Psychological Response to Injury, Recovery, and Social Support: A Survey of Athletes at an NCAA Division I University

According to the National Athletic Trainers’ Association, “In the last 10 years, college sports have flourished, with athletes required to train and compete year-round rather than seasonally . . .At the same time, athletes are getting bigger, stronger and more physical – which leads to a greater risk of injury.” Sports injury can be traumatic for many athletes because it is an important component of their self-identity. In addition to the physical pain of an injury, athletes struggle psychologically, however little is known about their emotional response, recovery, and need for social support. The Emotional Response of Athletes to Injury Questionnaire (ERAIQ) was adapted to collect information from athletes at an NCAA Division I university about their response to injury. Two hundred fifty varsity athletes volunteered to participate (127 males and 122 females, mean age = 19.9 years). The athletes represented 14 different teams included individuals who had experienced injuries and those who had not. Frustration and anger were the most strongly experienced emotions. Family and teammates were important sources of social support during recovery. The results suggest several important implications for resources the address the emotional as well as physical rehabilitation from sports injury. Recommendations for college athletic staff are discussed and questions for future research are offered

Activation of the Unfolded Protein Response by 2-Deoxy-d-Glucose Inhibits Kaposi's Sarcoma-Associated Herpesvirus Replication and Gene Expression

Lytic replication of the Kaposi's sarcoma-associated herpesvirus (KSHV) is essential for the maintenance of both the infected state and characteristic angiogenic phenotype of Kaposi's sarcoma and thus represents a desirable therapeutic target. During the peak of herpesvirus lytic replication, viral glycoproteins are mass produced in the endoplasmic reticulum (ER). Normally, this leads to ER stress which, through an unfolded protein response (UPR), triggers phosphorylation of the α subunit of eukaryotic initiation factor 2 (eIF2α), resulting in inhibition of protein synthesis to maintain ER and cellular homeostasis. However, in order to replicate, herpesviruses have acquired the ability to prevent eIF2α phosphorylation. Here we show that clinically achievable nontoxic doses of the glucose analog 2-deoxy-d-glucose (2-DG) stimulate ER stress, thereby shutting down eIF2α and inhibiting KSHV and murine herpesvirus 68 replication and KSHV reactivation from latency. Viral cascade genes that are involved in reactivation, including the master transactivator (RTA) gene, glycoprotein B, K8.1, and angiogenesis-regulating genes are markedly decreased with 2-DG treatment. Overall, our data suggest that activation of UPR by 2-DG elicits an early antiviral response via eIF2α inactivation, which impairs protein synthesis required to drive viral replication and oncogenesis. Thus, induction of ER stress by 2-DG provides a new antiherpesviral strategy that may be applicable to other viruses