Group cognitive behavioural therapy (GCBT) versus treatment as usual (TAU) in the treatment of irritable bowel syndrome (IBS): A study protocol for a randomized controlled trial

Background: Irritable bowel syndrome (IBS) is a common disease that affects the quality of life (QOL) and social functioning of sufferers. Visceral anxiety is currently considered a key factor in the onset and exacerbation of IBS, and cognitive-behavioural therapy (CBT) targeting visceral anxiety is thought to be effective. However, access to CBT is limited due to the lack of trained therapists, the substantial time required for therapy and the associated costs. Group CBT (GCBT) may solve some of these problems. We have therefore planned this trial to examine the efficacy of GCBT for IBS. Methods: The trial is a two-armed, parallel group, open label, stratified block randomized superiority trial. The study group will consist of 112 participants (aged 18–75 years) with IBS (Rome-III or IV criteria). Participants will be randomly allocated 1:1 to (i) the intervention group: ten-week GCBT plus treatment as usual (TAU) or (ii) the control group: waiting list (WL) plus TAU. The co-primary outcomes are the change in IBS severity or disease-specific quality of life from baseline to week 13 which is 1 month after the end of treatment. The efficacy of GCBT for IBS will be examined through mixed-effects repeated-measures analysis. Discussion: GCBT, if found effective, can address the issues of the shortage of therapists as well as the time required and the costs associated with individual CBT. Clinically, the findings will help make effective CBT programmes accessible to a large number of distressed IBS patients at lower costs. Theoretically, the results will clarify the relationship between IBS and psychological stress and will help elucidate the underlying mechanisms of IBS. Trial registration: UMIN, CTR-UMIN000031710. Registered on March 13, 2018

Major Factors Affecting Incidence of Childhood Thyroid Cancer in Belarus after the Chernobyl Accident: Do Nitrates in Drinking Water Play a Role?

One of the major health consequences of the Chernobyl Nuclear Power Plant accident in 1986 was a dramatic increase in incidence of thyroid cancer among those who were aged less than 18 years at the time of the accident. This increase has been directly linked in several analytic epidemiological studies to iodine-131 (131I) thyroid doses received from the accident. However, there remains limited understanding of factors that modify the 131Irelated risk. Focusing on post-Chernobyl pediatric thyroid cancer in Belarus, we reviewed evidence of the effects of radiation, thyroid screening, and iodine deficiency on regional differences in incidence rates of thyroid cancer. We also reviewed current evidence on content of nitrate in groundwater and thyroid cancer risk drawing attention to high levels of nitrates in open well water in several contaminated regions of Belarus, i.e. Gomel and Brest, related to the usage of nitrogen fertilizers. In this hypothesis generating study, based on ecological data and biological plausibility, we suggest that nitrate pollution may modify the radiationrelated risk of thyroid cancer contributing to regional differences in rates of pediatric thyroid cancer in Belarus. Analytic epidemiological studies designed to evaluate joint effect of nitrate content in groundwater and radiation present a promising avenue of research and may provide useful insights into etiology of thyroid cancer

Smoking and secondhand smoke exposure and prevalence of depressive symptoms during pregnancy in Japan : baseline data from the Kyushu Okinawa Maternal and Child Health Study

Background: Epidemiological evidence on the relationship between smoking and secondhand smoke (SHS) exposure and depressive symptoms during pregnancy has been limited. The present cross-sectional study examined this issue in Japan. Methods: Between April 2007 and March 2008, 1757 pregnant women who lived in one of seven prefectures on Kyushu Island in southern Japan or in Okinawa Prefecture, an island chain in the southwest of Japan, participated in the Kyushu Okinawa Maternal and Child Health Study, a prebirth cohort study. In the present study, data on 1745 pregnant women were available for analysis. Information on smoking, SHS exposure, depressive symptoms, and potential confounding factors was obtained through a self-administered questionnaire. Depressive symptoms were defined as present when subjects had a Center for Epidemiologic Studies Depression Scale score of 16 or higher. Adjustment was made for age, gestation, region of residence, number of children, family structure, household income, education, job type, history of depression, and family history of depression. Results: The prevalence of depressive symptoms during pregnancy was 19.2%. Compared with having never smoked, both former and current smoking was independently associated with a higher prevalence of depressive symptoms during pregnancy: the adjusted odds ratios (ORs) were 1.39 (95% CI: 1.06–1.83) and 2.49 (95% CI: 1.36–4.45), respectively. Also, 3.0 to 7.9 and 8.0 or more pack-years of smoking were independently positively related to depressive symptoms during pregnancy: the adjusted ORs were 1.55 (95% CI: 1.08–2.22) and 1.97 (95% CI: 1.26–3.03), respectively (P for trend = 0.0005). Among the 1183 subjects who had never smoked, current SHS exposure at home was independently positively associated with depressive symptoms during pregnancy: the adjusted OR was 1.51 (95% CI: 1.003–2.30). Conclusions: Former and current smoking, 3.0 or more pack-years of smoking, and current SHS exposure at home may be positively associated with depressive symptoms during pregnancy

The Effects of TGF-β Signaling on Cancer Cells and Cancer Stem Cells in the Bone Microenvironment

Background: Transforming growth factor-β (TGF-β) plays a key role in bone metastasis formation; we hypothesized the possible involvement of TGF-β in the induction of cancer stem cells (CSCs) in the bone microenvironment (micro-E), which may be responsible for chemo-resistance. Methods: Mouse mammary tumor cells were implanted under the dorsal skin flap over the calvaria and into a subcutaneous (subQ) lesions in female mice, generating tumors in the bone and subQ micro-Es. After implantation of the tumor cells, mice were treated with a TGF-β R1 kinase inhibitor (R1-Ki). Results: Treatment with R1-Ki decreased tumor volume and cell proliferation in the bone micro-E, but not in the subQ micro-E. R1-Ki treatment did not affect the induction of necrosis or apoptosis in either bone or subQ micro-E. The number of cells positive for the CSC markers, SOX2, and CD166 in the bone micro-E, were significantly higher than those in the subQ micro-E. R1-Ki treatment significantly decreased the number of CSC marker positive cells in the bone micro-E but not in the subQ micro-E. TGF-β activation of the MAPK/ERK and AKT pathways was the underlying mechanism of cell proliferation in the bone micro-E. BMP signaling did not play a role in cell proliferation in either micro-E. Conclusion: Our results indicated that the bone micro-E is a key niche for CSC generation, and TGF-β signaling has important roles in generating CSCs and tumor cell proliferation in the bone micro-E. Therefore, it is critically important to evaluate responses to chemotherapeutic agents on both cancer stem cells and proliferating tumor cells in different tumor microenvironments in vivo