Protection of Mice against Lethal Coxsackievirus B3 Infection by Using DNA Immunization

Vaccination with DNA and recombinant vaccinia viruses (rec.VV) has been studied with the coxsackievirus B3 (CVB3) model system. Plasmids encoding all structural proteins of CVB3, when injected intramuscularly, induced only low levels of virus-specific antibodies. However, DNA vaccination with the major structural protein VP1 protected 72.2% of mice from lethal challenge, whereas VP1 expressed by rec.VV was much less efficient.     

Mefluidide-chlorsulfuron-2,4-D surfactant combinations for roadside vegetation management

Using a combination of a primary growth retardant, mefluidide, a synergistic additive, chlorsulfuron, a detergent to enhance penetration (X-77), and a herbicide, 2,4-D, to provide for control of broadleaf weeds, full-season management of bluegrass (Poa pratensis L.)—tall fescue (Festuca arundinaceae Schreb.) mixtures along roadsides has been achieved. A single spray application is made in the spring, and no additional herbicide applications or mechanical mowing are needed. The treatment is effective with greater than 90% control of fescue seed heads. Those few seed heads that do form remain short. It is economical. The costs of materials and application are equal to or less than the cost of a single mowing cycle. The treatment is environmentally safe when applied in early spring before most agricultural crops have been planted. The effectiveness and low cost of the combination derive from laboratory and greenhouse observations that various materials, herein referred to as additives, often only weakly effective as growth retardants themselves, will interact synergistically with mefluidide to provide overall treatment effectiveness at application rates that are economical. Using this principle, a combination suitable for roadside vegetation management was devised, field-tested for 2 years under actual use conditions, and found to be effective for full-season vegetation management of mixed bluegrass—tall fescue turf to permit considerable cost savings when compared to three-cycle mechanical mowing.     

Environmental needs and social justice

Despite the growth in awareness and practical action to maintain biodiversity, environmental degradation and ecosystem destruction has continued at a high rate over the last 20 years. The roots of this lie in the predominant international economic order, underpinned by lifestyle demands for increased material consumption. Net flow of wealth from South (less developed) to North (more developed) nations has exacerbated a spiral of increased poverty and environmental degradation in the former. Global environmental conservation depends upon a radical change of direction with the principle of equity as the starting point. Notwithstanding the importance of continuing to add to local and small-scale conservation achievements, the prospect of radical change happening seems small, despite it being in the long-term self-interest of the North. The concept of equity is, apparently, unacceptable to Northern electorates.     

Global patterns of diversity among the specialist birds of riverine landscapes

1. Despite the growing view that biodiversity provides a unifying theme in river ecology, global perspectives on richness in riverine landscapes are limited. As a result, there is little theory or quantitative data on features that might have influenced global patterns in riverine richness, nor are there clear indications of which riverine landscapes are important to conservation at the global scale. As conspicuous elements of the vertebrate fauna of riverine landscapes, we mapped the global distributions of all of the world's specialist riverine birds and assessed their richness in relation to latitude, altitude, primary productivity and geomorphological complexity (surface configuration). 2. Specialist riverine birds, typical of high‐energy riverine landscapes and dependent wholly or partly on production from river ecosystems, occur in 16 families. They are represented by an estimated 60 species divided equally between the passerines and non‐passerines. Major radiation has occurred among different families on different continents, indicating that birds have evolved several times into the niches provided by riverine landscapes. 3. Continental richness varies from four species in Europe to 28 in Asia, with richness on the latter continent disproportionately larger than would be expected from a random distribution with respect to land area. Richness is greatest in mountainous regions at latitudes of 20–40°N in the riverine landscapes of the Himalayan mountains, where 13 species overlap in range. 4. Family, genus and species richness in specialist riverine birds all increase significantly with productivity and surface configuration (i.e. relief). However, family richness was the best single predictor of the numbers of species or genera. In keeping with the effect of surface configuration, river‐bird richness peaks globally at 1300–1400 m altitude, and most species occur typically on small, fast rivers where they feed predominantly on invertebrates. Increased lengths of such streams in areas of high relief and rainfall might have been responsible for species–area effects. 5. We propose the hypothesis that the diversity in channel forms and habitats in riverine landscapes, in addition to high temperature and primary productivity, have been prerequisites to the development of global patterns in the richness of specialist riverine organisms. We advocate tests of this hypothesis in other taxonomic groups. We draw attention, however, to the challenges of categorically defining riverine organisms in such tests because (i) rivers grade into many other habitat types across several different ecotones and (ii) `terrestrialisation' processes in riverine landscapes means that they offer habitat for organisms whose evolutionary origins are not exclusively riverine.     

Release of arachidonic acid from human endometrial cells in culture mediated by calcium ionophore (A23187) or fluoride.

Primary cultures of endometrial glands and stromal cells were labelled with [14C]-arachidonic acid for 4 h before exposure to either the calcium ionophore, A23187 (which activates phospholipase A2 (PLA2) by increasing intracellular calcium concentrations) or sodium fluoride (which activates a G-protein). Calcium ionophore (0.5-50 mumol/l) stimulated a dose- and time-dependent release of arachidonic acid from endometrial glands. Incubation with ionophore (10 mumol/l) for 1 h released 22% of the incorporated arachidonic acid. There was a corresponding decrease in phospholipids and no loss from triglycerides. Stromal cells were unresponsive to ionophore. Fluoride (10 mmol/l) stimulated a release of arachidonic acid from stromal cells and endometrial glands (6.5% of the total arachidonic acid incorporated). In stromal cells, arachidonic acid was released from triglycerides in Day-1 cultures and from phospholipids in Day-2 cultures. In both Day-1 and Day-2 cultures of endometrial glands, arachidonic acid was released from phospholipids, but not from triglycerides. Among the phospholipids, phosphatidylcholine was always the major source of arachidonic acid. Arachidonic acid release from endometrial glands and stromal cells may be mediated by activation of PLA2 (or phospholipase C) via a G-protein, but in glands calcium ionophore may have a direct effect on PLA2. The response to calcium ionophore may reflect the differences in calcium requirements of the two endometrial PLA2 isoenzymes.     

Prostaglandins do not mediate the actions of cholera toxin on pancreatic acini or gastric chief cells from the guinea pig

Recent reports suggest that prostaglandins, rather than cAMP, play a major role in mediating cholera toxin-induced water and electrolyte secretion from rabbit intestinal loops. We examined the role of prostaglandins in mediating toxin-induced pancreatic and gastric exocrine secretion. In these tissues, indomethacin, a potent inhibitor of prostaglandin synthesis, did not alter the stimulatory effects of cholera toxin on increases in cellular cAMP or enzyme secretion. Moreover, the addition of cholera toxin did not alter prostaglandin E2 release from either tissue. In contrast to their effects in rabbit intestinal loops, prostaglandins do not regulate cholera toxin-induced enzyme secretion from the guinea pig pancreas or stomach.