We aimed to know the risk-stratification-based prevalence of bacterial contamination of ambulance vehicle surfaces, equipment, and materials. This study was performed in a metropolitan area with fire-based single-tiered Basic Life Support ambulances. Total 13 out of 117 ambulances (11.1%) were sampled and 33 sites per each ambulance were sampled using a soft rayon swab and aseptic containers. These samples were then plated onto a screening media of blood agar and MacConkey agar. Specific identification with antibiotic susceptibility was performed. We categorized sampling sites into risk stratification-based groups (Critical, Semi-critical, and Non-critical equipment) related to the likelihood of direct contact with patients' mucosa. Total 214 of 429 samples showed positive results (49.9%) for any bacteria. Four of these were pathogenic (0.9%) (MRSA, MRCoNS, and K. pneumoniae), and 210 of these were environmental flora (49.0%). However, the prevalence (positive/number of sample) of bacterial contamination in critical, semi-critical airway, semi-critical breathing apparatus group was as high as 15.4% (4/26), 30.7% (16/52), and 46.2% (48/104), respectively. Despite current formal guidelines, critical and semi-critical equipments were contaminated with pathogens and normal flora. This study suggests the need for strict infection control and prevention for ambulance services.

EphAs and ephrin-As have been implicated in the morphogenesis of the developing brain. We found that EphA7 and ephrin-A5 are coexpressed in the dorsal midline (DM) of the diencephalon and anterior mesencephalon. Interestingly, programmed cell death (PCD) of the neural epithelial cells normally found in this region was reduced in ephrin-A5/ephrin-A2 dual-deficient embryos. In contrast, in vivo expression of ephrin-A5-Fc or full-length ephrin-A5 strongly induced apoptosis in neural epithelial cells and was accompanied by severe brain malformation during embryonic development. Expression of ephrinA5-Fc correlated with apoptosis of EphA7-expressing cells, whereas null mutation of ephrin-A5 resulted in the converse phenotype. Importantly, null mutation of caspase-3 or endogenous ephrin-A5 attenuated the PCD induced by ectopically overexpressed ephrin-A5. Together, our results suggest that brain region-specific PCD may occur in a region where EphAs cluster with neighboring ephrin-As through cell-cell contact.

The development of complex organs such as the eye requires a delicate and coordinated balance of cell division and cell death. Although apoptosis is prevalent in the proximoventral optic cup, the precise role it plays in eye development needs to be investigated further. In this study, we show that reduced apoptosis in the proximoventral optic cup prevents closure of the optic fissure. We also show that expression of ephrin A5 (Efna5) partially overlaps with Eph receptor B2 (Ephb2) expression in the proximoventral optic cup and that binding of EphB2 to ephrin A5 induces a sustained activation of JNK. This prolonged JNK signal promotes apoptosis and prevents cell proliferation. Thus, we propose that the unique cross-subclass interaction of EphB2 with ephrin A5 has evolved to function upstream of JNK signaling for the purpose of maintaining an adequate pool of progenitor cells to ensure proper closure of the optic fissure.

Endocytosis of Eph-ephrin complexes may be an important mechanism for converting cell-cell adhesion to a repulsive interaction. Here, we show that an endocytosisdefective EphA8 mutant forms a complex with EphAs and blocks their endocytosis in cultured cells. Further, we used bacterial artificial chromosome transgenic (Tg) mice to recapitulate the anterior4posterior gradient of EphA in the superior colliculus (SC). In mice expressing the endocytosis-defective EphA8 mutant, the nasal axons were aberrantly shifted to the anterior SC. In contrast, in Tg mice expressing wild-type EphA8, the nasal axons were shifted to the posterior SC, as predicted for the enhanced repellent effect of ephrinA reverse signalling. Importantly, Rac signalling was shown to be essential for EphAephrinA internalization and the subsequent nasal axonal repulsion in the SC. These results indicate that endocytosis of the Eph-ephrin complex is a key mechanism by which axonal repulsion is generated for proper guidance and topographic mapping.

The initial BD in pediatric trauma patients except severe brain injury was an independent predictor of mortality and blood transfusion requirement within 24 hours. Mortality and blood transfusion requirement were significantly high when initial BD was less than -8 mEq/L.