Moist turbulent Rayleigh-Benard convection with Neumann and Dirichlet boundary conditions

Turbulent Rayleigh-Benard convection with phase changes in an extended layer between two parallel impermeable planes is studied by means of three-dimensional direct numerical simulations for Rayleigh numbers between 10^4 and 1.5\times 10^7 and for Prandtl number Pr=0.7. Two different sets of boundary conditions of temperature and total water content are compared: imposed constant amplitudes which translate into Dirichlet boundary conditions for the scalar field fluctuations about the quiescent diffusive equilibrium and constant imposed flux boundary conditions that result in Neumann boundary conditions. Moist turbulent convection is in the conditionally unstable regime throughout this study for which unsaturated air parcels are stably and saturated air parcels unstably stratified. A direct comparison of both sets of boundary conditions with the same parameters requires to start the turbulence simulations out of differently saturated equilibrium states. Similar to dry Rayleigh-Benard convection the differences in the turbulent velocity fluctuations, the cloud cover and the convective buoyancy flux decrease across the layer with increasing Rayleigh number. At the highest Rayleigh numbers the system is found in a two-layer regime, a dry cloudless and stably stratified layer with low turbulence level below a fully saturated and cloudy turbulent one which equals classical Rayleigh-Benard convection layer. Both are separated by a strong inversion that gets increasingly narrower for growing Rayleigh number.Comment: 19 pages, 13 Postscript figures, Figures 10,11,12,13, in reduced qualit

Sclerostin: Current Knowledge and Future Perspectives

In recent years study of rare human bone disorders has led to the identification of important signaling pathways that regulate bone formation. Such diseases include the bone sclerosing dysplasias sclerosteosis and van Buchem disease, which are due to deficiency of sclerostin, a protein secreted by osteocytes that inhibits bone formation by osteoblasts. The restricted expression pattern of sclerostin in the skeleton and the exclusive bone phenotype of good quality of patients with sclerosteosis and van Buchem disease provide the basis for the design of therapeutics that stimulate bone formation. We review here current knowledge of the regulation of the expression and formation of sclerostin, its mechanism of action, and its potential as a bone-building treatment for patients with osteoporosis

A case report of delayed cortical infarction adjacent to sulcal clots after traumatic subarachnoid hemorrhage in the absence of proximal vasospasm

Background Cortical ischemic lesions represent the predominant pathomorphological pattern of focal lesions after aneurysmal subarachnoid hemorrhage (aSAH). Autopsy studies suggest that they occur adjacent to subarachnoid blood and are related to spasm of small cortical rather than proximal arteries. Recent clinical monitoring studies showed that cortical spreading depolarizations, which induce cortical arterial spasms, are involved in lesion development. If subarachnoid blood induces adjacent cortical lesions, it would be expected that (i) they also develop after traumatic subarachnoid hemorrhage (tSAH), and (ii) lesions after tSAH can occur in absence of angiographic vasospasm, as was found for aSAH. Case presentation An 86-year-old woman was admitted to our hospital with fluctuating consciousness after hitting her head during a fall. The initial computed tomography (CT) was significant for tSAH in cortical sulci. On day 8, the patient experienced a secondary neurological deterioration with reduced consciousness and global aphasia. Whereas the CT scan on day 9 was still unremarkable, magnetic resonance imaging (MRI) on day 10 revealed new cortical laminar infarcts adjacent to sulcal blood clots. Proximal vasospasm was ruled out using MR and CT angiography and Doppler sonography. CT on day 14 confirmed the delayed infarcts. Conclusions We describe a case of delayed cortical infarcts around sulcal blood clots after tSAH in the absence of proximal vasospasm, similar to results found previously for aSAH. As for aSAH, this case suggests that assessment of angiographic vasospasm is not sufficient to screen for risk of delayed infarcts after tSAH. Electrocorticography is suggested as a complementary method to monitor the hypothesized mechanism of spreading depolarizations