Pulmonary Pharmacology &amp Therapeutics Journal Impact Factor & Information

Publisher: Elsevier

Journal description

Current impact factor: 2.57

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 2.57
2012 Impact Factor 2.543
2011 Impact Factor 2.8
2010 Impact Factor 2.093
2009 Impact Factor 2.024
2008 Impact Factor 2.283
2007 Impact Factor 2.56
2006 Impact Factor 2.769
2005 Impact Factor 1.577
2004 Impact Factor 1.974
2003 Impact Factor 1.879
2002 Impact Factor 1.953
2001 Impact Factor 1.488
2000 Impact Factor 1.094
1999 Impact Factor 0.622
1998 Impact Factor 0.882

Impact factor over time

Impact factor
Year

Additional details

5-year impact 2.33
Cited half-life 5.00
Immediacy index 0.43
Eigenfactor 0.01
Article influence 0.71
Other titles Pulmonary pharmacology & therapeutics (Online), Pulmonary pharmacology & therapeutics, Pulmonary pharmacology and therapeutics
ISSN 1522-9629
OCLC 38867290
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Elsevier

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Pre-print allowed on any website or open access repository
    • Voluntary deposit by author of authors post-print allowed on authors' personal website, arXiv.org or institutions open scholarly website including Institutional Repository, without embargo, where there is not a policy or mandate
    • Deposit due to Funding Body, Institutional and Governmental policy or mandate only allowed where separate agreement between repository and the publisher exists.
    • Permitted deposit due to Funding Body, Institutional and Governmental policy or mandate, may be required to comply with embargo periods of 12 months to 48 months .
    • Set statement to accompany deposit
    • Published source must be acknowledged
    • Must link to journal home page or articles' DOI
    • Publisher's version/PDF cannot be used
    • Articles in some journals can be made Open Access on payment of additional charge
    • NIH Authors articles will be submitted to PubMed Central after 12 months
    • Publisher last contacted on 18/10/2013
  • Classification
    ​ green

Publications in this journal

  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Increased oxidative stress is supposed to be involved in the etiology of idiopathic pulmonary fibrosis (IPF). It was reported that oxidative stress values measured by a spectrophotometric technique (d-ROMs test) were significantly higher in IPF patients than in controls, and were negatively correlated with Forced Vital Capacity (FVC) and Carbon Monoxide Diffusing Capacity (DLCO). However, the relationship between progression of IPF over time and change in serum oxidative stress marker remains unclarified. This study aimed to investigate the change in serum oxidative stress marker during progression of IPF. The levels of oxidative stress in blood samples of 43 treatment-naïve IPF patients were measured by the d-ROMs test. FVC and DLCO were measured concurrently. The changes in oxidative stress and pulmonary function were evaluated in 27 untreated patients 6 months later. Oxidative stress levels of 13 patients with acute exacerbation of IPF (AE-IPF) and 30 healthy controls were also evaluated. Oxidative stress values [median, interquartile range (IQR); Carratelli units (U.CARR)] were significantly higher in 43 IPF patients than in controls (366, 339 -443 vs. 289, 257-329, p<0.01) and were significantly increased 6 months later in 27 untreated patients (353, 311-398 at baseline to 385, 345-417 at follow-up, p<0.01). The increase in oxidative stress values (24.0, 6.0-49.0 U.CARR/6 months) was negatively correlated with baseline DLCO (rs=-0.44, p<0.05) and FVC changes after 6 months (rs=-0.54, p<0.01). Oxidative stress values were significantly higher in IPF patients with acute exacerbation than in those with stable disease (587, 523-667 vs. 366, 339-443 U.CARR, respectively; p<0.01). Serum oxidative stress values increased with disease progression in IPF patients. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 04/2015; 183. DOI:10.1016/j.pupt.2015.03.005
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The prostaglandin D2 (PGD2) receptor, CRTH2, plays a role in allergic airway inflammation. The efficacy of BI 671800, a CRTH2 antagonist, was assessed in 2 separate trials in patients with asthma, in either the absence or the presence of inhaled corticosteroid (ICS) therapy. In this study, BI 671800 (50, 200 or 400 mg) and fluticasone propionate (220 μg) all given twice daily (bid) were compared with bid placebo in symptomatic controller-naïve adults with asthma (Trial 1), and BI 671800 400 mg bid compared with montelukast 10 mg once daily (qd), and matching placebo bid, in patients with asthma receiving inhaled fluticasone (88 μg bid) (Trial 2). The primary endpoint in both trials was change from baseline in trough forced expiratory volume in 1 second (FEV1) percent predicted. After 6 weeks' treatment, adjusted mean treatment differences (SE) for the primary endpoint compared with placebo in Trial 1 were 3.08% (1·65%), 3.59% (1·60%) and 3.98% (1·64%) for BI 671800 50, 200 and 400 mg bid, respectively, and 8.62% (1·68%) for fluticasone 220 μg bid (p = 0·0311, p = 0·0126, p = 0·0078 and p < 0·0001, respectively). In Trial 2, adjusted mean FEV1 (SE) treatment differences compared with placebo were 3.87% (1·49%) for BI 671800 400 mg bid and 2.37% (1·57%) for montelukast (p = 0·0050 and p = 0·0657, respectively). These findings suggest that BI 671800 is associated with a small improvement in FEV1 in symptomatic controller-naïve asthma patients, and in patients on ICS. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 04/2015; 227. DOI:10.1016/j.pupt.2015.03.003
  • [Show abstract] [Hide abstract]
    ABSTRACT: Phosphodiesterase type-5 inhibitors (PDE-5 inhibitors) have been suggested as a first-line drug for treating pulmonary arterial hypertension (PAH). The aim of present meta-analysis was to fully evaluate the efficacy and safety of treating PAH with PDE-5 inhibitors, focusing on the improvement of 6-min walk distance (6MWD). Studies were identified from The Cochrane Library, EMBASE, and PUBMED databases. We calculated odds ratios (OR) for dichotomous data and weighted mean differences with 95% confidence intervals (CI) for continuous data. Six studies with a total of 1056 patients (729 patients in PDE-5 inhibitors treatment group and 327 patients in placebo group) were included. All-cause mortality rate in the control group and PDE-5 inhibitors group was 2.6% and 0.7%, respectively. In an average of 12.3-week follow-up, PDE-5 inhibitors treatment was associated with a 71 % reduction in mortality (OR 0.29; 95 %CI 0.07-1.15; P = 0.08), and increased 6MWD by 40.17m, improved NYHA functional class and hemodynamic parameters. As for monotherapy and combination therapy patients, 6MWD has improved by 48.94m and 21.75m, respectively. The results of present meta-analysis suggest that treatment with PDE-5 inhibitors improves the 6MWD, clinical symptoms, hemodynamic parameters, and a tendency of survival benefits. In patients treated with PDE-5 inhibitor monotherapy, the 6MWD significantly increased when compared to combination therapies. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 04/2015; DOI:10.1016/j.pupt.2015.03.002
  • [Show abstract] [Hide abstract]
    ABSTRACT: Tuberculosis (TB) is one of the deadliest infectious diseases and comprises a global public health concern because co-infection with Human immunodeficiency virus (HIV) and, in particular, the continuous isolation of new Multidrug-resistant strains (MDR), rendering the discovery of novel anti-TB agents a strategic priority. One of the most effective first-line mycobactericidal drugs is Isoniazid (INH). Previously, we reported in vitro anti-mycobacterial activity against sensitive and MDR Mycobacterium tuberculosis strains of a new oxadiazole obtained from the hybridization of INH and palmitic acid. The present study evaluated the therapeutic potential of liposomes including Phosphatidylcholine (PC) and L-α Phosphatidic acid (PA) or PC and Cholesterol (Chol) containing 4-(5-pentadecyl-1,3,4-oxadiazol-2-yl)pyridine in BALB/c male mice infected by intratracheal (i.t.) route with drug-sensitive or MDR M. tuberculosis.
    Pulmonary Pharmacology &amp Therapeutics 04/2015; DOI:10.1016/j.pupt.2015.03.004
  • [Show abstract] [Hide abstract]
    ABSTRACT: Idiopathic pulmonary fibrosis (IPF) is a progressive disease with a high mortality rate. Signalling pathways activated by several tyrosine kinase receptors are known to be involved in lung fibrosis, and this knowledge has led to the development of the triple tyrosine kinase inhibitor nintedanib, an inhibitor of vascular endothelial growth factor receptor (VEGFR), platelet-derived growth factor receptor (PDGFR) and fibroblast growth factor receptor (FGFR), for the treatment of IPF. Pulmonary surfactant protein D (SP-D), an important biomarker of IPF, reportedly attenuates bleomycin-induced pulmonary fibrosis in mice. In this study, we investigated whether nintedanib modulates SP-D expression in human lung epithelial (A549) cells using quantitative real-time reverse transcriptase polymerase chain reaction and western blotting. To investigate the mechanisms underlying the effects of nintedanib, we evaluated the phosphorylation of c-Jun N-terminal kinase (JNK) and its downstream target c-Jun. The effect of the JNK inhibitor SP600125 on c-Jun phosphorylation was also tested. Activation of activator protein-1 (AP-1) was examined using an enzyme-linked immunosorbent assay-based test, and cell proliferation assays were performed to estimate the effect of nintedanib on cell proliferation. Furthermore, we treated mice with nintedanib to examine its in vivo effect on SP-D levels in lungs. These experiments showed that nintedanib up-regulated SP-D messenger RNA expression in a dose-dependent manner at concentrations up to 5 μM, with significant SP-D induction observed at concentrations of 3 μM and 5 μM, in comparison with that observed in vehicle controls. Nintedanib stimulated a rapid increase in phosphorylated JNK in A549 cells within 30 min of treatment and stimulated c-Jun phosphorylation, which was inhibited by the JNK inhibitor SP600125. Additionally, nintedanib was found to activate AP-1. A549 cell proliferation was not affected by nintedanib at any of the tested concentrations. Moreover, blocking FGFR, PDGFR, and VEGFR function did not affect nintedanib-induced SP-D expression, suggesting that nintedanib mediates its effects through a mechanism that is distinct from its known role as a tyrosine kinase inhibitor. Nintedanib is also reported to inhibit Src kinase although pre-treatment of cells with a Src kinase inhibitor had no effect on nintedanib-induced SP-D expression. Increased expression of SFTPD mRNA and SP-D protein in the lungs of nintedanib-treated mice was also observed. In this work, we demonstrated that nintedanib up-regulated SP-D expression in A549 cells via the JNK-AP-1 pathway and did not affect cell proliferation. This is the first report describing SP-D induction by nintedanib. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 04/2015; DOI:10.1016/j.pupt.2015.03.001
  • [Show abstract] [Hide abstract]
    ABSTRACT: Geranylgeranylacetone (GGA) has been clinically used as an anti-ulcer drug. In the present study, we explored the protective effects of GGA on lung ischemia/reperfusion injury (IRI) and the underlying mechanism. The results demonstrated that GGA ameliorated the lung biochemical and histological alterations induced by IRI, which was reversed by HSP70 inhibition. To further explore the mechanism of GGA action, we focused on NF-kB and thioredoxin (Trx) redox system. It was shown that GGA induced the HSP70 and Trx-1 expression, NF-kB nuclear translocation and activated thioredoxin reductase (TrxR). The Trx-1 expression and TrxR activity was suppressed by HSP70 and NF-kB inhibition, while the nuclear NF-kB p65 expression was suppressed by HSP70 inhibitor. These results indicated that GGA may protect rat lung against IRI by HSP70 and Trx redox system, in which NF-kB pathway may be involved. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 03/2015; DOI:10.1016/j.pupt.2015.02.009
  • [Show abstract] [Hide abstract]
    ABSTRACT: Inhalation is the preferred route of drug administration in chronic respiratory diseases because it optimises delivery of the active compounds to the targeted site and minimises side effects from systemic distribution. The choice of a device should be made after careful evaluation of the patient's clinical condition (degree of airway obstruction, comorbidities), as well as their ability to coordinate the inhalation manoeuvre and to generate sufficient inspiratory flow. These patient factors must be aligned with the specific advantages and limitations of each inhaler when making this important choice. Finally, adherence to treatment is not the responsibility of the patient alone, but should be shared also by clinicians. Clinicians have access to a wide selection of pressurised metered dose inhalers (pMDIs) and dry powder inhalers (DPIs) that can be used effectively when matched to the needs of individual patients; this should be perceived as an opportunity rather than a limitation. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 02/2015; DOI:10.1016/j.pupt.2015.02.006
  • [Show abstract] [Hide abstract]
    ABSTRACT: Reduced innate immunity responses as well as reduced T regulatory activities characterise bronchial asthma. In this study the effect of budesonide on the expression of TLR4 and TLR2 in T regulatory lymphocyte sub-population was assessed. TLR4 and TLR2 expression in total peripheral blood mononuclear cells (PBMC), in CD4+/CD25+ and in CD4+/CD25-was evaluated, by flow cytometric analysis, in mild intermittent asthmatics (n=14) and in controls (n=11). The in vitro effects of budesonide in modulating: TLR4 and TLR2 expression in controls and in asthmatics; IL-10 expression and cytokine release (IL-6 and TNF-α selected by a multiplex assay) in asthmatics were also explored. TLR4 and TLR2 were reduced in total PBMC from asthmatics in comparison to PBMC from controls. CD4+CD25+ cells expressed at higher extent TLR2 and TLR4 in comparison to CD4+CD25-cells. Budesonide was able to increase the expression of TLR4, TLR2 and IL-10 in CD4+/CD25highly+ cells from asthmatics. TLR4 ligand, LPS induced Foxp3 expression. Budesonide was also able to reduce the release of IL-6 and TNF-α by PBMC of asthmatics. Budesonide potentiates the activity of Treg by increasing TLR4, TLR2 and IL-10 expression. This event is associated to the decreased release of IL-6 and ΤΝF-α in PBMC treated with budesonide. These findings shed light on new mechanisms by which corticosteroids, drugs widely used for the clinical management of bronchial asthma, control T lymphocyte activation. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 02/2015; DOI:10.1016/j.pupt.2015.02.003
  • [Show abstract] [Hide abstract]
    ABSTRACT: Chronic obstructive pulmonary disease (COPD) is characterized by neutrophil-dominated airway mucosal inflammation and elevated neutrophil counts in sputum and lung tissue. CXC chemokine receptor 2 (CXCR2) is predominantly expressed on neutrophils and mediates the migration of neutrophils to inflammatory sites. AZD5069 is a small molecule CXCR2 antagonist with the potential to inhibit neutrophil migration into the airways in patients with COPD. This 4-week, randomized, double-blind, placebo-controlled, parallel-group, multi-center, Phase IIa study evaluated the safety and tolerability of AZD5069 in patients with moderate-to-severe COPD (ClinicalTrials.gov identifier: NCT01233232). The pharmacokinetics and effect of AZD5069 on blood neutrophil counts were also assessed. Patients completed daily diary cards and attended weekly clinic visits for safety assessments. 87 patients (mean FEV1 56% pred; mean age 64 years; 69% male) were randomized to receive placebo (n=29), AZD5069 50 mg bid (n=30) or AZD5069 80 mg bid (n=28) for 4 weeks. AZD5069 was well tolerated with adverse events (AEs) reported in 9 (31%), 10 (33%) and 6 (21%) patients in the placebo, AZD5069 50 mg and AZD5069 80 mg groups, respectively. AEs were generally mild or moderate in severity. The incidence of infections, the most commonly reported AE, was similar across the three groups (17%, 17% and 11% of patients in the placebo, AZD5069 50 and 80 mg groups, respectively). Blood neutrophil counts decreased on average from baseline by 14-40% and 13-36% in the AZD5069 50 mg and 80 mg groups, respectively, and 4 patients discontinued from the study due to decreased neutrophil count, 3 in the AZD5069 50 mg group and 1 in the 80 mg group. The systemic exposure (AUC and Cmax) of AZD5069 increased less than in proportion to the dose and there was a large overlap in the individual exposures between the two dose levels. AZD5069 was well tolerated overall in those patients who completed study treatment, with no increase in infection rates in either dosage group compared with placebo. Further studies with AZD5069 appear to be warranted. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 02/2015; 31. DOI:10.1016/j.pupt.2015.02.001
  • [Show abstract] [Hide abstract]
    ABSTRACT: Cough is one of the most common reasons that patients seek medical attention. Cough guidelines from numerous countries and societies are available to assist the clinician to investigate and manage patients with cough. We review some of the recent progress in the field of cough that may lead to revision of these guidelines. In adults with chronic cough, new causes such as obstructive sleep apnoea have been identified. A new terminology, cough hypersensitivity syndrome (CHS), has been proposed for patients with chronic cough, which emphasises cough reflex hypersensitivity as a key feature. New therapeutic options are now available, particularly for patients with refractory or idiopathic chronic cough, which include gabapentin, speech pathology management and morphine. There has been great progress in the assessment of cough with the development of validated quality of life questionnaires and cough frequency monitoring tools. In children, common aetiologies differ from adults and those managed according to guidelines have better outcomes compared to usual care. New diagnostic entities such as protracted bacterial bronchitis have been described. Paediatric-specific cough assessment tools such as the Parent/Child Quality of Life Questionnaire will help improve the assessment of patients. Further research is necessary to improve the evidence base for future clinical guideline recommendations. Guidelines in future should also aim to reach a wider audience that includes primary care physicians, non-specialists and patients. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 02/2015; DOI:10.1016/j.pupt.2015.01.007
  • Pulmonary Pharmacology &amp Therapeutics 02/2015; 31. DOI:10.1016/j.pupt.2015.01.003
  • [Show abstract] [Hide abstract]
    ABSTRACT: To determine the effects of montelukast added to maintenance inhaled steroids (ICS) therapy during the school year in children with stable asthma on the ICS use, frequency of exacerbations, lung function, asthma symptoms, fractional exhaled nitric oxide (FeNO) level and exercise-induced bronchoconstriction (EIB). Seventy six asthmatic children aged 6-14 years, allergic to house dust mites were randomized to a double-blinded trial comparing montelukast therapy to a matching placebo. We studied following end-points: the reduction in the ICS dose, the frequency of exacerbations, lung function, asthma control test score, and the change from baseline in FEV1 during a standardized exercise treadmill challenge. ICS dose was adjusted in a stepwise fashion to determine the lowest dose necessary to control asthma symptoms. We showed that children with baseline value of FeNO above 31 ppb and well controlled asthma symptoms on low doses of ICS, benefit the most from additive therapy with montelukast; their cumulative ICS dose is lower than in children treated with ICS only. Also, the addition of montelukast to regular treatment in asthmatic children resulted in a significant reduction in the frequency of exacerbations and EIB protection. It is reasonable to add montelukast to ICS therapy in asthmatic children during the school year, to lower cumulative ICS dose in children with well controlled asthma symptoms, as well as to reduce number of exacerbations, and to achieve better control of EIB. NCT01266772. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 01/2015; 31. DOI:10.1016/j.pupt.2015.01.004
  • [Show abstract] [Hide abstract]
    ABSTRACT: Randomized clinical trials (RCTs) are the gold standard for the assessment of any therapeutic intervention. Real-life (R-L) studies are needed to verify the provided results beyond the experimental setting. This review aims at comparing RCTs and R-L studies on omalizumab in adult severe allergic asthma, in order to highlight the concurring results and the discordant/missing data. The results of a selective literature research, including "omalizumab, controlled studies, randomized trial, real-life studies" as key words are discussed. Though some similarities between RCTs and R-L studies strengthen omalizumab efficacy and safety outcomes, significant differences concerning study population features, follow-up duration, local adverse events and drop-out rate for treatment inefficacy emerge between the two study categories. Furthermore the comparative analysis between RCTs and R-L studies highlights the need for further research, concerning in particular long-term effects of omalizumab and its impact on asthma comorbidities. Copyright © 2015. Published by Elsevier Ltd.
    Pulmonary Pharmacology &amp Therapeutics 01/2015; 31. DOI:10.1016/j.pupt.2015.01.006