8 research outputs found
Poa pratensis L., current status of the longest-established non-native vascular plant in the Antarctic
A single colony of the non-native grass Poa pratensis L., which was introduced inadvertently to Cierva Point, Antarctic Peninsula, during the 1954–1955 season, was still present during a survey in February 2012, making it the longest surviving non-native vascular plant colony known in Antarctica. Since 1991, the grass cover has roughly tripled in size, with an annual increase in area of approximately 0.016 m2, and an estimated maximum radial growth rate of 1.43 cm y−1. However, it remains restricted to the original site of introduction and its immediate surroundings (c. 1 m2). Annual flowering of the plants occurred during the 2010/2011 and 2011/2012 seasons; however, there has been no seed production and only incomplete development of the sexual structures. Current environmental conditions, including low temperatures, may inhibit sexual reproduction. Lack of effective vegetative dispersal may be influenced by the low level of human activity at the site, which limits opportunities for human-mediated dispersal. Although P. pratensis has existed at Cierva Point for almost 60 years, it has not yet become invasive. Scenarios for the potential future development of the species in Antarctica and the associated negative impacts upon the native vegetation from competition are discussed in the context of regional climate change. Finally, we describe the environmental risk presented by P. pratensis and argue that this non-native species should be eradicated as soon as possible in accordance with the Protocol on Environmental Protection to the Antarctic Treaty
Elimination of substances from the brain parenchyma: efflux via perivascular pathways and via the blood-brain barrier.
This review considers efflux of substances from brain parenchyma quantified as values of clearances (CL, stated in µL g-1 min-1). Total clearance of a substance is the sum of clearance values for all available routes including perivascular pathways and the blood-brain barrier. Perivascular efflux contributes to the clearance of all water-soluble substances. Substances leaving via the perivascular routes may enter cerebrospinal fluid (CSF) or lymph. These routes are also involved in entry to the parenchyma from CSF. However, evidence demonstrating net fluid flow inwards along arteries and then outwards along veins (the glymphatic hypothesis) is still lacking. CLperivascular, that via perivascular routes, has been measured by following the fate of exogenously applied labelled tracer amounts of sucrose, inulin or serum albumin, which are not metabolized or eliminated across the blood-brain barrier. With these substances values of total CL ≅ 1 have been measured. Substances that are eliminated at least partly by other routes, i.e. across the blood-brain barrier, have higher total CL values. Substances crossing the blood-brain barrier may do so by passive, non-specific means with CLblood-brain barrier values ranging from  1000 for water and CO2. CLblood-brain barrier values for many small solutes are predictable from their oil/water partition and molecular weight. Transporters specific for glucose, lactate and many polar substrates facilitate efflux across the blood-brain barrier producing CLblood-brain barrier values > 50. The principal route for movement of Na+ and Cl- ions across the blood-brain barrier is probably paracellular through tight junctions between the brain endothelial cells producing CLblood-brain barrier values ~ 1. There are large fluxes of amino acids into and out of the brain across the blood-brain barrier but only small net fluxes have been observed suggesting substantial reuse of essential amino acids and α-ketoacids within the brain. Amyloid-β efflux, which is measurably faster than efflux of inulin, is primarily across the blood-brain barrier. Amyloid-β also leaves the brain parenchyma via perivascular efflux and this may be important as the route by which amyloid-β reaches arterial walls resulting in cerebral amyloid angiopathy