983 resultados para 326-36


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Signatur des Originals: S 36/F11352

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"National Socialism": 1. Ankündigung einer Vorlesungsreihe November/Dezember 1941 von: Herbert Marcuse, A.R.L. Gurland, Franz Neumann, Otto Kirchheimer, Frederick Pollock. a) als Typoskript verfielfältigt, 1 Blatt, b) Typoskript, 1 Blatt; 2. Antwortbrief auf Einladungen zur Vorlesungsreihe, von Neilson, William A.; Packelis, Alexander H.; Michael, Jerome; McClung Lee, Alfred; Youtz, R.P.; Ginsburg, Isidor; Ganey, G.; Nunhauer, Arthur. 8 Blätter; "Autoritarian doctrines and modern European institutions" (1924): 1. Vorlesungs-Ankündigung Typoskript, 2 Blatt; 2. Ankündigungen der Vorlesungen von Neumann, Franz L.: "Stratification and Dominance in Germany"; "Bureaucracy as a Social and Political Institution", Typoskript, 2 Blatt; 3. Evans, Austin P.: 1 Brief (Abschrift) an Frederick Pollock, New York, 26.2.1924; "Eclipse of Reason", Fünf Vorlesungen 1943/44:; 1. I. Lecture. a) Typoskript mit eigenhändigen Korrekturen, 38 Blatt b) Typoskript, 29 Blatt c) Typoskript mit eigenhändigen und handschriftlichen Korrekturen, 31 Blatt d) Teilstück, Typoskript mit eigenhändigen Korrekturen, 2 Blatt e) Entwürfe, Typoskript mit eigenhändigen Korrekturen, 6 Blatt; 2. II. Lecture. a) Typoskript mit eigenhändigen Korrekturen, 27 Blatt, b) Typoskript mit handschriftlichen Korrekturen, 37 Blatt; 3. III. Lecture. Typoskript mit eigenhändigen Korrekturen, 27 Blatt; 4. IV. Lecture. Typoskript mit eigenhändigen Korrekturen, 23 Blatt; 5. V. Lecture. a) Typoskript mit eigenhändigen Korrekturen, 25 Blatt, b) Teilstücke, Typoskript mit eigenhändigen und handschriftlichen Korrekturen, 3 Blatt;

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6. Vorlesungen 1. - 5. mit dem Titel "Society and Reason". a) Typoskript mit handschriftlichen Randbemerkungen von Theodor W. Adorno, 139 Blatt b) Typoskript, 139 Blatt; 7. Teilstück, Typoskript mit eigenhändigen Korrekturen, 1 Blatt; 8. Eigenhändige Notizen, 4 Blatt; 9. Stichworte zu den Vorlesungen I-III. Typoskript mit eigenhändigen Ergänzungen, 2 Blatt a) Einladungskarte zur Vorlesungsreihe "Society and Reason". Als Typoskript vervielfältigt, 1 Blatt b) Gliederung. Typoskript, 1 Blatt; 10. "Über Probleme des wissenschaftlichen Stils". Reaktion auf ein Schriftstück (aus einem Brief an Friedrich Pollock). a) Typoskript, datiert: 28.11.1943, 3 Blatt b) Max Horkheimer: 1 Brief an Friedrich Pollock, ohne Ort, 28.11.1943, 5 Blatt; 11. Columbia University, New York: 1 Brief (Abschrift) an Max Horkheimer, New York, 5.3.1943, und Stichworte zu den Vorlesungen, 2 Blatt; 12. Zeitungsausschnitt, 1 Blatt.;

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1 Brief von Frederick Pollock an Hedwig Cornelius, 11.05.1948;

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1 Brief von Frederick Pollock an Walter Munding, 16.08.1950; 1 Brief von Frederick Pollock an Joseph Christ, 24.05.1950; 1 Brief von Albert Flegenheimer an Frederick Pollock, 18.05.1950; 2 Briefe von Frederick Pollock an E. Wehrle, 03.04.1950; 1 Brief von Margot von Mendelssohn an Max Horkheimer, 18.01.1950; 1 Brief von Nothern Life Insurance Co. (Seattle) an Max Horkheimer, 16.01.1950;

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2 Briefe zwischen A. P. Bersohn und Frederick Pollock, 1952; 1 Brief von Albert Ehrenzweig an Frederick Pollock, 01.06.1952; 1 Brief von Frederick Pollock an Leo Löwenthal, 20.12.1951; 1 Telegramm von Franz Neumann an Frederick Pollock, 11.05.1951;

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Vorbesitzer: Michelangelo Gualandi;

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Vorbesitzer: Johannes Matthaeus Valentini

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Vorbesitzer: M. G. T.;

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von Salomon Marcus Schiller,

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Previous research supports the hypothesis that a "rich" diet (i.e., high in fat and low in fiber) increases the risk of colon cancer. Previous research also supports the hypothesis that physical inactivity increases the risk of colon cancer, perhaps because physical inactivity decreases gut motility, thereby increasing tee time that carcinogens are in contact with the intestinal mucosa. Habitual physical inactivity, combined with rich diet, ordinarily results in chronic energy imbalance and gain in weight, except when energy balance is modified by disease or factors such as cigarette smoking. Cigarette smokers typically stay lean because of effects of smoking on the resting metabolic rate as well as on efficiency of caloric intake and storage. Therefore, if physical inactivity and rich diet do increase the risk of colon cancer, then weight gain during young adulthood should be positively associated with incidence of colon cancer during later life, especially in nonsmokers.^ This hypothesis was investigated in a cohort of 2,059 randomly selected middle-aged men who were employed at the Western Electric Company in Chicago and were free of clinically diagnosed cancer at initial examination in 1958. Body mass index (BMI) in middle age was calculated from measured height and weight at the initial examination. BMI at age 20 was estimated from weight at age 20 as recalled at the initial examination and height as measured at the initial examination. Change in BMI between age 20 and middle age was estimated by subtracting the BMI at 20 from the BMI in middle age. Forty-nine incident cases of colon cancer were detected during 25 years (43,326 person-years) at risk. When stratified by level of change in BMI from age 20 to middle age ($\le$1.9, 2.0-3.9, 4.0-5.9, $\ge$6.0 kg/m$\sp2$), age-adjusted relative hazards of colon cancer in never-smokers were 1.00, 1.22, 2.31, and 5.01, respectively (p for trend = 0.008); corresponding values in ever-smokers were 1.00, 0.95, 0.77, and 0.87, These associations did not change appreciably after further adjustment for BMI at age 20, subscapular-triceps skinfold ratio, cigarette smoking, consumption of alcohol, energy, fat, and calcium.^ We also investigated the hypothesis that the risk of colon cancer was higher in men who were lean at age 20 and became fat by middle age (lean-to-fat) than in men who were fat at age 20 and stayed fat in middle-age (fat-to-fat). "Lean" was defined as BMI $<$24 kg/m$\sp2$ at age 20 and as BMI $<$27.0 kg/m$\sp2$ in middle age. Among never-smokers, in comparison to men who were lean at age 20 and in middle age (lean-to-lean), the age-adjusted relative hazard of colon cancer was 1.43 in the fat-to-fat group (95% confidence interval (CI) 0.37-5.52) and 3.36 in the lean-to-fat group (95% CI 1.21-9.37). This investigation provides new results on the magnitude of risk of colon cancer associated with weight gain during adulthood (from age 20 to middle age). This relation was obscured or underestimated in previous studies due to effect-modification by cigarette smoking. Finally, the result supports the idea that a life-style characterized by chronic energy imbalance during young adulthood increases risk of colon cancer. ^

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Obesity has a complex, multi-factorial etiology. Infectious agents have recently emerged as a possible contributor to the current obesity epidemic. Seven viruses have demonstrated an association with obesity in animals; however, Adenovirus-36 (Ad-36) is the only known virus associated with obesity in humans. The primary aim of this research was to determine the association between Ad-36 infection and the expression of obesity related hormones in children. Additionally, this study proposed to compare the mean three year change in the level of obesity related hormones between Ad-36 positive and negative children. This study utilized pilot data collected from 98 children at baseline and year three of the Project Heartbeat! cohort. Fasting serum samples were analyzed for the concentration of adiponectin, insulin and leptin. The crude analysis uncovered Ad-36 positive children had significantly lower mean concentrations of insulin (p=0.039) and leptin (p=0.038) at baseline compared to Ad-36 negative children. The results of the adjusted analysis indicated the leptin association with Ad-36 infection at baseline was statistically significant even after controlling for age, sex, ethnicity, and BMI percentile. The longitudinal evaluation revealed individuals with a history of Ad-36 infection experienced a larger mean decrease in adiponectin, a larger mean increase in leptin, and a smaller mean increase in insulin levels over a three year period compared to individuals without a history of infection. These results suggest Ad-36 infection may produce changes in hormone expression. The only statistically significant findings in the crude and adjusted longitudinal analysis occurred at baseline when the children were younger, suggesting physical changes that occur during sexual maturation may mask or enhance Ad-36 induced changes in hormone expression. Furthermore, the longitudinal analysis revealed the duration and course of Ad-36 infection may influence changes in the expression of obesity-related hormones. Taken together, the results of this pilot study are suggestive of an association between Ad-36 infection and the expression of obesity-related hormones.^

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