment of analytes and also simultaneously performs real-time monitoring of hybridization of ZIKV gRNA on the sensor surface. Hence, the sensing procedures are simple with rapid turn-around time and good specificity and sensitivity. A series of experiments are conducted to optimize the sensor performance. The performance of the sensor is investigated for three different probes, two functionalization buffers, and different hybridization buffers. With the optimized sensing protocol, this method can detect spiked ZIKV gRNA from human serum within 30 s and reach a limit of detection of 78.8 copies/μL in analytical samples and as low as 287.5 copies/μL in neat serum. The sensors can successfully differentiate between the RNAs of the ZIKV and dengue virus, two viruses with similar transmission paths and symptoms. The sensor is simple to use and requires no labeling or sophisticated process typically involved in a polymerase chain reaction, hybridization chain reaction, or nucleic acid sequence-based amplification

Additional file 2 of Construction of a semi-automatic ICD-10 coding system

Additional file 2

Molecular Mechanism of Wide Photoabsorption Spectral Shifts of Color Variants of Human Cellular Retinol Binding Protein II

Color variants of human cellular retinol binding protein II (hCRBPII) created by protein engineering were recently shown to exhibit anomalously wide photoabsorption spectral shifts over ∼200 nm across the visible region. The remarkable phenomenon provides a unique opportunity to gain insight into the molecular basis of the color tuning of retinal binding proteins for understanding of color vision as well as for engineering of novel color variants of retinal binding photoreceptor proteins employed in optogenetics. Here, we report a theoretical investigation of the molecular mechanism underlying the anomalously wide spectral shifts of the color variants of hCRBPII. Computational modeling of the color variants with hybrid molecular simulations of free energy geometry optimization succeeded in reproducing the experimentally observed wide spectral shifts, and revealed that protein flexibility, through which the active site structure of the protein and bound water molecules is altered by remote mutations, plays a significant role in inducing the large spectral shifts

Circular RNA circVRK1 suppresses the proliferation, migration and invasion of osteosarcoma cells by regulating zinc finger protein ZNF652 expression via microRNA miR-337-3p

Circular RNA is an innovative kind of endogenous non-coding RNA, which could take part in tumorigenesis. Nonetheless, the potential molecular mechanisms of circVRK1 in the progression of osteosarcoma remain unresolved. In the current study, we initially investigated circVRK1 levels in osteosarcoma clinical samples and cell lines by qRT-PCR analysis and northern blot assay. RNase R treatments, RNA stability assay and nucleoplasmic separation assay were conducted to identify the characteristics of circVRK1. We adopted CCK-8, colony formation, wound-healing, and transwell assays to assess the biological effects of circVRK1 on the proliferation, migration, and invasiveness of osteosarcoma cells in vitro. We then constructed a xenograft model in nude mice to confirm the suppressive role of circVRK1 in vivo. Moreover, dual-luciferase reporter, RNA immunoprecipitation, and RNA pull-down assays were utilized to elucidate the underlying molecular mechanisms mediated by circVRK1. We demonstrated that circVRK1 was a stable circular transcript localized in the cytoplasm of osteosarcoma cells, and the down-regulation of circVRK1 in osteosarcoma tissues was related to poor outcome of patients. Meanwhile, over-expressed circVRK1 obviously restrained the growth, migration, and invasion of osteosarcoma in vitro and in vivo. Mechanistically, circVRK1 was assumed to be a microRNA sponge for miR-337-3p, and ZNF652 was the downstream gene of miR-337-3p. CircVRK1 overexpression or miR-337-3p knockdown accelerated ZNF652 expression, and up-regulated miR-337-3p efficiently abolished the promotion of ZNF652 induced by circVRK1. Moreover, rescue experiments have proved that circVRK1 inhibits the progression of osteosarcoma by modulating the miR-337-3p/ZNF652 axis. Therefore, we conclude that circVRK1 promotes ZNF652 expression by sponging miR-337-3p. CircVRK1 serves as a molecule sponge for miR-337-3p and mediates the ceRNA network to promote the expression of ZNF652, thus suppresses osteosarcoma proliferation, migration and invasion.</p

Additional file 1 of Construction of a semi-automatic ICD-10 coding system

Additional file 1

Depleted Oxygen Defect State Enhancing Tungsten Trioxide Photocatalysis: A Quantum Dynamics Perspective

Oxygen vacancies generally create midgap states in transition metal oxides, which are expected to decrease the photoelectrochemical water-splitting efficiency. Recent experiments defy this expectation but leave the mechanism unclear. Focusing on the photoanode WO3 as a prototypical system, we demonstrate using nonadiabatic molecular dynamics that an oxygen vacancy suppresses nonradiative electron–hole recombination, because the defect acts as an electron reservoir instead of a recombination center. The occupied midgap electrons prefer to be populated a priori compared to the band edge transition because of a larger transition dipole moment, converting to depleted/unoccupied trap states that rapidly accept conduction band electrons and then cause trap-assisted recombination by impeding the bandgap recombination regardless of oxygen vacancy configurations. The reported results provide a fundamental understanding of the “realistic” role of the oxygen vacancies and their influence on charge-phonon dynamics and carrier lifetime. The study generates valuable insights into the design of high-performance transition metal oxide photocatalysts

Molecular Mechanism of Wide Photoabsorption Spectral Shifts of Color Variants of Human Cellular Retinol Binding Protein II

Color variants of human cellular retinol binding protein II (hCRBPII) created by protein engineering were recently shown to exhibit anomalously wide photoabsorption spectral shifts over ∼200 nm across the visible region. The remarkable phenomenon provides a unique opportunity to gain insight into the molecular basis of the color tuning of retinal binding proteins for understanding of color vision as well as for engineering of novel color variants of retinal binding photoreceptor proteins employed in optogenetics. Here, we report a theoretical investigation of the molecular mechanism underlying the anomalously wide spectral shifts of the color variants of hCRBPII. Computational modeling of the color variants with hybrid molecular simulations of free energy geometry optimization succeeded in reproducing the experimentally observed wide spectral shifts, and revealed that protein flexibility, through which the active site structure of the protein and bound water molecules is altered by remote mutations, plays a significant role in inducing the large spectral shifts

Molecular Mechanism of Wide Photoabsorption Spectral Shifts of Color Variants of Human Cellular Retinol Binding Protein II

Color variants of human cellular retinol binding protein II (hCRBPII) created by protein engineering were recently shown to exhibit anomalously wide photoabsorption spectral shifts over ∼200 nm across the visible region. The remarkable phenomenon provides a unique opportunity to gain insight into the molecular basis of the color tuning of retinal binding proteins for understanding of color vision as well as for engineering of novel color variants of retinal binding photoreceptor proteins employed in optogenetics. Here, we report a theoretical investigation of the molecular mechanism underlying the anomalously wide spectral shifts of the color variants of hCRBPII. Computational modeling of the color variants with hybrid molecular simulations of free energy geometry optimization succeeded in reproducing the experimentally observed wide spectral shifts, and revealed that protein flexibility, through which the active site structure of the protein and bound water molecules is altered by remote mutations, plays a significant role in inducing the large spectral shifts