Publication:
Caveolin-1 Expression and Hemodynamics in COPD Patients

Date

Date

Date
2009
Journal Article
Published version

Abstract

Abstract

Abstract
Caveolin-1 is a regulator of both intracellular calcium homeostasis and endothelial nitric oxide synthase and may play a pathogenetic role in pulmonary hypertension. In the present study, we aimed to investigate the correlations between pulmonary hemodynamics and vessel morphology including the expression of Caveolin-1 in pulmonary arterioles from patients with chronic obstructive pulmonary disease (COPD) who underwent lung-volume reduction surgery. Staining and subsequent analysis was performed on paraffin-embedded lung tissue from C

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Downloads

83 since deposited on 2010-01-15
Acq. date: 2025-11-13

Views

195 since deposited on 2010-01-15
Acq. date: 2025-11-13

Additional indexing

Creators (Authors)

  • Huber, L C
    affiliation.icon.alt
  • Soltermann, A
    affiliation.icon.alt
  • Fischler, M
    affiliation.icon.alt
  • Gay, S
    affiliation.icon.alt
  • Weder, W
    affiliation.icon.alt
  • Russi, E W
    affiliation.icon.alt
  • Speich, R
    affiliation.icon.alt
  • Ulrich, S
    affiliation.icon.alt

Journal/Series Title

Journal/Series Title

Journal/Series Title

Volume

Volume

Volume
3

Page range/Item number

Page range/Item number

Page range/Item number
73

Page end

Page end

Page end
78

Item Type

Item Type

Item Type
Journal Article

Dewey Decimal Classifikation

Dewey Decimal Classifikation

Dewey Decimal Classifikation

Language

Language

Language
English

Publication date

Publication date

Publication date
2009

Date available

Date available

Date available
2010-01-15

Publisher

Publisher

Publisher

ISSN or e-ISSN

ISSN or e-ISSN

ISSN or e-ISSN
1874-3064

OA Status

OA Status

OA Status
Hybrid

Free Access at

Free Access at

Free Access at
Pubmed ID

PubMed ID

PubMed ID

PubMed ID

Metrics

Downloads

83 since deposited on 2010-01-15
Acq. date: 2025-11-13

Views

195 since deposited on 2010-01-15
Acq. date: 2025-11-13
Hybrid Open Access
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Files

Files

Files
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Files

Files

Files
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