Search

The purpose of this study was to investigate the effects of bumetanide, an inhibitor of NaCl cotransport on cisternal cerebral spinal fluid (CSF) acid-base balance during acute respiratory acidosis (ARA). We measured blood and CSF acid-base variables in two groups (N = 7 in each) of anesthetized paralyzed and mechanically ventilated dogs with bilateral ligation of renal pedicles (to eliminate saluresis). After baseline samples were obtained (-1 h) bumetanide (0.5 mg/kg) was administered intravenously within 15 min (group 2); group 1 received equal volume of diluted saline. ARA was induced 1 h later (0 h) and was maintained for 5 h. In both groups PaCO2 was maintained between 55 to 60 mm Hg. Mean cisternal CSF PCO2 was 42.8 +/- 2.6, and 43.8 +/- 2.5 mm Hg, respectively in group 1 and group 2 and rose approximately 20 mm Hg during ARA. In group 1, CSF [HCO3-] was 22.0 +/- 1.0, 24.8 +/- 0.6, and 25.4 +/- 1.6 mEq/L, respectively at 0, 2 1/2, and 5 h; respective values for group 2 were 22.9 +/- 1.5, 24.7 +/- 1.4, and 26.1 +/- 1.3 mEq/L. Comparing the two groups, respective values were not significantly different from each other. Similarly, between the two groups changes in CSF [Na(+)-Cl-] during ARA were not significantly different from each other. Based on our results we conclude that at the dose used in the present study bumetanide does not change ionic composition and acid-base balance of cisternal CSF when compared to controls. Because changes in CSF [Na(+)-Cl-] during ARA were similar in both groups, any inhibition of Cl- influx into CSF by bumetanide should have been proportional to that of Na+.

Our specific aim was to assess within-family clustering of high-density lipoprotein cholesterol (HDLC) levels in kindreds identified through probands with primary hypoalphalipoproteinemia, and to determine whether, and to what degree, familial aggregation of HDLC less than or equal to the tenth percentile represents a heritable trait, familial hypoalphalipoproteinemia. Our probands were selected arbitrarily by virtue of HDLC less than or equal to the age-sex-race-specific tenth percentile as the sole dyslipoproteinemia, with an additional requirement that they be normotriglyceridemic (triglyceride levels less than the 90th percentile). The probands were also required to have primary hypoalphalipoproteinemia, not secondary to diseases and/or drugs. Fifteen of the 16 probands were men; 12 were referred because of premature myocardial infarction, angina, or stroke, 2 because of family history of premature myocardial infarction or stroke, and 2 because of low HDLC observed on routine health examinations. Two of the 16 kindreds exhibited three-generation vertical transmission of bottom decile HDLC. In three kindreds, there was also three-generation vertical transmission of bottom decile HDLC, but top decile triglycerides accompanied bottom decile HDLC in one or more generations. Eight kindreds displayed two-generation vertical transmission of bottom decile HDLC. After excluding probands, there were 11 critical matings (bottom decile HDLC by normal), with 30 living offspring, all of whom were sampled. Of these 30 offspring, 13 had bottom decile HDLC, 17 had HDLC greater than tenth percentile. The ratio of offspring with bottom decile HDLC to those of HDLC greater than tenth percentile was 13:17 (0.76/1), not significantly different from the ratio of 1/1, the ratio predictive of a dominant trait, X2(1) = 0.53, P greater than 0.4. The nearly 1:1 segregation ratio for the group of offspring was not due to the aggregation of sibships with, in general, most of the sibs, or none of the sibs affected; within-family expression of low HDLC was also not sex-linked. The 13 hypoalphalipoproteinemic offspring of 11 critical matings included only two subjects whose bottom decile HDLC was accompanied by top decile triglyceride. Our data suggests that not only (by selection) was low HDLC in the probands the sole dyslipoproteinemia, but that the segregation of low HDLC in offspring of critical matings was primarily accounted for by isolated low HDLC, not by hypoalphalipoproteinemia secondary to hypertriglyceridemia. Familial hypoalphalipoproteinemia is a heritable disorder with a pattern of transmission not significantly different from that expected by a hypothesis of mendel

A heterofore strain-specific mammary carcinoma of the mouse was found to have acquired altered characteristics. The dbrB transplantable tumor originated in a DBA mouse as a spontaneous carcinoma in 1918. It was not until recently, when this tumor was transferred from mice to storage in the frozen state, that a marked transformation occurred both in vivo and in vitro. Certain morphologic differences were also noted.

D-Isoascorbic acid, an isomer of vitamin C, and betaine hydrate (quaternary amine) were found to inhibit mitoses of sarcoma 37, Ehrlich carcinoma, and L1210 leukemia cells in vitro. However, the combined effect of these compounds produced a greater inhibitory activity than when either was administered individually.

The effects of probiotics, nonantigenic fractions of normal and malignant cells on tumors, and of similar fractions of normal cells on bacteria and viruses are discussed. The effects are considered in relation to tumor growth and development. In a control group of mice given subcutaneous inoculations only of viable dbrB tumor cells in DBA/1 mice, 100% developed tumors. In a group receiving subcutaneous and intravenous injections of tumor cells and given the tumor fractions, 20% developed lung tumors and 53% developed subcutaneous tumors. In an experiment in which mice received only intravenous injections of viable tumor cells and the tumor fractions, 100% of the controls died with no deaths occurring in the treated group. It is concluded that nonantigenic cellular fractions (probiotics) effective in inducing resistance to some bacterial and viral diseases are effective in inducing resistance to tumors in an inbred strain of mice.