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Article: Keap1 modification and nuclear accumulation in response to S-nitrosocysteine.

Buckley, Barbara J / Li, Sheng / Whorton, A Richard

2007 Volume 44, Issue 4, Page(s) 692–698

Abstract: Keap1 is a key regulator of the Nrf2 transcription factor, which transactivates the antioxidant response element (ARE) and upregulates numerous proteins involved in antioxidant defense. Under basal conditions, Keap1 targets Nrf2 for ubiquitination and ... ...

Abstract	Keap1 is a key regulator of the Nrf2 transcription factor, which transactivates the antioxidant response element (ARE) and upregulates numerous proteins involved in antioxidant defense. Under basal conditions, Keap1 targets Nrf2 for ubiquitination and proteolytic degradation and as such is responsible for the rapid turnover of Nrf2. In response to oxidants and electrophiles, Nrf2 is stabilized and accumulates in the nucleus. The mechanism for this effect has been proposed to involve thiol-dependent modulation of Keap1 leading to loss of its ability to negatively regulate Nrf2. We have previously shown that nitric oxide and S-nitrosothiols cause nuclear accumulation of Nrf2 and upregulation of the ARE-regulated gene HO-1. Here we show that nitric oxide and S-nitrosocysteine (CSNO) cause time- and dose-dependent Keap1 thiol modification. These studies were carried out in HEK293 cells and in HEK293 cells overexpressing hemagglutinin-tagged Keap1. Furthermore we demonstrate that in response to CSNO Keap1 accumulates in the nucleus with a time course similar to that of Nrf2.
MeSH term(s)	Active Transport, Cell Nucleus ; Cell Nucleus/metabolism ; Cells, Cultured ; Cysteine/analogs & derivatives ; Cysteine/pharmacology ; Dithiothreitol/pharmacology ; Dose-Response Relationship, Drug ; Humans ; Intracellular Signaling Peptides and Proteins/metabolism ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2/metabolism ; S-Nitrosothiols/pharmacology ; Spermine/analogs & derivatives ; Spermine/pharmacology
Chemical Substances	Intracellular Signaling Peptides and Proteins ; KEAP1 protein, human ; Kelch-Like ECH-Associated Protein 1 ; NF-E2-Related Factor 2 ; NFE2L2 protein, human ; S-Nitrosothiols ; spermine nitric oxide complex (136587-13-8) ; Spermine (2FZ7Y3VOQX) ; S-nitrosocysteine (926P2322P4) ; Cysteine (K848JZ4886) ; Dithiothreitol (T8ID5YZU6Y)
Language	English
Publishing date	2007-11-13
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	807032-5
ISSN	1873-4596 ; 0891-5849
ISSN (online)	1873-4596
ISSN	0891-5849
DOI	10.1016/j.freeradbiomed.2007.10.055
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Zs.A 2109: Show issues

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Book: Survey of library and information plans

Buckley, Barbara J

(British Library R&D report ; 6128)

1993

Author's details	Barbara J. Buckley
Series title	British Library R&D report ; 6128
Language	English
Size	3 Mikrofiches
Document type	Book
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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Article: Nitric oxide stimulates Nrf2 nuclear translocation in vascular endothelium.

Buckley, Barbara J / Marshall, Zermeena M / Whorton, A R

Biochemical and biophysical research communications

2003 Volume 307, Issue 4, Page(s) 973–979

Abstract: Vascular endothelial cells respond to nitric oxide by activating MAPK pathways and upregulating stress-activated proteins such as gamma-glutamylcysteine synthetase (gamma-GCS) and heme oxygenase-1 (HO-1). Since consensus sequences for the antioxidant ... ...

Abstract	Vascular endothelial cells respond to nitric oxide by activating MAPK pathways and upregulating stress-activated proteins such as gamma-glutamylcysteine synthetase (gamma-GCS) and heme oxygenase-1 (HO-1). Since consensus sequences for the antioxidant response element (ARE) are found in the promoters of the gamma-GCS and HO-1 genes, we examined nuclear translocation of Nrf2, a CNC-bZIP protein which binds to and activates the ARE. We found a dramatic increase in Nrf2 nuclear translocation 1-8h following the nitric oxide donor spermine NONOate. Translocation was inhibited by pretreatment of cells with N-acetylcysteine suggesting involvement of an oxidative mechanism in this response. Translocation was also blocked by PD 98059 and SB 203580, inhibitors of ERK and p38 pathways, respectively. In addition to effects on Nrf2 subcellular localization, spermine NONOate increased Nrf2 protein levels by a mechanism which was inhibited by PD 98059. Pretreatment with N-acetylcysteine, PD 98059, and SB 203580 decreased HO-1 upregulation in spermine NONOate-treated cells. These results suggest that ERK and p38 pathways may regulate nitric oxide-mediated adaptive responses in vascular endothelium via translocation of Nrf2 and activation of the ARE.
MeSH term(s)	Active Transport, Cell Nucleus/drug effects ; Animals ; Cattle ; Cell Nucleus/metabolism ; Cells, Cultured ; DNA-Binding Proteins/metabolism ; Endothelium, Vascular/drug effects ; Endothelium, Vascular/enzymology ; Endothelium, Vascular/metabolism ; Enzyme Inhibitors/pharmacology ; Heme Oxygenase (Decyclizing)/biosynthesis ; Heme Oxygenase-1 ; MAP Kinase Signaling System/drug effects ; Mitogen-Activated Protein Kinases/antagonists & inhibitors ; Mitogen-Activated Protein Kinases/metabolism ; NF-E2-Related Factor 2 ; Nitric Oxide Donors/antagonists & inhibitors ; Nitric Oxide Donors/pharmacology ; Nitrogen Oxides ; Spermine/analogs & derivatives ; Spermine/antagonists & inhibitors ; Spermine/pharmacology ; Trans-Activators/metabolism ; Up-Regulation
Chemical Substances	DNA-Binding Proteins ; Enzyme Inhibitors ; NF-E2-Related Factor 2 ; Nitric Oxide Donors ; Nitrogen Oxides ; Trans-Activators ; spermine nitric oxide complex (136587-13-8) ; Spermine (2FZ7Y3VOQX) ; Heme Oxygenase (Decyclizing) (EC 1.14.14.18) ; Heme Oxygenase-1 (EC 1.14.14.18) ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2003-06-26
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	205723-2
ISSN	0006-291X ; 0006-291X
ISSN (online)	0006-291X
ISSN	0006-291X
DOI	10.1016/s0006-291x(03)01308-1
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Article: Multicenter, open-label, prospective evaluation of the conversion from previous opioid analgesics to extended-release hydromorphone hydrochloride administered every 24 hours to patients with persistent moderate to severe pain.

Weinstein, Sharon M / Shi, Minggao / Buckley, Barbara J / Kwarcinski, Monica A

Clinical therapeutics

2006 Volume 28, Issue 1, Page(s) 86–98

Abstract: Background: Hydromorphone hydrochloride is a mu-opioid agonist with dose-dependent analgesic properties. Extended-release hydromorphone hydrochloride (ER hydromorphone HCl) capsules have been developed for administration every 24 hours.: Objectives: ... ...

Abstract	Background: Hydromorphone hydrochloride is a mu-opioid agonist with dose-dependent analgesic properties. Extended-release hydromorphone hydrochloride (ER hydromorphone HCl) capsules have been developed for administration every 24 hours. Objectives: This prospective evaluation focused on the first (ie, conversion) phase of 2 identically designed, randomized, controlled studies that compared the safety and efficacy of once-daily ER hydromorphone HCl capsules with immediate-release hydromorphone hydrochloride (IR hydromorphone HCl) tablets administered 4 times daily in the treatment of persistent moderate to severe cancer- and noncancer-related pain. Methods: Patients being treated with opioid analgesics for persistent moderate to severe pain were converted to ER hydromorphone HCl using an 8:1 conversion ratio. The dose was titrated to attain an average pain intensity (API) score < or = 4 on a 0- to 10-point numeric rating scale. Supplemental oral IR hydromorphone HCl tablets were used as rescue medication at a dose of one eighth to one sixth of the daily ER hydromorphone HCl dose. Results: A total of 343 patients (272 [79%] with cancer pain; mean age, 57.8 years) were enrolled and converted to ER hydromorphone HCl from their previous opioids. About half (51%) were women. At baseline, the mean (SD) API score was 5.3 (2.1). Mean (SD) API scores were 4.7 (2.0) after the first 48 hours and 3.4 (2.1) by the end of titration. After 4 to 21 days of titration, 239 (70%) patients reached stabilization defined as a > or = 48-hour period with an API score of < or =4, unchanged ER hydromorphone HCl dose, and < or = 2 rescue doses per day. The stabilized patients had mean (SD) API scores of 2.7 (1.1) at the end of titration. At stabilization, 102 (43%) of 239 patients remained at their initial conversion dose, 129 (54%) had a dose increase, and 8 (3%) had a dose decrease. Frequent (> or =10% of patients) adverse events that occurred within the first 48 hours after conversion and during the entire titration phase were nausea, somnolence, headache, constipation, vomiting, and dizziness. Conclusion: In this prospective evaluation of the conversion and titration phase of 2 randomized, controlled studies, a conversion ratio of 8:1 mg of oral morphine to oral ER hydromorphone HCl was found to be clinically useful in patients with persistent moderate to severe cancer-related or noncancer-related pain.
MeSH term(s)	Administration, Oral ; Adult ; Aged ; Aged, 80 and over ; Analgesics, Opioid/administration & dosage ; Analgesics, Opioid/therapeutic use ; Clinical Trials as Topic ; Delayed-Action Preparations ; Double-Blind Method ; Drug Administration Schedule ; Female ; Follow-Up Studies ; Humans ; Hydromorphone/administration & dosage ; Hydromorphone/therapeutic use ; Male ; Middle Aged ; Neoplasms/complications ; Pain/diagnosis ; Pain/drug therapy ; Pain/etiology ; Pain Measurement ; Prospective Studies ; Severity of Illness Index ; Treatment Outcome
Chemical Substances	Analgesics, Opioid ; Delayed-Action Preparations ; Hydromorphone (Q812464R06)
Language	English
Publishing date	2006-01
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	603113-4
ISSN	1879-114X ; 0149-2918
ISSN (online)	1879-114X
ISSN	0149-2918
DOI	10.1016/j.clinthera.2006.01.010
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Zs.A 1435: 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)
Zs.MO 404: Show issues

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Article ; Online: A cross-disciplinary evaluation of evidence for multipollutant effects on cardiovascular disease.

Luben, Thomas J / Buckley, Barbara J / Patel, Molini M / Stevens, Tina / Coffman, Evan / Rappazzo, Kristen M / Owens, Elizabeth O / Hines, Erin P / Moore, Danielle / Painter, Kyle / Jones, Ryan / Datko-Williams, Laura / Wilkie, Adrien A / Madden, Meagan / Richmond-Bryant, Jennifer

Environmental research

2017 Volume 161, Page(s) 144–152

Abstract: Background: The current single-pollutant approach to regulating ambient air pollutants is effective at protecting public health, but efficiencies may be gained by addressing issues in a multipollutant context since multiple pollutants often have common ... ...

Abstract	Background: The current single-pollutant approach to regulating ambient air pollutants is effective at protecting public health, but efficiencies may be gained by addressing issues in a multipollutant context since multiple pollutants often have common sources and individuals are exposed to more than one pollutant at a time. Objective: We performed a cross-disciplinary review of the effects of multipollutant exposures on cardiovascular effects. Methods: A broad literature search for references including at least two criteria air pollutants (particulate matter [PM], ozone [O Discussion: Epidemiologic and experimental studies provide some evidence for O Conclusions: Overall, the evidence for multipollutant effects was often heterogeneous, and the limited number of studies inhibited making a conclusion about the nature of the relationship between pollutant combinations and cardiovascular disease.
MeSH term(s)	Air Pollutants/adverse effects ; Air Pollution ; Animals ; Cardiovascular Diseases/etiology ; Environmental Exposure ; Humans ; Particulate Matter
Chemical Substances	Air Pollutants ; Particulate Matter
Language	English
Publishing date	2017-11-13
Publishing country	Netherlands
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	205699-9
ISSN	1096-0953 ; 0013-9351
ISSN (online)	1096-0953
ISSN	0013-9351
DOI	10.1016/j.envres.2017.11.008
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Zs.A 726: Show issues

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Article: A cross-disciplinary evaluation of evidence for multipollutant effects on cardiovascular disease

Environmental research. 2018 Feb., v. 161

2018

Abstract: The current single-pollutant approach to regulating ambient air pollutants is effective at protecting public health, but efficiencies may be gained by addressing issues in a multipollutant context since multiple pollutants often have common sources and ... ...

Abstract	The current single-pollutant approach to regulating ambient air pollutants is effective at protecting public health, but efficiencies may be gained by addressing issues in a multipollutant context since multiple pollutants often have common sources and individuals are exposed to more than one pollutant at a time.We performed a cross-disciplinary review of the effects of multipollutant exposures on cardiovascular effects.A broad literature search for references including at least two criteria air pollutants (particulate matter [PM], ozone [O3], oxides of nitrogen, sulfur oxides, carbon monoxide) was conducted. References were culled based on scientific discipline then searched for terms related to cardiovascular disease. Most multipollutant epidemiologic and experimental (i.e., controlled human exposure, animal toxicology) studies examined PM and O3 together.Epidemiologic and experimental studies provide some evidence for O3 concentration modifying the effect of PM, although PM did not modify O3 risk estimates. Experimental studies of combined exposure to PM and O3 provided evidence for additivity, synergism, and/or antagonism depending on the specific health endpoint. Evidence for other pollutant pairs was more limited.Overall, the evidence for multipollutant effects was often heterogeneous, and the limited number of studies inhibited making a conclusion about the nature of the relationship between pollutant combinations and cardiovascular disease.
Keywords	air pollutants ; air pollution ; antagonism ; carbon monoxide ; cardiovascular diseases ; humans ; nitrogen oxides ; ozone ; particulates ; public health ; risk estimate ; sulfur oxides ; synergism ; toxicology
Language	English
Dates of publication	2018-02
Size	p. 144-152.
Publishing place	Elsevier Inc.
Document type	Article
ZDB-ID	205699-9
ISSN	1096-0953 ; 0013-9351
ISSN (online)	1096-0953
ISSN	0013-9351
DOI	10.1016/j.envres.2017.11.008
Database	NAL-Catalogue (AGRICOLA)

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Article ; Online: Particulate matter-induced health effects: who is susceptible?

Sacks, Jason D / Stanek, Lindsay Wichers / Luben, Thomas J / Johns, Douglas O / Buckley, Barbara J / Brown, James S / Ross, Mary

Environmental health perspectives

2010 Volume 119, Issue 4, Page(s) 446–454

Abstract: Background: Epidemiological, controlled human exposure, and toxicological studies have demonstrated a variety of health effects in response to particulate matter (PM) exposure with some of these studies indicating that populations with certain ... ...

Abstract	Background: Epidemiological, controlled human exposure, and toxicological studies have demonstrated a variety of health effects in response to particulate matter (PM) exposure with some of these studies indicating that populations with certain characteristics may be disproportionately affected. Objective: To identify populations potentially at greatest risk for PM-related health effects, we evaluated epidemiological studies that examined various characteristics that may influence susceptibility, while using results from controlled human exposure and toxicological studies as supporting evidence. Additionally, we formulated a definition of susceptibility, building from the varied and inconsistent definitions of susceptibility and vulnerability used throughout the literature. Data synthesis: We evaluated recent epidemiological studies to identify characteristics of populations potentially susceptible to PM-related health effects. Additionally, we evaluated controlled human exposure and toxicological studies to provide supporting evidence. We conducted a comprehensive review of epidemiological studies that presented stratified results (e.g., < 65 vs. ≥ 65 years of age), controlled human exposure studies that examined individuals with underlying disease, and toxicological studies that used animal models of disease. We evaluated results for consistency across studies, coherence across disciplines, and biological plausibility to assess the potential for increased susceptibility to PM-related health effects in a specific population or life stage. Conclusions: We identified a diverse group of characteristics that can lead to increased risk of PM-related health effects, including life stage (i.e., children and older adults), preexisting cardiovascular or respiratory diseases, genetic polymorphisms, and low-socioeconomic status. In addition, we crafted a comprehensive definition of susceptibility that can be used to encompass all populations potentially at increased risk of adverse health effects as a consequence of exposure to an air pollutant.
MeSH term(s)	Aged ; Air Pollutants/analysis ; Air Pollutants/toxicity ; Air Pollution/statistics & numerical data ; Cardiovascular Diseases/epidemiology ; Demography ; Disease Susceptibility/epidemiology ; Humans ; Middle Aged ; Particulate Matter/analysis ; Particulate Matter/toxicity ; Respiratory Tract Diseases/epidemiology ; Risk Assessment ; Socioeconomic Factors
Chemical Substances	Air Pollutants ; Particulate Matter
Language	English
Publishing date	2010-10-20
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S. ; Review
ZDB-ID	195189-0
ISSN	1552-9924 ; 0091-6765 ; 1078-0475
ISSN (online)	1552-9924
ISSN	0091-6765 ; 1078-0475
DOI	10.1289/ehp.1002255
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Zs.B 1360: 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)
Zs.MO 379: Show issues

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Article: Comparative efficacy of oral extended-release hydromorphone and immediate-release hydromorphone in patients with persistent moderate to severe pain: two randomized controlled trials.

Grosset, Alan B / Roberts, Michael S / Woodson, Mark E / Shi, Minggao / Swanton, Ruth E / Reder, Robert F / Buckley, Barbara J

Journal of pain and symptom management

2005 Volume 29, Issue 6, Page(s) 584–594

Abstract: Two multicenter, randomized, double-blind, crossover studies with identical designs evaluated the efficacy of oral extended-release hydromorphone (HHER) administered q24h compared with immediate-release hydromorphone (HHIR) dosed four times daily in ... ...

Abstract	Two multicenter, randomized, double-blind, crossover studies with identical designs evaluated the efficacy of oral extended-release hydromorphone (HHER) administered q24h compared with immediate-release hydromorphone (HHIR) dosed four times daily in patients with persistent moderate to severe pain. Patients titrated to a stable HHER dose were randomized to individualized doses of HHER or HHIR for 3 to 7 days before crossover to the second treatment. Primary efficacy end point was the mean of average pain intensity (API) scores, rated on a 0- to 10-point numeric scale, over the last 2 days before the pharmacokinetics/pharmacodynamics day of each double-blind period. Difference between treatments (HHER - HHIR) in study 1 was 0.17 with a 90% confidence interval (CI) (-0.01, 0.34); in study 2, difference was 0.07 with a 90% CI (-0.12, 0.26). There were no significant differences between treatments in API scores or amount of rescue medication used at any time interval within the 24-hour dosing period. No reduction in pain control occurred in patients administered HHER at the end of the 24-hour dosing period. Most treatment-emergent adverse events were opioid-related. In these studies, HHER administered q24h and HHIR dosed four times daily provided comparable analgesia at an equivalent total daily dose.
MeSH term(s)	Administration, Oral ; Adult ; Aged ; Aged, 80 and over ; Analgesics, Opioid/administration & dosage ; Analgesics, Opioid/adverse effects ; Delayed-Action Preparations ; Female ; Humans ; Hydromorphone/administration & dosage ; Hydromorphone/adverse effects ; Male ; Middle Aged ; Neoplasms/complications ; Pain/drug therapy ; Pain/etiology ; Terminal Care/methods
Chemical Substances	Analgesics, Opioid ; Delayed-Action Preparations ; Hydromorphone (Q812464R06)
Language	English
Publishing date	2005-06
Publishing country	United States
Document type	Clinical Trial ; Comparative Study ; Journal Article ; Multicenter Study ; Randomized Controlled Trial ; Research Support, Non-U.S. Gov't
ZDB-ID	639142-4
ISSN	0885-3924
ISSN	0885-3924
DOI	10.1016/j.jpainsymman.2004.10.008
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