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A direct numerical simulation of a temporally developing mixing layer with a passive scalar transport is performed for various Schmidt numbers (Sc = 0.25, 1, 4, and 8). Turbulent mixing is investigated near the turbulent/non-turbulent interface (TNTI), which is a layer consisting of the turbulent sublayer (TSL) and viscous superlayer (VSL). The irrotational boundary, which is close to the outer edge of the TNTI layer, is detected as the isosurface of small vorticity magnitude. The movement of fluid elements relative to the irrotational boundary movement is analyzed. Once the non-turbulent fluid is entrained into the VSL across the irrotational boundary by the viscous diffusion of vorticity, the fluid moves away from the irrotational boundary in the VSL in the normal direction of the irrotational boundary. After the fluid reaches the TSL, it is transported in the tangential direction of the irrotational boundary and is mixed with the fluid coming from the turbulent core (TC) region. The boundary between the TSL and VSL roughly separates the region (VSL) mostly consisting of the fluid entrained from the non-turbulent flow from the region (TSL) where the fluids from both the TC and non-turbulent regions coexist. Therefore, the scalar value in the VSL is close to the non-turbulent value especially for high Sc cases. Because of a large difference in the scalar between the TSL and VSL, a peak value of the conditional mean scalar dissipation rate appears near the boundary between the TSL and VSL independently of Sc.

Preeclampsia (PE) is a pregnancy-induced hypertension with proteinuria that typically develops after 20 weeks of gestation. A reduction in uterine blood flow causes placental ischemia and placental release of anti-angiogenic factors such as sFlt-1 followed by PE. Although the reduced uterine perfusion pressure (RUPP) model is widely used in rats, investigating the role of genes on PE using genetically engineered animals has been problematic because it has been difficult to make a useful RUPP model in mice. To establish a RUPP model of PE in mice, we bilaterally ligated ovarian vessels distal to ovarian branches, uterine vessels, or both in ICR-strain mice at 14.5 days post coitum (dpc). Consequently, these mice had elevated BP, increased urinary albumin excretion, severe endotheliosis, and mesangial expansion. They also had an increased incidence of miscarriage and premature delivery. Embryonic weight at 18.5 dpc was significantly lower than that in sham mice. The closer to the ligation site the embryos were, the higher the resorption rate and the lower the embryonic weight. The phenotype was more severe in the order of ligation at the ovarian vessels < uterine vessels < both. Unlike the RUPP models described in the literature, this model did not constrict the abdominal aorta, which allowed BP to be measured with a tail cuff. This novel RUPP model in mice should be useful for investigating the pathogenesis of PE in genetically engineered mice and for evaluating new therapies for PE.

Vortex stretching and compression, which cause enstrophy production by inviscid processes, are investigated near the turbulent/non-turbulent (T/NT) interface in a planar jet by using a direct numerical simulation (DNS). The enstrophy production is investigated by analysing the relationship among a vorticity vector, strain-rate eigenvectors and strain-rate eigenvalues. The statistics are calculated individually for three different interface orientations. The vorticity near the T/NT interface is oriented in the tangential direction to the interface. The enstrophy production is affected by the interface orientation because the intensity of vortex stretching depends on the interface orientation, and the alignment between the vorticity vector and the strain-rate eigenvectors is confined by the interface. The enstrophy production near the T/NT interface is analysed by considering the motion of turbulent fluid relative to that of the interface. The results show that the alignment between the interface and the strain-rate eigenvectors changes depending on the velocity field near the T/NT interface. When the turbulent fluid moves toward the T/NT interface, the enstrophy is generated by vortex stretching without being greatly affected by vortex compression. In contrast, when the turbulent fluid relatively moves away from the T/NT interface, large enstrophy reduction frequently occurs by vortex compression. Thus, it is shown that the velocity field near the T/NT interface affects the enstrophy production near the interface through the alignment between the vorticity and the strain-rate eigenvectors.