RESUMO
Large-eddy simulations of an observed single-layer Arctic mixed-phase cloud are analyzed to study the value of forward modeling of profiling millimeter-wave cloud radar Doppler spectral width for model evaluation. Individual broadening terms and their uncertainties are quantified for the observed spectral width and compared to modeled broadening terms. Modeled turbulent broadening is narrower than the observed values when the turbulent kinetic energy dissipation rate from the subgrid-scale model is used in the forward model. The total dissipation rates, estimated with the subgrid-scale dissipation rates and the numerical dissipation rates, agree much better with both the retrieved dissipation rates and those inferred from the power spectra of the simulated vertical air velocity. The comparison of the microphysical broadening provides another evaluative measure of the ice properties in the simulation. To accurately retrieve dissipation rates as well as each broadening term from the observations, we suggest a few modifications to previously presented techniques. First, we show that the inertial subrange spectra filtered with the radar sampling volume is a better underlying model than the unfiltered -5/3 law for the retrieval of the dissipation rate from the power spectra of the mean Doppler velocity. Second, we demonstrate that it is important to filter out turbulence and remove the layer-mean reflectivity-weighted mean fall speed from the observed mean Doppler velocity to avoid overestimation of shear broadening. Finally, we provide a method to quantify the uncertainty in the retrieved dissipation rates, which eventually propagates to the uncertainty in the microphysical broadening.
RESUMO
We investigated the alteration of coagulation state in a protein C (PC) deficiency pedigree and the impact of the PC gene mutations. The pedigree of a proband with cerebral hemorrhagic infarction had sixteen members with four generations. The plasma levels of PC activity (PC:A), protein S activity (PS:A), factor V:C and factor VIII:C, and routine coagulation tests were measured. Nine exons of the PC gene (PROC) were sequenced. Plasma PC:A and PC antigen (PC:Ag) of the proband were 26 and 18%, respectively, which was significantly lower than normal ranges. Two heterozygous missense mutations of PC in the proband were identified, T>G at site 6128 (exon 7) and G>C at site 8478 (exon 9) resulting in F139V and D255H, respectively. The family members with F139V (N = 4) or D255H (N = 4) had lower levels of PC:A and PC:Ag than members with wild-type PROC (N = 6). D255H mutation caused a more significant decrease in the levels of PC:A, PC:Ag and factor V:C as compared to F139V mutation (P < 0.05). Two independent mutations, F139V and D255H, of PROC reduce PC function. Compound heterozygous condition of the two mutations can cause synergistic PC deficiency, but resulting in later onset of cerebral thrombosis.