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Unmanned aerial vehicles (UAVs) have become an important technology for acquiring high-resolution remote sensing images. Because most space optical imaging systems of UAVs work in environments affected by vibrations, the optical axis motion and image plane jitter caused by these vibrations easily result in blurring of UAV images. In the paper; we propose an advanced UAV image deblurring method based on a discriminative model comprising a classifier for blurred and sharp UAV images which is embedded into the maximum a posteriori framework as a regularization term that constantly optimizes ill-posed problem of blind image deblurring to obtain sharper UAV images. Compared with other methods, the results show that in image deblurring experiments using both simulated and real UAV images the proposed method delivers sharper images of various ground objects. [ABSTRACT FROM AUTHOR]

Unmanned aerial vehicles (UAVs) are an inexpensive platform for collecting remote sensing images, but UAV images suffer from a content loss problem caused by noise. In order to solve the noise problem of UAV images, we propose a new methods to denoise UAV images. This paper introduces a novel deep neural network method based on generative adversarial learning to trace the mapping relationship between noisy and clean images. In our approach, perceptual reconstruction loss is used to establish a loss equation that continuously optimizes a min-max game theoretic model to obtain better UAV image denoising results. The generated denoised images by the proposed method enjoy clearer ground objects edges and more detailed textures of ground objects. In addition to the traditional comparison method, denoised UAV images and corresponding original clean UAV images were employed to perform image matching based on local features. At the same time, the classification experiment on the denoised images was also conducted to compare the denoising results of UAV images with others. The proposed method had achieved better results in these comparison experiments. [ABSTRACT FROM AUTHOR]

Tobacco use has one of the highest rates of addiction and relapse of any abused drug. Paradoxically, however, in animal models of reinforcement nicotine appears weak compared to other abused drugs. We report here that acetaldehyde, a major component of tobacco smoke, enhances nicotine self-administration. juvenile and adult male rats were implanted with intravenous catheters and tested for self-administration 4 days later at postnatal day 27 or 90, respectively. Animals were tested, without prior response training, in five daily 3-h sessions where each nose-poke d&ivered an intravenous injection followed by a 60-s timeout Animals (I 1- I 3/group) were offered one of the following solutions: nicotine (30 μg/lkg/inj)nicotine), acetaldehyde (16 μg/kg/inj), nicotine (30 μg/kg/inj) + acetaldehyde (16μ.g/kg/inj), or saline. The youngest animals responded significantly more for nic + acet than for saline or for either drug alone. Responding at the reinforced hole was significantly higher than at the nonreinforced hole or at the reinforced hole during noncontingent injections of nic + acet Tests with receptor antagonists indicated that these drug effects are mediated by central, but not peripheral, nicotinic receptors. There was an age-related decline in self-administration of nic + acet, but not for cocaine. Taken together, these results indicate that acetaldehyde, at the low concentrations found in tobacco smoke, interacts with nicotine to increase responding in a stringent self-administration acquisition test where nicotine alone is only weakly reinforcing, and that adolescent animals are more sensitive to these actions than adults. Animal models of tobacco addiction could be improved by combining acetaldehyde, and possibly other smoke components, with nicotine to more accurately reflect the pharmacological profile of tobacco smoke. [ABSTRACT FROM AUTHOR]

BACKGROUND: Majocchi granuloma is a cutaneous dermatophyte infection of the dermal and subcutaneous tissues characterized by chronic erythematous and indurated plaques, which are almost always the result of immunodeficiency and trauma. CASE: Disseminated dermatophyte Majocchi granuloma was diagnosed in a 19-year-old woman at 32 weeks of gestation and had no history of trauma or chronic illness. She was treated with topical antifungal medications until delivery, at which time systemic medications were started. The skin lesions resolved by the time of her 6-week postpartum visit. CONCLUSION: The altered immune state of pregnancy suggests that Majocchi granuloma should occur with some regularity in pregnancy. That this case is the second one described in the literature suggests that it may be underdiagnosed. Punch biopsy should be considered for diagnosis of unusual skin lesions during pregnancy. [ABSTRACT FROM AUTHOR]

Vascular endothelial cell premature senescence plays an important part in stroke. Many microRNAs (miRNAs) are known to be involved in the pathological process of vascular endothelial cell premature senescence. The present study aimed to investigate the mechanism of hydrogen peroxide (H~2O2)-induced premature senescence in human umbilical vein endothelial cells (HUVECs) and effect of miR-142-3p on hydrogen peroxide (H2O2)-induced premature senescence. HUVECs were exposed to H2O2 to establish a model premature senescence in endothelial cells. CCK-8 assay was performed to detect cell viability. Senescence-associated ß-galactosidase staining assay and senescence-related proteins p16 and p21 were used to detect changes in the degree of cell senescence. RT-qPCR and Western blot were conducted to measure mRNA and protein levels, respectively. The scratch wound-healing assay, transwell assay, and EdU assay were performed to evaluate the ability of migration and proliferation, respectively. miRNA-142-3p and silencing information regulator 2 related enzyme 1 (SIRT1) binding was verified using Targetscan software and a dual-luciferase assay. We found that miRNA-142-3p is abnormally up-regulated in HUVECs treated with H2O2. Functionally, miRNA-142-3p inhibition may mitigate the degree of HUVEC senescence and improve HUVEC migration and proliferation. Mechanistically, SIRT1 was validated to be targeted by miRNA-142-3p in HUVECs. Moreover, SIRT1 inhibition reversed the effects of miRNA-142-3p inhibition on senescent HUVECs exposed to H2O2. To our knowledge, this is the first study to show that miRNA-142-3p ameliorates H2O2-induced HUVECs premature senescence by targeting SIRT1 and may shed light on the role of the miR-142-3p/SIRT1 axis in stroke treatment. [ABSTRACT FROM AUTHOR]

High-voltage circuit breakers are the core equipment in power networks, and to a certain extent, are related to the safe and reliable operation of power systems. However, their core components are prone to mechanical faults. This study proposes a component separation method to detect multiple mechanical faults in circuit breakers that can achieve online real-time monitoring. First, a model and strategy are presented for obtaining mechanical voiceprint signals from circuit breakers. Subsequently, the component separation method was used to decompose the voiceprint signals of multiple faults into individual component signals. Based on this, the recognition of the features of a single-fault voiceprint signal can be achieved. Finally, multiple faults in high-voltage circuit breakers were identified through an experimental simulation and verification of the circuit breaker voiceprint signals collected from the substation site. The research results indicate that the proposed method exhibits excellent performance for multiple mechanical faults, such as spring structures and loose internal components of circuit breakers. In addition, it provides a reference method for the real-time online monitoring of high-voltage circuit breakers. [ABSTRACT FROM AUTHOR]

The mechanistic target of rapamycin (mTOR) forms two distinct complexes: rapamycin-sensitive mTOR complex 1 (mTORC1) and rapamycin-insensitive mTORC2. mTORC2 primarily regulates cell survival by phosphorylating Akt, though the upstream regulation of mTORC2 remains less welldefined than that of mTORC1. In this study, we show that NOP14, a 40S ribosome biogenesis factor and a target of the mTORC1-S6K axis, plays an essential role in mTORC2 signaling. Knockdown of NOP14 led to mTORC2 inactivation and Akt destabilization. Conversely, overexpression of NOP14 stimulated mTORC2-Akt activation and enhanced cell proliferation. Fractionation and coimmunoprecipitation assays demonstrated that the mTORC2 complex was recruited to the rough endoplasmic reticulum through association with endoplasmic reticulum-bound ribosomes. In vivo, high levels of NOP14 correlated with poor prognosis in multiple cancer types. Notably, cancer cells with NOP14 high expression exhibit increased sensitivity to mTOR inhibitors, because the feedback activation of the PI3K-PDK1-Akt axis by mTORC1 inhibition was compensated by mTORC2 inhibition partly through NOP14 downregulation. In conclusion, our findings reveal a spatial regulation of mTORC2-Akt signaling and identify ribosome biogenesis as a potential biomarker for assessing rapalog response in cancer therapy. [ABSTRACT FROM AUTHOR]

Alternative polyaclenylation (APA) has been found to be involved in tumorigenesis, development, and cell differentiation, as well as in the activation of several subsets of immune cells in vitro. Whether APA takes place in immune responses in vivo is largely unknown. We profiled the variation in tandem 3' untranslated regions (UTRs) in pathogen-challenged zebrafish and identified hundreds of APA genes with ~10% being immune response genes. The detected immune response APA genes were enriched in TLR signaling, apoptosis, and JAK-STAT signaling pathways. A greater number of microRNA target sites and AU-rich elements were found in the extended 3' UTRs than in the common 3' UTRs of these APA genes. Further analysis suggested that microRNA and AU-rich element-mediated posttranscriptional regulation plays an important role in modulating the expression of APA genes. These results indicate that APA is extensively involved in immune responses in vivo, and it may be a potential new' paradigm for immune regulation. [ABSTRACT FROM AUTHOR]

Studies have shown that the basal chordate amphioxus possesses an extraordinarily complex TLR system, including 39 TLRs and at least 40 Toll/IL-1R homologous region (TIR) adaptors. Besides homologs to MyD88 and TIR domain-containing adaptor molecule (TICAM), most amphioxus TIR adaptors exhibit domain architectures that are not observed in other species. To reveal how these novel TIR adaptors function in amphioxus Branchiostoma belcheri tsingtauense (bbt), four representatives, bbtTIRA, bbtTIRB, bbtTIRC, and bbtTIRD, were selected for functional analyses. We found bbtTIRA to show a unique inhibitory role in amphioxus TICAM-mediated pathway by interacting with bbtTICAM and bbt receptor interacting protein 1b, whereas bbtTIRC specifically inhibits the amphioxus MyD88-dependent pathway by interacting with bbtMyD88 and depressing the polyubiquitination of bbt TNFR-associated factor 6. Although both bbtTIRB and bbtTIRD are located on endosomes, the TIR domain of bbtTIRB can interact with bbtMyD88 in the cytosol, whereas the TIR domain of bbtTIRD is enclosed in endosome, suggesting that bbtTIRD may be a redundant gene in amphioxus. This study indicated that most expanded TIR adaptors play nonredundant regulatory roles in amphioxus TLR signaling, adding a new layer to understanding the diversity and complexity of innate immunity at basal chordate. [ABSTRACT FROM AUTHOR]

Animals exploit different germ-line-encoded proteins with various domain structures to detect the signature molecules of pathogenic microbes. These molecules are known as pathogen-associated molecular patterns (PAMPs), and the host proteins that react with PAMPs are called pattern recognition proteins (PRPs). Here, we present a novel type of protein domain structure capable of binding to bacterial peptidoglycan (PGN) and the minimal PGN motif muramyl dipeptide (GvlDP). This domain is designated as apextrin C-terminal domain (ApeC), and its presence was confirmed in several invertebrate phyla and subphyla. Two apextrin-like proteins (ALP1 and ALP2) were identified in a basal chordate, the Japanese amphioxus Branchiostoma japonicum (bj). bjALPI is a mucosal effector secreted into the gut lumen to agglutinate the Gram-positive bacterium Staphylococcus aureus via PGN binding. Neutralization of secreted bjALP1 by anti-bjALP1 monoclonal antibodies caused serious damage to the gut epithelium and rapid death of the animals after bacterial infection. bjALP2 is an intracellular PGN sensor that binds to TNF receptor-associated factor 6 (TRAF6) and prevents TRAF6 from self-ubiquitination and hence from NF-κB activation. MDP was found to compete with TRAF6 for bjALP2, which released TRAF6 to activate the NF-κB pathway. BjALPI and bjALP2 therefore play distinct and complementary functions in amphioxus gut mucosal immunity. In conclusion, discovery of the ApeC domain and the functional analyses of amphioxus ALP1 and ALP2 allowed us to define a previously undocumented type of PRP that is represented across different animal phyla. [ABSTRACT FROM AUTHOR]