Gut-focused hypnotherapy is an effective treatment for irritable bowel syndrome but is not widely available. This study assessed whether providing hypnotherapy by Skype might partially overcome this problem. Using a 50-point or more reduction in the IBS Symptom Severity Score as the primary outcome measure, 65% of subjects responded to Skype hypnotherapy with all other outcomes significantly improving. The primary outcome figure for face-to-face hypnotherapy was 76%. When other outcome scores for Skype and face-to-face treatment were compared, the mean changes were these: symptom severity (−94.1 vs. −129.2), noncolonic score (−52.3 vs. −64.8), quality of life (+56.4 vs. +66.2), anxiety (−3.3 vs. −3.0), depression (−1.7 vs. −2.5), and a 30% or more pain reduction (44% vs. 62%). Skype hypnotherapy is effective but slightly less so than face-to-face treatment. However, many patients would have been unable to access treatment without the Skype option.
BackgroundPhosphatidylinositol 3-kinase delta (PI3Kδ) and Janus-activated kinases (JAK) are both novel anti-inflammatory targets in asthma that affect lymphocyte activation. We have investigated the anti-inflammatory effects of PI3Kδ and JAK inhibition on cytokine release from asthma bronchoalveolar lavage (BAL) cells and T-cell activation, and measured lung PI3Kδ and JAK signalling pathway expression.MethodCells isolated from asthma patients and healthy subjects were treated with PI3Kδ or JAK inhibitors, and/or dexamethasone, before T-cell receptor stimulation. Levels of IFNγ, IL-13 and IL-17 were measured by ELISA and flow cytometry was used to assess T-cell activation. PI3Kδ, PI3Kγ, phosphorylated protein kinase B (pAKT) and Signal Transducer and Activator of Transcription (STAT) protein expression were assessed by immunohistochemistry in bronchial biopsy tissue from asthma patients and healthy subjects. PI3Kδ expression in BAL CD3 cells was measured by flow cytometry.ResultsJAK and PI3Kδ inhibitors reduced cytokine levels from both asthma and healthy BAL cells. Combining dexamethasone with either a JAK or PI3Kδ inhibitor showed an additive anti-inflammatory effect. JAK and PI3Kδ inhibitors were shown to have direct effects on T-cell activation. Immunohistochemistry showed increased numbers of PI3Kδ expressing cells in asthma bronchial tissue compared to controls. Asthma CD3 cells in BAL expressed higher levels of PI3Kδ protein compared to healthy cells.ConclusionsTargeting PI3Kδ or JAK may prove effective in reducing T-cell activation and the resulting cytokine production in asthma.Electronic supplementary materialThe online version of this article (doi:10.1186/s12931-016-0436-2) contains supplementary material, which is available to authorized users.
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