LIVIVO - Search results -

Search results

Result 1 - 10 of total 10

Search options

Article ; Online: Radiofrequency septal reduction in symptomatic hypertrophic obstructive cardiomyopathy.

Crossen, Karl / Jones, Marsha / Erikson, Christopher

2016 Volume 13, Issue 9, Page(s) 1885–1890

Abstract: Background: Alcohol septal ablation remains the only approved nonsurgical therapeutic alternative for patients with drug-resistant hypertrophic obstructive cardiomyopathy (HOCM). Radiofrequency (RF) ablation offers another option for treating HOCM.: ... ...

Abstract	Background: Alcohol septal ablation remains the only approved nonsurgical therapeutic alternative for patients with drug-resistant hypertrophic obstructive cardiomyopathy (HOCM). Radiofrequency (RF) ablation offers another option for treating HOCM. Objective: The purpose of this study was to determine whether irrigated RF ablation can reduce symptomatic outflow tract obstruction in adults with HOCM. Methods: Patients with symptomatic HOCM and an outflow gradient of >50 mm Hg despite medication were offered RF ablation. In 11 patients, the hypertrophied interventricular septum was localized on a 3-dimensional mapping system and ablated via a transmitral or retrograde aortic approach. Results: Ten of 11(91%) patients had a significant and persistent reduction in resting and provocable left ventricular outflow tract gradients. Mean resting gradients at 12 months postprocedure were reduced by 85% (66.7 mm Hg at baseline to 10.0 mm Hg at 12 months); mean provocable gradients were reduced by 85% from baseline (136.2 mm Hg at baseline to 20.0 mm Hg at 12 months). Functional New York Heart Association heart classification improved from class 3.0 ± 0.0 in all patients to class mean of 1.8 ± 0.8. Conclusion: RF septal ablation for the treatment of HOCM is a safe therapeutic option that allows for significant reduction in left ventricular outflow tract gradients, improvement in symptoms, and increase in efficacy rates comparable to reported rates for alcohol septal ablation.
Language	English
Publishing date	2016-09
Publishing country	United States
Document type	Journal Article
ZDB-ID	2229357-7
ISSN	1556-3871 ; 1547-5271
ISSN (online)	1556-3871
ISSN	1547-5271
DOI	10.1016/j.hrthm.2016.04.018
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6278: 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 ▾
- See ZB MED holdings
- Order with fees

Book: Wage differentials in Italy

Erikson, Christopher L / Ichino, Andrea

market forces, institutions, and inflation

(NBER working paper series ; working paper no. 4922)

1994

Institution	National Bureau of Economic Research
Author's details	Christopher L. Erikson, Andrea Ichino
Series title	NBER working paper series ; working paper no. 4922
Keywords	Wages ; Income distribution ; Wage differentials
Language	English
Size	44 p. :, ill. ;, 22 cm.
Publisher	National Bureau of Economic Research
Publishing place	Cambridge, MA
Document type	Book
Note	"November 1994."
Database	NAL-Catalogue (AGRICOLA)

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 ▾

Book: Wage differentials in Italy

Erikson, Christopher L / Ichino, Andrea

market forces, institutions, and inflation

(NBER working paper series ; 4922)

1994

Author's details	Christopher L. Erikson; Andrea Ichino
Series title	NBER working paper series ; 4922
Language	English
Size	44 S, graph. Darst
Publisher	National Bureau of Economic Research
Publishing place	Cambridge, Mass
Document type	Book
Note	Literaturverz. S. 42 - 44
Database	Library catalogue of the German National Library of Science and Technology (TIB), Hannover

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 ▾

Book: Wage differentials in Italy

Erikson, Christopher L / Ichino, Andrea

market forces, institutions, and inflation

(NBER working paper series ; 4922)

1994

Author's details	Christopher L. Erikson; Andrea Ichino
Series title	NBER working paper series ; 4922
Language	English
Size	44 S, graph. Darst
Publisher	National Bureau of Economic Research
Publishing place	Cambridge, Mass
Document type	Book
Note	Literaturverz. S. 42 - 44
Database	ECONomics Information System

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 ▾

Article: Involvement of A1 adenosine receptors and neural pathways in adenosine-induced bronchoconstriction in mice.

Hua, Xiaoyang / Erikson, Christopher J / Chason, Kelly D / Rosebrock, Craig N / Deshpande, Deepak A / Penn, Raymond B / Tilley, Stephen L

American journal of physiology. Lung cellular and molecular physiology

2007 Volume 293, Issue 1, Page(s) L25–32

Abstract: High levels of adenosine can be measured from the lungs of asthmatics, and it is well recognized that aerosolized 5'AMP, the precursor of adenosine, elicits robust bronchoconstriction in patients with this disease. Characterization of mice with elevated ... ...

Abstract	High levels of adenosine can be measured from the lungs of asthmatics, and it is well recognized that aerosolized 5'AMP, the precursor of adenosine, elicits robust bronchoconstriction in patients with this disease. Characterization of mice with elevated adenosine levels secondary to the loss of adenosine deaminase (ADA) expression, the primary metabolic enzyme for adenosine, further support a role for this ubiquitous mediator in the pathogenesis of asthma. To begin to identify pathways by which adenosine can alter airway tone, we examined adenosine-induced bronchoconstriction in four mouse lines, each lacking one of the receptors for this nucleoside. We show, using direct measures of airway mechanics, that adenosine can increase airway resistance and that this increase in resistance is mediated by binding the A(1) receptor. Further examination of this response using pharmacologically, surgically, and genetically manipulated mice supports a model in which adenosine-induced bronchoconstriction occurs indirectly through the activation of sensory neurons.
MeSH term(s)	Adenosine/analogs & derivatives ; Adenosine/pharmacology ; Adenosine-5'-(N-ethylcarboxamide)/pharmacology ; Anesthesia ; Animals ; Bronchoconstriction/drug effects ; In Vitro Techniques ; Mice ; Mice, Inbred C57BL ; Muscle Contraction/drug effects ; Muscle, Smooth/cytology ; Muscle, Smooth/drug effects ; Neural Pathways/metabolism ; Receptor, Adenosine A1/metabolism ; Respiratory System/cytology ; Respiratory System/drug effects ; Vagotomy
Chemical Substances	Receptor, Adenosine A1 ; Adenosine-5'-(N-ethylcarboxamide) (35920-39-9) ; Adenosine (K72T3FS567)
Language	English
Publishing date	2007-04-27
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00058.2007
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: 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.A 2749: 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: Identification of A3 receptor- and mast cell-dependent and -independent components of adenosine-mediated airway responsiveness in mice.

Tilley, Stephen L / Tsai, Mindy / Williams, Cara M / Wang, Z-S / Erikson, Christopher J / Galli, Stephen J / Koller, Beverly H

Journal of immunology (Baltimore, Md. : 1950)

2003 Volume 171, Issue 1, Page(s) 331–337

Abstract: Adenosine-induced bronchoconstriction is a well-recognized feature of atopic asthma. Adenosine acts through four different G protein-coupled receptors to produce a myriad of physiological effects. To examine the contribution of the A(3) adenosine ... ...

Abstract	Adenosine-induced bronchoconstriction is a well-recognized feature of atopic asthma. Adenosine acts through four different G protein-coupled receptors to produce a myriad of physiological effects. To examine the contribution of the A(3) adenosine receptor to adenosine-induced bronchoconstriction and to assess the contribution of mast cells to this process, we quantified airway responsiveness to aerosolized adenosine in wild-type, A(3) receptor-deficient, and mast cell-deficient mice. Compared with the robust airway responses elicited by adenosine in wild-type mice, both A(3)-deficient and mast cell-deficient mice exhibited a significantly attenuated response compared with their respective wild-type controls. Histological examination of the airways 4 h after adenosine exposure revealed extensive degranulation of airway mast cells as well as infiltration of neutrophils in wild-type mice, whereas these findings were much diminished in A(3)-deficient mice and were not different from those in PBS-treated controls. These data indicate that the airway responses to aerosolized adenosine in mice occur largely through A(3) receptor activation and that mast cells contribute significantly to these responses, but that activation of additional adenosine receptors on a cell type(s) other than mast cells also contributes to adenosine-induced airway responsiveness in mice. Finally, our findings indicate that adenosine exposure can result in A(3)-dependent airway inflammation, as reflected in neutrophil recruitment, as well as alterations in airway function.
MeSH term(s)	Adenosine/administration & dosage ; Adenosine/physiology ; Administration, Inhalation ; Aerosols ; Animals ; Bronchial Hyperreactivity/etiology ; Bronchial Hyperreactivity/genetics ; Bronchial Hyperreactivity/metabolism ; Bronchial Hyperreactivity/pathology ; Cell Degranulation/genetics ; Down-Regulation/genetics ; Inflammation/genetics ; Inflammation/metabolism ; Inflammation/pathology ; Lung/metabolism ; Lung/pathology ; Lung/physiology ; Mast Cells/metabolism ; Mast Cells/pathology ; Mast Cells/physiology ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Mutant Strains ; Neutrophil Infiltration/genetics ; Receptor, Adenosine A3 ; Receptors, Purinergic P1/deficiency ; Receptors, Purinergic P1/genetics ; Receptors, Purinergic P1/physiology ; Up-Regulation/genetics
Chemical Substances	Aerosols ; Receptor, Adenosine A3 ; Receptors, Purinergic P1 ; Adenosine (K72T3FS567)
Language	English
Publishing date	2003-06-09
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.171.1.331
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.37: 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.MG 28: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Genetic variation in body weight gain and composition in the intercross of Large (LG/J) and Small (SM/J) inbred strains of mice

Kramer Melissa G. / Vaughn Ty T. / Pletscher L. Susan / King-Ellison Kelly / Adams Emily / Erikson Christopher / Cheverud James M.

Genetics and Molecular Biology, Vol 21, Iss 2, Pp 211-

1998 Volume 218

Abstract: Strain intercross experiments provide a powerful means for mapping genes affecting complex quantitative traits. We report on the genetic variability of the intercross of the Large (LG/J) and Small (SM/J) inbred mouse strains as a guide to gene mapping ... ...

Abstract	Strain intercross experiments provide a powerful means for mapping genes affecting complex quantitative traits. We report on the genetic variability of the intercross of the Large (LG/J) and Small (SM/J) inbred mouse strains as a guide to gene mapping studies. Ten SM/J males were crossed to 10 LG/J females, after which animals were randomly mated to produce F1, F2, and F3 intercross generations. The 1632 F3 animals from 200 full-sib families were used to estimate heritabilities and genetic correlations of the traits measured. A subset of families was cross-fostered at birth to allow measurement of the importance of post-natal maternal effects. Data was collected on weekly body weight from one to 10 weeks and on organ weights, body weight, reproductive fat pad weight, and tail length at necropsy in the intercross generations. There was no heterosis for age-specific weights or necropsy traits, except that one-week weight was the highest in the F2 generation, indicating heterosis for maternal effect in the F1 mothers. We found moderate to high heritability for most age-specific weights and necropsy traits. Maternal effects were significant for age-specific weights from one to four weeks but disappeared completely at ten-week weight. Maternal effects for necropsy traits were low and not statistically significant. Age-specific weights showed a typical correlation pattern, with correlation declining as the difference in ages increased. Among necropsy traits, reproductive fat pad and body weights were very highly genetically correlated. Most other genetic correlations were low to moderate. The intercross between SM/J and LG/J inbred mouse strains provides a valuable resource for mapping quantitative trait loci for body size, composition, and morphology
Keywords	Genetics ; QH426-470 ; Biology (General) ; QH301-705.5 ; Science ; Q ; DOAJ:Genetics ; DOAJ:Biology ; DOAJ:Biology and Life Sciences
Subject code	630
Language	English
Publishing date	1998-01-01T00:00:00Z
Publisher	Sociedade Brasileira de Genética
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: Modulatory role for retinoid-related orphan receptor alpha in allergen-induced lung inflammation.

Jaradat, Maisa / Stapleton, Cliona / Tilley, Stephen L / Dixon, Darlene / Erikson, Christopher J / McCaskill, Joshua G / Kang, Hong Soon / Angers, Martin / Liao, Grace / Collins, Jennifer / Grissom, Sherry / Jetten, Anton M

American journal of respiratory and critical care medicine

2006 Volume 174, Issue 12, Page(s) 1299–1309

Abstract: Rationale: Nuclear receptors play a critical role in the regulation of inflammation, thus representing attractive targets for the treatment of asthma.: Objective: In this study, we assess the potential regulatory function of retinoid-related orphan ... ...

Abstract	Rationale: Nuclear receptors play a critical role in the regulation of inflammation, thus representing attractive targets for the treatment of asthma. Objective: In this study, we assess the potential regulatory function of retinoid-related orphan receptor alpha (RORalpha) in the adaptive immune response using ovalbumin (OVA)-induced airway inflammation as a model. Methods: Allergen-induced inflammation was compared between wild-type (WT) and staggerer (RORalpha(sg/sg)) mice, a natural mutant strain that is deficient in RORalpha expression. Measurements and main results: Despite robust increases in OVA-specific IgE, RORalpha(sg/sg) mice developed significantly less pulmonary inflammation, mucous cell hyperplasia, and eosinophilia compared with similarly treated WT animals. Induction of Th2 cytokines, including interleukin (IL)-4, IL-5, and IL-13, was also significantly less in RORalpha(sg/sg) mice. Microarray analysis using lung RNA showed increased expression of many genes, previously implicated in inflammation, in OVA-treated WT mice. These include mucin Muc5b, the chloride channel calcium-activated 3 (Clca3), macrophage inflammatory protein (MIP) 1alpha and 1beta, eotaxin-2, serum amyloid A3 (Saa3), and insulin-like growth factor 1 (Igf1). These genes were induced to a greater extent in OVA-treated WT mice relative to RORalpha(sg/sg) mice. Conclusions: Our study demonstrates that mice deficient in RORalpha exhibit an attenuated allergic inflammatory response, indicating that RORalpha plays a critical role in the development of Th2-driven allergic lung inflammation in mice, and suggests that this nuclear receptor should be further evaluated as a potential asthma target.
MeSH term(s)	Allergens ; Animals ; Asthma/physiopathology ; Chemokine CCL24 ; Chemokine CCL3 ; Chemokine CCL4 ; Chemokines, CC/genetics ; Chloride Channels/genetics ; Eosinophilia/etiology ; Inflammation/physiopathology ; Insulin-Like Growth Factor I/genetics ; Lung/physiopathology ; Macrophage Inflammatory Proteins/genetics ; Mice ; Mice, Mutant Strains ; Mucin-5B ; Mucins/genetics ; Mucoproteins/genetics ; Nuclear Receptor Subfamily 1, Group F, Member 1 ; Ovalbumin/immunology ; Receptors, Cytoplasmic and Nuclear/deficiency ; Receptors, Cytoplasmic and Nuclear/physiology ; Serum Amyloid A Protein/genetics ; Trans-Activators/deficiency ; Trans-Activators/physiology
Chemical Substances	Allergens ; Ccl24 protein, mouse ; Chemokine CCL24 ; Chemokine CCL3 ; Chemokine CCL4 ; Chemokines, CC ; Chloride Channels ; Clca3a1 protein, mouse ; Macrophage Inflammatory Proteins ; Mucin-5B ; Mucins ; Mucoproteins ; Nuclear Receptor Subfamily 1, Group F, Member 1 ; Receptors, Cytoplasmic and Nuclear ; Saa3 protein, mouse ; Serum Amyloid A Protein ; Trans-Activators ; Insulin-Like Growth Factor I (67763-96-6) ; Ovalbumin (9006-59-1)
Language	English
Publishing date	2006-09-14
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	1180953-x
ISSN	1535-4970 ; 1073-449X ; 0003-0805
ISSN (online)	1535-4970
ISSN	1073-449X ; 0003-0805
DOI	10.1164/rccm.200510-1672OC
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uh II Zs.80: 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

Details ▾
- See ZB MED holdings
- Order with fees

Article: Retinoid-related orphan receptor gamma controls immunoglobulin production and Th1/Th2 cytokine balance in the adaptive immune response to allergen.

Tilley, Stephen L / Jaradat, Maisa / Stapleton, Cliona / Dixon, Darlene / Hua, Xiaoyang / Erikson, Christopher J / McCaskill, Joshua G / Chason, Kelly D / Liao, Grace / Jania, Leigh / Koller, Beverly H / Jetten, Anton M

Journal of immunology (Baltimore, Md. : 1950)

2006 Volume 178, Issue 5, Page(s) 3208–3218

Abstract: The retinoid-related orphan receptors (ROR) comprise a distinct subfamily of nuclear receptors with the capacity to act as both repressors and activators of transcription. RORgamma, the most recently identified member of the ROR family, has been shown to ...

Abstract	The retinoid-related orphan receptors (ROR) comprise a distinct subfamily of nuclear receptors with the capacity to act as both repressors and activators of transcription. RORgamma, the most recently identified member of the ROR family, has been shown to be important for the development of normal lymphocyte compartments as well as organogenesis of some lymphoid organs. In this report, we examine the capacity of RORgamma-deficient mice to develop an adaptive immune response to Ag using OVA-induced inflammation in mice as a model for allergic airway disease. In sham-treated mice lacking RORgamma, low-grade pulmonary inflammation was observed and characterized by the perivascular accumulation of B and T lymphocytes, increased numbers of inflammatory cells in the lung lavage fluid, and polyclonal Ig activation. Following sensitization and challenge, the capacity of these animals to develop the allergic phenotype was severely impaired as evidenced by attenuated eosinophilic pulmonary inflammation, reduced numbers of CD4+ lymphocytes, and lower Th2 cytokines/chemokine protein and mRNA expression in the lungs. IFN-gamma and IL-10 production was markedly greater in splenocytes from RORgamma-deficient mice following in vitro restimulation with OVA compared with wild-type splenocytes, and a shift toward a Th1 immune response was observed in sensitized/challenged RORgamma-deficient animals in vivo. These data reveal a critical role for RORgamma in the regulation of Ig production and Th1/Th2 balance in adaptive immunity.
MeSH term(s)	Allergens/immunology ; Allergens/toxicity ; Animals ; Antibody Formation/genetics ; Antibody Formation/immunology ; Interferon-gamma/immunology ; Interleukin-10/immunology ; Mice ; Mice, Mutant Strains ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Receptors, Retinoic Acid/deficiency ; Receptors, Retinoic Acid/immunology ; Receptors, Thyroid Hormone/deficiency ; Receptors, Thyroid Hormone/immunology ; Respiratory Hypersensitivity/chemically induced ; Respiratory Hypersensitivity/genetics ; Respiratory Hypersensitivity/immunology ; Respiratory Hypersensitivity/pathology ; Th1 Cells/immunology ; Th1 Cells/pathology ; Th2 Cells/immunology ; Th2 Cells/pathology
Chemical Substances	Allergens ; Nuclear Receptor Subfamily 1, Group F, Member 3 ; Receptors, Retinoic Acid ; Receptors, Thyroid Hormone ; Rorc protein, mouse ; Interleukin-10 (130068-27-8) ; Interferon-gamma (82115-62-6)
Language	English
Publishing date	2006-10-05
Publishing country	United States
Document type	Comparative Study ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.178.5.3208
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.37: 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.MG 28: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article: Receptors and pathways mediating the effects of prostaglandin E2 on airway tone.

Tilley, Stephen L / Hartney, John M / Erikson, Christopher J / Jania, Corey / Nguyen, Mytrang / Stock, Jeffrey / McNeisch, John / Valancius, Cathy / Panettieri, Reynold A / Penn, Raymond B / Koller, Beverly H

American journal of physiology. Lung cellular and molecular physiology

2002 Volume 284, Issue 4, Page(s) L599–606

Abstract: Prostaglandin E(2) (PGE(2)) has complex effects on airway tone, and the existence of four PGE(2) [E-prostanoid (EP)] receptors, each with distinct signaling characteristics, has provided a possible explanation for the seemingly contradictory actions of ... ...

Abstract	Prostaglandin E(2) (PGE(2)) has complex effects on airway tone, and the existence of four PGE(2) [E-prostanoid (EP)] receptors, each with distinct signaling characteristics, has provided a possible explanation for the seemingly contradictory actions of this lipid mediator. To identify the receptors mediating the actions of PGE(2) on bronchomotor tone, we examined its effects on the airways of wild-type and EP receptor-deficient mice. In conscious mice the administration of PGE(2) increased airway responsiveness primarily through the EP1 receptor, although on certain genetic backgrounds a contribution of the EP3 receptor was detected. These effects of PGE(2) were eliminated by pretreatment with either atropine or bupivacaine and were undetectable in anesthetized mice or in denervated tracheal rings, where only EP2-mediated relaxation of airway smooth muscle was observed. Together, our findings are consistent with a model in which PGE(2) modulates airway tone by activating multiple receptors expressed on various cell populations and in which the relative contribution of these receptors might depend on the expression of modifier alleles. PGE(2)/EP1/EP3-induced airway constriction occurs indirectly through activation of neural pathways, whereas PGE(2)-induced bronchodilation results from direct activation of EP2 receptors on airway smooth muscle. This segregation of EP receptor function within the airway suggests that PGE(2) analogs that selectively activate the EP2 receptor without activating the EP1/EP3 receptors might prove useful in the treatment of asthma.
MeSH term(s)	Anesthesia ; Animals ; Bronchoconstriction/drug effects ; Bronchoconstriction/physiology ; Consciousness ; Dinoprostone/metabolism ; Dinoprostone/pharmacology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Inbred DBA ; Mice, Knockout ; Muscle, Smooth/drug effects ; Muscle, Smooth/physiology ; Receptors, Prostaglandin E/genetics ; Receptors, Prostaglandin E/metabolism ; Receptors, Prostaglandin E, EP1 Subtype ; Receptors, Prostaglandin E, EP3 Subtype ; Receptors, Prostaglandin E, EP4 Subtype ; Trachea/drug effects ; Trachea/innervation ; Trachea/physiology
Chemical Substances	Ptger1 protein, mouse ; Ptger3 protein, mouse ; Ptger4 protein, mouse ; Receptors, Prostaglandin E ; Receptors, Prostaglandin E, EP1 Subtype ; Receptors, Prostaglandin E, EP3 Subtype ; Receptors, Prostaglandin E, EP4 Subtype ; Dinoprostone (K7Q1JQR04M)
Language	English
Publishing date	2002-12-13
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, P.H.S.
ZDB-ID	1013184-x
ISSN	1522-1504 ; 1040-0605
ISSN (online)	1522-1504
ISSN	1040-0605
DOI	10.1152/ajplung.00324.2002
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Uc I Zs.89: 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.A 2749: 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

To top

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Inter-library loan at ZB MED

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

Inter-library loan at ZB MED

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

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito