Cooperative vehicular networks for intelligent transportation systems

University of Technology Sydney. Faculty of Engineering and Information Technology.Transportation systems are fundamental for the human society as they allow people and goods to move from one location to another. With an increasing volume of population and vehicles, current transportation systems are now facing a number of disruptive challenges such as congestion, crashes, air pollution and noise throughout the world. However, traditional solutions like expanding the present transportation systems by increasing the number of roads are recognized to be expensive, disruptive and involve protracted effort. Instead, intelligent transportation systems (ITS), with the goal of building a safer, more efficient and environmentally sustainable transportation system by incorporating state-of-the-art sensing, computing and communication technologies, is expected to be a better solution. ITS are complex systems and they function in a broad range of areas through smartly sensing, analysing and disseminating different kinds of traffic information. Vehicular networks, which incorporate advanced communication technology with intelligent vehicles equipped with on-board units (OBUs) and intelligent roadside infrastructure, realise the function of large scale traffic information dissemination for ITS through vehicle to vehicle (V2V), vehicle to infrastructure (V2I) and infrastructure to infrastructure (I2I) communications. Therefore, as one of the most enabling tools to support ITS, vehicular networks play a crucial role in improving road safety, relieving traffic congestion, enhancing driving experience and reducing pollution. Considering the critical impact information exchange poses on the transportation systems, vehicular network applications require particularly fast, reliable and secure message dissemination in the network. However, depending only on V2V or V2I communications may fail to meet these requirements. On one hand, the frequently changing topology of vehicular networks caused by the highly dynamic nature of vehicles and the lossy vehicular wireless channels resulting from fading, path loss and the fast movement of vehicles, would result in unreliable and intermittent V2V communications. On the other hand, V2I communications may have limited availability, especially in rural areas and in the initial deployment phase of vehicular networks due to the high cost of implementation and maintenance of infrastructure. These make research on employing cooperative communications within vehicular networks both interesting and important. In this thesis, we focus on the design of cooperative vehicular networks for ITS to satisfy the requirement of disseminating data quickly, reliably and securely, in the conditions of sparse roadside infrastructure, high mobility, and intermittent connectivity. Firstly, we propose a cooperative communication strategy that explores the combined use of V2I communications, V2V communications, mobility of vehicles, and cooperation among vehicles and infrastructure, to facilitate data dissemination in vehicular networks. The network performance, measured by the achievable throughput when there exists only one vehicle with a download request in the network, and the achievable capacity when there exist multiple vehicles with download requests in the network respectively, are analysed. The results show that the proposed cooperative communication strategy significantly boosts the throughput (or capacity) of vehicular networks. Secondly, to protect secure message dissemination, we investigate topological approaches to keep the message dissemination in vehicular networks robust against insider attackers who may tamper with the message content. As a novel approach, we take the network topology into consideration when designing algorithms to check the integrity and consistency of messages. Overall, our work provides guidance on the optimum design of cooperative vehicular networks for ITS to achieve fast, reliable and secure message dissemination

The role of Cdk5 in neurological disorders

Neurological disorders are a group of disorders with motor, sensory or cognitive damage, caused by dysfunction of the central or peripheral nervous system. Cyclin-dependent kinases 5 (Cdk5) is of vital significance for the development of the nervous system, including the migration and differentiation of neurons, the formation of synapses, and axon regeneration. However, when the nervous system is subject to pathological stimulation, aberrant activation of Cdk5 will induce abnormal phosphorylation of a variety of substrates, resulting in a cascade signaling pathway, and thus lead to pathological changes. Cdk5 is intimately related to the pathological mechanism of a variety of neurological disorders, such as A-β protein formation in Alzheimer’s disease, mitochondrial fragmentation in cerebral ischemia, and apoptosis of dopaminergic neurons in Parkinson’s disease. It is worth noting that Cdk5 inhibitors have been reported to have neuroprotective effects by inhibiting related pathological processes. Therefore, in this review, we will briefly introduce the physiological and pathological mechanisms of Cdk5 in the nervous system, focusing on the recent advances of Cdk5 in neurological disorders and the prospect of targeted Cdk5 for the treatment of neurological disorders

RIPK2: a promising target for cancer treatment

As an essential mediator of inflammation and innate immunity, the receptor-interacting serine/threonine-protein kinase-2 (RIPK2) is responsible for transducing signaling downstream of the intracellular peptidoglycan sensors nucleotide oligomerization domain (NOD)-like receptors 1 and 2 (NOD1/2), which will further activate nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) pathways, leading to the transcription activation of pro-inflammatory cytokines and productive inflammatory response. Thus, the NOD2-RIPK2 signaling pathway has attracted extensive attention due to its significant role in numerous autoimmune diseases, making pharmacologic RIPK2 inhibition a promising strategy, but little is known about its role outside the immune system. Recently, RIPK2 has been related to tumorigenesis and malignant progression for which there is an urgent need for targeted therapies. Herein, we would like to evaluate the feasibility of RIPK2 being the anti-tumor drug target and summarize the research progress of RIPK2 inhibitors. More importantly, following the above contents, we will analyze the possibility of applying small molecule RIPK2 inhibitors to anti-tumor therapy

Calonectria in the age of genes and genomes : towards understanding an important but relatively unknown group of pathogens

The genus Calonectria includes many aggressive plant pathogens causing diseases on various agricultural crops as well as forestry and ornamental tree species. Some species have been accidentally introduced into new environments via international trade of putatively asymptomatic plant germplasm or contaminated soil, resulting in significant economic losses. This review provides an overview of the taxonomy, population biology, and pathology of Calonectria species, specifically emerging from contemporary studies that have relied on DNA-based technologies. The growing importance of genomics in future research is highlighted. A life cycle is proposed for Calonectria species, aimed at improving our ability to manage diseases caused by these pathogens.The National Key R&D Program of China (China-South Africa Forestry Joint Research Centre Project); the National Ten-thousand Talents Program; the GuangDong Top Young Talents Program.http://wileyonlinelibrary.com/journal/mpphj2023BiochemistryForestry and Agricultural Biotechnology Institute (FABI)GeneticsMicrobiology and Plant Patholog

Linifanib (ABT-869) Potentiates the Efficacy of Chemotherapeutic Agents through the Suppression of Receptor Tyrosine Kinase-Mediated AKT/mTOR Signaling Pathways in Gastric Cancer

Gastric cancer, highly dependent on tumor angiogenesis, causes uncontrolled lethality, in part due to chemoresistance. Here, we demonstrate that linifanib (ABT-869), a novel multi-targeted receptor tyrosine kinase inhibitor, markedly augments cytotoxicity of chemotherapies in human gastric cancer. ABT-869 and chemotherapeutic agents exhibited a strong synergy to inhibit the viability of several gastric cancer cell lines, with combination index values ranging from 0.017 to 0.589. Additionally, the combination of ABT-869 and chemotherapeutic agents led to remarkable suppression of vascular endothelial growth factor (VEGF)-induced angiogenesis in vitro and in vivo. Importantly, in a preclinical gastric cancer xenograft mouse model, drug co-treatments led to increased mouse survival as well as a synergistic reduction in tumor size and the inhibition of tumor angiogenesis. Mechanistic studies further revealed that all of the co-treatments containing ABT-869 resulted in decreased activation of the VEGF receptor, the epidermal growth factor receptor and the insulin growth factor receptor. Inhibition of these receptor tyrosine kinases consequently attenuated the activation of the downstream AKT/mTOR signaling pathway both in cultured gastric cancer cells and in gastric cancer xenografts. Collectively, our findings suggest that the addition of ABT-869 to traditional chemotherapies may be a promising strategy for the treatment of human gastric cancer

Screening and Identification of APOC1 as a Novel Potential Biomarker for Differentiate of Mycoplasma pneumoniae in Children

Background: Although mycoplasma pneumoniae (MP) is a common cause of community-acquired pneumonia in children, the currently used diagnostic methods are not optimal. Proteomics is increasingly being used to study the biomarkers of infectious diseases. Methods: Label-free quantitative proteomics and liquid chromatography-mass/mass spectrometry were used to analyze the fold change of protein expression in plasma of children with MP pneumonia (MPP), infectious disease control (IDC), and healthy control (HC) groups. Selected proteins that can distinguish MPP from HC and IDC were further validated by enzyme-linked immunosorbent assay (ELISA).Results: After multivariate analyses, 27 potential plasma biomarkers were identified to be expressed differently among child MPP, HC, and IDC groups. Among these proteins, SERPINA3, APOC1, ANXA6, KNTC1, and CFLAR were selected for ELISA verification. SERPINA3, APOC1, and CFLAR levels were significantly different among the three groups and the ratios were consistent with the trends of proteomics results. A comparison of MPP patients and HC showed APOC1 had the largest area under the curve (AUC) of 0.853, with 77.6% sensitivity and 81.1% specificity. When APOC1 levels were compared between MPP and IDC patients, it also showed a relatively high AUC of 0.882, with 77.6% sensitivity and 88.3% specificity. Conclusion: APOC1 is a potential biomarker for the rapid and noninvasive diagnosis of MPP in children. The present finding may offer new insights into the pathogenesis and biomarker selection of MPP in children