1000 resultados para 330.31
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Sem medir o tempo não teria feito sentido falar-se, como tanto se falou na indústiia desde finais do século passado, pelo menos', em organização racional, ou científica, do trabalho. Foi empunhando o cronômetio que Frederick Winslow Taylor (1856-1915) observou as práticas de trabalho, experimentou e estabeleceu seqüências "racionais". Contando tempos, demonstrou a eficácia quantitativa da segmentação das tarefas e depuração dos gestos técnicos até ao estritamente necessário, com exclusão de todo o "desperdício" gestual susceptível de gerar lentidão ou atraso (Left-anc, 1975: 330-31; SainsauUeu, 1985: 374-76; Freire, 1993: 63-67, por exemplo).
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The present study aimed to examine the effects of thyroid hormone (TH), more precisely triiodothyronine (T3), on the modulation of leptin mRNA expression and the involvement of the phosphatidyl inositol 3 kinase (PI3K) signaling pathway in adipocytes, 3T3-L1, cell culture. We examined the involvement of this pathway in mediating TH effects by treating 3T3-L1 adipocytes with physiological (P=10nM) or supraphysiological (SI=100 nM) T3 dose during one hour (short time), in the absence or the presence of PI3K inhibitor (LY294002). The absence of any treatment was considered the control group (C). RT-qPCR was used for mRNA expression analyzes. For data analyzes ANOVA complemented with Tukey's test was used at 5% significance. T3 increased leptin mRNA expression in P (2.26 ± 0.36, p< 0.001), SI (1.99 ±0.22, p< 0.01) compared to C group (1± 0.18). This increase was completely abrogated by LY294002 in P (1.31±0.05, p< 0.001) and SI (1.33±0.31, p< 0.05). Western blotting confirmed these results at protein level, indicating the PI3K pathway dependency. To examine whether leptin is directly induced by T3, we used the translation inhibitor cycloheximide (CHX). In P, the presence of CHX maintained the levels mRNA leptin, but was completely abrogated in SI (1.14±0.09, p> 0.001). These results demonstrate that the activation of the PI3K signaling pathway has a role in TH-mediated direct and indirect leptin gene expression in 3T3-L1 adipocytes. © 2013 Oliveira et al.
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Bibliographical footnotes.
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FTO is the strongest known genetic susceptibility locus for obesity. Experimental studies in animals suggest the potential roles of FTO in regulating food intake. The interactive relation among FTO variants, dietary intake and body mass index (BMI) is complex and results from previous often small-scale studies in humans are highly inconsistent. We performed large-scale analyses based on data from 177,330 adults (154 439 Whites, 5776 African Americans and 17 115 Asians) from 40 studies to examine: (i) the association between the FTO-rs9939609 variant (or a proxy single-nucleotide polymorphism) and total energy and macronutrient intake and (ii) the interaction between the FTO variant and dietary intake on BMI. The minor allele (A-allele) of the FTO-rs9939609 variant was associated with higher BMI in Whites (effect per allele = 0.34 [0.31, 0.37] kg/m(2), P = 1.9 × 10(-105)), and all participants (0.30 [0.30, 0.35] kg/m(2), P = 3.6 × 10(-107)). The BMI-increasing allele of the FTO variant showed a significant association with higher dietary protein intake (effect per allele = 0.08 [0.06, 0.10] %, P = 2.4 × 10(-16)), and relative weak associations with lower total energy intake (-6.4 [-10.1, -2.6] kcal/day, P = 0.001) and lower dietary carbohydrate intake (-0.07 [-0.11, -0.02] %, P = 0.004). The associations with protein (P = 7.5 × 10(-9)) and total energy (P = 0.002) were attenuated but remained significant after adjustment for BMI. We did not find significant interactions between the FTO variant and dietary intake of total energy, protein, carbohydrate or fat on BMI. Our findings suggest a positive association between the BMI-increasing allele of FTO variant and higher dietary protein intake and offer insight into potential link between FTO, dietary protein intake and adiposity.
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1 Brief an Ernst Jacob von Max Horkheimer; 31 Briefe zwischen Stefan Jacobwicz und Max Horkheimer, 1936-1945; 1 Brief an die American Consul Lisabon von Max Horkheimer; 23 Briefe zwischen Heinz Jacoby, Lilli Jacoby und Max Horkheimer, 1936-1943; 1 Brief von Max Horkheimer an John B. Norman, 29.06.1942; 1 Brief von Max Horkheimer an George L. Warren; 1 Brief vom Service Social d'Aide aux Emigrants Paris an Heinz Jacobi, 18.01.1940; 1 Brief von Max Horkheimer an Jaeger , 29.09.1937; 5 Brief zwischen Philip C. Jessup und Max Horkheimer, 15.10.1940-1941; 3 Briefe an die Jewish National and University Library Jerusalem von Max Horkheimer, 1943, 1949; 5 Briefe zwischen der Jewish Telegraphic Agency New York und Max Horkheimer, 1940; 2 Briefe zwischen Ernest Jones und Max Horkheimer, 29.04.1938, 11.05.1938; 14 Briefe zwischen der Journal of Criminal Psychopathology, Woodbourne und Max Horkheimer,1940-1941; 1 Brief vom Journal of Philosophy and Phenomenological Research Bufallo N.Y. an Max Horkheimer, 19.11.1940; 1 Brief an das Jüdisches Schwesternheim Stuttgart an Max Horkheimer, 29.12.1937; 1 Brief von Jean Juget an Max Horkheimer, 25.11.1935; 2 Briefe zwischen der Juilliard School of Music New York und Theodor W. Adorno, 17.07.1940, 18.07.1940; 2 Briefe zwischen Gustave S. Juliber und Max Horkheimer, 09.10.1938, 01.11.1938;