A simple automatic kinetic enzyme immunoassay for digoxin.
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Biomedical subjects
Publications and source records attributed to D Seckinger.
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PURPOSE: To determine the advantages of using transcatheter sclerotherapy to treat renal allograft-related lymphoceles. MATERIALS AND METHODS: Eighteen patients first seen with symptomatic lymphoceles secondary to renal transplantation were treated with povidone-iodine percutaneous sclerotherapy. Percutaneous catheters were place by means of sonographic, computed tomographic, or combined fluoroscopic and sonographic guidance. Sclerotherapy was initiated while patients were in the hospital, and the patients then instilled povidone-iodine twice a day at home. RESULTS: One patient had an inadequate trial period of therapy and was not included in the analysis. Seventeen lymphoceles were adequately sclerosed. Average length of treatment was 35 days. Three lymphoceles recurred and were effectively treated percutaneously. Follow-up studies showed no recurrence 1 month to 2 years after completion of therapy. No patient needed surgery for lymphocele repair. CONCLUSION: Because of its safety and efficacy, percutaneous transcatheter sclerotherapy with povidone-iodine should be the treatment of choice in patients with lymphoceles that develop after renal transplantation.
The advent of the radioimmunoassay of Beta subunit chorionic gonadotropin (BhCG) has eliminated a major problem in following the patient with gestational trophoblastic neoplasia (GTN). Whole hCG cross reacts with luteinizing hormone (hLH) causing difficulties when GTN patient titers fall to levels coincidental with pituitary levels of hLH. The use of the Beta subunit of hCG in radioimmunoassay has eliminated this problem because there is essentially no cross reaction between the B-subunit of the hCG and hLH. A review of the use of this sensitive assay in the management of patients with GTN is presented.
Aphidicolin (AP) or hydroxyurea (HU) inhibited DNA repair and enhanced cytotoxicity in human ovarian carcinoma cells A2780 treated with L-phenylalanine mustard (L-PAM) combined with cisplatin or thioTEPA, and in the cells treated with cisplatin combined with thioTEPA. In cultures treated with L-PAM or cisplatin alone post-treatment with AP or HU had no effect on DNA repair and produced only additive cytotoxicity. Post-treatment with AP + HU inhibited DNA repair and enhanced cell killing in cultures treated with L-PAM alone. The inhibitor of protein synthesis cycloheximide protected cells from the cytotoxicity of AP + HU but had no effect on synergistic cell killing produced by DNA repair inhibition. In cisplatin-resistant cells A2780/CP post-treatment with AP + HU enhanced the cytotoxicity of L-PAM, but not of cisplatin. However, in resistant cells treated with cisplatin combined with L-PAM or thioTEPA DNA repair inhibitors decreased IC90 of cisplatin. Treatment of cells with two alkylating agents enhanced the sensitivity to DNA repair inhibitors and eliminated low sensitivity to inhibitors of repair associated with drug resistance.