Objective To evaluate the utility of the Point of Care Ultrasound (POCUS) Focused Assessment with Sonography for Trauma (FAST) examination for diagnosis of intra-abdominal injury (IAI) in children presenting with blunt abdominal trauma. Methods We searched medical literature from January 1966 to March 2018 in PubMed, EMBASE, and Web of Science. Prospective studies of POCUS FAST examinations in diagnosing IAI in pediatric trauma were included. Sensitivity, specificity, and likelihood ratios (LR) were calculated using a random-effects model (95% confidence interval). Study quality and bias risk were assessed, and test-treatment threshold estimates were performed. Results Eight prospective studies were included encompassing 2135 patients with a weighted prevalence of IAI of 13.5%. Studies had variable quality, with most at risk for partial and differential verification bias. The results from POCUS FAST examinations for IAI showed a pooled sensitivity of 35%, specificity of 96%, LR+ of 10.84, and LR− of 0.64. A positive POCUS FAST posttest probability for IAI (63%) exceeds the upper limit (57%) of our test-treatment threshold model for computed tomography of the abdomen with contrast. A negative POCUS FAST posttest probability for IAI (9%) does not cross the lower limit (0.23%) of our test-treatment threshold model. Conclusions In a hemodynamically stable child presenting with blunt abdominal trauma, a positive POCUS FAST examination result means that IAI is likely, but a negative examination result alone cannot preclude further diagnostic workup for IAI. The need for computed tomography scan may be obviated in a subset of low-risk pediatric blunt abdominal trauma patients presenting with a Glasgow Coma Scale of 14 to 15, a normal abdominal examination result, and a negative POCUS FAST result.

A strategy for activating transcription factor EB (TFEB) to restore autophagy flux may provide neuroprotection against Alzheimer's disease. Our previous study reported that gypenoside XVII (GP-17), which is a major saponin abundant in ginseng and Panax notoginseng, ameliorated amyloid-β (Aβ)25-35-induced apoptosis in PC12 cells by regulating autophagy. In the present study, we aimed to determine whether GP-17 has neuroprotective effects on PC12 cells expressing the Swedish mutant of APP695 (APP695swe) and APP/PS1 mice. We also investigated the underlying mechanism. We found that GP-17 could significantly increase Atg5 expression and the conversion of LC3-I to LC3-II in APP695 cells, which was associated with a reduction in p62 expression. GP-17 also elevated the number of LC3 puncta in APP695 cells transduced with pCMV-GFP-LC3. GP-17 promoted the autophagy-based elimination of AβPP, Aβ40, and Aβ42 in APP695swe cells and prevented the formation of Aβ plaques in the hippocampus and cortex of APP/PS1 mice. Furthermore, spatial learning and memory deficits were cured. Atg5 knockdown could abrogate the GP-17-mediated removal of AβPP, Aβ40, and Aβ42 in APP695swe cells. GP-17 upregulated LAMP-1, increased LysoTracker staining, and augmented LAMP-1/LC3-II co-localization. GP-17 could release TFEB from TFEB/14-3-3 complexes, which led to TFEB nuclear translocation and the induction of autophagy and lysosome biogenesis and resulted in the amelioration of autophagy flux. The knockdown of TFEB could abolish these effects of GP-17. In summary, these results demonstrated that GP-17 conferred protective effects to the cellular and rodent models of Alzheimer's disease by activating TFEB.

Background: To explore risk factors for no-reflow phenomenon after percutaneous coronary intervention in patients with acute