Thermal injury within the first 4 months of life.

AIM: To determine the incidence, magnitude of injury, fluid management, role of surgery and outcome in newborns and infants under 4 months of age admitted to a Burns Unit. METHOD: Retrospective analysis of patient records. RESULTS: 86 patients under the age of 4 months were admitted over a 37 year period (0.34% of admissions). Their injuries were caused by hot water in 45 and fire in 38, primitive heating devices in 2 and non-accidental paraffin burn in 1. Twenty-eight sustained superficial partial thickness burns, 12 deep partial thickness and 46 full thickness injuries. The total body surface area ranged from 1 to 55% with an average of 11.5%. Bacterial contamination of the burn wounds was present on admission in 52.3% and consisted of both gram positive and gram negative organisms. The resuscitation formula of 3.5 ml/kg/% burn on the first day and 1.5 ml/kg/% burn on the second day plus maintenance fluid at 30-120 ml/kg/day was not always adequate in maintaining haemodynamic stability. Three surgical methods were employed in 59 patients (69%). These included early tangential excision in 25, excision with or without allograft and delayed grafting in 27, and conventional therapy with eventual grafting in 7 patients. Releasing escharotomies were required in 9 children. Nineteen children required amputations. Three craniectomies, 2 tracheostomies and 1 colostomy were additional procedures. The mortality was 9.3%. Three causes of death were identified: magnitude of injury, sepsis and inhalation injury. CONCLUSION: Neonates and infants are very vulnerable and preventable environmental factors are often implicated. Fire and hot water are the most common causes resulting in significant physical trauma. Resuscitation especially during the first few days of life can be problematic. Wound infection and sepsis are common and surgery should be individualised. Long-term outcome is very satisfactory for those with small burns however those with larger burns may remain permanently disfigured.

Simian virus 5 V protein acts as an adaptor, linking DDB1 to STAT2, to facilitate the ubiquitination of STAT1.

The V protein of simian virus 5 (SV5) facilitates the ubiquitination and subsequent proteasome-mediated degradation of STAT1. Here we show, by visualizing direct protein-protein interactions and by using the yeast two-hybrid system, that while the SV5 V protein fails to bind to STAT1 directly, it binds directly and independently to both DDB1 and STAT2, two cellular proteins known to be essential for SV5-mediated degradation of STAT1. We also demonstrate that STAT1 and STAT2 interact independently of SV5 V and show that SV5 V protein acts as an adaptor molecule linking DDB1 to STAT2/STAT1 heterodimers, which in the presence of additional accessory cellular proteins, including Cullin 4a, can ubiquitinate STAT1. Additionally, we show that the avidity of STAT2 for V is relatively weak but is significantly enhanced by the presence of both STAT1 and DDB1, i.e., the complex of STAT1, STAT2, DDB1, and SV5 V is more stable than a complex of STAT2 and V. From these studies we propose a dynamic model in which SV5 V acts as a bridge, bringing together a DDB1/Cullin 4a-containing ubiquitin ligase complex and STAT1/STAT2 heterodimers, which leads to the degradation of STAT1. The loss of STAT1 results in a decrease in affinity of binding of STAT2 for V such that STAT2 either dissociates from V or is displaced from V by STAT1/STAT2 complexes, thereby ensuring the cycling of the DDB1 and SV5 V containing E3 complex for continued rounds of STAT1 ubiquitination and degradation.