Miracle-dz/UniFAR-FTUs huggingface dataset:
Fully Vertical GaN-on-Si power MOSFETs

We report the first demonstration of fully vertical power MOSFETs on 6.6-<inline-formula> <tex-math notation="LaTeX">$\mu \text{m}$ </tex-math></inline-formula>-thick GaN, grown on a 6-inch Si substrate by metal-organic chemical vapor deposition. A robust fabrication method was developed based on a selective and local removal of the Si substrate as well as the resistive GaN buffer layers, followed by a conformal deposition of a 35-<inline-formula> <tex-math notation="LaTeX">$\mu \text{m}$ </tex-math></inline-formula>-thick copper layer on the backside by electroplating, which provides excellent mechanical stability and electrical contact to the drain terminal. The fabrication process of the gate trench was optimized, improving considerably the effective mobility at the p-GaN channel and the output current of the devices. High-performance fully vertical GaN-on-Si MOSFETs are presented, with a low specific ON-resistance (<inline-formula> <tex-math notation="LaTeX">${R}_{\textsf {on,sp}}$ </tex-math></inline-formula>) of 5 <inline-formula> <tex-math notation="LaTeX">$\text{m}\Omega $ </tex-math></inline-formula>cm<sup>2</sup> and a high OFF-state breakdown voltage of 520 V. Our results reveal a major step toward the realization of high-performance GaN vertical power devices on cost-effective Si substrates.
Unipolar n-Type Conduction in Black Phosphorus Induced by Atomic Layer Deposited MgO

Two-dimensional black phosphorus (BP) holds great promise for future nanoscale field-effect transistors owing to its finite bandgap and expected high carrier mobility. Nevertheless, while most studies have reported unipolar p-type or ambipolar BP transistors with a hole conduction dominance, excellent n-type transport in BP has been a critical challenge. Here, we report unipolar n-type BP transistors realized by a MgO capping layer via atomic layer deposition. By coverage with 20-nm-thick MgO, remarkable electron conduction is obtained in transistors fabricated on BP flakes of thicknesses from 2.6 to 7.6 nm, accompanied by fully suppressed hole transport. Furthermore, the unipolar electron transport is found to retain (or even improve) after a period of six months, with the highest extrinsic electron mobility reaching 135.9 cm2/Vs. The effective approach to realizing unipolar n-FETs of BP demonstrated in this letter paves the way to the implementation of BP-based CMOS digital logic circuits.
Multiple mechanisms contribute to increased neutral lipid accumulation in yeast producing recombinant variants of plant diacylglycerol acyltransferase 1

The apparent bottleneck in the accumulation of oil during seed development in some oleaginous plant species is the formation of triacylglycerol (TAG) by the acyl-CoA–dependent acylation of sn-1,2-diacylglycerol catalyzed by diacylglycerol acyltransferase (DGAT, EC 2.3.1.20). Improving DGAT activity using protein engineering could lead to improvements in seed oil yield (e.g. in canola-type Brassica napus). Directed evolution of B. napus DGAT1 (BnaDGAT1) previously revealed that one of the regions where amino acid residue substitutions lead to higher performance in BnaDGAT1 is in the ninth predicted transmembrane domain (PTMD9). In this study, several BnaDGAT1 variants with amino acid residue substitutions in PTMD9 were characterized. Among these enzyme variants, the extent of yeast TAG production was affected by different mechanisms, including increased enzyme activity, increased polypeptide accumulation, and possibly reduced substrate inhibition. The kinetic properties of the BnaDGAT1 variants were affected by the amino acid residue substitutions, and a new kinetic model based on substrate inhibition and sigmoidicity was generated. Based on sequence alignment and further biochemical analysis, the amino acid residue substitutions that conferred increased TAG accumulation were shown to be present in the DGAT1-PTMD9 region of other higher plant species. When amino acid residue substitutions that increased BnaDGAT1 enzyme activity were introduced into recombinant Camelina sativa DGAT1, they also improved enzyme performance. Thus, the knowledge generated from directed evolution of DGAT1 in one plant species can be transferred to other plant species and has potentially broad applications in genetic engineering of oleaginous crops and microorganisms.
Mutagenic lesion bypass and two functionally different RecA proteins in Deinococcus deserti

RecA is essential for extreme radiation tolerance in Deinococcus radiodurans. Interestingly, Sahara bacterium Deinococcus deserti has three recA genes (recAC, recAP1, recAP3) that code for two different RecA proteins (RecAC, RecAP). Moreover, and in contrast to other sequenced Deinococcus species, D. deserti possesses homologues of translesion synthesis (TLS) DNA polymerases, including ImuY and DnaE2. Together with a lexA homologue, imuY and dnaE2 form a gene cluster similar to a widespread RecA/LexA‐controlled mutagenesis cassette. After having developed genetic tools, we have constructed mutant strains to characterize these recA and TLS polymerase genes in D. deserti. Both RecAC and RecAP are functional and allow D. deserti to survive, and thus repair massive DNA damage, after exposure to high doses of radiation. D. deserti is mutable by UV, which requires ImuY, DnaE2 and RecAC, but not RecAP. RecAC, but not RecAP, facilitates induced expression of imuY and dnaE2 following UV exposure. We propose that the extra recAP1 and recAP3 genes may provide higher levels of RecA protein for efficient error‐free repair of DNA damage, without further increasing error‐prone lesion bypass by ImuY and DnaE2, whereas limited TLS may contribute to adaptation to harsh conditions by generating genetic variability.
Toll-like receptor 4–induced ryanodine receptor 2 oxidation and sarcoplasmic reticulum Ca2+ leakage promote cardiac contractile dysfunction in sepsis

Studies suggest the potential role of a sarcoplasmic reticulum (SR) Ca2+ leak in cardiac contractile dysfunction in sepsis. However, direct supporting evidence is lacking, and the mechanisms underlying this SR leak are poorly understood. Here, we investigated the changes in cardiac Ca2+ handling and contraction in LPS-treated rat cardiomyocytes and a mouse model of polymicrobial sepsis produced by cecal ligation and puncture (CLP). LPS decreased the systolic Ca2+ transient and myocyte contraction as well as SR Ca2+ content. Meanwhile, LPS increased Ca2+ spark–mediated SR Ca2+ leak. Preventing the SR leak with ryanodine receptor (RyR) blocker tetracaine restored SR load and increased myocyte contraction. Similar alterations in Ca2+ handling were observed in cardiomyocytes from CLP mice. Treatment with JTV-519, an anti-SR leak drug, restored Ca2+ handling and improved cardiac function. In the LPS-treated cardiomyocytes, mitochondrial reactive oxygen species and oxidative stress in RyR2 were increased, whereas the levels of the RyR2-associated FK506-binding protein 1B (FKBP12.6) were decreased. The Toll-like receptor 4 (TLR4)–specific inhibitor TAK-242 reduced the oxidative stress in LPS-treated cells, decreased the SR leak, and normalized Ca2+ handling and myocyte contraction. Consistently, TLR4 deletion significantly improved cardiac function and corrected abnormal Ca2+ handling in the CLP mice. This study provides evidence for the critical role of the SR Ca2+ leak in the development of septic cardiomyopathy and highlights the therapeutic potential of JTV-519 by preventing SR leak. Furthermore, it reveals that TLR4 activation-induced mitochondrial reactive oxygen species production and the resulting oxidative stress in RyR2 contribute to the SR Ca2+ leak.
A multidimensional ELO model for matching learning objects

This research-to-practice full paper proposals a metric of multiple skills for learning of programming students. This kind of system often need to diagnose the student’s skill level. In the same way it needs to know the level of difficulty learning objects in its database. Such information makes it possible to make an appropriate match between student and the learning object. To model such tasks, we have adapted the ELO technique to apply a matchmaking process similar to that used in choosing opponents in chess tournaments or online matches. We used as a case study a virtual learning environment which has a repository with programming problems and the users interaction log. In this work we propose an extension to the traditional ELO model. In the classical model, ELO is a scalar value for each student and for each learning object. The extended model considers ELO as a multidimensional quantity, where each dimension is a skill in solving programming problems. The enumeration of the skills was made using the literature as well as statistical data of relevance of the attributes. The results are presented in this work.
Regulation of putative methyl‐sulphide methyltransferases in Methanosarcina acetivorans C2A

The regulation of the Methanosarcina acetivorans mtsD, mtsF and mtsH genes, which encode putative corrinoid/methyltransferase isozymes involved in methylsulphide metabolism, was examined by a variety of methods, suggesting that their expression is regulated at both the transcriptional and post‐transcriptional levels. Transcripts of all three genes, measured by quantitative reverse transcription PCR, were shown to be most abundant during growth on methanol with dimethylsulphide (DMS). Transcript levels were also high in media with CO or methylamines, but much lower with methanol. In contrast, translational fusions to mtsD showed high expression levels on CO or methanol with DMS, while the mtsF translational fusion showed highest reporter gene activity on methylamines with much lower expression on CO or methanol with DMS. The activity of mtsD and mtsF fusions was very low when the strains were grown in methanol or acetate. Expression of the mtsH fusion was not detected on any substrate, despite the presence of an mRNA transcript. The transcription start sites of all three genes were determined by 5′‐RACE revealing large leader sequences for each transcript. Characterization of deletion mutants lacking putative regulatory genes suggests that MA0862 (msrF), MA4383 (msrC) and MA4560 (msrG) act as transcriptional activators of mtsD, mtsF and mtsH respectively.
Pharmacological inhibition of myostatin suppresses systemic inflammation and muscle atrophy in mice with chronic kidney disease

Chronic kidney disease (CKD) and several other catabolic conditions are characterized by increased circulating inflammatory cytokines, defects in IGF‐1 signaling, abnormal muscle protein metabolism, and progressive muscle atrophy. In these conditions, no reliable treatments successfully block the development of muscle atrophy. In mice with CKD, we found a 2‐ to 3‐fold increase in myostatin expression in muscle. Its pharmacological inhibition by subcutaneous injections of an anti‐myostatin peptibody into CKD mice (IC50 ~1.2 nM) reversed the loss of body weight (≈5–7% increase in body mass) and muscle mass (~10% increase in muscle mass) and suppressed circulating inflammatory cytokines vs. results from CKD mice injected with PBS. Pharmacological myostatin inhibition also decreased the rate of protein degradation (16.38±1.29%;P<0.05), increased protein synthesis in extensor digitorum longus muscles (13.21±1.09%; P<0.05), markedly enhanced satellite cell function, and improved IGF‐1 intracellular signaling. In cultured muscle cells, TNF‐α increased myostatin expression via a NF‐κB‐dependent pathway, whereas muscle cells exposed to myostatin stimulated IL‐6 production via p38 MAPK and MEK1 pathways. Because IL‐6 stimulates muscle protein breakdown, we conclude that CKD increases myostatin through cytokine‐activated pathways, leading to muscle atrophy. Myostatin antagonism might become a therapeutic strategy for improving muscle growth in CKD and other conditions with similar characteristics. —Zhang, L. , Rajan, V. , Lin, E. , Hu, Z. , Han, H.Q. , Zhou, X. , Song, Y. , Min, H. , Wang, X. , Du, J., Mitch, W. E. Pharmacological inhibition of myostatin suppresses systemic inflammation and muscle atrophy in mice with chronic kidney disease. FASEB J. 25, 1653–1663 (2011). www.fasebj. org
MMANN: Multimodal Multilevel Attention Neural Network for Horror Clip Detection

Recently, the number of the online videos is booming. However, its openness gives the horror clips a chance to threaten children's physical and mental health. Therefore, it is necessary to design an algorithm to filter the horror clips in online videos. In this paper, we proposed a multimodal multilevel attention neural network for horror clip detection. Information from visual modality and auditory modality is used to describe the various factor of horror, including violence, bloody, deformed human, scream, sudden sound, etc. The temporal-level attention is designed to give the model the ability to capture horror moments. The modal-level attention automatically balances the weight on all modalities. We evaluate the model on the same dataset used in MediaEval 2017 Emotional Impact of Movies Task. The experimental result shows the advantages of our proposed model compared with other groups.
Two NDR kinase–MOB complexes function as distinct modules during septum formation and tip extension in Neurospora crassa

NDR kinases are important for growth and differentiation and require interaction with MOB proteins for activity and function. We characterized the NDR kinases and MOB activators in Neurospora crassa and identified two NDR kinases (COT1 and DBF2) and four MOB proteins (MOB1, MOB2A, MOB2B and MOB3/phocein) that form two functional NDR–MOB protein complexes. The MOB1–DBF2 complex is not only essential for septum formation in vegetative cells and during conidiation, but also functions during sexual fruiting body development and ascosporogenesis. The two MOB2‐type proteins interact with both COT1 isoforms and control polar tip extension and branching by regulating COT1 activity. The conserved region directly preceding the kinase domain of COT1 is sufficient for the formation of COT1–MOB2 heterodimers, but also for kinase homodimerization. An additional N‐terminal extension that is poorly conserved, but present in most fungal NDR kinases, is required for further stabilization of both types of interactions and for stimulating COT1 activity. COT1 lacking this region is degraded in a mob‐2 background. We propose a specific role of MOB3/phocein during vegetative cell fusion, fruiting body development and ascosporogenesis that is unrelated to the three other MOB proteins and NDR kinase signalling.
Bone proteins PHEX and DMP1 regulate fibroblastic growth factor Fgf23 expression in osteocytes through a common pathway involving FGF receptor (FGFR) signaling

Fibroblastic growth factor 23 (FGF23) is a circulating phosphaturic hormone. Inactivating mutations of the endopeptidase PHEX or the SIBLING protein DMP1 result in equivalent intrinsic bone mineralization defects and increased Fgf23 expression in osteocytes. The mechanisms whereby PHEX and DMP1 regulate Fgf23 expression are unknown. We examined the possibility that PHEX and DMP1 regulate Fgf23 through a common pathway by analyzing the phenotype of compound Phex and Dmp1 mutant mice (Hyp/Dmp1–/–). Compared to single‐mutant littermates, compound‐mutant Hyp/Dmp1–/– mice displayed nonadditive elevations of serum FGF23 (1912 ± 183, 1715 ± 178, and 1799 ± 181 pg/ml), hypophosphatemia (Pi: 6.0 ± 0.3, 5.8 ± 0.2, and 5.4 ±0.1 mg/dl), and severity of rickets/osteomalacia (bone mineral density: –36, –36, and –30%). Microarray analysis of long bones identified gene expression profiles implicating common activation of the FGFR pathway in all the mutant groups. Furthermore, inhibiting FGFR signaling using SU5402 in Hyp‐ and Dmp1–/– ‐derived bone marrow stromal cells prevented the increase in Fgf23 mRNA expression (129‐ and 124‐fold increase in Hyp and Dmp1–/– vs. 1.3‐fold in Hyp+SU5402 and 2.5‐fold in Dmp1–/– +SU5402, P<0.05). For all analyses, samples collected from nonmutant wild‐type littermates served as controls. These findings indicate that PHEX and DMP1 control a common pathway regulating bone mineralization and FGF23 production, the latter involving activation of the FGFR signaling in osteocytes. —Martin, A. , Liu, S. , David, V. , Li, H. , Karydis, A. , Feng, J. Q. , Quarles, L. D. Bone proteins PHEX and DMP1 regulate fibroblastic growth factor Fgf23 expression in osteocytes through a common pathway. FASEB J. 25, 2551–2562 (2011). www.fasebj. org
Transcriptional regulation of bone morphogenetic protein 4 by tumor necrosis factor and its relationship with age‐related macular degeneration

Bone morphogenetic protein‐4 (BMP4) may be involved in the molecular switch that determines which late form of age‐related macular degeneration (AMD) an individual develops. BMP4 expression is high in retinal pigment epithelium (RPE) cells in late, dry AMD patients, while BMP4 expression is low in the wet form of the disease, characterized by choroidal neovascularization (CNV). Here, we sought to determine the mechanism by which BMP4 is down‐regulated in CNV. BMP4 expression was decreased within laser‐induced CNV lesions in mice at a time when tumor necrosis factor (TNF) expression was high (7 d postlaser) and was reexpressed in RPE when TNF levels declined (14 d postlaser). We found that TNF, an important angiogenic stimulus, significantly down‐regulates BMP4 expression in cultured human fetal RPE cells, ARPE‐19 cells, and RPE cells in murine posterior eye cup explants. We identified two specificity protein 1 (Sp1) binding sites in the BMP4 promoter that are required for basal expression of BMP4 and its down‐regulation by TNF. Through c‐Jun NH2‐terminal kinase (JNK) activation, TNF modulates Sp1 phosphorylation, thus decreasing its affinity to the BMP4 promoter. The down‐regulation of BMP4 expression by TNF in CNV and mechanisms established might be useful for defining novel targets for AMD therapy. —Xu, J., Zhu, D. , He, S. , Spee, C. , Ryan, S. J., Hinton, D. R. Transcriptional regulation of bone morphogenetic protein 4 by tumor necrosis factor and its relationship with age‐related macular degeneration. FASEB J. 25, 2221‐2233 (2011). www.fasebj. org
Saliency Detection via Background Seeds by Object Proposals

In the recent research of saliency detection, many graph-based algorithms are applied, which use the border of an image as a background query. This frequently leads to undesired errors and retrieval outputs when the boundaries of the salient objects concerned touch, or connect with, the image's border. In this paper, we propose a novel bottom-up saliency-detection algorithm to tackle and overcome the above issue. First, we utilize object proposals to collect the background seeds reliably. Then, the Extended Random Walk algorithm is adopted to propagate the prior background labels to the rest of the pixels in an image. Finally, we refine the saliency map by taking both the textural and structural information into consideration simultaneously. Experiments on publicly available data sets show that our proposed approach achieves competitive results against the state-of-the-art methods.
Saliency Detection using Boundary Aware Regional Contrast Based Seam-map

Most of the saliency detection methods use the contrast and boundary prior to extract the salient region of an input image. These two approaches are followed in Boundary Aware Regional Contrast Based Visual Saliency Detection (BARC) [1] along with spatial distance information to achieve state of the art result. In this research, a more interesting cue is introduced to extract the salient region from an input image. Here, a combination of seam map and BARC [1] is presented to produce the saliency output. Seam importance map with boundary prior is also presented to measure the performance of this combination. Experiments with ten state of the art methods reveal that we get better saliency output by combining seam information of an input image with BARC [1].
Different roles for anti‐sigma factors in siderophore signalling pathways of Pseudomonas aeruginosa

Group IV (extracytoplasmic function) sigma factors direct the expression of a large number of regulons in bacteria. The activities of many Group IV sigma factors are inhibited by members of a family of anti‐sigma factor proteins, with appropriate environmental signals causing the sigma factor to be released for interaction with core RNA polymerase and consequent transcription of target genes. One subgroup of Group IV sigmas directs expression of genes for uptake of siderophores (iron‐chelating compounds) by Gram‐negative bacteria. The activities of these sigma factors are controlled by anti‐sigma factors that span the cytoplasmic membrane. Binding of siderophore by a receptor protein in the outer membrane results in signal transduction from the periplasmic portion to the cytoplasmic portion of the appropriate anti‐sigma factor, with consequent activity of the cognate sigma factor and upregulation of the gene encoding the receptor protein. We have investigated receptor/anti‐sigma/sigma factor signalling pathways for uptake of the siderophores ferrichrome and desferrioxamine by Pseudomonas aeruginosa. In these pathways the ‘anti‐sigma’ proteins are normally required for sigma factor activity and the cytoplasmic parts of the ‘anti‐sigmas’ have ‘pro‐sigma’ activity. We suggest that the family of anti‐sigma factor proteins may be better considered as ‘sigma regulators’.
Is eval () Evil : A study of JavaScript in PDF malware

Client-side attacks have become very popular in recent years. Consequently, third party client software, such as Adobe’s Acrobat Reader, remains a popular vector for infections. In order to support their malicious activities, PDF malware authors often turn to JavaScript. Because of this malicious intent, JavaScript from malicious PDF is markedly different than JavaScript from non-malicious PDF. This paper presents a detailed analysis of the content of JavaScript from two sources: malicious and non-malicious PDF files gathered from multiple extractions on VirusTotal Intelligence, in order to provide an overview of the significant differences in the distribution of keywords between the two types of JavaScript. The analysis shows that the obfuscation techniques and the generation of exploit triggering code used by malware authors create artefacts, such as the presence of seldom used functions that are not observable in normal files. Additionally, JavaScript from malicious PDF files lack the keywords associated with common PDF automation tasks such as getting new content from the web, interacting with the document or interacting with the user. This provides empirical confirmation of extrapolations into the detection of malicious JavaScript in PDF files from previous research and provides insight for the creation of a classifier based on keyword distributions.