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Biomedical subjects

C L Johnson

Publications and source records attributed to C L Johnson.

At least 235 records · Page 13Linked to original sources
PubMedDate not supplied

Indacrinone: natriuretic and uricosuric effects of various ratios of its enantiomers in healthy men.

Indacrinone is an investigational loop-acting diuretic. To evaluate the natriuretic and uricosuric effects of varying ratios of its enantiomers, 10 healthy men, on a controlled Na+ (100 mEq) and K+ (80 mEq) diet, participated in a double-blind, randomized, balanced incomplete block, multiple-dose (one week) study of a fixed daily dose (10 mg) of (-) enantiomer combined with increasing doses (40, 90 and 140 mg) of (+) enantiomer versus 50 mg hydrochlorothiazide and placebo. On day 1, mean 24-h urinary Na+ increased (p less than 0.01) comparably (approximately 285 mEq) after each enantiomer combination and hydrochlorothiazide; however, the enantiomer combinations had marked uricosuric and hypouricemic effects that were enhanced with increased (+) enantiomer doses. By day 7, while enantiomer combinations and hydrochlorothiazide demonstrated comparable natriuretic activity, mean serum uric acid levels (mg/dl), in comparison to placebo, were increased (p less than 0.05) with hydrochlorothiazide but progressively decreased with increases in (+) enantiomer. Thus varying the ratio [(+, uricosuric): (-, natriuretic)] of the enantiomers of indacrinone caused natriuresis similar to hydrochlorothiazide, but had an opposite effect on serum uric acid.

Adult↗
PubMedDate not supplied

Distributions and trends of serum lipid levels among United States children and adolescents ages 4-19 years: data from the Third National Health and Nutrition Examination Survey.

BACKGROUND: Atherosclerosis begins in childhood and progresses into adulthood. The reduction of cardiovascular risk factors, such as elevated serum total cholesterol and low-density lipoprotein cholesterol (LDL-C) levels, in childhood may reduce cardiovascular morbidity and mortality in adulthood. Lipid distributions among children and adolescents were examined using the most recent nationally representative data. METHODS: Data from 7,499 examinees in NHANES III (1988-1994) were used to estimate mean and percentile distributions of serum total cholesterol, LDL-C, high-density lipoprotein cholesterol (HDL-C), and triglycerides in children and adolescents aged 4 to 19 years. The estimates were analyzed by age, sex, and race/ethnic groups. Trends in mean total cholesterol were examined for 12- to 17-year-olds using data from NHES III (1966-1970), NHANES I (1971-1974), and NHANES III (1988-1994). RESULTS: For children and adolescents 4 to 19 years of age, the 95th percentile for serum total cholesterol was 216 mg/dL and the 75th percentile was 181 mg/dL. Mean age-specific total cholesterol levels peaked at 171 mg/dL at 9-11 years of age and fell thereafter. Females had significantly higher mean total cholesterol and LDL-C levels than did males (P < 0.005). Non-Hispanic black children and adolescents had significantly higher mean total cholesterol, LDL-C, and HDL-C levels compared to non-Hispanic white and Mexican American children and adolescents. The mean total cholesterol level among 12- to 17-year-olds decreased by 7 mg/dL from 1966-1970 to 1988-1994 and is consistent with, but less than, observed trends in adults. Black females have experienced the smallest decline between surveys. CONCLUSIONS: The findings provide a picture of the lipid distribution among U.S. children and adolescents and indicate that, like adults, adolescents have experienced a fall in total cholesterol levels. Total cholesterol levels in U.S. adolescents declined from the late 1960s to the early 1990s by an average of 7 mg/dL. This information is useful for planning programs targeting the prevention of cardiovascular disease beginning with the development of healthy lifestyles in childhood.

Adolescent↗
PubMedDate not supplied

The effect of TNFa on bradykinin receptor binding, phosphatidylinositol turnover and cell growth in human A431 epidermoid carcinoma cells.

In this study, we examined the effect of TNFa on bradykinin (BK) B2 receptor binding and function in human A431 epidermoid carcinoma cells. [3H]BK binds to a single class of receptors on A431 cells in a saturable and reversible manner. A binding affinity (KD) of 3.0 +/- 0.3 nM (n = 4) and a Bmax of 151 +/- 14 fmols/10(6) cells, representing approximately 90,000 BK receptors per cell, was observed. The rank order of potency for BK agonist peptides indicates that the A431 BK receptor appears to be of the B2 subtype. When A431 cells were incubated with TNFa (10 ng/ml) for 48 h prior to BK binding, a significant decrease in the number of BK receptors compared to control was observed. TNFa did not influence the affinity of BK binding to A431 cells and direct addition of TNFa to the binding assay did not effect BK binding. BK-stimulated IP1 formation appeared to be increased in TNFa treated cells compared to control whereas histamine-stimulated IP1 formation was not influenced. Both control and TNFa treated cells were greater than 95% viable. However, TNFa treated cells were blocked in the G1 phase of the cell cycle resulting in a decrease in DNA synthesis. This may be one mechanism for the TNFa-induced decrease in BK receptors in A431 cells.

Bradykinin↗
PubMedDate not supplied

Anti-Sdx: a "new" auto-agglutinin related to the Sda blood group.

Two examples of a "new" IgM saline-agglutinating auto-antibody are described. The antibodies bind complement, have the ability to cause in vivo hemolysis, and are most active at room temperature at a pH of about 6.5. Despite tests on more than 5,000 people, no nonreactive cell sample has been found. The reactive antigen is not denatured by neuraminidase, papain, or ficin, and is present on i adult red blood cells. The antibodies appear to be slightly inhibited by human saliva and milk, and more convincingly inhibited by urine from Sd(a+) persons. They are not inhibited by urine from Sd(a-) persons, but are strongly inhibited by guinea pig urine. The serologic characteristics indicate a relationship to the Sda blood group and the auto-antibody has been named antiSdx. Sdx antigen is present on red blood cells from some higher primates and is absent from rabbit, rhesus monkey, dog and sheep cells.

ABO Blood-Group System↗
PubMedDate not supplied

Duffy antigen changes on red blood cells stored at low temperature.

Red blood cells stored in saline solution for two weeks at 12 C lose some of their Fya, Fyb, and Fy3 antigenicity. At the same time substances with specific inhibitory activity against appropriate Duffy antibodies appear in the saline. Similar changes could not be recognized in time-expired commercial reagent red blood cell samples.

Blood Group Antigens↗
PubMedDate not supplied

Characterization of an anti-Dia antibody causing hemolytic disease in a newborn infant.

A case of hemolytic disease in a newborn infant caused by anti-Dia is described. The parents are Japanese. The antibody was an IgG of subclasses IgG1 and IgG3, did not bind complement, and gave a 27 percent phagocytosis rate when used to sensitize red blood cells for a macrophage binding assay. The antibody was not detected during antenatal serologic testing. This case suggests the need for reagent red blood cell panels selected to match antibody specificities likely to be encountered in a particular population.

Binding Sites, Antibody↗
PubMedDate not supplied

Depressed blood group antigens on red cells from a Mexican donor.

Red cells from a Mexican blood donor had depressed H, IF, ID, i, Sda, Sdx, D, LW, Dib, Vel and JMH antigens. A wide range of other blood group antigens had normal activity. The unusual red cell phenotype may be caused by a membrane anomaly that alters orientation of certain cell surface components. The specificities of the depressed red cell antigens in this phenomenon differ from those affected in Melanesians with ovalocytosis or in individuals with the In(Lu) inhibitor gene.

ABO Blood-Group System↗
PubMedDate not supplied

An individual with McLeod syndrome and the Kell blood group antigen K(K1).

McLeod syndrome is an X-linked condition in which individuals of McLeod blood group phenotype have weak Kell antigens, acanthocytic red cells, and a muscular disorder. We now report a family in which two brothers have McLeod syndrome. One is K:-1, while the other is the first known K:1 person with McLeod syndrome. The K1 gene in the latter is expressed weakly and was inherited from the father, in whom it is expressed normally. The brothers have the same clinical and laboratory manifestations of McLeod syndrome but have different Kell genes. Therefore, the Kell gene is unlikely to have any positive input into development of McLeod syndrome; its role is one of passive involvement in which its expression is modified.

Adult↗
PubMedDate not supplied

Isolation of Kell-active protein from the red cell membrane.

Kell blood-group-active protein has been isolated by labeling red cell surface proteins with 125I, sensitizing intact cells with anti-K1, anti-K2, anti-K7, or anti-K22, solubilizing the cell membranes, isolating immune complexes, and separating their components by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE). Each antibody separated a protein of approximately 93,000 daltons. Periodic-acid Schiff (PAS) staining of Kell protein showed that it was glycosylated. When separated under non-reducing conditions, Kell protein had different SDS-PAGE characteristics with protein bands of approximately 85,000 daltons and 115,000 daltons. This suggests that in the red cell membrane Kell protein is complexed with other proteins. Quantitative experiments made with anti-K7, anti-K22, and a mixture of anti-K7 and anti-K22 indicate that both antigen specificities are present in the same molecule. These biochemical data support serological studies which indicate that K22 is part of the Kell system.

Antigens, Surface↗
PubMedDate not supplied

The first example of autoanti-Kx.

An IgG autoantibody with Kx specificity was found in the blood of a 61-year-old white man. The antibody did not cause hemolysis of his own or transfused Kx-positive red cells. The patient is of common Kell blood type and does not exhibit any clinical or hematologic features of McLeod syndrome.

Antibody Specificity↗