Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The nutritional developmental origins of inflammatory bowel disease[s] (IBDs: Crohn's disease or Crohn disease [CD] and ulcerative colitis [UC]) and their diet-based treatments continue to receive increasing attention. There is growing evidence for the success of nutrition-based treatments, such as exclusive enteral nutrition [EEN] and the specific carbohydrate diet [SCD], in both paediatric and adult patients. Beyond these two dietary interventions, symptomatic benefit in IBD has also been shown from a gluten-free diet [GFD] and paleolithic diet [PALEO], among others. These nutritional therapies may point to critical factors in not only the pathology, but also the pathogenesis of the disease group. It is difficult, however, to discern a common element within the large number of diet-based causation theories [e.g. emulsifiers, processed foods, refrigeration, increased total fat intake, low fibre intake, carbohydrate dominant food, etc.] and the varied dietary treatments of IBD. This Viewpoint article highlights that carbohydrate variation links diet-based causation theories, and that carbohydrate monotony or persistence is the commonly shared characteristic of diet-based IBD therapy. Further research directed towards carbohydrate monotony may critically advance the prevention and treatment of these highly morbid conditions.
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PMID:Carbohydrate Monotony as Protection and Treatment for Inflammatory Bowel Disease. 3071 43

Emerging evidence indicates IBD is a risk factor for the increasing incidence of colorectal cancer (CRC) development. We used a system biology approach to identify common molecular signatures and pathways that interact between IBD and CRC and the indispensable pathological mechanisms. First, we identified 177 common differentially expressed genes (DEGs) between IBD and CRC. Gene set enrichment, protein-protein, DEGs-transcription factors, DEGs-microRNAs, protein-drug interaction, gene-disease association, Gene Ontology, pathway enrichment analyses were conducted to these common genes. The inclusion of common DEGs with bimolecular networks disclosed hub proteins (LYN, PLCB1, NPSR1, WNT5A, CDC25B, CD44, RIPK2, ASAP1), transcription factors (SCD, SLC7A5, IKZF3, SLC16A1, SLC7A11) and miRNAs (mir-335-5p, mir-26b-5p, mir-124-3p, mir-16-5p, mir-192-5p, mir-548c-3p, mir-29b-3p, mir-155-5p, mir-21-5p, mir-15a-5p). Analysis of the interaction between protein and drug discovered ASAP1 interacts with cysteine sulfonic acid and double oxidized cysteine drug compounds. Gene-disease association analysis retrieved ASAP1 also associated with pulmonary and bladder neoplasm diseases.
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PMID:Detection of molecular signatures and pathways shared in inflammatory bowel disease and colorectal cancer: A bioinformatics and systems biology approach. 3253 71