A New Solution to the Plasma Starved Event Horizon Magnetosphere: Application to the Forked Jet in M87

Very Long Baseline Interferometry observations at 86 GHz reveal an almost hollow jet in M87 with a forked morphology. The detailed analysis presented here indicates that the spectral luminosity of the central spine of the jet in M87 is a few percent of that of the surrounding hollow jet $200 -400 \mu\rm{as}$ from the central black hole. Furthermore, recent jet models in indicate that a hollow "tubular" jet can explain a wide range of plausible broadband spectra originating from jetted plasma located within $\sim 30\mu\rm{as}$ of the central black hole, including the 230 GHz correlated flux detected by the Event Horizon Telescope. Most importantly, these hollow jets from the inner accretion flow have an intrinsic power capable of energizing the global jet out to kiloparsec scales. Thus motivated, this paper considers new models of the event horizon magnetosphere (EHM) in low luminosity accretion systems. Contrary to some models, the spine is not an invisible powerful jet. It is an intrinsically weak jet. In the new EHM solution, the accreted poloidal magnetic flux is weak and the background photon field is weak. It is shown how this accretion scenario naturally results in the dissipation of the accreted poloidal magnetic flux in the EHM not the accumulation of poloidal flux required for a powerful jet. The new solution indicates less large scale poloidal magnetic flux (and jet power) in the EHM than in the surrounding accretion flow and cannot support significant EHM driven jets.Comment: To appear in Astronomy and Astrophysics. Revision fixes typos found during proof

Hypoglycemia and the Origin of Hypoxia-Induced Reduction in Human Fetal Growth

The most well known reproductive consequence of residence at high altitude (HA >2700 m) is reduction in fetal growth. Reduced fetoplacental oxygenation is an underlying cause of pregnancy pathologies, including intrauterine growth restriction and preeclampsia, which are more common at HA. Therefore, altitude is a natural experimental model to study the etiology of pregnancy pathophysiologies. We have shown that the proximate cause of decreased fetal growth is not reduced oxygen availability, delivery, or consumption. We therefore asked whether glucose, the primary substrate for fetal growth, might be decreased and/or whether altered fetoplacental glucose metabolism might account for reduced fetal growth at HA.Doppler and ultrasound were used to measure maternal uterine and fetal umbilical blood flows in 69 and 58 residents of 400 vs 3600 m. Arterial and venous blood samples from mother and fetus were collected at elective cesarean delivery and analyzed for glucose, lactate and insulin. Maternal delivery and fetal uptakes for oxygen and glucose were calculated.The maternal arterial – venous glucose concentration difference was greater at HA. However, umbilical venous and arterial glucose concentrations were markedly decreased, resulting in lower glucose delivery at 3600 m. Fetal glucose consumption was reduced by >28%, but strongly correlated with glucose delivery, highlighting the relevance of glucose concentration to fetal uptake. At altitude, fetal lactate levels were increased, insulin concentrations decreased, and the expression of GLUT1 glucose transporter protein in the placental basal membrane was reduced.Our results support that preferential anaerobic consumption of glucose by the placenta at high altitude spares oxygen for fetal use, but limits glucose availability for fetal growth. Thus reduced fetal growth at high altitude is associated with fetal hypoglycemia, hypoinsulinemia and a trend towards lactacidemia. Our data support that placentally-mediated reduction in glucose transport is an initiating factor for reduced fetal growth under conditions of chronic hypoxemia