Scaling analysis of unsteady natural convection boundary layer for ramp heating

A scaling analysis for the natural convection boundary layer adjacent to an inclined semi-infinite plate subject to a non-instantaneous heating in the form of an imposed wall temperature which increases linearly up to a prescribed steady value over a prescribed time is reported. The development of the flow from start-up to a steady-state has been described based on scaling analyses and verified by numerical simulations. The analysis reveals that, if the period of temperature growth on the wall is sufficiently long, the boundary layer reaches a quasisteady mode before the growth of the temperature is completed. In this mode the thermal boundary layer at first grows in thickness and then contracts with increasing time. However, if the imposed wall temperature growth period is sufficiently short, the boundary layer develops differently, but after the wall temperature growth is completed, the boundary layer develops as though the start up had been instantaneous. The steady state values of the boundary layer for both cases are ultimately the same.

Scaling analysis of unsteady natural convection boundary layer for instantaneous heating

Natural convection thermal boundary layer adjacent to an instantaneous heated inclined flat plate is investigated through a scaling analysis and verified by direct numerical simulations. It is revealed from the analysis that the development of the boundary layer may be characterized by three distinct stages, i.e. a start-up stage, a transitional stage and a steady state stage. These three stages can be clearly identified from the numerical simulations. Major scales including the flow velocity, flow development time, and the thermal and viscous boundary layer thicknesses are established to quantify the flow development at different stages and over a wide range of flow parameters. Details of the scaling analysis are described in this paper.

Genetic and gene expression analyses of the polycystic ovary syndrome candidate gene fibrillin-3 and other fibrillin family members in human ovaries

Several studies have demonstrated an association between polycystic ovary syndrome (PCOS) and the dinucleotide repeat microsatellite marker D19S884, which is located in intron 55 of the fibrillin-3 (FBN3) gene. Fibrillins, including FBN1 and 2, interact with latent transforming growth factor (TGF)-β-binding proteins (LTBP) and thereby control the bioactivity of TGFβs. TGFβs stimulate fibroblast replication and collagen production. The PCOS ovarian phenotype includes increased stromal collagen and expansion of the ovarian cortex, features feasibly influenced by abnormal fibrillin expression. To examine a possible role of fibrillins in PCOS, particularly FBN3, we undertook tagging and functional single nucleotide polymorphism (SNP) analysis (32 SNPs including 10 that generate non-synonymous amino acid changes) using DNA from 173 PCOS patients and 194 controls. No SNP showed a significant association with PCOS and alleles of most SNPs showed almost identical population frequencies between PCOS and control subjects. No significant differences were observed for microsatellite D19S884. In human PCO stroma/cortex (n = 4) and non-PCO ovarian stroma (n = 9), follicles (n = 3) and corpora lutea (n = 3) and in human ovarian cancer cell lines (KGN, SKOV-3, OVCAR-3, OVCAR-5), FBN1 mRNA levels were approximately 100 times greater than FBN2 and 200–1000-fold greater than FBN3. Expression of LTBP-1 mRNA was 3-fold greater than LTBP-2. We conclude that FBN3 appears to have little involvement in PCOS but cannot rule out that other markers in the region of chromosome 19p13.2 are associated with PCOS or that FBN3 expression occurs in other organs and that this may be influencing the PCOS phenotype.