Delivery Methods of Cognitive Behavior Therapy for Patients With Irritable Bowel Syndrome.

Irritable bowel syndrome (IBS) is the most commonly diagnosed gastrointestinal disorder and negatively impacts individuals' quality of life. Cognitive behavioral therapy appears effective for reducing symptoms in many irritable bowel syndrome patients. However, the optimal methods to deliver cognitive behavioral therapy and the effective treatment dosage for patients with IBS remain unclear. This article aims to provide an update on cognitive behavioral therapy research in IBS, particularly considering the dose of treatment, route of delivery (in-person vs. web- and telephone-based delivery), and outcome measures. A systematic literature review was conducted using databases of PubMed, CINAHL Complete, and Web of Science from 2008 through 2021. Twelve studies reporting randomized clinical trials comparing cognitive behavioral therapy delivered with in-person, telephone, and web for the management of IBS symptoms among adults with irritable bowel syndrome were found. The dose of treatment varied from 4 to 10 sessions. Six different scales measured various outcomes. No severe adverse reactions to cognitive behavioral therapy were reported. Cognitive behavioral therapy is an effective treatment for IBS symptoms regardless of the dose and the route of treatment. However, it is difficult to compare the effectiveness of these randomized clinical trials due to the various cognitive behavioral therapy protocols, combined routes of therapy delivery, and different outcome measures used.

Regulated proteolysis of the IFNaR2 subunit of the interferon-alpha receptor.

The type I interferons (IFNs) bind surface receptors, induce JAK kinases and activate STAT transcription factors to stimulate the transcription of genes downstream of IFN-stimulated response elements (ISREs). In this study, we demonstrate that IFNaR2, a subunit of the type I IFN receptor, is proteolytically cleaved in a regulated manner. Immunoblotting shows that multi-step cleavage occurs in response to phorbol ester (PMA) and IFN-alpha, generating both a transmembrane 'stub' and the intracellular domain (ICD), similar to Notch proteolysis. Isolated membrane fractions process IFNaR2 to release the ICD. A chimeric receptor construct is utilized to show that cleavage requires the presenilins and occurs in response to epidermal growth factor and protein kinase C-delta overexpression, as well as PMA and type I IFNs. Fluorescence microscopy demonstrates that a green fluorescent protein-ICD fusion localizes predominantly to the nucleus. A fusion between the ICD and the Gal4 DNA-binding domain represses transcription, in a histone deacetylase-dependent manner, of a Gal4 upstream activating sequence-regulated reporter, while overexpression of the ICD alone represses transcription of a reporter linked to an ISRE. Proteolytic cleavage events may facilitate receptor turnover or, more likely, function as a mechanism for signaling similar to that employed by Notch and the Alzheimer's precursor protein.