VIDAR-Based Road-Surface-Pothole-Detection Method.

This paper presents a VIDAR (a Vision-IMU based detection and ranging method)-based approach to road-surface pothole detection. Most potholes on the road surface are caused by the further erosion of cracks in the road surface, and tires, wheels and bearings of vehicles are damaged to some extent as they pass through the potholes. To ensure the safety and stability of vehicle driving, we propose a VIDAR-based pothole-detection method. The method combines vision with IMU to filter, mark and frame potholes on flat pavements using MSER to calculate the width, length and depth of potholes. By comparing it with the classical method and using the confusion matrix to judge the correctness, recall and accuracy of the method proposed in this paper, it is verified that the method proposed in this paper can improve the accuracy of monocular vision in detecting potholes in road surfaces.

Obstacle Detection Method Based on RSU and Vehicle Camera Fusion.

Road obstacle detection is an important component of intelligent assisted driving technology. Existing obstacle detection methods ignore the important direction of generalized obstacle detection. This paper proposes an obstacle detection method based on the fusion of roadside units and vehicle mounted cameras and illustrates the feasibility of a combined monocular camera inertial measurement unit (IMU) and roadside unit (RSU) detection method. A generalized obstacle detection method based on vision IMU is combined with a roadside unit obstacle detection method based on a background difference method to achieve generalized obstacle classification while reducing the spatial complexity of the detection area. In the generalized obstacle recognition stage, a VIDAR (Vision-IMU based identification and ranging) -based generalized obstacle recognition method is proposed. The problem of the low accuracy of obstacle information acquisition in the driving environment where generalized obstacles exist is solved. For generalized obstacles that cannot be detected by the roadside unit, VIDAR obstacle detection is performed on the target generalized obstacles through the vehicle terminal camera, and the detection result information is transmitted to the roadside device terminal through the UDP (User Data Protocol) protocol to achieve obstacle recognition and pseudo-obstacle removal, thereby reducing the error recognition rate of generalized obstacles. In this paper, pseudo-obstacles, obstacles with a certain height less than the maximum passing height of the vehicle, and obstacles with a height greater than the maximum passing height of the vehicle are defined as generalized obstacles. Pseudo-obstacles refer to non-height objects that appear to be "patches" on the imaging interface obtained by visual sensors and obstacles with a height less than the maximum passing height of the vehicle. VIDAR is a vision-IMU-based detection and ranging method. IMU is used to obtain the distance and pose of the camera movement, and through the inverse perspective transformation, it can calculate the height of the object in the image. The VIDAR-based obstacle detection method, the roadside unit-based obstacle detection method, YOLOv5 (You Only Look Once version 5), and the method proposed in this paper were applied to outdoor comparison experiments. The results show that the accuracy of the method is improved by 2.3%, 17.4%, and 1.8%, respectively, compared with the other four methods. Compared with the roadside unit obstacle detection method, the speed of obstacle detection is improved by 1.1%. The experimental results show that the method can expand the detection range of road vehicles based on the vehicle obstacle detection method and can quickly and effectively eliminate false obstacle information on the road.

Constitutive androstane receptor 1 is constitutively bound to chromatin and 'primed' for transactivation in hepatocytes.

The constitutive androstane receptor (CAR) is a xenobiotic sensor expressed in hepatocytes that activates genes involved in drug metabolism, lipid homeostasis, and cell proliferation. Much progress has been made in understanding the mechanism of activation of human CAR by drugs and xenobiotics. However, many aspects of the activation pathway remain to be elucidated. In this report, we have used viral constructs to express human CAR, its splice variants, and mutant CAR forms in hepatocytes from Car-/- mice in vitro and in vivo. We demonstrate CAR expression rescued the ability of Car-/- hepatocytes to respond to a wide range of CAR activators including phenobarbital. Additionally, two major splice isoforms of human CAR, CAR2 and CAR3, were inactive with almost all the agents tested. In contrast to the current model of CAR activation, ectopic CAR1 is constitutively localized in the nucleus and is loaded onto Cyp2b10 gene in the absence of an inducing agent. In studies to elucidate the role of threonine T38 in CAR regulation, we found that the T38D mutant was inactive even in the presence of CAR activators. However, the T38A mutant was activated by CAR inducers, showing that T38 is not essential for CAR activation. Also, using the inhibitor erlotinib, we could not confirm a role for the epidermal growth factor receptor in CAR regulation. Our data suggest that CAR is constitutively bound to gene regulatory regions and is regulated by exogenous agents through a mechanism which involves protein phosphorylation in the nucleus.

Measuring in vivo responses to endogenous and exogenous oxidative stress using a novel haem oxygenase 1 reporter mouse.

KEY POINTS: Haem oxygenase 1 (Hmox1) is a cytoprotective enzyme with anti-inflammatory and anti-oxidant properties that is induced in response to multiple noxious environmental stimuli and disease states. Tools to enable its expression to be monitored in vivo have been unavailable until now. In a new Hmox1 reporter model we provide high-fidelity, single-cell resolution blueprints for Hmox1 expression throughout the body of mice. We show for the first time that Hmox1 is constitutively expressed at barrier tissues at the interface between the internal and external environments, and that it is highly induced in muscle cells during systemic inflammation. These data suggest novel biological insights into the role of Hmox1 and pave the way for the use of the model to study the role of environmental stress in disease pathology. ABSTRACT: Hmox1 protein holds great promise as a biomarker of in vivo stress responses as it is highly induced in stressed or damaged cells. However, Hmox1 expression patterns have thus far only been available in simple model organisms with limited relevance to humans. We now report a new Hmox1 reporter line that makes it possible to obtain this information in mice, a premiere model system for studying human disease and toxicology. Using a state-of-the-art strategy, we expressed multiple complementary reporter molecules from the murine Hmox1 locus, including firefly luciferase, to allow long-term, non-invasive imaging of Hmox1 expression, and ß-galactosidase for high-resolution mapping of expression patterns post-mortem. We validated the model by confirming the fidelity of reporter expression, and its responsiveness to oxidative and inflammatory stimuli. In addition to providing blueprints for Hmox1 expression in mice that provide novel biological insights, this work paves the way for the broad application of this model to establish cellular stresses induced by endogenous processes and those resulting from exposure to drugs and environmental agents. It will also enable studies on the role of oxidative stress in the pathogenesis of disease and its prevention.

Regulation of alternative splicing of tau exon 10 by 9G8 and Dyrk1A.

Adult human brain expresses 6 isoforms of tau protein as a result of alternative splicing. Alternative splicing of exon 10 (E10) leads to tau isoforms containing either 3 (3R-tau) or 4 (4R-tau) microtubule-binding repeats. Imbalance in the 3R-tau/4R-tau ratio causes neurofibrillary degeneration and dementia. Here, we demonstrated that the dual-specificity tyrosine phosphorylation-regulated kinase 1A (Dyrk1A) interacted with the splicing factor 9G8 and phosphorylated it at several serine residues. Dyrk1A itself promoted tau E10 inclusion, whereas 9G8 inhibited E10 inclusion, and these actions were variable depending on the cell types. Coexpression of Dyrk1A and 9G8 led to their translocation from the nucleus to the cytoplasm and suppressed their ability to regulate tau exon 10 splicing. This action is probably due to their interaction-induced translocation from the nucleus, where the regulation of tau E10 splicing occurs, to the cytoplasm. These findings provide novel insights into the molecular mechanism of the regulation of tau E10 splicing and further our understanding of the neurodegeneration caused by dysregulation of tau E10 splicing.