Leisure Education and the Family

Having and utilizing free time is often a problem for individuals and for families. Family leisure education, focusing on lifestyles and leisure, or family wellness and the role of leisure may be a first step in addressing that problem. No other profession is specifically charged with the responsibility of educating for leisure; that charge is unique to the recreation and leisure profession. Families, as individuals and as a unit have significant time available for experiencing recreation and leisure, and their choices singularly and collectively impact on the unit as a whole. By exploring the components of leisure education, especially self and leisure awareness, the professional has an opportunity to assist family members in exploring intra and interpersonal transactions. Since most of the time families spend is off-work time, their primary interactions take place in the home and during free time, and it is during these times that they will come to know each other and come to bond or fragment as a group. The recreation and leisure choices made by each member and the group impact on how the unit will come to be defined. By exploring values, attitudes, behaviors and roles, the professional can help facilitate the meaning of recreation and leisure in the lives of the family unit. This paper focuses on the conceptual and practical design of a family leisure education model that can be used in various recreation settings including those settings which serve people with disabilities

Galectin-3 and N-acetylglucosamine promote myogenesis and improve skeletal muscle function in the mdx model of Duchenne muscular dystrophy

The muscle membrane, sarcolemma, must be firmly attached to the basal lamina. The failure of proper attachment results in muscle injury, which is the underlying cause of Duchenne muscular dystrophy (DMD), where mutations in the dystrophin gene disrupts the firm adhesion. In DMD patients, even moderate contraction causes damage, leading to progressive muscle degeneration. The damaged muscles are repaired through myogenesis. Consequently, myogenesis is highly active in DMD patients, and the repeated activation of myogenesis leads to the exhaustion of the myogenic stem cells. Therefore, approaches to reducing the risk of the exhaustion are to develop a treatment that strengthens the interaction between the sarcolemma and the basal lamina, and increases the efficiency of myogenesis. Galectin-3 is an oligosaccharide-binding protein and known to be involved in cell–cell interactions and cell–matrix interactions. Galectin-3 is expressed in myoblasts and skeletal muscle while its function in muscle remains elusive. In this study, we found evidence that galectin-3 and the monosaccharide N-acetylglucosamine, which increases the ligands (oligosaccharides) of galectin-3, promotes myogenesis in vitro. Moreover, in the mdx mouse model of DMD, treatment with N-acetylglucosamine increased the muscle force production. Our results demonstrate that treatment with N-acetylglucosamine can mitigate the burden of DMD

Dose-dependent spatiotemporal responses of mammalian cells to an alkylating agent.

Cultured cell populations are composed of heterogeneous cells, and previous single-cell lineage tracking analysis of individual HeLa cells provided empirical evidence for significant heterogeneity of the rate of cell proliferation and induction of cell death. Nevertheless, such cell lines have been used for investigations of cellular responses to various substances, resulting in incomplete characterizations. This problem caused by heterogeneity within cell lines could be overcome by investigating the spatiotemporal responses of individual cells to a substance. However, no approach to investigate the responses by analyzing spatiotemporal data is currently available. Thus, this study aimed to analyze the spatiotemporal responses of individual HeLa cells to cytotoxic, sub-cytotoxic, and non-cytotoxic doses of the well-characterized carcinogen, N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). Although cytotoxic doses of MNNG are known to induce cell death, the single-cell tracking approach revealed that cell death occurred following at least four different cellular events, suggesting that cell death is induced via multiple processes. We also found that HeLa cells exposed to a sub-cytotoxic dose of MNNG were in a state of equilibrium between cell proliferation and cell death, with cell death again induced through different processes. However, exposure of cells to a non-cytotoxic dose of MNNG promoted growth by reducing the cell doubling time, thus promoting the growth of a sub-population of cells. A single-cell lineage tracking approach could dissect processes leading to cell death in a spatiotemporal manner and the results suggest that spatiotemporal data obtained by tracking individual cells can be used as a new type of bioinformatics data resource that enables the examination of cellular responses to various external substances

Expanding perspectives on the poverty trap for smallholder farmers in Tanzania : the role of rural input supply chains

Smallholder farmers across rural landscapes remain trapped in a vicious cycle of endemic poverty where interconnected challenges limit their ability to improve their livelihoods. Our study of smallholder farmers’ relationships with suppliers and several stakeholders across the Tanzanian rural agro-input supply chain offers an extended perspective on the persistence of endemic poverty and broadens the discussion on the future of sustainable food production and smallholder livelihoods. Through interviews and focus groups, we use a grounded theory methodology to develop a systemic approach to understanding the complexities of this landscape as related to smallholder agro-input sourcing activities. Our causal loop diagram framework provides a unique perspective on the poverty trap experienced by smallholder farmers in this context. Our findings may be useful in targeting practical and sustainable directions towards overcoming the poverty trap, ultimately enabling smallholders to increase wealth and improve their livelihoods through sustainable practices

Galectin-3 enhances neutrophil motility and extravasation into the airways during Aspergillus fumigatus infection.

Aspergillus fumigatus is an opportunistic mold that infects patients who are immunocompromised or have chronic lung disease, causing significant morbidity and mortality in these populations. While the factors governing the host response to A. fumigatus remain poorly defined, neutrophil recruitment to the site of infection is critical to clear the fungus. Galectin-3 is a mammalian β-galactose-binding lectin with both antimicrobial and immunomodulatory activities, however the role of galectin-3 in the defense against molds has not been studied. Here we show that galectin-3 expression is markedly up-regulated in mice and humans with pulmonary aspergillosis. Galectin-3 deficient mice displayed increased fungal burden and higher mortality during pulmonary infection. In contrast to previous reports with pathogenic yeast, galectin-3 exhibited no antifungal activity against A. fumigatus in vitro. Galectin-3 deficient mice exhibited fewer neutrophils in their airways during infection, despite normal numbers of total lung neutrophils. Intravital imaging studies confirmed that galectin-3 was required for normal neutrophil migration to the airspaces during fungal infection. Adoptive transfer experiments demonstrated that stromal rather than neutrophil-intrinsic galectin-3 was necessary for normal neutrophil entry into the airspaces. Live cell imaging studies revealed that extracellular galectin-3 directly increases neutrophil motility. Taken together, these data demonstrate that extracellular galectin-3 facilitates recruitment of neutrophils to the site of A. fumigatus infection, and reveals a novel role for galectin-3 in host defense against fungal infections