Effects of body protection vests and experience levels in prevention of equestrian injuries.

OBJECTIVES: To investigate the risk reduction and benefit of wearing body protection/safety vests in equestrian sports. METHODS: A comparison of equestrians wearing body protective vests and those not wearing vests was performed using incident report data of 718 participants in the United States Pony Clubs during 2011-2017. Data obtained included age, gender, certification level of member, type of activity, description of incident, description of injuries, what protective equipment was worn and other possible contributing factors. RESULTS: While wearing body protective vests when riding on the flat or for show jumping was not correlated with a decrease in injuries, wearing vests for cross country was correlated with decrease in reported injuries (p=0.036) and showed a trend towards a lower incident severity level (p=0.062). Wearing body protection during cross country reduced the relative risk of injury by 56%. While the volume of incidents varied with a rider's experience level, the number of serious injuries did not appear to correlate with lesser equestrian experience. CONCLUSIONS: While equestrian sports are considered to have a certain degree of risk associated with them, there are ways to make them safer. Wearing safety equipment, such as helmets and body protection, and obtaining education and experience can lessen the chance of incurring serious injuries.

From Pipettes to Science Policy.

Science policy provides PhD-trained scientists with unique and rewarding opportunities to support the research community. Careers in science policy require broad scientific knowledge coupled with keen problem-solving, data-analysis, and communication skills. This article describes strategies for scientists to engage in policy discussions, both extramural and full-time.

Assessing the value of a Small Grants Program for behavioral research in cancer control.

In 1999, the National Cancer Institute (NCI) issued the first Small Grants Program (SGP) for Behavioral Research in Cancer Control (R03) funding opportunity announcement for investigators new to behavioral cancer prevention and control research. We explored whether the SGP was successful in its goals to encourage new investigators from a variety of disciplines to apply their skills to and promote career development in behavioral cancer prevention and control research. A quasi-experimental design examined applicant characteristics and outcome data by award status. Propensity score matching was used to compare awardees and non-awardees with similar impact scores as a control for application quality. Awardees were more likely than non-awardees to pursue and receive subsequent funding from the NCI and publish their research. Tailored small grant programs create benefit for both promoting and retaining new investigators.

Outcome evaluation of the National Cancer Institute career development awards program.

The National Cancer Institute (NCI) career development (K) awards program supports investigators to develop their cancer research programs and achieve independence. The NCI Center for Cancer Training conducted a K program evaluation by analyzing outcomes of awardees and individuals who applied to the program but were not funded. The evaluation covered seven NCI mechanisms (K01, K07, K08, K11, K22, K23, and K25) between 1980 and 2008. Descriptive statistics and regression modeling were performed on the full cohort (n = 2,893 individuals, 4,081 K applications) and a comparison cohort described herein. K awardees proportionately received more subsequent NIH grants and authored more publications, and time to first R01 grant was unaffected. Of those not pursuing research, K awardees were more likely to participate in activities signaling continued scientific engagement. The NCI K program had a positive impact, not only on participants' biomedical research careers but also on achieving outcomes significant to the scientific enterprise.

Adenovirus E1A targets p400 to induce the cellular oncoprotein Myc.

Adenovirus E1A drives oncogenesis by targeting key regulatory pathways that are critical for cellular growth control. The interaction of E1A with p400 is essential for many E1A activities, but the downstream target of this interaction is unknown. Here, we present evidence that the oncoprotein transcription factor Myc is the target of this interaction. We show that E1A stabilizes Myc protein via p400 and promotes the coassociation of Myc and p400 at Myc target genes, leading to their transcriptional induction. We also show that E1A requires Myc for its ability to activate Myc-dependent gene expression and induce apoptosis, and that forced expression of Myc is sufficient to rescue the activity of an E1A-mutant defective in p400 binding. Together, these findings establish that Myc, via p400, is an essential downstream target of E1A.

Defined genetic events associated with the spontaneous in vitro transformation of ElA/Ras-expressing human IMR90 fibroblasts.

In contrast to rodent cells, normal human fibroblasts are generally resistant to neoplastic transformation in vitro. Here, we report the derivation and characterization of a spontaneously transformed cell line from normal human IMR90 fibroblasts transduced with E1A and Ras oncogenes. Unlike the parental, non-tumorigenic E1A/Ras-expressing IMR90 cells, these spontaneously transformed cells displayed aberrant growth potential in vitro and were capable of tumorigenesis in vivo. In contrast to the parental E1A/Ras-expressing cells, both the spontaneously transformed cells and cells derived from resultant tumors displayed specific t(7q;8q) and t(5q;17) structural chromosomal changes. Chromosome 8q contains c-Myc, which is capable of activating the telomerase catalytic subunit hTERT. Notably, upregulation of c-Myc, hTERT and telomerase activity were detected only in the tumorigenic cells. Transduction of Myc siRNA into the tumorigenic cells led to a concomitant downregulation of hTERT. Furthermore, transduction of Myc or hTERT into the non-tumorigenic E1A/Ras-expressing IMR90 cells was able to confer tumorigenesis on these cells. These studies suggest that the t(7;8) translocation may result in Myc overexpression and its subsequent activation of hTERT, which may contribute to the tumorigenicity of the IMR90 cells. Furthermore, this report describes additional successful neoplastic transformation of human IMR90 fibroblasts by defined genetic elements. The spontaneously transformed cells we have derived provide a valuable model system for the study of neoplastic transformation.

Transformation of normal human cells in the absence of telomerase activation.

Our knowledge of the transformation process has emerged largely from studies of primary rodent cells and animal models. However, numerous attempts to transform human cells using oncogene combinations that are effective in rodents have proven unsuccessful. These findings strongly argue for the study of homologous experimental systems. Here we report that the combined expression of adenovirus E1A, Ha-RasV12, and MDM2 is sufficient to convert a normal human cell into a cancer cell. Notably, transformation did not require telomerase activation. Therefore, we provide evidence that activation of telomere maintenance strategies is not an obligate characteristic of tumorigenic human cells.