Improving Support for Non-Japanese Students Bullied in Japan\u27s Elementary Schools

The purpose of this applied study was to solve the problem of bullying for non-Japanese students in an elementary school in Japan and to design strategies, interventions, and training to address the problem. This research study utilized a multimethod approach to investigate the problem of bullying through participant interviews, focus group research, and an online survey in order to identify solutions to the study’s problem. Data analysis strategies involved analyzing transcribed participant responses from interviews and focus group research, coding, and interpreting survey participant data. This research project required the researcher to meet, interview, and survey participants in Japan who shared their experience involving the bullying of non-Japanese students in a Japanese elementary school. Based on the responses and data presented in this study, teacher professional development, program guidelines, curriculum resources, and student support strategies were created to address the research problem

THE IMPACT OF A PUSHRIM ACTIVATED POWER ASSIST WHEELCHAIR AMONG INDIVIDUALS WITH TETRAPLEGIA

The goal of this project was to test the influence of a pushrim activated power-assisted wheelchair (PAPAW) on the functional capabilities of individuals with cervical level spinal cord injuries (tetraplegia). This repeated measures design type study was divided into two phases, which included testing in two different laboratory settings: a biomechanics laboratory and an activities of daily living laboratory. Fifteen participants included in both phases were fulltime manual wheelchair users (MWUs) with tetraplegia. The purpose of the first phase of the study was to determine the differences in metabolic demands, stroke frequency, and upper extremity joint range of motion, during PAPAW propulsion and traditional manual wheelchair propulsion. Participants propelled both their own manual wheelchairs and a PAPAW through three different resistances (slight, moderate and high), on a computer controlled wheelchair dynamometer. Variables analyzed during this phase included: mean steady state oxygen consumption, ventilation, heart rate, mean stroke frequency, maximum upper extremity joint range of motion, and propulsion speed. Results from the first phase of the study revealed a significant improvement in kinematic, speed, and metabolic variables when participants were propelling with a PAPAW. In Phase II, participants propelled both their own manual wheelchairs and a PAPAW three times over an activities of daily living course. The course was constructed to reflect certain obstacles that a manual wheelchair user might encounter in his or her daily routine. PAPAWs received higher user ratings than the participant's own manual wheelchair for 10 out of 18 obstacles. Additionally, when using a PAPAW, participants were able to complete the course in the same amount of time while maintaining a lower mean heart rate. For individuals with tetraplegia, PAPAWs have the potential to decrease metabolic demands during propulsion, while increasing or maintaining function within ADLs. Use of this device could help MWUs maintain overall physical capacity while reducing the risk for pain and injuries to the upper extremities, which are often seen among manual wheelchair users with tetraplegia. Future studies with this device should focus on the ability of MWUs with tetraplegia to perform necessary activities of daily living within their home environment and community

IL-23 Contributes to Control of Chronic Helicobacter Pylori Infection and the Development of T Helper Responses in a Mouse Model1

The immune response to Helicobacter pylori involves a mixed T helper-1, T helper-2, and T helper-17 response. It has been suggested that T helper cells contribute to the gastric inflammatory response during infection, and that T helper 1 (Th1) and T helper 17 (Th17) subsets may be required for control of H. pylori colonization in the stomach. The relative contributions of these subsets to gastritis and control of infection are still under investigation. IL-23 plays a role in stabilizing and expanding Th17 cell cytokine expression. Expression of IL-23, which is induced in dendritic cells and macrophages following co-culture with H. pylori, has also been reported to increase during H. pylori infection in humans and animal models. To investigate the role of IL-23 in H. pylori, we infected IL-23p19 deficient mice (IL-23−/−) and wild-type littermates with H. pylori strain SS1. At various time points post-infection, we assessed colonization, gastric inflammation, and cytokine profiles in the gastric tissue. Specifically, H. pylori-infected IL-23−/− mice have higher levels of H. pylori in their stomachs, significantly less chronic gastritis, and reduced expression of IL-17 and IFNγ compared to H. pylori-infected wild-type mice. While many of these differences were significant, the H. pylori infected IL-23−/− had mild increases in our measurements of disease severity. Our results indicate that IL-23 plays a role in the activation of the immune response and induction of gastritis in response to H. pylori by contributing to the control of infection and severity of gastritis

Helicobacter pylori adaptation in vivoin response to a high salt diet

Helicobacter pylori exhibits a high level of intraspecies genetic diversity. In this study, we investigated whether the diversification of H. pylori is influenced by the composition of the diet. Specifically, we investigated the effect of a high salt diet (a known risk factor for gastric adenocarcinoma) on H. pylori diversification within a host. We analyzed H. pylori strains isolated from Mongolian gerbils fed either a high salt diet or a regular diet for four months, using proteomic and whole genome sequencing methods. Compared to the input strain and output strains from animals fed a regular diet, the output strains from animals fed a high salt diet produced higher levels of proteins involved in iron acquisition and oxidative stress resistance. Several of these changes were attributable to a non-synonymous mutation in fur (fur-R88H). Further experiments indicated that this mutation conferred increased resistance to high salt conditions and oxidative stress. We propose a model in which a high salt diet leads to high levels of gastric inflammation and associated oxidative stress in H. pylori-infected animals, and that these conditions along with the high intraluminal concentrations of sodium chloride lead to selection of H. pylori strains that are most fit for growth in this environment

Caregiver\u27s difficulty paying child\u27s healthcare bills and bullying victimization of adolescents with physical disabilities

Guided by the ecological systems perspective, the objective of the study was to examine whether caregivers\u27 difficulty paying their child\u27s health-care bills is associated with bullying victimization directly and indirectly through the mediating mechanisms of caregivers\u27 frustration, adolescents\u27 internalizing problems, and social difficulty focusing on adolescents with physical disabilities. The 2019 National Survey of Children\u27s Health dataset, which collected data on adolescents\u27 and caregivers\u27 demographic characteristics and health and well-being, was used. The study sample consisted of 368 caregivers of adolescents, 12–17 years of age with physical disabilities. No direct association between caregivers\u27 difficulty paying their child\u27s health-care bills and bullying victimization was found. However, caregivers\u27 frustration and adolescents\u27 internalizing problems were shown to have an indirect association with bullying victimization, which was mediated by difficulty making friends. In addition, adolescents\u27 difficulty making friends was positively associated with bullying victimization. Practitioners working with adolescents with physical disabilities are encouraged to foster collaborative processes across various ecological systems of the adolescent and family to address caregivers\u27 frustration and promote positive social and emotional development of the adolescent with physical disabilities, which can decrease their risk of bullying victimization

Tuning inflammation in tuberculosis: the role of decoy receptors

Decoy receptors are "silent scavengers" of CC chemokines and cytokines, which play a key role in damping inflammation and tissue damage. In this review we discuss on recent findings demonstrating that these receptors set the balance between antimicrobial resistance, immune activation and inflammatory response in Mycobacterium tuberculosis infection

A Case of Tuberculous Arthritis Following the Use of Etanercept

Etanercept is a tumor necrosis factor (TNF) inhibitor that has been used for the treatment of chronic inflammatory diseases including rheumatoid arthritis, ankylosing spondylitis and psoriatic arthritis. Because of its immunosuppressive activity, opportunistic infections have been noted in treated patients, most notably caused by Mycobacterium tuberculosis. Tuberculosis may present in an extrapulmonary or disseminated form. Since TNF-α inhibitors have been used in Korea, a few cases of TNF-α inhibitor associated tuberculosis have been described. However, tuberculous arthritis has not been previously reported. We describe a case of tuberculous arthritis in a 57-year-old woman with rheumatoid arthritis who was treated with etanercept

CCL3L1 copy number, CCR5 genotype and susceptibility to tuberculosis

Background: Tuberculosis is a major infectious disease and functional studies have provided evidence that both the chemokine MIP-1α and its receptor CCR5 play a role in susceptibility to TB. Thus by measuring copy number variation of CCL3L1, one of the genes that encode MIP-1α, and genotyping a functional promoter polymorphism -2459A > G in CCR5 (rs1799987) we investigate the influence of MIP-1α and CCR5, independently and combined, in susceptibility to clinically active TB in three populations, a Peruvian population (n = 1132), a !Xhosa population (n = 605) and a South African Coloured population (n = 221). The three populations include patients with clinically diagnosed pulmonary TB, as well as other, less prevalent forms of extrapulmonary TB. Methods and results: Copy number of CCL3L1 was measured using the paralogue ratio test and exhibited ranges between 0–6 copies per diploid genome (pdg) in Peru, between 0–12 pdg in !Xhosa samples and between 0–10 pdg in South African Coloured samples. The CCR5 promoter polymorphism was observed to differ significantly in allele frequency between populations (*A; Peru f = 0.67, !Xhosa f = 0.38, Coloured f = 0.48). Conclusions: The case–control association studies performed however find, surprisingly, no evidence for an influence of variation in genes coding for MIP-1α or CCR5 individually or together in susceptibility to clinically active TB in these populations

Current concepts on oxidative/carbonyl stress, inflammation and epigenetics in pathogenesis of chronic obstructive pulmonary disease

Chronic obstructive pulmonary disease (COPD) is a global health problem, and current therapy for COPD is poorly effective and the mainstays of pharmacotherapy are bronchodilators. A better understanding of the pathobiology of COPD is critical for the development of novel therapies. In the present review, we have discussed the roles of oxidative/aldehyde stress, inflammation/immunity, and chromatin remodeling in the pathogenesis of COPD. Imbalance of oxidant/antioxidant balance caused by cigarette smoke and other pollutants/biomass fuels plays an important role in the pathogenesis of COPD by regulating redox-sensitive transcription factors (e.g. NF-κB), autophagy and unfolded protein response leading to chronic lung inflammatory response. Cigarette smoke also activates canonical/alternative NF-κB pathways and their upstream kinases leading to sustained inflammatory response in lungs. Recently, epigenetic regulation has been shown to be critical for the development of COPD because the expression/activity of enzymes that regulate these epigenetic modifications have been reported to be abnormal in airways of COPD patients. Hence, the significant advances made in understanding the pathophysiology of COPD as described herein will identify novel therapeutic targets for intervening COPD