Does Specialty Training and Practice Setting Affect Adherence to the Pediatric Emergency Care Applied Research Network Criteria for Pediatric Head Trauma?

OBJECTIVE: The goal was to determine the effects of specialty training and practice settings on the adherence to the Pediatric Emergency Care Applied Research Network (PECARN) criteria. METHODS: A retrospective study was conducted on a 2-campus hospital. Chart documentation was used to determine adherence to PECARN criteria. Inclusion criteria were any traumatic head injury within 24 hours in patients younger than 18 years over a 1-year period. Specialty training was subdivided into 3 groups: pediatric emergency medicine, emergency medicine (EM), and general pediatrics. The 2 hospital campuses are distinctly different practice settings, one being an academic practice setting, which is also a trauma center that has a dedicated pediatric emergency department, staffed by pediatric emergency medicine, EM, and general pediatrics physicians, and the second campus is a community practice and is staffed solely by EM physicians. Statistical analysis was performed using χ and Cochran-Mantel-Haenszel tests. All analyses were 2-sided, and P < 0.05 was considered statistically significant. RESULTS: A total of 709 pediatric patients with traumatic head injuries were analyzed. Overall adherence to PECARN criteria was 93%. No statistical difference was found between different specialty training on the academic campus. In addition, the rate of adherence among EM physicians at the academic and community settings was 94.8% versus 86.5%, respectively (P = 0.004). CONCLUSIONS: Practice setting had an effect on adherence to PECARN criteria in pediatric patients with acute traumatic head injury. The same determination on adherence was not demonstrated among physicians with different specialty trainings.

Loss of lysosomal ion channel transient receptor potential channel mucolipin-1 (TRPML1) leads to cathepsin B-dependent apoptosis.

Mucolipidosis type IV (MLIV) is a lysosomal storage disease caused by mutations in the gene MCOLN1, which codes for the transient receptor potential family ion channel TRPML1. MLIV has an early onset and is characterized by developmental delays, motor and cognitive deficiencies, gastric abnormalities, retinal degeneration, and corneal cloudiness. The degenerative aspects of MLIV have been attributed to cell death, whose mechanisms remain to be delineated in MLIV and in most other storage diseases. Here we report that an acute siRNA-mediated loss of TRPML1 specifically causes a leak of lysosomal protease cathepsin B (CatB) into the cytoplasm. CatB leak is associated with apoptosis, which can be prevented by CatB inhibition. Inhibition of the proapoptotic protein Bax prevents TRPML1 KD-mediated apoptosis but does not prevent cytosolic release of CatB. This is the first evidence of a mechanistic link between acute TRPML1 loss and cell death.