mStroke: "Mobile Stroke"-Improving Acute Stroke Care with Smartphone Technology.

OBJECTIVE: This study aimed to evaluate the effect of method and time of system activation on clinical metrics in cases utilizing the Stop Stroke (Pulsara, Inc.) mobile acute stroke care coordination application. METHODS: A retrospective cohort analysis of stroke codes at 12 medical centers using Stop Stroke from March 2013 to May 2016 was performed. Comparison of metrics (door-to-needle time [DTN] and door-to-CT time [DTC], and rate of DTN ≤ 60 minutes [goal DTN]) was performed between subgroups based on method (emergency medical service [EMS] versus emergency department [ED]) and time of activation. Effects were adjusted for confounders (age, sex, National Institutes of Health Stroke Scale [NIHSS] score) using multiple linear and logistic regression. RESULTS: The final dataset included 2589 cases. Cases activated by EMS were more severe (median NIHSS score 8 versus 4, P < .0001) and more likely to receive recombinant tissue plasminogen activator (20% versus 12%, P < .0001) than those with ED activation. After adjustment, cases with EMS activation had shorter DTC (6.1 minutes shorter, 95% CI [-10.3, -2]) and DTN (12.8 minutes shorter, 95% CI [-21, -4.6]) and were more likely to meet goal DTN (OR 1.83, 95% CI [1.1, 3]). Cases between 1200 and 1800 had longer DTC (7.7 minutes longer, 95% CI [2.4, 13]) and DTN (21.1 minutes longer, 95% CI [9.3, 33]), and reduced rate of goal DTN (OR .3, 95% CI [.15, .61]) compared to those between 0000 and 0600. CONCLUSIONS: Incorporating real-time prehospital data obtained via smartphone technology provides unique insight into acute stroke codes. Activation of mobile electronic stroke coordination in the field appears to promote a more expedited and successful care process.

Choline inadequacy impairs trophoblast function and vascularization in cultured human placental trophoblasts.

Maternal choline intake during gestation may influence placental function and fetal health outcomes. Specifically, we previously showed that supplemental choline reduced placental and maternal circulating concentrations of the anti-angiogenic factor, fms-like tyrosine kinase-1 (sFLT1), in pregnant women as well as sFLT1 production in cultured human trophoblasts. The current study aimed to quantify the effect of choline on a wider array of biomarkers related to trophoblast function and to elucidate possible mechanisms. Immortalized HTR-8/SVneo trophoblasts were cultured in different choline concentrations (8, 13, and 28 µM [control]) for 96-h and markers of angiogenesis, inflammation, apoptosis, and blood vessel formation were examined. Choline insufficiency altered the angiogenic profile, impaired in vitro angiogenesis, increased inflammation, induced apoptosis, increased oxidative stress, and yielded greater levels of protein kinase C (PKC) isoforms δ and ϵ possibly through increases in the PKC activators 1-stearoyl-2-arachidonoyl-sn-glycerol and 1-stearoyl-2-docosahexaenoyl-sn-glycerol. Notably, the addition of a PKC inhibitor normalized angiogenesis and apoptosis, and partially rescued the aberrant gene expression profile. Together these results suggest that choline inadequacy may contribute to placental dysfunction and the development of disorders related to placental insufficiency by activating PKC.