ABSTRACT
A 2-year-old girl presented to the emergency department at 3:00 h with severe pain in her right eye and a rust coloured, blood stained frothy discharge that had woken her. An examination of her eye revealed a shiny metallic looking foreign body, which was immediately removed by the on-call ophthalmologist. That morning the patient underwent ocular examination under anaesthesia and was found to have severe tissue necrosis resulting from an electrochemical burn. She was treated with daily rodding for 3 days and betamethasone ointment four times a day, which was gradually tapered. At 3 months her only eye pathology was a mild symblepharon between the bulbar and tarsal conjunctiva. This is the first case of delayed symptoms after placement of a button battery into the conjunctival fornix. This case highlights the serious nature of button battery injuries to the eye and the potential to miss the diagnosis owing to a delayed onset of symptoms.
Subject(s)
Burns, Chemical , Conjunctiva/pathology , Conjunctival Diseases , Electric Power Supplies , Eye Injuries , Foreign Bodies , Betamethasone/therapeutic use , Burns, Chemical/diagnosis , Burns, Chemical/drug therapy , Burns, Chemical/etiology , Child, Preschool , Conjunctival Diseases/diagnosis , Conjunctival Diseases/drug therapy , Conjunctival Diseases/etiology , Eye Injuries/diagnosis , Eye Injuries/drug therapy , Eye Injuries/etiology , Female , HumansABSTRACT
Most chicken strains are highly susceptible to avian leukosis virus (ALV) induction of bursal lymphoma, involving proviral integration within the c-myc proto-oncogene, while certain strains are genetically resistant to lymphomagenesis. A nested PCR assay was developed to analyse the appearance of proviral c-myc integrations after ALV infection of lymphoma-susceptible birds, and to determine whether these integrations arise in lymphoma-resistant birds. Proviral c-myc integrations are detected in bursa and other tissues from 6 day-old lymphoma-susceptible birds infected as embryos. The abundance of bursal cells carrying these integrations increases roughly 40-fold by 35 days of age, indicating that these cells hyperproliferate within the bursal environment. Bursal cells with proviral c-myc integrations also arise soon after infection of lymphoma-resistant embryos. However, these cells expand much more slowly than cells from lymphoma-susceptible birds. Both strains show the same rate of viral infection, so that resistance to lymphomagenesis occurs at a step subsequent to proviral c-myc integration. Proviral c-erbB gene integrations arise at the same frequency in bursa and other tissues of both strains, and they do not increase in abundance during development. These findings indicate that the mechanism of resistance to lymphomagenesis involves specific inhibition of cells with proviral c-myc integrations within the bursa.
Subject(s)
Avian Leukosis Virus/genetics , Genes, myc , Virus Integration , Animals , Birds , Disease Susceptibility , Hematopoiesis , Immunity, Innate , Lymphoma , Proviruses/genetics , Receptor, ErbB-2/genetics , Tumor Cells, CulturedABSTRACT
Avian leukosis virus (ALV) infection induces bursal lymphomas in chickens after proviral integration within the c-myc proto-oncogene and induces erythroblastosis after integration within the c-erbB proto-oncogene. A nested PCR assay was used to analyze the appearance of these integrations at an early stage of tumor induction after infection of embryos. Five to eight distinct proviral c-myc integration events were amplified from bursas of infected 35-day-old birds, in good agreement with the number of transformed bursal follicles arising with these integrations. Cells containing these integrations are remarkably common, with an estimated 1 in 350 bursal cells having proviral c-myc integrations. These integrations were clustered within the 3' half of c-myc intron 1, in a pattern similar to that observed in bursal lymphomas. Bone marrow and spleen showed a similar number and pattern of integrations clustered within 3' c-myc intron 1, indicating that this region is a common integration target whether or not that tissue undergoes tumor induction. While all tissues showed equivalent levels of viral infection, cells with c-myc integrations were much more abundant in the bursa than in other tissues, indicating that cells with proviral c-myc integrations are preferentially expanded within the bursal environment. Proviral integration within the c-erbB gene was also analyzed, to detect clustered c-erbB intron 14 integrations associated with erythroblastosis. Proviral c-erbB integrations were equally abundant in the bone marrow, spleen, and bursa. These integrations were randomly situated upstream of c-erbB exon 15, indicating that cells carrying 3' intron 14 integrations must be selected during induction of erythroblastosis.
Subject(s)
Avian Leukosis Virus/genetics , Genes, erbB , Genes, myc , Virus Integration , Animals , Chickens , Polymerase Chain ReactionABSTRACT
The avian leukosis virus (ALV) long terminal repeat (LTR) contains a compact transcription enhancer that is active in many cell types. A major feature of the enhancer is multiple CCAAT/enhancer element motifs that could be important for the strong transcriptional activity of this unit. The contributions of the three CCAAT/enhancer elements to LTR function were examined in B cells, as this cell type is targeted for ALV tumor induction following integration of LTR sequences next to the c-myc proto-oncogene. One CCAAT/enhancer element, termed a3, was found to be the most critical for LTR enhancement in transiently transfected B lymphoma cells, while in chicken embryo fibroblasts all three elements contributed equally to enhancement. Gel shift assays demonstrated that vitellogenin gene-binding protein (VBP), a member of the PAR subfamily of C/EBP factors, is a major component of the nuclear proteins binding to the a3 CCAAT/enhancer element. VBP activated transcription through the a3 CCAAT/enhancer element, supporting the idea that VBP is important for LTR enhancement in B cells. A member of the Rel family of proteins was also identified as a component of the a3 protein binding complex in B cells. Gel shift and immunoprecipitation assays indicated that this factor is RelA. Gel shift assays demonstrated that while RelA does not bind directly to the LTR CCAAT/enhancer elements, it does interact with VBP to potentiate VBP DNA binding activity. The synergistic interaction of VBP and RelA increased CCAAT/enhancer element-mediated transcription, indicating that both factors may be important for viral LTR regulation and also for expression of many cellular genes.
Subject(s)
Avian Leukosis Virus/genetics , Avian Proteins , B-Lymphocytes/virology , Carrier Proteins/physiology , Enhancer Elements, Genetic , NF-kappa B/pharmacology , Transcription Factors/physiology , Transcription, Genetic , Animals , Base Sequence , Basic-Leucine Zipper Transcription Factors , Chick Embryo , Molecular Sequence Data , NF-kappa B/metabolism , Repetitive Sequences, Nucleic Acid , Transcription Factor RelAABSTRACT
Three adults are described who developed life-threatening hypotension following intravenous codeine phosphate. It is recommended that codeine phosphate should not be given intravenously to adults.
Subject(s)
Codeine/adverse effects , Hypotension/chemically induced , Intraoperative Complications/chemically induced , Adolescent , Codeine/administration & dosage , Female , Humans , Injections, Intravenous , Male , Middle AgedABSTRACT
A case report of biliary colic induced by narcotic premedication and reversed by naloxone administration is described and the literature reviewed.
