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Our previous studies showed that Insulin-like Growth Factor (IGF)-1 reduced blood brain barrier pemeability and decreased infarct volume caused by middle cerebral artery occlusion (MCAo) in middle aged female rats. Similarly, cultures of primary brain microvessel endothelial cells from middle-aged female rats and exposed to stroke-like conditions (oxygen glucose deprivation; OGD) confirmed that IGF-1 reduced dye transfer across this cell monolayer. Surprisingly, IGF-1 did not attenuate endothelial cell death caused by OGD. To reconcile these findings, the present study tested the hypothesis that, at the earliest phase of ischemia, IGF-1 promotes barrier function by increasing anchorage and stabilizing cell geometry of surviving endothelial cells. Cultures of human brain microvessel endothelial cells were subject to oxygen-glucose deprivation (OGD) in the presence of IGF-1, IGF-1+JB-1 (IGFR inhibitor) or vehicle. OGD disrupted the cell monolayer and reduced cell-cell interactions, which was preserved in IGF-1-treated cultures and reversed by concurrent treatment with JB-1. IGF-1-mediated preservation of the endothelial monolayer was reversed with LY294002 treatment, but not by Rapamycin, indicating that IGF-1s actions on cell-cell contacts are likely mediated via the PI3K pathway. In vivo, microvessel morphology was evaluated in middle-aged female rats that were subjected to ischemia by MCAo, and treated ICV with IGF-I, IGF-1 + JB-1, or artificial CSF (aCSF; vehicle) after reperfusion. Compared to vehicle controls, IGF-1 treated animals displayed larger microvessel diameters in the peri-infarct area and increased staining density for vinculin, an anchorage protein. Both these measures were reversed by concurrent IGF-1+JB-1 treatment. Moreover these effects were restricted to 24h after ischemia-reperfusion and no treatment effects were seen at 5d post stroke. Collectively, these data suggest that in the earliest hours during ischemia, IGF-I promotes receptor-mediated anchorage of endothelial cells, and its actions may be accurately characterized as vasculoprotective.

The effect of flow history on fluid phase entrapment during immiscible two-phase flow in Hele-Shaw cells packed with spherical and crushed glass beads is investigated. The wetting fluid is injected into an initially oil saturated cell at a welldefined capillary number. It is observed that the size and shape of the trapped clusters strongly depend on the history of flooding such that less oil was trapped in the medium when the injecting capillary number gradually increased to the final maximum capillary number compared to the case when the injection was started and maintained constant at the maximum capillary number. In addition, a comprehensive series of experiments were conducted to delineate the effects of the capillary number on the phase entrapment. Contrary to previously published data, our experimental data reveal that the residual oil saturation depends on capillary number nonmonotonically. A physically based relationship to scale the capillary desaturation curve is proposed.

The adsorption of Rh(CO) 2 (acac) (acac is acetylacetonate) on a TiO 2 (110) single crystal surface has been examined using a combination of scanning tunneling microscopy (STM) and density functional theory (DFT) calculations. When Rh(CO) 2 (acac) is deposited onto the TiO 2 (110) surface at room temperature, features are observed by STM suggesting monomeric species that bind preferentially to oxygen vacancy sites. DFT calculations suggest that these features must be partially deligated organometallic species and that oxygen vacancies are critical to the deligation process. Exposing the observed surface species to CO at 373 K results in the formation of clusters approximately 2−3 nm in diameter and 0.3−0.8 nm in height.

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