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Hitesh Handa - One of the best experts on this subject based on the ideXlab platform.
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S-Nitroso-N-Acetylpenicillamine (SNAP) Impregnated Endotracheal Tubes for Prevention of Ventilator-Associated Pneumonia.
Biotechnology and Bioengineering, 2020Co-Authors: Katie H. Homeyer, Marcus J Goudie, Priyadarshini Singha, Hitesh HandaAbstract:: The chances of ventilator-associated pneumonia (VAP) increases 6- to 20-fold when an endotracheal tube is placed in a patient. VAP is one of the most common hospital-acquired infections and comprises 86% of the nosocomial pneumonia cases. This work introduces the idea of nitric oxide-releasing endotracheal tubes (NORel-ETTs) fabricated by the incorporation of the nitric oxide (NO) donor S-Nitroso-N-Acetylpenicillamine (SNAP) into commercially available endotracheal tubes via solvent swelling. The impregnation of SNAP provides NO release over a 7-d period without altering the mechanical properties of the endotracheal tube. The NORel-ETTs successfully reduced the bacterial infection from a commonly found pathogen in VAP, P. aeruginosa, by 92.72 ± 0.97% when compared to the control endotracheal tubes. Overall, this study presents the incorporation of the active release of a bactericidal agent in endotracheal tubes as an efficient strategy to prevent the risk of VAP. This article is protected by copyright. All rights reserved.
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Multifunctional S-Nitroso-N-Acetylpenicillamine-Incorporated Medical-Grade Polymer with Selenium Interface for Biomedical Applications.
ACS Applied Materials & Interfaces, 2019Co-Authors: Arnab Mondal, Hitesh Handa, Priyadarshini Singha, Megan Douglass, Sean P. Hopkins, Martin Tran, Elizabeth J BrisboisAbstract:Modern crises in implantable or indwelling blood-contacting medical devices are mainly due to the dual problems of infection and thrombogenicity. There is a paucity of biomaterials that can address both problems simultaneously through a singular platform. Taking cues from the body’s own defense mechanism against infection and blood clotting (thrombosis) via the endogenous gasotransmitter nitric oxide (NO), both of these issues are addressed through the development of a layered S-Nitroso-N-Acetylpenicillamine (SNAP)-doped polymer with a blended selenium (Se)–polymer interface. The unique capability of the SNAP-Se-1 polymer composites to explicitly release NO from the SNAP reservoir as well as generate NO via the incorporated Se is reported for the first time. The NO release from the SNAP-doped polymer increased substantially in the presence of the Se interface. The Se interface was able to generate NO in the presence of S-nitrosoglutathione (GSNO) and glutathione (GSH), demonstrating the capability of gene...
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Nitric oxide‐releasing antibacterial albumin plastic for biomedical applications
Journal of Biomedical Materials Research Part A, 2018Co-Authors: Alexander Jones, Jitendra Pant, Eliza Lee, Joel Mansfield, Abhyuday Mandal, Suraj Sharma, Alexey Gruzd, Marcus J Goudie, Hitesh HandaAbstract:Designing innovative materials for biomedical applications is desired to prevent surface fouling and risk of associated infections arising in the surgical care patient. In the present study, albumin plastic was fabricated and nitric oxide (NO) donor, S-Nitroso-N-Acetylpenicillamine (SNAP), was incorporated through a solvent swelling process. The albumin-SNAP plastic was evaluated in terms of mechanical and thermal properties, and bacterial adhesion to the plastic surface. Thermal and viscoelastic analyses showed no significant difference between albumin-SNAP plastics and pure, water-plasticized albumin samples. Bacteria adhesion tests revealed that albumin-SNAP plastic can significantly reduce the surface-bound viable gram-positive Staphylococcus aureus and gram-negative Pseudomonas aeruginosa bacterial cells by 98.7 and 98.5%, respectively, when compared with the traditional polyvinyl chloride medical grade tubing material. The results from this study demonstrate NO-releasing albumin plastic's potential as a material for biomedical device applications. © 2018 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 106A: 1535-1542, 2018.
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tunable nitric oxide release from s nitroso n acetylpenicillamine via catalytic copper nanoparticles for biomedical applications
ACS Applied Materials & Interfaces, 2017Co-Authors: Jitendra Pant, Elizabeth J Brisbois, Marcus J Goudie, Sean P. Hopkins, Hitesh HandaAbstract:The quest for novel therapies to prevent bacterial infections and blood clots (thrombosis) is of utmost importance in biomedical research due to the exponential growth in the cases of thrombosis and blood infections and the emergence of multi-drug-resistant strains of bacteria. Endogenous nitric oxide (NO) is a cellular signaling molecule that plays a pivotal role in host immunity against pathogens, prevention of clotting, and regulation of systemic blood pressure, among several other biological functions. The physiological effect of NO is dose dependent, which necessitates the study of its tunable release kinetics, which is the objective of this study. In the present study, polymer composites were fabricated by incorporating S-Nitroso-N-Acetylpenicillamine (SNAP) in a medical-grade polymer, Carbosil, and top-coated with varying concentrations of catalytic copper nanoparticles (Cu-NPs). The addition of the Cu-NPs increased the NO release, as well as the overall antimicrobial activity via the oligodynamic ...
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Tunable Nitric Oxide Release from S-Nitroso-N-Acetylpenicillamine via Catalytic Copper Nanoparticles for Biomedical Applications.
ACS applied materials & interfaces, 2017Co-Authors: Jitendra Pant, Elizabeth J Brisbois, Marcus J Goudie, Sean P. Hopkins, Hitesh HandaAbstract:The quest for novel therapies to prevent bacterial infections and blood clots (thrombosis) is of utmost importance in biomedical research due to the exponential growth in the cases of thrombosis and blood infections and the emergence of multi-drug-resistant strains of bacteria. Endogenous nitric oxide (NO) is a cellular signaling molecule that plays a pivotal role in host immunity against pathogens, prevention of clotting, and regulation of systemic blood pressure, among several other biological functions. The physiological effect of NO is dose dependent, which necessitates the study of its tunable release kinetics, which is the objective of this study. In the present study, polymer composites were fabricated by incorporating S-Nitroso-N-Acetylpenicillamine (SNAP) in a medical-grade polymer, Carbosil, and top-coated with varying concentrations of catalytic copper nanoparticles (Cu-NPs). The addition of the Cu-NPs increased the NO release, as well as the overall antimicrobial activity via the oligodynamic effect of Cu. SNAP (10 wt %) composites without Cu-NP coatings showed a NO flux of 1.32 ± 0.6 × 10-10 mol min-1 cm-2, whereas Cu-NP-incorporated SNAP films exhibited fluxes of 4.48 ± 0.5 × 10-10, 4.84 ± 0.3 × 10-10, and 11.7 ± 3.6 × 10-10 mol min-1 cm-2 with 1, 3, and 5 wt % Cu-NPs, respectively. This resulted in a significant reduction (up to 99.8%) in both gram-positive and gram-negative bacteria, with very low platelet adhesion (up to 92% lower) as compared to that of the corresponding controls. Copper leachates from the SNAP films were detected using the inductively coupled plasma-mass spectrometry technique and were found to be significantly lower in concentration than the recommended safety limit by the FDA. The cell viability test performed on mouse fibroblast 3T3 cells provided supportive evidence for the biocompatibility of the material in vitro.
Nicole Morel - One of the best experts on this subject based on the ideXlab platform.
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The diacylglycerol lipase inhibitor RHC-80267 potentiates the relaxation to acetylcholine in rat mesenteric artery by anti-cholinesterase action.
European journal of pharmacology, 2005Co-Authors: Philippe Ghisdal, Marie-christine Hamaide, G. Vandenberg, Maurice Wibo, Nicole MorelAbstract:The diacylglycerol lipase inhibitor 1,6-bis(cyclohexyloximinocarbonylamino) hexane (RHC-80267) was tested for its effect on acetylcholine-evoked relaxation in rat mesenteric artery. In artery contracted with either noradrenaline or KCl, RHC-80267 (0.1-10 muM) potentiated the relaxation evoked by acetylcholine. The effect of RHC-80267 was not affected by nitric oxide synthase inhibition or by inhibitors of protein kinase C or of phospholipase A(2). The diacylglycerol analogue 1-oleoyl-2-acetyl-sn-glycerol did not change the relaxation to acetylcholine. RHC-80267 did not affect the relaxation evoked by carbachol, by the nitric oxide donor SNAP (S-Nitroso-N-Acetylpenicillamine) or by the K(+) channel opener cromakalim. Neostigmine, a cholinesterase inhibitor, produced the same effect as RHC-80267 on acetylcholine-evoked relaxation. When tested on cholinesterase in brain homogenate, RHC-80267 concentration-dependently inhibited cholinesterase activity with an IC(50) of 4 muM. These results indicate that the potentiation of acetylcholine-evoked responses by RHC-80267 in rat mesenteric artery is caused by the inhibition of the cholinesterase activity in the vascular wall.
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the diacylglycerol lipase inhibitor rhc 80267 potentiates the relaxation to acetylcholine in rat mesenteric artery by anti cholinesterase action
European Journal of Pharmacology, 2005Co-Authors: Philippe Ghisdal, Marie-christine Hamaide, G. Vandenberg, Maurice Wibo, Nicole MorelAbstract:The diacylglycerol lipase inhibitor 1,6-bis(cyclohexyloximinocarbonylamino) hexane (RHC-80267) was tested for its effect on acetylcholine-evoked relaxation in rat mesenteric artery. In artery contracted with either noradrenaline or KC), RHC-80267 (0.1 -10 mu M) potentiated the relaxation evoked by acetylcholine. The effect of RHC-80267 was not affected by nitric oxide synthase inhibition or by inhibitors of protein kinase C or of phospholipase A(2). The diacylglycerol analogue 1-oleoyl-2-acetyl-sn-glycerol did not change the relaxation to acetylcholine. R-HC-80267 did not affect the relaxation evoked by carbachol, by the nitric oxide donor SNAP (S-Nitroso-N-Acetylpenicillamine) or by the K+ channel opener cromakalim. Neostigmine, a cholinesterase inhibitor, produced the same effect as RHC-80267 on acetylcholine-evoked relaxation. When tested on cholinesterase in brain homogenate, RHC-80267 concentration-dependently inhibited cholinesterase activity with an IC50 of 4 mu M. These results indicate that the potentiation of acetylcholine-evoked responses by RHC-80267 in rat mesenteric artery is caused by the inhibition of the cholinesterase activity in the vascular wall. (c) 2005 Elsevier B.V. All rights reserved.
Vicente Felipo - One of the best experts on this subject based on the ideXlab platform.
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Chronic exposure to aluminum impairs neuronal glutamate-nitric oxide-cyclic GMP pathway
Journal of Neurochemistry, 2002Co-Authors: Carmen Cucarella, María-dolores Miñana, Carlos Hermenegildo, Carmina Montoliu, Rosana Sáez, Luigi Manzo, Vicente FelipoAbstract:Abstract: Humans are exposed to aluminum from environmental sources and therapeutic treatments. However, aluminum is neurotoxic and is considered a possible etiologic factor in Alzheimer's disease and other neurological disorders. The molecular mechanism of aluminum neurotoxicity is not understood. We tested the effects of aluminum on the glutamate-nitric oxide-cyclic GMP pathway in cultured neurons. Neurons were exposed to 50 µM aluminum in culture medium for short-term (4 h) or long-term (8–14 days) periods, or rats were prenatally exposed, i.e., 3.7% aluminum sulfate in the drinking water, during gestation. Chronic (but not short-term) exposure of neurons to aluminum decreased glutamate-induced activation of nitric oxide synthase by 38% and the formation of cyclic GMP by 77%. The formation of cyclic GMP induced by the nitric oxide-generating agent S-Nitroso-N-Acetylpenicillamine was reduced by 33%. In neurons from rats prenatally exposed to aluminum but not exposed to it during culture, glutamate-induced formation of cyclic GMP was inhibited by 81%, and activation of nitric oxide synthase was decreased by 85%. The formation of cyclic GMP induced by S-Nitroso-N-Acetylpenicillamine was not affected. These results indicate that chronic exposure to aluminum impairs glutamate-induced activation of nitric oxide synthase and nitric oxide-induced activation of guanylate cyclase. Impairment of the glutamate-nitric oxide-cyclic GMP pathway in neurons may contribute to aluminum neurotoxicity.
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Chronic exposure to aluminium impairs the glutamate-nitric oxide-cyclic GMP pathway in the rat in vivo
Neurochemistry International, 1999Co-Authors: Carlos Hermenegildo, Rosana Sáez, Luigi Manzo, Claudio Minoia, Vicente FelipoAbstract:Abstract Aluminium is neurotoxic and is considered a possible etiologic factor in Alzheimer’s disease, dialysis syndrome and other neurological disorders. The molecular mechanism of aluminium-induced impairment of neurological functions remains unclear. We showed that aluminium impairs the glutamate-nitric oxide-cGMP pathway in cultured neurons. The aim of this work was to assess by in vivo brain microdialysis whether chronic administration of aluminium in the drinking water (2.5% aluminium sulfate) also impairs the glutamate-nitric oxide-cGMP pathway in the cerebellum of rats in vivo. Chronic exposure to aluminium reduced NMDA-induced increase of extracellular cGMP by ca 50%. The increase in extracellular cGMP induced by the nitric oxide generating agent S -nitroso- N -acetylpenicillamine was higher (240%) in rats treated with aluminium than in controls. Immunoblotting experiments showed that aluminium reduced the cerebellar content of calmodulin and nitric oxide synthase by 34 and 15%, respectively. Basal activity of soluble guanylate cyclase was decreased by 66% in aluminium-treated rats, while the activity after stimulation with S -nitroso- N -acetylpenicillamine was similar to controls. Basal cGMP in the cerebellar extracellular space was decreased by 50% in aluminium-treated rats. These results indicate that chronic exposure to aluminium reduces the basal activity of guanylate cylcase and impairs the glutamate-nitric oxide-cGMP pathway in the animal in vivo.
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Modulation of Glutamine Synthesis in Cultured Astrocytes by Nitric Oxide
Cellular and Molecular Neurobiology, 1997Co-Authors: María-dolores Miñana, Elena Kosenko, Goizane Marcaida, Carlos Hermenegildo, Carmina Montoliu, Santiago Grisolía, Vicente FelipoAbstract:1. Previous results suggest that glutamine synthesis in brain could be modulated by nitrix oxide. The aim of this work was to assess this possibility. 2. As glutamine synthetase in brain is located mainly in astrocytes, we used primary cultures of astrocytes to assess the effects of increasing or decreasing nitrix oxide levels on glutamine synthesis in intact astrocytes. 3. Nitric oxide levels were decreased by adding nitroarginine, an inhibitor of nitric oxide synthase. To increase nitric oxide we used S -nitroso- N -acetylpenicillamine, a nitric oxide generating agent. 4. It is shown that S -nitroso- N -acetylpenicillamine decreases glutamine synthesis in intact astrocytes by ≈40–50%. Nitroarginine increases glutamine synthesis slightly in intact astrocytes. 5. These results indicate that brain glutamine synthesis may be modulated in vivo by nitric oxide.
Elizabeth J Brisbois - One of the best experts on this subject based on the ideXlab platform.
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Increasing the Lifetime of Insulin Cannula with Antifouling and Nitric Oxide Releasing Properties
ACS Applied Bio Materials, 2019Co-Authors: Manjyot Kaur Chug, Corbin Feit, Elizabeth J BrisboisAbstract:Many Type 1 diabetes patients utilize insulin pumps, which rely on a small subcutaneous insulin infusion cannula. However, insulin cannulas still suffer from infection and inflammation, which impacts the wear time of the insulin cannula, reduces the efficiency of insulin infusion, and requires frequent rotation of the insulin infusion site. Infection and inflammation of continuous insulin infusion pump therapy are growing issues and are estimated to cost billions of dollars globally each year. This study aims to develop a potent antibacterial and antifouling insulin cannula with a synergistic effect of bioinspired polymers, integrating antifouling Slippery, Liquid-Infused Porous Surface (SLIPs) technology with an active nitric oxide (NO) releasing polymer. The cannulas were developed by impregnating the NO donor molecule S-Nitroso-N-Acetylpenicillamine (SNAP) and silicone oil (Si) in commercial medical grade silicone rubber tubing (SR-SNAP-Si) via a solvent impregnation process. The efficiency of the SR-S...
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Multifunctional S-Nitroso-N-Acetylpenicillamine-Incorporated Medical-Grade Polymer with Selenium Interface for Biomedical Applications.
ACS Applied Materials & Interfaces, 2019Co-Authors: Arnab Mondal, Hitesh Handa, Priyadarshini Singha, Megan Douglass, Sean P. Hopkins, Martin Tran, Elizabeth J BrisboisAbstract:Modern crises in implantable or indwelling blood-contacting medical devices are mainly due to the dual problems of infection and thrombogenicity. There is a paucity of biomaterials that can address both problems simultaneously through a singular platform. Taking cues from the body’s own defense mechanism against infection and blood clotting (thrombosis) via the endogenous gasotransmitter nitric oxide (NO), both of these issues are addressed through the development of a layered S-Nitroso-N-Acetylpenicillamine (SNAP)-doped polymer with a blended selenium (Se)–polymer interface. The unique capability of the SNAP-Se-1 polymer composites to explicitly release NO from the SNAP reservoir as well as generate NO via the incorporated Se is reported for the first time. The NO release from the SNAP-doped polymer increased substantially in the presence of the Se interface. The Se interface was able to generate NO in the presence of S-nitrosoglutathione (GSNO) and glutathione (GSH), demonstrating the capability of gene...
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Development of S-Nitroso-N-Acetylpenicillamine Impregnated Medical Grade Polyvinyl Chloride for Antimicrobial Medical Device Interfaces
ACS Applied Bio Materials, 2019Co-Authors: Corbin Feit, Manjyot Kaur Chug, Elizabeth J BrisboisAbstract:In the clinical setting, polyvinyl chloride (PVC) accounts for 25% of all polymers used in medical device applications. However, medical devices fabricated with plasticized PVC, such as endotracheal tubes, extracorporeal circuits (ECCs), or intravenous catheters, can lead to thrombosis and infection complications. Mortality associated with hospital associated infections (HAIs) exceed 100,000 deaths each year. One method to overcome these challenges is to develop bioactive polymers with nitric oxide (NO) release. Nitric oxide exhibits many physiological roles including antibacterial, antithrombic, and anti-inflammatory activity. In this study, plasticized Tygon PVC tubing was impregnated with a NO donor molecule, S-Nitroso-N-Acetylpenicillamine (SNAP), via a simple solvent-swelling-impregnation method, where polymer samples were submerged in a SNAP impregnation solvent (methanol, acetone, plasticizer), rinsed, and dried. An additional topcoat of a biocompatible CarboSil 2080A (CB) was applied to reduce SNA...
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controlled light induced gas phase nitric oxide release from s nitrosothiol doped silicone rubber films
Nitric Oxide, 2019Co-Authors: Gergely Lautner, Blake Stringer, Elizabeth J Brisbois, Mark E Meyerhoff, Steven P SchwendemanAbstract:Abstract The light induced nitric oxide (NO) release properties of S-Nitroso-N-Acetylpenicillamine (SNAP) and S-nitrosoglutathione (GSNO) NO donors doped within polydimethylsiloxane (PDMS) films (PDMS-SNAP and PDMS-GSNO respectively) for potential inhaled NO (iNO) applications is examined. To achieve photolytic release of gas phase NO from the PDMS-SNAP and PDMS-GSNO films, narrow-band LED light sources are employed and the NO concentration in a N2 sweep gas above the film is monitored with an electrochemical NO sensor. The NO release kinetics using LED sources with different nominal wavelengths and optical power densities are reported. The effect of the NO donor loading within the PDMS films is also examined. The NO release levels can be controlled by the LED triggered release from the NO donor-doped silicone rubber films in order to generate therapeutic levels in a sweep gas for suitable durations potentially useful for iNO therapy. Hence this work may lay the groundwork for future development of a highly portable iNO system for treatment of patients with pulmonary hypertension, hypoxemia, and cystic fibrosis.
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tunable nitric oxide release from s nitroso n acetylpenicillamine via catalytic copper nanoparticles for biomedical applications
ACS Applied Materials & Interfaces, 2017Co-Authors: Jitendra Pant, Elizabeth J Brisbois, Marcus J Goudie, Sean P. Hopkins, Hitesh HandaAbstract:The quest for novel therapies to prevent bacterial infections and blood clots (thrombosis) is of utmost importance in biomedical research due to the exponential growth in the cases of thrombosis and blood infections and the emergence of multi-drug-resistant strains of bacteria. Endogenous nitric oxide (NO) is a cellular signaling molecule that plays a pivotal role in host immunity against pathogens, prevention of clotting, and regulation of systemic blood pressure, among several other biological functions. The physiological effect of NO is dose dependent, which necessitates the study of its tunable release kinetics, which is the objective of this study. In the present study, polymer composites were fabricated by incorporating S-Nitroso-N-Acetylpenicillamine (SNAP) in a medical-grade polymer, Carbosil, and top-coated with varying concentrations of catalytic copper nanoparticles (Cu-NPs). The addition of the Cu-NPs increased the NO release, as well as the overall antimicrobial activity via the oligodynamic ...
Philippe Ghisdal - One of the best experts on this subject based on the ideXlab platform.
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The diacylglycerol lipase inhibitor RHC-80267 potentiates the relaxation to acetylcholine in rat mesenteric artery by anti-cholinesterase action.
European journal of pharmacology, 2005Co-Authors: Philippe Ghisdal, Marie-christine Hamaide, G. Vandenberg, Maurice Wibo, Nicole MorelAbstract:The diacylglycerol lipase inhibitor 1,6-bis(cyclohexyloximinocarbonylamino) hexane (RHC-80267) was tested for its effect on acetylcholine-evoked relaxation in rat mesenteric artery. In artery contracted with either noradrenaline or KCl, RHC-80267 (0.1-10 muM) potentiated the relaxation evoked by acetylcholine. The effect of RHC-80267 was not affected by nitric oxide synthase inhibition or by inhibitors of protein kinase C or of phospholipase A(2). The diacylglycerol analogue 1-oleoyl-2-acetyl-sn-glycerol did not change the relaxation to acetylcholine. RHC-80267 did not affect the relaxation evoked by carbachol, by the nitric oxide donor SNAP (S-Nitroso-N-Acetylpenicillamine) or by the K(+) channel opener cromakalim. Neostigmine, a cholinesterase inhibitor, produced the same effect as RHC-80267 on acetylcholine-evoked relaxation. When tested on cholinesterase in brain homogenate, RHC-80267 concentration-dependently inhibited cholinesterase activity with an IC(50) of 4 muM. These results indicate that the potentiation of acetylcholine-evoked responses by RHC-80267 in rat mesenteric artery is caused by the inhibition of the cholinesterase activity in the vascular wall.
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the diacylglycerol lipase inhibitor rhc 80267 potentiates the relaxation to acetylcholine in rat mesenteric artery by anti cholinesterase action
European Journal of Pharmacology, 2005Co-Authors: Philippe Ghisdal, Marie-christine Hamaide, G. Vandenberg, Maurice Wibo, Nicole MorelAbstract:The diacylglycerol lipase inhibitor 1,6-bis(cyclohexyloximinocarbonylamino) hexane (RHC-80267) was tested for its effect on acetylcholine-evoked relaxation in rat mesenteric artery. In artery contracted with either noradrenaline or KC), RHC-80267 (0.1 -10 mu M) potentiated the relaxation evoked by acetylcholine. The effect of RHC-80267 was not affected by nitric oxide synthase inhibition or by inhibitors of protein kinase C or of phospholipase A(2). The diacylglycerol analogue 1-oleoyl-2-acetyl-sn-glycerol did not change the relaxation to acetylcholine. R-HC-80267 did not affect the relaxation evoked by carbachol, by the nitric oxide donor SNAP (S-Nitroso-N-Acetylpenicillamine) or by the K+ channel opener cromakalim. Neostigmine, a cholinesterase inhibitor, produced the same effect as RHC-80267 on acetylcholine-evoked relaxation. When tested on cholinesterase in brain homogenate, RHC-80267 concentration-dependently inhibited cholinesterase activity with an IC50 of 4 mu M. These results indicate that the potentiation of acetylcholine-evoked responses by RHC-80267 in rat mesenteric artery is caused by the inhibition of the cholinesterase activity in the vascular wall. (c) 2005 Elsevier B.V. All rights reserved.
