PubMed Health⌕ Search

Biomedical subjects

K Woodward

Publications and source records attributed to K Woodward.

28 records · Page 2Linked to original sources
PubMed1987

Diagnosing gonorrhea. A comparison of standard and rapid techniques.

A timely and accurate technique for diagnosing gonorrhea is necessary if prompt therapy is to be instituted. We screened 567 adolescents who presented for routine gynecologic care or for specific gynecologic or urologic problems. Each patient was tested by standard culture, Gonozyme (Abbott Labs), and Gram's stain. One hundred five patients (18.5%) had an ELISA immunoassay or culture evidence of infection. Overall sensitivity was 90% for Gonozyme and 56% for Gram's stain (females 41%, males 94%). Overall specificity was 97% for Gonozyme and 99% for Gram's stain. No increase in sensitivity of either test was found in women with signs of upper genital tract involvement. The predictive value of a negative Gonozyme was 98% and 85% for a positive result compared to Gram's stain values of 99% and 95%, respectively. Overall clinical efficacy was 96% for Gonozyme and 93% for Gram's stain. Gonozyme, although a sensitive and specific test, has a limited role in the diagnosis of gonorrhea. Gram's stain, although more limited in women, may serve as a useful adjunct in diagnosing gonorrhea.

Adolescent↗
PubMed1982

Inhibition of phorbol ester-receptor binding by a factor from human serum.

The inhibition of receptor binding of [3H]phorbol-12,13-dibutyrate (PDBu) by a factor from human serum was characterized. The serum factor inhibited [3H]PDBu binding in intact monolayer cultures of the rat embryo cell line CREF N and in a subcellular system containing membranes from these cells. Inhibition occurred at both 37 and 4 degrees C and was rapid and reversible. An analysis of [3H]PDBu binding in the presence of the serum factor indicated that inhibition of [3H]PDBu binding by the serum factor was noncompetitive. Using gel filtration to separate the serum factor from free [3H]PDBu, we obtained evidence that the serum factor does not act by binding or trapping the [3H]PDBu. Unlike the phorbol ester tumor promoters, the serum factor alone did not stimulate the release of choline or arachidonic acid from cellular phospholipids, nor did it inhibit the binding of 125I-labeled epidermal growth factor to cellular receptors. The factor did, however, antagonize the inhibition of epidermal growth factor binding induced by PDBu. Sera from pregnant women were, in general, more inhibitory of [3H]PDBu binding than were those from nonpregnant women, which were more inhibitory than those from men. During these studies we found that CREF N cells responded to being grown in the presence of PDBu by partial down regulation of the phorboid receptor. The 50% effective dose for down regulation was 8 nM PDBu, and the maximum effect occurred after 6 h. Taken together, our results indicate that the serum factor inhibits [3H]PDBu binding by a direct physical effect at the level of the phorboid receptors or their associated membranes. It would appear that if this factor acts in vivo, then it might antagonize certain effects of this class of tumor promoters.

Animals↗
PubMed1981

New HLA-D alleles associated with DR1 and DR2.

The present study describes two new HLA-D specificities : LD 13, associated with DR1, and LD14 associated with DR2. LD13 is defined by an HTC who is the bc offspring of an a: A25, B18, DR7, Dw7/b: A33, B14, DR1, Dx father, and of a c: A24, B14, Dr1, Dx/d: A26, B41, DR5, Dw5 mother. This HTC was included both as a responder and as a stimulator in our cross-reference studies of 8W HTCs. While failing to cluster with any other 8W HTC, it typed 2 of 64 panel members carrying a "blank" HLA-D, linked to DR1. To exclude the possibility that HTC-LD13 might be a split of Dwl, the entire family was tested with the Family Set of 8W HTCs. No typing responses to any 8W Dw1 HTCs were observed. Furthermore, checkerboard experiments between HTC-LD13 and 8WDw1 HTCs showed strong reciprocal stimulation. The LD13 specificity was only found in Ashkenazi Jews and may be in linkage disequilibrium with HLA-B14. LD14 is defined by three, SD different, HTCs deriving from the same family of Sicilian descent. The family was included in the 8th Workshop and each HTC was shown to have inherited DR2, MT1 from both parents. When tested as stimulators, on our HLA-D reference panel, these cells were clustered in a distinct group, LD14, associated with DR2. None of the 8W HTCs appeared to belong to this cluster. The antigen frequency of LD14 is 0.03.

Alleles↗