Identification of plant leaf diseases by deep learning based on channel attention and channel pruning.

Plant diseases cause significant economic losses and food security in agriculture each year, with the critical path to reducing losses being accurate identification and timely diagnosis of plant diseases. Currently, deep neural networks have been extensively applied in plant disease identification, but such approaches still suffer from low identification accuracy and numerous parameters. Hence, this paper proposes a model combining channel attention and channel pruning called CACPNET, suitable for disease identification of common species. The channel attention mechanism adopts a local cross-channel strategy without dimensionality reduction, which is inserted into a ResNet-18-based model that combines global average pooling with global max pooling to effectively improve the features' extracting ability of plant leaf diseases. Based on the model's optimum feature extraction condition, unimportant channels are removed to reduce the model's parameters and complexity via the L1-norm channel weight and local compression ratio. The accuracy of CACPNET on the public dataset PlantVillage reaches 99.7% and achieves 97.7% on the local peanut leaf disease dataset. Compared with the base ResNet-18 model, the floating point operations (FLOPs) decreased by 30.35%, the parameters by 57.97%, the model size by 57.85%, and the GPU RAM requirements by 8.3%. Additionally, CACPNET outperforms current models considering inference time and throughput, reaching 22.8 ms/frame and 75.5 frames/s, respectively. The results outline that CACPNET is appealing for deployment on edge devices to improve the efficiency of precision agriculture in plant disease detection.

Preosteoblast-enriched lnc-Evf2 facilitates osteogenic differentiation by targeting Notch.

Ossification of ligaments (OL) and osteoporosis (OP) are multifactorial disorders without definitive clinical biomarkers. Long non-coding RNAs (lncRNAs) are known to involve in regulating pathogenesis. Here, we have identified a preosteoblast-enriched lnc-Evf2 that was overexpressed in ossified ligamentum flavum (OLF) and down-expressed in OP. lnc-Evf2 is gradually upregulated during osteogenic induction, correlating with the enhanced expression of osteogenic marker genes and matrix mineralization. Moreover, knockdown of lnc-Evf2 significantly inhibits the expression of osteogenic differentiation markers and delays the osteoblastic mineralization process, indicating that this molecule is involved in osteogenesis. Mechanistically, we demonstrated that silencing of lnc-Evf2 decreases the protein level but not the mRNA levels of Notch2, Notch3, and Hes1, all of which correlate with osteogenesis. Taken together, our data demonstrate that lnc-Evf2 promotes osteogenic differentiation and bone formation through the Notch signaling, revealing that lnc-Evf2 may serve as a novel potential clinical target of OL and OP.

Estimation of Peanut Leaf Area Index from Unmanned Aerial Vehicle Multispectral Images.

Leaf area index (LAI) is used to predict crop yield, and unmanned aerial vehicles (UAVs) provide new ways to monitor LAI. In this study, we used a fixed-wing UAV with multispectral cameras for remote sensing monitoring. We conducted field experiments with two peanut varieties at different planting densities to estimate LAI from multispectral images and establish a high-precision LAI prediction model. We used eight vegetation indices (VIs) and developed simple regression and artificial neural network (BPN) models for LAI and spectral VIs. The empirical model was calibrated to estimate peanut LAI, and the best model was selected from the coefficient of determination and root mean square error. The red (660 nm) and near-infrared (790 nm) bands effectively predicted peanut LAI, and LAI increased with planting density. The predictive accuracy of the multiple regression model was higher than that of the single linear regression models, and the correlations between Modified Red-Edge Simple Ratio Index (MSR), Ratio Vegetation Index (RVI), Normalized Difference Vegetation Index (NDVI), and LAI were higher than the other indices. The combined VI BPN model was more accurate than the single VI BPN model, and the BPN model accuracy was higher. Planting density affects peanut LAI, and reflectance-based vegetation indices can help predict LAI.

Field evaluation of an unmanned aerial vehicle (UAV) sprayer: effect of spray volume on deposition and the control of pests and disease in wheat.

BACKGROUND: Unmanned aerial vehicles (UAVs) are a recently developed aerial spraying technology. However, the effect of spray volume variation on deposition and pesticide control efficacy is unknown. The effect of three UAV spray volumes (9.0, 16.8 and 28.1 L ha-1 ) using three different nozzle sizes on droplet deposition and wheat aphid and powdery mildew control efficacy was assessed. An electric air-pressure knapsack (EAP) sprayer was used as a comparison. RESULTS: Different spray volumes significantly influenced the deposition and control efficacy of the UAV and EAP. For the UAV, a low spray volume of 9.0 L ha-1 with a fine nozzle (nozzle LU120-01) resulted in lower deposition and control efficacy. Optimal control efficacy was achieved with coarser nozzles (nozzles LU120-02, -03) at > 16.8 L ha-1 volume with systemic insecticide, and at 28.1 L ha-1 with contact insecticide and fungicide. For EAP, a high spray volume led to run-off, and a spray volume of 225 L ha-1 achieved better deposition and control efficacy. CONCLUSION: The UAV had comparable deposition and efficacy control to the EAP at a higher spray volume (> 16.8 L ha-1 ) with coarse nozzles, but exhibited inferior deposition and efficacy control at a lower spray volume (<9.0 L ha-1 ) with fine nozzles. © 2019 Society of Chemical Industry.

Low Dielectric Poly(imide siloxane) Films Enabled by a Well-Defined Disiloxane-Linked Alkyl Diamine.

This paper presents an efficient pathway to achieve the dielectric constant as low as 2.48 @ 25 °C, 1 MHz for nonporous poly(imide siloxane) films with mechanical and thermal robustness. A symmetric disiloxane-linked alkyl diamine, bis(aminopropyl)tetramethyldisiloxane (BATMS) with a well-defined molecular formula NH2CH2CH2CH2Si(CH3)2OSi(CH3)2CH2CH2CH2NH2, has been used to controllably reduce the dielectric constant of the polymer films by adjusting the loading of BATMS. The thermal stability of all the polymer films remains robust with T 5 and T 10 no less than 458 and 472 °C, respectively, while the glass-transition temperature decreases with increasing incorporation of flexible disiloxane-alkyl segments into a polymer backbone. There exists a consistent regularity between the thermal, optical, and dielectric properties with the loading amount of BATMS in the polymer films, inferring that the disiloxane-alkyl segments are homogeneously distributed in the polymer backbone. Charge-transfer complex inhibition of polymer films by disiloxane segments has been revealed by an enlarged d-spacing in wide-angle X-ray diffraction spectra and a blue shift in film fluorescence emission spectra. The combined low dielectric constant, robust mechanical and thermal stability, and improved hydrophobicity make the series of BATMS-resulting poly(imide siloxane) films promising candidates for sophisticated flexible microelectronic application.

The Parenteral Vitamin C Improves Sepsis and Sepsis-Induced Multiple Organ Dysfunction Syndrome via Preventing Cellular Immunosuppression.

Cellular immunosuppression appears to be involved in sepsis and sepsis-induced multiple organ dysfunction syndrome (MODS). Recent evidence showed that parenteral vitamin C (Vit C) had the ability to attenuate sepsis and sepsis-induced MODS. Herein, we investigated the impact of parenteral Vit C on cellular immunosuppression and the therapeutic value in sepsis. Using cecal ligation and puncture (CLP), sepsis was induced in WT and Gulo-/- mice followed with 200 mg/Kg parenteral Vit C administration. The immunologic functions of CD4+CD25+ regulatory T cells (Tregs) and CD4+CD25- T cells, as well as the organ functions, were determined. Administration of parenteral Vit C per se markedly improved the outcome of sepsis and sepsis-induced MODS of WT and Gulo-/- mice. The negative immunoregulation of Tregs was inhibited, mainly including inhibiting the expression of forkhead helix transcription factor- (Foxp-) 3, cytotoxic T lymphocyte associated antigen- (CTLA-) 4, membrane associated transforming growth factor-ß (TGF-ßm+), and the secretion of inhibitory cytokines [including TGF-ß and interleukin- (IL-) 10], as well as CD4+ T cells-mediated cellular immunosuppression which was improved by parenteral Vit C in WT and Gulo-/- septic mice. These results suggested that parenteral Vit C has the ability to improve the outcome of sepsis and sepsis-induced MODS and is associated with improvement in cellular immunosuppression.

Doxorubicin-Induced Systemic Inflammation Is Driven by Upregulation of Toll-Like Receptor TLR4 and Endotoxin Leakage.

Doxorubicin is one of the most effective chemotherapeutic agents used for cancer treatment, but it causes systemic inflammation and serious multiorgan side effects in many patients. In this study, we report that upregulation of the proinflammatory Toll-like receptor TLR4 in macrophages by doxorubicin is an important step in generating its toxic side effects. In patient serum, doxorubicin treatment resulted in leakage of endotoxin and inflammatory cytokines into circulation. In mice, doxorubicin damaged the intestinal epithelium, which also resulted in leakage of endotoxin from the gut flora into circulation. Concurrently, doxorubicin increased TLR4 expression in macrophages both in vitro and in vivo, which further enhanced the sensitivity of these cells to endotoxin. Either depletion of gut microorganisms or blockage of TLR4 signaling effectively decreased doxorubicin-induced toxicity. Taken together, our findings suggest that doxorubicin-triggered leakage of endotoxin into the circulation, in tandem with enhanced TLR4 signaling, is a candidate mechanism underlying doxorubicin-induced systemic inflammation. Our study provides new insights for devising relevant strategies to minimize the adverse effects of chemotherapeutic agents such as doxorubicin, which may extend its clinical uses to eradicate cancer cells. Cancer Res; 76(22); 6631-42. ©2016 AACR.

G-protein-coupled receptors mediate ω-3 PUFAs-inhibited colorectal cancer by activating the Hippo pathway.

Colorectal cancer (CRC) is one of the most common cancers leading to high mortality. However, long-term administration of anti-tumor therapy for CRC is not feasible due to the side effects. Omega-3 polyunsaturated fatty acids (ω-3 PUFAs), particularly DHA and EPA, exert protection against CRC, but the mechanisms are unclear. Here, we show that ω-3 PUFAs inhibit proliferation and induce apoptosis of CRC cells in vitro and alleviate AOM/DSS-induced mice colorectal cancer in vivo. Moreover, ω-3 PUFAs promote phosphorylation and cytoplasmic retention of YAP and this effect was mediated by MST1/2 and LATS1, suggesting that the canonical Hippo Pathway is involved in ω-3 PUFAs function. We further confirmed that increase of pYAP by ω-3 PUFAs was mediated by GPRs, including GPR40 and GPR120, which subsequently activate PKA via Gαs, thus inducing the Hippo pathway activation. These data provide a novel DHA/EPA-GPR40/120-Gαs-PKA-MST1/2-LATS1-YAP signaling pathway which is linked to ω-3 PUFAs-induced inhibition of cell proliferation and promotion of apoptosis in CRC cells, indicating a mechanism that could explain the anti-cancer action of ω-3 PUFAs.

Extracellular control of intracellular drug release for enhanced safety of anti-cancer chemotherapy.

The difficulty of controlling drug release at an intracellular level remains a key challenge for maximising drug safety and efficacy. We demonstrate herein a new, efficient and convenient approach to extracellularly control the intracellular release of doxorubicin (DOX), by designing a delivery system that harnesses the interactions between the system and a particular set of cellular machinery. By simply adding a small-molecule chemical into the cell medium, we could lower the release rate of DOX in the cytosol, and thereby increase its accumulation in the nuclei while decreasing its presence at mitochondria. Delivery of DOX with this system effectively prevented DOX-induced mitochondria damage that is the main mechanism of its toxicity, while exerting the maximum efficacy of this anti-cancer chemotherapeutic agent. The present study sheds light on the design of drug delivery systems for extracellular control of intracellular drug delivery, with immediate therapeutic implications.

Upstream regulators and downstream effectors of NF-κB in Alzheimer's disease.

Since Alzheimer's disease (AD) is becoming the prevalent dementia in the whole world, more underlying mechanisms are emerging. Long time has the transcription factor NF-κB been identified to participate in AD pathogenesis, various studies have focused on the causes and effects of AD that are linked to NF-κB. In this review we discuss diverse environmental stimuli including oxidative stress, neuroinflammation and metabolism, involved signaling pathways such as PI3K/AKT, MAPK and AGE/RAGE/GSK-3 and newly found ncRNAs that mediate neuron toxicity or neuron protection through NF-κB activation and the following response associated with the same factors in AD. These may provide future orientation of investigation at transcription level and support efficient treatment to AD by a better understanding of the upstream regulators and downstream effectors of NF-κB.

Hypoxia-regulated lncRNAs in cancer.

Hypoxic regions are common in solid tumors and have an impact on tumor progression and on the therapeutic response. However, the underlying mechanism for hypoxic tumor microenvironment has not been entirely elucidated. Recently, long noncoding RNAs (lncRNAs) are being increasingly recognized to contribute to carcinogenesis through diverse mechanisms. To date, several lncRNAs have been described in hypoxia-associated cancer process, implying a potential role in maintaining cellular homeostasis and enabling an adaptive survival under hypoxic stress conditions. While it has been widely accepted that a complex cellular network of gene products, such as protein and miRNA, take part in hypoxic cancer progression, it remains largely elusive how lncRNAs participate in it. In this review, we introduce an update view of lncRNAs, focusing on hypoxia-related lncRNAs. We hereby summarize the cause and consequence of hypoxia-modulated lncRNAs in cancer as well as their functional mechanisms, highlighting the specific roles of lncRNAs in hypoxia response in cancer.

YAP and TAZ Take Center Stage in Cancer.

The Hippo pathway was originally identified and named through screening for mutations in Drosophila, and the core components of the Hippo pathway are highly conserved in mammals. In the Hippo pathway, MST1/2 and LATS1/2 regulate downstream transcription coactivators YAP and TAZ, which mainly interact with TEAD family transcription factors to promote tissue proliferation, self-renewal of normal and cancer stem cells, migration, and carcinogenesis. The Hippo pathway was initially thought to be quite straightforward; however, recent studies have revealed that YAP/TAZ is an integral part and a nexus of a network composed of multiple signaling pathways. Therefore, in this review, we will summarize the latest findings on events upstream and downstream of YAP/TAZ and the ways of regulation of YAP/TAZ. In addition, we also focus on the crosstalk between the Hippo pathway and other tumor-related pathways and discuss their potential as therapeutic targets.

Docosahexaenoic acid inhibits the growth of hormone-dependent prostate cancer cells by promoting the degradation of the androgen receptor.

Epidemiological and preclinical data have demonstrated the preventative effects of ω-3 polyunsaturated fatty acids, including docosahexaenoic acid (DHA), on prostate cancer. However, there are inconsistencies in these previous studies and the underlying mechanisms remain to be elucidated. In the present study, the androgen receptor (AR), which is a transcription factor involved in cell proliferation and prostate carcinogenesis, was identified as a target of DHA. It was revealed that DHA inhibited hormone­dependent growth of LNCaP prostate cancer cells. Reverse transcription-quantitative polymerase chain reaction analysis revealed that treatment with DHA caused no alteration in the transcribed mRNA expression levels of the AR gene. However, immunoblotting revealed that this treatment reduces the protein expression level of the AR. The androgen­induced genes were subsequently repressed by treatment with DHA. It was demonstrated that DHA exhibits no effect on the translation process of the AR, however, it promotes the proteasome­mediated degradation of the AR. Therefore, the present study provided a novel mechanism by which DHA exhibits an inhibitory effect on growth of prostate cancer cells.

Targeted depletion of tumour-associated macrophages by an alendronate-glucomannan conjugate for cancer immunotherapy.

Tumour-associated macrophages (TAMs) are a set of macrophages residing in the tumour microenvironment. They play essential roles in mediating tumour angiogenesis, metastasis and immune evasion. Delivery of therapeutic agents to eliminate TAMs can be a promising strategy for cancer immunotherapy but an efficient vehicle to target these cells is still in pressing need. In this study, we developed a bisphosphonate-glucomannan conjugate that could efficiently target and specifically eliminate TAMs in the tumour microenvironment. We employed the polysaccharide from Bletilla striata (BSP), a glucomannan affinitive for macrophages that express abundant mannose receptors, to conjugate alendronate (ALN), a bisphosphonate compound with in vitro macrophage-inhibiting activities. In both in vitro and in vivo tests, the prepared ALN-BSP conjugate could preferentially accumulate in macrophages and induced them into apoptosis. In the subcutaneous S180 tumour-bearing mice model, the treatment using ALN-BSP effectively eliminated TAMs, remarkably inhibited angiogenesis, recovered local immune surveillance, and eventually suppressed tumour progression, without eliciting any unwanted effect such as systematic immune response. Interestingly, ALN alone failed to exhibit any anti-TAM activity in vivo, probably because this compound was susceptible to the mildly acidic tumour microenvironment. Taken together, these results demonstrate the potential of ALN-BSP as a safe and efficient tool targeted at direct depletion of TAMs for cancer immunotherapy.

The ways of action of long non-coding RNAs in cytoplasm and nucleus.

Over the past fifteen years, small regulatory RNAs, such as siRNA and miRNA, have been extensively investigated and the underlying molecular mechanisms have been well documented, suggesting that ncRNAs play a major function in many cellular processes. An expanding body of evidence reveals that long non-coding RNAs (lncRNAs), once described as dark matter, are involved in diverse cellular progresses, including regulation of gene expression, dosage compensation, genomic imprinting, nuclear organization and nuclear-cytoplasm trafficking via a number of complex mechanisms. The emerging links between lncRNAs and diseases as well as their tissue-specific expression patterns also indicate that lncRNAs comprise a core transcriptional regulatory circuitry. The function of lncRNAs is based on their sequence and structure; and they can combine with DNA, RNA, and proteins both in the nucleus and the cytoplasm. However, detailed insights into their biological and mechanistic functions are only beginning to emerge. In this review, we will mainly talk about diverse ways of action of lncRNAs in different sub-cellular locations and provide clues for following studies.