LIVIVO - Search results -

Search results

Result 1 - 10 of total 25

Search options

Article ; Online: Repair Mechanisms in Oxidant-Driven Chronic Inflammatory Disease.

Deeb, Ruba S / Hajjar, David P

2016 Volume 186, Issue 7, Page(s) 1736–1749

Abstract: The interplay that governs chronic diseases through pathways specifically associated with chronic inflammation remains undefined. Many metabolic events have been identified during the injury and repair process. Nonetheless, the cellular events that ... ...

Abstract	The interplay that governs chronic diseases through pathways specifically associated with chronic inflammation remains undefined. Many metabolic events have been identified during the injury and repair process. Nonetheless, the cellular events that control the pathogenesis of inflammation-induced disease have not been fully characterized. We and others reason that chronic inflammatory diseases associated with a cascade of complex network mediators, such as nitric oxide, arachidonic acid metabolites, cytokines, and reactive oxygen species, play a significant role in the governance of alterations in homeostasis, oxidative stress, and thromboatherosclerosis. In this context, we discuss lipid mediators associated with the maintenance of health, including the specialized proresolving mediators that help drive cellular repair. Emphasis is placed on the pathophysiology of chronic metabolic insults involving both the airways and the cardiovascular system during oxidant-driven inflammatory disease. In this review, we highlight new pathways of inquiry that show promise for the identification of those metabolic targets that can improve therapy for chronic inflammation.
MeSH term(s)	Animals ; Chronic Disease ; Humans ; Inflammation/physiopathology ; Oxidants/adverse effects ; Oxidative Stress/physiology
Chemical Substances	Oxidants
Language	English
Publishing date	2016
Publishing country	United States
Document type	Journal Article ; Review ; Research Support, Non-U.S. Gov't
ZDB-ID	2943-9
ISSN	1525-2191 ; 0002-9440
ISSN (online)	1525-2191
ISSN	0002-9440
DOI	10.1016/j.ajpath.2016.03.001
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ud II Zs.76: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Details ▾

Article ; Online: Bridging medical simulation with computer science and engineering: A growing field of study.

Papp, Carol / Deeb, Ruba S / Booth, Christine / El-Sayed, Ahmed / Freilicher, Tina

Nurse education today

2018 Volume 71, Page(s) 1–6

Abstract: Background: Medical simulation has become an essential educational tool in the curricula of healthcare professionals. A literature review revealed a knowledge gap in healthcare simulation education with respect to the technological expertise required to ...

Abstract	Background: Medical simulation has become an essential educational tool in the curricula of healthcare professionals. A literature review revealed a knowledge gap in healthcare simulation education with respect to the technological expertise required to operate highly sophisticated simulation equipment. With this motivation, a case study was designed to determine if implementing on-site technological expertise allows for the facile navigation of high fidelity manikins. Next, a research study was conducted to evaluate engineering students understanding of simulation, and their interest to attend a program in medical simulation. Objectives: To determine if on-site technological expertise lifts barriers associated with manikin use and to assess levels of understanding and interest among engineering students following exposure to the technology used in healthcare simulation. Design: A prospective, descriptive study with pre-post surveys. Settings: The Nursing Skills and Simulation Center at a New England University campus. Participants: Engineering students attending 6 different engineering programs (Computer Science, Computer Engineering, Mechanical Engineering, Biomedical Engineering, Electrical Engineering and Technology Management) and having different educational levels (undergraduate and graduate). Methods: Two assessments were applied to engineering students attending a class on technology used in healthcare simulation. A pre-test measured the understanding and interest of students in the engineering/computer science courses before attending a simulation class. A post-test assessment measured their improvement in understanding and interest to learn more about simulation technologies. Results: Statistical analysis and comparisons of pre-and post-test assessments show a 23% gain in understanding of this field following exposure to the healthcare simulation class. Furthermore, post test results show greater than 67% of those surveyed have an interest in attending a program in healthcare simulation. Conclusions: The results indicate the collaboration of nursing and engineering has lifted known barriers to simulation education, and reveal engineering students have an interest in the field of medical simulation.
MeSH term(s)	Computer Simulation/trends ; Education, Nursing, Baccalaureate/methods ; Education, Nursing, Baccalaureate/trends ; Educational Measurement/methods ; Engineering/education ; Humans ; Manikins ; New England ; Prospective Studies ; Students/statistics & numerical data ; Surveys and Questionnaires
Language	English
Publishing date	2018-09-04
Publishing country	Scotland
Document type	Journal Article
ZDB-ID	1062570-7
ISSN	1532-2793 ; 0260-6917
ISSN (online)	1532-2793
ISSN	0260-6917
DOI	10.1016/j.nedt.2018.08.011
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 3117: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Serum Metabolite Biomarkers Discriminate Healthy Smokers from COPD Smokers.

Chen, Qiuying / Deeb, Ruba S / Ma, Yuliang / Staudt, Michelle R / Crystal, Ronald G / Gross, Steven S

PloS one

2015 Volume 10, Issue 12, Page(s) e0143937

Abstract: COPD (chronic obstructive pulmonary disease) is defined by a fixed expiratory airflow obstruction associated with disordered airways and alveolar destruction. COPD is caused by cigarette smoking and is the third greatest cause of mortality in the US. ... ...

Abstract	COPD (chronic obstructive pulmonary disease) is defined by a fixed expiratory airflow obstruction associated with disordered airways and alveolar destruction. COPD is caused by cigarette smoking and is the third greatest cause of mortality in the US. Forced expiratory volume in 1 second (FEV1) is the only validated clinical marker of COPD, but it correlates poorly with clinical features and is not sensitive enough to predict the early onset of disease. Using LC/MS global untargeted metabolite profiling of serum samples from a well-defined cohort of healthy smokers (n = 37), COPD smokers (n = 41) and non-smokers (n = 37), we sought to discover serum metabolic markers with known and/or unknown molecular identities that are associated with early-onset COPD. A total of 1,181 distinct molecular ions were detected in 95% of sera from all study subjects and 23 were found to be differentially-expressed in COPD-smokers vs. healthy-smokers. These 23 putative biomarkers were differentially-correlated with lung function parameters and used to generate a COPD prediction model possessing 87.8% sensitivity and 86.5% specificity. In an independent validation set, this model correctly predicted COPD in 8/10 individuals. These serum biomarkers included myoinositol, glycerophopshoinositol, fumarate, cysteinesulfonic acid, a modified version of fibrinogen peptide B (mFBP), and three doubly-charged peptides with undefined sequence that significantly and positively correlate with mFBP levels. Together, elevated levels of serum mFBP and additional disease-associated biomarkers point to a role for chronic inflammation, thrombosis, and oxidative stress in remodeling of the COPD airways. Serum metabolite biomarkers offer a promising and accessible window for recognition of early-stage COPD.
MeSH term(s)	Adult ; Biomarkers ; Case-Control Studies ; Chromatography, Liquid ; Cluster Analysis ; Female ; Forced Expiratory Volume ; Healthy Volunteers ; Humans ; Male ; Mass Spectrometry ; Metabolome ; Metabolomics/methods ; Middle Aged ; Pulmonary Disease, Chronic Obstructive/blood ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Reproducibility of Results ; Respiratory Function Tests ; Smoking/blood
Chemical Substances	Biomarkers
Language	English
Publishing date	2015
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0143937
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Full text

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Details ▾
- Full text online
- Order with fees

Article ; Online: Silent Partner in Blood Vessel Homeostasis? Pervasive Role of Nitric Oxide in Vascular Disease.

Deeb, Ruba S / Lamon, Brian D / Hajjar, David P

Current hypertension reviews

2010 Volume 5, Issue 4, Page(s) 273–282

Abstract: The endothelium generates powerful mediators that regulate blood flow, temper inflammation and maintain a homeostatic environment to prevent both the initiation and progression of vascular disease. Nitric oxide (NO) is arguably the single most ... ...

Abstract	The endothelium generates powerful mediators that regulate blood flow, temper inflammation and maintain a homeostatic environment to prevent both the initiation and progression of vascular disease. Nitric oxide (NO) is arguably the single most influential molecule in terms of dictating blood vessel homeostasis. In addition to direct effects associated with altered NO production (e.g. vasoconstriction, excessive inflammation, endothelial dysfunction), NO is a critical modulator of vaso-relevant pathways including cyclooxygenase (COX)-derived prostaglandin production and angiotensin II generation by the renin-angiotensin system. Furthermore, NO may influence the selectivity of COX-2 inhibitors and ultimately contribute to controversies associated with the use of these drugs. Consistent with a central role for NO in vascular disease, disruptions in the production and bioavailability of NO have been linked to hypertension, diabetes, hypercholesterolemia, obesity, aging, and smoking. The ability of the vessel wall to control disease-associated oxidative stress may be the most critical determinant in maintaining homeostatic levels of NO and subsequently the prospect of stroke, myocardial infarction and other CV abnormalities. To this end, investigation of mechanisms that alter the balance of protective mediators, including pathways that are indirectly modified by NO, is critical to the development of effective therapy in the treatment of CV disease.
Language	English
Publishing date	2010-04-06
Publishing country	United Arab Emirates
Document type	Journal Article
ISSN	1875-6506
ISSN (online)	1875-6506
DOI	10.2174/157340209789587726
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Smoking-Associated Disordering of the Airway Basal Stem/Progenitor Cell Metabotype.

Deeb, Ruba S / Walters, Matthew S / Strulovici-Barel, Yael / Chen, Qiuying / Gross, Steven S / Crystal, Ronald G

American journal of respiratory cell and molecular biology

2016 Volume 54, Issue 2, Page(s) 231–240

Abstract: The airway epithelium is a complex pseudostratified multicellular layer lining the tracheobronchial tree, functioning as the primary defense against inhaled environmental contaminants. The major cell types of the airway epithelium include basal, ... ...

Abstract	The airway epithelium is a complex pseudostratified multicellular layer lining the tracheobronchial tree, functioning as the primary defense against inhaled environmental contaminants. The major cell types of the airway epithelium include basal, intermediate columnar, ciliated, and secretory. Basal cells (BCs) are the proliferating stem/progenitor population that differentiate into the other specialized cell types of the airway epithelium during normal turnover and repair. Given that cigarette smoke delivers thousands of xenobiotics and high levels of reactive molecules to the lung epithelial surface, we hypothesized that cigarette smoke broadly perturbs BC metabolism. To test this hypothesis, primary airway BCs were isolated from healthy nonsmokers (n = 11) and healthy smokers (n = 7) and assessed by global metabolic profiling by liquid chromatography-mass spectrometry. The analysis identified 52 significant metabolites in BCs differentially expressed between smokers and nonsmokers (P < 0.05). These changes included metabolites associated with redox pathways, energy production, and inflammatory processes. Notably, BCs from smokers exhibited altered levels of the key enzyme cofactors/substrates nicotinamide adenine dinucleotide, flavin adenine dinucleotide, acetyl coenzyme A, and membrane phospholipid levels. Consistent with the high burden of oxidants in cigarette smoke, glutathione levels were diminished, whereas 3-nitrotyrosine levels were increased, suggesting that protection of airway epithelial cells against oxidative and nitrosative stress is significantly compromised in smoker BCs. It is likely that this altered metabotype is a reflection of, and likely contributes to, the disordered biology of airway BCs consequent to the stress cigarette smoking puts on the airway epithelium.
MeSH term(s)	Adult ; Biomarkers/metabolism ; Case-Control Studies ; Cells, Cultured ; Chromatography, High Pressure Liquid ; Epithelial Cells/drug effects ; Epithelial Cells/metabolism ; Epithelial Cells/pathology ; Female ; Humans ; Male ; Metabolomics/methods ; Middle Aged ; Oxidation-Reduction ; Oxidative Stress/drug effects ; Respiratory Mucosa/drug effects ; Respiratory Mucosa/metabolism ; Respiratory Mucosa/pathology ; Smoking/adverse effects ; Smoking/metabolism ; Smoking/pathology ; Spectrometry, Mass, Electrospray Ionization ; Stem Cells/drug effects ; Stem Cells/metabolism ; Stem Cells/pathology ; Young Adult
Chemical Substances	Biomarkers
Language	English
Publishing date	2016-02
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1025960-0
ISSN	1535-4989 ; 1044-1549
ISSN (online)	1535-4989
ISSN	1044-1549
DOI	10.1165/rcmb.2015-0055OC
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 2851: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Untargeted Metabolite Profiling of Cerebrospinal Fluid Uncovers Biomarkers for Severity of Late Infantile Neuronal Ceroid Lipofuscinosis (CLN2, Batten Disease).

Sindelar, Miriam / Dyke, Jonathan P / Deeb, Ruba S / Sondhi, Dolan / Kaminsky, Stephen M / Kosofsky, Barry E / Ballon, Douglas J / Crystal, Ronald G / Gross, Steven S

Scientific reports

2018 Volume 8, Issue 1, Page(s) 15229

Abstract: Late infantile neuronal ceroid lipofuscinosis (CLN2 disease) is a rare lysosomal storage disorder caused by a monogenetic deficiency of tripeptidyl peptidase-1 (TPP1). Despite knowledge that lipofuscin is the hallmark disease product, the relevant TPP1 ... ...

Abstract	Late infantile neuronal ceroid lipofuscinosis (CLN2 disease) is a rare lysosomal storage disorder caused by a monogenetic deficiency of tripeptidyl peptidase-1 (TPP1). Despite knowledge that lipofuscin is the hallmark disease product, the relevant TPP1 substrate and its role in neuronal physiology/pathology is unknown. We hypothesized that untargeted metabolite profiling of cerebrospinal fluid (CSF) could be used as an effective tool to identify disease-associated metabolic disruptions in CLN2 disease, offering the potential to identify biomarkers that inform on disease severity and progression. Accordingly, a mass spectrometry-based untargeted metabolite profiling approach was employed to differentiate CSF from normal vs. CLN2 deficient individuals. Of 1,433 metabolite features surveyed, 29 linearly correlated with currently employed disease severity scores. With tandem mass spectrometry 8 distinct metabolite identities were structurally confirmed based on retention time and fragmentation pattern matches, vs. standards. These putative CLN2 biomarkers include 7 acetylated species - all attenuated in CLN2 compared to controls. Because acetate is the major bioenergetic fuel for support of mitochondrial respiration, deficient acetylated species in CSF suggests a brain energy defect that may drive neurodegeneration. Targeted analysis of these metabolites in CSF of CLN2 patients offers a powerful new approach for monitoring CLN2 disease progression and response to therapy.
MeSH term(s)	Acetates/metabolism ; Adolescent ; Adult ; Aged ; Aminopeptidases/cerebrospinal fluid ; Aminopeptidases/genetics ; Animals ; Biomarkers/cerebrospinal fluid ; Brain/metabolism ; Brain/pathology ; Child ; Child, Preschool ; Dipeptidyl-Peptidases and Tripeptidyl-Peptidases/cerebrospinal fluid ; Dipeptidyl-Peptidases and Tripeptidyl-Peptidases/genetics ; Disease Models, Animal ; Female ; Humans ; Male ; Metabolome/genetics ; Metabolomics ; Middle Aged ; Mitochondria/metabolism ; Mitochondria/pathology ; Neuronal Ceroid-Lipofuscinoses/cerebrospinal fluid ; Neuronal Ceroid-Lipofuscinoses/genetics ; Neuronal Ceroid-Lipofuscinoses/metabolism ; Neuronal Ceroid-Lipofuscinoses/pathology ; Neurons/metabolism ; Neurons/pathology ; Serine Proteases/cerebrospinal fluid ; Serine Proteases/genetics ; Severity of Illness Index ; Young Adult
Chemical Substances	Acetates ; Biomarkers ; Serine Proteases (EC 3.4.-) ; Aminopeptidases (EC 3.4.11.-) ; Dipeptidyl-Peptidases and Tripeptidyl-Peptidases (EC 3.4.14.-) ; tripeptidyl-peptidase 1 (EC 3.4.14.9)
Language	English
Publishing date	2018-10-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2615211-3
ISSN	2045-2322 ; 2045-2322
ISSN (online)	2045-2322
ISSN	2045-2322
DOI	10.1038/s41598-018-33449-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Untargeted Metabolite Profiling of Cerebrospinal Fluid Uncovers Biomarkers for Severity of Late Infantile Neuronal Ceroid Lipofuscinosis (CLN2, Batten Disease)

Miriam Sindelar / Jonathan P. Dyke / Ruba S. Deeb / Dolan Sondhi / Stephen M. Kaminsky / Barry E. Kosofsky / Douglas J. Ballon / Ronald G. Crystal / Steven S. Gross

Scientific Reports, Vol 8, Iss 1, Pp 1-

2018 Volume 12

Abstract: Abstract Late infantile neuronal ceroid lipofuscinosis (CLN2 disease) is a rare lysosomal storage disorder caused by a monogenetic deficiency of tripeptidyl peptidase-1 (TPP1). Despite knowledge that lipofuscin is the hallmark disease product, the ... ...

Abstract	Abstract Late infantile neuronal ceroid lipofuscinosis (CLN2 disease) is a rare lysosomal storage disorder caused by a monogenetic deficiency of tripeptidyl peptidase-1 (TPP1). Despite knowledge that lipofuscin is the hallmark disease product, the relevant TPP1 substrate and its role in neuronal physiology/pathology is unknown. We hypothesized that untargeted metabolite profiling of cerebrospinal fluid (CSF) could be used as an effective tool to identify disease-associated metabolic disruptions in CLN2 disease, offering the potential to identify biomarkers that inform on disease severity and progression. Accordingly, a mass spectrometry-based untargeted metabolite profiling approach was employed to differentiate CSF from normal vs. CLN2 deficient individuals. Of 1,433 metabolite features surveyed, 29 linearly correlated with currently employed disease severity scores. With tandem mass spectrometry 8 distinct metabolite identities were structurally confirmed based on retention time and fragmentation pattern matches, vs. standards. These putative CLN2 biomarkers include 7 acetylated species – all attenuated in CLN2 compared to controls. Because acetate is the major bioenergetic fuel for support of mitochondrial respiration, deficient acetylated species in CSF suggests a brain energy defect that may drive neurodegeneration. Targeted analysis of these metabolites in CSF of CLN2 patients offers a powerful new approach for monitoring CLN2 disease progression and response to therapy.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2018-10-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: Complex "cross talk" involving nitric oxide metabolites: who's listening?

Hajjar, David P / Deeb, Ruba S / Upmacis, Rita K

Current atherosclerosis reports

2006 Volume 8, Issue 5, Page(s) 347–348

MeSH term(s)	Animals ; Atherosclerosis/metabolism ; Eicosanoids/biosynthesis ; Humans ; Nitric Oxide/metabolism ; Nitric Oxide Synthase Type II/metabolism ; Oxidative Stress/physiology ; Signal Transduction
Chemical Substances	Eicosanoids ; Nitric Oxide (31C4KY9ESH) ; Nitric Oxide Synthase Type II (EC 1.14.13.39)
Language	English
Publishing date	2006-07-10
Publishing country	United States
Document type	Journal Article
ZDB-ID	2057369-8
ISSN	1523-3804
ISSN	1523-3804
DOI	10.1007/s11883-006-0029-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Zs.A 5534: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (2.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾

Article ; Online: Serum Metabolite Biomarkers Discriminate Healthy Smokers from COPD Smokers.

Qiuying Chen / Ruba S Deeb / Yuliang Ma / Michelle R Staudt / Ronald G Crystal / Steven S Gross

PLoS ONE, Vol 10, Iss 12, p e

2015 Volume 0143937

Abstract	COPD (chronic obstructive pulmonary disease) is defined by a fixed expiratory airflow obstruction associated with disordered airways and alveolar destruction. COPD is caused by cigarette smoking and is the third greatest cause of mortality in the US. Forced expiratory volume in 1 second (FEV1) is the only validated clinical marker of COPD, but it correlates poorly with clinical features and is not sensitive enough to predict the early onset of disease. Using LC/MS global untargeted metabolite profiling of serum samples from a well-defined cohort of healthy smokers (n = 37), COPD smokers (n = 41) and non-smokers (n = 37), we sought to discover serum metabolic markers with known and/or unknown molecular identities that are associated with early-onset COPD. A total of 1,181 distinct molecular ions were detected in 95% of sera from all study subjects and 23 were found to be differentially-expressed in COPD-smokers vs. healthy-smokers. These 23 putative biomarkers were differentially-correlated with lung function parameters and used to generate a COPD prediction model possessing 87.8% sensitivity and 86.5% specificity. In an independent validation set, this model correctly predicted COPD in 8/10 individuals. These serum biomarkers included myoinositol, glycerophopshoinositol, fumarate, cysteinesulfonic acid, a modified version of fibrinogen peptide B (mFBP), and three doubly-charged peptides with undefined sequence that significantly and positively correlate with mFBP levels. Together, elevated levels of serum mFBP and additional disease-associated biomarkers point to a role for chronic inflammation, thrombosis, and oxidative stress in remodeling of the COPD airways. Serum metabolite biomarkers offer a promising and accessible window for recognition of early-stage COPD.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2015-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article: Reprint of "oxidative alterations of cyclooxygenase during atherogenesis" [Prostag. Oth. Lipid. M. 80 (2006) 1-14].

Upmacis, Rita K / Deeb, Ruba S / Hajjar, David P

Prostaglandins & other lipid mediators

2007 Volume 82, Issue 1-4, Page(s) I–XIV

Abstract: ... activation. Other post-translational modifications of COX by NOx species include S-nitrosation of cysteine ...

Abstract	Nitric oxide (NO) and eicosanoids are critical mediators of physiological and pathophysiological processes. They include inflammation and atherosclerosis. NO production and eicosanoid synthesis become disrupted during atherosclerosis and thus, it is important to understand the mechanisms that may contribute to this outcome. We, and others, have shown that nitrogen oxide (NOx) species modulate cyclooxygenase (COX; also known as prostaglandin H2 synthase) activity and alter eicosanoid production. We have determined that peroxynitrite (ONOO-) has multiple effects on COX activity. ONOO- can provide the peroxide tone necessary for COX activation, such that simultaneous exposure of COX to its arachidonic acid substrate and ONOO- results in increased eicosanoid production. Alternatively, in the absence of arachidonic acid, ONOO- can modify COX through nitration of an essential tyrosine residue (Tyr385) such that it is incapable of catalysis. In this regard, we have shown that COX nitration occurs in human atherosclerotic tissue and in aortic lesions from ApoE-/- mice kept on a high fat diet. Additionally, we have demonstrated that Tyr nitration in ApoE-/- mice is dependent on the inducible form of NO synthase (iNOS). Under conditions where ONOO- persists and arachidonic acid is not immediately available, the cell may try to correct the situation by responding to ONOO- and releasing arachidonic acid via a signaling pathway to favor COX activation. Other post-translational modifications of COX by NOx species include S-nitrosation of cysteine (Cys) residues (which may have an activating effect) and Cys oxidation. The central focus of this review will include a discussion of how NOx species alter COX activity at the molecular level and how these modifications may contribute to altered eicosanoid output during atherosclerosis and lesion development.
Language	English
Publishing date	2007-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	1426962-4
ISSN	2212-196X ; 1098-8823 ; 0090-6980
ISSN (online)	2212-196X
ISSN	1098-8823 ; 0090-6980
DOI	10.1016/S1098-8823(06)00182-1
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 815: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
Jg. 1995 - 2021: Lesesall (1.OG)
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

To top

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito