Dispersal of soredia from individual soralia of the lichen Hypogymnia physodes (L.) Nyl. in a simple wind tunnel

Dispersal of soredia from individual soralia of the lichen Hypogymnia physodes (L.) Nyl. was studied using a simple wind tunnel constructed in the field. Individual lobes with terminal soralia were placed in the wind tunnel on the adhesive surface of dust particle collectors. Air currents produced by a fan were directed over the surface of the lobes. The majority of soredia were deposited within 5 cm of the source soralium but some soredia were dispersed to at least 80 cm at a wind speed of 6 m s-1. Variation in wind speed had no statistically significant effect on the total number of soredial clusters deposited averaged over soralia but the mean size of cluster and the distance dispersed were greater at higher wind speeds. The number of soredia deposited was dependent on the orientation of the soralium to the air currents. More soredia were deposited with the soralium facing the fan at a wind speed of 9 m s-1. Moisture in the form of a fine mist reduced substantially the number of soredia deposited at a wind speed of 6 m s-1 but had no effect on the mean number of soredia per cluster or on the mean distance dispersed. The data suggest: (1) that wind dispersal from an individual soralium is influenced by wind speed, the location of the soralium on the thallus and the level of moisture and (2) that air currents directed over the surfaces of thalli located on the upper branches of trees would effectively disperse soredia of H. physodes vertically and horizontally within a tree canopy. © 1994.

Placenta growth factor-1 exerts time-dependent stabilization of adherens junctions following VEGF-induced vascular permeability

Increased vascular permeability is an early event characteristic of tissue ischemia and angiogenesis. Although VEGF family members are potent promoters of endothelial permeability the role of placental growth factor (PlGF) is hotly debated. Here we investigated PlGF isoforms 1 and 2 and present in vitro and in vivo evidence that PlGF-1, but not PlGF-2, can inhibit VEGF-induced permeability but only during a critical window post-VEGF exposure. PlGF-1 promotes VE-cadherin expression via the trans-activating Sp1 and Sp3 interaction with the VE-cadherin promoter and subsequently stabilizes transendothelial junctions, but only after activation of endothelial cells by VEGF. PlGF-1 regulates vascular permeability associated with the rapid localization of VE-cadherin to the plasma membrane and dephosphorylation of tyrosine residues that precedes changes observed in claudin 5 tyrosine phosphorylation and membrane localization. The critical window during which PlGF-1 exerts its effect on VEGF-induced permeability highlights the importance of the translational significance of this work in that PLGF-1 likely serves as an endogenous anti-permeability factor whose effectiveness is limited to a precise time point following vascular injury. Clinical approaches that would pattern nature's approach would thus limit treatments to precise intervals following injury and bring attention to use of agents only during therapeutic windows.

Tunnel monitoring using multicore displacement sensor

In this paper, we report the first demonstration of multiplexed fibre Bragg grating strain sensors in a multicore fibre for shape measurement and their application to structural monitoring. Sets of gratings, acting as strain gauges, are co-located in the multicore fibre such that they enable the curvature to be determined via differential strain measurement. Multiple sets of these gratings allow the curvature to be measured at several points along the fibre. In this paper, the multicore fibre is configured to measure the deflection of a simple mechanical beam arising from the displacement of concrete tunnel sections. Laboratory tests are presented in which the system was demonstrated capable of displacement measurement with a resolution of ±0.1 mm over a range of several millimetres. © 2006 IOP Publishing Ltd.

Role of transglutaminase 1 in stabilisation of intercellular junctions of the vascular endothelium

Microvascular endothelial monolayers from mouse myocardium (MyEnd) cultured for up to 5 days postconfluency became increasingly resistant to various barrier-compromising stimuli such as low extracellular Ca2+ and treatment with the Ca2+ ionophore A23187 and with the actin depolymerising compound cytochalasin D. In contrast, microvascular endothelial monolayers from mouse lung microvessels (PulmEnd) remained sensitive to these conditions during the entire culture period which corresponds to the well-known in vivo sensitivity of the lung microvasculature to Ca2+depletion and cytochalasin D treatment. One molecular difference between pulmonary and myocardial endothelial cells was found to be transglutaminase 1 (TGase1) which is strongly expressed in myocardial endothelial cells but is absent from pulmonary endothelial cells. Resistance of MyEnd cells to barrier-breaking conditions correlated strongly with translocation of TGase1 to intercellular junctions. Simultaneous inhibition of intracellular and extracellular TGase activity by monodansylcadaverine (MDC) strongly weakened barrier properties of MyEnd monolayers, whereas inhibition of extracellular TGases by the membrane-impermeable active site-directed TGase inhibitor R281 did not reduce barrier properties. Weakening of barrier properties could be also induced in MyEnd cells by downregulation of TGase1 expression using RNAi-based gene silencing. These findings suggest that crosslinking activity of intracellular TGase1 at intercellular junctions may play a role in controlling barrier properties of endothelial monolayers.