The characterization of cycad palm toxicosis and treatment effects in 130 dogs.

The purpose of this retrospective study is to characterize the clinical signs, laboratory values, treatment modalities and mortality outcomes related to cycad palm toxicosis in dogs and to identify medical interventions that potentially correlate with mortality. Dogs with confirmed cycad palm ingestion were identified by reviewing medical records from two private veterinary referral centres for key terms and phrases indicative of cycad palm toxicosis. Of 130 dogs included, 107 (82.3%) presented with clinical signs. A total of 2 (1.5%) died and 14 (10.8%) were euthanized. Diarrhea, lethargy and mortality were all associated with an elevated initial alanine transaminase (ALT) concentration. Overall mortality was 12.3%, with a significantly higher proportion of dogs with an ALT concentration <125 U/L surviving compared to dogs with an elevated ALT concentration. Treatment with activated charcoal reduced the odds of death among all dogs by 82% and was even more protective among dogs with an elevated initial ALT concentration. Among dogs that had an initial platelet count performed, the presence of thrombocytopenia (<200,000/µL) was a negative prognostic indicator and was associated with a significant increase in mortality. Given the high mortality rates reported for cycad palm toxicosis, it is imperative to identify early clinical indicators of mortality as well as treatments that reduce mortality.

Xrel3 is required for head development in Xenopus laevis.

The Rel/NF-kappa B gene family encodes a large group of transcriptional activators involved in myriad differentiation events, including embryonic development. We have shown previously that Xrel3, a Xenopus Rel/NF-kappa B-related gene, is expressed in the forebrain, dorsal aspect of the mid- and hindbrain, the otocysts and notochord of neurula and larval stage embryos. Overexpression of Xrel3 causes formation of embryonic tumours. We now show that Xrel3-induced tumours and animal caps from embryos injected with Xrel3 RNA express Otx2, Shh and Gli1. Heterodimerisation of a C-terminally deleted mutant of Xrel3 with wild-type Xrel3 inhibits in vitro binding of wild-type Xrel3 to Rel/NF-kappa B consensus DNA sequences. This dominant interference mutant disrupts Shh, Gli1 and Otx2 mRNA patterning and inhibits anterior development when expressed in the dorsal side of zygotes, which is rescued by co-injecting wild-type Xrel3 mRNA. In chick development, Rel activates Shh signalling, which is required for normal limb formation; Shh, Gli1 and Otx2 encode important neural patterning elements in vertebrates. The activation of these genes in tumours by Xrel3 overexpression and the inhibition of their expression and head development by a dominant interference mutant of Xrel3 indicates that Rel/NF-kappa B is required for activation of these genes and for anterior neural patterning in Xenopus.