Relevant bibliographies by topics / Nitric oxide resistance

Academic literature on the topic 'Nitric oxide resistance'

Author: Grafiati
Published: 10 December 2022
Last updated: 29 January 2023

Create a spot-on reference in APA, MLA, Chicago, Harvard, and other styles

Select a source type:

Contents

Consult the lists of relevant articles, books, theses, conference reports, and other scholarly sources on the topic 'Nitric oxide resistance.'

Next to every source in the list of references, there is an 'Add to bibliography' button. Press on it, and we will generate automatically the bibliographic reference to the chosen work in the citation style you need: APA, MLA, Harvard, Chicago, Vancouver, etc.

You can also download the full text of the academic publication as pdf and read online its abstract whenever available in the metadata.

Journal articles on the topic "Nitric oxide resistance"

1

Nathan, Carl. "Natural resistance and nitric oxide." Cell 82, no. 6 (September 1995): 873–76. http://dx.doi.org/10.1016/0092-8674(95)90019-5.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Benzing, Albert, Torsten Loop, Georg Mols, and Klaus Geiger. "Unintended Inhalation of Nitric Oxide by Contamination of Compressed Air." Anesthesiology 91, no. 4 (October 1, 1999): 945. http://dx.doi.org/10.1097/00000542-199910000-00013.

Full text
Abstract:
Background Compressed air from a hospital's central gas supply may contain nitric oxide as a result of air pollution. Inhaled nitric oxide may increase arterial oxygen tension and decrease pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. Therefore, the authors wanted to determine whether unintentional nitric oxide inhalation by contamination of compressed air influences arterial oxygen tension and pulmonary vascular resistance and interferes with the therapeutic use of nitric oxide. Methods Nitric oxide concentrations in the compressed air of a university hospital were measured continuously by chemiluminescence during two periods (4 and 2 weeks). The effects of unintended nitric oxide inhalation on arterial oxygen tension (n = 15) and on pulmonary vascular resistance (n = 9) were measured in patients with acute lung injury and acute respiratory distress syndrome by changing the source of compressed air of the ventilator from the hospital's central gas supply to a nitric oxide-free gas tank containing compressed air. In five of these patients, the effects of an additional inhalation of 5 ppm nitric oxide were evaluated. Results During working days, compressed air of the hospital's central gas supply contained clinically effective nitric oxide concentrations (> 80 parts per billion) during 40% of the time. Change to gas tank-supplied nitric oxide-free compressed air decreased the arterial oxygen tension by 10% and increased pulmonary vascular resistance by 13%. The addition of 5 ppm nitric oxide had a minimal effect on arterial oxygen tension and pulmonary vascular resistance when added to hospital-supplied compressed air but improved both when added to tank-supplied compressed air. Conclusions Unintended inhalation of nitric oxide increases arterial oxygen tension and decreases pulmonary vascular resistance in patients with acute lung injury and acute respiratory distress syndrome. The unintended nitric oxide inhalation interferes with the therapeutic use of nitric oxide.
APA, Harvard, Vancouver, ISO, and other styles
3

Lee, Alexandra, and Warwick Butt. "Nitric oxide: a new role in intensive care." Critical Care and Resuscitation 22, no. 1 (March 2, 2020): 72–79. http://dx.doi.org/10.51893/2020.1.sr1.

Full text
Abstract:
Inhaled nitric oxide has been used for 30 years to improve oxygenation and decrease pulmonary vascular resistance. In the past 15 years, there has been increased understanding of the role of endogenous nitric oxide on cell surface receptors, mitochondria, and intracellular processes involving calcium and superoxide radicals. This has led to several animal and human experiments revealing a potential role for administered nitric oxide or nitric oxide donors in patients with systemic inflammatory response syndrome or ischaemia–reperfusion injury, and in patients for whom exposure of blood to artificial surfaces has occurred.
APA, Harvard, Vancouver, ISO, and other styles
4

Wu, Guoyao, and Cynthia J. Meininger. "Nitric oxide and vascular insulin resistance." BioFactors 35, no. 1 (January 2009): 21–27. http://dx.doi.org/10.1002/biof.3.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Perez-Rojas, Jazmin M., Kamal M. Kassem, William H. Beierwaltes, Jeffrey L. Garvin, and Marcela Herrera. "Nitric oxide produced by endothelial nitric oxide synthase promotes diuresis." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 298, no. 4 (April 2010): R1050—R1055. http://dx.doi.org/10.1152/ajpregu.00181.2009.

Full text
Abstract:
Extracellular fluid volume is highly regulated, at least in part, by peripheral resistance and renal function. Nitric oxide (NO) produced by NO synthase type 3 (NOS 3) in the nonrenal vasculature may promote fluid retention by reducing systemic vascular resistance and arterial pressure. In contrast, NO produced by renal NOS 3 promotes water excretion by reducing renal vascular resistance, increasing glomerular filtration, and inhibiting reabsorption along the nephron. Thus, the net effect of NO from NOS 3 on urinary volume (UV) is unclear. We hypothesized that NO produced by NOS 3 promotes water excretion primarily due to renal tubular effects. We gave conscious wild-type and NOS 3 −/− mice an acute volume load and measured UV, blood pressure, plasma renin concentration (PRC), Na+, vasopressin, and urinary Na+ and creatinine concentrations. To give the acute volume load, we trained mice to drink a large volume of water while in metabolic cages. On the day of the experiment, water was replaced with 1% sucrose, and mice had access to it for 1 h. Volume intake was similar in both groups. Over 3 h, wild-type mice excreted 62 ± 10% of the volume load, but NOS 3 −/− excreted only 42 ± 5% ( P < 0.05). Blood pressure in NOS 3 −/− was 118 ± 3 compared with 110 ± 2 mmHg in wild-type mice ( P < 0.05), but it did not change following volume load in either strain. PRC, vasopressin, and glomerular filtration rate were similar between groups. Urinary Na+ excretion was 49.3 ± 7.0 in wild-type vs. 37.8 ± 6.4 μmol/3 h in NOS 3 −/− mice ( P < 0.05). Bumetanide administration eliminated the difference in volume excretion between wild-type and NOS 3 −/− mice. We conclude that 1) NO produced by NOS 3 promotes water and Na+ excretion and 2) the renal epithelial actions of NO produced by NOS 3 supersede the systemic and renal vascular actions.
APA, Harvard, Vancouver, ISO, and other styles
6

Ramya K, Gowri Sethu, and Dhanasekar T. "Is Nitric oxide the missing link in glucose homeostasis? A study on correlation of Nitric oxide and Insulin Resistance in Obstructive Sleep Apnoea." International Journal of Research in Pharmaceutical Sciences 10, no. 2 (April 15, 2019): 820–25. http://dx.doi.org/10.26452/ijrps.v10i2.258.

Full text
Abstract:
Nitric oxide is associated with glucose homeostasis. An independent relationship between Nitric oxide and insulin resistance in Prediabetic and Obstructive sleep apnea patients without pre-existing diabetes mellitus are equivocally linked to increased risk of type II diabetes. A reciprocal relationship seems to exist between nitric oxide and insulin resistance. Aim of this present study is to determine relationship between nitric oxide and glucose parameters in control, prediabetic and Obstructive sleep apnea. A cross sectional study was performed in 150. They were divided into, group I (control), group II (prediabetics) and group III (OSA). Fasting blood sugar (FBS), fasting insulin, HbA1c and nitric oxide were measured in these subjects and insulin resistance calculated by HOMA-IR. Data was analyzed statistically using Pearson’s correlation coefficient analysis, the significant value being P<0.05. Negative correlation was observed between the NO and insulin resistance in prediabetic (r=-0.627, P =<0.001) and OSA (r= -0.416, P=0.003) respectively. Nitric oxide is significantly inversely associated with insulin resistance in Prediabetic and Obstructive sleep apnea.
APA, Harvard, Vancouver, ISO, and other styles
7

Green, Shawn J., Libia F. Scheller, Michael A. Marletta, Matthew C. Seguin, Francis W. Klotz, Mike Slayter, Barbara J. Nelson, and Carol A. Nacy. "Nitric oxide: Cytokine-regulation of nitric oxide in host resistance to intracellular pathogens." Immunology Letters 43, no. 1-2 (December 1994): 87–94. http://dx.doi.org/10.1016/0165-2478(94)00158-8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Kuzhebaeva, U., Irina Donnik, Maksim Petropavlovskiy, S. Kanatbaev, and Birzhan Nurgaliev. "Nitric oxide as an indicator for assessing the resistance and susceptibility of cattle to leukemia." Agrarian Bulletin of the 213, no. 10 (November 26, 2021): 48–54. http://dx.doi.org/10.32417/1997-4868-2021-213-10-48-54.

Full text
Abstract:
Abstract. The role of allelic variability of inducible nitric oxide synthase (iNOS) is significant in the study of the resistance and susceptibility of animals to leukemia infection. After analyzing the literature data, it can be stated that in the iNOS gene, allele A (with genotype AA) is responsible for resistance to the leukemia virus, and allele B (with genotype BB) is responsible for susceptibility. This is due to the frequency of occurrence of alleles and their genotypes of the polymorphic marker AN13-1 of the inducibeal nitric oxide synthase gene. The iNOS gene is capable of producing a large amount of nitric oxide, compared to other isoforms. In turn, nitric oxide causes death or can stop the growth of pathogenic microorganisms, including viruses. The purpose of this work is to further study nitric oxide as an indicator for determining the resistance and susceptibility of animals to leukemia, as well as the selection of specific primers for PCR-PDRF used in genotyping. Methods. The iNOS gene sequence was analyzed and a pair of specific primers were selected and synthesized using the Vector NTI program. Scientific novelty of this work lies in the fact that we have selected specific primers that are important for the analysis of cattle genotyping by allelic variants of the polymorphic marker AH13-1 of the iNOS gene. Results. Based on this work, a pair of primers iNOSF_new and iNOSR_new, with a calculated annealing temperature of 52 °C, were selected and synthesized, giving an amplicon with a length of 186 bp. The amplicon contains a polymorphic site that distinguishes the A and B alleles. During PCR-RFLP, the following genotype-specific fragments are formed: AA-47/139 bp; AB -186/139/47 bp; BB-186 bp.
APA, Harvard, Vancouver, ISO, and other styles
9

Bigatello, Luca M., and William E. Hurford. "Inhaled nitric oxide and pulmonary vascular resistance." Critical Care Medicine 27, no. 9 (September 1999): 2060–61. http://dx.doi.org/10.1097/00003246-199909000-00075.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Mohteshamzadeh, Mobin, and T. H. Tomas. "HYPERTENSION, INSULIN RESISTANCE AND NITRIC OXIDE SYNTHASE." Journal of Hypertension 22, Suppl. 1 (February 2004): S49. http://dx.doi.org/10.1097/00004872-200402001-00199.

Full text
APA, Harvard, Vancouver, ISO, and other styles
More sources

Dissertations / Theses on the topic "Nitric oxide resistance"

1

Razavi, Habib M. "Conduit versus resistance blood vessels, adrenoceptors and nitric oxide." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0011/MQ40846.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Cremona, George Ian. "Nitric oxide and pulmonary vascular resistance in health and disease." Thesis, University of Cambridge, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360748.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Brown, Claire. "The regulation of the pulmonary vasculature of the rat by 5-hydroxytryptamine." Thesis, Glasgow Caledonian University, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337868.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Lo, Jeannette. "Characterization of novel nitroplatinum(iv) complexes for the treatment of cancer." [Tampa, Fla.] : University of South Florida, 2004. http://purl.fcla.edu/fcla/etd/SFE0000619.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Brillante, Divina Graciela Clinical School St George Hospital Faculty of Medicine UNSW. "Modulation of arterial stiffness by angiotensin receptors and nitric oxide in the insulin resistance syndrome." Publisher:University of New South Wales. Clinical School - St George Hospital, 2008. http://handle.unsw.edu.au/1959.4/41849.

Full text
Abstract:
The insulin resistance syndrome [INSR] is associated with increased cardiovascular risk and affects up to 25% of the Australian population. The mechanism underlying the relationship between the INSR and increased cardiovascular risk is controversial. We postulated that perturbations in the renin-angiotensin system [RAS] and endothelium-derived NO may be implicated in the development of early vascular changes in the INSR. Repeated measurements of arterial stiffness [using digital photoplethysmography] and haemodynamic parameters in response to vasoactive medications were used to demonstrate the functional expression of angiotensin II [Ang II] receptors and NO synthase [NOS]. Ang II acts via two main receptor sub-types: the Ang II type 1 [AT1] and Ang II type 2 [AT2] receptors. The AT1 receptor is central to the development of arterial stiffness and endothelial dysfunction. The role of AT2 receptors in humans is controversial but is postulated to counter-act AT1 receptor mediated effects in diseased vascular beds. We demonstrated increased AT1 and AT2 receptor-mediated effects in small to medium-sized arteries of subjects with early INSR [Chapter 6]. In addition, functional expression of AT2 receptors in adult insulin resistant humans [Chapter 5], but not in healthy volunteers [Chapter 4] was demonstrated. AT1 receptor blockade in subjects with early INSR resulted in improvements in vascular function, with a consequent functional down-regulation of AT2 receptors [Chapter 7]. Functional NOS expression was demonstrated to be increased in subjects with early INSR compared with healthy controls [Chapter 6]. This was postulated to be a homeostatic response to counteract early vascular changes in subjects with early INSR. AT1 receptor blockade in these subjects reduced functional NOS expression [Chapter 8]. In conclusion, patients with early INSR represent a model of early disease where early intervention may be able to reverse the process incited by the initial exposure to multiple cardiovascular risk factors. Early vascular changes in these individuals are mediated at least in part, by increased AT1 receptor activity and/or expression, and may be detected by changes in arterial stiffness indices and non-invasive vascular reactivity studies. There is a compensatory increase in AT2 receptor and NOS expression/activity to counter-act these vascular changes.
APA, Harvard, Vancouver, ISO, and other styles
6

Hu, Xiaochen, Juichi Sato, Gustavo Bajotto, Oyun Khookhor, Isao Ohsawa, Yoshiharu Oshida, and Yuzo Sato. "Goshajinkigan (Chinese Herbal Medicine Niu-Che-Sen-Qi-Wan) Improves Insulin Resistance in Diabetic Rats via the Nitric Oxide Pathway." Nagoya University School of Medicine, 2010. http://hdl.handle.net/2237/12907.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Matthews, Nicola Elizabeth. "A novel mechanism of hypoxia-induced drug resistance, evidence that nitric oxide is a primary mediator of chemosensitivity." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/MQ59389.pdf.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Freeman, Philip. "The influence of nitric oxide and nitrite on coronary vascular resistance, platelet function and inflammation in patients undergoing revascularisation after NSTEMI and stable angina." Thesis, Cardiff University, 2018. http://orca.cf.ac.uk/114152/.

Full text
Abstract:
Coronary blood flow (CBF) is principally controlled by changes in coronary vascular resistance (CVR). Low CVR helps to maintain myocardial perfusion in the presence of epicardial stenosis, therefore factors that impair the reduction of CVR will have a direct effect on CBF leading to either a narrower “effective” perfusion pressure range or reduced ability to compensate for increased demand on myocardial contraction. There are several mechanisms which may be important in the control CVR in humans including both endothelial dependent production of NO and reduction of the simple anion inorganic nitrite (a metabolite of NO) back to NO (via several putative mechanisms). The synthesis of NO by both nitric oxide synthase (NOS) and the reduction of nitrite in the coronary circulation has been the subject of many animal and human clinical studies. Reduced systemic endothelial dependent production of NO has an association with worse cardiovascular outcomes in humans, the number of potential mechanisms are large and perhaps central is the effect on CVR. The reduction of nitrite to NO is seen, in some ways, to be the perfect compensatory mechanism, particularly when endothelial function is impaired. It is easy to hypothesise that this stoichiometric balance of NO production might be responsible for the perfect regulation of CVR and thus CBF. Methods This thesis investigates the influence and effect of both endothelial production of NO and the reduction of nitrite to NO on CVR in man. First, an observational study assessing the impact of these mechanisms in patients undergoing percutaneous coronary intervention (PCI), in the treatment of both non-ST-elevation myocardial infarction and stable angina. Specifically, the metabolites of NO were measured from aortic root to coronary sinus together with the associated CVR both before and after PCI. Second, using a systemic infusion of sodium nitrite (NaNO2) in NSTEMI patients to assess the effect of nitrite reduction on CVR during PCI. The systemic nitrite concentration was increased 8-fold in the same experimental conditions as the observational study. Third, beyond CVR control the influence of NO and nitrite was also assessed in terms of platelet reactivity and systemic inflammatory cytokines in the NSTEMI cohort both with and without NaNO2 infusion. Results NSTEMI patients have a net increase in NO metabolites across the coronary circulation unlike healthy controls (historical data) and stable angina patients. This net increase is lost following PCI and is associated with a significant rise in CVR. Stable angina patients appear to compensate with increase collateral circulation and not NO synthesis. An 8-fold increase in nitrite concentration has no effect on CVR or platelet reactivity in NSTEMI patients. Conclusions In NSTEMI patients a net aorta to coronary sinus NO synthesis appears to be important to maintain a low CVR and thus CBF when haemodynamically significant epicardial disease is present. After the epicardial disease is treated this net increase in NOx (Nitric Oxide metabolites), is lost and is associated with an acute increase in CVR. Stable angina patients have no net increase in NOx across the coronary circulation and after revascularisation have no change in CVR, this may reflect an alternate mechanism of compensation and microvascular perfusion maintained by collateral circulation as evident by the increase CFI. Despite the perfect environment for the reduction of nitrite to NO we saw no influence of an 8-fold increase in serum nitrite concentration on CVR in patients with NSTEMI either before or after PCI, suggesting that nitrite reduction to NO plays no role in CBF regulation in NSTEMI patients. Nitrite reduction depends on conditions that are found predominantly in the capillary bed or venules, thus any mechanism would need to rely on a feedback mechanism to signal back to the arterioles (where much of resistance change is created). Despite hypotheses by others that this may occur by the close arrangement of venules to arterioles, this appears not to be the case in NSTEMI patients. Other clinically relevant and important mechanisms also appear to be unaffected by this increase in serum nitrite, residual platelet function and cytokine concentrations at 24 hours.
APA, Harvard, Vancouver, ISO, and other styles
9

Anumba, Dilichukwu Okeoma C. "The role of nitric oxide in the modulation of the peripheral vascular resistance changes of pregnancy and pre-eclampsia." Thesis, University of Newcastle Upon Tyne, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.311136.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Zecchin, Henrique Gottardello. "Transmissão do sinal de insulina e acetilcolina na aorta de modelos animais e resistencia a insulina." [s.n.], 2007. http://repositorio.unicamp.br/jspui/handle/REPOSIP/311235.

Full text
Abstract:
Orientador: Mario Jose Abdalla Saad
Tese (doutorado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas
Made available in DSpace on 2018-08-08T15:02:32Z (GMT). No. of bitstreams: 1 Zecchin_HenriqueGottardello_D.pdf: 4518336 bytes, checksum: db2ce3333dfb7dda86b0298470e924ca (MD5) Previous issue date: 2007
Resumo: A resistência seletiva à insulina através da via IRS/PI3-K/Akt/eNOS associada à ativação normal ou exacerbada da via de crescimento MAPK tem sido proposta como um possível elo entre situações de resistência à insulina e doença cardiovascular. Inicialmente demonstramos que animais com resistência à insulina e doença cardiovascular (o rato espontaneamente hipertenso, SHR) apresentam menor ativação da via IRS/PI3-K/Akt/eNOS e hiperativação/hiperexpressão da via da MAPK na aorta torácica, enquanto a ativação normal da via IRS/PI3-K/Akt/eNOS pode proteger o animal obeso, resistente à insulina e que não apresenta doença cardiovascular. Posteriormente, outras vias estimulatórias do crescimento celular, como a via JAK/STAT, foram estudadas no vaso de outro modelo animal de resistência à insulina e doença cardiovascular - o rato com obesidade induzida por dieta. Este modelo demonstrou que a redução da ativação da via PI3-K/Akt/eNOS ocorre em paralelo à hiperativação das vias da MAPK e JAK/STAT, e isso pode desempenhar função importante da patogênese da doença cardiovascular neste estado patológico. Em outro estudo foi demonstrado pela primeira vez que a acetilcolina pode ativar a eNOS de maneira cálcio-independente, através da via IRS/PI3-K/Akt utilizando para isso uma tirosina quinase intracelular, a JAK2. Em ratos com obesidade induzida por dieta, resistentes à insulina e com disfunção endotelial, foi demonstrado que há resistência na via da PI3-K/Akt/eNOS tanto em resposta à insulina quanto à acetilcolina, em decorrência de maior fosforilação inibitória do IRS-1 e da redução dos níveis teciduais da eNOS. Assim, o desequilíbrio entre a ativação reduzida da via IRS/PI3-K/Akt/eNOS e a maior ativação das vias de crescimento (MAPK e JAK/STAT) pode contribuir para o desenvolvimento de doença cardiovascular em estados de resistência à insulina
Abstract: The actions of acetylcholine on endothelium are mainly mediated through muscarinic receptors, which are members of the G protein-coupled receptor family. In the present study we show that acetylcholine induces rapid tyrosine phosphorylation and activation of Janus kinase 2 (JAK2) in rat aorta. Upon JAK2 activation, tyrosine phosphorylation of insulin receptor substrate-1 (IRS-1) is detected. In addition, acetylcholine induces JAK2/IRS-1 and IRS-1/phosphatidylinositol (PI) 3-kinase associations, downstream activation of Akt/protein kinase B, endothelial cell-nitric oxide synthase (eNOS), and extracellular signal-regulated kinase (ERK1/2). The pharmacological blockade of JAK2 or PI 3-kinase reduced acetylcholine-stimulated eNOS phosphorylation, NOS activity and aorta relaxation. These data indicate a new signal transduction pathway for IRS-1/PI 3- kinase/Akt/eNOS activation and ERK1/2 by means of JAK2 tyrosine phosphorylation stimulated by acetylcholine in vessels. Moreover, we demonstrate that, in aorta of obese rats (high-fat diet), there is an impairment in insulin- and acetylcholinestimulated IRS-1/PI 3-kinase pathway, leading to reduced activation with lower protein levels of eNOS associated with a hyperactivated ERK/MAP kinase pathway. These results suggest that in aorta of obese rats, there is not only insulin resistance, but also acetylcholine resistance, probably mediated by a common signaling pathway that controls the activity and the protein levels of eNOS
Doutorado
Medicina Experimental
Doutor em Fisiopatologia Medica
APA, Harvard, Vancouver, ISO, and other styles
More sources

Books on the topic "Nitric oxide resistance"

1

Kenneth, Weir E., Archer Stephen L, and Reeves John T, eds. Nitric oxide and radicals in the pulmonary vasculature. Armonk, NY: Futura Pub. Co. Inc., 1996.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
2

Conduit versus resistance blood vessels: Adrenoceptors and nitric oxide. Ottawa: National Library of Canada, 1998.

Find full text
APA, Harvard, Vancouver, ISO, and other styles
3

1941-, Ryan Una S., and Rubanyi Gabor M. 1947-, eds. Endothelial regulation of vascular tone. New York: M. Dekker, 1992.

Find full text
APA, Harvard, Vancouver, ISO, and other styles

Book chapters on the topic "Nitric oxide resistance"

1

BrüNe, B., A. Von Knethen, and K. Sandau. "Mechanisms of Cellular Resistance Against Nitric Oxide." In Nitric Oxide, 159–75. Berlin, Heidelberg: Springer Berlin Heidelberg, 2000. http://dx.doi.org/10.1007/978-3-642-57077-3_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Efferth, Thomas. "Role of Nitric Oxide for Modulation of Cancer Therapy Resistance." In Nitric Oxide (NO) and Cancer, 265–82. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1432-3_14.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Garbán, Hermes J. "Breaking Resistance: Role of Nitric Oxide in the Sensitization of Cancer Cells to Chemo- and immunotherapy." In Nitric Oxide (NO) and Cancer, 283–90. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1432-3_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Bonavida, Benjamin, Stavroula Baritaki, Sara Huerta-Yepez, Mario I. Vega, Ali R. Jazirehi, and James Berenson. "Nitric Oxide Donors Are a New Class of Anti-cancer Therapeutics for the Reversal of Resistance and Inhibition of Metastasis." In Nitric Oxide (NO) and Cancer, 459–77. New York, NY: Springer New York, 2010. http://dx.doi.org/10.1007/978-1-4419-1432-3_24.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Koller, Akos, Dong Sun, An Huang, and Gabor Kaley. "Exercise Training Augments EDRF (Nitric Oxide) Synthesis in Skeletal Muscle Arterioles." In The Resistance Arteries, 153–61. Totowa, NJ: Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4757-2296-3_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
6

Lee, Tony J. F., and Raj Mishra. "Nitrergic Neurogenic Control of Resistance Blood Vessels." In Nitric Oxide and Free Radicals in Peripheral Neurotransmission, 160–82. Boston, MA: Birkhäuser Boston, 2000. http://dx.doi.org/10.1007/978-1-4612-1328-4_7.

Full text
APA, Harvard, Vancouver, ISO, and other styles
7

Kawasaki, Hiromu, and Makoto Takenaga. "Is There Neural Control of Peripheral Resistance Arteries by Nitrergic Nerves?" In Nitric Oxide and Free Radicals in Peripheral Neurotransmission, 183–98. Boston, MA: Birkhäuser Boston, 2000. http://dx.doi.org/10.1007/978-1-4612-1328-4_8.

Full text
APA, Harvard, Vancouver, ISO, and other styles
8

Delledonne, M., Y. Xia, R. A. Dixon, C. Lorenzoni, and C. Lamb. "Nitric oxide signalling in the plant hypersensitive disease resistance response." In Developments in Plant Breeding, 127–33. Dordrecht: Springer Netherlands, 1999. http://dx.doi.org/10.1007/978-94-011-4475-9_15.

Full text
APA, Harvard, Vancouver, ISO, and other styles
9

Matthew, John D., and Roger M. Wadsworth. "Nitric Oxide and Vasoactive Intestinal Peptide as Dual Mediators of Neurogenic Relaxation in the Sheep Middle Cerebral Artery." In The Resistance Arteries, 183–93. Totowa, NJ: Humana Press, 1994. http://dx.doi.org/10.1007/978-1-4757-2296-3_18.

Full text
APA, Harvard, Vancouver, ISO, and other styles
10

Klessig, Daniel F., Jörg Durner, Roy Navarre, Dhirendra Kumar, Jyoti Shah, Jun Ma Zhou, Shuqun Zhang, et al. "Salicylic Acid- And Nitric Oxide-Mediated Signal Transduction In Disease Resistance." In Signal Transduction in Plants, 201–7. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1365-0_20.

Full text
APA, Harvard, Vancouver, ISO, and other styles

Conference papers on the topic "Nitric oxide resistance"

1

Borland, CD, F. Bottrill, H. Dunningham, A. Vuylsteke, C. Yilmaz, DM Dane, and CC Hsia. "Significant Erythrocyte Membrane Resistance to Nitric Oxide Diffusion in the Lung." In American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a2088.

Full text
APA, Harvard, Vancouver, ISO, and other styles
2

Yastreb, T. O., Yu E. Kolupaev, A. I. Kokorev, and A. P. Dmitriev. "ROLE OF JASMONATE AND NITRIC OXIDE- INDUCED OF STOMATA CLOSURE IN ARABIDOPSIS THALIANA." In The All-Russian Scientific Conference with International Participation and Schools of Young Scientists "Mechanisms of resistance of plants and microorganisms to unfavorable environmental". SIPPB SB RAS, 2018. http://dx.doi.org/10.31255/978-5-94797-319-8-850-854.

Full text
APA, Harvard, Vancouver, ISO, and other styles
3

Borland, Colin D., Fiona Bottrill, Aled Jones, Chris Sparkes, and Alain Vuylsteke. "The Blood Resistance To Nitric Oxide Transfer In The Lung Lies Within The Red Cell." In American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a2052.

Full text
APA, Harvard, Vancouver, ISO, and other styles
4

Lovich, Mark A., Natalie K. Bruno, Abraham E. Wei, and Richard J. Gilbert. "Ultra Pure Nitric Oxide Generated Through Ascorbic Acid Reduction Of Nitrogen Dioxide Reverses Pulmonary Hypertension And Pulmonary Vascular Resistance In Hypoxemic Swine." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a5973.

Full text
APA, Harvard, Vancouver, ISO, and other styles
5

Abdelsalam, Shahenda Salaheldine, and Abdelali Agouni. "Protein Tyrosine Phosphatase (PTP) 1B Inhibition Improves Endoplasmic Reticulum Stress-Induced Apoptosis and Impaired Angiogenic Response in Endothelial Cells." In Qatar University Annual Research Forum & Exhibition. Qatar University Press, 2021. http://dx.doi.org/10.29117/quarfe.2021.0110.

Full text
Abstract:
Insulin is not only important for glucose homeostasis, but also plays a critical role in the activation of endothelial nitric oxide synthase (eNOS) to synthesize nitric oxide (NO) and keeping the endothelium functional. Conditions which result in insulin resistance, such as diabetes and obesity, cause impairment of endothelial function, a condition known as endothelial dysfunction that features a reduced release of NO. Protein tyrosine phosphatase (PTP) 1B, is a known negative regulator of insulin receptor, that has been implicated in the pathogenesis of insulin resistance and endothelial dysfunction. Owing to its critical location at the surface of the endoplasmic reticulum (ER), PTP1B has been found to play an important role in ER stress response. However, the role of ER stress in PTP1B-mediated endothelial dysfunction is not fully elucidated. Toa address this, ER stress was induced pharmacologically in endothelial cells using thapsigargin, in the presence or absence of either a small molecule inhibitor of PTP1B or silencing siRNA duplexes, followed by the assessment of the expression of key ER stress markers, angiogenic capacity and apoptotic signals. We report here, that PTP1B inhibition protected cells against ER stress and ER stress-induced impairment in eNOS activation and angiogenic capacity. PTP1B inhibition or silencing also protected against ER stress-induced endothelial cell apoptosis. Moreover, PTP1B blockade also suppressed ER stress-activated autophagy. Our data emphasize on the critical role of PTP1B in ER stress-mediated endothelial cell dysfunction and highlights the therapeutic potential of PTP1B inhibition against ER stress-mediated cell death and impairment of endothelial function to prevent cardiovascular disease in pathologies charactereized by the activation of ER stress such as diabetes.
APA, Harvard, Vancouver, ISO, and other styles
6

Ajdelsztajn, L., A. Sickinger, and J. M. Schoenung. "Nanostructured NiTi Coatings Produced by Low Pressure Plasma Spraying." In ITSC2005, edited by E. Lugscheider. Verlag für Schweißen und verwandte Verfahren DVS-Verlag GmbH, 2005. http://dx.doi.org/10.31399/asm.cp.itsc2005p1441.

Full text
Abstract:
Abstract This work describes the synthesis and characterization of nanostructured coatings produced by low pressure plasma spraying (LPPS) of cryomilled NiTi powder. Ni and Ti powders (60 and 40 wt %, respectively) were cryomilled together and LPPS sprayed onto stainless steel substrates. The elemental powders reacted and alloyed during cryomilling forming a nanocrystalline grain structure with nanodispersed oxide and nitride phases. These nanodispersoids are formed due to contamination by the milling media (liquid nitrogen). After spray deposition, the coatings presented a nanostructured microstructure with enhanced mechanical properties when compared with conventional NiTi coatings sprayed under the same conditions. High hardness and toughness values together with intrinsic corrosion resistance of the NiTi alloy lead to the formation of an attractive coating material for applications where corrosion and wear resistance are required. The ability to synthesize the NiTi from elemental Ni and Ti powders and the refinement of the microstructure achieved during milling makes the cryomilling process together with thermal spray of the nanostructured NiTi coatings a unique process and coating to be used in engineering applications. Abstract only; no full-text paper available.
APA, Harvard, Vancouver, ISO, and other styles
7

Wang, Yiguang, and Linan An. "Polymer Derived SiAlCN for Environmental Barrier Coatings." In ASME Turbo Expo 2005: Power for Land, Sea, and Air. ASMEDC, 2005. http://dx.doi.org/10.1115/gt2005-68172.

Full text
Abstract:
Silicon-based ceramics and composites are one of the most promising candidates for high temperature structural components in next generation gas turbines due to their excellent thermo-mechanical properties. However, these materials severely degraded when used in high temperature oxidizing environments, particularly, in the presence of corrosive species such as alkali elements or water vapor. Currently, the most promising approach with near-term benefits is to employ environmental barrier coatings (EBCs) that prevent direct contact between silicon-based materials and aggressive environments exist in turbine engines. Previous work on EBCs has primarily focused on using oxide coatings because oxides are in general more resistant to corrosive environments than Silicon-based ceramics. In this study, we propose to develop polymer-derived SiAlCN amorphous ceramics for EBC applications. Our research revealed that the oxidation rate of the SiAlCN ceramics is about 10 times lower than the lowest values observed on chemical vapor deposition (CVD) silicon carbide/nitride. Furthermore, the SiAlCN also exhibited good corrosion resistance to alkali salt at elevated temperatures.
APA, Harvard, Vancouver, ISO, and other styles
8

Yang, J., L. Kong, X. Cui, Y. Tao, T. Li, and T. Xiong. "Oxidation Behavior of TiAl3-Al Composite Coating on γ-TiAl Based Alloy at 950 °C." In ITSC 2012, edited by R. S. Lima, A. Agarwal, M. M. Hyland, Y. C. Lau, C. J. Li, A. McDonald, and F. L. Toma. ASM International, 2012. http://dx.doi.org/10.31399/asm.cp.itsc2012p0568.

Full text
Abstract:
Abstract TiAl3-Al composite coating on γ-TiAl alloy was prepared by cold spray and subsequent heat-treatment. The Oxidation test, which was carried out at 950 °C in air, indicated that the bare alloy exhibited poor oxidation resistance, significant weight loss was observed after oxidation for 70 h. The oxides formed were the mixture of TiO2 /Al2O3. For the specimen with the TiAl3–Al coating, great improvement in oxidation resistance was observed. Approximate parabolic oxidation kinetics was observed for the oxidation period. The microstructure analysis showed a dense TiAl2 interlayer and a reticular Cr rich phase formed between the composite coating and the substrate. The oxides in the oxidized coating were mainly alumina, with only trace of titanium dioxide and titanium nitrides after oxidation up to 1000 h. A certain amount of TiAl3 phase in the coating remained unoxidized and unconsumed. The EPMA analyses of the coated samples showed that no trend of oxygen or nitride diffusion into the substrate and no oxide formed beneath the TiAl2 interlayer.
APA, Harvard, Vancouver, ISO, and other styles
9

Fedorischeva, M., T. Dorofeeva, M. Dorofeeva, T. Gubaidulina, and V. Sergeev. "Multilayer corrosion-resistant ceramic-metal coatings on stainless steel obtained by magnetron sputtering." In 8th International Congress on Energy Fluxes and Radiation Effects. Crossref, 2022. http://dx.doi.org/10.56761/efre2022.c3-p-041404.

Full text
Abstract:
In this work, multilayer ceramic-metal coatings (Metal/nitride ceramics/ Metal/oxide ceramics) with increased corrosion resistance were obtained. The structure of each layer of the obtained coatings was researched using the transmission electron microscope JEOL JEM-2100. The metal layers had a columnar crystal structure, the layers of nitride ceramics predominantly had a nanocrystalline structure (grain size was about 15 nm), the layers of oxide ceramics were amorphous. Corrosion resistance was evaluated on a potentiostat P-45X in a 0.5 M NaCl solution using a three-electrode cell. The created coating reduced the corrosion rate of the stainless steel substrate by an order of magnitude.
APA, Harvard, Vancouver, ISO, and other styles
10

Bao, Y., D. T. Gawne, and T. Zhang. "The Influence of Matrix Phase Viscosity on the Plasma-Spray Deposition of Silicon-Nitride Composite Coatings." In ITSC2003, edited by Basil R. Marple and Christian Moreau. ASM International, 2003. http://dx.doi.org/10.31399/asm.cp.itsc2003p0263.

Full text
Abstract:
Abstract Non-oxide ceramics, such as silicon nitride, have a unique combination of high strength, toughness, wear resistance, thermal and chemical stability. However, the use of these materials as thick protective coatings on engineering components has been severely restricted by their decomposition behavior. Silicon nitride, for instance, does not melt but decomposes at ~1900oC and so thermal spraying of pure silicon nitride powder is impracticable. A limited amount of research has been carried out on depositing silicon nitride in various metallic or ceramic matrix materials but none have produced adequate coating microstructures or coating properties. This paper concerns the design of oxide matrix systems for silicon nitride composite coatings. A quantitative model is developed for the viscous flow of two-phase feedstock particles on impact with the substrate and is applied to the deposition of silicon nitride – ceramic matrix coatings. A number of matrix systems are investigated including a series of yttria-alumina and yttria-alumina -silica compositions. The research shows that the oxide matrices successfully protect the silicon nitride from decomposition but that the matrix composition and particle loading have a critical influence on splat flow and coating quality.
APA, Harvard, Vancouver, ISO, and other styles
You might also be interested in the extended bibliographies on the topic 'Nitric oxide resistance' for particular source types:
Journal articles Dissertations / Theses
We offer discounts on all premium plans for authors whose works are included in thematic literature selections. Contact us to get a unique promo code!

To the bibliography