2,178 research outputs found

    Army Retirees at the Hunter Army Airfield Chapel in Savannah, Georgia, Will Gain the Confidence and the Basic Skills Necessary to Form Spiritual Mentoring Relationships With Young Soldiers Through a Constructivist Interview and Back-brief Process

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    Army retirees choose to live in close proximity to a military installation, because living close provides many benefits, such as: continuing to shop in the discounted commissary, remaining in the military medical system, enjoying many other recreational benefits offered at military installations, and remaining as close as possible to the world they love. Thus, most Army garrisons across the entire Army enterprise have retirees who have chosen to permanently remain close to the Army posts at which they honorably served. Homesteading near a military installation gives a retiree the opportunity to live among those with whom they existentially identify. Some choose to continue to faithfully attend Army chapels, however, they are often under-utilized as mentors for young soldiers due to the lack of training and leadership opportunities across the entire army chapel system

    The God Plant and other stories

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    Mad2 and Mad3 Cooperate to Arrest Budding Yeast in Mitosis

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    Background: The spindle checkpoint ensures accurate chromosome transmission by delaying chromosome segregation until all chromosomes are correctly aligned on the mitotic spindle. The checkpoint is activated by kinetochores that are not attached to microtubules or are attached but not under tension and arrests cells at metaphase by inhibiting the anaphase-promoting complex (APC) and its coactivator Cdc20. Despite numerous studies, we still do not understand how the checkpoint proteins coordinate with each other to inhibit APCCdc20APC^{Cdc20} activity. Results: To ask how the checkpoint components induce metaphase arrest, we constructed fusions of checkpoint proteins and expressed them in the budding yeast Saccharomyces cerevisiae to mimic possible protein interactions during checkpoint activation. We found that expression of a Mad2-Mad3 protein fusion or noncovalently linked Mad2 and Mad3, but not the overexpression of the two separate proteins, induces metaphase arrest that is independent of functional kinetochores or other checkpoint proteins. We further showed that artificially tethering Mad2 to Cdc20 also arrests cells in metaphase independently of other checkpoint components. Conclusion: Our results suggest that Mad3 is required for the stable binding of Mad2 to Cdc20 in vivo, which is sufficient to inhibit APC activity and is the most downstream event in spindle checkpoint activation.Molecular and Cellular Biolog

    Developing and Piloting a Design Guide for Outdoor Classrooms in Utah

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    The outdoor classroom design guide can help applicants successfully apply for the Utah Outdoor Classroom Grant introduced by the Office of Outdoor Recreation (OOR) in 2021. The design guide includes case studies, design resources, and critical information for community involvement from statewide locations and will serve as a free public resource

    Increased prevalence of precancerous changes in relatives of gastric cancer patients: critical role of H. pylori

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    Background & Aims:Helicobacter pylori is believed to predispose to gastric cancer by inducing gastric atrophy and hypochlorhydria. First-degree relatives of patients with gastric cancer have an increased risk of developing gastric cancer. The aim of this study was to determine the prevalence of atrophy and hypochlorhydria and their association with H. pylori infection in first-degree relatives of patients with gastric cancer. Methods:H. pylori status, gastric secretory function, and gastric histology were studied in 100 first-degree relatives of patients with noncardia gastric cancer and compared with those of controls with no family history of this cancer. Results: Compared with healthy controls, relatives of patients with gastric cancer had a higher prevalence of hypochlorhydria (27% vs. 3%) but a similar prevalence of H. pylori infection (63% vs. 64%). Relatives of cancer patients also had a higher prevalence of atrophy (34%) than patients with nonulcer dyspepsia (5%) matched for H. pylori prevalence. Among the relatives of cancer patients, the prevalence of atrophy and hypochlorhydria was increased only in those with evidence of H. pylori infection, was greater in relatives of patients with familial cancer than in relatives of sporadic cancer index patients, and increased with age. Eradication of H. pylori infection produced resolution of the gastric inflammation in each subject and resolution of hypochlorhydria and atrophy in 50% of the subjects. Conclusions: Relatives of patients with gastric cancer have an increased prevalence of precancerous gastric abnormalities, but this increase is confined to those with H. pylori infection. Consequently, prophylactic eradication of the infection should be offered to such subjects

    Disruption of PCNA-lamins A/C interactions by prelamin A induces DNA replication fork stalling

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    The accumulation of prelamin A is linked to disruption of cellular homeostasis, tissue degeneration and aging. Its expression is implicated in compromised genome stability and increased levels of DNA damage, but to date there is no complete explanation for how prelamin A exerts its toxic effects. As the nuclear lamina is important for DNA replication we wanted to investigate the relationship between prelamin A expression and DNA replication fork stability. In this study we report that the expression of prelamin A in U2OS cells induced both mono-ubiquitination of proliferating cell nuclear antigen (PCNA) and subsequent induction of Pol η, two hallmarks of DNA replication fork stalling. Immunofluorescence microscopy revealed that cells expressing prelamin A presented with high levels of colocalisation between PCNA and γH2AX, indicating collapse of stalled DNA replication forks into DNA double-strand breaks. Subsequent protein-protein interaction assays showed prelamin A interacted with PCNA and that its presence mitigated interactions between PCNA and the mature nuclear lamina. Thus, we propose that the cytotoxicity of prelamin A arises in part, from it actively competing against mature lamin A to bind PCNA and that this destabilises DNA replication to induce fork stalling which in turn contributes to genomic instability
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