ABSTRACT
The present research was aimed to investigate the effectiveness of mindfulness training and dietary regime on weight loss in obese people. The research was quasi-experimental with posttest-pretest that used control group. The population consisted of all the individuals who attended two clinics of nutrition advice and diet therapy in Karaj. 60 individuals, whose BMI was more than 30, were selected by using the random sampling method. Moreover, they were evaluated by using the SCL-90 test in order to neglect them in case there existed any other significant disorder. Next, they were selected based on age, sex, and education. After explaining the individuals the ongoing research and collecting the informed consent written by them, the samples were placed in four groups (15 in each group). The groups that received mindfulness training attended the nutrition center for eight to 120-minute sessions. In addition, since all the participants referred to the center were motivated to lose weight, individuals who were placed in the control group and those who received mindfulness training were asked not to follow any specific diet for two months. Moreover, the in depth relaxation CD was prepared for those who asked, in order to train themselves at home. Descriptive statistical methods were employed in order to analyze the data and ANACOVA and variance analysis with frequent measurement were used. The research findings indicated that mindfulness training was accompanied by diet, which resulted in weight loss in obese patients. In addition, the findings of the two-month follow-up indicated lasting results.
ABSTRACT
Our gastrointestinal tract is a portal of entry for a number of bacteria and viruses. Thus, this tissue must develop ways to induce antigen-specific T cell and antibody responses quickly. Intestinal epithelial cells are a central player in barrier function and also in communicating signals from invading pathogens to the underlying immune tissue. Here we demonstrate that activation of Toll-like receptor 1 (TLR1) in the epithelium leads to the upregulation of the chemokine CCL20 during oral infection with Yersinia enterocolitica. Further, both neutralization of CCL20 using polyclonal antibody treatment and deletion of TLR1 resulted in a defect in CCR6+ dendritic cells (DCs), which produce innate cytokines that help to induce anti-Yersinia-specific T helper 17 (TH17) cells and IgA production. These data demonstrate a novel role for TLR1 signaling in the intestinal epithelium and demonstrate that together TLR1 and CCL20 are critical mediators of TH17 immunity through the activation and recruitment of DCs.
Subject(s)
Chemokine CCL20/immunology , Dendritic Cells/immunology , Intestinal Mucosa/immunology , Th17 Cells/immunology , Toll-Like Receptor 1/immunology , Yersinia Infections/immunology , Yersinia enterocolitica/immunology , Animals , Antibodies, Blocking/administration & dosage , Antibody Formation/drug effects , Cells, Cultured , Chemokines/metabolism , Dendritic Cells/drug effects , Immunity, Mucosal/drug effects , Immunoglobulin A/blood , Lymphocyte Activation/drug effects , Mice, Inbred C57BL , Mice, Knockout , Receptors, CCR6/metabolism , Th17 Cells/drug effectsABSTRACT
Mice were stressed by swimming for 3 min in water at 20 degrees C and antinociception was assessed by the tail-flick test. The stress-induced antinociception was potentiated by intraperitoneal administration of different doses of theophylline. The effect of the drug was dose-dependent. 5'-N-Ethylcarboxamidoadenosine administration also increased the stress response dose-dependently. N6-Phenyl-isopropyladenosine decreased the antinociception induced by swim-stress as well as after stress plus theophylline. Administration of dipyridamole caused a decrease of antinociception induced by stress or stress plus theophylline. It may be concluded that activation of A2 adenosine receptors increased whereas activation of A1 adenosine sites decreased the stress-induced antinociception. The responses of A2 or A1 activation may be irrelevant to changes in cAMP levels. Because the adenosine agonists and antagonists employed were not selective at the receptor level, other possibilities are not excluded.