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Data publikacji: 4 czerwca 2021
Data aktualizacji: 20 lutego 2023

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1

Nguyen, Yen Hoang Le Dervan Peter B. Gray Harry B. "Wiring inducible nitric oxide synthase /". Diss., Pasadena, Calif. : California Institute of Technology, 2007. http://resolver.caltech.edu/CaltechETD:etd-09262006-134259.

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2

Fairley, Brian. "Porphyrin models for nitric oxide synthase". Thesis, Heriot-Watt University, 2001. http://hdl.handle.net/10399/534.

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3

Pluciennick, Cecile. "Biomimetic models for nitric oxide synthase". Thesis, Heriot-Watt University, 2002. http://hdl.handle.net/10399/439.

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4

Feng, Gui-jie. "Regulation of inducible nitric oxide synthase". Thesis, University of Glasgow, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.360104.

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5

Wei, Xiao-qing. "Inducible nitric oxide synthase gene targeting". Thesis, University of Glasgow, 1995. http://theses.gla.ac.uk/8351/.

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Nitric oxide (NO) is a critical mediator of a variety of biological functions, including vascular and muscle relaxation, platelet aggregation, neuronal-cell function, microbicidal and tumoricidal activity, and a range of immunopathologies. NO is derived from L-arginine and molecular oxygen in a reaction catalysed by NO synthase (NOS). Three isoforms of NOS have been identified; neuronal constitutive NOS (ncNOS), endothelial constitutive NOS (ecNOS), and inducible NOS (iNOS). ncNOS and ecNOS are calcium-dependent, present constitutively in a variety of tissues and produce physiological concentrations of NO. However, large amounts NO are produced by iNOS which are expressed in cells such as macrophage after stimulation with a number of cytokines, including interferon-gamma (IFN-γ), tumour necrosis factor-alpha (TNF-α), and bacterial lipopolysaccharide (LPS). Findings of iNOS biological functions are based mainly on experiments using L-arginine analogues such as L-NG monomethyl arginine (L-NMMA) which competitively inhibits NO Synthase. These inhibitors are not NOS isoform selective and have differential bioavailability, and hence often render interpretation of results difficult. To directly define the iNOS biological functions, I constructed a strain of iNOS gene targeted mice. The first step of a gene targeting experiment is typically cDNA cloning and sequencing. A cDNA library was constructed in the vector λ ZAPII using mRNA isolated from J774 macrophages activated with IFN-? and LPS. Six independent positive colonies were found in the screen with both 5' and 3' specific probes and were subcloned in pBluescript. A full-length iNOS cDNA was constructed using the clones isolated from the library. Double strand cDNA sequence analysis showed that the J774 iNOS clone was identical to that of the Raw 264.7 macrophages iNOS cDNA sequence. A replacement-type targeting construct was prepared from 129/sv genomic DNA. A single targeted clone was identified amongst 636 screened after two independent electroporations of the CGR8 embryonic stem cell line. Gene replacement was detected by both 5' and 3' specific external probes. Five of ten chimeras generated gave germ line transmission. No homozygous mice were found by Southern blot analysis with 5' and 3' external probe in the offspring from heterozygous mice (FI) breedings. The iNOS gene had been altered by replacement with gene targeting construct and 5' iNOS gene translocation which could be detected by internal probe Southern blot analysis. Using the internal probe, mutant homozygous, heterozygous and wild-type mice were found in the offspring from heterozygous breedings. The ratio of these three genotypes was 21:47:25. Northern blot analysis with 5' iNOS cDNA probe showed that a large messenger appeared in the macrophages of homozygous mice when the cells were activated with IFN-γ and LPS in vitro. However there was no detectable iNOS protein translation by western blot analysis using monoclonal or polyclonal anti-iNOS antibodies.
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6

Lahiri, Mayurika. "Characterisation of nitric oxide synthase isoforms and nitric oxide synthase activity in human breast cancer cell lines". Thesis, University of Wolverhampton, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.391489.

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7

Molinari, Micol Ariella. "Nitric oxide synthase and the contribution of nitric oxide to vertebrate motor contol /". St Andrews, 2008. http://hdl.handle.net/10023/489.

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8

Åkesson, Björn. "Islet constitutive nitric oxide synthase and nitric oxide production modulatory effects on insulin and glucagon secretion /". Diss., Lund, Sweden : Dept. of Pharmacology, University of Lund, 1998. http://catalog.hathitrust.org/api/volumes/oclc/41383563.html.

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9

Lane, Paul B. "Molecular regulation of endothelial nitric oxide synthase". Thesis, University of Surrey, 2000. http://epubs.surrey.ac.uk/848628/.

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The three isoforms of nitric oxide synthase (NOS) are classified based on their mode of regulation by calmodulin (CaM). The "calcium-independent" inducible isoform (iNOS) contains tightly-bound CaM and is active at all levels of intracellular calcium. In contrast, the two calcium-dependent isoforms (neuronal, nNOS and endothelial eNOS) are activated by CaM-binding following stimulus-evoked increases in intracellular calcium. However, both the structural basis for these differences in regulation and the molecular basis for CaM-induced cNOS activation remained unclear. Given that the regulation of calmodulin regulated enzyme systems often involves the displacement of an intrinsic autoinhibitory domain, we attempted to identify regions of eNOS which may fulfill this autoinhibory function. Herein, I describe the identification of two autoinhibitory control elements (ACEs) in eNOS, one within the FMN binding domain (ACE-I) and one located at the C-terminus (ACE-2). Together with CaM, these form a tripartite system for the regulation of eNOS. ACE-lIACE-2 exerting negative effects to attenuate catalytic activity, which are overcome by the conformational changes induced by CaM-binding. The mechanism of ACE-lIACE-2-mediated inhibition and the alleviation of this inhibition were investigated.
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10

Wang, Tingting. "Molecular Regulation of Inducible Nitric Oxide Synthase". The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1353684453.

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11

Hope, Bruce Thomas. "Neuronal NADPH-diaphorase is a nitric oxide synthase". Thesis, University of British Columbia, 1991. http://hdl.handle.net/2429/30932.

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The enzyme responsible for the neuronal NADPH-diaphorase histochemical reaction was identified in rat brain by employing a variety of histochemical and biochemical techniques. The histochemical reaction catalyzes the NADPH-dependent reduction of tetrazolium dyes to colored insoluble formazans. Although the histochemical reaction has been widely employed in neuroanatomical and neuropathological studies, the identity of the enzyme responsible for the reaction has been unknown. Previous attempts to determine the identity of the enzyme have failed due to the lack of a specific biochemical assay. Some biochemical characteristics of the histochemical reaction in rat striatum were determined in order to develop a specific biochemical assay for neuronal NADPH-diaphorase. The histochemical reaction used several different analogs of NADPH but did not use β-NADH. All tetrazolium analogs with redox potentials above that for β-NADPH were reduced, although the reduction of some tetrazoliums was oxygen-sensitive. The reaction appeared not to require metal ions, flavins, peroxides, or superoxide anions as all methods to remove these factors did not influence staining. The DT-diaphorase activator, menadione, and the inhibitor, dicumarol, did not affect neuronal NADPH-diaphorase. Electron microscopic results suggested neuronal NADPH-diaphorase was membrane-bound, particularly with the endoplasmic reticulum. These results correlate with no known enzymes, including those previously proposed as neuronal NADPH-diaphorase. Employing an antiserum which specifically detected neuronal NADPH-diaphorase, we found the enzyme to be nitric oxide (NO) synthase. NO synthase produces the membrane-permeable second messenger NO. Immunoreactive NADPH-diaphorase activity was copurified to apparent homogeneity with NO synthase activity. The antiserum specifically immunoprecipitated both NO synthase and NADPH-diaphorase activities and specifically labelled a 150 kD band on Western blots, similar to NO synthase from previous reports. The NADPH-diaphorase substrate, NBT, competed with the NO synthase substrate, arginine, for electrons from NADPH. As expected, immunoreactivity for citrulline was found only in NADPH-diaphorase neurons. Citrulline is produced along with NO from the substrate, arginine. NADPH-diaphorase activity was weak to moderate in the cerebellum even though this region contains high levels of NO synthase. The cerebellum also had no citrulline- or NADPH-diaphorase immunoreactivity. We suggest the NO synthase in the cerebellum is a different form from that in the rest of the brain. We conclude that the neuronal NADPH-diaphorase histochemical reaction is due to a form of NO synthase and therefore NADPH-diaphorase is a histochemical marker of NO synthase in the brain. The product NO is the endogenous activator of soluble gu any late cyclase in the brain. This allows a discussion of the anatomical and functional relationships between NO synthase/NADPH-diaphorase and guanylate cyclase to determine the possible functions of these enzymes and their second messenger products in the brain.
Medicine, Faculty of
Graduate
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12

Stevenson, Thirza Helen. "Structural and functional studies of nitric oxide synthase". Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29830.

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The oxygenase domains of rat brain nNOS (amino acids 221-724) and murine macrophage iNOS (residues 66-498) have been expressed and purified from Escherichia coli (E. coli). The two haem domain proteins have been characterised with respect to substrate and cofactor binding. The nNOS protein could not be purified to a high degree and bound less haem and BH4 than expected. The purified iNOS haem domain, however, contained its full complement of iron and zinc, had an optimal subunit:haem: BH4 stoichiometry of 1:1:1 and bound L-arginine with a similar affinity as the E. coli-generated full-length murine iNOS. Optical perturbation spectroscopy and NMR paramagnetic relaxation experiments were used to study the interaction between NOS substrates, or inhibitors, and the reactive centre of the murine iNOS haem domain. Type I ligands, such as the substrates L-arginine bound near the haem and converted any hexa-co-ordinate low-spin haem iron to a penta-co-ordinate high-spin form. Type II ligands, such as imidazole, however, co-ordinated directly to the iNOS haem iron resulting in enzyme with a six-co-ordinate low-spin haem iron. To obtain information on the orientation of ligands within the iNOS active site, the NMR experiments required ligands to be weakly binding and in fast-exchange on the NMR timescale with the iNOS haem domain. Although spectral titrations identified ligands with near millimolar binding affinities, NMR experiments indicated that the ligands did not satisfy the fast-exchange criteria. Laser flash photolysis and stopped-flow spectroscopy were used to examine the kinetics of ligand binding to the iNOS haem domain. Studies of Type I ligand binding to the iNOS haem domain-CO complex supported the view that the haem domain exists in different conformational states, corresponding to 'open' and 'closed' forms of the ligand access channel. In the absence of a Type I ligand and BH4, the iNOS haem domain appeared to have a relatively open distal pocket that allowed CO to bind unhindered. In the presence of BH4 and Type I ligand, however, the enzyme adopted a more closed structure that greatly reduced ligand access to the haem iron.
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13

Akbar, Muhammad Naveed. "Analogues of BH4 and nitric oxide synthase activators". Thesis, University of Strathclyde, 2017. http://digitool.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=28866.

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Nitric oxide synthase (NOS) is an enzyme that catalyses the synthesis of nitric oxide (NO)from L-arginine. There are three kinds of nitric oxide synthase enzymes: neuronal NOS (nNOS), endothelial NOS (eNOS) and inducible NOS (iNOS). Nitric oxide is a biological messenger molecule and a potent vasodilator which controls many biological processes, such as hypertension, stroke, memory, learning disorders and many more. The Nobel Prize in Physiology and Medicine was granted for the discovery and identification of the endothelium-derived relaxing factor as nitric oxide. 5,6,7,8-Tetrahydrobiopterin (BH4) is an essential cofactor of nitric oxide synthases (NOSs) and presumably is present in every cell or tissue of higher organisms. Oxidation of BH4, in diabetes and in different chronic vasoinflammatory diseases can produce cofactor deficiency. This decreased level of BH4 can result in uncoupling of endothelial nitric oxide synthase where this enzyme produces superoxide and thus nitric oxide production is suppressed. BH4 in its active, reduced form is highly unstable and therefore not suitable for oral administration. BH4 does not readily pass across the blood brain barrier; also it cannot be utilized to improve the central neurotransmitter insufficiency in case of BH4 deficiency. This defect of BH4 owes to its hydrophilic nature; however, lipophilic particles can readily pass this brain barrier. If we can have a molecule that is not easily oxidized, and is more lipophilic so that it can cross the blood brain barrier and is also a nitric oxide synthase activator, we can treat all diseases which are caused due to deficiency of nitric oxide especially in old age, when the body starts producing less of nitric oxide. In other words, we can find a cure for diseases which are caused by nitric oxide deficiency. When I started my PhD, Prof Suckling group has already discovered an active pteridine called as WSG1002 1.2 which is more stable to oxidation and has greater solubility than BH41.1. It was an improvement but still not an ideal molecule; both stability and solubility needed to improve. We worked to develop an oxidatively stable and lipophilic pteridine molecule which can act as a cofactor for nitric oxide synthase (NOS) and can correct BH4 deficiency in selected diseases. The following substitutions at WSG1002 (1.2) were considered for my research project. i) N8-deaza ii) C6-unsubstituted iii) 2H at C7 instead of methyl groups. iv) At C6 methyl, hydroxymethyl, acetoxymethyl, acetyl and 1, 2-dihydroxypropyl. This research project provided 8-alkyl and 8-deaza analogues for for nitric oxide synthase enzyme essay, the biological assays for these compounds will be discussed Chapter 3. The investigation of these compounds also made possible studies of the mechanism of action of NOS. Chapter 1 describes nitric oxide and how it is formed from NOS enzymes along with NOS structures and mechanism. It also describes the role of BH4 and its drawbacks. The stucture of the cofactor plays an important role for binding and NOS activity which has been discussed with examples along with requirements for a better molecule. Chapter 2 is about synthesis of important molecules which can help us to understand the mechanism of NO formation and the possibility of finding an ideal drug with better medicinal properties. Although the reactions were challenging, we have prepared many new molecules, many them have been evaluated, and some of them were found to be active and oxidatively stable which is one of the problems with these molecules. 8-Alkyl and 8-deaza analogues have been successfully synthesized. Chapter 3 describes biological results of our compounds which were screened for nitric oxide synthase assays in collaboration with Dr. Simon Daff at the University of Edinburgh. In addition to NOS activity, a number of molecues were also submitted for antibacterial and microbial activity in SIPBS and some of them were found to be active. Chapter 4 describes the experiments for the synthesis of our desired compounds. The methods for the preparation and their characterisation have been given in detail. The last Chapter lists the references.
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14

Altawallbeh, Ghaith. "Endothelial Nitric Oxide Synthase on Nanoscale Phospholipid Bilayers". Cleveland State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=csu1480640206186696.

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15

Gotoh, Kazuo. "Nitric oxide synthase immunoreactivity in the edematous brain". Kyoto University, 1999. http://hdl.handle.net/2433/181695.

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16

Dai, Yue. "Study of Electron Transfer through the Reductase Domain of Neuronal Nitric Oxide Synthase and Development of Bacterial Nitric Oxide Synthase Inhibitors". Cleveland State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=csu1472477836.

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17

Woo, Wai-hong Connie, i 胡偉康. "Regulation of nitric oxide production in macrophages". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2003. http://hub.hku.hk/bib/B26662103.

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18

Leung, Tung-ming. "An in vivo study on the distinctive role of inducible and endothelial nitric oxide synthase in carbon tetrachloride-induced liver injury". Click to view the E-thesis via HKUTO, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36846806.

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19

Levy, Dan. "Local nitric oxide synthase expression and nitric oxide action in an animal model of neuropathic pain". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape7/PQDD_0034/NQ38484.pdf.

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20

Gahm, Caroline. "Nitric oxide in brain contusion /". Stockholm, 2005. http://diss.kib.ki.se/2005/91-7140-392-2/.

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21

Sandström, Per A. "Nitric oxide, arginine and acute pancreatitis /". Linköping : Univ, 2004. http://www.bibl.liu.se/liupubl/disp/disp2004/med866s.pdf.

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22

Chen, Wei-Kang. "Analysis of neural gene expression glutamine synthetase and nitric oxide synthas I /". Columbus, Ohio : Ohio State University, 2003. http://rave.ohiolink.edu/etdc/view?acc%5num=osu1061581254.

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Thesis (Ph. D.)--Ohio State University, 2003.
Title from first page of PDF file. Document formatted into pages; contains xi, 174 p. : ill. (some col.). Advisor: Anthony Young, Molecular, Cellular, and Developmental Biology Program. Includes bibliographical references (p. 154-174).
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23

Padayachee, Eden Rebecca. "Neuronal nitric oxide synthase : a biomarker for Alzheimers disease : interaction of neuronal nitric oxide synthase with beta-amyloid peptides in the brain". Thesis, Rhodes University, 2011. http://hdl.handle.net/10962/d1007677.

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High levels of the amino acid arginine and low levels of the product citrulline in the cerebrospinal fluid of Alzheimer's patients could mean that there is a decrease in the enzymes that metabolize this amino acid. One such enzyme is neuronal nitric oxide synthase (nNOS). In this study, neuronal nitric oxide synthase (nNOS), sourced from bovine brain was extracted and concentrated using two methods of precipitation: poly (ethylene glycol) 20 000 (PEG) and ammonium sulphate [(NH₄)₂S0₄). These two techniques gave no increase in yield nor fold purification and hence were abandoned in favour of ion exchange chromatography by DEAE-Sepharose. The enzyme was then successfully purified by anion-exchange and after dialysis produced a 38% yield and three fold purification and yielded the highest specific activity of 2.27 U/mg. Neuronal nitric oxide synthase (nNOS) was a heterodimeric protein with a total molecular mass of ± 225 kDa (95 and 130 kDa monomers). The temperature and pH optima of the enzyme were 40⁰C and 6.5, respectively. The kinetic parameters (KM and Vmax) of nNOS were 70 μM and 0.332 μmol.min⁻¹, respectively. Moreover neuronal nitric oxide synthase (nNOS) was relatively stable at 40⁰C (t½ = 3 h). It was also confirmed that β-amyloid peptides inhibited nNOS when bound to the enzyme and that nNOS behaved as a catalyst in fibril formation through association-dissociation between enzyme and β-amyloid peptide. It was further shown that Aβ₁₇₋₂₈ inhibited nNOS the most with a Ki of 1.92 μM and also had the highest Stern-Volmer value (Ksv) of 0.11 μM⁻¹ indicating tight binding affinity to nNOS and easier accessibility to fluor molecules during binding. Congo red, turbidity, thioflavin-T assays and transmission electron microscopy were successfully used to detect and visualize the presence of fibrils by studying the process of fibrillogenesis. Computerized molecular modeling successfully studied protein dynamics and conformational changes of nNOS. These results correlated with resonance energy transfer (FRET) results which revealed the distance of tryptophan residues from the arginine bound at enzyme active site. Both the aforementioned techniques revealed that in the natural state of the enzyme with arginine bound at the active site, the tryptophan residues (TRP₆₂₅ and TRP₇₂₁) were positioned at the surface of the enzyme 28 Å away from the active site. When the amyloid peptide (Aβ₁₇₋₂₈) was bound to the active site, these same two amino acids moved 14 Å closer to the active site. A five residue hydrophobic fragment Aβ₁₇₋₂₁ [Leu₁₇ - Val₁₈ - Phe₁₉ - Phe₂₀ - Ala₁] within Aβ₁₇₋₂₈ was shown by computer modeling to be critical to the binding of the peptide to the active site of nNOS.
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24

Cheung, Filly. "Regulation of nitric oxide synthase expression in mammalian cells /". Hong Kong : University of Hong Kong, 2001. http://sunzi.lib.hku.hk:8888/cgi-bin/hkuto%5Ftoc%5Fpdf?B23425866.

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25

Faughn, Jonathan David. "Regulation of Endothelial Nitric Oxide Synthase in Pulmonary Myofibroblasts". TopSCHOLAR®, 2011. http://digitalcommons.wku.edu/theses/1088.

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Idiopathic pulmonary fibrosis (IPF) is an interstitial lung disease leading to decreased lung volume and eventual respiratory failure. At present, the median post-diagnosis lifespan is between three and six years. Myofibroblasts are collagen-secreting cells essential for wound healing, but also implicated in the fibroproliferation and extra cellular matrix deposition commonly seen in IPF. The nitric oxide (NO) signaling pathway is implicated in protomyofibroblast to myofibroblast transition and regulation. Previous work has shown that in pulmonary myofibroblasts, endothelial nitric oxide synthase (eNOS) is the primary NOS isoform expressed. The current study used cultured rat pulmonary myofibroblasts between passages two and five as a cell model. The cells were grown in normal growth media (DMEM + 10% FBS) or serum starved (DMEM + 0% FBS) to induce cellular differentiation. In this study, immunocytochemistry was used to show localization of eNOS is dependent on cellular differentiation, with protomyofibroblasts expressing eNOS primarily in the nucleus and protomyofibroblasts expressing eNOS in the perinuclear region. We also show catalytic activity and localization of eNOS are correlated by visualizing nitric oxide production in the cells using a permeable fluorescein chromophore. By using western blot analysis on fractionated cell lysates we found eNOS expressed in the nucleus under normal growth conditions. eNOS is at least partially regulated by intracellular calcium (Ca2+) and calmodulin (CaM). Western blot analysis using native eNOS and phospho-specific eNOS antibodies on fractionated cells treated with the protein kinase C (PKC) activator phorbal 12-myristate 13-acetate (PMA) with and without addition of its antagonist ethylene glycol tetraacetic acid (EGTA) was conducted to investigate PKC’s role in eNOS regulation by phosphorylation. Indeed, PKC activation was found to mitigate expression in the nucleus, while inhibition of the activator restored the activity expression above basal levels. This finding correlates with previous data from our lab showing a decrease in activity in myofibroblasts treated with PMA and assayed amperometrically with an NO electrode.
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26

Wilson, Neil Martin McCall. "Towards a biomimetic porphyrin model for nitric oxide synthase". Thesis, Heriot-Watt University, 2008. http://hdl.handle.net/10399/2173.

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Hum, Kathleen O. "Nitric oxide synthase expression and murine mammary tumour progression". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/mq30798.pdf.

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Yan, Zhong-qun. "Inducible nitric oxide synthase : in vascular smooth muscle cells /". Stockholm, 1998. http://diss.kib.ki.se/1998/91-826-3177-1/.

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29

Wu, Chin-Chen. "Role of inducible nitric oxide synthase in septic shock". Thesis, Queen Mary, University of London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.362801.

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30

Edgar, K. S. "The role of nitric oxide synthase in retinal angiogenesis". Thesis, Queen's University Belfast, 2012. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.557406.

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Neovascularisation occurs in response to tissue ischemia in conditions including ischaemic retinopathy, with new vessels often infiltrating the transparent vitreous by a poorly understood mechanism. Nitric oxide produced by eNOS is a downstream mediator of VEGF function and plays a crucial role in vascular formation and maturation; therefore, we investigated the role of NOS using transgenic models in the murine model of oxygen induced retinopathy (aiR). Using eNOS over-expressing eNOS-GFP mice, we investigated vascular growth during retinal development, during aiR and also using an in-vitro model and found that eNOS over-expression increased angiogenesis. Over-expression of eNOS in the eNOS-GFP mice resulted in an increase in vaso-obliteration following hyperoxia exposure, which was followed by an increased neovascular response and improved revascularisation of the ischaemic retina. There was evidence of dysfunction of NOS in the eNOS-GFP animals, with an increase in oxidative stress which may contribute to the neovascular formation. Using the BH4 deficient hph-l mouse model we investigated the role of this NOS co-factor in the development of the retinal vasculature and the pathology of ischaemic retinopathy. We found that there was a reduced severity of both the vaso-obliterative . and neovascular phases of ischaemic retinopathy. A reduction in NOS activity due to the BH4 deficiency was demonstrated in-vitro in microglial cells from the hph-l animals and could explain the reduced angiogenesis seen in the hph-l animals. Our results demonstrate that the pathology of ischaemic retinopathy is altered by changes in NOS expression and function with eNOS over-expression resulting in more severe vaso-obliteration, followed by improved retinal revascularisation, while a deficiency in BH4 results in reduced severity of both the vaso-obliterative and neovascular phases of ischaemic retinopathy, but with a delayed revascularisation. These results indicate that selective alteration of NOS expression at different stages of ischaemic retinopathy may reduce the severity of the vaso-obliterative stage and help promote recovery of the ischaemic retina.
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31

McKendrick, Joyce Dickson. "Induction of nitric oxide synthase in vascular smooth muscle". Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.484166.

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32

張婓怡 i Filly Cheung. "Regulation of nitric oxide synthase expression in mammalian cells". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B31241554.

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33

Wakefield, Ian D. "Nitric oxide synthase inhibition : effects on the cardiovascular system". Thesis, University of Nottingham, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.438285.

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34

Stevenson, L. "Regulation of Nitric Oxide Synthase Isoforms in Retinal Angiogenesis". Thesis, Queen's University Belfast, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501408.

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35

Ashraf, Haroon. "RNAI knockdown of nitric oxide synthase in manduca sexta". Thesis, The University of Arizona, 2009. http://hdl.handle.net/10150/192283.

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36

Gribbe, Örjan. "Experimental skin flaps and nitric oxide /". Stockholm, 2006. http://diss.kib.ki.se/2006/91-7357-043-5/.

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37

Soneja, Amit. "Restoration of the nitric oxide/peroxynitrite balance in the acceleration of wound healing /". View abstract, 2006. http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:3248458.

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Keen, Jeremy T. "Dietary nitrate supplementation augments nitric oxide synthase mediated cutaneous vasodilation during local heating in healthy humans". Thesis, Kansas State University, 2013. http://hdl.handle.net/2097/15438.

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Master of Science
Department of Kinesiology
Brett J. Wong
Nitrate supplementation in the form of beetroot juice (BRJ) has been shown to increase nitric oxide (NO), where nitrate can be reduced to nitrite and NO through both nitric oxide synthase (NOS) independent and dependent pathways. We tested the hypothesis that BRJ would augment the NO component of cutaneous thermal hyperemia. Dietary intervention consisted of one shot of BRJ for three days. Six subjects were equipped with two microdialysis fibers on the ventral forearm and randomly assigned to lactated Ringer’s (control) or continuous infusion of 20mM L-NAME (NOS inhibitor). The control site was subsequently perfused with L-NAME once a plateau in the local heating response was achieved to quantify NOS-dependent cutaneous vasodilation. Skin blood flow via laser-Doppler flowmetry (LDF) and mean arterial pressure (MAP) were measured; cutaneous vascular conductance (CVC) was calculated as LDF/MAP and normalized to %CVCmax. Maximal vasodilation was achieved via local heating to 43°C and 54mM sodium nitroprusside infusion. There was a significant decrease in DBP after BRJ (Pre-BRJ:74 ± 1 mmHg vs. Post-BRJ: 61 ± 2 mmHg; p < 0.05) and significant reduction in MAP after BRJ (Pre-BRJ: 90 ± 1 mmHg vs. Post-BRJ: 80 ± 2 mmHg; p < 0.05). The initial peak and secondary plateau phase of cutaneous thermal hyperemia were attenuated at sites with continuous LNAME; however, there was no effect of BRJ on either the initial peak at control sites (Pre-BRJ: 76 ± 3%CVCmax vs. Post-BRJ: 75 ± 4%CVCmax) or L-NAME sites (Pre-BRJ: 60 ± 4%CVCmax vs. Post-BRJ: 59 ± 5%CVCmax) or the secondary plateau phaseat control sites (Pre-BRJ: 88 ± 4%CVCmax vs. Post-BRJ: 90 ± 4%CVCmax) or L-NAME sites (Pre-BRJ: 45 ± 5%CVCmax vs. Post-BRJ: 51 ± 3%CVCmax). The decrease in %CVCmax to L-NAME infusion during the plateau of local heating (i.e. post-L-NAME drop) was greater after BRJ (Pre-BRJ: 36 ± 2%CVCmax vs. Post-BRJ: 28 ± 1%CVCmax; p < 0.05). This resulted in a greater contribution of NOS to the plateau phase of local heating (Pre-BRJ: 57±3%CVCmax vs. Post-BRJ: 64±2%CVCmax; p < 0.05). These data suggest BRJ modestly improves NOS-dependent vasodilation to local heating in the cutaneous vasculature of healthy humans.
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39

Huang, Kan. "Impact of the short-term consumption of a moderately high fat diet on nitric oxide production and bioavailability". [Huntington, WV : Marshall University Libraries], 2009. http://www.marshall.edu/etd/descript.asp?ref=986.

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Schön, Thomas. "Nitric oxide in tuberculosis and leprosy /". Linköping, 2002. http://www.bibl.liu.se/liupubl/disp/disp2002/med749s.pdf.

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Fitzpatrick, Brian. "The role of inducible nitric oxide synthase and nitric oxide in tumour cells and their response to therapy". Thesis, University of Manchester, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.511755.

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Erdely, Aaron. "Progression of chronic renal disease in several animal models possible role of decreased renal nitric oxide production as a primary causative factor /". Morgantown, W. Va. : [West Virginia University Libraries], 2002. http://etd.wvu.edu/templates/showETD.cfm?recnum=2740.

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43

Song, Wook. "Exercise training reverses age-induced inducible nitric oxide synthase upregulation". Diss., Texas A&M University, 2003. http://hdl.handle.net/1969.1/1609.

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The risk of injury, inflammation, and oxidative stress increases in skeletal muscle with aging. It has been postulated that pro-oxidant signaling, including upregulation of inducible nitric oxide synthase (iNOS) contributes to inflammation, pathology, and aging in the brain, liver and heart. Exercise training reduces the risk of injury and inflammation. The purpose of this study was: 1) to identify the mechanisms that upregulate iNOS, pro-oxidant and pro-inflammatory signaling in skeletal muscle, and 2) to identify the mechanisms by which exercise training reduces pro-oxidant signaling. Protein levels and activity of iNOS were measured in 4 groups of male Fischer-344 rats (5 mo and 24 mo, n=10/group), old-control (OC), old-trained (OT), young-control (YC), and young-trained (YT). Exercise training protocol was 60 min at 15 m/min at 15° incline for 5 d/wk for 12 wk. Both iNOS protein expression and activity were significantly higher in OC compared to YC, but exercise training reversed the elevation of iNOS levels lower than OC in tibialis anterior. Surprisingly, NF-κB DNA binding activity was significantly lower in OC than YC, while increased with exercise training in white and red gastrocnemius in both OT and YT. In contrast, protein expression of p65, a regulatory subunit of NF-κB was significantly greater in OC than YC, while exercise training significantly reduced p65 in OT compared to OC from the white gastrocnemius. These data indicate that regulation of NF-κB activity with aging is post-translational and alterations in iNOS expression may result from alternative NF-κB pathways. As decreased NF-κB activity with aging could result in downstream increase in pro-apoptotic signaling, we tested follow-up hypotheses that aging would increase pro-apoptotic regulator Bax and decrease the anti-apoptotic regulator Bcl-2. Bax increased while Bcl-2 decreased in OC in white gastrocnemius when compared to YC. In contrast, exercise training resulted in a dramatic upregulation of Bcl-2 and downregulation of Bax protein expression in OT when compared to OC. These novel results indicate that alterations in pro-inflammatory and pro-apoptotic signaling occur in skeletal muscle during the aging process. Importantly, our findings strongly support the hypothesis that exercise training reverses age-induced changes in pro-inflammatory and pro-apoptotic signaling.
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Rao, Morthala Raghavendar. "The synthesis and study of novel nitric oxide synthase activators". Thesis, University of Strathclyde, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486538.

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Nitric oxide (NO) is an essential molecule for the maintenance of blood pressure and vascular tone In mammals including humans. NO is produced by three different nitric oxide synthases (NOSs): Neuronal NOS (nNOS), inducible NOS (iNOS) and endothelial NOS (eNOS). Tetrahydrobiopterin (BH4) 1.1 is one of the important cofactors of these three NOSs: The deficiency of BH4 causes reduced nitric oxide production which in turn contributes to the hypertension, diabetes, oxidative stress etc. Biologists from various groups suggested that the dihydrobiopterin BH2 5.1. is an inhibitor of all three NOSs. However one of our library compounds 1.2 (WSG1002) in BH4 deficient tissues, although in dihydro oxidation state as 5.1, had shown similar action as natural BH4 by producing nitric oxide. Thus. WSG1002 has become lead compound for this PhD study. The main aim of my PhD study was to synthesise different blocked dihydropteridines with variation at positions 2, 6 and 7 in 1.2 to identify a '!lore efficient and selective eNOS activator, and to study the .mechanism behind the unusual activation ofNOSs by these dihydropteridines. Chapter One gives an introduction to the project. In this, a review of nitric oxide synthase enzymes,. mechanism of nitric oxide synthesis and introduction to the pteridines are covered. Chapter Two describes the synthesis of blocked dihydropteridines; most of the discussion is devoted to the challenges faced in the construction of sterically highly demanding a,a-disubstituted amino ketones. After considering various synthetic routes, a highly flexible and divergent synthetic route has been developed. In pursuit of diversity at C2 in pteridi!1e 1.2, a new synthetic route has b~en developed. starting from trichloropyrimidine 3.102. In this a stepwise regioselective nucleophilic substitution of three chlorines In 3.102 has been successful. Consequently a new pteridine 3.110 with variation at C2 was constructed. Chapter Four is dedicated to the asymmetric alkylation of alanine derivative 4.36. This chapter starts with a brief review of enantioselective alkylation of Schiff bases of glycine and alanine esters with variety of phase transfer catalysts. In the results and discussion section, syntheses of the cinchonidine-derived catalyst 4.13 and the usubstituted alanine derivative 2.120 with >99 % ee is discussed in detail. In Chapter Five, the biological results of blocked dihydro and tetrahydropteridines from nNOS assays have been demonstrated. In this project tetrahydropteridines 2.183b and 2.183d have shown excellent activity in nNOS by producing nitric oxide. Chapter Six provides detailed experimental procedures and characterisation data of compounds discussed in chapters from two to five.
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Scott, Jeremy Alexander. "Alteration and regulation of nitric oxide synthase isozymes in sepsis". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp04/NQ58233.pdf.

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Bishop-Bailey, David. "Induction of cyclo-oxygenase and nitric oxide synthase in vessels". Thesis, Imperial College London, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.286016.

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Castillo, Joel. "Design and synthesis of inhibitors of inducible nitric oxide synthase". Thesis, University of Newcastle Upon Tyne, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.270170.

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Wilson, Natalie Jane. "Molecular and biochemical characterisation of a FUGU nitric oxide synthase". Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.393853.

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Stebbing, John French. "Nitric oxide synthase neurones and neuromuscular behaviour of the anorectum". Thesis, King's College London (University of London), 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.266007.

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Ahmetaj-Shala, Blerina. "The role of nitric oxide synthase inhibitors on macrophage function". Thesis, Kingston University, 2013. http://eprints.kingston.ac.uk/27732/.

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Asymmetrically methylated forms of arginine (asymmetric dimethylarginine, ADMA and L-N-monomethylarginine, L-NMMA) are competitive inhibitors of all three isoforms of nitric oxide synthase (NOS). These molecules are produced endogenously in all cells by a process that involves protein arginine methyltransferase (PRMT)-catalysed methylation of certain arginine residues in proteins and the subsequent proteolysis of these methylated proteins. Free methylarginines accumulate in the cytosol where they are actively metabolized to citrulline and methylamines by the enzyme dimethylarginine dimethylaminohydrolase (DDAH1 and 2). ADMA and L-NMMA have been shown to be elevated in patients with cardiovascular and renal disease, however, their role in immune cells and in particular macrophages is yet to be confirmed. The aim of this project was to determine the effect of increased ADMA, both endogenous and exogenous, on macrophage function. U937-derived macrophages (a human monocytic cell line) and primary peritoneal macrophages extracted from wild type (DDAH2+/+), global DDAH2 knock-out (DDAH2-/-) and macrophage-specific DDAH2 knock-out (DDAH2flox/flox LysM-Cre) mice were used. Their NO production, motility, phagocytosis, chemotaxis, and cytokine levels was determined using the Griess assay, real-time imaging, a fluorescently labelled E-coli phagocytosis assay, a transwell migration assay and RNA-sequencing respectively. Here we show that, in contrast to endothelial cells, DDAH2 is the only DDAH isoform expressed in primary murine macrophages basally or following cytokine stimulation of the cells. Results showed that DDAH2 metabolises methylarginines in macrophages through a VEGF-independent mechanism and significantly attenuates cytokine-stimulated NO synthesis. Both the pharmacological addition of ADMA and genetic deletion of DDAH2 in macrophages results in impaired macrophage function (as assessed by motility, phagocytosis and cytokine production). These data identify DDAH2 as a key regulator of macrophage NO synthesis and demonstrate the potential therapeutic utility of DDAH2-selective inhibitors.
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