National Defense Medical Center

To share our 20-year experience in major burn management and the impact of a newly implemented burn protocol since 2015 at Tri-Service General Hospital (TSGH).

We performed a retrospective cohort study of severely burned patients who were admitted to the intensive care unit (ICU) at TSGH from January 2003 to September 2023. Data regarding demographics, complications, and mortality were collected and analyzed. We compared the patient data before (pre-implementation) and after 2015 (post-implementation), when the new major burn management protocol was introduced.

No statistically significant differences were observed in the mean total body surface area of the burns between the groups. The post-implementation group had younger age (34.62 vs 45.06, P < 0.001) and lower rate of inhalation injury (60.8 % vs 82.5 %, P = 0.005). No statistically significant difference was observed in the ICU stays between the groups. The post-implementation group had a statistically significant lower all-cause mortality (8.1 % vs 47.6 %, P < 0.0001) and lower rate of renal replacement therapy (RRT) (20.3 % vs 42.9 %, P = 0.004) but earlier initiation of RRT.

The new TSGH Burns Protocol revolutionized the care of major burns by introducing tailored, multidisciplinary burn management and improved patient outcomes.

Preterm infants with intraventricular hemorrhage (IVH) are at a risk of developing neurodevelopmental disabilities. Few studies have examined the effects of oxygen saturation (SpO₂) changes and intubation procedures on the risk of IVH.

We examined the effects of intubation and the rates of three thresholds of hypoxemia on the occurrence of IVH in preterm infants during their first week in the neonatal intensive care unit (NICU).

In this prospective observational cohort study, preterm infants with a gestational age (GA) of <37 weeks were included from two Level III NICUs in Taiwan. Continuous electrocardiography was used to monitor SpO₂ changes, and cranial ultrasonography was used to monitor IVH. Thresholds of hypoxemia (SpO₂ levels of <80 %, <85 %, and <90 %) were screened by digitally sampling data at 10-s intervals. Generalized estimating equations were used with logistic regression to analyze the effects of intubation and the rates of the three thresholds of hypoxemia on the risk of IVH during the first week after birth.

In all preterm infants (N = 73), the mean GA was 31.55 weeks, and the mean birth weight was 1508.86 g. Intubation within 3 days of birth, duration of mechanical ventilation and oxygen use, hypoxemia rate, and maternal use of magnesium sulfate before and during delivery were significantly associated with IVH. A multivariate analysis revealed that intubation was a key factor associated with the occurrence of IVH across different thresholds of hypoxemia (p = 0.004).

Although the rate of hypoxemia, duration of mechanical ventilation and oxygen use, and maternal use of magnesium sulfate were significantly associated with IVH, intubation within 3 days of birth was the key factor responsible for increased IVH risk.

Tetrabromobisphenol A (TBBPA), a brominated flame retardant (BFR), has been implicated as the neurotoxic effects in mammalian. However, the exact mechanisms underlying TBBPA-induced neurotoxicity remain unclear. In the present study, Neuro-2a cells, a mouse neural crest-derived cell line, were used to examine the mechanism of TBBPA-induced neuronal cytotoxicity. TBBPA exposure caused alterations in cell viability and mitochondrial membrane potential (MMP) and induction of apoptotic events, such as increased apoptotic cell population and cleaved caspase-3, -7, -9, and poly (ADP-ribose) polymerase (PARP) protein expression). TBBPA exposure triggered CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP) activation. Transfection with CHOP-specific small interfering RNA (siRNA) obviously prevented the expression of CHOP protein and markedly attenuated MMP loss, and caspase-3 and -7 activation in TBBPA-exposed Neuro-2a cells. In addition, TBBPA exposure significantly evoked the phosphorylation of c-Jun N-terminal kinase (JNK), extracellular-signal regulated kinase1/2 (ERK1/2), p38-mitogen-activated protein kinase (p38-MAPK), and AMP-activated protein kinase (AMPK)α proteins. Pretreatment of cells with pharmacological inhibitors of p38-MAPK (SB203580) and AMPK (compound C), but not inhibitors of JNK (SP600125) or ERK1/2 (PD98059), effectively prevented the increase in caspase-3 activity, MMP loss, and activated CHOP and cleaved caspase-3 and -7 protein expression in TBBPA-treated cells. Notably, transfection with either p38α-MAPK- or AMPKα1/2-specific siRNAs markedly attenuated the expression of CHOP, and cleaved caspase-3 and -7. Interestingly, transfection with each siRNA significantly reduced the TBBPA-induced phosphorylation of p38-MAPK and AMPKα proteins. Collectively, these findings suggest that CHOP activation-mediated mitochondria-dependent apoptosis contributes to TBBPA-induced neurotoxicity. An interdependent p38-MAPK and AMPKα signaling-regulated apoptotic pathway may provide new insights into the mechanism understanding TBBPA-elicited neurotoxicity.