Experimental observations on metal-like carrier transport and Mott hopping conduction behaviours in boron-doped Si nanocrystal multilayers.

Studies on the carrier transport characteristics of semiconductor nanomaterials are the important and interesting issues which are helpful for developing the next generation of optoelectronic devices. In this work, we fabricate B-doped Si nanocrystals/SiO2multilayers by plasma enhanced chemical vapor deposition with subsequent high temperature annealing. The electronic transport behaviors are studied via Hall measurements within a wide temperature range (30-660 K). It is found that when the temperature is above 300 K, all the B-doped Si nanocrystals with the size near 4.0 nm exhibit the semiconductor-like conduction characteristics, while the conduction of Si nanocrystals with large size near 7.0 nm transforms from semiconductor-like to metal-like at high B-doping ratios. The critical carrier concentration of conduction transition can reach as high as 2.2 × 1020cm-3, which is significantly higher than that of bulk counterpart and may be even higher for the smaller Si nanocrystals. Meanwhile, the Mott variable-range hopping dominates the carrier transport when the temperature is below 100 K. The localization radius of carriers can be regulated by the B-doping ratios and Si NCs size, which is contributed to the metallic insulator transition.

Oxidative Modification of miR-184 Enables It to Target Bcl-xL and Bcl-w.

MicroRNAs (miRNAs) are small non-coding RNAs, and they bind to complementary sequences in the three prime untranslated regions (3' UTRs) of target mRNA transcripts, thereby inhibiting mRNA translation or promoting mRNA degradation. Excessive reactive oxygen species (ROS) can cause cell-damaging effects through oxidative modification of macromolecules leading to their inappropriate functions. Such oxidative modification is related to cancers, aging, and neurodegenerative and cardiovascular diseases. Here we report that miRNAs can be oxidatively modified by ROS. We identified that miR-184 upon oxidative modification associates with the 3' UTRs of Bcl-xL and Bcl-w that are not its native targets. The mismatch of oxidized miR-184 with Bcl-xL and Bcl-w is involved in the initiation of apoptosis in the study with rat heart cell line H9c2 and mouse models. Our results reveal a model of ROS in regulating cellular events by oxidatively modifying miRNA.

VIDAR-Based Road-Surface-Pothole-Detection Method.

This paper presents a VIDAR (a Vision-IMU based detection and ranging method)-based approach to road-surface pothole detection. Most potholes on the road surface are caused by the further erosion of cracks in the road surface, and tires, wheels and bearings of vehicles are damaged to some extent as they pass through the potholes. To ensure the safety and stability of vehicle driving, we propose a VIDAR-based pothole-detection method. The method combines vision with IMU to filter, mark and frame potholes on flat pavements using MSER to calculate the width, length and depth of potholes. By comparing it with the classical method and using the confusion matrix to judge the correctness, recall and accuracy of the method proposed in this paper, it is verified that the method proposed in this paper can improve the accuracy of monocular vision in detecting potholes in road surfaces.

Obstacle Detection Method Based on RSU and Vehicle Camera Fusion.

Road obstacle detection is an important component of intelligent assisted driving technology. Existing obstacle detection methods ignore the important direction of generalized obstacle detection. This paper proposes an obstacle detection method based on the fusion of roadside units and vehicle mounted cameras and illustrates the feasibility of a combined monocular camera inertial measurement unit (IMU) and roadside unit (RSU) detection method. A generalized obstacle detection method based on vision IMU is combined with a roadside unit obstacle detection method based on a background difference method to achieve generalized obstacle classification while reducing the spatial complexity of the detection area. In the generalized obstacle recognition stage, a VIDAR (Vision-IMU based identification and ranging) -based generalized obstacle recognition method is proposed. The problem of the low accuracy of obstacle information acquisition in the driving environment where generalized obstacles exist is solved. For generalized obstacles that cannot be detected by the roadside unit, VIDAR obstacle detection is performed on the target generalized obstacles through the vehicle terminal camera, and the detection result information is transmitted to the roadside device terminal through the UDP (User Data Protocol) protocol to achieve obstacle recognition and pseudo-obstacle removal, thereby reducing the error recognition rate of generalized obstacles. In this paper, pseudo-obstacles, obstacles with a certain height less than the maximum passing height of the vehicle, and obstacles with a height greater than the maximum passing height of the vehicle are defined as generalized obstacles. Pseudo-obstacles refer to non-height objects that appear to be "patches" on the imaging interface obtained by visual sensors and obstacles with a height less than the maximum passing height of the vehicle. VIDAR is a vision-IMU-based detection and ranging method. IMU is used to obtain the distance and pose of the camera movement, and through the inverse perspective transformation, it can calculate the height of the object in the image. The VIDAR-based obstacle detection method, the roadside unit-based obstacle detection method, YOLOv5 (You Only Look Once version 5), and the method proposed in this paper were applied to outdoor comparison experiments. The results show that the accuracy of the method is improved by 2.3%, 17.4%, and 1.8%, respectively, compared with the other four methods. Compared with the roadside unit obstacle detection method, the speed of obstacle detection is improved by 1.1%. The experimental results show that the method can expand the detection range of road vehicles based on the vehicle obstacle detection method and can quickly and effectively eliminate false obstacle information on the road.

Circular RNAs: Biogenesis, Biological Functions, and Roles in Myocardial Infarction.

Non-coding RNAs have been excavated as important cardiac function modulators and linked to heart diseases. Significant advances have been obtained in illuminating the effects of microRNAs and long non-coding RNAs. Nevertheless, the characteristics of circular RNAs are rarely mined. Circular RNAs (circRNAs) are widely believed to participate in cardiac pathologic processes, especially in myocardial infarction. In this review, we round up the biogenesis of circRNAs, briefly describe their biological functions, and summarize the latest literature on multifarious circRNAs related to new therapies and biomarkers for myocardial infarction.

A Transformer-Based Channel Estimation Method for OTFS Systems.

Orthogonal time frequency space (OTFS) is a novel modulation scheme that enables reliable communication in high-mobility environments. In this paper, we propose a Transformer-based channel estimation method for OTFS systems. Initially, the threshold method is utilized to obtain preliminary channel estimation results. To further enhance the channel estimation, we leverage the inherent temporal correlation between channels, and a new method of channel response prediction is performed. To enhance the accuracy of the preliminary results, we utilize a specialized Transformer neural network designed for processing time series data for refinement. The simulation results demonstrate that our proposed scheme outperforms the threshold method and other deep learning (DL) methods in terms of normalized mean squared error and bit error rate. Additionally, the temporal complexity and spatial complexity of different DL models are compared. The results indicate that our proposed algorithm achieves superior accuracy while maintaining an acceptable computational complexity.

Enhanced subband light emission from Si quantum dots/SiO2 multilayers via phosphorus and boron co-doping.

Seeking light sources from Si-based materials with an emission wavelength meeting the requirements of optical telecommunication is a challenge nowadays. It was found that the subband emission centered near 1200 nm can be achieved in phosphorus-doped Si quantum dots/SiO2 multilayers. In this work, we propose the phosphorus/boron co-doping in Si quantum dots/SiO2 multilayers to enhance the subband light emission. By increasing the B co-doping ratio, the emission intensity is first increased and then decreased, while the strongest integrated emission intensity is almost two orders of magnitude stronger than that of P solely-doped sample. The enhanced subband light emission in co-doped samples can be attributed to the passivation of surface dangling bonds by B dopants. At high B co-doping ratios, the samples transfer to p-type and the subband light emission from phosphorus-related deep level is suppressed but the emission centered around 1400 nm is appeared.

Characterization of the heterogeneity of endothelial cells in bleomycin-induced lung fibrosis using single-cell RNA sequencing.

The loss of normal alveolar capillary and deregulated angiogenesis occurs simultaneously in idiopathic pulmonary fibrosis (IPF); however the contributions of specific endothelial subpopulations in the development of pulmonary fibrosis are poorly understood. Herein, we perform single-cell RNA sequencing to characterize the heterogeneity of endothelial cells (ECs) in bleomycin (BLM)-induced lung fibrosis in rats. One subpopulation, characterized by the expression of Nos3 and Cav1, is mostly distributed in non-fibrotic lungs and also highly expresses genes related to the "response to mechanical stimulus" and "lung/heart morphogenesis" processes. Another subpopulation of ECs expanded in BLM-treated lungs, characterized by Cxcl12, is observed to be closely related to the pro-fibrotic process in the transcriptome data, such as "regulation of angiogenesis," "collagen binding," and "chemokine activity," and spatially localized to BLM-induced neovascularization. Using CellPhoneDB software, we generated a complex cell-cell interaction network, which predicts the potential roles of EC subpopulations in recruiting monocytes, inducing the proliferation of fibroblasts and promoting the production and remolding of the extracellular matrix (ECM). Taken together, our data demonstrate the high degree of heterogeneity of ECs in fibrotic lung and it is proposed that the interaction between ECs, macrophages, and stromal cells contributes to pathologic IPF.

East-West differences in clinical manifestations of COVID-19 patients: A systematic literature review and meta-analysis.

The coronavirus disease 2019 (COVID-19) pandemic is currently not under control. We aimed to assess whether there are differences in clinical manifestations between COVID-19 patients from the East (East and South-East Asian countries including China, South Korea, and Thailand) and the West (North American, European, and Middle East countries, including the United States, Italy, France, and Iran). For this meta-analysis, we searched for eligible studies about COVID-19 in three databases: PubMed, EMBASE, and the Cochrane Library. Studies were divided into two cohorts for analysis: the East and the West. Stata 13.1 software was used for the meta-analysis. Of the 1527 studies initially identified by the literature search, 169 full-text articles were retrieved and screened for eligibility. Fifty-seven of these, describing 19,353 patients, were deemed eligible for inclusion. Of these, 45 studies with 8416 patients were from the East while 12 studies with 10,937 patients were from the West. The results indicated that the incidences of cough, headache, dizziness, nasal congestion, and digestive symptoms in COVID-19 patients from the East were lower than those in the West. The laboratory data showed that there were no significant differences in the levels of lymphocytes, leukocytes, C-reactive protein, and platelet counts between the two groups. In addition, our results also showed that the incidence of cardiac and kidney injury, as well as increased levels of creatinine, alanine transaminase, and aspartate transaminase, were significantly higher in patients from the West than from the East. Our meta-analysis indicated that there are differences in the clinical manifestations of COVID-19 in patients from the East and the West. COVID-19 patients from the West appear to suffer more severe liver, kidney, and heart damage due to SARS-CoV-2.

A polymorphism rs3746444 within the pre-miR-499 alters the maturation of miR-499-5p and its antiapoptotic function.

microRNAs (miRNAs) are non-coding RNAs that function as post-transcriptional regulators of cardiac development and cardiovascular diseases. Single nucleotide polymorphisms (SNPs) in miRNA genes are a novel class of genetic variations in the human genome that confer the risk of cardiovascular diseases. Here, we identified a polymorphism A→G (rs3746444) in miR-499 precursor (pre-miR-499) that affects the maturation of miR-499-5p and alters its antiapoptotic function by converting stable A-U base pair to wobble G-U base pair in pre-miR-499 secondary structure. Furthermore, our results showed that the concentrations of plasma miR-499-5p could be correlated with myocardial infarction (MI) and heart failure (HF) patients in comparison with control subjects and polymorphism rs3746444 in miR-499 could influence its abundance in plasma. Finally, our results also showed that the variant of polymorphism in miR-499 influenced the severity of the myocardial infarction significantly. This is the first report to highlight the biological significance of this polymorphism on the maturation of miR-499-5p and its antiapoptotic role during MI. These findings may pave a way to better understand the individual variability based on miRNA SNPs in heart diseases and may contribute to better treatment for disease severity on a personalized level.

Silicon Nanowire/Polymer Hybrid Solar Cell-Supercapacitor: A Self-Charging Power Unit with a Total Efficiency of 10.5.

An integrated self-charging power unit, combining a hybrid silicon nanowire/polymer heterojunction solar cell with a polypyrrole-based supercapacitor, has been demonstrated to simultaneously harvest solar energy and store it. By efficiency enhancement of the hybrid nanowire solar cells and a dual-functional titanium film serving as conjunct electrode of the solar cell and supercapacitor, the integrated system is able to yield a total photoelectric conversion to storage efficiency of 10.5%, which is the record value in all the integrated solar energy conversion and storage system. This system may not only serve as a buffer that diminishes the solar power fluctuations from light intensity, but also pave its way toward cost-effective high efficiency self-charging power unit. Finally, an integrated device based on ultrathin Si substrate is demonstrated to expand its feasibility and potential application in flexible energy conversion and storage devices.

MDRL lncRNA regulates the processing of miR-484 primary transcript by targeting miR-361.

Long noncoding RNAs (lncRNAs) are emerging as new players in gene regulation, but whether lncRNAs operate in the processing of miRNA primary transcript is unclear. Also, whether lncRNAs are involved in the regulation of the mitochondrial network remains to be elucidated. Here, we report that a long noncoding RNA, named mitochondrial dynamic related lncRNA (MDRL), affects the processing of miR-484 primary transcript in nucleus and regulates the mitochondrial network by targeting miR-361 and miR-484. The results showed that miR-361 that predominantly located in nucleus can directly bind to primary transcript of miR-484 (pri-miR-484) and prevent its processing by Drosha into pre-miR-484. miR-361 is able to regulate mitochondrial fission and apoptosis by regulating miR-484 levels. In exploring the underlying molecular mechanism by which miR-361 is regulated, we identified MDRL and demonstrated that it could directly bind to miR-361 and downregulate its expression levels, which promotes the processing of pri-miR-484. MDRL inhibits mitochondrial fission and apoptosis by downregulating miR-361, which in turn relieves inhibition of miR-484 processing by miR-361. Our present study reveals a novel regulating model of mitochondrial fission program which is composed of MDRL, miR-361 and miR-484. Our work not only expands the function of the lncRNA pathway in gene regulation but also establishes a new mechanism for controlling miRNA expression.

A circular RNA protects the heart from pathological hypertrophy and heart failure by targeting miR-223.

AIMS: Sustained cardiac hypertrophy accompanied by maladaptive cardiac remodelling represents an early event in the clinical course leading to heart failure. Maladaptive hypertrophy is considered to be a therapeutic target for heart failure. However, the molecular mechanisms that regulate cardiac hypertrophy are largely unknown. METHODS AND RESULTS: Here we show that a circular RNA (circRNA), which we term heart-related circRNA (HRCR), acts as an endogenous miR-223 sponge to inhibit cardiac hypertrophy and heart failure. miR-223 transgenic mice developed cardiac hypertrophy and heart failure, whereas miR-223-deficient mice were protected from hypertrophic stimuli, indicating that miR-223 acts as a positive regulator of cardiac hypertrophy. We identified ARC as a miR-223 downstream target to mediate the function of miR-223 in cardiac hypertrophy. Apoptosis repressor with CARD domain transgenic mice showed reduced hypertrophic responses. Further, we found that a circRNA HRCR functions as an endogenous miR-223 sponge to sequester and inhibit miR-223 activity, which resulted in the increase of ARC expression. Heart-related circRNA directly bound to miR-223 in cytoplasm and enforced expression of HRCR in cardiomyocytes and in mice both exhibited attenuated hypertrophic responses. CONCLUSIONS: These findings disclose a novel regulatory pathway that is composed of HRCR, miR-223, and ARC. Modulation of their levels provides an attractive therapeutic target for the treatment of cardiac hypertrophy and heart failure.

The Role of MicroRNAs in Myocardial Infarction: From Molecular Mechanism to Clinical Application.

MicroRNAs (miRNAs) are a class of small single-stranded and highly conserved non-coding RNAs, which are closely linked to cardiac disorders such as myocardial infarction (MI), cardiomyocyte hypertrophy, and heart failure. A growing number of studies have demonstrated that miRNAs determine the fate of the heart by regulating cardiac cell death and regeneration after MI. A deep understanding of the pathophysiology of miRNA dependent regulatory pathways in these processes is required. The role of miRNAs as diagnostic, prognostic, and therapeutic targets also needs to be explored in order to utilize them in clinical settings. This review summarizes the role of miRNAs in myocardial infarction and focuses mainly on their influence on cardiomyocyte regeneration and cell death including apoptosis, necrosis, and autophagy. In addition, the targets of pro- and anti-MI miRNAs are comparatively described. In particular, the possibilities of miRNA-based diagnostic and therapeutic strategies for myocardial infarction are discussed in this review.

PEDF and 34-mer inhibit angiogenesis in the heart by inducing tip cells apoptosis via up-regulating PPAR-γ to increase surface FasL.

Pigment epithelial-derived factor (PEDF) is a potent anti-angiogenic factor whose effects are partially mediated through the induction of endothelial cell apoptosis. However, the underlying mechanism for PEDF and the functional PEDF peptides 34-mer and 44-mer to inhibit angiogenesis in the heart has not been fully established. In the present study, by constructing adult Sprague-Dawley rat models of acute myocardial infarction (AMI) and in vitro myocardial angiogenesis, we showed that PEDF and 34-mer markedly inhibits angiogenesis by selectively inducing tip cells apoptosis rather than quiescent cells. Peptide 44-mer on the other hand exhibits no such effects. Next, we identified Fas death pathway as essential downstream regulators of PEDF and 34-mer activities in inhibiting angiogenesis. By using peroxisome proliferator-activated receptor γ (PPAR-γ) siRNA and PPAR-γ inhibitor, GW9662, we found the effects of PEDF and 34-mer were extensively blocked. These data suggest that PEDF and 34-mer inhibit angiogenesis via inducing tip cells apoptosis at least by means of up-regulating PPAR-γ to increase surface FasL in the ischemic heart, which might be a novel mechanism to understanding cardiac angiogenesis after AMI.

Measurement of complex refractive index of turbid media by scanning focused refractive index.

We present the application of scanning focused refractive index microscopy in the complex refractive index measurement of turbid media. An extra standard scattering layer is placed in front of the detector to perform scattering transformation on the reflected light. The principle of the scattering transformation is elaborated theoretically. The influence of the sample scattering is deeply and effectively suppressed experimentally. As a proof of the feasibility and accuracy of the proposed method, we demonstrate experimental data of 20% and 30% Intralipid solutions that are commonly used as phantom media for light propagation studies.

The long noncoding RNA CHRF regulates cardiac hypertrophy by targeting miR-489.

RATIONALE: Sustained cardiac hypertrophy is often accompanied by maladaptive cardiac remodeling leading to decreased compliance and increased risk for heart failure. Maladaptive hypertrophy is considered to be a therapeutic target for heart failure. MicroRNAs (miRNAs) and long noncoding RNAs (lncRNAs) have various biological functions and have been extensively investigated in past years. OBJECTIVE: We identified miR-489 and lncRNAs (cardiac hypertrophy related factor, CHRF) from hypertrophic cardiomyocytes. Here, we tested the hypothesis that miR-489 and CHRF can participate in the regulation of cardiac hypertrophy in vivo and in vitro. METHODS AND RESULTS: A microarray was performed to analyze miRNAs in response to angiotensin II treatment, and we found miR-489 was substantially reduced. Enforced expression of miR-489 in cardiomyocytes and transgenic overexpression of miR-489 both exhibited reduced hypertrophic response on angiotensin II treatment. We identified myeloid differentiation primary response gene 88 (Myd88) as a miR-489 target to mediate the function of miR-489 in cardiac hypertrophy. Knockdown of Myd88 in cardiomyocytes and Myd88-knockout mice both showed attenuated hypertrophic responses. Furthermore, we explored the molecular mechanism by which miR-489 expression is regulated and found that an lncRNA that we named CHRF acts as an endogenous sponge of miR-489, which downregulates miR-489 expression levels. CHRF is able to directly bind to miR-489 and regulate Myd88 expression and hypertrophy. CONCLUSIONS: Our present study reveals a novel cardiac hypertrophy regulating model that is composed of CHRF, miR-489, and Myd88. The modulation of their levels may provide a new approach for tackling cardiac hypertrophy.

Hybrid silicon honeycomb/organic solar cells with enhanced efficiency using surface etching.

Silicon (Si) nanostructure-based photovoltaic devices are attractive for their excellent optical and electrical performance, but show lower efficiency than their planar counterparts due to the increased surface recombination associated with the high surface area and roughness. Here, we demonstrate an efficiency enhancement for hybrid nanostructured Si/polymer solar cells based on a novel Si honeycomb (SiHC) structure using a simple etching method. SiHC structures are fabricated using a combination of nanosphere lithography and plasma treatment followed by a wet chemical post-etching. SiHC has shown superior light-trapping ability in comparison with the other Si nanostructures, along with a robust structure. Anisotropic tetramethylammonium hydroxide etching not only tunes the final surface morphologies of the nanostructures, but also reduces the surface roughness leading to a lower recombination rate in the hybrid solar cells. The suppressed recombination loss, benefiting from the reduced surface-to-volume ratio and roughness, has resulted in a high open-circuit voltage of 600 mV, a short-circuit current of 31.46 mA cm(-2) due to the light-trapping ability of the SiHCs, and yields a power conversion efficiency of 12.79% without any other device structure optimization.

PEDF and PEDF-derived peptide 44mer stimulate cardiac triglyceride degradation via ATGL.

BACKGROUND: Pigment epithelium-derived factor (PEDF) is a 50-kDa secreted glycoprotein that is highly expressed in cardiomyocytes. A variety of peptides derived from PEDF exerts diverse physiological activities including anti-angiogenesis, antivasopermeability, and neurotrophic activities. Recent studies demonstrated that segmental functional peptides of PEDF, 44mer peptide (Val78-Thr121), show similar neurotrophic and cytoprotective effect to that of the holoprotein. We found that PEDF can reduce infarct size and protect cardiac function after acute myocardial infarction (AMI). However, the effects of PEDF on cardiac triglyceride (TG) accumulation after AMI remain unknown. The present study was performed to demonstrate the influence of PEDF and its functional peptides 44mer on TG degradation in AMI. METHODS: The left ascending coronary artery (LAD) was ligated to induce AMI. PEDF-small interfering RNA (siRNA)-lentivirus (PEDF-RNAi-LV) or PEDF-LV was delivered to the ischemic myocardium in order to knock down or overexpress PEDF, respectively. Oil Red O staining and a TG assay kit were used to analyze the TG content in cardiomyocytes and infarcted areas. RESULTS: The TG content significantly decreased in the PEDF-overexpressing heart compared to the sham group (P < 0.05). Both rPEDF and 44mer administration stimulate the TG degradation in cultured cardiomyocytes (P < 0.05). Adipose triglyceride lipase (ATGL)-specific inhibitor, atglistatin, attenuated the PEDF or 44mer-induced TG lipolysis activation of cardiomyocytes at 10 µmol/L. The effects of PEDF and 44mer on myocardial TG degradation were also abolished when ATGL was downregulated. CONCLUSIONS: We conclude that PEDF and 44mer promote TG degradation in cardiomyocytes after AMI via ATGL. The substitution of PEDF and 44mer may be a novel therapeutic strategy for cardiac TG accumulation after AMI.

[Quality Analysis of Peanut Seed by Visible/Near-Infrared Spectra].

In this paper, three representative varieties of peanut seeds were selected for the experiment based on visible/near-infrared reflectance spectroscopy living in the wavelength rang from 600 to 1 100 nm. Firstly, spectral datas ware collected by the near-infrared fiber optic spectrometer, and the spectral features of the original spectral dates were extracted by the wavelet analysis. Then the principal component analysis (PCA) was used for cluster analysis of spectral features. Finally, the four principal components were applied as the inputs, the varieties category as the output and the Mahalanobis distance as the discriminant function of the recognition model, so a linear discriminant analysis model was established. In the 50 samples of each varieties, 30 samples were randomly selected as the training set, and the remaining 20 samples as the predictor set. The recognition model for three peanut varieties have a recognition rate of 95% on average. As the experimental results show that this method is reliable and effectively, and a new method to distinguish and discriminate the quality of peanut seeds was put forword.