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<rdf:RDF xmlns:rdf="http://www.w3.org/1999/02/22-rdf-syntax-ns#" xmlns:dcterms="http://purl.org/dc/terms/" xmlns:prism="http://prismstandard.org/namespaces/1.2/basic/" xmlns:dc="http://purl.org/dc/elements/1.1/" xmlns="http://purl.org/rss/1.0/"><channel rdf:about="http://www.annallergy.org/?rss=yes"><title>Annals of Allergy, Asthma &amp; Immunology</title><description>Annals of Allergy, Asthma &amp; Immunology RSS feed: Current Issue. The  Annals of Allergy, Asthma &amp; Immunology  is a scholarly medical journal published monthly by the American College of 
Allergy, Asthma &amp; Immunology. The purpose of the Annals is to serve as an objective evidence-based forum for the allergy/immunology 
specialist to keep up to date on current clinical science (both research and practice-based) in the fields of allergy, asthma, and immunology. 
The emphasis of the journal will be to provide clinical and research information that is readily applicable to both the clinician and 
the researcher. Each issue of the Annals shall also provide opportunities to participate in accredited continuing medical education activities 
to enhance overall clinical proficiency.</description><link>http://www.annallergy.org/?rss=yes</link><dc:publisher>Elsevier Inc.</dc:publisher><dc:language>en</dc:language><dc:rights> © 2010 Published by Elsevier Inc.  </dc:rights><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:issn>1081-1206</prism:issn><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:publicationDate>September 2010</prism:publicationDate><prism:copyright> © 2010 Published by Elsevier Inc.  </prism:copyright><prism:rightsAgent>healthpermissions@elsevier.com</prism:rightsAgent><items><rdf:Seq><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS108112061000195X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610001985/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610006435/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610006575/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610001997/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610006587/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610006393/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610006423/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610006848/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610006708/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610006411/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610006812/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610005521/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610006691/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS108112061000668X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610007180/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610007192/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS108112061000726X/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610007209/abstract?rss=yes"/><rdf:li rdf:resource="http://www.annallergy.org/article/PIIS1081120610007222/abstract?rss=yes"/></rdf:Seq></items></channel><item rdf:about="http://www.annallergy.org/article/PIIS108112061000195X/abstract?rss=yes"><title>The role of vitamin D in asthma</title><link>http://www.annallergy.org/article/PIIS108112061000195X/abstract?rss=yes</link><description>Objective: To review the current literature on vitamin D and asthma, discussing the possible roles of vitamin D on asthma pathogenesis and the potential consequences of vitamin D deficiency.Data Sources: PubMed database was searched from 1950 to 2009. Keywords used included asthma, vitamin D, inflammation, airway smooth muscle and cytokines.Study Selection: Articles were selected based on relevance to the subject.Results: Vitamin D deficiency has been associated with epidemiologic patterns observed in the asthma epidemic. Vitamin D deficiency is more common with obesity, African American ethnicity, and westernization of countries with higher-risk populations for asthma. Evidence suggests that vitamin D deficiency is associated with increased airway hyperresponsiveness, lower pulmonary functions, worse asthma control, and possibly steroid resistance. Lung epithelial cells express high baseline levels of 1α-hydroxylase. This allows the conversion of inactive calcidiol to active calcitriol locally within the lung. Calcitriol has been shown to inhibit the synthesis and release of certain cytokines, such as RANTES, platelet-derived growth factor, and matrix metalloproteinases, from bronchial smooth muscle cells, thereby leading to decreased lung inflammation and smooth muscle cell proliferation. Vitamin D also increases synthesis of interleukin 10 by CD4+CD25+Foxp3+ T-regulatory cells and dendritic cells, while concurrently inhibiting dendritic cell activation by downregulating expression of costimulatory molecules CD40 and CD80/86. Vitamin D is also capable of inducing the expression of several anti-infective molecules, such as cathelicidin. Thus, vitamin D has a number of biologic effects that are likely important in regulating key mechanisms in asthma.Conclusions: We hypothesize that vitamin D supplementation may lead to improved asthma control by inhibiting the influx of inflammatory cytokines in the lung and increasing the secretion of interleukin 10 by T-regulatory cells and dendritic cells.</description><dc:title>The role of vitamin D in asthma</dc:title><dc:creator>Manbir S. Sandhu, Thomas B. Casale</dc:creator><dc:identifier>10.1016/j.anai.2010.01.013</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-03-02</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-03-02</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>CME Review Article</prism:section><prism:startingPage>191</prism:startingPage><prism:endingPage>199</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610001985/abstract?rss=yes"><title>CME Examination</title><link>http://www.annallergy.org/article/PIIS1081120610001985/abstract?rss=yes</link><description></description><dc:title>CME Examination</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.anai.2010.01.016</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>CME Review Article</prism:section><prism:startingPage>200</prism:startingPage><prism:endingPage>200</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610006435/abstract?rss=yes"><title>Development of a nomogram for identification of asthma among adults in epidemiologic studies</title><link>http://www.annallergy.org/article/PIIS1081120610006435/abstract?rss=yes</link><description>Background: The criteria used to identify persons with asthma in epidemiologic studies are varying and, depending on the method used, can be challenging and resource consuming.Objective: To develop a nomogram (scoring system) to identify adult patients with asthma using a combination of variables collected via a validated questionnaire.Methods: We studied the first 268 women aged 40 to 69 years in the Shanghai Women's Asthma and Allergy Study who reported signs and symptoms of asthma and underwent either methacholine challenge testing or test of reversibility during the asthma screening survey between 2003 and 2007. These women were defined as having definite asthma (n = 106) or not (n = 162). Multivariable logistic regression analysis was performed to develop a predictive model for identifying asthma using survey information alone.Results: Clinically relevant questions were used for the predictive multivariable logistic regression model and included the following: ever wheezing or whistling in the chest, current medication use for asthma, self-reported ever asthma, self-reported ever allergic rhinitis, family history of allergy, and age. The area under the receiver operating characteristic curve of the prediction model was 0.75 (95% confidence interval, 0.69–0.81). A nomogram was developed to assess the individual probability of asthma based on individually weighted variables in the predictive model.Conclusions: In clinical or epidemiologic studies, this asthma nomogram could be used as a tool to assess the probability of asthma for an individual patient by incorporating asthma-related predictor variables obtained through a field questionnaire.</description><dc:title>Development of a nomogram for identification of asthma among adults in epidemiologic studies</dc:title><dc:creator>Xinqing Deng, Tebeb Gebretsadik, Meiling Jin, Yu-Tang Gao, Chunxue Bai, John W. Christman, Wanqing Wen, William D. Dupont, Dale Plummer, Jeremy Stephens, Xiao Ou Shu, Tina V. Hartert</dc:creator><dc:identifier>10.1016/j.anai.2010.06.020</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Asthma, Lower Airway Diseases</prism:section><prism:startingPage>203</prism:startingPage><prism:endingPage>210</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610006575/abstract?rss=yes"><title>Risk of perinatal mortality associated with asthma during pregnancy: a 2-stage sampling cohort study</title><link>http://www.annallergy.org/article/PIIS1081120610006575/abstract?rss=yes</link><description>Background: The association between maternal asthma during pregnancy and perinatal mortality has been investigated in 21 studies, and a significantly increased risk among asthmatic women was found in 4 studies. However, these studies have methodologic limitations, such as lack of adjustment for cigarette smoking, a major risk factor for perinatal mortality.Objective: To evaluate whether maternal asthma during pregnancy increases the risk of perinatal mortality.Methods: From the linkage of 3 administrative databases from Québec, Canada, a cohort including 13,100 asthmatic and 28,042 nonasthmatic women who had at least 1 pregnancy between 1990 and 2002 was constructed. We used a 2-stage sampling cohort design to obtain information on cigarette smoking and other potential confounders from the medical records of 1,247 selected mothers.Results: In the cohort, 353 cases of perinatal mortality were identified, and we were able to retrieve the medical record of the mother for 304 cases. A significantly increased crude risk of perinatal mortality of 34% among asthmatic women compared with nonasthmatic women was found, but the odds ratio did not remain significant after adjustment for placental abruption and cigarette smoking (odds ratio, 1.12; 95% confidence interval, 0.87–1.45).Conclusion: The risk of perinatal mortality was not found to be significantly associated with maternal asthma after the effect of smoking was removed.</description><dc:title>Risk of perinatal mortality associated with asthma during pregnancy: a 2-stage sampling cohort study</dc:title><dc:creator>Marie-Claude Breton, Marie-France Beauchesne, Catherine Lemière, Évelyne Rey, Amélie Forget, Lucie Blais</dc:creator><dc:identifier>10.1016/j.anai.2010.06.021</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Asthma, Lower Airway Diseases</prism:section><prism:startingPage>211</prism:startingPage><prism:endingPage>217</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610001997/abstract?rss=yes"><title>Answers to CME examination—Annals of Allergy, Asthma &amp; Immunology, September 2010</title><link>http://www.annallergy.org/article/PIIS1081120610001997/abstract?rss=yes</link><description></description><dc:title>Answers to CME examination—Annals of Allergy, Asthma &amp; Immunology, September 2010</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/j.anai.2010.01.017</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Asthma, Lower Airway Diseases</prism:section><prism:startingPage>217</prism:startingPage><prism:endingPage>217</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610006587/abstract?rss=yes"><title>Premenstrual asthma and atopy markers</title><link>http://www.annallergy.org/article/PIIS1081120610006587/abstract?rss=yes</link><description>Background: The frequency of atopy in women with premenstrual asthma (PMA) and its possible effect on the premenstrual exacerbation of asthma are unknown.Objective: To analyze the relation between atopy markers (total IgE, Phadiatop, and specific IgE) and PMA.Methods: Asthmatic women of reproductive age completed a questionnaire about respiratory symptoms and recorded peak flow during an entire menstrual cycle to be classified as asthmatic patients with or without PMA. Their asthma severity was graded according to the 2005 Global Initiative for Asthma scale. PMA was defined as a clinical or functional exacerbation (≥20%) in the premenstrual phase compared with the preovulatory phase. Blood tests for several atopy markers were conducted for: total IgE and screening for aeroallergens (Phadiatop) and specific IgE.Results: Blood determinations were performed in 59 asthmatic women, of whom 31 (53%) had PMA. Twenty-six patients with PMA (84%) and 12 without PMA (43%) had total IgE values greater than 100 kU/L (P = .001). Twenty-one patients with PMA (68%) and 14 without PMA (50%) tested positive for Phadiatop (P = .17). Those who were positive for Phadiatop were also tested for specific IgE. No relation was found between specific IgE and PMA; values for ryegrass (63%), olive (60%), and Dermatophagoides pteronyssinus (54%) exceeded 0.35 kU/L.Conclusions: PMA seems to be closely linked to total IgE levels but not to specific allergens. The atopy affects the clinical manifestations of PMA in women of reproductive age.</description><dc:title>Premenstrual asthma and atopy markers</dc:title><dc:creator>Antonio Pereira-Vega, José L. Sánchez, José A. Maldonado, Fátima Borrero, Ignacio Vázquez Rico, Rosa Vázquez, Francisco Álvarez, José M. Ignacio, Pedro Romero, Francisco L. Gil</dc:creator><dc:identifier>10.1016/j.anai.2010.06.022</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Asthma, Lower Airway Diseases</prism:section><prism:startingPage>218</prism:startingPage><prism:endingPage>222</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610006393/abstract?rss=yes"><title>Bridging allergologic and botanical knowledge in seasonal allergy: a role for phenology</title><link>http://www.annallergy.org/article/PIIS1081120610006393/abstract?rss=yes</link><description>Background: Grass pollen is a worldwide cause of respiratory allergy. Identifying the causative species is essential, for example for choosing the appropriate immunotherapy, because not all grass allergens are totally cross-reacting, and the pollen calendars provide only a gross estimate. Phenologic analyses allow identification of the pollen release for each individual grass.Objectives: To assess, using phenologic analyses, the true flowering periods of grasses and to compare the data with the standard pollen calendar.Methods: Phenologic analyses were performed of the following grasses: black grass, sweet vernal grass, common wild oat, barren brome, cocksfoot, tall fescue, Yorkshire fog, ryegrass, Timothy grass, bulbous meadow-grass, Kentucky bluegrass, and Bermuda grass. Sampling was performed every 10 days, starting in April 2009, at 50 stations distributed across Italy. The flowering phase was assessed using a stereomicroscopy-based method for the detection of spreading stamens. The official pollen calendar was used for comparison.Results: Relevant differences were found between grass pollen count and effective flowering of the grass species. Only some species contributed to the pollen peak, and a relevant pollen load for other species was also present out of the peak. Important Pooideae, such as Timothy grass, were not present during the pollen peak in northern and central Italy, and the same occurred with Bermuda grass.Conclusions: The various species of grasses release their pollen grains at different times during the pollen season, and this information is missing with pollen calendars. This may have a relevant effect on the choice of an appropriate immunotherapy.</description><dc:title>Bridging allergologic and botanical knowledge in seasonal allergy: a role for phenology</dc:title><dc:creator>Giuseppe Frenguelli, Giovanni Passalacqua, Sergio Bonini, Alessandro Fiocchi, Cristoforo Incorvaia, Francesco Marcucci, Emma Tedeschini, Giorgio Walter Canonica, Franco Frati</dc:creator><dc:identifier>10.1016/j.anai.2010.06.016</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Mechanisms of Allergic and Immune Diseases</prism:section><prism:startingPage>223</prism:startingPage><prism:endingPage>227</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610006423/abstract?rss=yes"><title>Dog characteristics and allergen levels in the home</title><link>http://www.annallergy.org/article/PIIS1081120610006423/abstract?rss=yes</link><description>Background: Comprehensive analyses on the effect of household dogs on dog allergen levels in the home are lacking.Objective: To identify environmental factors and dog-specific characteristics that influence the accumulation of Canis familiaris 1 (Can f 1) in homes.Methods: Dust samples were collected from the floor of infants' bedrooms at a Wayne County Health, Environment, Allergy, &amp; Asthma Longitudinal Study birth cohort study home visit and processed for Can f 1 using a standardized protocol. Dog characteristics were based on maternal report. Homes with 1 dog were included in detailed analyses, including characterization of the dog based on coat type, dander level, and shedding.Results: Households with dogs had higher levels of dog allergen in the home than those without dogs; however, the number of dogs in the home was not related to dog allergen levels. Homes with exclusively outdoor dogs had significantly higher dog allergen levels than homes without any dogs but significantly lower levels of dog allergen than homes with indoor dogs. Homes where the dog was allowed in the infant's bedroom had significantly higher Can f 1 levels on the child's bedroom floor than homes where it was not. The homes of altered dogs had higher Can f 1 levels than did their unaltered counterparts.Conclusions: Dogs in the home corresponded to dog allergen in the home. Time the dog was indoors and whether it was allowed on the vacuumed surface mattered. No dog characteristic, other than altered status, was associated with allergen levels in the home.</description><dc:title>Dog characteristics and allergen levels in the home</dc:title><dc:creator>Charlotte Nicholas, Ganesa Wegienka, Suzanne Havstad, Edward Zoratti, Dennis Ownby, Christine Cole Johnson</dc:creator><dc:identifier>10.1016/j.anai.2010.06.019</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Mechanisms of Allergic and Immune Diseases</prism:section><prism:startingPage>228</prism:startingPage><prism:endingPage>233</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610006848/abstract?rss=yes"><title>Induction of interleukin 8 by American cockroach allergens from human airway epithelial cells via extracellular signal regulatory kinase and jun N-terminal kinase but not p38 mitogen-activated protein kinase</title><link>http://www.annallergy.org/article/PIIS1081120610006848/abstract?rss=yes</link><description>Background: Cockroaches are potent aeroallergens associated with asthma. Several reports suggest that a novel group of G protein–linked receptors, protease-activated receptors (PARs), may be involved in the intracellular signaling pathway induced by aeroallergens of the epithelial cells.Objective: To investigate the mechanisms of American cockroach allergens (CraA) on interleukin 8 (IL-8) in human pulmonary epithelial cells.Methods: Protease activities of CraA were quantified by the Azocoll method. The gene and protein expressions of IL-8 from CraA-stimulated A549 cells were quantified by real-time polymerase chain reaction and enzyme-linked immunosorbent assay, respectively. The activity of different mitogen-activated protein kinases (MAPKs) was assessed by Western blot.Results: CraA-induced A549 cell IL-8 secretion in a dose-dependent manner at both the messenger RNA and protein levels. CraA-induced IL-8 secretion can be blocked by serine protease inhibitors, phenylmethane sulfonyl fluoride, and aprotinin but not by other protease inhibitors. Blocking antibodies against the cleavage sites of PAR-2 and PAR-3, but not of PAR-1, inhibited CraA-induced IL-8 production. CraA induced significant PAR-2 and PAR-3 messenger RNA upregulation and extracellular-regulated kinase (ERK/1/2) and Jun N-terminal kinase (JNK) phosphorylation but not p38 MAPK. Furthermore, ERK1/2 (U0126) and JNK (SP600125) inhibitors inhibited CraA-induced IL-8 secretion by 100% and 45%, respectively.Conclusions: Both PAR-2 and PAR-3 might play a role in CraA-induced IL-8 secretion from human airway epithelial cells. It signals mainly through the ERK1/2 and partly from the JNK pathways. The key receptors and signaling molecules mediate cytokine release from the respiratory epithelium and can be potential therapeutic targets in treating cockroach allergy.</description><dc:title>Induction of interleukin 8 by American cockroach allergens from human airway epithelial cells via extracellular signal regulatory kinase and jun N-terminal kinase but not p38 mitogen-activated protein kinase</dc:title><dc:creator>Mey-Fann Lee, Nancy M. Wang, Szu-Wei Liu, Shyh-Jye Lin, Yi-Hsing Chen</dc:creator><dc:identifier>10.1016/j.anai.2010.07.008</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Mechanisms of Allergic and Immune Diseases</prism:section><prism:startingPage>234</prism:startingPage><prism:endingPage>240</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610006708/abstract?rss=yes"><title>Anaphylaxis Induced by Fosfomycin</title><link>http://www.annallergy.org/article/PIIS1081120610006708/abstract?rss=yes</link><description>Fosfomycin or l-cis-1,2-epoxypropylphosphoric acid has a unique mechanism of antimicrobial action that involves the inhibition of UDP-N-acetylglucosamine enolpyruvyl transferase, an enzyme that catalyzes the first step in bacterial cell wall synthesis within the cell. Fosfomycin is a unique antibiotic that is chemically unrelated to any other known antimicrobial agent. Fosfomycin has a broad spectrum of antimicrobial activity, including gram-negative and gram-positive aerobic bacteria.</description><dc:title>Anaphylaxis Induced by Fosfomycin</dc:title><dc:creator>Leticia Sánchez-Morillas, Patricia Rojas Pérez-Ezquerra, Mar Reaño-Martos, Cristobalina Mayorga, José Julio Laguna-Martínez</dc:creator><dc:identifier>10.1016/j.anai.2010.07.004</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>241</prism:startingPage><prism:endingPage>241</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610006411/abstract?rss=yes"><title>Acute Generalized Exanthematous Pustulosis: The First Pediatric Case Caused by a Contrast Agent</title><link>http://www.annallergy.org/article/PIIS1081120610006411/abstract?rss=yes</link><description>Acute generalized exanthematous pustulosis (AGEP) is a rare exfoliative dermatitis characterized by a generalized eruption of sterile, nonfollicular pustules on erythematous, edematous skin. It is associated with neutrophilia, fever, and, sometimes, hemodynamic instability, with mortality of 2%. AGEP is more common in the adult population and is usually caused by medications, traditionally antibiotics. We describe a 4-year-old boy who developed AGEP on 3 separate occasions after receiving an infusion of nonionic ioversol-containing radiocontrast dye. To our knowledge, he represents the first pediatric case of AGEP due to ioversol.</description><dc:title>Acute Generalized Exanthematous Pustulosis: The First Pediatric Case Caused by a Contrast Agent</dc:title><dc:creator>Nina Poliak, Matthew Elias, Antonella Cianferoni, James Treat</dc:creator><dc:identifier>10.1016/j.anai.2010.06.018</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>242</prism:startingPage><prism:endingPage>243</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610006812/abstract?rss=yes"><title>Returning the Athlete to Sports After a Near-Fatal Asthma Event</title><link>http://www.annallergy.org/article/PIIS1081120610006812/abstract?rss=yes</link><description>Near-fatal asthma events in athletes present a significant problem to treating physicians, and a management strategy for safely returning athletes with near-fatal asthma exacerbations to sports has not been previously described. We describe a near-fatal asthma event in an elite adolescent athlete and our approach to returning him safely to sports.</description><dc:title>Returning the Athlete to Sports After a Near-Fatal Asthma Event</dc:title><dc:creator>Joseph P. Forester, Michael S. Tankersley</dc:creator><dc:identifier>10.1016/j.anai.2010.07.005</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Letters</prism:section><prism:startingPage>243</prism:startingPage><prism:endingPage>244</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610005521/abstract?rss=yes"><title>Multiple Treatment Cycles of High-Dose Intravenous Immunoglobulin for Chronic Spontaneous Urticaria</title><link>http://www.annallergy.org/article/PIIS1081120610005521/abstract?rss=yes</link><description>We commend Mitzel-Kaoukhov et al for their study of high-dose intravenous immunoglobulin (IVIG) therapy for chronic spontaneous urticaria (CSU), in which patients received 2 g/kg across 2 days at monthly intervals (for 5 of 6 patients). Four of 6 patients had complete remission after 2 to 4 cycles, maintaining remission for 10 to 24 months without IVIG therapy. However, their favorable results contrast with our experience using IVIG in 3 patients with corticosteroid-dependent CSU. Our patients achieved only partial remission with subsequent relapse, similar to the results of Asero.</description><dc:title>Multiple Treatment Cycles of High-Dose Intravenous Immunoglobulin for Chronic Spontaneous Urticaria</dc:title><dc:creator>Todd Hrabak, Christopher W. Calabria</dc:creator><dc:identifier>10.1016/j.anai.2010.05.018</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Correspondence</prism:section><prism:startingPage>245</prism:startingPage><prism:endingPage>245</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610006691/abstract?rss=yes"><title>Intravenous Immunoglobulin as a Third-Line Therapy in Chronic Spontaneous Urticaria</title><link>http://www.annallergy.org/article/PIIS1081120610006691/abstract?rss=yes</link><description>Author Response: We thank you for your annotation to our series about intravenous immunoglobulin (IVIG) therapy. Of course, observations such as case report series are not comparable with big controlled studies. For different reasons (eg, costs), there is no chance of obtaining results across large randomized studies in the near future.</description><dc:title>Intravenous Immunoglobulin as a Third-Line Therapy in Chronic Spontaneous Urticaria</dc:title><dc:creator>Heidrun Mitzel-Kaoukhov, Petra Staubach, Tina Müller-Brenne</dc:creator><dc:identifier>10.1016/j.anai.2010.07.003</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Correspondence</prism:section><prism:startingPage>245</prism:startingPage><prism:endingPage>246</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS108112061000668X/abstract?rss=yes"><title></title><link>http://www.annallergy.org/article/PIIS108112061000668X/abstract?rss=yes</link><description>Have you ever wondered why during the grass pollen season, allergy-like symptoms can be observed (often referred to the allergist) but after skin testing the patients are found to be negative to the various aeroallergens, including grass pollen, and, thus, considered as a nonallergic form of conjunctivitis? Today, more than ever, it is increasingly important to understand the allergic response of the eye interaction with overlapping disorders, such as tear film dysfunction, also known as dry eye syndrome (DES). One of the most clinically established high prevalence diseases worldwide, DES is a complex and multifactorial condition, similar to allergy. With the recent Food and Drug Administration approval of a specific immunomodulator medication, topical cyclosporine, as a treatment for DES and additional agents being considered by the Food and Drug Administration, it is important for allergists and clinical immunologists to be more aware of DES.</description><dc:title></dc:title><dc:creator>Leonard Bielory</dc:creator><dc:identifier>10.1016/j.anai.2010.07.002</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Book Review</prism:section><prism:startingPage>247</prism:startingPage><prism:endingPage>247</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610007180/abstract?rss=yes"><title>Information for Readers</title><link>http://www.annallergy.org/article/PIIS1081120610007180/abstract?rss=yes</link><description>Annals of Allergy, Asthma &amp; Allergy (ISSN 1081-1206) is published monthly by Elsevier Inc., 360 Park Avenue South, New York, NY 10010. Business Office: 1600 John F. Kennedy Blvd., Ste. 1800, Philadelphia, PA 19103-2899. Editorial Office: 360 Park Avenue South, New York, NY 10010. Customer Services Office: 3251 Riverport Lane, Maryland Heights, MO 63043. Periodicals postage paid at New York, NY, and at additional mailing offices.</description><dc:title>Information for Readers</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1081-1206(10)00718-0</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A10</prism:startingPage><prism:endingPage>A10</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610007192/abstract?rss=yes"><title>Table of Contents</title><link>http://www.annallergy.org/article/PIIS1081120610007192/abstract?rss=yes</link><description></description><dc:title>Table of Contents</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1081-1206(10)00719-2</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A11</prism:startingPage><prism:endingPage>A11</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS108112061000726X/abstract?rss=yes"><title>On The Cover – Horse Dander</title><link>http://www.annallergy.org/article/PIIS108112061000726X/abstract?rss=yes</link><description>Most horses in existence today are strains of the domesticated horse, Equus caballus. Domestication is believed to have been begun around 4000 BCE, and been widespread by 3000 BCE. The only true remaining wild horses are found on the Chinese-Mongolian steppes, and these face the threat of extinction. Wild horses of the North American continent and other places are descendents of escaped domesticated horses. Horses have been bred for various purposes to include pulling or carrying burdens, herding, jumping, or racing. Human exposure to horses, then, may come in the agricultural arena or with various equestrian pastimes. Until it became apparent that immunological adverse reactions could occur to horse serum, horses were frequently used to raise antitoxin antibodies.</description><dc:title>On The Cover – Horse Dander</dc:title><dc:creator>Richard W. Weber</dc:creator><dc:identifier>10.1016/j.anai.2010.08.001</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>On the Cover</prism:section><prism:startingPage>A12</prism:startingPage><prism:endingPage>A12</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610007209/abstract?rss=yes"><title>Editorial Board</title><link>http://www.annallergy.org/article/PIIS1081120610007209/abstract?rss=yes</link><description></description><dc:title>Editorial Board</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1081-1206(10)00720-9</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A19</prism:startingPage><prism:endingPage>A19</prism:endingPage></item><item rdf:about="http://www.annallergy.org/article/PIIS1081120610007222/abstract?rss=yes"><title>Instructions for Authors</title><link>http://www.annallergy.org/article/PIIS1081120610007222/abstract?rss=yes</link><description>The Annals of Allergy, Asthma &amp; Immunology is a scholarly medical journal published monthly by the American College of Allergy, Asthma &amp; Immunology. The purpose of the Annals is to serve as an objective evidence-based forum for the allergy/immunology specialist to keep up to date on current clinical science (both research and practice-based) in the fields of allergy, asthma, and immunology. The emphasis of the journal will be to provide clinical and research information that is readily applicable to both the clinician and the researcher. Each issue of the Annals shall also provide opportunities to participate in accredited continuing medical education activities to enhance overall clinical proficiency.</description><dc:title>Instructions for Authors</dc:title><dc:creator></dc:creator><dc:identifier>10.1016/S1081-1206(10)00722-2</dc:identifier><dc:source>Annals of Allergy, Asthma &amp; Immunology 105, 3 (2010)</dc:source><dc:date>2010-09-01</dc:date><prism:publicationName>Annals of Allergy, Asthma &amp; Immunology</prism:publicationName><prism:publicationDate>2010-09-01</prism:publicationDate><prism:volume>105</prism:volume><prism:number>3</prism:number><prism:issueIdentifier>S1081-1206(10)X0010-2</prism:issueIdentifier><prism:section>Frontmatter</prism:section><prism:startingPage>A20</prism:startingPage><prism:endingPage>A20</prism:endingPage></item></rdf:RDF>