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        <title>BMC Pulmonary Medicine - Latest Articles</title>
        <link>http://www.biomedcentral.com/bmcpulmmed/</link>
        <description>The latest research articles published by BMC Pulmonary Medicine</description>
        <dc:date>2012-05-31T00:00:00Z</dc:date>
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                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2466/12/22" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2466/12/21" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2466/12/20" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2466/12/19" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2466/12/18" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2466/12/17" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2466/12/16" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2466/12/15" />
                                <rdf:li rdf:resource="http://www.biomedcentral.com/1471-2466/12/14" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2466/12/22">
        <title>Determinants of high-sensitivity cardiac troponin T during acute exacerbation of chronic obstructive pulmonary disease: a prospective cohort study</title>
        <description>Background:
A high-sensitivity cardiac troponin T (hs-cTnT) concentration above the 99th percentile (i.e. 14 ng/L) is common during Acute Exacerbation of Chronic Obstructive Pulmonary Disease (AECOPD) and associated with increased mortality. The objective of the study was to identify factors associated with hs-cTnT levels during AECOPD.
Methods:
We included 99 patients with AECOPD on admission. As 41 patients had one or more repeat admissions, there were 202 observations in the final analysis. We recorded clinical and biochemical data, medication, spirometry, chest radiographs, and ECGs. The data were analysed for cross-sectional and longitudinal associations using ordinary least square as well as linear mixed models with the natural logarithm of hs-cTnT as the dependent variable.
Results:
Mean age at inclusion was 71.5 years, mean FEV1/FVC was 45%, and median hs-cTnT was 27.0 ng/L. In a multivariable model there was a 24% relative increase in hs-cTnT per 10 years increase in age (p &lt; 0.0001), a 6% increase per 10 mumol/L increase in creatinine (p = 0.037), and a 2% increase per month after enrollment (p = 0.046). Similarly, the ratios of hs-cTnT between patients with and without tachycardia (heart rate [greater than or equal to]100/min) and with and without history of arterial hypertension were 1.25 (p = 0.042) and 1.44 (p = 0.034), respectively. We found no significant association between arterial hypoxemia and elevated hs-cTnT.
Conclusion:
Age, arterial hypertension, tachycardia, and serum creatinine are independently associated with the level of hs-cTnT on admission for AECOPD.</description>
        <link>http://www.biomedcentral.com/1471-2466/12/22</link>
                <dc:creator>Arne Didrik Høiseth</dc:creator>
                <dc:creator>Torbjørn Omland</dc:creator>
                <dc:creator>Tor-Arne Hagve</dc:creator>
                <dc:creator>Pål Brekke</dc:creator>
                <dc:creator>Vidar Søyseth</dc:creator>
                <dc:source>BMC Pulmonary Medicine 2012, null:22</dc:source>
        <dc:date>2012-05-31T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2466-12-22</dc:identifier>
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                <prism:publicationName>BMC Pulmonary Medicine</prism:publicationName>
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        <prism:startingPage>22</prism:startingPage>
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        <item rdf:about="http://www.biomedcentral.com/1471-2466/12/21">
        <title>Predictors for length of hospital stay in patients with community-acquired Pneumonia: 
Results from a Swiss Multicenter study
</title>
        <description>Background:
Length of hospital stay (LOS) in patients with community-acquired pneumonia (CAP) is variable and directly related to medical costs. Accurate estimation of LOS on admission and during follow-up may result in earlier and more efficient discharge strategies.
Methods:
This is a prospective multicenter study including patients in emergency departments of 6 tertiary care hospitals in Switzerland between October 2006 and March 2008. Medical history, clinical data at presentation and health care insurance class were collected. We calculated univariate and multivariate cox regression models to assess the association of different characteristics with LOS. In a split sample analysis, we created two LOS prediction rules, first including only admission data, and second including also additional inpatient information.
Results:
The mean LOS in the 875 included CAP patients was 9.8 days (95%CI 9.3-10.4). Older age, respiratory rate &gt;20pm, nursing home residence, chronic pulmonary disease, diabetes, multilobar CAP and the pneumonia severity index class were independently associated with longer LOS in the admission prediction model. When also considering follow-up information, low albumin levels, ICU transfer and development of CAP-associated complications were additional independent risk factors for prolonged LOS. Both weighted clinical prediction rules based on these factors showed a high separation of patients in Kaplan Meier Curves (p logrank &lt;0.001 and &lt;0.001) and a good calibration when comparing predicted and observed results.
Conclusions:
Within this study we identified different baseline and follow-up characteristics to be strong and independent predictors for LOS. If validated in future studies, these factors may help to optimize discharge strategies and thus shorten LOS in CAP patients.</description>
        <link>http://www.biomedcentral.com/1471-2466/12/21</link>
                <dc:creator>Isabelle Suter-Widmer</dc:creator>
                <dc:creator>Mirjam Christ-Crain</dc:creator>
                <dc:creator>Werner Zimmerli</dc:creator>
                <dc:creator>Werner Albrich</dc:creator>
                <dc:creator>Beat Mueller</dc:creator>
                <dc:creator>Philipp Schuetz</dc:creator>
                <dc:source>BMC Pulmonary Medicine 2012, null:21</dc:source>
        <dc:date>2012-05-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2466-12-21</dc:identifier>
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                <prism:publicationName>BMC Pulmonary Medicine</prism:publicationName>
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        <prism:startingPage>21</prism:startingPage>
        <prism:publicationDate>2012-05-20T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.biomedcentral.com/1471-2466/12/20">
        <title>Assessing health status in COPD. A head-to-head
comparison between the COPD assessment test
(CAT) and the clinical COPD questionnaire (CCQ)</title>
        <description>Background:
Health status provides valuable information, complementary to spirometry and improvementof health status has become an important treatment goal in COPD management. Wecompared the usefulness and validity of the COPD Assessment Test (CAT) and the ClinicalCOPD Questionnaire (CCQ), two simple questionnaires, in comparison with the St. GeorgeRespiratory Questionnaire (SGRQ).
Methods:
We administered the CAT, CCQ and SGRQ in patients with COPD stage I-IV during threevisits. Spirometry, 6 MWT, MRC scale, BODE index, and patients perspectives onquestionnaires were recorded in all visits. Standard Error of Measurement (SEM) was used tocalculate the Minimal Clinical Important Difference (MCID) of all questionnaires.
Results:
We enrolled 90 COPD patients. Cronbach&apos;s alpha for both CAT and CCQ was high (0.86 and0.89, respectively). Patients with severe COPD reported worse health status compared tomilder subgroups. CAT and CCQ correlated significantly (rho =0.64, p &lt; 0.01) and both withthe SGRQ (rho = 0.65; CAT and rho = 0.77; CCQ, p &lt; 0.01). Both questionnaires exhibited aweak correlation with lung function (rho = 0.35;CAT and rho = 0.41; CCQ, p &lt; 0.01). Theirreproducibility was high; CAT: ICC = 0.94 (CI 0.92-0.96), total CCQ ICC = 0.95 (0.92-0.96)and SGRQ = 0.97 (CI 0.95-0.98). The MCID calculated using the SEM method showedresults similar to previous studies of 3.76 for the CAT, 0.41 for the CCQ and 4.84 for SGRQ.Patients suggested both CAT and CCQ as easier tools than SGRQ in terms of complexity andtime considerations. More than half of patients preferred CCQ instead of CAT.
Conclusions:
The CAT and CCQ have similar psychometric properties with a slight advantage for CCQbased mainly on patients&apos; preference and are both valid and reliable questionnaires to assesshealth status in COPD patients.</description>
        <link>http://www.biomedcentral.com/1471-2466/12/20</link>
                <dc:creator>Ioanna Tsiligianni</dc:creator>
                <dc:creator>Thys van der Molen</dc:creator>
                <dc:creator>Despoina Moraitaki</dc:creator>
                <dc:creator>Ilaine Lopez</dc:creator>
                <dc:creator>Janwillem Kocks</dc:creator>
                <dc:creator>Konstantinos Karagiannis</dc:creator>
                <dc:creator>Nikolaos Siafakas</dc:creator>
                <dc:creator>Nikolaos Tzanakis</dc:creator>
                <dc:source>BMC Pulmonary Medicine 2012, null:20</dc:source>
        <dc:date>2012-05-20T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2466-12-20</dc:identifier>
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        <prism:startingPage>20</prism:startingPage>
        <prism:publicationDate>2012-05-20T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2466/12/19">
        <title>Increased hospitalizations among sarcoidosis patients from 1998 to 2008: a population-based cohort study</title>
        <description>Background:
Diagnostic and treatment approaches for sarcoidosis have changed dramatically over the past decade. Yet, the most recent reports of trends in hospitalizations of sarcoidosis patients are over ten years old. The objectives of this study were to determine the incidence of sarcoidosis among hospitalized patients and to analyze recent trends and seasonality of hospitalizations in sarcoidosis patients.
Methods:
We performed a retrospective cohort study of the Nationwide Inpatient Sample from 1998 through 2008. We identified all hospitalizations with a primary or secondary diagnosis of sarcoidosis (ICD-9-CM code 135). Incidence was modeled as a seasonal time series about a linear trend.
Results:
Time series analysis of the monthly number of hospitalizations revealed a distinct positive linear trend. Over the study period, the number of hospitalized patients with sarcoidosis increased from 37,516 to 70,947 cases. Trends were most pronounced in patients older than 55 years (p &lt; 0.0001), African Americans (p &lt; 0.0001), females (p = 0.0289), and non-Medicaid populations (p &lt; 0.0001). Hospitalizations are seasonal with highest incidence in January through March.
Conclusions:
Hospitalizations among sarcoidosis patients have almost doubled during the past decade, with disproportionate rate increases in African Americans, women, and older patients. The rate also increases among patients with insurance other than Medicaid. This study indicates the need for heightened surveillance of sarcoidosis patients given the unknown consequences of evolving treatment approaches. Our results point to a need for research investigating risk factors for hospitalization, including medications, co-morbidities, demographics, and socioeconomic status.</description>
        <link>http://www.biomedcentral.com/1471-2466/12/19</link>
                <dc:creator>Alicia Gerke</dc:creator>
                <dc:creator>Ming Yang</dc:creator>
                <dc:creator>Fan Tang</dc:creator>
                <dc:creator>Joseph Cavanaugh</dc:creator>
                <dc:creator>Philip Polgreen</dc:creator>
                <dc:source>BMC Pulmonary Medicine 2012, null:19</dc:source>
        <dc:date>2012-05-14T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2466-12-19</dc:identifier>
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                <prism:publicationName>BMC Pulmonary Medicine</prism:publicationName>
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        <prism:startingPage>19</prism:startingPage>
        <prism:publicationDate>2012-05-14T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2466/12/18">
        <title>Comparison of human lung tissue mass measurements from Ex Vivo lungs and high resolution CT software analysis</title>
        <description>Background:
Quantification of lung tissue via analysis of computed tomography (CT) scans is increasingly common for monitoring disease progression and for planning of therapeutic interventions. The current study evaluates the quantification of human lung tissue mass by software analysis of a CT to physical tissue mass measurements.
Methods:
Twenty-two ex vivo lungs were scanned by CT and analyzed by commercially available software. The lungs were then dissected into lobes and sublobar segments and weighed. Because sublobar boundaries are not visually apparent, a novel technique of defining sublobar segments in ex vivo tissue was developed. The tissue masses were then compared to measurements by the software analysis.
Results:
Both emphysematous (n = 14) and non-emphysematous (n = 8) bilateral lungs were evaluated. Masses (Mean +/- SD) as measured by dissection were 651 +/- 171 g for en bloc lungs, 126 +/- 60 g for lobar segments, and 46 +/- 23 g for sublobar segments. Masses as measured by software analysis were 598 +/- 159 g for en bloc lungs, 120 +/- 58 g for lobar segments, and 45 +/- 23 g for sublobar segments. Correlations between measurement methods was above 0.9 for each segmentation level. The Bland-Altman analysis found limits of agreement at the lung, lobe and sublobar levels to be 13.11% to 4.22%, -13.59% to 4.24%, and -45.85% to 44.56%.
Conclusion:
The degree of concordance between the software mass quantification to physical mass measurements provides substantial evidence that the software method represents an appropriate non-invasive means to determine lung tissue mass.</description>
        <link>http://www.biomedcentral.com/1471-2466/12/18</link>
                <dc:creator>Erik Henne</dc:creator>
                <dc:creator>Joseph Anderson</dc:creator>
                <dc:creator>Norma Lowe</dc:creator>
                <dc:creator>Steven Kesten</dc:creator>
                <dc:source>BMC Pulmonary Medicine 2012, null:18</dc:source>
        <dc:date>2012-05-14T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2466-12-18</dc:identifier>
                                <prism:require>/content/figures/1471-2466-12-18-toc.gif</prism:require>
                <prism:publicationName>BMC Pulmonary Medicine</prism:publicationName>
        <prism:issn>1471-2466</prism:issn>
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        <prism:startingPage>18</prism:startingPage>
        <prism:publicationDate>2012-05-14T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>PDF</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2466/12/17">
        <title>Prevalence of asthma and other allergic conditions in Colombia 2009-2010: a cross-sectional study</title>
        <description>Background:
While it is suggested that the prevalence of asthma in developed countries may have stabilized, this is not clear in currently developing countries. Current available information for both adults and children simultaneously on the burden and impact of allergic conditions in Colombia and in many Latin American countries is limited. The objectives of this study were to estimate the prevalence for asthma, allergic rhinitis (AR), atopic eczema (AE), and atopy in six colombian cities; to quantify costs to the patient and her/his family; and to determine levels of Immunoglobulin E (IgE) in asthmatic and healthy subjects
Methods:
We conducted a cross-sectional, population-based study in six cities during the academic year 2009-2010. We used a school-based design for subjects between 5-17 years old. We carried out a community-based strategy for subjects between 1-4 years old and adults between 18-59 years old. Serum samples for total and antigen-specific (IgE) levels were collected using a population-based, nested, case-control design.
Results:
We obtained information on 5978 subjects. The largest sample of subjects was collected in Bogota (2392). The current prevalence of asthma symptoms was 12% (95% CI, 10.5-13.7), with 43% (95% CI, 36.3-49.2) reporting having required an emergency department visit or hospitalization in the past 12 months. Physician diagnosed asthma was 7% (95% CI, 6.1-8.0). The current prevalence of AR symptoms was 32% (95% CI, 29.5-33.9), and of AE symptoms was 14% (95% CI, 12.5-15.3). We collected blood samples from 855 subjects; 60.2% of asthmatics and 40.6% of controls could be classified as atopic.
Conclusions:
In Colombia, symptom prevalence for asthma, AR and AE, as well as levels of atopy, are substantial. Specifically for asthma, symptom severity and absence from work or study due to symptoms are important. These primary care sensitive conditions remain an unmet public health burden in developing countries such as Colombia.</description>
        <link>http://www.biomedcentral.com/1471-2466/12/17</link>
                <dc:creator>Rodolfo Dennis</dc:creator>
                <dc:creator>Luis Caraballo</dc:creator>
                <dc:creator>Elizabeth García</dc:creator>
                <dc:creator>María Rojas</dc:creator>
                <dc:creator>Martín Rondón</dc:creator>
                <dc:creator>Adriana Pérez</dc:creator>
                <dc:creator>Gustavo Aristizabal</dc:creator>
                <dc:creator>Augusto Peñaranda</dc:creator>
                <dc:creator>Ana Barragan</dc:creator>
                <dc:creator>Velky Ahumada</dc:creator>
                <dc:creator>Silvia Jimenez</dc:creator>
                <dc:source>BMC Pulmonary Medicine 2012, null:17</dc:source>
        <dc:date>2012-05-02T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2466-12-17</dc:identifier>
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        <item rdf:about="http://www.biomedcentral.com/1471-2466/12/16">
        <title>Non drowsy obstructive sleep apnea as a potential cause of resistant hypertension: a case report</title>
        <description>Background:
Obstructive sleep apnea (OSA) and arterial hypertension (AH) are common and underrecognized medical disorders. OSA is a potential risk factor for the development of AH and/or may act as a factor complicating AH management. The symptoms of excessive daytime sleepiness (EDS) are considered essential for the initiation of continuous positive airway pressure (CPAP) therapy, which is a first line treatment of OSA. The medical literature and practice is controversial about the treatment of people with asymptomatic OSA. Thus, OSA patients without EDS may be left at increased cardiovascular risk.Case presentationThe report presents a case of 42year old Asian woman with symptoms of heart failure and angina like chest pain upon admission. She didnt experience symptoms of EDS, and the Epworth Sleepiness Scale was seven points. Snoring was reported on direct questioning. The patient had prior medical history of three unsuccessful pregnancies complicated by gestational AH and preeclampsia with C-section during the last pregnancy. The admission blood pressure (BP) was 200/120mm Hg. The patients treatment regimen consisted of five hypotensive medications including diuretic. However, a target BP wasnt achieved in about one and half month. The patient was offered to undergo a polysomnography (PSG) study, which she rejected. One month after discharge the PSG study was done, and this showed an apnea-hypopnea index (AHI) of 46 events per hour. CPAP therapy was initiated with a pressure of 11H20cm. After 2months of compliant CPAP use, adherence to pharmacologic regimen and lifestyle modifications the patients BP decreased to 134/82mm Hg.
Conclusions:
OSA and AH are common and often underdiagnosed medical disorders independently imposing excessive cardiovascular risk on a diseased subject. When two conditions coexist the cardiovascular risk is likely much greater. This case highlights a possible clinical phenotype of OSA without EDS and its association with resistant AH. Most importantly a good hypotensive response to medical treatment in tandem with CPAP therapy was achieved in this patient. Thus, it is reasonable to include OSA in the differential list of resistant AH, even if EDS is not clinically obvious.</description>
        <link>http://www.biomedcentral.com/1471-2466/12/16</link>
                <dc:creator>Aibek Mirrakhimov</dc:creator>
                <dc:source>BMC Pulmonary Medicine 2012, null:16</dc:source>
        <dc:date>2012-04-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2466-12-16</dc:identifier>
                                <prism:require>/content/figures/1471-2466-12-16-toc.gif</prism:require>
                <prism:publicationName>BMC Pulmonary Medicine</prism:publicationName>
        <prism:issn>1471-2466</prism:issn>
        <prism:volume>${item.volume}</prism:volume>
        <prism:startingPage>16</prism:startingPage>
        <prism:publicationDate>2012-04-25T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.biomedcentral.com/1471-2466/12/15">
        <title>The surfactant protein C mutation A116D alters cellular processing, stress tolerance, surfactant lipid composition, and immune cell activation</title>
        <description>Background:
Surfactant protein C (SP-C) is important for the function of pulmonary surfactant. Heterozygous mutations in SFTPC, the gene encoding SP-C, cause sporadic and familial interstitial lung disease (ILD) in children and adults. Mutations mapping to the BRICHOS domain located within the SP-C proprotein result in perinuclear aggregation of the proprotein. In this study, we investigated the effects of the mutation A116D in the BRICHOS domain of SP-C on cellular homeostasis. We also evaluated the ability of drugs currently used in ILD therapy to counteract these effects.
Methods:
SP-CA116D was expressed in MLE-12 alveolar epithelial cells. We assessed in vitro the consequences for cellular homeostasis, immune response and effects of azathioprine, hydroxychloroquine, methylprednisolone and cyclophosphamide.
Results:
Stable expression of SP-CA116D in MLE-12 alveolar epithelial cells resulted in increased intracellular accumulation of proSP-C processing intermediates. SP-CA116D expression further led to reduced cell viability and increased levels of the chaperones Hsp90, Hsp70, calreticulin and calnexin. Lipid analysis revealed decreased intracellular levels of phosphatidylcholine (PC) and increased lyso-PC levels. Treatment with methylprednisolone or hydroxychloroquine partially restored these lipid alterations. Furthermore, SP-CA116D cells secreted soluble factors into the medium that modulated surface expression of CCR2 or CXCR1 receptors on CD4+ lymphocytes and neutrophils, suggesting a direct paracrine effect of SP-CA116D on neighboring cells in the alveolar space.
Conclusions:
We show that the A116D mutation leads to impaired processing of proSP-C in alveolar epithelial cells, alters cell viability and lipid composition, and also activates cells of the immune system. In addition, we show that some of the effects of the mutation on cellular homeostasis can be antagonized by application of pharmaceuticals commonly applied in ILD therapy. Our findings shed new light on the pathomechanisms underlying SP-C deficiency associated ILD and provide insight into the mechanisms by which drugs currently used in ILD therapy act.</description>
        <link>http://www.biomedcentral.com/1471-2466/12/15</link>
                <dc:creator>Ralf Zarbock</dc:creator>
                <dc:creator>Markus Woischnik</dc:creator>
                <dc:creator>Christiane Sparr</dc:creator>
                <dc:creator>Tobias Thurm</dc:creator>
                <dc:creator>Suncana Kern</dc:creator>
                <dc:creator>Eva Kaltenborn</dc:creator>
                <dc:creator>Andreas Hector</dc:creator>
                <dc:creator>Dominik Hartl</dc:creator>
                <dc:creator>Gerhard Liebisch</dc:creator>
                <dc:creator>Gerd Schmitz</dc:creator>
                <dc:creator>Matthias Griese</dc:creator>
                <dc:source>BMC Pulmonary Medicine 2012, null:15</dc:source>
        <dc:date>2012-03-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2466-12-15</dc:identifier>
                            <dc:title>Effects of SP-C mutation in vitro</dc:title>
                            <dc:description>Mutations to the gene encoding Surfactant protein C (SP-C) are implicated in interstitial lung disease; the A116D mutation impairs processing of proSP-C in vitro, leading to altered cell viability, surfactant lipid composition and activation of immune cells.</dc:description>
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        <item rdf:about="http://www.biomedcentral.com/1471-2466/12/14">
        <title>Utilization and responsiveness of the asthma control test (ACT) at the initiation of therapy for patients with asthma: A randomized controlled trial</title>
        <description>Background:
The aim of this study was to assess the responsiveness of the asthma control test (ACT) to detect changes at the initiation of therapy and its utilization in the initiation of asthma treatment.
Methods:
This study was designed as a randomized clinical trial conducted in a primary care setting. The subjects were asthma patients who had not received controller therapy for at least two months. The patients were randomized into two groups: The Saudi Initiative for Asthma (SINA) group and the Global Initiative for Asthma (GINA) group. Treatment in the SINA group was initiated at step1 when the ACT scores &#8805; 20, step 2 when the score between16-19, and step 3 when the score &lt; 16 began at step 3. The GINA group patients were started on step 2 when they had persistent asthma symptoms or step 3 when they had severely uncontrolled disease.
Results:
Forty-five patients were analyzed in each group. The improvement in ACT score after treatment initiation was significantly higher when the SINA approach was used (2.9 in the SINA group compared to 1.7 in the GINA group (p = 0.04)). The improvement in FEV1 was 5.8% in the SINA group compared to 3.4% in the GINA group (p = 0.46). The number of patients who achieved asthma control at the follow-up visit and required no treatment adjustment was 33 (73.3%) in the SINA group and 27 (60%) in the GINA group (p = 0.0125).
Conclusion:
The ACT was responsive to change at the initiation of asthma treatment and was useful for the initiation of asthma treatment.Trial Registration numberISRCTN31998214</description>
        <link>http://www.biomedcentral.com/1471-2466/12/14</link>
                <dc:creator>Mohamed Al-Moamary</dc:creator>
                <dc:creator>Ahmed Al-Kordi</dc:creator>
                <dc:creator>Mohamed Al Ghobain</dc:creator>
                <dc:creator>Hani Tamim</dc:creator>
                <dc:source>BMC Pulmonary Medicine 2012, null:14</dc:source>
        <dc:date>2012-03-26T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2466-12-14</dc:identifier>
                            <dc:title>Utilisation of the ACT in primary care</dc:title>
                            <dc:description>In a primary care setting, the Asthma Control Test (ACT) is responsive to changes in lung function at the initiation of asthma treatment, and may be useful for the initiation of asthma treatment.</dc:description>
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                <prism:publicationName>BMC Pulmonary Medicine</prism:publicationName>
        <prism:issn>1471-2466</prism:issn>
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        <prism:startingPage>14</prism:startingPage>
        <prism:publicationDate>2012-03-26T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.biomedcentral.com/1471-2466/12/12">
        <title>Lung function decline in relation to diagnostic criteria for airflow obstruction in respiratory symptomatic subjects</title>
        <description>Background:
Current COPD guidelines advocate a fixed &lt; 0.70 FEV1/FVC cutpoint to define airflow obstruction. We compared rate of lung function decline in respiratory symptomatic 40+ subjects who were &apos;obstructive&apos; or &apos;non-obstructive&apos; according to the fixed and/or age and gender specific lower limit of normal (LLN) FEV1/FVC cutpoints.
Methods:
We studied 3,324 respiratory symptomatic subjects referred to primary care diagnostic centres for spirometry. The cohort was subdivided into four categories based on presence or absence of obstruction according to the fixed and LLN FEV1/FVC cutpoints. Postbronchodilator FEV1 decline served as primary outcome to compare subjects between the respective categories.
Results:
918 subjects were obstructive according to the fixed FEV1/FVC cutpoint; 389 (42%) of them were non-obstructive according to the LLN cutpoint. In smokers, postbronchodilator FEV1 decline was 21 (SE 3) ml/year in those non-obstructive according to both cutpoints, 21 (7) ml/year in those obstructive according to the fixed but not according to the LLN cutpoint, and 50 (5) ml/year in those obstructive according to both cutpoints (p = 0.004).
Conclusion:
This study showed that respiratory symptomatic 40+ smokers and non-smokers who show FEV1/FVC values below the fixed 0.70 cutpoint but above their age/gender specific LLN value did not show accelerated FEV1 decline, in contrast with those showing FEV1/FVC values below their LLN cutpoint.</description>
        <link>http://www.biomedcentral.com/1471-2466/12/12</link>
                <dc:creator>Reinier Akkermans</dc:creator>
                <dc:creator>Marvin Berrevoets</dc:creator>
                <dc:creator>Ivo Smeele</dc:creator>
                <dc:creator>Annelies Lucas</dc:creator>
                <dc:creator>Bart Thoonen</dc:creator>
                <dc:creator>Joke Grootens-Stekelenburg</dc:creator>
                <dc:creator>Yvonne Heijdra</dc:creator>
                <dc:creator>Chris van Weel</dc:creator>
                <dc:creator>Tjard Schermer</dc:creator>
                <dc:source>BMC Pulmonary Medicine 2012, null:12</dc:source>
        <dc:date>2012-03-22T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1471-2466-12-12</dc:identifier>
                                <prism:require>/content/figures/1471-2466-12-12-toc.gif</prism:require>
                <prism:publicationName>BMC Pulmonary Medicine</prism:publicationName>
        <prism:issn>1471-2466</prism:issn>
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        <prism:startingPage>12</prism:startingPage>
        <prism:publicationDate>2012-03-22T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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