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Article: Stezenie przedsionkowego peptydu natriuretycznego w stabilnym i zaostrzonym okresie przewlekłej obturacyjnej choroby płuc.

Skwarski, K / Lee, M / MacNee, W

1996 Volume 64, Issue 9-10, Page(s) 627–637

Abstract: Plasma Atrial Natriuretic Peptide (ANP) levels are elevated in patients wish chronic obstructive pulmonary disease (COPD) and can play a role in oedema formation. Plasma ANP levels measured in 60 patients with COPD were compared with results of pulmonary ...

Title translation	Levels of atrial natriuretic peptide in stable and exacerbated chronic obstructive pulmonary disease.
Abstract	Plasma Atrial Natriuretic Peptide (ANP) levels are elevated in patients wish chronic obstructive pulmonary disease (COPD) and can play a role in oedema formation. Plasma ANP levels measured in 60 patients with COPD were compared with results of pulmonary haemodynamics, with therapeutic response to treatment in the time of exacerbation of COPD and with physiologic status of patients with stable COPD. Plasma ANP levels did not correlate with right atrial and pulmonary artery pressure, but were significantly related with right ventricular end diastolic volume and with right ventricular wall volume measured by magnetic resonance imaging. Oxygen breathing (2 l/min by nasal prongs in 30 min.) did not change either mean pulmonary artery pressure or ANP levels. Among patients studied during an acute exacerbation of COPD, plasma ANP levels were higher in patients with oedema (302 +/- 185 pg/ml) than in patients without oedema (87 +/- 43 pg/ml). Oxygen therapy applied in one hour did not influence plasma ANP levels. Plasma ANP levels decreased during first three days of treatment in patients with oedema. This decrease was related to the body weight. In the group of patients with hypoxemia in stable COPD, plasma ANP levels (120 +/- 50 pg/ml) were higher in patients with the history of hypercapnia and oedema than in others (54 +/- 15 pg/ml).
MeSH term(s)	Aged ; Atrial Natriuretic Factor/blood ; Edema/etiology ; Humans ; Lung Diseases, Obstructive/blood ; Lung Diseases, Obstructive/complications ; Lung Diseases, Obstructive/diagnosis ; Lung Diseases, Obstructive/therapy ; Middle Aged ; Oxygen/blood ; Oxygen Inhalation Therapy ; Respiratory Function Tests
Chemical Substances	Atrial Natriuretic Factor (85637-73-6) ; Oxygen (S88TT14065)
Language	Polish
Publishing date	1996
Publishing country	Poland
Document type	English Abstract ; Journal Article
ZDB-ID	1173936-8
ISSN	2299-8292 ; 0867-7077
ISSN (online)	2299-8292
ISSN	0867-7077
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Zs.B 493: Show issues

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Article ; Online: Beta-Blockers in COPD - A Controversy Resolved?

MacNee, William

The New England journal of medicine

2019 Volume 381, Issue 24, Page(s) 2367–2368

MeSH term(s)	Adrenergic beta-Antagonists ; Humans ; Metoprolol ; Pulmonary Disease, Chronic Obstructive
Chemical Substances	Adrenergic beta-Antagonists ; Metoprolol (GEB06NHM23)
Language	English
Publishing date	2019-10-20
Publishing country	United States
Document type	Editorial ; Comment
ZDB-ID	207154-x
ISSN	1533-4406 ; 0028-4793
ISSN (online)	1533-4406
ISSN	0028-4793
DOI	10.1056/NEJMe1912664
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Ua VI Zs.34: Show issues

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Article ; Online: Is Chronic Obstructive Pulmonary Disease an Accelerated Aging Disease?

MacNee, William

Annals of the American Thoracic Society

2016 Volume 13 Suppl 5, Page(s) S429–S437

Abstract: Aging is one of the most important risk factors for most chronic diseases. The worldwide increase in life expectancy has been accompanied by an increase in the prevalence of age-related diseases that result in significant morbidity and mortality and ... ...

Abstract	Aging is one of the most important risk factors for most chronic diseases. The worldwide increase in life expectancy has been accompanied by an increase in the prevalence of age-related diseases that result in significant morbidity and mortality and place an enormous burden on healthcare and resources. Aging is a progressive degeneration of the tissues that has a negative impact on the structure and function of vital organs. The lung ages, resulting in decreased function and reduced capacity to respond to environmental stresses and injury. Many of the changes that occur in the lungs with normal aging, such as decline in lung function, increased gas trapping, loss of lung elastic recoil, and enlargement of the distal air spaces, also are present in chronic obstructive pulmonary disease (COPD). The prevalence of COPD is two to three times higher in people over the age of 60 years than in younger age groups. Indeed, COPD has been considered a condition of accelerated lung aging. Several mechanisms associated with aging are present in the lungs of patients with COPD. Cell senescence is present in emphysematous lungs and is associated with shortened telomeres and decreased antiaging molecules, suggesting accelerated aging in the lungs of patients with COPD. Increasing age leads to elevated basal levels of inflammation and oxidative stress (inflammaging) and to increased immunosenescence associated with changes in both the innate and adaptive immune responses. These changes are similar to those that occur in COPD and may enhance the activity of the disease as well as increase susceptibility to exacerbations in patients with COPD. Understanding the mechanism of age-related changes in COPD may identify novel therapies for this condition.
MeSH term(s)	Adaptive Immunity ; Aging/immunology ; Aging/physiology ; Humans ; Immunity, Innate ; Immunosenescence/immunology ; Immunosenescence/physiology ; Inflammation ; Lung/immunology ; Lung/physiopathology ; Oxidative Stress ; Pulmonary Disease, Chronic Obstructive/immunology ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Telomere Shortening
Language	English
Publishing date	2016-12-21
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	2717461-X
ISSN	2325-6621 ; 1943-5665 ; 2325-6621
ISSN (online)	2325-6621 ; 1943-5665
ISSN	2325-6621
DOI	10.1513/AnnalsATS.201602-124AW
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Zs.A 5828: Show issues

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Article ; Online: Computed tomography-derived pathological phenotypes in COPD.

MacNee, William

The European respiratory journal

2016 Volume 48, Issue 1, Page(s) 10–13

MeSH term(s)	Humans ; Phenotype ; Pulmonary Disease, Chronic Obstructive ; Pulmonary Emphysema ; Tomography, X-Ray Computed
Language	English
Publishing date	2016-06-30
Publishing country	England
Document type	Editorial ; Comment
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/13993003.00958-2016
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Zs.A 2322: 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)
Zs.MO 292: Show issues

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Article ; Online: Premature vascular ageing in cystic fibrosis.

Macnee, W

The European respiratory journal

2009 Volume 34, Issue 6, Page(s) 1217–1218

MeSH term(s)	Adult ; Aorta/physiopathology ; Arteries/physiopathology ; Brachial Artery/physiopathology ; Cross-Sectional Studies ; Cystic Fibrosis/complications ; Cystic Fibrosis/physiopathology ; Female ; Humans ; Inflammation ; Male ; Pulmonary Disease, Chronic Obstructive/complications ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Pulmonary Medicine/methods ; Vascular Diseases/etiology ; Vascular Diseases/physiopathology
Language	English
Publishing date	2009-12
Publishing country	England
Document type	Comment ; Editorial
ZDB-ID	639359-7
ISSN	1399-3003 ; 0903-1936
ISSN (online)	1399-3003
ISSN	0903-1936
DOI	10.1183/09031936.00155209
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Zs.A 2322: 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)
Zs.MO 292: Show issues

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Article ; Online: The recognition of lung disease in coal workers: The role of Gough-Wentworth whole lung sections.

Donaldson, Ken / Wallace, William A / MacNee, William / Henry, Christopher / Seaton, Anthony

The journal of the Royal College of Physicians of Edinburgh

2022 Volume 52, Issue 1, Page(s) 65–72

Abstract: From the identification of a specific lung disease caused by coal dust exposure in miners in 1831 until the demonstration of the association of that exposure to risk of emphysema in 1984, there was continuous argument about the harmfulness of coal dust. ... ...

Abstract	From the identification of a specific lung disease caused by coal dust exposure in miners in 1831 until the demonstration of the association of that exposure to risk of emphysema in 1984, there was continuous argument about the harmfulness of coal dust. Ill health in miners was attributed variously to tuberculosis, quartz exposure or cigarette smoking. An acceptance that coal dust was harmful only started with investigative radiology and pathology in the 1920s, and physiology in the 1950s. Most of the early investigations were in South Wales, the centre of the most important coal field in Great Britain. Among the investigators was Professor Jethro Gough who, with his technician James Wentworth, introduced a technique for making thick sections of whole, inflated lungs on paper backing. Here, we describe this method and its central role in understanding the relationships between coal dust exposure, pneumoconiosis, emphysema and lung dysfunction in miners.
MeSH term(s)	Coal/adverse effects ; Coal Mining ; Dust ; Emphysema/pathology ; Humans ; Lung/diagnostic imaging ; Lung/pathology ; Lung Diseases ; Pulmonary Emphysema/pathology ; Quartz
Chemical Substances	Coal ; Dust ; Quartz (14808-60-7)
Language	English
Publishing date	2022-09-23
Publishing country	England
Document type	Journal Article
ZDB-ID	2866363-9
ISSN	2042-8189 ; 0953-0932
ISSN (online)	2042-8189
ISSN	0953-0932
DOI	10.1177/14782715221088982
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Zs.A 3088 -Suppl.-: Show issues

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Article ; Online: Right heart function in COPD.

Macnee, William

Seminars in respiratory and critical care medicine

2010 Volume 31, Issue 3, Page(s) 295–312

Abstract: Pulmonary hypertension is a common complication in patients with severe hypoxic COPD, but the elevation in pulmonary arterial pressure (PAP) is usually relatively mild, although its presence indicates a poor prognosis. A minority of patients have severe ... ...

Abstract	Pulmonary hypertension is a common complication in patients with severe hypoxic COPD, but the elevation in pulmonary arterial pressure (PAP) is usually relatively mild, although its presence indicates a poor prognosis. A minority of patients have severe pulmonary hypertension, whose prognosis is very poor with the development of right heart failure. Pulmonary hypertension in COPD is thought to result from hypoxic pulmonary vasoconstriction leading to structural remodeling of all layers of the pulmonary arterial walls. The simple hypothesis that hypoxemia in patients with chronic lung disease results in pulmonary hypertension, which adversely affects right ventricular function and hence increases morbidity and decreases exercise tolerance, leading to the development of peripheral edema and increased mortality, is still somewhat controversial. Whether therapeutic interventions that directly affect PAP or right ventricular function have a significant effect on long-term survival in patients with pulmonary hypertension secondary to hypoxic lung disease is still a matter of debate. Furthermore, whether such interventions will have an effect on symptoms or exercise tolerance remains unproven. Present therapies are limited to the correction of hypoxemia over the long term, which has been shown to have proven benefits on survival. Further studies are required of more specific pulmonary vasodilators or therapies to improve right ventricular function in these patients.
MeSH term(s)	Exercise Tolerance ; Humans ; Hypertension, Pulmonary/etiology ; Hypertension, Pulmonary/physiopathology ; Hypertension, Pulmonary/therapy ; Hypoxia/physiopathology ; Hypoxia/therapy ; Prognosis ; Pulmonary Disease, Chronic Obstructive/complications ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Severity of Illness Index ; Survival ; Ventricular Dysfunction, Right/etiology ; Ventricular Dysfunction, Right/physiopathology ; Ventricular Dysfunction, Right/therapy
Language	English
Publishing date	2010-06
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1183617-9
ISSN	1098-9048 ; 1069-3424
ISSN (online)	1098-9048
ISSN	1069-3424
DOI	10.1055/s-0030-1254070
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Zs.A 1555: Show issues

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Article ; Online: Role of Inflammation and Oxidative Stress in the Pathology of Ageing in COPD: Potential Therapeutic Interventions.

Choudhury, Gourab / MacNee, William

COPD

2016 Volume 14, Issue 1, Page(s) 122–135

Abstract: Ageing is defined as a progressive decline of homeostasis that occurs after the reproductive phase of life is complete, which is thought to arise because of impaired DNA repair following damage. This leads to an increased risk of disease or death. Ageing ...

Abstract	Ageing is defined as a progressive decline of homeostasis that occurs after the reproductive phase of life is complete, which is thought to arise because of impaired DNA repair following damage. This leads to an increased risk of disease or death. Ageing is one of the most important risk factors for most chronic diseases. Chronic obstructive pulmonary disease (COPD) represents an important component of the increasingly prevalent multiple chronic debilitating diseases that are a major cause of morbidity and mortality, particularly in the elderly. There is increasing evidence that the pathogenesis of COPD is linked to an accelerated ageing process. This review discusses the evidence supporting a number of mechanisms, including oxidative stress and ageing, in the pathogenesis of COPD. Greater understanding of these mechanisms leads to novel therapeutic interventions targeted at this heterogeneous disease.
MeSH term(s)	Aging/physiology ; Anti-Inflammatory Agents/therapeutic use ; Antioxidants/therapeutic use ; Apoptosis ; Autophagy ; Cellular Senescence ; Glycation End Products, Advanced/metabolism ; Humans ; Inflammation/complications ; Inflammation/genetics ; Lung/pathology ; Mitochondria/physiology ; NF-kappa B/genetics ; NF-kappa B/metabolism ; Oxidative Stress/physiology ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Disease, Chronic Obstructive/etiology ; Reactive Nitrogen Species/toxicity ; Reactive Oxygen Species/toxicity ; Sirtuins/metabolism ; Telomere Shortening ; Unfolded Protein Response
Chemical Substances	Anti-Inflammatory Agents ; Antioxidants ; Glycation End Products, Advanced ; NF-kappa B ; Reactive Nitrogen Species ; Reactive Oxygen Species ; Sirtuins (EC 3.5.1.-)
Language	English
Publishing date	2016-09-13
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2171107-0
ISSN	1541-2563 ; 1541-2555
ISSN (online)	1541-2563
ISSN	1541-2555
DOI	10.1080/15412555.2016.1214948
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Zs.A 5990: Show issues

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Article ; Online: Systemic inflammatory biomarkers and co-morbidities of chronic obstructive pulmonary disease.

MacNee, William

Annals of medicine

2013 Volume 45, Issue 3, Page(s) 291–300

Abstract: Chronic obstructive pulmonary disease (COPD) can no longer be considered as a disease affecting only the lungs. Increasing evidence supports the presence of a systemic inflammatory component which is thought to provide the link between COPD and the co- ... ...

Abstract	Chronic obstructive pulmonary disease (COPD) can no longer be considered as a disease affecting only the lungs. Increasing evidence supports the presence of a systemic inflammatory component which is thought to provide the link between COPD and the co-morbidities commonly associated with this disease. These include cardiovascular disorders, skeletal muscle dysfunction, diabetes, and osteoporosis. The majority of current therapies for COPD have been developed to improve airway obstruction or to target airway inflammation, leaving an unmet medical need with respect to the systemic inflammatory component of COPD and its extra-pulmonary manifestations. This review describes systemic biomarkers in COPD and their relationship with both the local lung and systemic manifestations of the disease. A summary is provided of the most promising biomarkers that have been investigated in COPD and its co-morbidities. Such biomarkers may be used to assess and manage the systemic effects of COPD, and may guide future development of novel therapeutic interventions to provide a more holistic approach to treating this multi-faceted disease.
MeSH term(s)	Adiponectin/blood ; Aging ; Airway Remodeling ; Biomarkers/blood ; C-Reactive Protein/analysis ; CD40 Ligand/blood ; Cachexia/etiology ; Cardiovascular Diseases/blood ; Cardiovascular Diseases/complications ; Chemokines, CC/blood ; Cytokines/blood ; Desmosine/metabolism ; Fibrinogen/analysis ; Humans ; Inflammation/blood ; Inflammation/complications ; Intercellular Adhesion Molecule-1/blood ; Isodesmosine/metabolism ; Lung Neoplasms/complications ; Matrix Metalloproteinases/blood ; Natriuretic Peptide, Brain/blood ; Osteoprotegerin/blood ; Pulmonary Disease, Chronic Obstructive/blood ; Pulmonary Disease, Chronic Obstructive/complications ; Pulmonary Disease, Chronic Obstructive/drug therapy ; Pulmonary Surfactant-Associated Protein D/blood ; Serum Amyloid A Protein/analysis ; Severity of Illness Index ; Telomere/physiology ; Uteroglobin/blood
Chemical Substances	Adiponectin ; Biomarkers ; CCL18 protein, human ; Chemokines, CC ; Cytokines ; Osteoprotegerin ; Pulmonary Surfactant-Associated Protein D ; SCGB1A1 protein, human ; Serum Amyloid A Protein ; Desmosine (11003-57-9) ; Natriuretic Peptide, Brain (114471-18-0) ; Intercellular Adhesion Molecule-1 (126547-89-5) ; CD40 Ligand (147205-72-9) ; Fibrinogen (9001-32-5) ; C-Reactive Protein (9007-41-4) ; Uteroglobin (9060-09-7) ; Isodesmosine (991-01-5) ; Matrix Metalloproteinases (EC 3.4.24.-)
Language	English
Publishing date	2013-05
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1004226-x
ISSN	1365-2060 ; 1651-2219 ; 0785-3890 ; 1743-1387
ISSN (online)	1365-2060 ; 1651-2219
ISSN	0785-3890 ; 1743-1387
DOI	10.3109/07853890.2012.732703
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Zs.A 680: Show issues

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Article: Pathogenesis of chronic obstructive pulmonary disease.

Macnee, William

Clinics in chest medicine

2007 Volume 28, Issue 3, Page(s) 479–513, v

Abstract: The pathogenesis of chronic obstructive pulmonary disease (COPD) encompasses a number of injurious processes, including an abnormal inflammatory response in the lungs to inhaled particles and gases. Other processes, such as failure to resolve ... ...

Abstract	The pathogenesis of chronic obstructive pulmonary disease (COPD) encompasses a number of injurious processes, including an abnormal inflammatory response in the lungs to inhaled particles and gases. Other processes, such as failure to resolve inflammation, abnormal cell repair, apoptosis, abnormal cellular maintenance programs, extracellular matrix destruction (protease/antiprotease imbalance), and oxidative stress (oxidant/antioxidant imbalance) also have a role. The inflammatory responses to the inhalation of active and passive tobacco smoke and urban and rural air pollution are modified by genetic and epigenetic factors. The subsequent chronic inflammatory responses lead to mucus hypersecretion, airway remodeling, and alveolar destruction. This article provides an update on the cellular and molecular mechanisms of these processes in the pathogenesis of COPD.
MeSH term(s)	Forced Expiratory Flow Rates/physiology ; Humans ; Prognosis ; Pulmonary Disease, Chronic Obstructive/etiology ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Risk Factors ; Smoking/adverse effects
Language	English
Publishing date	2007-09
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Review
ZDB-ID	447455-7
ISSN	1557-8216 ; 0272-5231
ISSN (online)	1557-8216
ISSN	0272-5231
DOI	10.1016/j.ccm.2007.06.008
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