University of Kentucky

About: University of Kentucky is a education organization based out in Lexington, Kentucky, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 43933 authors who have published 92195 publications receiving 3256087 citations. The organization is also known as: UK.

Internet of Vehicles: Architecture, Protocols, and Security

Abstract: Today, vehicles are increasingly being connected to the Internet of Things which enable them to provide ubiquitous access to information to drivers and passengers while on the move. However, as the number of connected vehicles keeps increasing, new requirements (such as seamless, secure, robust, scalable information exchange among vehicles, humans, and roadside infrastructures) of vehicular networks are emerging. In this context, the original concept of vehicular ad-hoc networks is being transformed into a new concept called the Internet of Vehicles (IoV). We discuss the benefits of IoV along with recent industry standards developed to promote its implementation. We further present recently proposed communication protocols to enable the seamless integration and operation of the IoV. Finally, we present future research directions of IoV that require further consideration from the vehicular research community.

Mouse Models of Abdominal Aortic Aneurysms

Abstract: Many mouse models of abdominal aortic aneurysms have been developed that use a diverse array of methods for producing the disease, including genetic manipulation and chemical induction. These models could provide insight into potential mechanisms in the development of this disease. Although experimental studies on abdominal aortic aneurysms (AAAs) have used a variety of mammalian and avian approaches, there is an increasing reliance on the use of mice. The models recapitulate some facets of the human disease including medial degeneration, inflammation, thrombus formation, and rupture. Most of the mouse models of AAA are evoked either by genetically defined approaches or by chemical means. The genetic approaches are spontaneous and engineered mutations. These include defects in extracellular matrix maturation, increased degradation of elastin and collagen, aberrant cholesterol homeostasis, and enhanced production of angiotensin peptides. The chemical approaches include the intraluminal infusion of elastase, periaortic incubations of calcium chloride, and subcutaneous infusion of AngII. A common feature of these models is the reduction of AAA incidence and severity by the prophylactic administration of matrix metalloproteinase (MMP) inhibitors or genetically engineered deficiencies of specific members of this proteolytic protein family. The validation of mouse models of AAAs will provide insight into the mechanisms of progression of the human disease.

The glial glutamate transporter, GLT-1, is oxidatively modified by 4-hydroxy-2-nonenal in the Alzheimer's disease brain: the role of Aβ1–42

Abstract: Glutamate transporters are involved in the maintenance of synaptic glutamate concentrations Because of its potential neurotoxicity, clearance of glutamate from the synaptic cleft may be critical for neuronal survival Inhibition of glutamate uptake from the synapse has been implicated in several neurodegenerative disorders In particular, glutamate uptake is inhibited in Alzheimer's disease (AD); however, the mechanism of decreased transporter activity is unknown Oxidative damage in brain is implicated in models of neurodegeneration, as well as in AD Glutamate transporters are inhibited by oxidative damage from reactive oxygen species and lipid peroxidation products such as 4-hydroxy-2-nonenal (HNE) Therefore, we have investigated a possible connection between the oxidative damage and the decreased glutamate uptake known to occur in AD brain Western blots of immunoprecipitated HNE-immunoreactive proteins from the inferior parietal lobule of AD and control brains suggest that HNE is conjugated to GLT-1 to a greater extent in the AD brain A similar analysis of beta amyloid (Abeta)-treated synaptosomes shows for the first time that Abeta1-42 also increases HNE conjugation to the glutamate transporter Together, our data provide a possible link between the oxidative damage and neurodegeneration in AD, and supports the role of excitotoxicity in the pathogenesis of this disorder Furthermore, our data suggests that Abeta may be a possible causative agent in this cascade

Immunology of age-related macular degeneration

Abstract: Age-related macular degeneration (AMD) is a leading cause of blindness in aged individuals. Recent advances have highlighted the essential role of immune processes in the development, progression and treatment of AMD. In this Review we discuss recent discoveries related to the immunological aspects of AMD pathogenesis. We outline the diverse immune cell types, inflammatory activators and pathways that are involved. Finally, we discuss the future of inflammation-directed therapeutics to treat AMD in the growing aged population.