Pseudointimal development and vascular prosthesis' susceptibility to bacteremic infection.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to B Bean.
Explore the source record for details and available documents.
Three classes of 5-fluorpyrimidine-resistant mutants of Diplococcus pneumoniae have been characterized. The mutant strain upp is resistant to high concentrations of the fluoropyrimidine bases fluorouracil (FU) and fluorocytosine (FC); strain upp has a defective uridine monophosphate pyrophosphorylase. The mutant strain udk is resistant to inhibition by fluorouridine (FUR) and exhibits defective uridine kinase activity. The mutant strain fun is resistant to inhibition by the nucleosides fluorodeoxyuridine, fluorodeoxycytidine, and FUR, but shows normal activity for all pyrimidine pathway enzymes tested. This strain may be defective in the activity of a transport system that governs the cellular uptake of pyrimidine ribo- and deoxyribonucleosides. Biochemical studies on wild-type and fluoropyrimidine-resistant pneumococci are discussed with respect to the transport and early metabolism of preformed pyrimidine precursors by this organism.
When pyrimidine deoxyribonucleosides are supplied to growing cultures of Diplococcus pneumoniae, they are selectively used for incorporation into deoxyribonucleic acid (DNA). Differently labeled molecules of deoxyuridine, thymidine, and deoxycytidine were used to study the precursor pathways of this organism. Each of these preformed pyrimidine deoxynucleosides is incorporated intact (i.e., without cleavage of the glycosidic bond) and is predominantly recoverable as DNA thymidine. During the utilization of deoxycytidine and deoxyuridine by pneumococci, large proportions of the available precursor are converted to free thymidine, which is secreted back into the growth medium. The biochemical pathways for selective incorporation into DNA and the regulation of concentrations of intracellular thymidine compounds by excretion of free thymidine are discussed.
5-Fluorouracil (FU), 5-fluorocytosine, and the riboside and deoxyriboside derivatives of these fluoropyrimidines each exhibit a different spectrum of inhibitory effects in pneumococci. The biochemical basis of this finding seems to be the extremely low level of nucleoside phosphorylase (hydrolase) and N-trans-deoxyribosylase activity in pneumococcus and the consequent, relatively limited metabolic interconversion of the different fluoropyrimidines, which can therefore selectively affect one or the other of the several drug-sensitive biochemical reactions in this bacterium. Special attention was paid to the effect of fluoropyrimidines on the metabolism of cytosine and thymidine. In spite of the fact that FU is converted to both fluorouridine triphosphate and fluorocytidine triphosphate, only fluorouridylate but no fluorocytidylate can be detected in the ribonucleic acid Exogenous FU and fluorouridine also inhibit the synthesis of cytosine nucleotides from supplied uridine in a pyrimidine auxotroph. Thymidine was found to be a poor reversing agent for any of the fluoropyrimidine inhibitions. In both the wild type and in a thymidine-requiring (thymidylate-synthetase deficient) mutant, growing with supplied thymidine in the medium, fluorodeoxyuridine (FUdR) treatment caused cell death and inhibition of the incorporation of radioactive thymidine, adenosine, or uracil into deoxyribonucleic acid. It is suggested that FUdR (or a metabolic derivative) inhibits the transport of phosphorylation of thymidine in this microorganism.
Acute lymphatic filariasis developed in an American traveling recreationally to Asia. The illness was characterized by fatigue, eosinophilia, and lymphedema of the arm and chest wall, but no lymphangitis, lymphadenitis, or pain. Complete resolution occurred over 1-2 years. We discuss this syndrome and describe the use of new diagnostic tests in its diagnosis and management.
Acyclovir is a specific antiviral agent. The triphosphate form inhibits viral DNA replication by competing for incorporation into the replicating DNA chain or by inhibiting viral DNA polymerase. Cells not infected with herpesvirus are generally unaffected. Oral acyclovir inhibits most herpes simplex virus types 1 and 2, and varicella-zoster virus at concentrations used clinically. Oral acyclovir has an average plasma half-life of three hours and is eliminated primarily by renal mechanisms. Peak plasma concentrations occur 1.5 to 2.5 hours after administration and the oral bioavailability is 15 to 30 percent. Acyclovir distributes into most body tissues, including vesicular fluid and the central nervous system. Oral acyclovir is effective treatment of initial and recurrent genital herpes and can suppress frequently recurring genital herpes in both immunocompetent and immunocompromised patients. It is also effective for acute herpes zoster in the immunocompetent and possibly immunocompromised patient. No role is established in either Epstein-Barr virus or cytomegalovirus infections. Oral acyclovir appears to be effective and relatively safe, nontoxic therapy when administered in doses of 1-4 g/d. Oral acyclovir represents a major therapeutic advance in the treatment of herpesvirus infections.
Explore the source record for details and available documents.
To help identify and characterize antigens involved in sperm functions and immune infertility, monoclonal antibodies (mAbs) were raised against human sperm antigens. The immunoglobulin G (IgG) fraction of serum from a male donor with a spontaneous high titer of IgG-positive antisperm reactivity (as determined by immunobead binding) was purified by ammonium sulfate precipitation. This IgG preparation was coupled to Sepharose 4B and was used for immunoaffinity purification of antigens from a detergent-solubilized extract of pooled normal human sperm. The affinity-purified antigens were used to immunize female mice, and the resultant spleen cells were fused with SP 2/0 mouse myeloma cells to generate hybridomas. A single-step semisolid methylcellulose method was used to isolate hybridomas for the selection of positive clones, which were determined by enzyme-linked immunosorbent assay. Thirty-two positive hybridoma lines were selected for immunolocalization and cross-reactivity studies using an avidin-biotin complex assay. Distinctive staining patterns and distribution of sperm antigens were observed for 10 mAbs. Among them, the cross-reactivity with human lymphocytes was not observed for four mAbs.