EXPERIENCE WITH VIPERINE ENVENOMATION

Two hundred and twenty one cases of viperine envenomation, who presented to hospital without specific treatment, seen over an twenty five years period, have been presented. Mild, moderate and severe envenomation was encountered in 33 per cent, 47 per cent and 20 per cent respectively. Bites on feet and ankles were seen in 85.5 per cent of cases. The average time interval between bite and hospitalisation was 4.8 hours, range being 15 minutes to 7 days. Local swelling was observed in 97.7 per cent, hematuria in 62 per cent, mucosal haemorrhages in 24.8 per cent and haematemesis in 19 per cent of patients. Average Antisnake Venom (ASV) required in mild, moderate and severe envenomation was 50 ml, 147.5 ml and 324 ml respectively. Major complications observed were renal failure in 10, intracompartmental syndrome in 3, intracerebral bleed and septicaemia in 2 each. One patient each developed finger gangrene, osteomyelitis, perirenal haematoma, sinus bradycardia and uncontrolled bleeding. Blood transfusion was required in 32 patients. Reactions to ASV were seen in 12 patients and overall there were 5 deaths.KEY WORDS: Antisnake venom, Viperine envenomation     

The UTX gene escapes X inactivation in mice and humans

We recently have identified a ubiquitously transcribed mouse Y chromosome gene, Uty , which encodes a tetratricopeptide repeat (TPR) protein. A peptide derived from the UTY protein confers H-Y antigenicity on male cells. Here we report the characterization of a widely transcribed X-linked homologue of Uty , called Utx , which maps to the proximal region of the mouse X chromosome and which detects a human X-linked homologue at Xp11.2. Given that Uty is ubiquitously transcribed, we assayed for Utx expression from the inactive X chromosome (Xi) in mice and found that Utx escapes X chromosome inactivation. Only Smcx and the pseudoautosomal Sts gene on the mouse X chromosome have been reported previously to escape inactivation. The human UTX gene was also found to be expressed from Xi. We discuss the significance of these data for our understanding of dosage compensation of X-Y homologous genes in humans and mice.      

L1 knockout mice show dilated ventricles, vermis hypoplasia and impaired exploration patterns

L1 is a neural cell adhesion molecule mainly involved in axon guidance and neuronal migration during brain development. Mutations in the human L1 gene give rise to a complex clinical picture, with mental retardation, neurologic abnormalities and a variable degree of hydrocephalus. Recently, a transgenic mouse model with a targeted null mutation in the L1 gene was generated. These knockout (KO) mice show hypoplasia of the corticospinal tract. Here we have performed further studies of these KO mice including magnetic resonance imaging of the brain, neuropathological analysis and behavioral testing. The ventricular system was shown to be abnormal with dilatation of the lateral ventricles and the 4th ventricle, and an altered shape of the Sylvius aqueduct. Additionally, the cerebellar vermis of the KO mice is hypoplastic. Their exploratory behavior is characterized by stereotype peripheral circling reminiscent of that of rodents with induced cerebellar lesions.