An Evaluation of Size-Resolved Cloud Microphysics Scheme Numerics for Use with Radar Observations. Part I: Collision-Coalescence

This study evaluates some available schemes designed to solve the stochastic collection equation (SCE) for collision-coalescence of hydrometeors using a size-resolved (bin) microphysics approach, and documents their numerical properties within the framework of a box model. Comparing three widely used SCE schemes, we find that all converge to almost identical solutions at sufficiently fine mass grids. However, one scheme converges far slower than the other two and shows pronounced numerical diffusion at the large-drop tail of the size distribution. One of the remaining two schemes is recommended on the basis that it is well-converged on a relatively coarse mass grid, stable for large time steps, strictly mass-conservative, and computationally efficient. To examine the effects of SCE scheme choice on simulating clouds and precipitation, two of the three schemes are compared in large-eddy simulations of a drizzling stratocumulus field. A forward simulator that produces Doppler spectra from the large-eddy simulation results is used to compare the model output directly with radar observations. The scheme with pronounced numerical diffusion predicts excessively large mean Doppler velocities and overly broad and negatively skewed spectra compared with observations, consistent with numerical diffusion demonstrated in the box model. Statistics obtained using the recommended scheme are closer to observations, but notable differences remain, indicating that factors other than SCE scheme accuracy are limiting simulation fidelity

Unique transcriptomic landscapes identified in idiopathic spontaneous and infection related preterm births compared to normal term births.

Preterm birth (PTB) is leading contributor to infant death in the United States and globally, yet the underlying mechanistic causes are not well understood. Histopathological studies of preterm birth suggest advanced villous maturity may have a role in idiopathic spontaneous preterm birth (isPTB). To better understand pathological and molecular basis of isPTB, we compared placental villous transcriptomes from carefully phenotyped cohorts of PTB due to infection or isPTB between 28-36 weeks gestation and healthy term placentas. Transcriptomic analyses revealed a unique expression signature for isPTB distinct from the age-matched controls that were delivered prematurely due to infection. This signature included the upregulation of three IGF binding proteins (IGFBP1, IGFBP2, and IGFBP6), supporting a role for aberrant IGF signaling in isPTB. However, within the isPTB expression signature, we detected secondary signature of inflammatory markers including TNC, C3, CFH, and C1R, which have been associated with placental maturity. In contrast, the expression signature of the gestational age-matched infected samples included upregulation of proliferative genes along with cell cycling and mitosis pathways. Together, these data suggest an isPTB molecular signature of placental hypermaturity, likely contributing to the premature activation of inflammatory pathways associated with birth and providing a molecular basis for idiopathic spontaneous birth