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Will Systems Biology Transform Clinical Decision Support?
Published in Paul Cerrato, John Halamka, Reinventing Clinical Decision Support, 2020
Transcriptome. Advances in transcriptomics are likewise providing insights into the pathophysiology of asthma. The transcriptome refers to RNA strands in our cells. Body proteins that carry out essential biological functions are created through a 3-step process: DNA provides the basic building blocks—the genes. These genes then go through the process of transcription, in which they are “converted” into RNA, which in turn undergoes the process of translation, which results in the generation of body proteins, including enzymes. As Bunyavanich and Shadt explain, “Transcriptomics offers a complementary and synergistic approach to GWAS for studying disease, as RNA reflects the more dynamic processes at play in a given tissue or tissues that underlie pathophysiology.”18 RNA sequencing has identified gene transcripts linked to eosinophilic esophagitis, a form of allergic inflammation of the esophagus, which are consistent with GWAS of patients with eosinophilic esophagitis. The GWAS also reveal relevant genetic variants on chromosome 5 (5q22). Similarly, RNA sequencing of airway biopsies has found several specific expressed genes, including SLC26A4, POSTN, and BCL2.
Shape of epithelia
Published in A. Šiber, P. Ziherl, Cellular Patterns, 2018
These deformation modes are observed in animal tubular epithelia. A convincing example of the longitudinal mode are the ridges seen in eosinophilic esophagitis, a condition caused by accumulation of white blood cells within the epithelium that lines the esophagus (Figure 4.11a). Panels bd in Figure 4.11 show the cross‐section of lengthwise folds characteristic of the circumferential mode in the developing chick gut. Apart from this, an important feature of this model is that the ratios of shear moduli as well as the growth ratios required to reproduce these patterns are realistic, not departing very dramatically from 1. Experimental reports suggest that μen/μme may typically range from about 10% to about 70% [115] and that the endoderm/mesoderm growth ratio may reach 1.5 or so [116].
Evaluation of Food and Food Contaminants
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
The incidence and prevalence of allergy-related diseases, including asthma,3 atopic dermatitis,4 hay fever,5 food allergy,6–8 atopic conjunctivitis,9 and eosinophilic esophagitis10 have escalated considerably in the last two decades as has vascular inflammation as shown in the previous chapters. There has been increasing recognition, however, that not all sensitivities, including many types of food intolerance and chemical hypersensitivity reactions, are related to the classically understood concept of allergic phenomenon involving immunoglobulin (Ig)-E antibody-mediated allergic responses.11–13 Food intolerance, for example, can precipitate a variety of outcomes, including headache, eczema, rhinosinusitis, vascular spasm, and cardiac arrhythmia that are unrelated to atopic disease.14 To others working in the field, this increase in sensitivity is due to pollutant overload in our air, food, and water triggering the intracellular mechanisms making Ca2+ combining with protein kinase A and C and then being phosphorylated. Many of the other clinical phenomena include multiple neurovascular syndromes such as small vessel vasculopathy colitis, enteritis myotoxicity, neuritis, neuropathy, encephalopathy, and so on. For all of these, food sensitivity is part of the problem.
A comprehensive summary of disease variants implicated in metal allergy
Published in Journal of Toxicology and Environmental Health, Part B, 2022
These symptoms and the immunological mechanisms responsible for SNAS are believed to involve both cell-mediated effects, as well as prototypical Th2-type responses. The existence of nickel-reactive T-cell populations is a common feature of the disease, and subjects with SNAS often exhibit a significant increase in number of CD45RO+ memory cells present in the GI mucosa (Falagiani et al. 2008). Similarly, while established populations of nickel-specific regulatory T-cells may be detected in healthy individuals, this tolerogenic cell type is non-existent in SNAS patients. Although T-cells play a prominent role in the pathogenesis of SNAS, the simultaneous involvement of several critical Th2-associated effector functions led to the classification of this disease as a mixed-type hypersensitivity response initiated by Ni (Di Gioacchino et al. 2018). Accordingly, one of the major cytokines responsible for SNAS responses is IL-5. Consistent with this molecule’s role in immediate-type allergic responses, the enhanced production of IL-5 detected in SNAS patients leads to eosinophilic-dominant inflammation (Falagiani et al. 2008). As a result, many patients develop eosinophilic esophagitis and other eosinophil-mediated reactions in the GI tract.