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- Paying for telemedicine. [JOURNAL ARTICLE]
- Am J Manag Care 2014 Dec; 20(12):983-985.
Objectives We used the 2003-2009 Medical Expenditure Panel Survey to evaluate average annual total and out-of-pocket expenditures by nonelderly adults with asthma. Study Design We divided patients diagnosed with asthma into 4 groups, based on whether or not they had had an asthma attack in the previous year (a crude marker for disease severity) and whether or not they reported using treatment for their asthma. Methods For each group we calculated total and out-of-pocket average annual spending for hospital inpatient, hospital outpatient, emergency department, and physician office care, as well as for prescription drugs. These averages were adjusted to account for differences in respondents' overall health (presence of other co-morbidities, self-reported health status, and self-reported activity limitations), sociodemographic characteristics (age, sex, race/ethnicity, income), and insurance status. Results We found that among the 4 groups, those who were receiving treatment but continued to experience asthma attacks had the highest total and out-of-pocket expenditures in all categories, consistent with their likely higher illness severity. However, patients who reported receiving treatment and did not experience attacks also reported relatively high adjusted total and out-of-pocket expenditures-most notably $536 per year out of pocket for prescription medications and $231 per year out of pocket for physician office visits. After adjustment, about the same proportion of patients in these 2 groups (13.5% who did not get treated and had attacks, and 13.8% who did get treated and avoided attacks) reported high financial burden. Conclusions Patients may experience financial challenges to appropriate self-management of asthma, even when they are able to avoid exacerbations.
- A risk-based approach to reducing exposure of staff to laboratory animal allergens. [JOURNAL ARTICLE]
- Lab Anim (NY) 2014 Dec 19; 44(1):32-38.
Within the biomedical research industry, people who work with laboratory animals may be at risk of developing laboratory animal allergy, which can lead to occupational asthma. Under UK and EU laws, employers must prevent or adequately control exposure to any hazardous substance, which includes animal allergens, so far as reasonably practicable, for the protection of all people on the premises. This can be achieved in part by reviewing the risk of allergen exposure in specific areas of a facility and implementing appropriate infrastructure, environmental and performance controls to minimize that risk. The authors describe the approach used at their institution to stratify risk of allergen exposure in various areas of the animal facility and to implement appropriate controls. They also discuss their use of a monitoring program to evaluate allergen concentrations in low- and high-risk areas of the animal facility and explain how the monitoring results can be applied to determine which controls are needed to minimize risk of exposure and to provide a safe working environment.
- Pulse Oxygen Saturation Values in a Healthy School-Aged Population. [JOURNAL ARTICLE]
- Pediatr Emerg Care 2014 Dec 18.
The purpose of this study was to determine the normal values of oxygen saturation in a healthy school-aged pediatric population.This study enrolled students in grades K-8 at an elementary and middle school in Los Angeles. Although all students were invited to participate, only pulse oximetry results among healthy students were included. Healthy students were defined as not having asthma, bronchitis, a recent cold or pneumonia within the past week, any chronic lung disease, or any heart condition.Two hundred forty-eight students participated in the study, and 246 students met the inclusion criteria. Pulse oxygen saturation values ranged from 97% to 100% with a mean of 98.7% (95% confidence interval [CI], 98.6%-99.8%) and median of 99%. The distribution of measured pulse oximetry values were 97%: 16 (95% CI, 6.5%), 98%: 45 (95% CI, 18.3%), 99%: 184 (95% CI, 74.8%), and 100%: 1 (95% CI, 0.4%).Although the conventional wisdom is that pulse oximetry values 95% or greater are normal, these data suggest that the normal oxygen saturation range should be between 97% and 100%. Values of 95% and 96% should increase clinical suspicion of underlying disease.
- The Monascus secondary metabolites monascin and ankaflavin inhibit the allergic reaction in RBL-2H3 cells. [JOURNAL ARTICLE]
- J Agric Food Chem 2014 Dec 19.
Monascus-fermented products have been used as dietary food and traditional medicine due to their beneficial effects on circulation and digestive systems in Asia for thousands of years. Besides, monascin and ankaflavin, the secondary metabolites from Monascus-fermented products, have been proved their anti-inflammatory and immunomodulatory effect. In previous research, monascin and ankaflavin ameliorated ovalbumin-induced airway allergic reaction often used as type I allergy asthma model. Additionally, mast cells plays critical roles in type I allergy. Therefore, we used RBL-2H3 cells as the mast cell model to understand that whether the improving effects of asthma of monascin and ankaflavin came from influencing mast cells. We found 40 μM monascin and ankaflavin inhibited PMA/ionomycin-induced mast cell degranulation and TNF-α secretion through suppressing the phosphorylation of PKC and MAPK family ERK, JNK, and p38. Consequently, monascin and ankaflavin affected the activation of mast cell and may have the potential to improve type I allergy.
- Targeting Immune Pathways for Therapy in Asthma and Chronic Obstructive Pulmonary Disease. [JOURNAL ARTICLE]
- Ann Am Thorac Soc 2014 Dec; 11(Supplement 5):S322-S328.
Asthma and chronic obstructive pulmonary disease (COPD) are highly prevalent chronic inflammatory diseases of the airways, with differences in etiology, pathogenesis, immunologic mechanisms, clinical presentation, comorbidities, prognosis, and response to treatment. In mild to moderate early-onset allergic asthma, the Th2-driven eosinophilic airway inflammation and the ensuing disease can be well controlled with maintenance treatment with inhaled corticosteroids (ICS). In real-life settings, asthma control can be improved by facilitating adherence to ICS treatment and by optimizing inhaler technique. In patients with uncontrolled severe asthma, old and novel therapies targeting specific immunologic pathways should be added according to the underlying endotype/phenotype. In COPD, there is a high unmet need for safe and effective antiinflammatory treatments that not only prevent exacerbations but also have a beneficial impact on the course of the disease and improve survival. Although several new approaches aim to target the chronic neutrophilic pulmonary inflammation per se in patients with COPD, strategies that target the underlying causes of the pulmonary neutrophilia (e.g., smoking, chronic infection, and oxidative stress) might be more successful. In both chronic airway diseases (especially in more difficult, complex cases), the choice of the optimal treatment should be based not only on arbitrary clinical labels but also on the underlying immunopathology.
- Vitamin D Influences Asthmatic Pathology through Its Action on Diverse Immunological Pathways. [JOURNAL ARTICLE]
- Ann Am Thorac Soc 2014 Dec; 11(Supplement 5):S314-S321.
The prevalence of vitamin D insufficiency and deficiency has increased markedly in recent decades to current epidemic levels (Hyppönen E, et al. Am J Clin Nutr 2007;85:860-868). In parallel, there has been an increase in the incidence of a range of immune-mediated conditions ranging from cancer to autoimmune and respiratory diseases, including chronic obstructive pulmonary disease and asthma (Holick MF. N Engl J Med 2007;357:266-281; Finklea et al. Adv Nutr 2011;2:244-253). There is also an association with increased respiratory infections, which are the most common cause of asthma exacerbations (Finklea et al. Adv Nutr 2011;2:244-253). Together, this has resulted in considerable interest in the therapeutic potential of vitamin D to prevent and improve treatment of asthma and other respiratory diseases. To this end, data from clinical trials involving supplementation with active vitamin D, or more commonly a precursor, are starting to emerge. This review considers mechanisms by which vitamin D may act on the immune system to dampen inappropriate inflammatory responses in the airway while also promoting tolerance and antimicrobial defense mechanisms that collectively maintain respiratory health.
- Gas6'ing the Innate Immune Response during Experimental Asthma. [JOURNAL ARTICLE]
- Ann Am Thorac Soc 2014 Dec; 11(Supplement 5):S303-S305.
Growth arrest-specific gene 6 (Gas6) binds Tyro3, Axl, and Mertk (TAM) receptors and exerts prominent effects in many diseases, but little is known about its role in asthma. Herein, we examined the role of Gas6 and TAM receptors differentially in an experimental asthma model driven by Aspergillus fumigatus. A. fumigatus-sensitized mice were challenged with live A. fumigatus conidia, and airway hyperresponsiveness and airway remodeling were determined 28 days later. When administered to mice from Days 14 to 28 after conidia challenge, anti-Axl monoclonal antibody, but not anti-Mertk monoclonal antibody, treatment significantly inhibited airway hyperresponsiveness and airway remodeling compared with the appropriate control IgG group. These results demonstrate that Gas6 has modulatory functions in fungal asthma via Axl receptor activation in immune and nonimmune cells.
- Pulmonary Immunity during Respiratory Infections in Early Life and the Development of Severe Asthma. [JOURNAL ARTICLE]
- Ann Am Thorac Soc 2014 Dec; 11(Supplement 5):S297-S302.
Asthma affects 10% of the population in Westernized countries, being most common in children. It is a heterogeneous condition characterized by chronic allergic airway inflammation, mucus hypersecretion, and airway hyperresponsiveness (AHR) to normally innocuous antigens. Combination therapies with inhaled corticosteroids and bronchodilators effectively manage mild to moderate asthma, but there are no cures, and patients with severe asthma do not respond to these treatments. The inception of asthma is linked to respiratory viral (respiratory syncytial virus, rhinovirus) and bacterial (Chlamydia, Mycoplasma) infections. The examination of mouse models of early-life infections and allergic airway disease (AAD) provides valuable insights into the mechanisms of disease inception that may lead to the development of more effective therapeutics. For example, early-life, but not adult, Chlamydia respiratory infections in mice permanently modify immunity and lung physiology. This increases the severity of AAD by promoting IL-13 expression, mucus hypersecretion, and AHR. We have identified novel roles for tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) and IL-13 in promoting infection-induced pathology in early life and subsequent chronic lung disease. Genetic deletion of TRAIL or IL-13 variously protected against neonatal infection-induced inflammation, mucus hypersecretion, altered lung structure, AHR, and impaired lung function. Therapeutic neutralization of these factors prevented infection-induced severe AAD. Other novel mechanisms and avenues for intervention are also being explored. Such studies indicate the immunological mechanisms that may underpin the association between early-life respiratory infections and the development of more severe asthma and may facilitate the development of tailored preventions and treatments.
- Linking Acute Infection to Chronic Lung Disease. The Role of IL-33-Expressing Epithelial Progenitor Cells. [JOURNAL ARTICLE]
- Ann Am Thorac Soc 2014 Dec; 11(Supplement 5):S287-S291.
Respiratory infection is a common feature of the major human airway diseases, such as asthma and chronic obstructive pulmonary disease, but the precise link between acute infection and chronic lung disease is still undefined. In a mouse model of this process, parainfluenza virus infection is followed by long-term induction of IL-33 expression and release and in turn innate immune cell generation of IL-13 and consequent airway disease signified by excess mucus formation. IL-33 induction was traceable to a subset of secretoglobin-positive airway epithelial cells linked to progenitor/stem cell function. In corresponding studies of humans with chronic obstructive pulmonary disease, an increase in IL-33 production was also detected in concert with up-regulation of IL-13 and airway mucus formation. In this case, increased IL-33 production was localized to a subset of airway basal cells that maintain an endogenous capacity for increased pluripotency and ATP-regulated release of IL-33 even ex vivo. The results provide evidence of a sustainable epithelial cell population that may be activated by environmental danger signals to release IL-33 and thereby lead to IL-13-dependent disease. The progenitor nature of this IL-33-expressing ATP-responsive cell population could explain an acquired susceptibility to chronic airway disease. The findings may therefore provide a new paradigm to explain the role of viral infection and the innate immune system in chronic lung disease based on the influence of long-term epithelial progenitor cells programmed for excess IL-33 production. Further studies are needed to address the basis for this type of postviral reprogramming and the means to correct it and thereby restore airway mucosal immune function to normal.
- Airway Fibrinogenolysis and the Initiation of Allergic Inflammation. [JOURNAL ARTICLE]
- Ann Am Thorac Soc 2014 Dec; 11(Supplement 5):S277-S283.
The past 15 years of allergic disease research have produced extraordinary improvements in our understanding of the pathogenesis of airway allergic diseases such as asthma. Whereas it was previously viewed as largely an immunoglobulin E-mediated process, the gradual recognition that T cells, especially Type 2 T helper (Th2) cells and Th17 cells, play a major role in asthma and related afflictions has inspired clinical trials targeting cytokine-based inflammatory pathways that show great promise. What has yet to be clarified about the pathogenesis of allergic inflammatory disorders, however, are the fundamental initiating factors, both exogenous and endogenous, that drive and sustain B- and T-cell responses that underlie the expression of chronic disease. Here we review how proteinases derived from diverse sources drive allergic responses. A central discovery supporting the proteinase hypothesis of allergic disease pathophysiology is the role played by airway fibrinogen, which in part appears to serve as a sensor of unregulated proteinase activity and which, when cleaved, both participates in a novel allergic signaling pathway through Toll-like receptor 4 and forms fibrin clots that contribute to airway obstruction. Unresolved at present is the ultimate source of airway allergenic proteinases. From among many potential candidates, perhaps the most intriguing is the possibility such enzymes derive from airway fungi. Together, these new findings expand both our knowledge of allergic disease pathophysiology and options for therapeutic intervention.