A LINEAR THEORY FOR LEEWAVE ROTORS

A linear theory for the prediction of rotor formation under trapped lee waves has been developed. The theory is based on the assumption that the flow can be divided into two layers: an outer region in which the flow is inviscid, and an inner region close to the ground where turbulent stresses are important. The flow in the inner region is driven by the pressure gradient due to lee waves aloft. A simple mixing-length turbulence closure is assumed and for a given lee-wave pressure field, analytic solutions to the inner-region flow are obtained. Results from the linear theory are compared with a series of two-dimensional numerical simulations in which a sharp temperature inversion is present upwind of a ridge. Lee waves may form on the inversion, which when of sufficient amplitude, give rise to flow separation and rotors underneath the wave crests. The point at which linear theory predicts flow separation underneath the wave crests is shown to correspond, approximately, to the occurrence of lee-wave rotors in the numerical results and a flow regime diagram based on linear theory is constructed and compared to that obtained from the simulations

Setdb1-mediated H3K9 methylation is enriched on the inactive X and plays a role in its epigenetic silencing

Background: The presence of histone 3 lysine 9 (H3K9) methylation on the mouse inactive X chromosome has been controversial over the last 15 years, and the functional role of H3K9 methylation in X chromosome inactivation in any species has remained largely unexplored. Results: Here we report the first genomic analysis of H3K9 di- and tri-methylation on the inactive X: we find they are enriched at the intergenic, gene poor regions of the inactive X, interspersed between H3K27 tri-methylation domains found in the gene dense regions. Although H3K9 methylation is predominantly non-genic, we find that depletion of H3K9 methylation via depletion of H3K9 methyltransferase Set domain bifurcated 1 (Setdb1) during the establishment of X inactivation, results in failure of silencing for around 150 genes on the inactive X. By contrast, we find a very minor role for Setdb1-mediated H3K9 methylation once X inactivation is fully established. In addition to failed gene silencing, we observed a specific failure to silence X-linked long-terminal repeat class repetitive elements. Conclusions: Here we have shown that H3K9 methylation clearly marks the murine inactive X chromosome. The role of this mark is most apparent during the establishment phase of gene silencing, with a more muted effect on maintenance of the silent state. Based on our data, we hypothesise that Setdb1-mediated H3K9 methylation plays a role in epigenetic silencing of the inactive X via silencing of the repeats, which itself facilitates gene silencing through alterations to the conformation of the whole inactive X chromosome.Andrew Keniry, Linden J. Gearing, Natasha Jansz, Joy Liu, Aliaksei Z. Holik, Peter F. Hickey, Sarah A. Kinkel, Darcy L. Moore, Kelsey Breslin, Kelan Chen, Ruijie Liu, Catherine Phillips, Miha Pakusch, Christine Biben, Julie M. Sheridan, Benjamin T. Kile, Catherine Carmichael, Matthew E. Ritchie, Douglas J. Hilton and Marnie E. Blewit

Consensus on the use and interpretation of cystic fibrosis mutation analysis in clinical practice

It is often challenging for the clinician interested in cystic fibrosis (CF) to interpret molecular genetic results, and to integrate them in the diagnostic process. The limitations of genotyping technology, the choice of mutations to be tested, and the clinical context in which the test is administered can all influence how genetic information is interpreted. This paper describes the conclusions of a consensus conference to address the use and interpretation of CF mutation analysis in clinical settings

Computer Simulations of Hyperbranched Polymers: the Influence of the Wiener Index on the Intrinsic Viscosity and Radius of Gyration

The influence of the Wiener index on solution properties of trifunctional hyperbranched polymers has been investigated using Brownian dynamics simulations with excluded volume and hydrodynamic interactions. A range of degrees of polymerization (N) and degrees of branching (DB) were used. For each DB and N, several molecules with different Wiener indices (W) were simulated, where W depends on the arrangement of branch points. The intrinsic viscosity and the radius of gyration (Rg) of HPs were both observed to scale with W at a constant N via a power law relationship, as found in the literature. Through their relationships to W, an expression relating intrinsic viscosity to Rg was obtained. This relationship is found to fall centrally between the predictions of Flory and Fox for linear polymers and that of Zimm and Kilb for branched polymers. Molecular shape in solution is also found to depend on W and N, as observed through the W dependence of the ratio of Rg to the hydrodynamic radius, Rh

Clinical and pathological features associated with mutations in MICU1

Neurological Motor Disorder