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Search Results: 1 - 10 of 221589 matches for " Jan L?tvall "
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Welcome to Clinical and Translational Allergy
Jan Ltvall, Victoria Cardona
Clinical and Translational Allergy , 2011, DOI: 10.1186/2045-7022-1-1
Abstract: The aim of CTA is to provide a platform for the dissemination of original allergy-immunology research, exciting reviews as well as EAACI-developed position papers. Today, at the launch of the journal, one position paper and three exciting reviews are published, and several recently submitted original research papers are under consideration. Firstly, a very long-term effort in developing an EAACI position paper on diagnostic tools in rhinology is published in CTA [1]. This publication has taken several years to develop, and is the most comprehensive publication on the topic to date. Three review articles are discussing different interesting aspects and theories in allergy. One, by Woo and Bahna [2], discusses the different types of reactions that can be induced by shellfish ingestion, and the clinical misinterpretations that can evolve. Another review article, by Chaudhary and Marr [3], considers the impact that Aspergillus Fumigatus can have on respiratory disease. Lastly, an overview article by Mattila and colleagues [4], examines the role of respiratory and conjunctival epithelium in airway allergic disease. These fundamentally different topics not only contribute to the literature, but also illustrate the width of topics that CTA will publish. Beyond clinical experimental research and epidemiology, CTA will certainly also accept any studies using animal models of any allergic process, and immunological research related to allergic disease.The field of allergy concerns the most common group of diseases globally. Allergic diseases have grown rapidly in prevalence in the industrialized world, and are now rapidly growing in developing countries. It is considered that diseases of the immune system, such as allergic diseases, are best explained through a clear grasp of normal immune mechanisms and the ways by which these processes become dysfunctional. This is one of the explanations of selecting the name of the journal, including the key word "translational", since it
Comparing the effects of two inhaled glucocorticoids on allergen-induced bronchoconstriction and markers of systemic effects, a randomised cross-over double-blind study
Jan Ltvall, Mona Palmqvist, Peter Arvidsson
Clinical and Translational Allergy , 2011, DOI: 10.1186/2045-7022-1-12
Abstract: Twelve patients with documented early and late asthmatic responses (EAR and LAR) to inhaled allergen at a screening visit were randomized in a double-blind fashion to treatment with mometasone (200 μg × 2 or 400 μg × 2), budesonide (400 μg × 2) or placebo in a double-blind crossover fashion for a period of seven days. Challenge with the total allergen dose causing both an EAR and LAR was given on the last day of treatment taken in the morning. Lung function was assessed using FEV1, and systemic glucocorticoid activity was quantified using 24 h urinary cortisol.Mometasone and budesonide attenuate both EAR and LAR to allergen to a similar degree. No significant dose-related effects on the lung function parameters were observed. Both treatments reduced the relative amount of sputum eosinophils (%) after allergen. At the dose of 800 μg daily, mometasone reduced 24 h urinary cortisol by approximately 35%. Both drugs were well tolerated.Mometasone and budesonide are equieffective in reducing early and late asthmatic responses induced by inhaled allergen challenge. Mometasone 800 μg given for seven days partially affects the HPA axis.Asthmatic patients with allergies often develop early (EAR) and in some patients also a late asthmatic response (LAR) when a relevant allergen is inhaled [1-3]. Allergen exposure can also increase non-specific bronchial hyperresponsiveness to stimuli such as methacholine or histamine [4]. The LAR and the bronchial hyperresponsiveness are often associated with increase of eosinophils in the blood, and influx of eosinophils into the airways [3,5].The anti-inflammatory effects of inhaled glucocorticoids in asthma are well documented [1,6,7], shown by attenuation of the EAR, LAR and allergen-induced sputum eosinophils. Glucocorticoids are also more effective than anti-leukotrienes in attenuating the LARs and improve the bronchial hyperresponsiveness in mild asthmatic patients [8]. Mometasone and budesonide are corticosteroids that have been shown
Inhaled steroid/long-acting β2 agonist combination products provide 24 hours improvement in lung function in adult asthmatic patients
Jan Ltvall, Stephen Langley, Ashley Woodcock
Respiratory Research , 2006, DOI: 10.1186/1465-9921-7-110
Abstract: The purpose of these studies was to evaluate and compare the duration of bronchodilation of both combination products up to 24 hours after a single dose.Two randomised, double blind, placebo-controlled, crossover studies were performed. Study A was conducted in 33 asthmatic adults receiving 400–1200 mcg of budesonide or equivalent. Serial forced expiratory volume in one second (FEV1) was measured over 24 hours to determine the duration of effect of both SFC (50/100 mcg) and FBC (4.5/160 mcg). Study B was conducted in 75 asthmatic adults receiving 800–1200 mcg of budesonide or equivalent and comprised a 4 week run-in of 400 mcg bd Becotide? followed by 4 weeks treatment with either SFC 50/100 mcg bd or FBC 4.5/160 mcg bd taken in a cross-over manner. Serial 24-hour FEV1 was measured after the first dose and the last dose after each 4-weeks treatment period to determine the offset of action of each treatment.In study A, a single inhalation of SFC and FBC produced a sustained bronchodilation at 16 hours with an adjusted mean increase in FEV1 from pre-dose of 0.22 L (95% CI 0.19, 0.35 L) for SFC and 0.25 L (95% CI 0.21, 0.37 L) for FBC, which was significantly greater than placebo for both treatments (-0.05 L; p < 0.001). In study B, the slope of decline in FEV1 from 2–24 hours post dose was -16.0 ml/hr for SFC and -14.2 ml/hr for FBC. The weighted mean AUC over 24 hours was 0.21 Lxmin and 0.22 Lxmin and mean change from pre-dose FEV1 at 12 hours was 0.21 L for SFC and 0.20 L for FBC respectivelyBoth SFC and FBC produced a similar sustained bronchodilator effect which was prolonged beyond 12 hours post dose and was clearly measurable at 24 h.The benefit of adding a long-acting β2-agonist (LABA) to inhaled corticosteroid therapy (ICS) in the treatment of asthma is well-established [1-3]. Two such combinations, salmeterol xinafoate and fluticasone propionate (SFC, Seretide?) and formoterol and budesonide (FBC, Symbicort?) are widely used and have been shown to be effectiv
Reviewer acknowledgement 2012
Ltvall Jan,Panettieri Reynold A
Respiratory Research , 2013, DOI: 10.1186/1465-9921-14-12
Abstract: Contributing reviewers The editors of Respiratory Research would like to thank all of our reviewers who have contributed to the journal in Volume 13 (2012).
The Influence of Personality Traits on Reported Adherence to Medication in Individuals with Chronic Disease: An Epidemiological Study in West Sweden
Malin Axelsson,Eva Brink,Jesper Lundgren,Jan Ltvall
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0018241
Abstract: Limited research exists exploring the influence of personality on adherence behaviour. Since non-adherence is a major obstacle in treating prevalent chronic diseases the aim was to determine whether personality traits are related to reported adherence to medication in individuals with chronic disease.
Motivational foci and asthma medication tactics directed towards a functional day
Malin Axelsson, Jan Ltvall, Jesper Lundgren, Eva Brink
BMC Public Health , 2011, DOI: 10.1186/1471-2458-11-809
Abstract: This was a qualitative study; data collection and analysis procedures were conducted according to Grounded Theory methodology. Eighteen persons, aged 22 with asthma and regular asthma medication treatment, were interviewed.The emerged theoretical model illustrated that adherence to asthma medication was motivated by three foci, all directed towards a desired outcome in terms of a functional day as desired by the patient. A promotive focus was associated with the ambition to achieve a positive asthma outcome by being adherent either to the received prescription or to a self-adjusted dosage. A preventive focus was intended to ensure avoidance of a negative asthma outcome either by sticking to the prescription or by preventively overusing the medication. A permissive focus was associated with unstructured adherence behaviour in which medication intake was primarily triggered by asthma symptoms.As all participants had consciously adopted functioning medication tactics that directed them towards the desired goal of a functional day. In an effort to bridge the gap between a patient- and a medical adherence perspective, patients need support in defining their desired functionality and guidance in developing a person-based medication tactic.A novel trend direction in health care has been established in recent years. It is seen in the transition from disease-oriented care [1] to a more patient-centred approach [2], which is intended to result in a shared decision about treatment between the patient and the caregiver [1]. It has been argued that a patient-centred approach is crucial for encouraging adherence to treatment [3]. With reference to asthma medication treatment, several studies have reported figures showing lower adherence than prescribed [4-8]. From a medical perspective, deviating from a medication prescription could seem rather irrational, because it could constitute the missing link between a prescribed treatment and an efficacious outcome [9]. Inadequate adhere
Multi-symptom asthma is closely related to nasal blockage, rhinorrhea and symptoms of chronic rhinosinusitis-evidence from the West Sweden Asthma Study
Jan Ltvall, Linda Ekerljung, Bo Lundb?ck
Respiratory Research , 2010, DOI: 10.1186/1465-9921-11-163
Abstract: This study analyzed data on asthma symptoms, rhinitis, and chronic rhinosinusitis from the 2008 West Sweden Asthma Study, which is an epidemiologically based study using the OLIN and GA2LEN respiratory and allergy focused questionnaires.Multi-symptom asthma was present in 2.1% of the general population. Subjects with multi-symptom asthma had more than double the risk of having night-time awakenings caused by asthma compared with those with fewer asthma symptoms (P < 0.001). The prevalence of allergic rhinitis was similar in the fewer- and multi-symptom asthma groups, but nasal blockage and rhinorrhea were significantly increased in those with multi- versus fewer-symptom asthma (odds ratio 2.21; 95% confidence interval 1.64-2.97, versus 1.49; 1.10-2.02, respectively). Having any, or one to four symptoms of chronic rhinosinusitis significantly increased the risk of having multi- versus fewer-symptom asthma (P < 0.01).An epidemiologically identified group of individuals with multiple asthma symptoms harbour to greater extent those with signs of severe asthma. The degree of rhinitis, described by the presence of symptoms of nasal blockage or rhinorrhea, as well as the presence of any or several signs of chronic rhinosinusitis, significantly increases the risk of having multi-symptom asthma.Asthma is a common chronic disease with a prevalence of approximately 5-10% in different populations [1-6]. We have recently shown that the prevalence of asthma in West Sweden is approximately 8.5%, based on a large epidemiological survey [6]. Importantly, our data argue that there has been no further increase in the prevalence of asthma over the last 18 years in this part of Europe, and moreover that the overall degree of airway symptoms have decreased over this period [6]. However, in the current survey we identify a large population of individuals with multiple asthma symptoms, which amounts to approximately 25% of all asthmatics, and 2% of the general population [6].Asthma is asso
Repeated allergen exposure reduce early phase airway response and leukotriene release despite upregulation of 5-lipoxygenase pathways
Zhi-Hua Cui, Madeleine R?dinger, Margareta Sj?strand, Jan Ltvall
Clinical and Translational Allergy , 2012, DOI: 10.1186/2045-7022-2-7
Abstract: A trimellitic anhydride (TMA) sensitized guinea pig model was used to investigate the effects of low dose repeated allergen exposure on cholinergic airway responsiveness, early phase airway response and plasma exudation, as well as local airway production of mast cell derived cysteinyl leukotrienes and thromboxane B2 (TXB2) after allergen challenge.Repeated low dose allergen exposure increased cholinergic airway responsiveness. In contrast, early phase airway response and plasma exudation in response to a high-dose allergen challenge were strongly attenuated after repeated low dose allergen exposure. Inhibition of the airway response was unspecific to exposed allergen and independent of histamine receptor blocking. Furthermore, a significant reduction of cysteinyl leukotrienes and TXB2 was found in the airways of animals repeatedly exposed to a low dose allergen. However, in vitro stimulation of airway tissue from animals repeatedly exposed to a low dose allergen with arachidonic acid and calcium ionophore (A23187) induced production of cysteinyl leukotrienes and TXB2, suggesting enhanced activity of 5-lipoxygenase and cyclooxygenase pathways.The inhibition of the early phase airway response, cysteinyl leukotriene and TXB2 production after repeated allergen exposure may result from unresponsive effector cells.Early phase airway response to allergen and airway plasma exudation are predominantly mediated by inflammatory mediators including histamine, cysteinyl leukotrienes (cysLTs) and thromboxane A2 (TXA2) [1-3] released from mast cells in the response to allergen challenge [4-7]. In asthmatic patients, the concentrations of cysLTs and TXA2 are increased in plasma, urine and BAL fluid during asthma exacerbation and after experimental allergen challenges [8-11]. Thus, these mediators can induce both airway constriction and airway plasma exudation in several species [3,12-14]. Production of these mediators needs the substrate arachidonic acid and enzymes such as 5-lipo
Quantitative expression of osteopontin in nasal mucosa of patients with allergic rhinitis: effects of pollen exposure and nasal glucocorticoid treatment
Serena E O'Neil, Carina Malmh?ll, Konstantinos Samitas, Teet Pullerits, Apostolos Bossios, Jan Ltvall
Allergy, Asthma & Clinical Immunology , 2010, DOI: 10.1186/1710-1492-6-28
Abstract: Subjects with AR were randomised to receive treatment with fluticasone propionate (FP) (n = 12) or a placebo (n = 16) over the grass pollen season and nasal biopsies were taken prior to, and during the season. OPN expression in the nasal mucosa was examined with immunohistochemistry. Healthy non-AR controls (n = 5) were used as a comparator.OPN expression was detected in epithelial cells, subepithelial infiltrating/inflammatory cells and cells lining the vessels and glands of all subjects. Comparison of the pre- and peak-pollen season biopsy sections in placebo treated patients revealed no increase in OPN expression during the grass pollen season (5.7% vs 6.4%). Treatment with a local glucocorticosteroid did not alter the expression of OPN during pollen exposure (6.2% vs 6.7%).OPN has been increasingly associated with the pathogenesis of various Th2-mediated diseases. However, our finding that the OPN expression in the nasal mucosa of AR patients is not significantly affected by allergen exposure and is comparable to that of the healthy controls, suggests that intracellular OPN is not directly involved in the pathogenesis of allergic rhinitis.The inflammatory process in allergic rhinitis (AR) involves many different inflammatory cells, cytokines, chemokines and other regulatory molecules [1]. It is well known that exposure to allergens, including natural pollen exposure, primarily enhances eosinophilic inflammation in the nose [2] and increases cytokine release [1]. Furthermore, local glucocorticoids are efficient in attenuating the allergen-induced inflammation and the cytokine expression, as we and others have documented in nasal mucosal studies [2-6].OPN is a pleiotropic cytokine normally expressed by many cell types [7], which has been implicated in various diseases [8], including asthma [9-11] and chronic rhinosinusitis [12]. OPN can be expressed in eosinophils, which could argue its involvement in allergic eosinophilic inflammation [13]. Studies of OPN express
Patterns of airway inflammation and MMP-12 expression in smokers and ex-smokers with COPD
Agne Babusyte, Kristina Stravinskaite, Jolanta Jeroch, Jan Ltvall, Raimundas Sakalauskas, Brigita Sitkauskiene
Respiratory Research , 2007, DOI: 10.1186/1465-9921-8-81
Abstract: 39 COPD outpatients – smokers (n = 22) and ex-smokers (n = 17) were studied. 8 'healthy' smokers and 11 healthy never-smokers were tested as the control groups. IS and BAL samples were obtained for differential and MMP-12+-macrophages count analysis.The number of IS neutrophils was higher in both COPD groups compared to both controls. The amount of BAL neutrophils was higher in COPD smokers compared to healthy never-smokers. The number of BAL MMP-12+-macrophages was higher in COPD smokers (1.6 ± 0.3 × 106/ml) compared to COPD ex-smokers, 'healthy' smokers and healthy never-smokers (0.9 ± 0.4, 0.4 ± 0.2, 0.2 ± 0.1 × 106/ml respectively, p < 0.05).The lower amount of BAL neutrophils in COPD ex-smokers, compared to COPD smokers, suggests positive alterations in alveolar compartment after smoking cessation. Smoking and disease itself may stimulate MMP-12 expression in airway compartments (IS and BAL) from COPD patients.Smoking is the major known risk factor for the development of chronic obstructive pulmonary disease (COPD), which is characterized by progressive and not fully reversible airflow limitation [1]. The pathogenesis of COPD is multifactor, involving airway inflammation, associated with an infiltration of inflammatory cells and protease-antiprotease imbalance [2,3].Over 85% COPD patients have been regular smokers [4,5]. It is well known, that inflammation initiated by smoking leads to a changes in both – airways and lung parenchyma. The main known contribution of smoking is activation and recruitment of inflammatory cells to the lungs [6-8]. We have previously observed a tendency of neutrophils to be increased in the airways of stable COPD patients [9]. Other studies have also shown that cigarette smoke produces an increase of neutrophils in bronchoalveolar lavage (BAL) and lung tissue [10-12]. Although, the major environmental risk factor – smoking, for COPD development is well known, the changes of COPD induced by inflammation after smoking cessation are les
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