55 resultados para Montrose
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I. Waverley.-II. Guy Mannering.-III. The antiquary.-IV. Rob Roy.-V. Black dwarf. Old Mortality.-VI. Heart of Mid-Lothian.-VII. Bride of Lammermoor. A legend of Montrose.-VIII. Ivanhoe.-IX. The monastery.-X. The abbot.-XI. Kenilworth.-XII. The pirate.-XIII. The fortunes of Nigel. -XIV. Peveril of the peak.-XV. Quentin Durward.-XVI. St. Ronan's well.-XVII. Redgauntlet.-XVIII. Tales of the crusaders.-XIX. Woodstock.-XX. Chronicles of Canongate. XXI. St. Valentine's Day..-XXII. Anne of Geierstein.-XXIII. Count Robert of Paris.-XXIV. Castle Dangerous. Tales of a grandfather. First series.-XXV. Tales of a grandfather. Second series.-XXVI. Tales of a grandfather. Third series.-XXVII. Tales of a grandfather. Fourth series.
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cont. VI. The application of standard measurements to school administration. [By] D.C. Bliss. VII. A half-year's progress in the achievement of one school system. A. The progress as measured by the Thorndike visual vocabulary test. B. The progress as measured by the Courtis tests, series B. [By] H.G. Childs. VIII. Courtis tests in arithmetic: value to superintendents and teacher. [By] S.A. Courtis. IX. Use of standard tests at Salt Lake City, Utah. [By] E. P. Cubberley. X. Reading. [By] C.H. Judd. XI. Studies by the Bureau of research and efficiency of Kansas City, Mo. [By] George Melcher. XII. The effects of efficiency tests in reading on a city school system. [By] E.E. Oberholtzer. XIII. Investigation of spelling in the schools of Oakland, Cal. [By] J.B. Sears. XIV. Standard tests as aids in the classification and promotion of pupils. [By] Daniel Starch. XV. The use of mental tests in the school. [By] G.M. Whipple.
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Vol. III contains also A legend of Montrose.
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Mode of access: Internet.
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Binder's title.
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Bibliography: p. 311-341.
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Nonalcoholic fatty liver disease is the most common of all liver diseases. The hepatic disposition [H-3]palmitate and its low-molecular-weight metabolites in perfused normal and steatotic rat liver were studied using the multiple indicator dilution technique and a physiologically based slow diffusion/bound pharmacokinetic model. The steatotic rat model was established by administration of 17alpha-ethynylestradiol to female Wistar rats. Serum biochemistry markers and histology of treated and normal animals were assessed and indicated the presence of steatosis in the treatment group. The steatotic group showed a significantly higher alanine aminotransferase-to-aspartate aminotransferase ratio, lower levels of liver fatty acid binding protein and cytochrome P-450, as well as microvesicular steatosis with an enlargement of sinusoidal space. Hepatic extraction for unchanged [H-3]palmitate and production of low-molecular-weight metabolites were found to be significantly decreased in steatotic animals. Pharmacokinetic analysis suggested that the reduced extraction and sequestration for palmitate and its metabolites was mainly attributed to a reduction in liver fatty acid binding protein in steatosis.
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Systemic inflammation is known to affect drug disposition in the liver. This study sought to relate and quantitate changes in hepatic pharmacokinetics of propranolol with changes in hepatic architecture and physiology in adjuvant-treated rats. Transmission electron microscopy was used to assess morphological changes in mitochondria and lysosomes of adjuvant-treated rat livers. The disposition of propranolol was assessed in the perfused rat liver using the multiple indicator dilution technique. Hepatic extraction and mean transit time were determined from outflow-concentration profiles using a nonparametric method. Kinetic parameters were derived from a two-phase physiologically based organ pharmacokinetic model. Possible relationships were then explored between the changes in hepatic drug disposition and cytochrome P-450 activity and iron concentration. Adjuvant treatment induced the appearance of mitochondrial inclusions/tubularization and irregularly shaped lysosomes in rat livers. Livers from adjuvant-treated rats had (relative to normal) significantly higher alpha(1)-acid glycoprotein (orosomucoid) and iron tissue concentrations but lower cytochrome P-450 content. The hepatic extraction, metabolism, and ion trapping of propranolol were significantly impaired in adjuvant-treated rats and could be correlated with altered iron store and cytochrome P-450 activity. It is concluded that adjuvant-induced systemic inflammation alters hepatocellular morphology and biochemistry and consequently influences hepatic disposition of propranolol.