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Search Results: 1 - 10 of 237687 matches for " John L Wallace "
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Nitric oxide as a regulator of inflammatory processes
Wallace, John L;
Memórias do Instituto Oswaldo Cruz , 2005, DOI: 10.1590/S0074-02762005000900002
Abstract: nitric oxide (no) plays an important role in mediating many aspects of inflammatory responses. no is an effector molecule of cellular injury, and can act as an anti-oxidant. it can modulate the release of various inflammatory mediators from a wide range of cells participating in inflammatory responses (e.g., leukocytes, macrophages, mast cells, endothelial cells, and platelets). it can modulate blood flow, adhesion of leukocytes to the vascular endothelium and the activity of numerous enzymes, all of which can have an impact on inflammatory responses. in recent years, no-releasing drugs have been developed, usually as derivatives of other drugs, which exhibit very powerful anti-inflammatory effects.
Mechanisms, prevention and clinical implications of nonsteroidal anti-inflammatory drug-enteropathy
John L Wallace
World Journal of Gastroenterology , 2013, DOI: 10.3748/wjg.v19.i12.1861
Abstract: This article reviews the latest developments in understanding the pathogenesis, detection and treatment of small intestinal damage and bleeding caused by nonsteroidal anti-inflammatory drugs (NSAIDs). With improvements in the detection of NSAID-induced damage in the small intestine, it is now clear that this injury and the associated bleeding occurs more frequently than that occurring in the stomach and duodenum, and can also be regarded as more dangerous. However, there are no proven-effective therapies for NSAID-enteropathy, and detection remains a challenge, particularly because of the poor correlation between tissue injury and symptoms. Moreover, recent studies suggest that commonly used drugs for protecting the upper gastrointestinal tract (i.e., proton pump inhibitors) can significantly worsen NSAID-induced damage in the small intestine. The pathogenesis of NSAID-enteropathy is complex, but studies in animal models are shedding light on the key factors that contribute to ulceration and bleeding, and are providing clues to the development of effective therapies and prevention strategies. Novel NSAIDs that do not cause small intestinal damage in animal models offer hope for a solution to this serious adverse effect of one of the most widely used classes of drugs.
COX-2: A Pivotal Enzyme in Mucosal Protection and Resolution of Inflammation
John L. Wallace
The Scientific World Journal , 2006, DOI: 10.1100/tsw.2006.122
Abstract:
Nitric oxide as a mediator of gastrointestinal mucosal injury?—Say it ain't so
Paul Kubes,John L. Wallace
Mediators of Inflammation , 1995, DOI: 10.1155/s0962935195000640
Abstract:
Enhanced Synthesis and Diminished Degradation of Hydrogen Sulfide in Experimental Colitis: A Site-Specific, Pro-Resolution Mechanism
Kyle L. Flannigan, Jose G. P. Ferraz, Rui Wang, John L. Wallace
PLOS ONE , 2013, DOI: 10.1371/journal.pone.0071962
Abstract: Hydrogen sulfide (H2S) is produced throughout the gastrointestinal tract, and it contributes to maintenance of mucosal integrity, resolution of inflammation, and repair of damaged tissue. H2S synthesis is elevated in inflamed and damaged colonic tissue, but the enzymatic sources of that synthesis are not completely understood. In the present study, the contributions of three enzymatic pathways to colonic H2S synthesis were determined, with tissues taken from healthy rats and rats with colitis. The ability of the colonic tissue to inactivate H2S was also determined. Colonic tissue from rats with hapten-induced colitis produced significantly more H2S than tissue from healthy controls. The largest source of the H2S synthesis was the pathway involving cysteine amino transferase and 3-mercaptopyruvate sulfurtransferase (an α-ketoglutarate-dependent pathway). Elevated H2S synthesis occurred specifically at sites of mucosal ulceration, and was not related to the extent of granulocyte infiltration into the tissue. Inactivation of H2S by colonic tissue occurred rapidly, and was significantly reduced at sites of mucosal ulceration. This correlated with a marked decrease in the expression of sulfide quinone reductase in these regions. Together, the increased production and decreased inactivation of H2S at sites of mucosal ulceration would result in higher H2S levels at these sites, which promotes of resolution of inflammation and repair of damaged tissue.
Gastrointestinal-Sparing Effects of Novel NSAIDs in Rats with Compromised Mucosal Defence
Rory Blackler, Stephanie Syer, Manlio Bolla, Ennio Ongini, John L. Wallace
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0035196
Abstract: Nonsteroidal anti-inflammatory drugs are among the most commonly used prescription and over-the-counter medications, but they often produce significant gastrointestinal ulceration and bleeding, particularly in elderly patients and patients with certain co-morbidities. Novel anti-inflammatory drugs are seldom tested in animal models that mimic the high risk human users, leading to an underestimate of the true toxicity of the drugs. In the present study we examined the effects of two novel NSAIDs and two commonly used NSAIDs in models in which mucosal defence was expected to be impaired. Naproxen, celecoxib, ATB-346 (a hydrogen sulfide- and naproxen-releasing compound) and NCX 429 (a nitric oxide- and naproxen-releasing compound) were evaluated in healthy, arthritic, obese, and hypertensive rats and in rats of advanced age (19 months) and rats co-administered low-dose aspirin and/or omeprazole. In all models except hypertension, greater gastric and/or intestinal damage was observed when naproxen was administered in these models than in healthy rats. Celecoxib-induced damage was significantly increased when co-administered with low-dose aspirin and/or omeprazole. In contrast, ATB-346 and NCX 429, when tested at doses that were as effective as naproxen and celecoxib in reducing inflammation and inhibiting cyclooxygenase activity, did not produce significant gastric or intestinal damage in any of the models. These results demonstrate that animal models of human co-morbidities display the same increased susceptibility to NSAID-induced gastrointestinal damage as observed in humans. Moreover, two novel NSAIDs that release mediators of mucosal defence (hydrogen sulfide and nitric oxide) do not induce significant gastrointestinal damage in these models of impaired mucosal defence.
A unique therapeutic approach to emesis and itch with a proanthocyanidin-rich genonutrient
Mark JS Miller, Brian K Reuter, John L Wallace, Keith A Sharkey
Journal of Translational Medicine , 2008, DOI: 10.1186/1479-5876-6-3
Abstract: Emesis was induced in ferrets with morphine-6-glucuronide (0.05 mg/kg sc) in the presence of Zangrado (3 mg/kg, ip) and the cannabinoid receptor 1 antagonist, AM 251 (5 mg/kg, ip). Topical Zangrado (1%) was assessed for anti-pruretic actions in the 5-HT-induced scratching model in rats and evaluated in capsaicin-induced gastric hyperemia as measured by laser doppler flow. In the ApcMinmouse model of precancerous adenomatosis polyposis, mice received Zangrado (100 μg/ml in drinking water) from the age of 6 – 16 weeks for effects on polyp number. In RAW 264.7 cells Zangrado was examined for effects on lipopolysaccharide-induced nitrite production.Zangrado was a highly effective anti-emetic, reducing morphine-induced vomiting and retching by 77%. These benefits were not associated with sedation or hypothermia and were not reversed by cannabinoid receptor antagonism. Itch responses were blocked in both the morphine and 5-HT models. Zangrado did not exacerbate the ApcMincondition rather health was improved. Capsaicin-induced hyperemia was blocked by Zangrado, which also attenuated the production of nitric oxide by activated macrophages.Zangrado is an effective anti-emetic and anti-itch therapy that is devoid of common side-effects, cannabinoid-independent and broadly suppresses sensory afferent nerve activation. This complementary medicine represents a promising new approach to the management of nausea, itch and irritable bowel syndrome.The latex of the Amazonian traditional medicine Croton palanostigma and related Croton species is traditionally used in the treatment of inflammation, pain, itch, and a number of gastrointestinal afflictions that are common in the rainforest [1]. This traditional medicine is derived from a fast growing tree that is known by different names in various countries: in Peru it is called sangre de grado and in Ecuador, sangre de drago. We have found substantial scientific support for a number of these ethnomedical applications [2-4]. A central
A protease activated receptor-2 (PAR-2) activating peptide, tc-LIGRLO-NH2, induces protease release from mast cells: role in TNF degradation
Alshurafa Hashem N,Stenton Grant R,Wallace John L,Hollenberg Morley D
BMC Pharmacology , 2004, DOI: 10.1186/1471-2210-4-12
Abstract: Background Mast cell (MC)-derived serine proteases have been implicated in a variety of inflammatory processes. We have previously shown that rat peritoneal MC (PMC) express mRNA for protease activated receptor 2 (PAR-2), a G-coupled receptor activated by trypsin-like proteases. Recent evidence also suggests that MC-induced inflammation can be mediated through PAR. Therefore, we hypothesized that specific PAR-2 agonist peptides (PAR-2ap) induce protease release from PMC. Results Western blot analysis of PMC supernatants revealed that a PAR-2ap, tc-LIGRLO (10 μM), stimulated the release of rat MC protease (RMCP)-1, RMCP-5 and carboxypeptidase-A. The release was evident by 20 min but further increased up to 8 h. To study the biological effects of protease release we tested supernatants from tc-LIGRLO, tc-OLRGIL (inactive control peptide) and antigen-activated PMC for proteolytic activity by seeding with TNF (150 pg/ml), incubating for 8 h at 37°C, and measuring TNF remaining in the supernatants. Supernatants from tc-LIGRLO-stimulated PMC degraded 44 % of seeded TNF (n = 5). Moreover, this TNF proteolysis was dependent on the concentration of tc-LIGRLO used to stimulate PMC, and was significantly inhibited (94 %) by soybean trypsin inhibitor. Antigen and tc-OLRGIL induced no significant release of such proteolytic activity. Conclusions These data indicate that a PAR-2ap induces the release of proteases from mast cells, which may degrade extracellular cytokines and other substrates thus modulating the inflammatory response.
Behavior, design, and modeling of structural walls and coupling beams — Lessons from recent laboratory tests and earthquakes
John W. Wallace
International Journal of Concrete Structures and Materials , 2012, DOI: 10.1007/s40069-012-0001-4
Abstract: Observed wall damage in recent earthquakes in Chile and New Zealand, where modern building codes exist, exceeded expectations. In these earthquakes, structural wall damage included boundary crushing, reinforcement fracture, and global wall buckling. Recent laboratory tests also have demonstrated inadequate performance in some cases, indicating a need to review code provisions, identify shortcomings and make necessary revisions. Current modeling approaches used for slender structural walls adequately capture nonlinear flexural behavior; however, strength loss due to buckling of reinforcement and nonlinear and shear-flexure interaction are not adequately captured. Additional research is needed to address these issues. Recent tests of reinforced concrete coupling beams indicate that diagonally-reinforced beams detailed according to ACI 318-111 can sustain plastic rotations of about 6% prior to significant strength loss and that relatively simple modeling approaches in commercially available computer programs are capable of capturing the observed responses. Tests of conventionally-reinforced beams indicate less energy dissipation capacity and strength loss at approximately 4% rotation.
Electrodynamics in Iron and Steel
John Paul Wallace
Physics , 2009,
Abstract: In order to calculate the reflected EM fields at low amplitudes in iron and steel, more must be understood about the nature of long wavelength excitations in these metals. A bulk piece of iron is a very complex material with microstructure, a split band structure, magnetic domains and crystallographic textures that affect domain orientation. Probing iron and other bulk ferromagnetic materials with weak reflected and transmitted inductive low frequency fields is an easy operation to perform but the responses are difficult to interpret because of the complexity and variety of the structures affected by the fields. First starting with a simple single coil induction measurement and classical EM calculation to show the error is grossly under estimating the measured response. Extending this experiment to measuring the transmission of the induced fields allows the extraction of three dispersion curves which define these internal fields. One dispersion curve yielded an exceedingly small effective mass of 1.8 10^{-39}kg (1.3 10^{-9} m_e) for those spin waves. There is a second distinct dispersion curve more representative of the density function of a zero momentum bound state rather than a propagating wave. The third dispersion curve describes a magneto-elastic coupling to a very long wave length propagating mode. These experiments taken together display the characteristics of a high temperature Bose-Einstein like condensation that can be initiated by pumping two different states. A weak time dependent field drives the formation of coupled J=0 spin wave pairs with the reduced effective mass reflecting the increased size of the coherent state. These field can dominate induction measurements well past the Curie temperature.
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