Search

Context: Balance testing is a vital component in the evaluation and management of sport-related concussion. Few studies have examined the use of objective, low-cost, force-plate balance systems and changes in balance after a competitive season. Objective: To examine the extent of preseason versus postseason static balance changes using the Balance Tracking System (BTrackS) force plate in college athletes. Design: Pretest, posttest design. Setting: Athletic training facility. Participants: A total of 47 healthy, Division-I student-athletes (33 males and 14 females; age 18.4 [0.5] y, height 71.8 [10.8] cm, weight 85.6 [21.7] kg) participated in this study. Main Outcome Measures: Total center of pressure path length was measured preseason and postseason using the BTrackS force plate. A Wilcoxon signed-rank test was conducted to examine preseason and postseason changes. SEM and minimal detectable change were also calculated. Results: There was a significant difference in center of pressure path length differed between preseason (24.6 [6.8] cm) and postseason (22.7 [5.4] cm) intervals (P = .03), with an SEM of 3.8 cm and minimal detectable change of 10.5 cm. Conclusions: Significant improvements occurred for center of pressure path length after a competitive season, when assessed using the BTrackS in a sample of college athletes. Further research is warranted to determine the effectiveness of the BTrackS as a reliable, low-cost alternative to force-plate balance systems. In addition, clinicians may need to update baseline balance assessments more frequently to account for improvements.

Herein we report the synthesis and characterization of a novel series of N-phenylsulfonyl-1H-pyrrole picolinamides as novel positive allosteric modulators of mGlu4. We detail our work towards finding phenyl replacements for the core scaffold of previously reported phenyl sulfonamides and phenyl sulfone compounds. Our efforts culminated in the identification of N-(1-((3,4-dimethylphenyl)sulfonyl)-1H-pyrrol-3-yl)picolinamide as a potent PAM of mGlu4.

Background Traumatic brain injury (TBI) induces arachidonic acid (ArA) release from cell membranes. ArA metabolites form a class of over 50 bioactive eicosanoids that can induce both adaptive and/or maladaptive brain responses. The dynamic metabolism of ArA to eicosanoids, and how they affect the injured brain, is poorly understood due to their diverse activities, trace levels, and short half-lives. The eicosanoids produced in the brain postinjury depend upon the enzymes present locally at any given time. Eicosanoids are synthesized by heme-containing enzymes, including cyclooxygenases, lipoxygenases, and arachidonate monoxygenases. The latter comprise a subset of the cytochrome P450 “Cyp” gene family that metabolize fatty acids, steroids, as well as endogenous and exogenous toxicants. However, for many of these genes neither baseline neuroanatomical nor injury-related temporal expression have been studied in the brain. In a rat model of parietal cortex TBI, Cyp and eicosanoid-related mRNA levels were determined at 6 h, 24 h, 3d, and 7d postinjury in parietal cortex and hippocampus, where dynamic changes in eicosanoids have been observed. Quantitative real-time polymerase chain reaction with low density arrays were used to assay 62 rat Cyps, 37 of which metabolize ArA or other unsaturated fatty acids; 16 eicosanoid-related enzymes that metabolize ArA or its metabolites; 8 eicosanoid receptors; 5 other inflammatory- and recovery-related genes, plus 2 mouse Cyps as negative controls and 3 highly expressed “housekeeping” genes. Results Sixteen arachidonate monoxygenases, 17 eicosanoid-related genes, and 12 other Cyps were regulated in the brain postinjury (p Conclusions The results suggest complex regulation of ArA and other lipid metabolism after TBI. Due to the temporal nature of brain injury-induced Cyp gene induction, manipulation of each gene (or its products) at a given time after TBI will be required to assess their contributions to secondary injury and/or recovery. Moreover, a better understanding of brain region localization and cell type-specific expression may be necessary to deduce the role of these eicosanoid-related genes in the healthy and injured brain.