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.

Magnetic Field-Induced Phase Transformation in NiMnCoIn Magnetic Shape-Memory Alloys—A New Actuation Mechanism with Large Work Output

Abstract: Magnetic shape memory alloys (MSMAs) have recently been developed into a new class of functional materials that are capable of magnetic-field-induced actuation, mechanical sensing, magnetic refrigeration, and energy harvesting. In the present work, the magnetic field-induced martensitic phase transformation (FIPT) in Ni{sub 45}Mn{sub 36.5}Co{sub 5}In{sub 13.5} MSMA single crystals is characterized as a new actuation mechanism with potential to result in ultra-high actuation work outputs. The effects of the applied magnetic field on the transformation temperatures, magnetization, and superelastic response are investigated. The magnetic work output of NiMnCoIn alloys is determined to be more than 1 MJ m{sup -3} per Tesla, which is one order of magnitude higher than that of the most well-known MSMAs, i.e., NiMnGa alloys. In addition, the work output of NiMnCoIn alloys is orientation independent, potentially surpassing the need for single crystals, and not limited by a saturation magnetic field, as opposed to NiMnGa MSMAs. Experimental and theoretical transformation strains and magnetostress levels are determined as a function of crystal orientation. It is found that [111]-oriented crystals can demonstrate a magnetostress level of 140 MPa T{sup -1} with 1.2% axial strain under compression. These field-induced stress and strain levels are significantly higher than those from existingmore » piezoelectric and magnetostrictive actuators. A thermodynamical framework is introduced to comprehend the magnetic energy contributions during FIPT. The present work reveals that the magnetic FIPT mechanism is promising for magnetic actuation applications and provides new opportunities for applications requiring high actuation work-outputs with relatively large actuation frequencies. One potential issue is the requirement for relatively high critical magnetic fields and field intervals (1.5-3 T) for the onset of FIPT and for reversible FIPT, respectively.« less

Nutritional approaches to combat oxidative stress in Alzheimer's disease.

Abstract: Alzheimer's disease (AD) brains are characterized by extensive oxidative stress. Additionally, large depositions of amyloid -peptide (A) are observed, and many researchers opine that A is central to the pathogenesis of AD. Our laboratory combined these two observations in a comprehensive model for neurodegeneration in AD brains centered around A-induced oxidative stress. Given the oxidative stress in AD and its potentially important role in neurodegeneration, considerable research has been conducted on the use of antioxidants to slow or reverse the pathology and course of AD. One source of antioxidants is the diet. This review examines the literature of the effects of endogenous and exogenous, nutritionally-derived antioxidants in relation to AD. In particular, studies of glutathione and other SH-containing antioxidants, vitamins, and polyphenolic compounds and their use in AD and modulation of A-induced oxidative stress and neurotoxicity are reviewed. © 2002 Elsevier Science Inc. All rights reserved.

Sex differences in phenotypic plasticity affect variation in sexual size dimorphism in insects: from physiology to evolution.

Abstract: Males and females of nearly all animals differ in their body size, a phenomenon called sexual size dimorphism (SSD). The degree and direction of SSD vary considerably among taxa, including among populations within species. A considerable amount of this variation is due to sex differences in body size plasticity. We examine how variation in these sex differences is generated by exploring sex differences in plasticity in growth rate and development time and the physiological regulation of these differences (e.g., sex differences in regulation by the endocrine system). We explore adaptive hypotheses proposed to explain sex differences in plasticity, including those that predict that plasticity will be lowest for traits under strong selection (adaptive canalization) or greatest for traits under strong directional selection (condition dependence), but few studies have tested these hypotheses. Studies that combine proximate and ultimate mechanisms offer great promise for understanding variation in SSD and sex differences in body size plasticity in insects.

Mitochondrial permeability transition in CNS trauma: cause or effect of neuronal cell death?

Abstract: Experimental traumatic brain injury (TBI) and spinal cord injury (SCI) result in a rapid and significant necrosis of neuronal tissue at the site of injury. In the ensuing hours and days, secondary injury exacerbates the primary damage, resulting in significant neurologic dysfunction. It is believed that alterations in excitatory amino acids (EAA), increased reactive oxygen species (ROS), and the disruption of Ca(2+) homeostasis are major factors contributing to the ensuing neuropathology. Mitochondria serve as the powerhouse of the cell by maintaining ratios of ATP:ADP that thermodynamically favor the hydrolysis of ATP to ADP + P(i), yet a byproduct of this process is the generation of ROS. Proton-pumping by components of the electron transport system (ETS) generates a membrane potential (DeltaPsi) that can then be used to phosphorylate ADP or sequester Ca(2+) out of the cytosol into the mitochondrial matrix. This allows mitochondria to act as cellular Ca(2+) sinks and to be in phase with changes in cytosolic Ca(2+) levels. Under extreme loads of Ca(2+), however, opening of the mitochondrial permeability transition pore (mPTP) results in the extrusion of mitochondrial Ca(2+) and other high- and low-molecular weight components. This catastrophic event discharges DeltaPsi and uncouples the ETS from ATP production. Cyclosporin A (CsA), a potent immunosuppressive drug, inhibits mitochondrial permeability transition (mPT) by binding to matrix cyclophilin D and blocking its binding to the adenine nucleotide translocator. Peripherally administered CsA attenuates mitochondrial dysfunction and neuronal damage in an experimental rodent model of TBI, in a dose-dependent manner. The underlying mechanism of neuroprotection afforded by CsA is most likely via interaction with the mPTP because the immunosuppressant FK506, which has no effect on the mPT, was not neuroprotective. When CsA was administrated after experimental SCI at the same dosage and regimen used TBI paradigms, however, it had no beneficial neuroprotective effects. This review takes a comprehensive and critical look at the evidence supporting the role for mPT in central nervous system (CNS) trauma and highlights the differential responses of CNS mitochondria to mPT induction and the implications this has for therapeutically targeting the mPT in TBI and SCI.