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33 records – page 1 of 4.

Airway inflammation among compost workers exposed to actinomycetes spores.

https://arctichealth.org/en/permalink/ahliterature271518
Source
Ann Agric Environ Med. 2015;22(2):253-8
Publication Type
Article
Date
2015
Author
Kari Kulvik Heldal
Lene Madsø
Wijnand Eduard
Source
Ann Agric Environ Med. 2015;22(2):253-8
Date
2015
Language
English
Publication Type
Article
Keywords
Actinobacteria - chemistry
Adult
Aerosols - toxicity
Air Pollutants, Occupational - toxicity
Biomarkers - blood
Female
Humans
Male
Middle Aged
Norway - epidemiology
Occupational Exposure
Pulmonary Surfactant-Associated Protein A - blood
Pulmonary Surfactant-Associated Protein D - blood
Respiratory Hypersensitivity - epidemiology - microbiology
Sewage
Spores, Bacterial - chemistry
Uteroglobin - blood
Abstract
To study the associations between exposure to bioaerosols and work-related symptoms, lung function and biomarkers of airway inflammation in compost workers.
Personal full-shift exposure measurements were performed on 47 workers employed at five windrow plants (n=20) and five reactor plants (n=27). Samples were analyzed for endotoxins, bacteria, fungal and actinomycetes spores. Health examinations were performed on workers and 37 controls before and after work on the day exposure was measured. The examinations included symptoms recorded by questionnaire, lung function by spirometry and nasal dimensions by acoustic rhinometry (AR). The pneumoproteins CC16, SP-D and SP-A were measured in a blood sample drawn at the end of the day.
The levels of endotoxins (median 3 EU/m(3), range 0-730 EU/m(3)) and actinomycetes spores (median 0.2 ? 10(6) spores/m(3), range 0-590 ? 10(6) spores/m(3)) were significantly higher in reactor plants compared to windrow plants. However, windrow composting workers reported more symptoms than reactor composting workers, probably due to use of respiratory protection. Exposure-response relationships between actinomycetes spores exposure and respiratory effects, found as cough and nose irritation during a shift, was significantly increased (OR 4.3, 95% CI 1.1-16, OR 6.1, 95% CI 1.5-25, respectively, p
PubMed ID
26094519 View in PubMed
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Association between surfactant protein A gene locus and severe respiratory syncytial virus infection in infants.

https://arctichealth.org/en/permalink/ahliterature58561
Source
J Infect Dis. 2002 Feb 1;185(3):283-9
Publication Type
Article
Date
Feb-1-2002
Author
Johan Löfgren
Mika Rämet
Marjo Renko
Riitta Marttila
Mikko Hallman
Author Affiliation
Department of Pediatrics and Biocenter Oulu, University of Oulu, Oulu, FIN-90014 Finland. johann.lofgren@oulu.fi
Source
J Infect Dis. 2002 Feb 1;185(3):283-9
Date
Feb-1-2002
Language
English
Publication Type
Article
Keywords
Alleles
Chromosome Mapping
Female
Genotype
Haplotypes
Humans
Infant, Newborn
Male
Proteolipids - chemistry - genetics
Pulmonary Surfactant-Associated Protein A
Pulmonary Surfactant-Associated Proteins
Pulmonary Surfactants - chemistry - genetics
Research Support, Non-U.S. Gov't
Respiratory Syncytial Virus Infections - genetics
Abstract
Respiratory syncytial virus (RSV) causes seasonal epidemics of bronchiolitis among susceptible infants. Surfactant protein A (SP-A), a lung C-type lectin involved in innate host defense, opsonizes RSV and enhances phagocytosis. The candidate gene approach was used to investigate association of SP-A polymorphism with susceptibility to severe RSV infection. Genotype analysis was done for 86 infants with severe RSV infection and 95 matched control subjects. A significant difference in the frequency of SP-A2 was observed. The SP-A2 allele 1A(3) was overrepresented in RSV-infected infants, compared with control subjects (5% vs. 0.5%; P =.006), whereas allele 1A was underrepresented (1% vs. 6%; P =.011). The allele pool in which lysine was amino acid 223 was overrepresented in infants with severe RSV infection (28% vs. 18%; P =.023), whereas the allele pool in which proline was amino acid 99 was underrepresented (5% vs. 16%; P =.001). These results indicate that a genetic association exists between SP-A gene locus and severe RSV infection.
PubMed ID
11807709 View in PubMed
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Association between the surfactant protein A (SP-A) gene locus and respiratory-distress syndrome in the Finnish population.

https://arctichealth.org/en/permalink/ahliterature58782
Source
Am J Hum Genet. 2000 May;66(5):1569-79
Publication Type
Article
Date
May-2000
Author
M. Rämet
R. Haataja
R. Marttila
J. Floros
M. Hallman
Author Affiliation
Department of Pediatrics and Biocenter Oulu, University of Oulu, FIN-90014, Oulu, Finland.
Source
Am J Hum Genet. 2000 May;66(5):1569-79
Date
May-2000
Language
English
Publication Type
Article
Keywords
Alleles
Birth weight
Female
Finland
Gene Frequency - genetics
Genetic Predisposition to Disease - genetics
Genotype
Gestational Age
Glucocorticoids - therapeutic use
Haplotypes - genetics
Humans
Infant, Newborn
Infant, Premature
Introns - genetics
Logistic Models
Male
Matched-Pair Analysis
Proteolipids - genetics - physiology
Pulmonary Surfactant-Associated Protein A
Pulmonary Surfactant-Associated Proteins
Pulmonary Surfactants - genetics - physiology
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S.
Respiratory Distress Syndrome, Newborn - genetics
Risk factors
Sequence Deletion - genetics
Sex Characteristics
Abstract
Respiratory-distress syndrome (RDS) in the newborn is a major cause of neonatal mortality and morbidity. Although prematurity is the most-important risk factor for RDS, the syndrome does not develop in many premature infants. The main cause of RDS is a deficiency of pulmonary surfactant, which consists of phospholipids and specific proteins. The genes underlying susceptibility to RDS are insufficiently known. The candidate-gene approach was used to study the association between the surfactant protein A (SP-A) gene locus and RDS in the genetically homogeneous Finnish population. In the present study, 88 infants with RDS and 88 control infants that were matched for degree of prematurity, prenatal glucocorticoid therapy, and sex were analyzed for SP-A genotypes. We show that certain SP-A1 alleles (6A2 and 6A3) and an SP-A1/SP-A2 haplotype (6A2/1A0) were associated with RDS. The 6A2 allele was overrepresented and the 6A3 allele was underrepresented in infants with RDS. These associations were particularly strong among small premature infants born at gestational age
PubMed ID
10762543 View in PubMed
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Association between the surfactant protein D (SFTPD) gene and subclinical carotid artery atherosclerosis.

https://arctichealth.org/en/permalink/ahliterature278404
Source
Atherosclerosis. 2016 Mar;246:7-12
Publication Type
Article
Date
Mar-2016
Author
Grith L Sorensen
Else Marie Bladbjerg
Rudi Steffensen
Qihua Tan
Jens Madsen
Thomas Drivsholm
Uffe Holmskov
Source
Atherosclerosis. 2016 Mar;246:7-12
Date
Mar-2016
Language
English
Publication Type
Article
Keywords
Asymptomatic Diseases
Carotid Arteries - diagnostic imaging
Carotid Artery Diseases - blood - diagnostic imaging - genetics
Carotid Intima-Media Thickness
Chi-Square Distribution
Denmark
Female
Genetic Association Studies
Genetic Predisposition to Disease
Humans
Linear Models
Logistic Models
Male
Middle Aged
Multivariate Analysis
Phenotype
Plaque, Atherosclerotic
Polymorphism, Single Nucleotide
Pulmonary Surfactant-Associated Protein D - blood - genetics
Risk assessment
Risk factors
Smoking - adverse effects
Abstract
Surfactant protein D (SP-D) is a defense collectin with inflammation-modulating properties. SP-D deficiency inhibits atherosclerosis in vivo, and the circulatory SP-D levels have been previously associated with cardiovascular disease mortality. We hypothesized that plasma SP-D (pSP-D) and SP-D gene (SFTPD) single nucleotide polymorphisms (SNPs) are risk factors for atherosclerosis.
We evaluated individuals who were all 60 years old and participated in The Glostrup Population Study. Subclinical atherosclerosis was diagnosed based on the ultrasonographic measurement of intima-media thickness (IMT) and protruding plaques in the right carotid artery. Associations between cardiovascular traits and the levels of pSP-D (n = 687) or two coding SFTPD SNPs rs3088308 and rs721917 (n = 396) were investigated using multiple linear regressions and logistic regressions.
There was no significant association between pSP-D and the presence of plaques or IMT. The SFTPD SNP rs3088308 was nominally associated with the presence of plaques, and rs721917 was nominally associated with IMT. The directions of effects of associations were markedly dependent on current smoking status.
The results do not support that pSP-D levels influence the development of subclinical atherosclerosis. However, the SFTPD SNP data support previous observations from animal studies that SP-D plays a role in the etiology of atherosclerotic disease development. The nominal significant effects are likely to be mediated by structural variant SP-D modulation of effects of tobacco smoking and are independent of pSP-D levels. The data warrant confirmation in larger cohorts.
PubMed ID
26748346 View in PubMed
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[Association of polymorphism genes of surfactant proteins in patients with influenza].

https://arctichealth.org/en/permalink/ahliterature271090
Source
Zh Mikrobiol Epidemiol Immunobiol. 2015 Nov-Dec;(6):71-7
Publication Type
Article
Author
Dudina KR
Kutateladze MM
Bokova NO
Znoiko OO
Abramov DD
Kelly EI
Yuschuk ND
Source
Zh Mikrobiol Epidemiol Immunobiol. 2015 Nov-Dec;(6):71-7
Language
Russian
Publication Type
Article
Keywords
Adult
Cardiovascular Diseases - epidemiology - mortality
Case-Control Studies
Comorbidity
Endocrine System Diseases - epidemiology - mortality
Female
Gene Expression
Genetic Association Studies
Humans
Influenza A Virus, H1N1 Subtype - genetics - immunology - isolation & purification
Influenza A Virus, H3N2 Subtype - genetics - immunology - isolation & purification
Influenza, Human - epidemiology - mortality
Lung Diseases - epidemiology - mortality
Male
Polymorphism, Single Nucleotide
Pulmonary Surfactant-Associated Protein A - genetics
Pulmonary Surfactant-Associated Protein B - genetics
Russia - epidemiology
Abstract
Evaluate role of gene polymorphisms of surfactant proteins in susceptibility and severity of influenza infection course in representatives of Moscow population. MATERIALS AND METHODS; 320 influenza patients, infected with various influenza virus strains, and 115 healthy individuals (control group),, were included into the study. Human DNA samples genotyping for determination of SFTPA2 gene rs1965708 and rs1059046, SFTPB gene rs1130866 polymorphisms was carried out using a modified method of "adjacent samples".
Most of the individuals of the control group and influenza patients are carries of alleles and genotypes rs1965708 and rs1059046 of SFTPA2 gene, rs1130866 of SFTPB gene, that have, based on scientific literature data, shown association with severe course of influenza A(H1N1) pdm09 and other inflammatory diseases of the respiratory tract. Generally, significant differences in frequency of occurrence of unfavorable genotypes CC rs1965708, AA rs1059046 of SFTPA2 gene and CC rs1130866 of SFTPB gene in influenza patients in comparison with individuals of the control group were not detected, that gives evidence on a high (from 19 to 51%) prevalence of these genotypes in the studied population. Allele C and genotype CC rs1965708 of SFTPA2 gene, allele A and genotype AA rs1059046 of SFTPA2 gene, allele C and genotype CC rs1130866 of SFTPB gene did not shown an association with severe course of A(H1N1) pdm09 influenza. The following pathology registered in most (88%) of the patients with severe course of influenza A (H1N1)pdm09: diseases of cardiovascilar (44%), endocrine (36%) and respiratory (12%) systems.
Because in most of the deceased patients due to severe course of A (H1N1)pdm09 influenza, diseases of cardiovascular, respiratory and endocrine system were detected, and an association of unfavorable disease outcome with the studied genetic markers was not detected, dominating risk factor of development of severe course and lethal outcome for A(H1N1)pdm09 influenza in the studied cohort was comorbidity.
PubMed ID
26950992 View in PubMed
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Circulating surfactant protein D is associated to mortality in elderly women: a twin study.

https://arctichealth.org/en/permalink/ahliterature120460
Source
Immunobiology. 2013 May;218(5):712-7
Publication Type
Article
Date
May-2013
Author
Helle Wulf-Johansson
Mikael Thinggaard
Qihua Tan
Sofie Lock Johansson
Anders Schlosser
Kaare Christensen
Uffe Holmskov
Grith Lykke Sorensen
Author Affiliation
Cardiovascular and Renal Research, Institute of Molecular Medicine, University of Southern Denmark, J.B. Winsløws Vej 25, 5000 Odense, Denmark. hwulf@health.sdu.dk
Source
Immunobiology. 2013 May;218(5):712-7
Date
May-2013
Language
English
Publication Type
Article
Keywords
Aged
Aged, 80 and over
Biological Markers - blood
Body mass index
Denmark - epidemiology
Female
Health status
Humans
Incidence
Longitudinal Studies
Male
Mortality
Probability
Pulmonary Surfactant-Associated Protein D - blood
Risk factors
Smoking - mortality
Survival Analysis
Abstract
Surfactant protein D (SP-D) is produced in the lungs and additional mucosal surfaces. Systemic SP-D levels are previously associated to aging-related- and lifestyle-related disorders and predicts mortality in cardiovascular and lung diseases. However, the association between higher serum SP-D levels and mortality in the general population is unknown. We hypothesized that increased systemic levels of SP-D may be used as prognostic factor for assessing the mortality in the elderly.
SP-D serum levels were measured in 689 elderly subjects and mortality ratios were investigated after a 13-year follow-up period. Survival analysis showed that increasing quartiles of serum SP-D levels were associated to mortality in 70+ year old women (hazard ratio [HR], 1.29; 95% confidence interval [CI], 0.93-1.78; p = 0.032) adjusted for age, smoking and BMI. Women with SP-D levels above 2100 ng/ml had significantly increased mortality when compared to elderly women with SP-D levels equal to or below 2100 ng/ml (HR, 1.45; 95% CI, 1.12-1.88; p = 0.005). The likelihood that the female twin with the highest SP-D level died first increased with increasing SP-D levels (p = 0.031) - that is, the bigger intra-pair difference in SP-D level, the higher the probability that the twin with the highest measure died first (odds ratio [OR], 1.66; p = 0.047).
The study demonstrates that higher circulating SP-D levels are associated with increased mortality rate in elderly women in this population-based cohort study. SP-D may serve as a biomarker to track the cardio-pulmonary health status in elderly women.
PubMed ID
22999473 View in PubMed
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Data mining and multiparameter analysis of lung surfactant protein genes in bronchopulmonary dysplasia.

https://arctichealth.org/en/permalink/ahliterature58277
Source
Hum Mol Genet. 2004 Jun 1;13(11):1095-104
Publication Type
Article
Date
Jun-1-2004
Author
Meri Rova
Ritva Haataja
Riitta Marttila
Vesa Ollikainen
Outi Tammela
Mikko Hallman
Author Affiliation
Department of Paediatrics and Biocenter Oulu, University of Oulu, Oulu, Finland.
Source
Hum Mol Genet. 2004 Jun 1;13(11):1095-104
Date
Jun-1-2004
Language
English
Publication Type
Article
Keywords
Bronchopulmonary Dysplasia - genetics
Case-Control Studies
Computational Biology
DNA Fingerprinting
Gene Frequency
Genetic Predisposition to Disease
Genetic Screening
Humans
Infant
Infant, Newborn
Population - genetics
Pulmonary Surfactant-Associated Proteins - genetics
Research Support, Non-U.S. Gov't
Transcription Factors - genetics
Abstract
Bronchopulmonary dysplasia (BPD), the most common chronic lung disease in infancy, is influenced by a number of antenatal and postnatal risk factors and is mostly preceded by respiratory distress syndrome (RDS) in the newborn. Surfactant protein (SP-A, -B, -C and -D) gene variations may play a role in both BPD and RDS. An association study between these candidate genes and BPD was performed. A total of 365 preterm Finnish infants in a high-risk population with gestational age
PubMed ID
15102713 View in PubMed
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Degree of lung maturity determines the direction of the interleukin-1- induced effect on the expression of surfactant proteins.

https://arctichealth.org/en/permalink/ahliterature63986
Source
Am J Respir Cell Mol Biol. 2000 Mar;22(3):280-8
Publication Type
Article
Date
Mar-2000
Author
V. Glumoff
O. Väyrynen
T. Kangas
M. Hallman
Author Affiliation
Department of Pediatrics and Biocenter Oulu, University of Oulu, Oulu, Finland.
Source
Am J Respir Cell Mol Biol. 2000 Mar;22(3):280-8
Date
Mar-2000
Language
English
Publication Type
Article
Keywords
Amniotic Fluid - chemistry
Animals
Blotting, Western
Cycloheximide - pharmacology
Dactinomycin - pharmacology
Female
Fetus - chemistry - physiology
Gene Expression Regulation, Developmental - drug effects - physiology
Interleukin-1 - pharmacology
Lung - chemistry - growth & development - physiology
Organ Culture Techniques
Pregnancy
Protein Synthesis Inhibitors - pharmacology
Proteolipids - analysis - genetics
Pulmonary Surfactant-Associated Protein A
Pulmonary Surfactant-Associated Proteins
Pulmonary Surfactants - analysis - genetics
RNA, Messenger - analysis - genetics
Rabbits
Research Support, Non-U.S. Gov't
Abstract
Intra-amniotic interleukin (IL)-1 increases surfactant components in immature fetal lung, whereas high IL-1 after birth is associated with surfactant dysfunction. Our aim was to investigate whether the fetal age influences the responsiveness of surfactant proteins (SPs) to IL-1. Rabbit lung explants from fetuses at 19, 22, 27, and 30 d of gestation and 1-d-old newborns were cultured in serum-free medium in the presence of recombinant human (rh) IL-1alpha or vehicle. The influence of IL-1alpha on SP-A, -B, and -C messenger RNA (mRNA) content was dependent on the conceptional age. In very immature lung on Day 19, rhIL-1alpha (570 ng/ml for 20 h) increased SP-A, -B, and -C mRNA by 860+/-15%, 314+/-108%, and 64+/-17%, respectively. The increase in SP-A mRNA was evident within 4 to 6 h. IL-1alpha increased the SP-A concentration in alveolar epithelial cells and in the culture medium within 20 h. In contrast, at 27 to 30 d of gestation and in newborns, IL-1alpha decreased SP-C, -B, and -A mRNA by means of 64 to 67%, 48 to 59%, and 12 to 15%, respectively. SP-B protein decreased by 45 to 60%. The decrease in mRNA became evident within 8 to 12 h and was dependent on IL-1 concentration. On Day 27, IL-1alpha accelerated the degradation of SP-B mRNA in the presence of actinomycin D. IL-1 did not increase the degradation rate of SP-A mRNA unless both actinomycin D and cycloheximide were added to the explants. The present findings may explain some of the contrasting associations between inflammatory cytokines and lung diseases during the perinatal period. The determinants of the direction of the IL-1 effect on the expression of SPs remain to be identified.
PubMed ID
10696064 View in PubMed
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The effects of fluticasone with or without salmeterol on systemic biomarkers of inflammation in chronic obstructive pulmonary disease.

https://arctichealth.org/en/permalink/ahliterature158537
Source
Am J Respir Crit Care Med. 2008 Jun 1;177(11):1207-14
Publication Type
Article
Date
Jun-1-2008
Author
Don D Sin
S F Paul Man
Darcy D Marciniuk
Gordon Ford
Mark FitzGerald
Eric Wong
Ernest York
Rajesh R Mainra
Warren Ramesh
Lyle S Melenka
Eric Wilde
Robert L Cowie
Dave Williams
Wen Q Gan
Roxanne Rousseau
Author Affiliation
Department of Medicine, Respiratory Division, University of British Columbia, Vancouver, Canada.
Source
Am J Respir Crit Care Med. 2008 Jun 1;177(11):1207-14
Date
Jun-1-2008
Language
English
Publication Type
Article
Keywords
Administration, Inhalation
Adrenergic beta-Agonists - administration & dosage
Aged
Albuterol - administration & dosage - analogs & derivatives
Androstadienes - administration & dosage
Anti-Inflammatory Agents - administration & dosage
Biological Markers - metabolism
C-Reactive Protein - metabolism
Canada
Double-Blind Method
Drug Combinations
Female
Humans
Interleukin-6 - metabolism
Male
Middle Aged
Pulmonary Disease, Chronic Obstructive - drug therapy - metabolism - pathology
Pulmonary Surfactant-Associated Protein D - metabolism
Respiratory Function Tests
Treatment Outcome
Abstract
Small studies have suggested that inhaled corticosteroids can suppress systemic inflammation in chronic obstructive pulmonary disease (COPD).
To determine the effect of inhaled corticosteroids with or without long-acting beta(2)-adrenergic agonist on systemic biomarkers of inflammation.
We conducted a double-blind randomized placebo-controlled trial across 11 centers (n = 289 patients with FEV(1) of 47.8 +/- 16.2% of predicted) to compare the effects of inhaled fluticasone alone or in combination with salmeterol against placebo on circulating biomarkers of systemic inflammation over 4 weeks. The primary endpoint was C-reactive protein (CRP) level. Secondary molecules of interest were IL-6 and surfactant protein D (SP-D).
Neither fluticasone nor the combination of fluticasone/salmeterol had a significant effect on CRP or IL-6 levels. There was, however, a significant reduction in SP-D levels with fluticasone and fluticasone/salmeterol compared with placebo (P = 0.002). Health status also improved significantly in both the fluticasone and fluticasone/salmeterol groups compared with placebo, driven mostly by improvements in the symptom scores. Changes in the circulating SP-D levels were related to changes in health status scores. FEV(1) improved significantly only in the fluticasone/salmeterol group compared with placebo.
ICS in conjunction with long-acting beta(2)-adrenergic agonist do not reduce CRP or IL-6 levels in serum of patients with COPD over 4 weeks. They do, however, significantly reduce serum SP-D levels. These data suggest that these drugs reduce lung-specific but not generalized biomarkers of systemic inflammation in COPD.
Notes
Comment In: Am J Respir Crit Care Med. 2008 Jun 1;177(11):1177-818487618
Comment In: Am J Respir Crit Care Med. 2009 Jan 15;179(2):170; author reply 170-119119152
Comment In: Expert Opin Pharmacother. 2008 Dec;9(18):3271-319040347
PubMed ID
18310480 View in PubMed
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Genetic influences and neonatal lung disease.

https://arctichealth.org/en/permalink/ahliterature58414
Source
Semin Neonatol. 2003 Feb;8(1):19-27
Publication Type
Article
Date
Feb-2003
Author
Mikko Hallman
Ritva Haataja
Author Affiliation
Department of Pediatrics, University of Oulu, Kajaanintie 52A PL 5000, 90014, Oulu, Finland. mikko.hallman@oulu.fi
Source
Semin Neonatol. 2003 Feb;8(1):19-27
Date
Feb-2003
Language
English
Publication Type
Article
Keywords
Genetic Predisposition to Disease
Humans
Infant, Newborn
Mutation
Polymorphism, Genetic
Pulmonary Surfactant-Associated Protein A - genetics
Pulmonary Surfactant-Associated Protein B - genetics
Pulmonary Surfactant-Associated Proteins - genetics
Respiratory Distress Syndrome, Newborn - genetics
Abstract
Neonatal lung diseases may have a genetic background. The available studies mainly concentrate on surfactant proteins (SP-A, SP-B) and respiratory distress syndrome. Specific alleles of the SP-A and SP-B genes associate interactively with susceptibility to respiratory distress syndrome. This genetic impact on the condition is influenced by environmental, acquired and inherited factors. Other alleles and genotypes of SP-A and SP-D associate with severe respiratory infections in early infancy. Rare mutations causing an absence of the SP-B protein result in progressive respiratory failure. Dominant mutations of SP-C associate with chronic lung disease, with variable manifestations. The first steps towards unraveling the genetic network influencing the susceptibility to neonatal lung diseases are now being taken. Genes encoding multifunctional proteins in the distal lung are prime candidates for causing susceptibility to neonatal lung disease, including bronchopulmonary dysplasia.
PubMed ID
12667827 View in PubMed
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33 records – page 1 of 4.