ABSTRACT
UNLABELLED: Life-threatening anaphylaxis developed in a 5-y-old boy with septic shock within minutes of receiving his first intravenous injection of ceftriaxone. Hypersensivity could not be demonstrated by skin testing and ceftriaxone-specific IgE. However, an in vivo, controlled, intravenous challenge was clearly positive. CONCLUSION: Clinicians should be aware of the possibility of anaphylaxis occurring with the first dose of ceftriaxone, especially since such a reaction could go unnoticed in patients with life-threatening infections and unstable vital signs.
Subject(s)
Anaphylaxis/chemically induced , Ceftriaxone/adverse effects , Drug Hypersensitivity/etiology , Shock, Septic/drug therapy , Ceftriaxone/administration & dosage , Child, Preschool , Drug Hypersensitivity/diagnosis , Follow-Up Studies , Humans , Injections, Intravenous , Male , Patch Tests , Risk Assessment , Severity of Illness IndexABSTRACT
The Plk gene encodes a serine/threonine protein kinase believed to be important for the normal progression of mammalian cells through the cell cycle. In this paper, we report the genomic organization of the mouse Plk gene. The mouse Plk gene encompasses 16 kb of the mouse genome and is organised into 10 exons. Based on homology with the human PLK1 promoter region, the putative mouse promoter region includes a CCAAT motif but lacks the conventional TATA motif. The proposed promoter region contains consensus binding sites for several transcriptional regulators, including Sp1 and AP2. In addition to the active copy of Plk, Plk exists as a processed pseudogene. Using RFLP analysis, we have localized the active Plk gene to mouse Chromosome 7 and the processed pseudogene to mouse Chromosome 5. Southern blot analysis of DNA from a limited number of other mammalian species suggests that the duplication is confined to the mouse. Parsimony analysis suggests that the gene duplication leading to the mouse Plk pseudogene occurred after the rat-mouse split.
