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Articles 1 - 12 of 12
Full-Text Articles in Social and Behavioral Sciences
Dissociation Of Β1 And Β2 Adrenergic Receptor Subtypes In Retrieval And Reconsolidation Of A Cocaine Conditioned Place Preference, Michael Fitzgerald
Dissociation Of Β1 And Β2 Adrenergic Receptor Subtypes In Retrieval And Reconsolidation Of A Cocaine Conditioned Place Preference, Michael Fitzgerald
Theses and Dissertations
Drug-seeking behavior is maintained by encounters with drug-associated cues, and disrupting retrieval or reconsolidation of the drug-cue associations could reduce the risk of relapse. Previous work has shown beta-adrenergic receptor (beta-AR) antagonists can prevent retrieval or reconsolidation of a cocaine conditioned place preference (CPP) when administered either before or after test, respectively (Otis and Mueller, 2011; Otis et al., 2013). However, the specific beta-AR subtypes that mediate retrieval and reconsolidation of a cocaine CPP remain unknown. Here we used selective blockade of & beta-1 or beta-2-AR subtypes to determine the effects on retrieval and reconsolidation of a cocaine CPP. During …
Extracellular Chaperones Modulate The Effects Of Alzheimer's Patient Cerebrospinal Fluid On A Beta(1-42) Toxicity And Uptake , Justin J. Yerbury, Mark R. Wilson
Extracellular Chaperones Modulate The Effects Of Alzheimer's Patient Cerebrospinal Fluid On A Beta(1-42) Toxicity And Uptake , Justin J. Yerbury, Mark R. Wilson
Mark R Wilson
Alzheimer's disease is characterised by the inappropriate death of brain cells and accumulation of the A beta peptide in the brain. Thus, it is possible that there are fundamental differences between Alzheimer's disease patients and healthy individuals in their abilities to clear A beta from brain fluid and to protect neurons from A beta toxicity. In the present study, we examined (1) the cytotoxicity of Alzheimer's disease cerebrospinal fluid (CSF) compared to control CSF, (2) the ability of Alzheimer's disease and control CSF to protect cells from A beta toxicity and to promote cell-mediated clearance of A beta and lastly …
Diets High In Oat-Derived Beta-Glucan Promote Negative Energy Regulatory Pathway Of Hypothalamic Npy System In Chronic Diet-Induced Obesity In Mice, Xu-Feng Huang, Timothy South, Eleanor Beck, Marijka Batterham, K. Grinter, Linda Tapsell
Diets High In Oat-Derived Beta-Glucan Promote Negative Energy Regulatory Pathway Of Hypothalamic Npy System In Chronic Diet-Induced Obesity In Mice, Xu-Feng Huang, Timothy South, Eleanor Beck, Marijka Batterham, K. Grinter, Linda Tapsell
Xu-Feng Huang
No abstract provided.
Am 251 And Beta-Funaltrexamine Reduce Fat Intake In A Fat-Preferring Strain Of Mouse, Xu-Feng Huang, Chao Deng, Timothy South
Am 251 And Beta-Funaltrexamine Reduce Fat Intake In A Fat-Preferring Strain Of Mouse, Xu-Feng Huang, Chao Deng, Timothy South
Xu-Feng Huang
No abstract provided.
Alphab-Crystallin Inhibits The Cell Toxicity Associated With Amyloid Fibril Formation By Kappa-Casein And The Amyloid-Beta Peptide, Francis C. Dehle, Heath Ecroyd, Ian F. Musgrave, John A. Carver
Alphab-Crystallin Inhibits The Cell Toxicity Associated With Amyloid Fibril Formation By Kappa-Casein And The Amyloid-Beta Peptide, Francis C. Dehle, Heath Ecroyd, Ian F. Musgrave, John A. Carver
Heath Ecroyd
Amyloid fibril formation is associated with diseases such as Alzheimer’s, Parkinson’s, and prion diseases. Inhibition of amyloid fibril formation by molecular chaperone proteins, such as the small heat-shock protein αB-crystallin, may play a protective role in preventing the toxicity associated with this form of protein misfolding. Reduced and carboxymethylated κ-casein (RCMκ-CN), a protein derived from milk, readily and reproducibly forms fibrils at physiological temperature and pH. We investigated the toxicity of fibril formation by RCMκ-CN using neuronal model PC12 cells and determined whether the inhibition of fibril formation altered its cell toxicity. To resolve ambiguities in the literature, we also …
Wild Type And Tangier Disease Abca1 Mutants Modulate Cellular Amyloid-Beta Production Independent Of Cholesterol Efflux Activity, Kim S. Woojin, Andrew F. Hill, Michael L. Fitzgerald, Mason W. Freeman, Genevieve Evin, Brett Garner
Wild Type And Tangier Disease Abca1 Mutants Modulate Cellular Amyloid-Beta Production Independent Of Cholesterol Efflux Activity, Kim S. Woojin, Andrew F. Hill, Michael L. Fitzgerald, Mason W. Freeman, Genevieve Evin, Brett Garner
Faculty of Science - Papers (Archive)
Cerebral amyloid-β (Aβ) deposition is a critical feature of Alzheimer’s disease. Aβ is derived from the amyloid-β protein precursor (AβPP) via two sequential cleavages that are mediated by β-secretase and the γ-secretase complex. Such amyloidogenic AβPP processing occurs in lipid raft microdomains of cell membranes and it is thought that modulating the distribution of lipids in rafts may regulate AβPP processing and Aβ production. Certain ATP-binding cassette (ABC) transporters regulate lipid transport across cell membranes and, as recent studies reveal, within membrane microdomains. ABCA1 also regulates Aβ metabolism in the brain although its direct impact on AβPP remains an open …
Dipyridyl Beta-Diketonate Complexes: Versatile Polydentate Metalloligands For Metal-Organic Frameworks And Hydrogen-Bonded Networks, Andrew D. Burrows, Christopher G. Frost, Mary F. Mahon, Paul R. Raithby, Catherine L. Renouf, Christopher Richardson, Anna J. Stevenson
Dipyridyl Beta-Diketonate Complexes: Versatile Polydentate Metalloligands For Metal-Organic Frameworks And Hydrogen-Bonded Networks, Andrew D. Burrows, Christopher G. Frost, Mary F. Mahon, Paul R. Raithby, Catherine L. Renouf, Christopher Richardson, Anna J. Stevenson
Faculty of Science - Papers (Archive)
The Group 13 metal complexes [M(L-2)(3)], where M is Al or Ga and L-2 is 1,3-di(4-pyridyl)-1,3-propanedionato, are hexatopic metalloligands that have been used to prepare mixed-metalorganic frameworks containing interpenetrated primitive cubic networks. In contrast, the europium complex [Eu(HL2)(3)-(H2L2)]Cl-4 center dot EtOH forms a hydrogen-bonded network following partial protonation of the pyridyl groups.
Extracellular Chaperones Modulate The Effects Of Alzheimer's Patient Cerebrospinal Fluid On A Beta(1-42) Toxicity And Uptake , Justin J. Yerbury, Mark R. Wilson
Extracellular Chaperones Modulate The Effects Of Alzheimer's Patient Cerebrospinal Fluid On A Beta(1-42) Toxicity And Uptake , Justin J. Yerbury, Mark R. Wilson
Faculty of Science - Papers (Archive)
Alzheimer's disease is characterised by the inappropriate death of brain cells and accumulation of the A beta peptide in the brain. Thus, it is possible that there are fundamental differences between Alzheimer's disease patients and healthy individuals in their abilities to clear A beta from brain fluid and to protect neurons from A beta toxicity. In the present study, we examined (1) the cytotoxicity of Alzheimer's disease cerebrospinal fluid (CSF) compared to control CSF, (2) the ability of Alzheimer's disease and control CSF to protect cells from A beta toxicity and to promote cell-mediated clearance of A beta and lastly …
Alphab-Crystallin Inhibits The Cell Toxicity Associated With Amyloid Fibril Formation By Kappa-Casein And The Amyloid-Beta Peptide, Francis C. Dehle, Heath Ecroyd, Ian F. Musgrave, John A. Carver
Alphab-Crystallin Inhibits The Cell Toxicity Associated With Amyloid Fibril Formation By Kappa-Casein And The Amyloid-Beta Peptide, Francis C. Dehle, Heath Ecroyd, Ian F. Musgrave, John A. Carver
Faculty of Science - Papers (Archive)
Amyloid fibril formation is associated with diseases such as Alzheimer’s, Parkinson’s, and prion diseases. Inhibition of amyloid fibril formation by molecular chaperone proteins, such as the small heat-shock protein αB-crystallin, may play a protective role in preventing the toxicity associated with this form of protein misfolding. Reduced and carboxymethylated κ-casein (RCMκ-CN), a protein derived from milk, readily and reproducibly forms fibrils at physiological temperature and pH. We investigated the toxicity of fibril formation by RCMκ-CN using neuronal model PC12 cells and determined whether the inhibition of fibril formation altered its cell toxicity. To resolve ambiguities in the literature, we also …
Crystallization And Diffraction Data Of 1h-3-Hydroxy-4-Oxoquinoline 2,4-Dioxygenase: A Cofactor-Free Oxygenase Of The Alpha/Beta-Hydrolase Family, Ruhu Qi, Susanne Fetzner, Aaron J. Oakley
Crystallization And Diffraction Data Of 1h-3-Hydroxy-4-Oxoquinoline 2,4-Dioxygenase: A Cofactor-Free Oxygenase Of The Alpha/Beta-Hydrolase Family, Ruhu Qi, Susanne Fetzner, Aaron J. Oakley
Faculty of Science - Papers (Archive)
1H-3-Hydroxy-4-oxoquinoline 2,4-dioxygenase (QDO) from Pseudomonas putida 33/1 catalyses the oxygenolysis of 1H-3-hydroxy-4-oxoquinoline to form N-formylanthranilic acid and carbon monoxide without the aid of cofactors. Both N-terminally His6-tagged and native QDO were overexpressed in Escherichia coli and purified by conventional chromatographic procedures. Untagged QDO, but not His6-tagged QDO, was crystallized by the vapour-diffusion method, giving hexagonal bipyramid crystals belonging to space group P6(1)22. Selenomethionine-containing native QDO was prepared and crystallized under identical conditions. The unit-cell parameters were a = b = 90.1, c = 168.6 A, alpha = beta = 90, gamma = 120 degrees. Using synchrotron radiation, these crystals diffract …
Amyloid Fibril Formation By Bovine Milk Kappa-Casein And Its Inhibition By The Molecular Chaperones Alpha-S And Beta-Casein, Mark Wilson, David Thorn, Agata Rekas, S. L Gras, Christopher Dobson, Sarah Meehan, Cait Macphee, M Sunde
Amyloid Fibril Formation By Bovine Milk Kappa-Casein And Its Inhibition By The Molecular Chaperones Alpha-S And Beta-Casein, Mark Wilson, David Thorn, Agata Rekas, S. L Gras, Christopher Dobson, Sarah Meehan, Cait Macphee, M Sunde
Mark R Wilson
No abstract provided.
Lymphotoxin-Beta Receptor-Dependent Genes In Lymph Node And Follicular Dendritic Cell Transcriptomes, Mark Wilson, C. Huber, C. Thielen, Y. Fu, E. Heinen, A Aguzzi, G Miele
Lymphotoxin-Beta Receptor-Dependent Genes In Lymph Node And Follicular Dendritic Cell Transcriptomes, Mark Wilson, C. Huber, C. Thielen, Y. Fu, E. Heinen, A Aguzzi, G Miele
Mark R Wilson
No abstract provided.