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Items 1 to 10 of about 1236303
1. Feng JX, Lin Y, Lin J, He SS, Chen MF, Wu XM, Xu YZ: Relationship between Fractional Exhaled Nitric Oxide Level and Efficacy of Inhaled Corticosteroid in Asthma-COPD Overlap Syndrome Patients with Different Disease Severity. J Korean Med Sci; 2017 Mar;32(3):439-447
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Relationship between Fractional Exhaled Nitric Oxide Level and Efficacy of Inhaled Corticosteroid in Asthma-COPD Overlap Syndrome Patients with Different Disease Severity.
  • This study explored the relationship between the fractional exhaled nitric oxide (FeNO) level and the efficacy of inhaled corticosteroid (ICS) in asthma-chronic obstructive pulmonary disease (COPD) overlap syndrome (ACOS) patients with different disease severity.
  • We compared FeNO levels, pulmonary function parameters including percentage of forced expiratory volume in 1 second (FEV1) to predicted value (FEV1%pred), ratio of FEV1 to forced vital capacity (FEV1/FVC), inspiratory capacity to total lung capacity (IC/TLC) and residual volume to total lung capacity (RV/TLC), arterial blood gas parameters, including PH, arterial partial pressure of oxygen (PaO₂) and arterial partial pressure of carbon dioxide (PaCO₂), total serum immunoglobulin E (IgE), induced sputum eosinophil (EOS), plasma surfactant protein A (SP-A), plasma soluble receptor for advanced glycation end products (sRAGE), sputum myeloperoxidase (MPO), sputum neutrophil gelatinase-associated lipocalin (NGAL) and Asthma Control Test (ACT) scores, and COPD Assessment Test (CAT) scores.
  • [MeSH-major] Adrenal Cortex Hormones / therapeutic use. Asthma / drug therapy. Nitric Oxide / analysis. Pulmonary Disease, Chronic Obstructive / drug therapy
  • [MeSH-minor] Administration, Inhalation. Adult. Advanced Glycosylation End Product-Specific Receptor / blood. Aged. Biomarkers / blood. Biomarkers / metabolism. Blood Gas Analysis. Case-Control Studies. Female. Forced Expiratory Volume. Humans. Immunoglobulin E / blood. Lipocalin-2 / metabolism. Male. Middle Aged. Peroxidase / metabolism. Pulmonary Surfactant-Associated Protein A / blood. Respiratory Function Tests. Severity of Illness Index. Sputum / enzymology. Sputum / metabolism

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  • (PMID = 28145647.001).
  • [ISSN] 1598-6357
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Adrenal Cortex Hormones; 0 / Advanced Glycosylation End Product-Specific Receptor; 0 / Biomarkers; 0 / Lipocalin-2; 0 / Pulmonary Surfactant-Associated Protein A; 31C4KY9ESH / Nitric Oxide; 37341-29-0 / Immunoglobulin E; EC 1.11.1.7 / Peroxidase
  • [Keywords] NOTNLM ; Asthma-Chronic Obstructive Pulmonary Disease Overlap Syndrome / Efficacy / Fractional Exhaled Nitric Oxide / Inhaled Corticosteroid
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2. Albert M, Corsilli D, Williamson DR, Brosseau M, Bellemare P, Delisle S, Nguyen AQ, Varin F: Comparison of inhaled milrinone, nitric oxide and prostacyclin in acute respiratory distress syndrome. World J Crit Care Med; 2017 Feb 04;6(1):74-78

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Comparison of inhaled milrinone, nitric oxide and prostacyclin in acute respiratory distress syndrome.
  • METHODS: Open-label prospective cross-over pilot study where fifteen adult patients with hypoxemic failure meeting standard ARDS criteria and monitored with a pulmonary artery catheter were recruited in an academic 24-bed medico-surgical intensive care unit.
  • Thereafter, inhaled milrinone (1 mg/mL) alone followed by inhaled milrinone in association with inhaled nitric oxide (iNO) was administered.
  • RESULTS: The majority of ARDS were of pulmonary cause (<i>n</i> = 13) and pneumonia (<i>n</i> = 7) was the leading underlying initial disease.
  • Other pulmonary causes of ARDS were: Post cardiopulmonary bypass (<i>n</i> = 2), smoke inhalation injury (<i>n</i> = 1), thoracic trauma and pulmonary contusions (<i>n</i> = 2) and aspiration (<i>n</i> = 1).
  • Two patients had an extra pulmonary cause of ARDS: A polytrauma patient and an intra-abdominal abscess Inhaled nitric oxide, epoprostenol, inhaled milrinone and the combination of inhaled milrinone and iNO had no impact on systemic hemodynamics.

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  • (PMID = 28224110.001).
  • [Journal-full-title] World journal of critical care medicine
  • [ISO-abbreviation] World J Crit Care Med
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; Acute respiratory distress syndrome / Hypoxemia / Inhaled milrinone / Nitric oxide / Prostacyclin / Pulmonary hypertension
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3. Pereira ML, D'ancona CA, Rojas-Moscoso JA, Ramos AC Filho, Monica FZ, Antunes E: Effects of nitric oxide inhibitors in mice with bladder outlet obstruction. Int Braz J Urol; 2017 Mar-Apr;43(2):356-366

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effects of nitric oxide inhibitors in mice with bladder outlet obstruction.
  • PURPOSE: To investigate the lower urinary tract changes in mice treated with L-NAME, a non-selective competitive inhibitor of nitric oxide synthase (NOS), or aminoguanidine, a competitive inhibitor of inducible nitric oxide synthase (iNOS), after 5 weeks of partial bladder outlet obstruction (BOO), in order to evaluate the role of constitutive and non-constitutive NOS in the pathogenesis of this experimental condition.
  • RESULTS: BOO animals showed increase of non-voiding contractions (NVC) and bladder capacity, and also less contractile response to Carbachol and Electric Field Stimulation.

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  • [Copyright] Copyright® by the International Brazilian Journal of Urology.
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  • (PMID = 28328190.001).
  • [ISSN] 1677-6119
  • [Journal-full-title] International braz j urol : official journal of the Brazilian Society of Urology
  • [ISO-abbreviation] Int Braz J Urol
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Brazil
  • [Keywords] NOTNLM ; NG-Nitroarginine Methyl Ester / Nitric Oxide / Urinary Bladder
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4. Ko SY, Chang YS, Park WS: Clinical response to inhaled nitric oxide in persistent pulmonary hypertension of the newborn. J Korean Med Sci; 1998 Oct;13(5):500-6
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Clinical response to inhaled nitric oxide in persistent pulmonary hypertension of the newborn.
  • We observed clinical response to inhaled nitric oxide (iNO) in 12 neonates with persistent pulmonary hypertension of the newborn (PPHN).
  • Two infants showed no response to iNO (one diaphragmatic hernia and one suspected pulmonary hypoplasia).
  • We conclude that iNO therapy could improve oxygenation in high percentage of newborn infants with severe PPHN of various underlying conditions except pulmonary hypoplasia.
  • [MeSH-major] Nitric Oxide / therapeutic use. Persistent Fetal Circulation Syndrome / therapy. Vasodilator Agents / therapeutic use

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  • (PMID = 9811179.001).
  • [ISSN] 1011-8934
  • [Journal-full-title] Journal of Korean medical science
  • [ISO-abbreviation] J. Korean Med. Sci.
  • [Language] eng
  • [Publication-type] Journal Article; Research Support, Non-U.S. Gov't
  • [Publication-country] Korea (South)
  • [Chemical-registry-number] 0 / Vasodilator Agents; 31C4KY9ESH / Nitric Oxide
  • [Other-IDs] NLM/ PMC3054528
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5. Maccallini C, Amoroso R: Targeting neuronal nitric oxide synthase as a valuable strategy for the therapy of neurological disorders. Neural Regen Res; 2016 Nov;11(11):1731-1734

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Targeting neuronal nitric oxide synthase as a valuable strategy for the therapy of neurological disorders.
  • In this short review we analyze some promising advancements in the search of new bioactive molecules targeting neuronal nitric oxide synthase (nNOS), an enzyme deputed to the biosynthesis of nitric oxide (NO).

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  • (PMID = 28123402.001).
  • [ISSN] 1673-5374
  • [Journal-full-title] Neural regeneration research
  • [ISO-abbreviation] Neural Regen Res
  • [Language] eng
  • [Publication-type] Journal Article; Review
  • [Publication-country] India
  • [Keywords] NOTNLM ; NMDAR / PSD95 / amidines / carbonic anhydrase / inhibitors / neurological diseases / neuronal nitric oxide synthase
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6. Kozij NK, Granton JT, Silkoff PE, Thenganatt J, Chakravorty S, Johnson SR: Exhaled Nitric Oxide in Systemic Sclerosis Lung Disease. Can Respir J; 2017;2017:6736239

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exhaled Nitric Oxide in Systemic Sclerosis Lung Disease.
  • Exhaled nitric oxide (eNO) is a potential biomarker to distinguish systemic sclerosis (SSc) associated pulmonary arterial hypertension (PAH) and interstitial lung disease (ILD).
  • We evaluated the discriminative validity, feasibility, methods of eNO measurement, and magnitude of differences across lung diseases, disease-subsets (SSc, systemic lupus erythematosus), and healthy-controls. <i>Methods</i>.
  • Consecutive subjects in the UHN Pulmonary Hypertension Programme were recruited.
  • Exhaled nitric oxide was measured at 50 mL/s intervals using chemiluminescent detection.

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  • (PMID = 28293128.001).
  • [ISSN] 1916-7245
  • [Journal-full-title] Canadian respiratory journal
  • [ISO-abbreviation] Can. Respir. J.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Egypt
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7. Jin L, Gao H, Wang J, Yang S, Wang J, Liu J, Yang Y, Yan T, Chen T, Zhao Y, He Y: Role and regulation of autophagy and apoptosis by nitric oxide in hepatic stellate cells during acute liver failure. Liver Int; 2017 May 15;

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Role and regulation of autophagy and apoptosis by nitric oxide in hepatic stellate cells during acute liver failure.
  • BACKGROUND & AIMS: We previously found that hepatic stellate cell activation induced by autophagy maintains the liver architecture to prevent collapse during acute liver failure.
  • Nitric oxide has shown to induce hepatic stellate cell apoptosis.
  • Whether and how nitric oxide is involved in acute liver failure and autophagy remains unclear.
  • METHODS: Acute liver failure patients were recruited to investigate the correlation between plasma nitric oxide levels and clinical features.
  • The expression of nitric oxide synthases and hepatic stellate cell activation (alpha-SMA), and autophagic activity (LC3) were investigated by immunohistochemistry.
  • Autophagy and apoptosis were investigated by immunoblot analysis, confocal microscopy, and flow cytometry in hepatic stellate cells treated with nitric oxide donors.
  • RESULTS: Plasma nitric oxide level was significantly increased in patients with acute liver failure compared to those with cirrhosis (53.60±19.74 μM vs 19.40±9.03 μM, Z=-7.384, P<.001) and positively correlated with MELD-Na score (r=.539, P<.001), implicating nitric oxide in acute liver failure.
  • At least some Nitric oxide was produced by overexpression of inducible nitric oxide synthases and endothelial nitric oxide synthases, but not neuronal nitric oxide synthases in the liver tissue.
  • In vivo observation revealed that autophagy was inhibited in hepatic stellate cells based on decreased LC3 immunostaining, and in vitro experiments demonstrated that Nitric oxide can inhibit autophagy.
  • Moreover, nitric oxide promoted hepatic stellate cell apoptosis, which was rescued by an autophagy inducer.
  • CONCLUSIONS: Increased nitric oxide synthases/ nitric oxide promotes apoptosis through autophagy inhibition in hepatic stellate cells during acute liver failure, providing a novel strategy for the treatment of patients with acute liver failure.

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  • [Copyright] © 2017 John Wiley & Sons A/S. Published by John Wiley & Sons Ltd.
  • (PMID = 28508586.001).
  • [ISSN] 1478-3231
  • [Journal-full-title] Liver international : official journal of the International Association for the Study of the Liver
  • [ISO-abbreviation] Liver Int.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] United States
  • [Keywords] NOTNLM ; acute liver failure / autophagy / hepatic stellate cell / nitric oxide
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8. Al-Ali MK, Howarth PH: Exhaled nitric oxide levels in exacerbations of asthma, chronic obstructive pulmonary disease and pneumonia. Saudi Med J; 2001 Mar;22(3):249-53
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Exhaled nitric oxide levels in exacerbations of asthma, chronic obstructive pulmonary disease and pneumonia.
  • OBJECTIVE: Nitric oxide is known to be present in the exhaled air of normal subjects and at higher concentrations in asthmatics.
  • The aim of this study was to measure exhaled nitric oxide levels in patients admitted to hospital with acute exacerbations of asthma, or chronic obstructive pulmonary disease, or with pneumonia.
  • METHODS: Within 24 hours of admission exhaled nitric oxide levels were measured by a chemiluminescent analyzer in 11 patients with acute sever asthma, 19 patients with acute exacerbation of chronic obstructive pulmonary disease, and in 12 patients with pneumonia.
  • RESULTS: On admission median exhaled nitric oxide levels (range) were significantly higher in asthmatics 22 (9.3-74) parts per billion in comparison to patients with chronic obstructive pulmonary disease 10.3 (2.7-34) parts per billion; p < 0.01, pneumonia 7 (4-17) parts per billion; p<0.001, and normal subjects 8.7 (5-13.3) parts per billion; p < 0.001.
  • Following treatment the asthmatics had a significant reduction in their exhaled nitric oxide levels from 22 (9.3-74) parts per billion on day 1 to 9.7 (5.7-18.3) parts per billion on day 28; p = 0.005.
  • A strong negative correlation existed between peak expiratory flow rate measurements and exhaled nitric oxide levels in asthmatics on day 28 (r = -0.70; p = 0.017).
  • CONCLUSION: Acute exacerbations of asthma are associated with increased levels of exhaled nitric oxide in contrast to exacerbations of chronic obstructive pulmonary disease and acute pneumonia.
  • Exhaled nitric oxide may be a useful indirect marker of asthmatic airway inflammation.
  • The differing time course of response of nitric oxide to peak flow measures suggests that these two measures are reflecting differing airway events.
  • [MeSH-major] Asthma / metabolism. Breath Tests. Lung Diseases, Obstructive / metabolism. Nitric Oxide / analysis. Pneumonia / metabolism


9. Gupta S, Ghosh S, Gupta S, Sakhuja P: Effect of curcumin on the expression of p53, transforming growth factor-β, and inducible nitric oxide synthase in oral submucous fibrosis: A pilot study. J Investig Clin Dent; 2016 Dec 17;
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  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Effect of curcumin on the expression of p53, transforming growth factor-β, and inducible nitric oxide synthase in oral submucous fibrosis: A pilot study.
  • AIM: The purpose of the present study was to find out the expression of p53, transforming growth factor-β TGF-β), and inducible nitric oxide synthase (iNOS) in oral submucous fibrosis (OSMF), proteins implicated in its pathophysiology, as well as malignant transformation.

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  • [Copyright] © 2016 John Wiley & Sons Australia, Ltd.
  • (PMID = 27989010.001).
  • [ISSN] 2041-1626
  • [Journal-full-title] Journal of investigative and clinical dentistry
  • [ISO-abbreviation] J Investig Clin Dent
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] Australia
  • [Keywords] NOTNLM ; inducible nitric oxide synthase / oral squamous cell carcinoma / oral submucous fibrosis / p53 / transforming growth factor-β
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10. Liu X, Guo P, Liu A, Wu Q, Xue X, Dai M, Hao H, Qu W, Xie S, Wang X, Yuan Z: Nitric oxide (NO)-mediated mitochondrial damage plays a critical role in T-2 toxin-induced apoptosis and growth hormone deficiency in rat anterior pituitary GH3 cells. Food Chem Toxicol; 2017 Apr;102:11-23
Hazardous Substances Data Bank. T-2 TOXIN .

  • [Source] The source of this record is MEDLINE®, a database of the U.S. National Library of Medicine.
  • [Title] Nitric oxide (NO)-mediated mitochondrial damage plays a critical role in T-2 toxin-induced apoptosis and growth hormone deficiency in rat anterior pituitary GH3 cells.
  • T-2 toxin, a major compound of trichothecenes, induces cell apoptosis and growth hormone (GH) deficiency and causes considerable growth retardation in animals and human cells.
  • Recent studies have suggested that ROS induced cell apoptosis and animal feed intake reduction, but there are limited reports on the role of RNS in T-2 toxin-mediated mitochondrial damage, cell apoptosis and growth retardation.
  • Herein, T-2 toxin-induced GH3 cell damage and apoptosis were tested by MTT assay, LDH leakage and flow cytometry, respectively.
  • The results clearly revealed that T-2 toxin caused significant increases in NO generation, cell apoptosis, GH deficiency, increased iNOS activity, upregulation of inflammatory factors and caspase pathway, decreases in ΔΨm and morphosis damage.
  • These data suggest that mitochondria are a primary target of T-2 toxin-induced NO, and NO is a key mediator of T-2 toxin-induced cell apoptosis and GH deficiency via the mitochondria-dependent pathway in cells.
  • [MeSH-major] Growth Hormone / deficiency. Mitochondria / drug effects. Nitric Oxide / metabolism. Somatotrophs / drug effects. T-2 Toxin / toxicity
  • [MeSH-minor] Animals. Apoptosis / drug effects. Caspases / metabolism. Membrane Potential, Mitochondrial / drug effects. Nitric Oxide Synthase Type II / metabolism. Oxidative Stress / drug effects. Pituitary Gland, Anterior / cytology. Rats. Signal Transduction / drug effects

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  • [Copyright] Copyright © 2017 Elsevier Ltd. All rights reserved.
  • (PMID = 28130091.001).
  • [ISSN] 1873-6351
  • [Journal-full-title] Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association
  • [ISO-abbreviation] Food Chem. Toxicol.
  • [Language] eng
  • [Publication-type] Journal Article
  • [Publication-country] England
  • [Chemical-registry-number] 31C4KY9ESH / Nitric Oxide; 9002-72-6 / Growth Hormone; EC 1.14.13.39 / Nitric Oxide Synthase Type II; EC 1.14.13.39 / Nos2 protein, rat; EC 3.4.22.- / Caspases; I3FL5NM3MO / T-2 Toxin
  • [Keywords] NOTNLM ; Caspase pathway / Cell apoptosis / Growth hormone deficiency / Mitochondrial damage / NO / T-2 toxin
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