Food-specific IgG Antibody-guided Elimination Diets Followed by Resolution of Asthma Symptoms and Reduction in Pharmacological Interventions in Two Patients: A Case Report.

Asthma is one of the most common causes of office visits in the primary care and emergency care settings. Individuals are often able to maintain symptomatic control with long-term pharmacological therapy. Exacerbations of asthma commonly occur due to exposure to triggers such as viruses, pollutants, and allergens. While it is widely accepted that exposure to immunoglobulin E food allergens can exacerbate asthma symptoms, there is little evidence examining delayed immunoglobulin G-mediated reactions to food. Here we present two clinical cases of individuals who experienced a reduction in asthma symptoms, decreased dependence on pharmacological therapies, and increased quality of life by eliminating foods that demonstrated reactivity to immunoglobulin G levels identified through serum testing.

El asma es una de las causas más frecuentes de visita a la consulta del médico de atención primaria y a urgencias. A menudo los pacientes pueden controlar sus síntomas con tratamiento farmacológico de larga duración. Las exacerbaciones del asma ocurren por lo general debido a exposición a desencadenantes como virus, contaminantes y alérgenos. Si bien se acepta por lo general que la exposición a alérgenos alimentarios que causan la producción de inmunoglobulina E puede exacerbar los síntomas de asma, hay poca evidencia al examinar las reacciones retardadas a alimentos mediadas por inmunoglobulina G. Presentamos aquí dos casos clínicos de individuos que experimentaron una reducción de los síntomas de asma, disminución en su dependencia a tratamientos farmacológicos y una mejora en su calidad de vida eliminando alimentos que demostraron reactividad a los niveles de inmunoglobulina G identificados mediante análisis de suero.

An insertional trap for conditional gene expression in Toxoplasma gondii: identification of TAF250 as an essential gene.

Toxoplasmosis is characterized by fast lytic replication cycles leading to severe tissue lesions. Successful host cell invasion is essential for pathogenesis. The division cycle of Toxoplasma gondii is characterized by an unusual cell cycle progression and a distinct internal budding mechanism. To identify essential genes involved in the lytic cycle we devised an insertional gene trapping strategy using the Tet-transactivator system. In essence, a random, active promoter is displaced with a tetracycline regulatable promoter, which if in an essential gene, will result in a conditionally lethal phenotype upon tetracycline addition. We isolated eight mutants with growth defects, two of which displayed modest invasion defects, one of which had an additional cell cycle defect. The trapped loci were identified using expression microarrays, exploiting the tetracycline dependent expression of the trapped genes. In mutant 3.3H6 we identified TCP-1, a component of the chaperonin protein folding machinery under the control of the Tet promoter. However, this gene was not critical for growth of mutant 3.3H6. Subsequently, we identified a suppressor gene encoding a protein with a hypothetical function by guided cosmid complementation. In mutant 4.3B13, we identified TAF250, an RNA polymerase II complex component, as the trapped, essential gene. Furthermore, by mapping the plasmid insertion boundaries we identified multiple genomic rearrangements, which hint at a potential replication dependent DNA repair mechanism. Furthermore, these rearrangements provide an explanation for inconsistent locus rescue results observed by molecular biological approaches. Taken together, we have added an approach to identify and study essential genes in Toxoplasma.