SF-CNN: Signal Filtering Convolutional Neural Network for Precipitation Intensity Estimation.

Precipitation intensity estimation is a critical issue in the analysis of weather conditions. Most existing approaches focus on building complex models to extract rain streaks. However, an efficient approach to estimate the precipitation intensity from surveillance cameras is still challenging. This study proposes a convolutional neural network known as the signal filtering convolutional neural network (SF-CNN) to handle precipitation intensity using surveillance-based images. The SF-CNN has two main blocks, the signal filtering block (SF block) and the gradually decreasing dimension block (GDD block), to extract features for the precipitation intensity estimation. The SF block with the filtering operation is constructed in different parts of the SF-CNN to remove the noise from the features containing rain streak information. The GDD block continuously takes the pair of the convolutional operation with the activation function to reduce the dimension of features. Our main contributions are (1) an SF block considering the signal filtering process and effectively removing the useless signals and (2) a procedure of gradually decreasing the dimension of the feature able to learn and reserve the information of features. Experiments on the self-collected dataset, consisting of 9394 raining images with six precipitation intensity levels, demonstrate the proposed approach's effectiveness against the popular convolutional neural networks. To the best of our knowledge, the self-collected dataset is the largest dataset for monitoring infrared images of precipitation intensity.

Tire⁻Pavement Contact-Aware Weight Estimation for Multi-Sensor WIM Systems.

Accurately estimating the weight of a moving vehicle at normal speed remains a challenging problem due to the complex vehicle dynamics and vehicle-pavement interaction. The weighing technique based on multiple sensors has proven to be an effective approach to this task. To improve the accuracy of weigh-in-motion (WIM) systems, this paper proposes a neural network-based method integrating identification and predication. A backpropagation neural network for signal classification (BPNN-i) was designed to identify ideal samples acquired by load sensors closest to the tire-pavement contact area. After that, ideal samples were used to predict the gross vehicle weight by using another backpropagation neural network (BPNN-e). The dataset for training and evaluation was collected from a multiple-sensor WIM (MS-WIM) system deployed in a public road. In our experiments, 96.89% of samples in the test set had an estimation error of less than 5%.

Isovitexin alleviates liver injury induced by lipopolysaccharide/d-galactosamine by activating Nrf2 and inhibiting NF-κB activation.

The aim of this study was to investigate the protective effects and mechanism of isovitexin, a glycosylflavonoid isolated from rice hulls of Oryza sativa, on Lipopolysaccharide (LPS)/d-galactosamine (D-Gal)-induced acute liver injury. The mice were randomly divided into five groups: control group, LPS/D-Gal group, and LPS/D-Gal + isovitexin groups. The mice of LPS/D-Gal group were received of LPS (50 µg/kg) and D-gal (800 mg/kg) intraperitoneal. The mice of LPS/D-Gal + isovitexin groups were received isovitexin (25, 50, 100 mg/kg) 1 h before LPS/D-Gal treatment. The results showed that the severity of liver injury was attenuated by treatment of isovitexin, as confirmed by the decreased liver histopathologic changes, as well as serum AST and ALT levels. Furthermore, the levels of TNF-α in serum and liver tissues, MPO activity and MDA content were significantly inhibited by isovitexin. In addition, isovitexin significantly attenuated NF-κB phosphorylation induced by LPS/D-Gal. The expression of Nrf2 and HO-1 were significantly up-regulated by isovitexin. In conclusion, isovitexin could protect against LPS/D-Gal-induced liver injury by inhibiting inflammatory and oxidative responses. Isovitexin also had protective effects against carbon tetrachloride (CCl4)-induced liver injury. Isovitexin may used as a potential agent for the treatment of liver injury.

Effects of Sensor Location on Dynamic Load Estimation in Weigh-in-Motion System.

In recent years, weigh-in-motion systems based on embedded sensor networks have received a lot of attention. However, how to improve the accuracy of multi-sensor weigh-in-motion (WIM) systems while keeping costs low remains a challenge. In this paper, a numerical simulation method is presented to analyze the relationship between sensor location and the accuracy of static weight estimation. The finite element model of a WIM system is developed, which consists of three parts: a pavement model, a moving load model and two types of sensor models. Analysis of simulation results shows that the ability of sensing dynamic load is closely related to the installation depth of sensors and pavement material. Moreover, the distance between the moving wheel and sensors has a great impact on estimating performance. Gaussian curve fitting could be used to reduce weighing error within a limited range. Our work suggests that much more attention should be paid to the design of the sensor layout of a WIM system.

Esculentoside A inhibits LPS-induced acute kidney injury by activating PPAR-γ.

Acute kidney injury (AKI) is a major clinical problem associated with high morbidity and mortality. Esculentoside A (EsA), a kind of saponin isolated from the root of the Chinese herb Phytolaca esculenta, has been reported to have anti-inflammatory effect. In this study, we aimed to investigate the protective effects of EsA on LPS-induced AKI in mice. The protective effects of EsA was evaluated by detecting kidney histological change, blood urea nitrogen (BUN) and creatinine levels, and inflammatory cytokines production. The results showed that EsA significantly attenuated LPS-induced kidney histological change, as well as BUN and creatinine levels. EsA also inhibited LPS-induced TNF-α, IL-1ß, and IL-6 production. LPS-induced NF-κB activation was significantly suppressed by treatment of EsA. In addition, EsA up-regulated the expression of PPAR-γ in a dose-dependent manner. In conclusion, EsA protected mice effectively from LPS-induced AKI by PPAR-γ, which subsequently inhibited LPS-induced inflammatory response.

Saikosaponin a Inhibits Cigarette Smoke-Induced Oxidant Stress and Inflammatory Responses by Activation of Nrf2.

Saikosaponin a (SSa), a triterpenoid saponin, has numerous pharmacological properties, including anti-inflammatory and antioxidant effects. The purpose of this study was to investigate whether and how SSa protected against cigarette smoke (CS)-induced lung inflammation in mice. The mice were exposed to CS and SSa was administered by an intraperitoneal (i.p.) injection 1 h before CS treatment for 5 consecutive days. The results showed that SSa significantly inhibited CS-induced inflammatory cell infiltration, NO, TNF-α, and IL-1ß production in BALF. SSa also inhibited CS-induced MPO and MDA contents in lung tissues. Furthermore, SSa significantly inhibited CS-induced NF-κB and upregulated the expression of Nrf2 and HO-1. In conclusion, these results support a therapeutic potential for SSa in CS-induced lung inflammation.

Dexmedetomidine attenuates lipopolysaccharide-induced acute lung injury by inhibiting oxidative stress, mitochondrial dysfunction and apoptosis in rats.

Previous studies have identified that dexmedetomidine (DEX) treatment can ameliorate the acute lung injury (ALI) induced by lipopolysaccharide and ischemia-reperfusion. However, the molecular mechanisms by which DEX ameliorates lung injury remain unclear. The present study investigated whether DEX, which has been reported to exert effects on oxidative stress, mitochondrial permeability transition pores and apoptosis in other disease types, can exert protective effects in lipopolysaccharide (LPS)­induced ALI by inhibiting oxidative stress, mitochondrial dysfunction and mitochondrial­dependent apoptosis. It was revealed that LPS­challenged rats exhibited significant lung injury, characterized by the deterioration of histopathology, vascular hyperpermeability, wet­to­dry weight ratio and oxygenation index (PaO2/FIO2), which was attenuated by DEX treatment. DEX treatment inhibited LPS­induced mitochondrial dysfunction, as evidenced by alleviating the cellular ATP and mitochondrial membrane potential in vitro. In addition, DEX treatment markedly prevented the LPS­induced mitochondrial­dependent apoptotic pathway in vitro (increases of cell apoptotic rate, cytosolic cytochrome c, and caspase 3 activity) and in vivo (increases of |terminal deoxynucleotidyl transferase dUTP nick­end labeling positive cells, cleaved caspase 3, Bax upregulation and Bcl­2 downregulation). Furthermore, DEX treatment markedly attenuated LPS­induced oxidative stress, as evidenced by downregulation of cellular reactive oxygen species in vitro and lipid peroxides in serum. Collectively, the present results demonstrated that DEX ameliorates LPS­induced ALI by reducing oxidative stress, mitochondrial dysfunction and mitochondrial-dependent apoptosis.

Shikonin protects against D-Galactosamine and lipopolysaccharide-induced acute hepatic injury by inhibiting TLR4 signaling pathway.

Shikonin, a naphthoquinone isolated from the root of medical herb Lithospermum erythrorhizon, has been reported to have anti-inflammatory effect. However, there is no related research for the treatment of shikonin on hepaic injury. The purpose of this study was to investigate the effects of shikonin on D-Galactosamine and Lipopolysaccharide-induced hepatic injury in mice. Male BALB/c mice were pretreated with shikonin 1 h before LPS/D-GalN treatment. The pathological changes of hepatic injury were detected by H&E staining. The levels of TNF-α and IL-1ß in hepatic tissues were detected by ELISA. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were also measured in this study. In addition, the expression of TLR4 and NF-κB were determined by western blot analysis. These results suggest that shikonin effectively prevents LPS/D-GalN-induced liver injury by inhibiting AST and ALT levels, as well as inflammatory cytokines TNF-α and IL-1ß production. The expression of TLR4 and NF-κB activation induced by LPS/D-GalN were also inhibited by treatment of shikonin. In vitro, shikonin significantly inhibited LPS-induced TNF-α and IL-1ß production, as well as TLR4 expression and NF-κB activation. In conclusion, the results of the present study suggest that shikonin attenuates LPS/D-GalN-induced hepatic injury by inhibiting TLR4 signaling pathway.

Effects of Angelicin on Ovalbumin (OVA)-Induced Airway Inflammation in a Mouse Model of Asthma.

Angelicin, a furocoumarin found in Psoralea corylifolia L. fruit, has been reported to have anti-inflammatory activity. The purpose of this study was to determine the protective effects of angelicin on allergic asthma induced by ovalbumin (OVA) in mice. Mice were sensitized to OVA (on days 0 and 14) and challenged with OVA three times (on days 21 to 23). Angelicin (2.5, 5, 10 mg/kg) was given intraperitoneally 1 h before OVA treatment after the initial OVA sensitization. The production of IL-4, IL-5, and IL-13 in BALF and IgE in the serum were measured by ELISA. Lung histological changes were detected by using hematoxylin and eosin (H&E) stain. The results showed that angelicin significantly inhibited inflammatory cells infiltration into the lungs. Histological studies showed that angelicin significantly attenuated OVA-induced lung injury. Meanwhile, treatment of angelicin dose-dependently inhibited OVA-induced the production of IL-4, IL-5, and IL-13 in BALF and IgE in the serum. Furthermore, angelicin was found to inhibit airway hyperresponsiveness and NF-kB activation. In conclusion, our results suggested that angelicin inhibited allergic airway inflammation and hyperresponsiveness by inhibiting NF-kB activation.

[Effects of curcumin on the expression of nuclear factor-kappaB and intercellular adhesion molecular 1 in rats with cerebral ischemia-reperfusion injury].

OBJECTIVE: To investigate the effects of curcumin on the expression of nuclear factor-kappaB (NF-kappaB) and intercellular adhesion molecular 1 (ICAM-1) in rats with cerebral ischemia-reperfusion (IR) injury. METHODS: A total of 160 SD rats were randomized equally into sham-operated group, IR model group, curcumin treatment group and solvent control group. Global cerebral ischemia/reperfusion injury was induced in the latter 3 groups with subsequent corresponding treatment. At 6 h and 1, 3, and 7 days after the injury, 10 rats from each group were sacrificed, and brain sections were prepare for HE staining, immunohistochemical staining for NF-kappaB, and enzyme-linked immunosorbent assay for ICAM-1 expression. RESULTS: In the IR model group, the contour of the pyramidal cells in hippocampal CA1 region was almost indistinguishable after the injury, whereas more than 70% of the pyramidal cells retained distinct cell contour and nuclear boundary in curcumin treatment group. At 6 h and 1, 3, and 7 days after the IR injury, the expression of NF-kappaB in curcumin treatment group showed significantly reduction in comparison with that in the IR model and solvent control groups (P<0.05), and the content of ICAM-1 protein was also reduced, which was especially obvious at 1 and 3 days (P<0.05). CONCLUSION: Curcumin can ameliorate cerebral pathological changes in the event of IR injury by suppressing the expressions of NF-kappaB and ICAM-1.