467 resultados para Lancaster
Resumo:
Mode of access: Internet.
Resumo:
Mode of access: Internet.
Resumo:
Editors vary: v. 1-4, J. H. Stanning -- v. 5-6, John Brownbill.
Resumo:
Twenty-eighth report of the Council of the Chetham society, 1870/71, and list of members, 1871/72, appended to v. 1.
Resumo:
On cover: Illustrated history of Preston and its environs.
Resumo:
Editors : 1883-Nov. 1887 H. C. Brubaker, C. I. Landis ; Dec. 1887- G. R. Eshleman (with I. C. Arnold, Dec. 1887-Nov. 1888)
Resumo:
"Substantially a reprint of the second edition of 1824."
Resumo:
Relief shown by hachures.
Resumo:
Resistance training results in skeletal muscle hypertrophy, but the molecular signalling mechanisms responsible for this altered phenotype are incompletely understood. We used a resistance training (RT) protocol consisting of three sessions [day 1 (d1), day 3 (d3), day 5 (d5)] separated by 48 h recovery (squat exercise, 4 sets × 10 repetitions, 3 min recovery) to determine early signalling responses to RT in rodent skeletal muscle. Six animals per group were killed 3 h after each resistance training session and 24 and 48 h after the last training session (d5). There was a robust increase in TNF? protein expression, and IKKSer180/181 and p38MAPK Thr180/Tyr182 phosphorylation on d1 (P < 0.05), which abated with subsequent RT, returning to control levels by d5 for TNF? and IKK Ser180/181. There was a trend for a decrease in MuRF-1 protein expression, 48 h following d5 of training (P = 0.08). Notably, muscle myofibrillar protein concentration was elevated compared to control 24 and 48 h following RT (P < 0.05). AktSer473 and mTORSer2448 phosphorylation were unchanged throughout RT. Phosphorylation of p70S6k Thr389 increased 3 h post-exercise on d1, d3 and d5 (P < 0.05), whilst phosphorylation of S6Ser235/236 increased on d1 and d3 (P < 0.05). Our results show a rapid attenuation of inflammatory signalling with repeated bouts of resistance exercise, concomitant with summation in translation initiation signalling in skeletal muscle. Indeed, the cumulative effect of these signalling events was associated with myofibrillar protein accretion, which likely contributes to the early adaptations in response to resistance training overload in the skeletal muscle.
Resumo:
PURPOSE: Regulation of skeletal muscle mass is highly dependent on contractile loading. The purpose of this study was to examine changes in growth factor and inflammatory pathways following high-frequency resistance training. METHODS: Using a novel design in which male Sprague-Dawley rats undertook a "stacked" resistance training protocol designed to generate a summation of transient exercise-induced signaling responses (four bouts of three sets × 10 repetitions of squat exercise, separated by 3 h of recovery), we determined the effects of high training frequency on signaling pathways and transcriptional activity regulating muscle mass. RESULTS: The stacked training regimen resulted in acute suppression of insulin-like growth factor 1 mRNA abundance (P < 0.05) and Akt phosphorylation (P < 0.05), an effect that persisted 48 h after the final training bout. Conversely, stacked training elicited a coordinated increase in the expression of tumor necrosis factor alpha, inhibitor kappa B kinase alpha/beta activity (P < 0.05), and p38 mitogen-activated protein kinase phosphorylation (P < 0.05) at 3 h after each training bout. In addition, the stacked series of resistance exercise bouts induced an increase in p70 S6 kinase phosphorylation 3 h after bouts ×3 and ×4, independent of the phosphorylation state of Akt. CONCLUSIONS: Our results indicate that high resistance training frequency extends the transient activation of inflammatory signaling cascades, concomitant with persistent suppression of key mediators of anabolic responses. We provide novel insights into the effects of the timing of exercise-induced overload and recovery on signal transduction pathways and transcriptional activity regulating skeletal muscle mass in vivo.
Resumo:
After nearly fifteen years of the open access (OA) movement and its hard-fought struggle for a more open scholarly communication system, publishers are realizing that business models can be both open and profitable. Making journal articles available on an OA license is becoming an accepted strategy for maximizing the value of content to both research communities and the businesses that serve them. The first blog in this two-part series celebrating Data Innovation Day looks at the role that data-innovation is playing in the shift to open access for journal articles.
Resumo:
Frances Pinter and I have been visiting fellows at the Big Innovation Centre for more than a year now. Tucked away in a corner, inspired by BIC’s open innovation vision, we have been attempting to solve a problem that continues to perplex many in the era of digital affordance: creating sustainable markets for high quality new content that include free access for end users.
Resumo:
The world is increasingly moving towards more open models of publishing and communication. The UK government has demonstrated a firm commitment to ensuring that academic research outputs are made available to all who might benefit from access to them, and its open access policy attempts to make academic publications freely available to readers, rather than being locked behind pay walls or only available to researchers with access to well-funded university libraries. Open access policies have an important role to play in fostering an open innovation ecosystem and ensuring that maximum value is derived from investments in university-based research. But are we ready to embrace this change?