Chapter 1 contemporary advancements in Flocculation exams (pages 1–10): N. F. Maclagan
Chapter 2 Lyophilic houses of Sera in Liver ailment (pages 11–21): Ch. Wunderly and F. Wuhrmann
Chapter three Amino?Acid Metabolism in Liver sickness (pages 1–10): C. E. Dent and J. M. Walshe
Chapter four alterations within the materials of the Liver cellphone in Early Choline and Protein Deficiencies (pages 32–73): H. W. Kosterlitz
Chapter five Experimental Hepatic Cirrhosis (pages 74–80): L. E. Glynn
Chapter 6 results of Antibiotics and diet B12 in Cirrhosis and Necrosis of the Liver (pages 81–89): P. Gyorgy
Chapter 7 Histological reports on Fatty Infiltration of the Liver in Choline?Deficient Rats (pages 90–100): W. S. Hartroft
Chapter eight Needle Biopsy reports of the Liver in Cirrhosis and different stipulations (pages 101–122): L. Schiff
Chapter nine The Relation of convinced Mechanical elements to the construction of Ascites (pages 123–129): W. Volwiler
Chapter 10 elements within the Mechanism of Ascites (pages 130–135): H. G. Kunkel
Chapter eleven The Pathogenesis of Ascites (pages 136–144): Poul Iversen
Chapter 12 Observations at the Surgical difficulties in Portal high blood pressure (pages 145–201): A. I. S Macpherson
Chapter thirteen Bile Pigment Metabolism (pages 202–210): Torben okay. With
Chapter 14 Appendix: the organic importance of the Direct Diazo response (pages 211–221): Torben okay. With
Chapter 15 Relation of Liver Blood circulate to adjustments in Carbohydrate Metabolism (pages 222–234): Sheila Sherlock
Chapter sixteen stories on Viral Hepatitis (pages 235–246): J. Stokes
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Extra resources for Ciba Foundation Symposium - Liver Disease
M, mean ; F, fasted 2448 hr. ; L,10 per cent fat diets ; H,40 per cent fat diets ; HO, protein-free 40 per cent fat diets ; H32, 32 per cent casein 40 per cent fat diet, for one and four weeks respectively. The figures below the columns indicate the number of rats in each group. the rats fed on the diet containing 32 per cent casein and 40 per cent fat for four weeks. In these animals the DNA P content of the liver was smaller than that calculated from the regression equation. However, as these animals gained weight excessively during the experimental period, this discrepancy is probably only apparent, the true body weight being lower than the measured one.
We found that all showed responses similar to those of our liver patients, usually reaching a peak about three days after the operation. This certainly requires some interpretation and further study. We suggest that it probably indicates a true liver dysfunction but we cannot yet say if i t is R direct effect of the anzesthetic on the liver, or if it is more in the nature of a stress reaction, as a part of the negative nitrogen balance which has long been known to occur. It is clear that we have little here to help us in the diagnosis of these milder types of liver damage.
Simultaneously with the injection of s2P,any food left over was removed. It was found that the specific activity of the lipoid P, viz. , rose with decreasing protein and therefore decreasing phospholipin content of the liver. A t the same time, however, there was a similar change in the specific activity of inorganic P, a fact which in itself would cause a rise of the specific activity of lipoid P. In Fig. 4 the logarithms of the specific activities of inorganic P and of lipoid P are plotted against the ratios N/DNA P.