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        <title>Clinical and Molecular Allergy - Most accessed articles</title>
        <link>http://www.clinicalmolecularallergy.com</link>
        <description>The most accessed research articles published by Clinical and Molecular Allergy</description>
        <dc:date>2010-02-23T00:00:00Z</dc:date>
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        <item rdf:about="http://www.clinicalmolecularallergy.com/content/8/1/1">
        <title>Non-allergic rhinitis: a case report and review</title>
        <description>Rhinitis is characterized by rhinorrhea, sneezing, nasal congestion, nasal itch and/or postnasal drip. Often the first step in arriving at a diagnosis is to exclude or diagnose sensitivity to inhalant allergens. Non-allergic rhinitis (NAR) comprises multiple distinct conditions that may even co-exist with allergic rhinitis (AR). They may differ in their presentation and treatment. As well, the pathogenesis of NAR is not clearly elucidated and likely varied. There are many conditions that can have similar presentations to NAR or AR, including nasal polyps, anatomical/mechanical factors, autoimmune diseases, metabolic conditions, genetic conditions and immunodeficiency. Here we present a case of a rare condition initially diagnosed and treated as typical allergic rhinitis vs. vasomotor rhinitis, but found to be something much more serious. This case illustrates the importance of maintaining an appropriate differential diagnosis for a complaint routinely seen as mundane. The case presentation is followed by a review of the potential causes and pathogenesis of NAR.</description>
        <link>http://www.clinicalmolecularallergy.com/content/8/1/1</link>
                <dc:creator>Cyrus Nozad</dc:creator>
                <dc:creator>L. Madison Michael</dc:creator>
                <dc:creator>D. Betty Lew</dc:creator>
                <dc:creator>Christie Michael</dc:creator>
                <dc:source>Clinical and Molecular Allergy 2010, 8:1</dc:source>
        <dc:date>2010-02-03T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7961-8-1</dc:identifier>
        <prism:publicationName>Clinical and Molecular Allergy</prism:publicationName>
        <prism:issn>1476-7961</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>1</prism:startingPage>
        <prism:publicationDate>2010-02-03T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.clinicalmolecularallergy.com/content/6/1/3">
        <title>Incense smoke: clinical, structural and molecular effects on airway disease</title>
        <description>In Asian countries where the Buddhism and Taoism are mainstream religions, incense burning is a daily practice. A typical composition of stick incense consists of 21% (by weight) of herbal and wood powder, 35% of fragrance material, 11% of adhesive powder, and 33% of bamboo stick. Incense smoke (fumes) contains particulate matter (PM), gas products and many organic compounds. On average, incense burning produces particulates greater than 45 mg/g burned as compared to 10 mg/g burned for cigarettes. The gas products from burning incense include CO, CO2, NO2, SO2, and others. Incense burning also produces volatile organic compounds, such as benzene, toluene, and xylenes, as well as aldehydes and polycyclic aromatic hydrocarbons (PAHs). The air pollution in and around various temples has been documented to have harmful effects on health. When incense smoke pollutants are inhaled, they cause respiratory system dysfunction. Incense smoke is a risk factor for elevated cord blood IgE levels and has been indicated to cause allergic contact dermatitis. Incense smoke also has been associated with neoplasm and extracts of particulate matter from incense smoke are found to be mutagenic in the Ames Salmonella test with TA98 and activation. In order to prevent airway disease and other health problem, it is advisable that people should reduce the exposure time when they worship at the temple with heavy incense smokes, and ventilate their house when they burn incense at home.</description>
        <link>http://www.clinicalmolecularallergy.com/content/6/1/3</link>
                <dc:creator>Ta-Chang Lin</dc:creator>
                <dc:creator>Guha Krishnaswamy</dc:creator>
                <dc:creator>David Chi</dc:creator>
                <dc:source>Clinical and Molecular Allergy 2008, 6:3</dc:source>
        <dc:date>2008-04-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7961-6-3</dc:identifier>
        <prism:publicationName>Clinical and Molecular Allergy</prism:publicationName>
        <prism:issn>1476-7961</prism:issn>
        <prism:volume>6</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2008-04-25T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.clinicalmolecularallergy.com/content/2/1/10">
        <title>Autoimmune progesterone dermatitis in a patient with endometriosis: case report and review of the literature</title>
        <description>Autoimmune progesterone dermatitis (APD) is a condition in which the menstrual cycle is associated with a number of skin findings such as urticaria, eczema, angioedema, and others. In affected women, it occurs 3&#8211;10 days prior to the onset of menstrual flow, and resolves 2 days into menses. Women with irregular menses may not have this clear correlation, and therefore may be missed. We present a case of APD in a woman with irregular menses and urticaria/angioedema for over 20 years, who had not been diagnosed or correctly treated due to the variable timing of skin manifestations and menses. In addition, we review the medical literature in regards to clinical features, pathogenesis, diagnosis, and treatment options.</description>
        <link>http://www.clinicalmolecularallergy.com/content/2/1/10</link>
                <dc:creator>Alan Baptist</dc:creator>
                <dc:creator>James Baldwin</dc:creator>
                <dc:source>Clinical and Molecular Allergy 2004, 2:10</dc:source>
        <dc:date>2004-08-02T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7961-2-10</dc:identifier>
        <prism:publicationName>Clinical and Molecular Allergy</prism:publicationName>
        <prism:issn>1476-7961</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>10</prism:startingPage>
        <prism:publicationDate>2004-08-02T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.clinicalmolecularallergy.com/content/8/1/3">
        <title>Regulation and dysregulation of immunoglobulin E:  a molecular and clinical perspective</title>
        <description>Background:
Altered levels of Immunoglobulin E (IgE) represent a dysregulation of IgE synthesis and may be seen in a variety of immunological disorders. The object of this review is to summarize the historical and molecular aspects of IgE synthesis and the disorders associated with dysregulation of IgE production.
Methods:
Articles published in Medline/PubMed were searched with the keyword Immunoglobulin E and specific terms such as class switch recombination, deficiency and/or specific disease conditions (atopy, neoplasia, renal disease, myeloma, etc.). The selected papers included reviews, case reports, retrospective reviews and molecular mechanisms. Studies involving both sexes and all ages were included in the analysis.
Results:
Both very low and elevated levels of IgE may be seen in clinical practice. Major advancements have been made in our understanding of the molecular basis of IgE class switching including roles for T cells, cytokines and T regulatory (or Treg) cells in this process. Dysregulation of this process may result in either elevated IgE levels or IgE deficiency.
Conclusion:
Evaluation of a patient with elevated IgE must involve a detailed differential diagnosis and consideration of various immunological and non-immunological disorders. The use of appropriate tests will allow the correct diagnosis to be made. This can often assist in the development of tailored treatments.</description>
        <link>http://www.clinicalmolecularallergy.com/content/8/1/3</link>
                <dc:creator>Mariah Pate</dc:creator>
                <dc:creator>John Smith</dc:creator>
                <dc:creator>David Chi</dc:creator>
                <dc:creator>Guha Krishnaswamy</dc:creator>
                <dc:source>Clinical and Molecular Allergy 2010, 8:3</dc:source>
        <dc:date>2010-02-23T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7961-8-3</dc:identifier>
        <prism:publicationName>Clinical and Molecular Allergy</prism:publicationName>
        <prism:issn>1476-7961</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>3</prism:startingPage>
        <prism:publicationDate>2010-02-23T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.clinicalmolecularallergy.com/content/8/1/2">
        <title>Basophil sensitivity through CD63 or CD203c is a functional measure for specific immunotherapy </title>
        <description>Background:
Subcutaneous Immunotherapy (SCIT) modifies the allergic response and relieves allergic symptoms. SCIT is the only and a very effective treatment for insect venom allergy. We hypothesized that basophil sensitivity, measured through the basophil activation test, would decrease during SCIT up dosing. Expression of CD203c was compared to CD63 as marker for basophil activation, using a Bland Altman plot and ROC curves.
Methods:
Patients (n = 18) starting subcutaneous SCIT for wasp allergy with an up dosing scheme of 7 to 11 weeks were enrolled. Heparinised blood samples were drawn at weeks 1-4, 7 and at the first maintenance visit. Basophils were stimulated at 7 log dilutions of V. vespula allergen for 15 min, and were stained with CD203c and CD63. Basophils were identified as CD203c+ leukocytes, and the proportion of CD63+ and CD203c+ cells were plotted against allergen concentration. A sigmoid curve was fitted to the points, and the allergen concentration at which half of the maximal activation was achieved, LC50, was calculated. In another series of experiments, LC50 calculated in whole blood (AP) was subtracted from LC50 calculated with basophils suspended in plasma from a nonatopic donor (HS) to determine the protective effect of soluble factors in blood of patients treated with SCIT.
Results:
Heparin blood basophil activation was similar through CD63 and CD203c. Basophils were significantly more sensitized three weeks after initiation of SCIT compared to baseline (p &lt; 0,01). The difference in LC50 increased by 1,04 LC50 units (p = 0,04) in patients that had just achieved maintenance dose compared with patients before initiating SCIT. When maintenance allergen concentrations had been reached, an increase in the protective plasma component was documented. Blood basophil concentration was marginally reduced by SCIT.
Conclusion:
Basophil activation is a versatile and sensitive tool that measures changes in the humoral immune response to allergen during SCIT.</description>
        <link>http://www.clinicalmolecularallergy.com/content/8/1/2</link>
                <dc:creator>Susan Mikkelsen</dc:creator>
                <dc:creator>Bo Martin Bibby</dc:creator>
                <dc:creator>Mette Konow Bogebjerg Dolberg</dc:creator>
                <dc:creator>Ronald Dahl</dc:creator>
                <dc:creator>Hans Jurgen Hoffmann</dc:creator>
                <dc:source>Clinical and Molecular Allergy 2010, 8:2</dc:source>
        <dc:date>2010-02-16T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7961-8-2</dc:identifier>
        <prism:publicationName>Clinical and Molecular Allergy</prism:publicationName>
        <prism:issn>1476-7961</prism:issn>
        <prism:volume>8</prism:volume>
        <prism:startingPage>2</prism:startingPage>
        <prism:publicationDate>2010-02-16T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.clinicalmolecularallergy.com/content/2/1/5">
        <title>Dermatology for the practicing allergist: Tinea pedis and its complications</title>
        <description>Tinea pedis is a chronic fungal infection of the feet, very often observed in patients who are immuno-suppressed or have diabetes mellitus. The practicing allergist may be called upon to treat this disease for various reasons. Sometimes tinea infection may be mistaken for atopic dermatitis or allergic eczema. In other patients, tinea pedis may complicate allergy and asthma and may contribute to refractory atopic disease. Patients with recurrent cellulitis may be referred to the allergist/immunologist for an immune evaluation and discovered to have tinea pedis as a predisposing factor. From a molecular standpoint, superficial fungal infections may induce a type2 T helper cell response (Th2) that can aggravate atopy. Th2 cytokines may induce eosinophil recruitment and immunoglobulin E (IgE) class switching by B cells, thereby leading to exacerbation of atopic conditions. Three groups of fungal pathogens, referred to as dermatophytes, have been shown to cause tinea pedis: Trychophyton sp, Epidermophyton sp, and Microsporum sp. The disease manifests as a pruritic, erythematous, scaly eruption on the foot and depending on its location, three variants have been described: interdigital type, moccasin type, and vesiculobullous type. Tinea pedis may be associated with recurrent cellulitis, as the fungal pathogens provide a portal for bacterial invasion of subcutaneous tissues. In some cases of refractory asthma, treatment of the associated tinea pedis infection may induce remission in airway disease. Very often, protracted topical and/or oral antifungal agents are required to treat this often frustrating and morbid disease. An evaluation for underlying immuno-suppression or diabetes may be indicated in patients with refractory disease.</description>
        <link>http://www.clinicalmolecularallergy.com/content/2/1/5</link>
                <dc:creator>Muhannad Al Hasan</dc:creator>
                <dc:creator>S. Matthew Fitzgerald</dc:creator>
                <dc:creator>Mahnaz Saoudian</dc:creator>
                <dc:creator>Guha Krishnaswamy</dc:creator>
                <dc:source>Clinical and Molecular Allergy 2004, 2:5</dc:source>
        <dc:date>2004-03-29T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7961-2-5</dc:identifier>
        <prism:publicationName>Clinical and Molecular Allergy</prism:publicationName>
        <prism:issn>1476-7961</prism:issn>
        <prism:volume>2</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2004-03-29T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.clinicalmolecularallergy.com/content/3/1/9">
        <title>The basophil activation test by flow cytometry: recent developments in clinical studies, standardization and emerging perspectives</title>
        <description>The diagnosis of immediate allergy is mainly based upon an evocative clinical history, positive skin tests (gold standard) and, if available, detection of specific IgE. In some complicated cases, functional in vitro tests are necessary. The general concept of those tests is to mimic in vitro the contact between allergens and circulating basophils. The first approach to basophil functional responses was the histamine release test but this has remained controversial due to insufficient sensitivity and specificity. During recent years an increasing number of studies have demonstrated that flow cytometry is a reliable tool for monitoring basophil activation upon allergen challenge by detecting surface expression of degranulation/activation markers (CD63 or CD203c). This article reviews the recent improvements to the basophil activation test made possible by flow cytometry, focusing on the use of anti-CRTH2/DP2 antibodies for basophil recognition. On the basis of a new triple staining protocol, the basophil activation test has become a standardized tool for in vitro diagnosis of immediate allergy. It is also suitable for pharmacological studies on non-purified human basophils. Multicenter studies are now required for its clinical assessment in large patient populations and to define the cut-off values for clinical decision-making.</description>
        <link>http://www.clinicalmolecularallergy.com/content/3/1/9</link>
                <dc:creator>Radhia Boumiza</dc:creator>
                <dc:creator>Anne-lise Debard</dc:creator>
                <dc:creator>Guillaume Monneret</dc:creator>
                <dc:source>Clinical and Molecular Allergy 2005, 3:9</dc:source>
        <dc:date>2005-06-30T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7961-3-9</dc:identifier>
        <prism:publicationName>Clinical and Molecular Allergy</prism:publicationName>
        <prism:issn>1476-7961</prism:issn>
        <prism:volume>3</prism:volume>
        <prism:startingPage>9</prism:startingPage>
        <prism:publicationDate>2005-06-30T00:00:00Z</prism:publicationDate>
                <prism:versionidentifier>XML</prism:versionidentifier>
                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
    </item>
        <item rdf:about="http://www.clinicalmolecularallergy.com/content/7/1/7">
        <title>Genetics of asthma: a molecular biologist perspective

</title>
        <description>Asthma belongs to the category of classical allergic diseases which generally arise due to IgE mediated hypersensitivity to environmental triggers. Since its prevalence is very high in developed or urbanized societies it is also referred to as &quot;disease of civilizations&quot;. Due to its increased prevalence among related individuals, it was understood quite long back that it is a genetic disorder. Well designed epidemiological studies reinforced these views. The advent of modern biological technology saw further refinements in our understanding of genetics of asthma and led to the realization that asthma is not a disorder with simple Mendelian mode of inheritance but a multifactorial disorder of the airways brought about by complex interaction between genetic and environmental factors. Current asthma research has witnessed evidences that are compelling researchers to redefine asthma altogether. Although no consensus exists among workers regarding its definition, it seems obvious that several pathologies, all affecting the airways, have been clubbed into one common category called asthma. Needless to say, genetic studies have led from the front in bringing about these transformations. Genomics, molecular biology, immunology and other interrelated disciplines have unearthed data that has changed the way we think about asthma now. In this review, we center our discussions on genetic basis of asthma; the molecular mechanisms involved in its pathogenesis. Taking cue from the existing data we would briefly ponder over the future directions that should improve our understanding of asthma pathogenesis.</description>
        <link>http://www.clinicalmolecularallergy.com/content/7/1/7</link>
                <dc:creator>Amrendra Kumar</dc:creator>
                <dc:creator>Balaram Ghosh</dc:creator>
                <dc:source>Clinical and Molecular Allergy 2009, 7:7</dc:source>
        <dc:date>2009-05-06T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7961-7-7</dc:identifier>
        <prism:publicationName>Clinical and Molecular Allergy</prism:publicationName>
        <prism:issn>1476-7961</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>7</prism:startingPage>
        <prism:publicationDate>2009-05-06T00:00:00Z</prism:publicationDate>
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                <cc:license rdf:resource="http://creativecommons.org/licenses/by/2.0/" />
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        <item rdf:about="http://www.clinicalmolecularallergy.com/content/7/1/5">
        <title>T regulatory cells: an overview and intervention techniques to modulate allergy outcome</title>
        <description>Dysregulated immune response results in inflammatory symptoms in the respiratory mucosa leading to asthma and allergy in susceptible individuals. The T helper type 2 (Th2) subsets are primarily involved in this disease process. Nevertheless, there is growing evidence in support of T cells with regulatory potential that operates in non-allergic individuals. These regulatory T cells occur naturally are called natural T regulatory cells (nTregs) and express the transcription factor Foxp3. They are selected in the thymus and move to the periphery. The CD4 Th cells in the periphery can be induced to become regulatory T cells and hence called induced or adaptive T regulatory cells. These cells can make IL-10 or TGF-b or both, by which they attain most of their suppressive activity. This review gives an overview of the regulatory T cells, their role in allergic diseases and explores possible interventionist approaches to manipulate Tregs for achieving therapeutic goals.</description>
        <link>http://www.clinicalmolecularallergy.com/content/7/1/5</link>
                <dc:creator>Subhadra Nandakumar</dc:creator>
                <dc:creator>Christopher Miller</dc:creator>
                <dc:creator>Uday Kumaraguru</dc:creator>
                <dc:source>Clinical and Molecular Allergy 2009, 7:5</dc:source>
        <dc:date>2009-03-12T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7961-7-5</dc:identifier>
        <prism:publicationName>Clinical and Molecular Allergy</prism:publicationName>
        <prism:issn>1476-7961</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>5</prism:startingPage>
        <prism:publicationDate>2009-03-12T00:00:00Z</prism:publicationDate>
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        <item rdf:about="http://www.clinicalmolecularallergy.com/content/7/1/10">
        <title>Oral mite anaphylaxis by Thyreophagus entomophagus in a child: a case report</title>
        <description>Sensitization to Thyreophagus entomophagus, a storage mite, is uncommon and might produce occupational respiratory disorders in farmers. We present the first case of a child suffering anaphylaxis produced by ingestion of contaminated flour with Thyreophagus entomophagus.</description>
        <link>http://www.clinicalmolecularallergy.com/content/7/1/10</link>
                <dc:creator>Javier Iglesias-Souto</dc:creator>
                <dc:creator>Inmaculada Sanchez-Machin</dc:creator>
                <dc:creator>Victor Iraola</dc:creator>
                <dc:creator>Paloma Poza</dc:creator>
                <dc:creator>Ruperto Gonzalez</dc:creator>
                <dc:creator>Victor Matheu</dc:creator>
                <dc:source>Clinical and Molecular Allergy 2009, 7:10</dc:source>
        <dc:date>2009-11-25T00:00:00Z</dc:date>
        <dc:identifier>doi:10.1186/1476-7961-7-10</dc:identifier>
        <prism:publicationName>Clinical and Molecular Allergy</prism:publicationName>
        <prism:issn>1476-7961</prism:issn>
        <prism:volume>7</prism:volume>
        <prism:startingPage>10</prism:startingPage>
        <prism:publicationDate>2009-11-25T00:00:00Z</prism:publicationDate>
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