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[ 89 Articles ]   1  2  3  5  6  7  8  9 
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For Health Professionals Laypersons Organisation Moderate Childhood Asthma In Peru Not Induced By Allergens

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Asthma and asthma symptoms among children living in Lima, Peru, do not appear to be related to atopy, according to researchers.

LinkMedica   United Kingdom

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Commercial Organisation's Site Moderate Childhood Exposure To Allergens Reduces Incidence Of Allergies

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Children who come into regular contact with farm animals may have long term protection from allergic illnesses, according to the results of a new study.

A news report.

Doctor's Guide to Asthma Information and Resources   USA

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For Health Professionals Professional Organisation's Site Excellent Class I Chitinases and the Latex-Fruit Syndrome

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The prevalence of sensitization to natural rubber latex in the general population is around 1%. However, occupational latex allergy is considerably higher in people who work wearing latex gloves. Furthermore, almost 50% of these allergic patients also show hypersensitivity to some plant foods, especially chestnut, banana, and avocado, but also to kiwi, papaya, tomato and others. The name "latex-fruit syndrome" has been proposed to describe this type of cross-reactivity. We review here the role of class I chitinases of chestnut, avocado and banana, as major allergens implicated in the latex-fruit syndrome. These enzymes have an N-terminal domain homologous to hevein, one of the major allergens of latex. Thus, there should be common IgE-binding epitopes in latex hevein and the hevein-like domain of class I chitinases. Homologous class II enzymes lacking the hevein domain are not reactive either in vitro or in vivo.

This type of protein is widely distributed in plants and it has been demonstrated that in many other foods, like fruits and legumes, there are also IgE-binding class I chitinases. We propose them as panallergens responsible for the latex-fruit syndrome. They are inactivated by heat treatment, which probably explains why only fresh consumed foods are associated with the syndrome. The amount of these allergens may vary dramatically because class I chitinases are induced by ethylene. This plant hormone acts during the ripening of climacteric fruits and is commercially used to hasten ripening of fruits and vegetables. The increase in the allergenicity of these fruits due to ethylene treatment could explain in part the rise in the prevalence of latex-fruit allergy.

R. SÁNCHEZ-MONGE, A. DIAZ-PERALES, C. BLANCO, G. SALCEDO

Internet Symposium on Food Allergens   Germany

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Commercial Organisation's Site Moderate Common Allergens

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Most common cause of allergic asthma are pollen particularly grass pollen, house dust particularly the mites in the dust, and the animals. Molds, fumes and dust encountered in industry, drugs and food are other important causes of asthma.

Following are some the common allergens causing allergic diseases.

Asthma Cure   India

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Commercial Organisation's Site Moderate Controlling Irritants and FAQ

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A brief overview of the control of allergens and irritants, and answers to how often should the Honeywell filter be changed, bedding washed, etc.

Allergy Clean Environments   USA

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Commercial Organisation's Site Excellent Controlling The Environment

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An excellent overview of ways to reduce triggers and allergens in the bedroom, rest of the house, car and elsewhere. Also includes tips on odours, epidermal allergies, and hepa filters.

Allergy Web - Asthma & Allergy Associates of Florida, PA.   USA

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For Health Professionals Professional Organisation's Site Excellent Cow's Milk

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Cow's milk allergy (CMA) can be defined as any adverse reaction mediated by immunological mechanisms to cow's milk proteins. CMA can be divided in IgE-mediated reactions (IgE-CMA) and non-IgE-mediated reactions (non-IgE-CMA) which may involve other immunoglobulins, immune complexes and cell-mediated reactions. Patients with non-IgE-CMA and digestive symptoms can present with the following well defined clinical pictures: milk- induced enterocolitis, milk- induced proctitis, milk- induced enteropathy, or eosinophilic allergic gastro- enteritis. CMA should be differentiated from cow's milk intolerance (CMI) reactions due to lactase deficiency or other non immune mediated causes which are not subject of the present review. Most CMA has its onset in the first year of life, and becomes apparent at the time of weaning from breastfeeding.
Prevalences of CMA range from 1.6% to 2.8% in randomly selected children younger than 2 years of age (elimination / challenge proven). Oral tolerance is frequently acquired in about 50 to 90% of children with CMA within the first 6 years of life. However, severe CMA may persist into adulthood. The frequency of sensitization to cow's milk in adults has recently been estimated by RAST to be 0.7% and 1.2% in Scandinavian countries.

According to the onset of symptoms after milk ingestion CMA can be classified as immediate or delayed- type. The clinical picture can vary from mild to severe, involving the skin (eczema, hives, angioedema), gastrointestinal tract (oral pruritis, colic, vomiting, diarrhea, constipation), respiratory tract (cough, stridor, wheezing), and cardiovascular system (anaphylactic shock).
No single laboratory test is diagnostic of CMA. Clinical manifestations supported by skin tests and in vitro parameters are valuable. The diagnosis is confirmed by well-defined elimination and subsequent challenge procedures. If there is evidence of anaphylaxis, challenge should be avoided. The inadvertent ingestion of small amounts of cow's milk allergens hidden in foods can result in severe life- threatening clinical reactions. Cow's milk allergens could be present in breast milk, infant formulas, milk and milk products like cheese and yogurt, as well as in "non- dairy" foods occurring as contaminants or unlabeled additives. The most effective treatment of CMA is allergen avoidance. Besides the optimal choice of breast milk, suitable milk substitutes in the nutrition of infants with CMA are soy hydrolyzed formulas, extensively casein and whey hydrolyzed formulas, and amino acid formulas. The exact frequency of sensitization to soy protein in children with CMA is still controversial. Soy allergy seems to be rare in IgE-CMA, while approximately 60% of children with milk- induced enterocolitis are sensitive to soybean. However, severe anaphylactic reactions to extensively hydrolyzed casein and partially hydrolyzed whey formulas can occur in highly sensitized infants with IgE-mediated cow’s milk allergy. Due to the high homology of protein composition sheep's and goat's milk are cross- reactive in approximately 80% of subjects with CMA while mare's milk is only rarely cross- reactive with cow's milk (4% in subjects with CMA). In addition, sheep’s milk may cause severe IgE-mediated allergic reactions in children not affected by CMA. IgE antibodies from children allergic to cow’s milk are capable of recognizing milk proteins from mammals bred in European countries (ewe, goat, buffalo). Cross-reactivity of camel’s milk proteins has not been recognized. Therefore, due to clinically important residual allergenicity in some hypoallergenic formulas and milk allergen cross-reactivity between species, clinical testing in a safe medically- supervised environment is necessary in each cow’s milk sensitive infant before use.

In infants and children the major cow's milk allergens are casein (CAS), beta- lactoglobulin (beta-LG), and alpha- lactalbumin (alpha-LA). Caseins (alpha-, beta-, kappa-CAS) are the most important in children and adults. Other allergens involved in CMA are bovine serum albumin (BSA) and bovine immunoglobulins. Several IgE- binding epitopes of alpha-LA, beta-LG, alpha- and beta-CAS have been described. Knowledge of the immunodominant epitopes of the major allergens may be useful in identifying children who will have persistent CMA and children who are likely to outgrow CMA.
The present data collection summarizes the following topics in tabular form: prevalences of CMA, diagnostic and therapeutic features, molecular biological and allergenic properties of cow's milk allergens, stability and hidden presence of allergens, the use of infant formulas in therapy and prevention of CMA and other atopic diseases.

Internet Symposium on Food Allergens   Germany

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Commercial Organisation's Site Excellent Creating a Safe Harbor - a Home Allergen Audit

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An excellent interactive guide to remove allergens from the home including soot!

Priorities   USA

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For Health Professionals Professional Organisation's Site Excellent Determination of Hidden Allergens in Foods by Immunoassays

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Hidden food allergens present a potential threat to allergic individuals. In Europe mandatory labelling of the most important food allergens is in preparation (Amendment of EU Food Labeling Directive). On the other hand there are only a few validated methods for the detection and quantitation of minute amounts of allergens in foods. Immunological methods can involve either human IgE or animal antisera. Dot- immunblotting and SDS-PAGE / immunoblotting are sufficient for qualitative detection of food allergens, while Rocket- immunoelectrophoresis and Enzyme-linked immunosorbent assays (ELISA) are applications to quantitate hidden food allergens. The performance of the methods such as their sensitivity, specificity, limit of detection, recovery and reproducability are reviewed in detail.

Internet Symposium on Food Allergens   Germany

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For Health Professionals Professional Organisation's Site Excellent Effects of in vitro Digestion on the IgE-binding Activity of Proteins from Hazelnuts (Corylus avellana)

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The allergenicity of hazelnuts treated with different proteolytic enzymes was examined and compared by SDS-PAGE / immunoblotting and EAST- inhibition experiments using sera of 16 hazelnut allergic individuals. 30 min treatment with the enzymes protease, elastase and trypsin eliminated the allergenicity of the hazelnut proteins, which can be shown by means of immunoblotting experiments. EAST- inhibition experiments reveal only a reduction of allergenicity. Treatment with pancreatin led to a slight decrease in the IgE binding activity of the main hazelnut allergens after 30 min and to an elimination after 60 min. Hydrolysis with pepsin at pH 1.2 resulted in a slight decrease of allergenic activity after 60 min. A complete elimination did not even appear in two of seven patients' sera after 240 min of hydrolysis with pepsin. The results
reveal that the IgE-binding proteins in hazelnuts are not very stable to in vitro digestion with proteolytic enzymes.

M. WIGOTZKI, S. SCHUBERT, H. STEINHART, A. PASCHKE

Internet Symposium on Food Allergens   Germany

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