Hydrogen Peroxide-Dependent Uptake of Iodine by Marine Flavobacteriaceae Bacterium Strain C-21

The cells of the marine bacterium strain C-21, which is phylogenetically closely related to Arenibacter troitsensis, accumulate iodine in the presence of glucose and iodide (I⁻). In this study, the detailed mechanism of iodine uptake by C-21 was determined using a radioactive iodide tracer, ¹²⁵I⁻. In addition to glucose, oxygen and calcium ions were also required for the uptake of iodine. The uptake was not inhibited or was only partially inhibited by various metabolic inhibitors, whereas reducing agents and catalase strongly inhibited the uptake. When exogenous glucose oxidase was added to the cell suspension, enhanced uptake of iodine was observed. The uptake occurred even in the absence of glucose and oxygen if hydrogen peroxide was added to the cell suspension. Significant activity of glucose oxidase was found in the crude extracts of C-21, and it was located mainly in the membrane fraction. These findings indicate that hydrogen peroxide produced by glucose oxidase plays a key role in the uptake of iodine. Furthermore, enzymatic oxidation of iodide strongly stimulated iodine uptake in the absence of glucose. Based on these results, the mechanism was considered to consist of oxidation of iodide to hypoiodous acid by hydrogen peroxide, followed by passive translocation of this uncharged iodine species across the cell membrane. Interestingly, such a mechanism of iodine uptake is similar to that observed in iodine-accumulating marine algae.     

The urokinase-type plasminogen activator receptor is not required for skeletal muscle inflammation or regeneration

The hypothesis of this study was the urokinase-type plasminogen activator receptor (uPAR) is required for accumulation of inflammatory cells in injured skeletal muscle and for efficient muscle regeneration. Expression of uPAR was elevated at 1 and 3 days after cardiotoxin-induced muscle injury in wild-type mice before returning to baseline levels. Neutrophil accumulation peaked 1 day postinjury in muscle from both wild-type (WT) and uPAR null mice, while macrophage accumulation peaked between 3 and 5 days postinjury, with no differences between strains. Histological analyses confirmed efficient muscle regeneration in both wild-type and uPAR null mice, with no difference between strains in the formation or growth of regenerating fibers, or recovery of normal morphology. Furthermore, in vitro experiments demonstrated that chemotaxis is not different between WT and uPAR null macrophages. Finally, fusion of cultured satellite cells into multinucleated myotubes was not different between cells isolated from WT and uPAR null mice. These results demonstrate that uPAR is not required for the accumulation of inflammatory cells or the regeneration of skeletal muscle following injury, suggesting uPA can act independently of uPAR to regulate events critical for muscle regeneration.     

Impending disaster or sliver of hope for Southeast Asian forests? The devil may lie in the details

Here, I report on how forest area in Southeast Asia has changed for different types of forest and across different countries between the periods of 1990–2000 and 2000–2005. The loss of old growth forests has accelerated in Indonesia, Cambodia and Vietnam but have ceased in Thailand, Malaysia, Laos and the Philippines. Secondary forests continue to be lost in Malaysia, Cambodia, Laos, Myanmar, Indonesia, Thailand and the Philippines. Plantation forests have increased in area by 25.0% from 1990 to 2005 but still comprise only 6.2% of the total forest area in Southeast Asia. Overall, the loss of native forests (old growth and secondary forests) has slowed down in Thailand, the Philippines and Brunei but has worsened in Laos, Myanmar, Indonesia, Malaysia and Cambodia.     

Unreported yet massive deforestation driving loss of endemic biodiversity in Indian Himalaya

Deforestation is a primary driver of biotic extinctions in the tropics. The impacts of deforestation in tropical biodiversity hotspots are of particular concern because these regions contain high concentrations of globally endemic species. However, the effects of large-scale deforestation on native biotas within the biodiversity hotspot of Himalaya remain poorly documented. Here we report on an alarming trend of deforestation in the Indian Himalaya and project the likely consequential extinctions of endemic taxa (species and subspecies) by 2100 across a broad range of taxonomic groups, including gymnosperms, angiosperms, fishes, amphibians, reptiles, birds, and mammals. With the current level of deforestation, by 2100 only about 10% of the land area of the Indian Himalaya will be covered by dense forest (>40% canopy cover)—a scenario in which almost a quarter of the endemic species could be wiped out, including 366 endemic vascular plant taxa and 35 endemic vertebrate taxa. We also show that inaccurate reporting of forest cover data by governmental institutions can result in underestimations of the biological impacts of deforestation, as well as potential miscalculations in land-use decisions (e.g., the construction of hydroelectric dams). Large-scale conservation efforts, including forest protection and reforestation, are urgently needed to avoid the impending deforestation-driven biodiversity losses in the Himalaya.     

3D pharmacophore based virtual screening of T-type calcium channel blockers

Virtual screening of the commercial databases was done by using a three dimensional pharmacophore previously developed for T-type calcium channel blockers using CATALYSTtrade mark program. Biological evaluation of 25 selected virtual hits resulted in the discovery of a highly potent compound VH04 with IC(50) value of 0.10 microM, eight times as potent as the known selective T-type calcium channel blocker, mibefradil. Search for similar compounds yielded several hits with micro-molar IC(50) values and high T-type calcium channel selectivity. Based on the structure of the virtual hits, small molecule libraries with novel scaffolds were designed, synthesis and biological evaluation of which are currently in progress. This result shows a successful example of ligand based drug discovery of potent T-type calcium channel blockers.     

Sphingosine-1-phosphate initiates rapid retraction of pseudopodia by localized RhoA activation

Lysophosphatidic acid (LPA) stimulates sphingosine-1-phosphate (S1P)-sensitive motility in NIH3T3 clone7 cells. S1P inhibits motility only when added to the bottom well of the Boyden chamber, suggesting that pseudopodia can respond to their microenvironment. In order to study and localize this effect, we utilized a Transwell insert system to isolate pseudopodia. LPA stimulates protrusion of pseudopodia that are enriched in RhoA compared to cell bodies. Removal of LPA results in slow retraction with loss of vinculin-rich adhesion complexes and prolonged activation of RhoA. However, RhoA, ROCK and mDia are not required for this process. In contrast, rapid retraction, induced by adding S1P to the bottom well, is associated with a quick spike of activated RhoA and coalescence of adhesion complexes that colocalize with the ends of stress fibers. S1P-induced retraction requires RhoA and ROCK but is only delayed by inhibition of mDia. These data indicate that pseudopodia sense and integrate signals initiated by localized bioactive lipids, affecting both cellular polarity and their own function in motility.