Oneilrossi5450

Background We examined whether telecommunication-device-based distance interviews are inferior to face-to-face interviews in terms of facilitating behavioral changes and disease management in patients with diabetic nephropathy. We also examined the feasibility of a newly designed six-month telenursing program. Methods This study represents a post-hoc analysis of data from a randomized controlled trial, in which we compared the efficacy of remote self-management education with that of direct education for patients with diabetic nephropathy. The participants were 40 company employees, who were randomly divided into two groups. Over 6 months, the intervention group (n = 21) received three distance interviews using a tablet computer. Meanwhile, the control group (n = 19) received three face-to-face interviews. In addition, both groups received biweekly nine telephone calls. A triangulation approach was used. We first compared the two groups in inferiority tests. Then, we analyzed data from semi-structured intervicators, we found that the distance method is not inferior to the direct face-to-face method. However, when considering long-term effects, based on the respective degrees of improvement in behavioral change, the direct method seems to be more effective. Trial registration The trial was registered with the University Hospital Medical Information Network clinical trial registry (No. UMIN000026568) on March 15, 2017, retrospectively. © The Author(s). 2020.A joint is the point of connection between two bones in our body. Inflammation of the joint leads to several diseases, including osteoarthritis, which is the concern of this review. Osteoarthritis is a common chronic debilitating joint disease mainly affecting the elderly. Several studies showed that inflammation triggered by factors like biomechanical stress is involved in the development of osteoarthritis. Barasertib cost This stimulates the release of early-stage inflammatory cytokines like interleukin-1 beta (IL-1β), which in turn induces the activation of signaling pathways, such as nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), phosphoinositide 3-kinase/protein kinase B (PI3K/AKT), and mitogen-activated protein kinase (MAPK). These events, in turn, generate more inflammatory molecules. Subsequently, collagenase like matrix metalloproteinases-13 (MMP-13) will degrade the extracellular matrix. As a result, anatomical and physiological functions of the joint are altered. This review is aimed at summarizing the previous studies highlighting the involvement of inflammation in the pathogenesis of osteoarthritis. Copyright © 2020 Yoke Yue Chow and Kok-Yong Chin.Smoking is a major risk factor for pulmonary diseases that include chronic obstructive pulmonary diseases (COPD) and cancer. Nicotine is the toxic and addictive component of tobacco products, like cigarettes, that negatively affects the immune system. Here, we examined the effect of nicotine on the IL-22 pathway that protects lung function by increasing transepithelial resistance and epithelial cell regeneration and repair. Our results indicate that exposure to nicotine impairs the regenerative capacity of primary bronchial epithelial cells in scratch assays. IL-22 at 100 ng/ml significantly improved wound healing in epithelial cells; however, the exposure to nicotine hampered the IL-22-mediated effect of wound healing. Investigation into the mechanisms showed that IL-22 receptor, IL-22Rα1, was downregulated in the presence of nicotine as determined by q-PCR and flow cytometry. We also investigated the effect of nicotine on IL-22 production by T cells. Results indicate that nicotine inhibited the secretion of IL-22 from T cells in response to aryl hydrocarbon receptor (AHR) ligand, FICZ. Altogether, the data suggests that nicotine negatively influences the IL-22-IL-22R axis. This impairment may contribute to the nicotine-mediated detrimental effects on lung function. Copyright © 2020 Hannah My-Hanh Nguyen et al.Rheumatoid arthritis is characterised by a chronic inflammatory response resulting in destruction of the joint and significant pain. Although a range of treatments are available to control disease activity in RA, bone destruction and joint pain exist despite suppression of inflammation. This study is aimed at assessing the effects of parthenolide (PAR) on paw inflammation, bone destruction, and pain-like behaviour in a mild collagen antibody-induced arthritis (CAIA) mouse model. CAIA was induced in BALB/c mice and treated daily with 1 mg/kg or 4 mg/kg PAR. Clinical paw inflammation was scored daily, and mechanical hypersensitivity was assessed on alternate days. At end point, bone volume and swelling in the paws were assessed using micro-CT. Paw tissue sections were assessed for inflammation and pre-/osteoclast-like cells. The lumbar spinal cord and the periaqueductal grey (PAG) and rostral ventromedulla (RVM) regions of the brain were stained for glial fibrillary acidic protein (GFAP) and ionised calcium-binding adaptor molecule 1 (IBA1) to assess for glial reactivity. Paw scores increased in CAIA mice from days 5-10 and were reduced with 1 mg/kg and 4 mg/kg PAR on days 8-10. Osteoclast-like cells on the bone surface of the radiocarpal joint and within the soft tissue of the hind paw were significantly lower following PAR treatment (p less then 0.005). GFAP- and IBA1-positive cells in the PAG and RVM were significantly lower following treatment with 1 mg/kg (p less then 0.0001 and p = 0.0004, respectively) and 4 mg/kg PAR (p less then 0.0001 and p = 0.001, respectively). In the lumbar spinal cord, IBA1-positive cells were significantly lower in CAIA mice treated with 4 mg/kg PAR (p = 0.001). The findings indicate a suppressive effect of both low- and moderate-dose PAR on paw inflammation, osteoclast presence, and glial cell reactivity in a mild CAIA mouse model. Copyright © 2020 B. Williams et al.Inflammation and oxidative stress play key roles in the process of aging and age-related diseases. Since serine availability plays important roles in the support of antioxidant and anti-inflammatory defense system, we explored whether serine deficiency affects inflammatory and oxidative status in D-galactose-induced aging mice. Male mice were randomly assigned into four groups mice fed a basal diet, mice fed a serine- and glycine-deficient (SGD) diet, mice injected with D-galactose and fed a basal diet, and mice injected with D-galactose and fed an SGD diet. The results showed that D-galactose resulted in oxidative and inflammatory responses, while serine deficiency alone showed no such effects. However, serine deficiency significantly exacerbated oxidative stress and inflammation in D-galactose-treated mice. The composition of fecal microbiota was affected by D-galactose injection, which was characterized by decreased microbiota diversity and downregulated ratio of Firmicutes/Bacteroidetes, as well as decreased proportion of Clostridium XIVa.