Ex. 279-US-438

A report on the Summary of Stream Surveys in the Upper Sprague River, Klamath Basin, Oregon, 1991-1994

Risk of Low Energy Availability, Disordered Eating, and Menstrual Dysfunction in Female Collegiate Runners

Collegiate female distance runners may be at risk for low energy availability (LEA) due to increased exercise energy expenditure with or without decreased energy intake. Furthermore, this population has increased risk of disordered eating (DE), which can lead to LEA and negative health consequences, such as menstrual dysfunction (MD). Purpose: The purpose of this study was to: 1) investigate risk of LEA and DE and 2) compare DE, training volume, and weight dissatisfaction among female collegiate runners athletes at risk vs not at risk for LEA. Methods: Female runners (n = 287) who competed on an NCAA Division I, II, or III cross-country and/or track team completed an online questionnaire (45 questions). The questionnaire included the Low Energy Availability in Females Questionnaire (LEAF-Q) which examines incidence of stress fractures, occurrence and frequency of menstrual cycles within the previous 12 months, contraceptive use, and gastrointestinal function. The Disordered Eating Screening Assessment (DESA-6) was used to examine risk of DE and weight dissatisfaction. Results: 54.5% (n = 156) of runners were at risk for LEA (score \u3e 8 on LEAF-Q), and 40.8% (n = 117) were at risk for DE (DESA-6 score \u3e 3), and 56.5% (n = 162) reported MD (LEAF-Q subsection MD score \u3e 4). Athletes “at risk” for LEA had significantly higher DESA-6 scores than athletes “not at risk” for LEA (p \u3c 0.001). Athletes “at risk” for LEA had significantly greater weight dissatisfaction than those not at risk for LEA (X23, 156 = 15.92, p = 0.001). Higher weekly training volumes was not associated with risk for LEA (X22, 156 = 4.20, p = 0.112). Conclusion: Consistent with previous literature, a substantial percentage of collegiate female runners were found to be at risk for LEA, DE, and report MD. These findings demonstrate that risk for DE, MD, and weight dissatisfaction are associated with risk for LEA

Ex. 279-US-438

A report on the Summary of Stream Surveys in the Upper Sprague River, Klamath Basin, Oregon, 1991-1994

Interleukin 31 mediates MAP kinase and STAT1/3 activation in intestinal epithelial cells and its expression is upregulated in inflammatory bowel disease

Background/aim: Interleukin 31 (IL31), primarily expressed in activated lymphocytes, signals through a heterodimeric receptor complex consisting of the IL31 receptor alpha (IL31R\textgreeka) and the oncostatin M receptor (OSMR). The aim of this study was to analyse IL31 receptor expression, signal transduction, and specific biological functions of this cytokine system in intestinal inflammation.Methods: Expression studies were performed by RT-PCR, quantitative PCR, western blotting, and immunohistochemistry. Signal transduction was analysed by western blotting. Cell proliferation was measured by MTS assays, cell migration by restitution assays.Results: Colorectal cancer derived intestinal epithelial cell (IEC) lines express both IL31 receptor subunits, while their expression in unstimulated primary murine IEC was low. LPS and the proinflammatory cytokines TNF-\textgreeka, IL1\textgreekb, IFN-\textgreekg, and sodium butyrate stimulation increased IL31, IL31R\textgreeka, and OSMR mRNA expression, while IL31 itself enhanced IL8 expression in IEC. IL31 mediates ERK-1/2, Akt, STAT1, and STAT3 activation in IEC resulting in enhanced IEC migration. However, at low cell density, IL31 had significant antiproliferative capacities (p<0.005). IL31 mRNA expression was not increased in the TNF\textgreekDARE mouse model of ileitis but in inflamed colonic lesions compared to non-inflamed tissue in patients with Crohn's disease (CD; average 2.4-fold increase) and in patients with ulcerative colitis (UC; average 2.6-fold increase) and correlated with the IL-8 expression in these lesions (r = 0.564 for CD; r = 0.650 for UC; total number of biopsies analysed: n = 88).Conclusion: IEC express the functional IL31 receptor complex. IL31 modulates cell proliferation and migration suggesting a role in the regulation of intestinal barrier function particularly in intestinal inflammation

Ex. 280-US-421

A stream report from the Oregon Department of Fish and Wildlife acquatic inventory project of the Sprague River

Ex. 280-US-421

A stream report from the Oregon Department of Fish and Wildlife acquatic inventory project of the Sprague River

Can the fast bone loss in osteoporotic and osteopenic patients be stopped with active vitamin D metabolites?

The aim of this study was to evaluate whether fast trabecular bone loss in osteoporotic and osteopenic patients can effectively be treated with active vitamin D metabolites. Thirty-one osteoporotic and osteopenic patients were monitored between 4 and 22 months before and between 8 and 18 months during the treatment. Fast bone losers were designated as osteoporotic or osteopenic patients with a loss of trabecular bone density in the radius of 3% or more calculated for 1 year. For this differentiation, the high precise peripheral quantitative computed tomography system (DENSISCAN 1000) was used (reproducability 0.3% in mixed collectives). The pretreatment loss and the "gain” under treatment with active vitamin D metabolites was calculated for 1 year. The treatment consisted of either 0.5 μg calcitriol daily or 1 μg of alfacalcidol daily. Before treatment, the trabecular bone loss in the radius/year was −6.6 ± 0.5% (mean ± SEM). After treatment with vitamin D metabolites, the trabecular bone gain in the radius/year was 0.01 ± 0.6% (mean ± SEM). The difference was highly significant (P < 0.001). In contrast to this, the loss of cortical bone density before treatment was −1.8 ± 0.3% (mean ± SEM) and the reduced loss after treatment −0.2 ± 0.4% (mean ± SEM), both values calculated for 1 year. This difference was less significant (P < 0.05). This study shows that the treatment with active vitamin D metabolites is very effective in slowing fast trabecular bone loss in osteoporotic and osteopenic patient