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This study assesses an asset-based approach to international teaching assistant (ITA) training at a public research institution. The program is a peer mentorship-based learning community that facilitates ITAs' cultural awareness and pedagogic development. Survey results indicate the program positively impacted participants' teaching skills, confidence, and view of their international background.

Background The possibility that ε4 may modulate the effects of fitness in the brain remains controversial. The present exploratory FDG-PET study aimed to better understand the relationship among ε4, fitness and cerebral metabolism in 18 healthy aged females (9 Carriers, 9 Non-carriers) during working memory. Methods Participants underwent VO2 max, CVLT and FDG-PET, collected at rest and during completion of the Sternberg Working Memory Task. Results Resting FDG-PET did not differ between carriers and non-carriers. Significant effects of fitness on FDG-PET during working memory was noted in the ε4 carriers only. High Fit ε4 carriers had greater glucose uptake than the Low Fit in the temporal lobe, but Low Fit had greater glucose uptake in the frontal and parietal lobes. Conclusion(s) We demonstrate that fitness differentially affects cerebral metabolism in ε4 carriers only, consistent with previous findings that the effects of fitness may be more pronounced in populations genetically at risk for cognitive decline.

Objective. The purpose of this study was to examine the association of the alpha-actinin-3 (ACTN3) R577X polymorphism on muscle function and physical performance in older adults. Methods. We measured knee extensor torque, midthigh muscle cross-sectional area, muscle quality, short physical performance battery score, and 400-meter walk time at baseline and after 5 years in white older adults aged 70-79 years in the Health, Aging and Body Composition Study cohort (n = 1367). Incident persistent lower extremity limitation (PLL) over 5 years was additionally assessed. We also examined white men in the Osteoporotic Fractures in Men Study, a longitudinal, observational cohort (n = 1152) of men 65 years old or older as a validation cohort for certain phenotypes. Results. There were no significant differences between genotype groups in men or women for adjusted baseline phenotypes. Male X-homozygotes had a significantly greater adjusted 5-year increase in their 400-meter walk time compared to R-homozygotes and heterozygotes (p = .03). In women, X-homozygotes had a ~35% greater risk of incident PLL compared to R-homozygotes (hazard ratio = 0.65, 95% confidence interval = 0.44-0.94). There were no other significant associations between any of the phenotypes and ACTN3 genotype with aging in either cohort. Conclusions. The ACTN3 polymorphism may influence declines in certain measures of physical performance with aging in older white adults, based on longitudinal assessments. However, the influence of the ACTN3 R577X polymorphism does not appear to have a strong effect on skeletal muscle-related phenotypes based on the strength and consistency of the associations and lack of replication with regard to specific phenotypes. Key Words: Genetics--Elderly--Sarcopenia--Skeletal muscle.

In endothelial cells, [NF-[kappa]B is an important intracellular signaling molecule by which changes in wall shear stress are transduced into the nucleus to initiate downstream endothelial nitric oxide synthase (NOS3) gene expression. We investigated whether NF-[kappa] light-chain gene enhancer in B cells 1 (NFKB 1) promoter polymorphism ([sup.-94]NFKB1 I/D, where I is the insertion allele and D is the deletion allele) was associated with 1) NOS3 gene expression in endothelial cells under physiological levels of unidirectional laminar shear stress (LSS) and 2) endothelial function in prehypertensive and stage I hypertensive individuals before and after a 6-mo supervised endurance exercise intervention. Competitive EMSAs revealed that proteins present in the nuclei of endothelial cells preferentially bound to the I allele NFKB1 promoter compared with the D allele. Reporter gene assays showed that the I allele promoter had significantly higher activity than the D allele. In agreement with these observations, homozygous II genotype cells had higher p50 expression levels than homozygous DD genotype cells. Cells with the homozygous II genotype showed a greater increase in NOS3 protein expression than did homozygous DD genotype cells under LSS. Functional experiments on volunteers confirmed higher baseline reactive hyperemic forearm blood flow, and, furthermore, the subgroup analysis revealed that DD homozygotes were significantly less prevalent in the exercise responder group compared with II and ID genotypes. We conclude that the [sup.-94]NFKB1 I/D promoter variation contributes to the modulation of vascular function and adaptability to exercise-induced flow shear stress, most likely due to differences in NFKB1 gene transactivity. nuclear factor-[kappa] light-chain gene enhancer in B cells 1; nitric oxide synthase 3; shear stress

Background. There is little information regarding the effects of strength training on intermuscular fat (IMF). This study examines changes in IMF in response to strength training in carriers of the adrenergic receptor (ADR) [Beta]2Glu27 polymorphism versus noncarriers and between carriers of ADR[Alpha]2b [Glu.sup.9] polymorphism versus noncarriers. Methods. Midthigh IMF and muscle area were measured by computed tomography (CT) before and after 10 weeks of single-leg strength training in healthy, sedentary middle-aged and older (50-83 years) men ([Eta] = 46) and women ([Eta] = 52) in both their trained and untrained (control) legs. Results. The strength training program resulted in a substantial increase in one-repetition maximum strength (p < .001) and muscle area (p < .001), but no significant changes in IMF in the whole group. However, IMF was significantly reduced with strength training in participants carrying ADR[Beta]2 Glu27 (-2. 3 [+ or -] 1.0 [cm.sup.2], p = .028), but no significant change was observed with ADR[Beta]2 Glu27 noncarriers. The decrease in IMF in ADR[Alpha]2b [Glu.sup.9] carriers (-1.9 [+ or -] 1.0 [cm.sup.2], p = .066) was significantly different (-2.9 [+ or -] 1.5 [cm.sup.2], p - .043) from a nonsignificant increase in ADR[Alpha]2b [Glu.sup.9] noncarriers. ADR[Beta] Glu27 carriers who also carried ADR[Alpha]2b [Glu.sup.9] significantly lost IMF with strength training (-3.8 [+ or -] 1.5 [cm.sup.2], p = .018). Conclusion. ADR genotype influences IMF response to strength training.

Background. The alpha-actinin-3 (ACTN3) R577X polymorphism has been associated with muscle power performance in cross-sectional studies. Methods. We examined baseline knee extensor concentric peak power (PP) and PP change with ~10 weeks of unilateral knee extensor strength training (ST) using air-powered resistance machines in 71 older men (65 [standard deviation = 8] years) and 86 older women (64 [standard deviation = 9] years). Results. At baseline in women, the XX genotype group had an absolute (same resistance) PP that was higher than the RR (p = .005) and RX genotype groups (p = .02). The women XX group also had a relative (70% of one-repetition maximum [1-RM]) PP that was higher than that in the RR (p = .002) and RX groups (p = .008). No differences in baseline absolute or relative PP were observed between ACTN3 genotype groups in men. In men, absolute PP change with ST in the RR (n = 16) group approached a significantly higher value than in the XX group (n = 9; p = .07). In women, relative PP change with ST in the RR group (n = 16) was higher than in the XX group (n = 17; p = .02). Conclusions. The results indicate that the ACTN3 R577X polymorphism influences the response of quadriceps muscle power to ST in older adults.

In its role as an endothelial cell proliferation and migration factor, vascular endothelial growth factor (VEGF) can affect peripheral circulation and therefore impact maximal oxygen consumption (V[O.sub.2 max]). Because of the role of VEGF, and because variation in the VEGF gene has the ability to alter VEGF gene expression and VEGF protein level, we hypothesized that VEGF gene polylnorphisms are related to VEGF gene expression in human myoblasts and V[O.sub.2 max] before and after aerobic exercise training. We analyzed the effects of the VEGF -2578/ -1154/-634 protnoter region haplotype on VEGF gene expression by using a luciferase reporter assay in cultured human myoblasts and found that the AAG and CGC haplotypes resulted m significantly higher hypoxia-stimulated VEGF gene expression than the AGG and CGG haplotypes. Consistent with these results, we found that individuals with at least one copy of the AAG or CGC haplotype had higher V[O.sub.2 max] before and after aerobic exercise training than did subjects with only the AGG and/or CGG haplotype. In conclusion, we found that VEGF-2578/-1154/-634 haplotype impacts VEGF gene expression in human myoblasts and is associated with V[O.sub.2 max]. These results have potential implications for aerobic exercise training and may prove relevant in the study of pathological conditions that can be affected by angiogenesis, such as coronary artery disease and peripheral artery disease. angiogenesis; exercise; genetics; polymorphism

We investigated the association of vitamin D receptor (VDR) genotype with fat-free mass (FFM) in a cohort of 302 older (aged 58-93 years) Caucasian men who underwent body composition analysis by dual-energy X-ray absorptiometry, and completed questionnaires addressing comorbidities, physical activity, and dietary intake. All participants were genotyped for a VDR translation start site (FokI) polymorphism [FF (37.7%), Ff (48.4%), and ff (13.9%)] and the previously studied BsmI polymorphism [BB (24.9%), Bb (37.7%), and bb (37.4%)]. The BsmI polymorphism was not associated with FFM in any analysis; however, the Fokl polymorphism was significantly associated with total FFM, appendicular FFM, and relative (kg/[m.sup.2]) appendicular FFM (all p < .05), with the FF group demonstrating significantly lower FFM than the Ff and ff groups (e.g., total FFM: FF = 57.6 [+ or -] 0.4, Ff = 59.4 [+ or -] 0.4, if= 59.4 [+ or -] 0.7 kg; p < .02). Age-adjusted logistic regression revealed a 2.17-fold higher risk for sarcopenia (defined previously as appendicular FFM

We studied the association of the G- 174C promoter polymorphism in the interleukin-6 gene (IL6) with total body fat and fat-free mass (FFM) in 242 men and women (IL6 genotypes: G/G, n = 87; G/C, n = 100; C/C, n = 55) across the adult age span (21-92 years). In men, but not women (significant genotype by sex interactions; p = .023-.048), the C/C group exhibited significantly lower total FFM than the G/G group (54.7 [+ or -] 0.8 kg vs 57.2 [+ or -] 0.7 kg, respectively, p = .020), as well as significantly lower FFM of the lower limbs compared with the G/G group (18.4 [+ or -) 0.3 kg vs 19.8 [+ or -] 0.3 kg, respectively, p = .004). No significant genotype differences were observed in total body fat mass in either men or women. The results indicate that the IL6 G-174C polymorphism is significantly associated with FFM in men but not women.

Testosterone (T) supplementation in men induces muscle fiber hypertrophy. We hypothesized that T-induced increase in muscle fiber size is associated with a dose-dependent increase in satellite cell number. We quantitated satellite cell and myonuclear number by using direct counting and spatial orientation methods in biopsies of vastus lateralis obtained at baseline and after 20 wk of treatment with a gonadotropin-releasing hormone agonist and a 125-, 300-, or 600-mg weekly dose oft enanthate. T administration was associated with a significant increase in myonuclear number in men receiving 300- and 600-mg doses. The posttreatment percent satellite cell number, obtained by direct counting, differed significantly among the three groups (ANCOVA P < 0.000001); the mean posttreatment values (5.0 and 15.0%) in men treated with 300- and 600-mg doses were greater than baseline (2.5 and 2.5%, respectively, P < 0.05 vs. baseline). The absolute satellite cell number measured by spatial orientation at 20 wk (1.5 and 4.0/mm) was significantly greater than baseline (0.3 and 0.6/mm) in men receiving the 300- and 600-mg doses (P < 0.05). The change in percent satellite cell number correlated with changes in total (r = 0.548) and free T concentrations (r = 0.468). Satellite cell and mitochondrial areas were significantly higher and the nuclear-to-cytoplasmic ratio lower after treatment with 300- and 600-mg doses. We conclude that T-induced muscle fiber hypertrophy is associated with an increase in satellite cell number, a proportionate increase in myonuclear number, and changes in satellite cell ultrastructure. anabolic steroids; anabolic effects of androgens; mechanisms of androgen action; testosterone effects on muscle stem cells