Using a Historical Tour to Teach Extension Audiences About Diversity and Human Rights

Idaho\u27s Journey for Diversity and Human Rights is a traveling workshop designed to teach about the roots of the state\u27s people and their human rights challenges. Designers planned to acquaint participants with the richness and diversity of Idaho\u27s past and broaden their perspective on the way in which past residents coped with issues not much different from those current residents face. Participants report gains in knowledge of Idaho\u27s past and present challenges of human rights and diversity and plan to apply that knowledge in their daily lives. Educators can modify and replicate Idaho\u27s Journey to fit any state or region

Interview of Susan Traver by Kevlin Haire

Interview conducted at The Ohio State University Archives, Columbus, Ohio.Susan Traver was the first of her family to attend college, and she began at the Lima branch of The Ohio State University. At the time, classes met in a high school since no buildings had been constructed yet for the branch. After transferring to the Columbus campus, Traver attended classes while working, first as a keypunch operator, then in a social services position with the state of Ohio. She also recalls friends getting arrested during the 1970 demonstrations for missing curfew, and she describes the stress and pressure felt by students throughout the Vietnam War era. After graduating in 1972, she moved to Toledo where she worked as a rehabilitation counselor, and she earned a master’s degree at the University of Toledo in 1992

Building new computational models to support health behavior change and maintenance:new opportunities in behavioral research

Adverse and suboptimal health behaviors and habits are responsible for approximately 40 % of preventable deaths, in addition to their unfavorable effects on quality of life and economics. Our current understanding of human behavior is largely based on static "snapshots" of human behavior, rather than ongoing, dynamic feedback loops of behavior in response to ever-changing biological, social, personal, and environmental states. This paper first discusses how new technologies (i.e., mobile sensors, smartphones, ubiquitous computing, and cloud-enabled processing/computing) and emerging systems modeling techniques enable the development of new, dynamic, and empirical models of human behavior that could facilitate just-in-time adaptive, scalable interventions. The paper then describes concrete steps to the creation of robust dynamic mathematical models of behavior including: (1) establishing "gold standard" measures, (2) the creation of a behavioral ontology for shared language and understanding tools that both enable dynamic theorizing across disciplines, (3) the development of data sharing resources, and (4) facilitating improved sharing of mathematical models and tools to support rapid aggregation of the models. We conclude with the discussion of what might be incorporated into a "knowledge commons," which could help to bring together these disparate activities into a unified system and structure for organizing knowledge about behavior

A randomized trial of adjunct testosterone for cancer‐related muscle loss in men and women

Abstract Background Cancer cachexia negatively impacts cancer‐related treatment options, quality of life, morbidity, and mortality, yet no established therapies exist. We investigated the anabolic properties of testosterone to limit the loss of body mass in late stage cancer patients undergoing standard of care cancer treatment. Methods A randomized, double‐blind, placebo‐controlled phase II clinical trial was undertaken to assess the potential therapeutic role of adjunct testosterone to limit loss of body mass in patients with squamous cell carcinoma of the cervix or head and neck undergoing standard of care treatment including chemotherapy and chemoradiation. Patients were randomly assigned in blocks to receive weekly injections of either 100 mg testosterone enanthate or placebo for 7 weeks. The primary outcome was per cent change in lean body mass, and secondary outcomes included assessment of quality of life, tests of physical performance, muscle strength, daily activity levels, resting energy expenditure, nutritional intake, and overall survival. Results A total of 28 patients were enrolled, 22 patients were studied to completion, and 21 patients were included in the final analysis (12 placebo, nine testosterone). Adjunct testosterone increased lean body mass by 3.2% (95% confidence interval [CI], 0–7%) whereas those receiving placebo lost 3.3% (95% CI, −7% to 1%, P = 0.015). Although testosterone patients maintained more favourable body condition, sustained daily activity levels, and showed meaningful improvements in quality of life and physical performance, overall survival was similar in both treatment groups. Conclusions In patients with advanced cancer undergoing the early phase of standard of care therapy, adjunct testosterone improved lean body mass and was also associated with increased quality of life, and physical activity compared with placebo

The Kruppel-like factor KLF4 is a critical regulator of monocyte differentiation

Monocyte differentiation involves the participation of lineage-restricted transcription factors, although the mechanisms by which this process occurs are incompletely defined. Within the hematopoietic system, members of the Kruppel-like family of factors (KLFs) play essential roles in erythrocyte and T lymphocyte development. Here we show that KLF4/GKLF is expressed in a monocyte-restricted and stage-specific pattern during myelopoiesis and functions to promote monocyte differentiation. Overexpression of KLF4 in HL-60 cells confers the characteristics of mature monocytes. Conversely, KLF4 knockdown blocked phorbol ester-induced monocyte differentiation. Forced expression of KLF4 in primary common myeloid progenitors (CMPs) or hematopoietic stem cells (HSCs) induced exclusive monocyte differentiation in clonogenic assays, whereas KLF4 deficiency inhibited monocyte but increased granulocyte differentiation. Mechanistic studies demonstrate that KLF4 is a target gene of PU.1. Consistently, KLF4 can rescue PU.1−/− fetal liver cells along the monocytic lineage and can activate the monocytic-specific CD14 promoter. Thus, KLF4 is a critical regulator in the transcriptional network controlling monocyte differentiation

Biallelic mutations in the 3' exonuclease TOE1 cause pontocerebellar hypoplasia and uncover a role in snRNA processing.

Deadenylases are best known for degrading the poly(A) tail during mRNA decay. The deadenylase family has expanded throughout evolution and, in mammals, consists of 12 Mg2+-dependent 3'-end RNases with substrate specificity that is mostly unknown. Pontocerebellar hypoplasia type 7 (PCH7) is a unique recessive syndrome characterized by neurodegeneration and ambiguous genitalia. We studied 12 human families with PCH7, uncovering biallelic, loss-of-function mutations in TOE1, which encodes an unconventional deadenylase. toe1-morphant zebrafish displayed midbrain and hindbrain degeneration, modeling PCH-like structural defects in vivo. Surprisingly, we found that TOE1 associated with small nuclear RNAs (snRNAs) incompletely processed spliceosomal. These pre-snRNAs contained 3' genome-encoded tails often followed by post-transcriptionally added adenosines. Human cells with reduced levels of TOE1 accumulated 3'-end-extended pre-snRNAs, and the immunoisolated TOE1 complex was sufficient for 3'-end maturation of snRNAs. Our findings identify the cause of a neurodegenerative syndrome linked to snRNA maturation and uncover a key factor involved in the processing of snRNA 3' ends