No abstract

155gen content has entered the lipide extract. Cirrhosis affects the lipide content so that it increases above normal but not as high as the normal fasted liver cytoplasm. The phospholipide in the cirrhotic liver decreases, but here also there seems to be a lipide present with a high nitrogen content.The iodine value of both the normal fasted and the cirrhotic-fasted liver cytoplasms decreased below that of normal. These results are in accord with those of WinteP in that he found that after feeding carbon tetrachloride to rats the iodine value of the liver fatty acids decreased from 11 1 to 100.Summary and discussion. Chemical changes in the cytoplasm of the mouse liver cell after a short fast and at cirrhosis are reported. These changes occur most dramatically in the lipide fraction during a 24 hour fast resulting in an increase of 3 to 4 fold above normal. ~ ~ ~-12TS'intcr, J. C., J . Hiol. Cheni., 1939, 128, 283.This lipide is non-phospholipide in character. Fasted cirrhotic liver differs from the fasted normal liver cytoplasm in that the lipide does not increase so markedly and the phospholipide decreases to about 60% of the normal fasted value. The iodine values of the normal-fasted and the cirrhotic-fasted liver cytoplasm fatty acids decrease below that of the normal values.In addition to a lipide increase in the fasted-cirrhotic liver cytoplasm there is also a decrease of "ribonucleic acid" and phospholipide in one gram wet weight of the ground fasted cirrhotic liver.It is possible that there is an interchange of phospholipide during a fast as evidenced by the lipide nitrogen to phosphorus ratio. This interchange would consist of substituting normal phospholipide with a lipide or phospholipide which contains a great deal of nitrogen. P Electrical Alternation in Experimental Coronary Artery Occlusion.

The prevalence and incidence of CHD, defined by ECG abnormalities according to the Tecumseh criteria for Minnesota Codes, were determined in Pima Indians greater than or equal to 25 yr of age. In a cross-sectional analysis, the age-sex-adjusted prevalence (+/- SE) of ECG abnormalities was higher in 1454 NIDDM patients (6.86 +/- 0.65%) than in 1696 nondiabetic subjects (3.23 +/- 0.63%; prevalence rate ratio = 2.12; 95% CI 1.39-3.25). In a prospective analysis, the age-sex-adjusted incidence (+/- SE) of ECG abnormalities was higher in 824 NIDDM patients (12.77 +/- 1.67) than in 935 nondiabetic subjects (5.93 +/- 1.43 cases/1000 person-yr; incidence rate ratio = 2.15; 95% CI 1.26-3.69). The prevalence of ECG abnormalities in insulin-treated NIDDM patients was significantly higher than in NIDDM patients not treated with insulin (age-sex-adjusted OR = 2.83; 95% CI 1.84-4.33); and this association persisted when adjusted for other factors such as sBP, BMI, duration of diabetes, serum cholesterol concentration, and oral hypoglycemic agents (OR = 2.12; 95% CI 1.34-3.37). In the prospective analysis, the incidence of ECG abnormalities in NIDDM patients treated with insulin was higher than in those NIDDM patients not treated with insulin, but, when controlled for age, sex, duration of diabetes, and oral hypoglycemic agents in a proportional-hazards model, the relationship with insulin treatment was not statistically significant (incidence rate ratio = 1.36; 95% CI 0.80-2.31). This suggests that insulin treatment may be a marker of more severe diabetes, and that factors associated with clinical indications for insulin treatment, rather than insulin treatment per se, are related causally to CHD. On the other hand, endogenous fasting and 2-h postload serum insulin concentrations were not associated with ECG abnormalities among 761 NIDDM patients not treated with insulin nor among 1226 nondiabetic subjects. Furthermore, in the prospective study, neither endogenous fasting nor 2-h postload serum insulin was associated with the subsequent development of ECG abnormalities in NIDDM patients or nondiabetic subjects.

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