Multifunctional 2-bit coded reconfigurable metasurface based on graphene-vanadium dioxide.

In this paper, a graphene-vanadium dioxide-based reconfigurable metasurface unit structure is proposed. Using the change at a graphene Fermi energy level on the surface of the unit structure to satisfy the 2-bit coding condition, four reflection units with a phase difference of 90 ∘ can be discovered. The modulating impact of the multi-beam reflection wave with 1-bit coding is then confirmed. Then we study the control of a single-beam reflected wave by metasurfaces combined with a convolution theorem in a 2-bit coding mode. Finally, when vanadium dioxide is in an insulating condition, the structure can also be transformed into a terahertz absorber. It is possible to switch between a reflection beam controller and a terahertz multifrequency absorber simply by changing the temperature of the vanadium dioxide layer without retooling a new metasurface. Moreover, compared with the 1-bit coded metasurface, it increases the ability of single-beam regulation, which makes the device more powerful for beam regulation.

Data-Augmented Deep Learning Models for Abnormal Road Manhole Cover Detection.

Anomalous road manhole covers pose a potential risk to road safety in cities. In the development of smart cities, computer vision techniques use deep learning to automatically detect anomalous manhole covers to avoid these risks. One important problem is that a large amount of data are required to train a road anomaly manhole cover detection model. The number of anomalous manhole covers is usually small, which makes it a challenge to create training datasets quickly. To expand the dataset and improve the generalization of the model, researchers usually copy and paste samples from the original data to other data in order to achieve data augmentation. In this paper, we propose a new data augmentation method, which uses data that do not exist in the original dataset as samples to automatically select the pasting position of manhole cover samples and predict the transformation parameters via visual prior experience and perspective transformations, making it more accurately capture the actual shape of manhole covers on a road. Without using other data enhancement processes, our method raises the mean average precision (mAP) by at least 6.8 compared with the baseline model.

[Establishment of a complex alcoholic liver fibrosis mouse model and investigation of OPN and TGF-beta1 hepatic expression].

OBJECTIVE: To create a convenient method to establish an alcoholic liver fibrosis model in mice and use it to explore the putative pathogenic mechanisms involving the immunomodulatory proteins osteopontin (OPN) and transforming growth factor-betal (TGF-beta1). METHODS: Forty C57BLI6J mice were fed the Lieber-DeCarli 4% ethanol-containing liquid diet for four weeks, followed by an additional four weeks of the 4% ethanol diet combined with intraperitoneal injection of carbon tetrachloride (CC14 5% solution in olive oil; 2ml/ kg body weight, 2 times/week) to induce alcoholic liver fibrosis. Control groups (n = 6 each) included: normal diet; normal diet plus CCl4 injections; ethanol diet alone; ethanol diet plus solvent (olive oil) injections. Model establishment was monitored by sacrificing six mice at model inception (week 0), and weeks 4, 5, 6, 7, and 8 of modeling to collect liver tissues and blood for histological and biochemical analyses. Extent of hepatic steatosis, inflammation, and fibrosis was assessed by hematoxylin-eosin and Masson staining. Liver function markers, serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels, were tested by automated enzymatic assays. Alpha-smooth muscle actin (alpha-SMA) expression was detected by immunohistochemistry. The mRNA and protein expression of OPN and TGF-beta1 was detected by real-time quantitative reverse transcription-PCR and western blotting, respectively. Significance of differences between multiple groups was assessed by one-way ANOVA analysis followed by least significant difference t-test or Kruskal-Wallis H test followed by the Mann-Whitney U test. RESULTS: Compared to the control groups, the group of mice administrated ethanol and CCl4 developed mild to moderate hepatic steatosis at week 4 of modeling, progressive necroinflammation and perisinusoidal and portal fibrosis from weeks 5-8, and irregular necrosis and bridging fibrosis at week 8. In addition, the model group showed progressive up-regulation of a-SMA expression in the activated hepatic stellate cells (HSCs) and fibrotic areas from weeks 5-8. Both hepatic OPN and TGF-beta1 showed significantly increasing trends in mRNA and protein expressions from weeks 5-8 (OPN mRNA: 1.83 +/- 0.25, 2.94 +/- 0.19, 3.45 +/- 0.31, and 5.99 +/- 0.17 (F= 476.27, P < 0.001); OPN protein: 0.52 +/- 0.06, 1.02 +/- 0.10, 1.52 +/- 0.11 and 1.50 +/- 0.08 (F= 298.03, P< 0.001); TGF-beta1 mRNA: 13.19 +/- 0.40, 3.31 +/- 0.28, 1.58 +/- 0.18 and 2.08 +/- 0.26 (F= 85.55, P < 0.001); TGF-P31 protein: 1.26 +/- 0.16, 0.96 +/- 0.12, 1.09 +/- 0.25 and 1.10 +/- 0.20 (F = 43.64, P < 0.001). CONCLUSION: Feeding C57BL/6J mice the Lieber-DeCarli ethanol-containing liquid diet combined with CCl4 intraperitoneal injection is a convenient method to establish a model of alcoholic liver fibrosis within a relatively short amount of time (eight weeks). Progression of alcoholic liver fibrosis is accompanied by increased hepatic expression of OPN and TGF-beta1, which may contribute to the pathogenic mechanism of this disease and may be targets of future molecular therapies.

[Activation of Fas/FasL and its downstream signaling pathway promotes development of alcoholic steatohepatitis and liver fibrosis in mice].

OBJECTIVE: To explore the role and mechanism of the Fas/Fas ligand (FasL) system and its downstream signaling pathway related to the progression of alcoholic steatohepatitis and liver fibrosis. METHODS: Eighteen C57BL/6J mice were randomly divided into three groups: controls; alcoholic steatohepatitis model, given four-weeks of a 4% ethanol-containing Lieber-DeCarli liquid diet; alcoholic steatohepatitis and liver fibrosis model, given the four-week alcohol diet followed by twice weekly intraperitoneal injections of carbon tetrachloride (5% olive oil solution; 2 mL/kg dose) during the fifth to eighth weeks. Mice in the model groups were sacrificed at the end of week 4 and 8, respectively, along with control mice for comparative analyses. Liver tissue sections were evaluated for hepatocellular apoptosis by terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) assay. The mRNA expression of Fas, FasL, cysteine aspartate-specific proteases 3 (caspase 3), and cytochrome P450 2E1 (CYP 2E1) in liver tissues was detected by reverse transcription (RT)-PCR, visualized by ethidium bromide staining, and normalized to the gray-value of GAPDH expression. The protein expression of Fas and caspase 3 were detected by western blotting (b-actin normalized), and of FasL and CYP 2E1 by immunohistochemistry staining. Intergroup differences and statistical significance were evaluated by single factor analysis of variance and the least squares difference-t test or the Kruskal-Wallis H test and the Mann-Whitney U test. RESULTS: The number of apoptotic cells in the liver sections was significantly higher in both model groups with alcoholic steatohepatitis (vs. controls) and the amount in the alcoholic steatohepatitis plus liver fibrosis model was significantly higher than that in the model with only alcoholic steatohepatitis. In addition, activation of Fas, FasL and its downstream signaling pathway showed an increasing trend with extent of liver injury. The hepatic mRNA (by RT-PCR) and protein (by western blotting) normalized expression levels in the controls, alcoholic steatohepatitis models, and alcoholic steatohepatitis plus liver fibrosis models were, respectively: Fas mRNA: 0.50+/-0.05, 0.61+/-0.10, 0.76+/-0.03 (H=12.137, P less than 0.05), protein: 0.52+/-0.14, 0.86+/-0.10, 0.99+/-0.09 (F=12.758, P less than 0.01); FasL mRNA: 0.31+/-0.03, 0.53+/-0.02, 1.02+/-0.04 (F=153.260, P less than 0.01); caspase 3 mRNA: 0.86+/-0.11, 0.85+/-0.05, 1.33+/-0.16 (F=8.740, P less than 0.01), protein: 0.40+/-0.03, 0.69+/-0.06, 1.02+/-0.10 (F=90.785, P less than 0.01); CYP 2E1 mRNA: 0.72+/-0.14, 1.00+/-0.15, 1.30+/-0.20 (H=4.713, P less than 0.01). The changes in hepatic FasL and CYP 2E1 expression detected by immunohistochemistry were consistent with the mRNA expression. CONCLUSION: Activation of Fas/FasL and its downstream signaling pathway, which induces hepatocellular apoptosis, contributes to the development of alcoholic steatohepatitis and liver fibrosis.

Fuzheng Huayu recipe prevents nutritional fibrosing steatohepatitis in mice.

BACKGROUND: Fuzheng Huayu recipe (FZHY), a compound of Chinese herbal medicine, was reported to improve liver function and fibrosis in patients with hepatitis B virus infection. However, its effect on nutritional fibrosing steatohepatitis is unclear. We aimed to elucidate the role and molecular mechanism of FZHY on this disorder in mice. METHODS: C57BL/6 J mice were fed with methionine-choline deficient (MCD) diet for 8 weeks to induce fibrosing steatohepatitis. FZHY and/or heme oxygenase-1 (HO-1) chemical inducer (hemin) were administered to mice, respectively. The effect of FZHY was assessed by comparing the severity of hepatic injury, levels of hepatic lipid peroxides, activation of hepatic stellate cells (HSCs) and the expression of oxidative stress, inflammatory and fibrogenic related genes. RESULTS: Mice fed with MCD diet for 8 weeks showed severe hepatic injury including hepatic steatosis, necro-inflammation and fibrosis. Administration of FZHY or hemin significantly lowered serum levels of alanine aminotransferase, aspartate aminotransferase, reduced hepatic oxidative stress and ameliorated hepatic inflammation and fibrosis. An additive effect was observed in mice fed MCD supplemented with FZHY or/and hemin. These effects were associated with down-regulation of pro-oxidative stress gene cytochrome P450 2E1, up-regulation of anti-oxidative gene HO-1; suppression of pro-inflammation genes tumor necrosis factor alpha and interleukin-6; and inhibition of pro-fibrotic genes including α-smooth muscle actin, transforming growth factor beta 1, collagen type I (Col-1) and Col-3. CONCLUSIONS: Our study demonstrated the protective role of FZHY in ameliorating nutritional fibrosing steatohepatitis. The effect was mediated through regulating key genes related to oxidative stress, inflammation and fibrogenesis.

Activation of peroxisome proliferator activated receptor alpha ameliorates ethanol induced steatohepatitis in mice.

BACKGROUND: Peroxisome proliferator activated receptor alpha (PPARα) regulates lipids metabolism and inhibits inflammatory response. However, the role of PPARα in alcoholic liver disease is largely unknown. We aim to elucidate the effect and the molecular basis of PPARα in ethanol induced hepatic injury in mice. RESULTS: C57BL/6J mice fed with 4% ethanol-containing Lieber-DeCarli liquid diet for 12 weeks exhibited hepatocyte steatosis, necrosis and inflammatory infiltration, accompanied with elevated serum alanine aminotransferase (ALT) and aspartic transaminase (AST) levels, decreased hepatic expression of PPARα, lipids oxidation promoting genes and anti-inflammatory factors, as well as enhanced hepatic expression of fatty acids synthesis promoting genes and pro-inflammatory cytokines. Induction of PPARα by PPARα agonist WY14643 treatment for 2 weeks ameliorated the severity of liver injury and restored expression of genes altered by ethanol treatment. However, administration of PPARα antagonist GW6471 for 2 weeks promoted the inflammatory response. CONCLUSIONS: The present study provided the evidence for the protective role of PPARα in ameliorating ethanol induced liver injury through modulation of the genes related to lipid metabolism and inflammatory response.

Higher plant antioxidants and redox signaling under environmental stresses.

Main antioxidants in higher plants include glutathione, ascorbate, tocopherol, proline, betaine, and others, which are also information-rich redox buffers and important redox signaling components that interact with biomembrane-related compartments. As an evolutionary consequence of aerobic life for higher plants, reactive oxygen species (ROS) are formed by partial reduction of molecular oxygen. The above enzymatic and non-enzymatic antioxidants in higher plants can protect their cells from oxidative damage by scavenging ROS. In addition to crucial roles in defense system and as enzyme cofactors, antioxidants influence higher plant growth and development by modifying processes from mitosis and cell elongation to senescence and death. Most importantly, they provide essential information on cellular redox state, and regulate gene expression associated with biotic and abiotic stress responses to optimize defense and survival. An overview of the literature is presented in terms of main antioxidants and redox signaling in plant cells. Special attention is given to ROS and ROS-antioxidant interaction as a metabolic interface for different types of signals derived from metabolism and from the changing environment, which regulates the appropriate induction of acclimation processes or, execution of cell death programs, which are the two essential directions for higher plants.

Joint tumor growth prediction and tumor segmentation on therapeutic follow-up PET images.

Tumor response to treatment varies among patients. Patient-specific prediction of tumor evolution based on medical images during the treatment can help to build and adapt patient's treatment planning in a non-invasive way. Personalized tumor growth modeling allows patient-specific prediction by estimating model parameters based on individual's images. The model parameters are often estimated by optimizing a cost function constructed based on the tumor delineations. In this paper, we propose a joint framework for tumor growth prediction and tumor segmentation in the context of patient's therapeutic follow ups. Throughout the treatment, a series of sequential positron emission tomography (PET) images are acquired for tumor response monitoring. We propose to take into account the predicted information, which is used in combination with the random walks (RW) algorithm, to develop an automatic tumor segmentation method on PET images. Moreover, we propose an iterative scheme of RW, making the segmentation more performant. Furthermore, the obtained segmentation is applied to the process of model parameter estimation so as to get the model based prediction of tumor evolution. We evaluate our methods on 7 lung tumor patients, totaling 29 PET exams, under radiotherapy by comparing the obtained tumor prediction and tumor segmentation with manual tumor delineation by expert. Our system produces promising results when compared to the state-of-the-art methods.

Robust feature selection to predict tumor treatment outcome.

OBJECTIVE: Recurrence of cancer after treatment increases the risk of death. The ability to predict the treatment outcome can help to design the treatment planning and can thus be beneficial to the patient. We aim to select predictive features from clinical and PET (positron emission tomography) based features, in order to provide doctors with informative factors so as to anticipate the outcome of the patient treatment. METHODS: In order to overcome the small sample size problem of datasets usually met in the medical domain, we propose a novel wrapper feature selection algorithm, named HFS (hierarchical forward selection), which searches forward in a hierarchical feature subset space. Feature subsets are iteratively evaluated with the prediction performance using SVM (support vector machine). All feature subsets performing better than those at the preceding iteration are retained. Moreover, as SUV (standardized uptake value) based features have been recognized as significant predictive factors for a patient outcome, we propose to incorporate this prior knowledge into the selection procedure to improve its robustness and reduce its computational cost. RESULTS: Two real-world datasets from cancer patients are included in the evaluation. We extract dozens of clinical and PET-based features to characterize the patient's state, including SUV parameters and texture features. We use leave-one-out cross-validation to evaluate the prediction performance, in terms of prediction accuracy and robustness. Using SVM as the classifier, our HFS method produces accuracy values of 100% and 94% on the two datasets, respectively, and robustness values of 89% and 96%. Without accuracy loss, the prior-based version (pHFS) improves the robustness up to 100% and 98% on the two datasets, respectively. CONCLUSIONS: Compared with other feature selection methods, the proposed HFS and pHFS provide the most promising results. For our HFS method, we have empirically shown that the addition of prior knowledge improves the robustness and accelerates the convergence.

Modulation of IKKß/NF-κB and TGF-ß1/Smad via Fuzheng Huayu recipe involves in prevention of nutritional steatohepatitis and fibrosis in mice.

OBJECTIVES: Fuzheng Huayu recipe (FZHY) exerts significant protective effects against liver fibrosis by strengthening the body's resistance and removing blood stasis. However, the molecular mechanisms through which FZHY affects liver fibrosis are still unclear. In this study, we examined the expression levels of factors involved in the inhibitor κB kinase-ß (IKK-ß)/nuclear factor-κB (NF-κB) and transforming growth factor beta 1 (TGF-ß1)/Smad signaling pathways to elucidate whether FZHY could attenuate nutritional steatohepatitis and fibrosis in mice. MATERIALS AND METHODS: C57BL/6J mice were fed with methionine-choline deficient (MCD) diet for 8 weeks to induce fibrotic steatohepatitis. FZHY and/or heme oxygenase-1 (HO-1) chemical inducer (hemin) were administered to mice. The effects of FZHY alone and in combination with hemin were assessed by comparing the severity of hepatic injury, activation of hepatic stellate cells (HSCs), and the expression of oxidative stress, inflammation and fibrogenesis related genes. RESULTS: Administration of FZHY, hemin and FZHY plus hemin significantly ameliorated liver injury. Additionally, our analysis indicated that administration of these agents significantly attenuated oxidative stress, downregulated the expression of pro-inflammatory and pro-fibrotic genes, including IKK-ß, NF-κB, monocyte chemoattractant protein-1 (MCP-1), α-smooth muscle actin (α-SMA), TGF-ß1, Smad3 and Smad4, and upregulated the expression of the antifibrogenic gene Smad7 (P< 0.001). CONCLUSION: FZHY-containing therapies prevented nutritional steatohepatitis and fibrosis through modulating the expression of factors associated with the IKKß/NF-κB and TGF-ß1/Smad signaling pathways and oxidative stress related genes.

Prediction of lung tumor evolution during radiotherapy in individual patients with PET.

We propose a patient-specific model based on partial differential equation to predict the evolution of lung tumors during radiotherapy. The evolution of tumor cell density is formulated by three terms: 1) advection describing the advective flux transport of tumor cells, 2) proliferation representing the tumor cell proliferation modeled as Gompertz differential equation, and 3) treatment quantifying the radiotherapeutic efficacy from linear quadratic formulation. We consider that tumor cell density variation can be derived from positron emission tomography images, the novel idea is to model the advection term by calculating 3D optical flow field from sequential images. To estimate patient-specific parameters, we propose an optimization between the predicted and observed images, under a global constraint that the tumor volume decreases exponentially as radiation dose increases. A thresholding on the predicted tumor cell densities is then used to define tumor contours, tumor volumes and maximum standardized uptake values (SUVmax). Results obtained on seven patients show a satisfying agreement between the predicted tumor contours and those drawn by an expert.