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Search Results: 1 - 10 of 217314 matches for " L. Charles Murrin "
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Mitochondrial Fragmentation Is Involved in Methamphetamine-Induced Cell Death in Rat Hippocampal Neural Progenitor Cells
Changhai Tian, L. Charles Murrin, Jialin C. Zheng
PLOS ONE , 2009, DOI: 10.1371/journal.pone.0005546
Abstract: Methamphetamine (METH) induces neurodegeneration through damage and apoptosis of dopaminergic nerve terminals and striatal cells, presumably via cross-talk between the endoplasmic reticulum and mitochondria-dependent death cascades. However, the effects of METH on neural progenitor cells (NPC), an important reservoir for replacing neurons and glia during development and injury, remain elusive. Using a rat hippocampal NPC (rhNPC) culture, we characterized the METH-induced mitochondrial fragmentation, apoptosis, and its related signaling mechanism through immunocytochemistry, flow cytometry, and Western blotting. We observed that METH induced rhNPC mitochondrial fragmentation, apoptosis, and inhibited cell proliferation. The mitochondrial fission protein dynamin-related protein 1 (Drp1) and reactive oxygen species (ROS), but not calcium (Ca2+) influx, were involved in the regulation of METH-induced mitochondrial fragmentation. Furthermore, our results indicated that dysregulation of ROS contributed to the oligomerization and translocation of Drp1, resulting in mitochondrial fragmentation in rhNPC. Taken together, our data demonstrate that METH-mediated ROS generation results in the dysregulation of Drp1, which leads to mitochondrial fragmentation and subsequent apoptosis in rhNPC. This provides a potential mechanism for METH-related neurodegenerative disorders, and also provides insight into therapeutic strategies for the neurodegenerative effects of METH.
Impairment of brain endothelial glucose transporter by methamphetamine causes blood-brain barrier dysfunction
P M Abdul Muneer, Saleena Alikunju, Adam M Szlachetka, L Charles Murrin, James Haorah
Molecular Neurodegeneration , 2011, DOI: 10.1186/1750-1326-6-23
Abstract: In this study, we demonstrate that METH-induced disruption of glucose uptake by endothelium lead to BBB dysfunction. Our data indicate that a low concentration of METH (20 μM) increased the expression of glucose transporter protein-1 (GLUT1) in primary human brain endothelial cell (hBEC, main component of BBB) without affecting the glucose uptake. A high concentration of 200 μM of METH decreased both the glucose uptake and GLUT1 protein levels in hBEC culture. Transcription process appeared to regulate the changes in METH-induced GLUT1 expression. METH-induced decrease in GLUT1 protein level was associated with reduction in BBB tight junction protein occludin and zonula occludens-1. Functional assessment of the trans-endothelial electrical resistance of the cell monolayers and permeability of dye tracers in animal model validated the pharmacokinetics and molecular findings that inhibition of glucose uptake by GLUT1 inhibitor cytochalasin B (CB) aggravated the METH-induced disruption of the BBB integrity. Application of acetyl-L-carnitine suppressed the effects of METH on glucose uptake and BBB function.Our findings suggest that impairment of GLUT1 at the brain endothelium by METH may contribute to energy-associated disruption of tight junction assembly and loss of BBB integrity.Methamphetamine (METH), a highly addictive drug is a potent CNS stimulant that produces euphoric effects by promoting the release of dopamine, serotonin and norepinephrine [1]. METH abuse and trafficking are increasing law enforcement and social health problems in the United States, particularly in the mid-western states where the rates of METH users among teenagers (12-17 years) and young adults (18-25 years) are highest in the country [2]. The escalating problems due to METH abuse are enormous financial and health burdens to family and society. The ability of METH to stimulate the release of dopamine rapidly from dopaminergic neurons in the reward regions of the brain produces intense eupho
Semi-classical properties of geometric quantization with metaplectic correction
L. Charles
Mathematics , 2006, DOI: 10.1007/s00220-006-0155-5
Abstract: The geometric quantization of a symplectic manifold endowed with a prequantum bundle and a metaplectic structure is defined by means of an integrable complex structure. We prove that its semi-classical limit does not depend on the choice of the complex structure. We show this in two ways. First, by introducing unitary identifications between the quantum spaces associated to the various complex polarizations and second, by defining an asymptotically flat connection in the bundle of quantum spaces over the space of complex structures. Furthermore Berezin-Toeplitz operators are intertwined by these identifications and have principal and subprincipal symbols defined independently of the complex structure. The relation with Schrodinger equation and the group of prequantum bundle automorphisms is considered as well.
Symbolic calculus for Toeplitz operators with half-forms
L. Charles
Mathematics , 2006,
Abstract: This paper is devoted to the use of half-form bundles in the symbolic calculus of Berezin-Toeplitz operators on Kahler manifolds. We state the Bohr-Sommerfeld conditions and relate them to the functional calculus of Toeplitz operators, a trace formula and the characteristic classes in deformation quantization. We also develop the symbolic calculus of Lagrangian sections, with the crucial estimate of the subprincipal terms.
Toeplitz operators and Hamiltonian torus action
L. Charles
Mathematics , 2004,
Abstract: This paper is devoted to semi-classical aspects of symplectic reduction. Consider a compact prequantizable Kahler manifold M with a Hamiltonian torus action. Guillemin and Sternberg introduced an isomorphism between the invariant part of the quantum space associated to M and the quantum space associated to the symplectic quotient of M, provided this quotient is non-singular. We prove that this isomorphism is a Fourier integral operator and that the Toeplitz operators of M descend to Toeplitz operators of the reduced phase space. We also extend these results to the case where the symplectic quotient is an orbifold and estimate the spectral density of a reduced Toeplitz operator, a result related to the Riemann-Roch-Kawazaki theorem.
Aged rat heart: Modulation of age-related respiratory defects decreases ischemic-reflow injury  [PDF]
Edward J. Lesnefsky, Charles L. Hoppel
Health (Health) , 2013, DOI: 10.4236/health.2013.51001

Myocardial injury increases in the elderly heart during ischemia and reperfusion. Mitochondria, the key targets and sources of injury during ischemia and reperfusion, sustain ischemic damage to the electron transport chain that is superimposed upon age-related defects. In the adult heart, interventions to activate endogenous cytoprotective signaling systems meet in mitochondria to decrease cardiac injury. Unfortunately, these systems are largely ineffective in the aged heart. Thus, new treatment concepts are needed to reduce injury in the aged heart. Our group chose a strategy to directly treat the effector of cardiac injury in the aged heart, the mitochondria. We further utilized a novel approach to ask if the reversal of aging defects in cardiac mitochondria before ischemia could decrease ischemia-reperfusion injury in the heart. Three hours following treatment with the small molecule, nutriceutical acetylcarnitine (AcCN), oxidative phosphorylation as well as age-induced defects in electron transport chain complexes III and IV was corrected in the heart. When such hearts were then exposed to ischemia and reperfusion, cardiac injury was markedly reduced. Contraction during reperfusion improved and recovery became similar to that in adult hearts. Cardiac cell death was substantially reduced. Thus, age-related defects in electron transport are a key mechanism of the increased myocardial injury in the elderly heart during ischemia and reperfusion. Modulation of aging-induced defects in mitochondrial metabolism reduces cardiac injury from ischemia and reperfusion, and is a novel strategy to protect myocardium in the elderly patient at risk for an acute myocardial infarction.

Effectiveness of Cognitive Therapy and Mindfulness Tools in Reducing Depression and Anxiety: A Mixed Method Study  [PDF]
Valerie L. Alexander, B. Charles Tatum
Psychology (PSYCH) , 2014, DOI: 10.4236/psych.2014.515178
Abstract: Depression and anxiety continue to be among the most common mental disorders. This study looked at three tracks of participants diagnosed with a mood disorder. The three tracks were Cognitive Therapy (CT), Mindfulness Training (MT), and Treatment As Usual (TAU). All participants had been trained in CT and then randomly separated into three groups. These three tracks were assessed at 3, 6, and 12 months in terms of their stated level of depression (measured on the Beck Depression Inventory) and anxiety (measured by the Beck Anxiety Inventory). This study was a follow-up to two previous studies (Alexander et al., 2012; Alexander & Tatum, 2013). In the current study, the participants reported the tools and skills they used to manage their mood and anxiety and then the effectiveness of these tools/skills was examined. Two tools were identified by three independent coders as the most frequently used by the participants. Both of these tools related to thought management (“thought records” and “thought distortions”). The two tools were combined into a single category (“thought tools”) and the frequency of their use was examined in relation to reductions in depression and anxiety. The results showed that a high use of these tools was connected to a significant reduction in reported depression. There was also a reduction in reported anxiety, but this effect was not statistically significant. Other tools that were reported (e.g., mood tracking, relaxation) showed no significant effects on depression and anxiety. Future research will now focus not on reported tool use, but rather on manipulating the incidence of tool use and determine the direct causal path between using a thought tool and reductions in negative moods.
Modeling the signaling endosome hypothesis: Why a drive to the nucleus is better than a (random) walk
Charles L Howe
Theoretical Biology and Medical Modelling , 2005, DOI: 10.1186/1742-4682-2-43
Abstract: Using large-scale Monte Carlo simulations of diffusing STAT-3 molecules coupled with probabilistic modeling of dephosphorylation kinetics we found that predicted theoretical measures of STAT-3 diffusion likely overestimate the effective range of this signal. Compared to the inherently nucleus-directed movement of retrogradely transported signaling endosomes, diffusion of STAT-3 becomes less efficient at information transfer in spatial domains greater than 200 nanometers from the plasma membrane.Our model suggests that cells might utilize two distinct information transmission paradigms: 1) fast local signaling via diffusion over spatial domains on the order of less than 200 nanometers; 2) long-distance signaling via information packets associated with the cytoskeletal transport apparatus. Our model supports previous observations suggesting that the signaling endosome hypothesis is a subset of a more general hypothesis that the most efficient mechanism for intracellular signaling-at-a-distance involves the association of signaling molecules with molecular motors that move along the cytoskeleton. Importantly, however, cytoskeletal association of membrane-bounded complexes containing ligand-occupied transmembrane receptors and downstream effector molecules provides the ability to regenerate signals at any point along the transmission path. We conclude that signaling endosomes provide unique information transmission properties relevant to all cell architectures, and we propose that the majority of relevant information transmitted from the plasma membrane to the nucleus will be found in association with organelles of endocytic origin.The transmission of signals from the extracellular surface of the plasma membrane to the nucleus is a complex process that involves a large repertoire of trafficking-related and signal-transducing proteins. A highly dynamic and carefully orchestrated series of molecular events has evolved to ensure that signals emanating from outside the cell
The Biology of Nearctic Lepidoptera—Part I: Foodplants and Life-Histories of Colorado Papilionoidea
Charles L. Remington
Psyche , 1952, DOI: 10.1155/1952/61092
The Biology of Nearctic Lepidoptera—Part II: Foodplant and Pupa of Hemiargus Isolus
Charles L. Remington
Psyche , 1952, DOI: 10.1155/1952/81347
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