A Prospective Evaluation of the Accuracy of Weight Estimation Using the Broselow Tape in Overweight and Obese Pediatric Patients in the Emergency Department.

OBJECTIVES: The aims of the study were to examine the predictive accuracy of Broselow tape (BT) weight estimation and body mass index-based weight categorization in overweight and obese pediatric patients and to develop an adjustment factor that improves the BT weight estimate in overweight and obese pediatric patients. METHODS: A prospective observational study was conducted. We enrolled noncritical pediatric patients presenting to a tertiary care pediatric emergency department with nonurgent complaints. Patients had their weights, heights, abdominal circumferences, and actual BT measurements documented by research staff. RESULTS: One hundred seventy-eight patients aged 2 to 18 years were enrolled. Using the Centers for Disease Control and Prevention's definition of body mass index classification, 71 patients (39.89%) had normal BMI, 43 patients (24.16%) were overweight, and 64 patients (35.96%) were obese. The accuracy of the BT-estimated weight range, compared with the actual weight, is 40.5% in our study population. When stratified by BMI classification, the accuracy proportions were the following: 71.8% for normal, 41.9% for overweight, and 4.7% for obese patients. The adjustment formula ([0.014 × waistline in cm + 0.3] × BT weight) improved overall weight estimation from 40.5% to 65.2%. The greatest improvement was noted in obese children, where the BT accuracy improved from 4.7% to 59.4%. CONCLUSIONS: The growing pediatric obesity epidemic has challenged the BT's ability to accurately estimate the weights in overweight and obese pediatric patients. Our study demonstrated inverse relationship between the accuracy of BT and body weight. An adjustment factor significantly improved BT accuracy in obese children.

Kaposi's sarcoma-associated herpesvirus K7 induces viral G protein-coupled receptor degradation and reduces its tumorigenicity.

The Kaposi's sarcoma-associated herpesvirus (KSHV) genome encodes a G protein-coupled receptor (vGPCR). vGPCR is a ligand-independent, constitutively active signaling molecule that promotes cell growth and proliferation; however, it is not clear how vGPCR is negatively regulated. We report here that the KSHV K7 small membrane protein interacts with vGPCR and induces its degradation, thereby dampening vGPCR signaling. K7 interaction with vGPCR is readily detected in transiently transfected human cells. Mutational analyses reveal that the K7 transmembrane domain is necessary and sufficient for this interaction. Biochemical and confocal microscopy studies indicate that K7 retains vGPCR in the endoplasmic reticulum (ER) and induces vGPCR proteasomeal degradation. Indeed, the knockdown of K7 by shRNA-mediated silencing increases vGPCR protein expression in BCBL-1 cells that are induced for KSHV lytic replication. Interestingly, K7 expression significantly reduces vGPCR tumorigenicity in nude mice. These findings define a viral factor that negatively regulates vGPCR protein expression and reveal a post-translational event that modulates GPCR-dependent transformation and tumorigenicity.