Parallel declines in species and genetic diversity in tropical forest fragments

The potential for parallel impacts of habitat change on multiple biodiversity levels has important conservation implications. We report on the first empirical test of the 'species-genetic diversity correlation' across co-distributed taxa with contrasting ecological traits in the context of habitat fragmentation. In a rainforest landscape undergoing conversion to oil palm, we show that depauperate species richness in fragments is mirrored by concomitant declines in population genetic diversity in the taxon predicted to be most susceptible to fragmentation. This association, not seen in the other species, relates to fragment area rather than isolation. While highlighting the over-simplification of extrapolating across taxa, we show that fragmentation presents a double jeopardy for some species. For these, conserving genetic diversity at levels of pristine forest could require sites 15-fold larger than those needed to safeguard species numbers. Importantly, however, each fragment contributes to regional species richness, with larger ones tending to contain more species.     

The Maintenance of Discrete Bacterial Colonies on the Surface of Objects Embedded in Agar

Summary: Bacterial colonies grown on objects embedded in agar sometimes show a tendency to become confluent. Glass coverslips and polytetrafluorethylene (Teflon) discs were inoculated with Staphylococcus lactis and completely embedded in serum agar. If the surface of the agar were flooded with broth before the plates were incubated the colonies had a tendency to run together, but not if the plates were incubated after thorough drying. Drying also prevented confluence occurring when broth had been injected on to the surface of the embedded object. Drying the poured plate probably acts by removing fluid squeezed out at the interface.     

The pH-independent effect of aluminum on cultures of phytoplankton from an acidic Wisconsin lake

Negative correlations between aluminum and planktonic algal abundance have been reported in acidic lakes. Natural assemblages of phytoplankton from a low-pH, low-Al lake (Franklin Lake, WI) were grown in semi-continuous cultures consisting of four treatments at pH 5.7 with 0.0, 50, 100, and 200 μg Al L⁻¹ and one treatment at pH 4.7 with no Al added. Asterionella ralfsii var. americana (a common diatom plankter in acidic lakes) grew well at both pH 4.7 and 5.7 when no Al was added but declined in all other treatments and so may be useful as an indicator of acidic, low monomeric-Al conditions. Other common plankters that showed this pattern included: Arthrodesmus indentatus, Ar. octocornus, Ar. quiriferus, Staurastrum arachne var. curvatum, S. longipes var. contractum, and S. pentacerum. Common taxa showing no toxic effects of Al were Dinobryon bavaricum, Peridinium limbatum, Stenokalyx monilifera, Elaktothrix sp. and Oedogonium sp. We hypothesize that metal toxicity as a pulse at spring snowmelt could dramatically change algal succession in moderately acidic lakes. The experimental results agreed well with field observations. These types of experiments are useful for predicting the responses of natural phytoplankton communities to increases in Al concentration.     

Role of interleukin-4 in regulation of age-related inflammatory changes in the hippocampus

It is well documented that long term potentiation (LTP) is impaired in the hippocampus of the aged animal. Among the changes that contribute to this impairment is an increase in hippocampal concentration of the pro-inflammatory cytokine interleukin-1beta (IL-1beta), and increased IL-1beta-induced signaling. In this study we investigated the possibility that these changes were a consequence of decreased concentration of the anti-inflammatory cytokine, IL-4, and decreased IL-4-stimulated signaling. We report that functional IL-4 receptors are expressed on granule cells of the dentate gyrus and that receptor activation results in phosphorylation of JAK1 and STAT6. Hippocampal IL-4 concentration was decreased with age, and this was accompanied by a decrease in phosphorylation of JAK1 and STAT6. The evidence indicates that IL-4 modulates expression of IL-1beta mRNA and protein and that it attenuates IL-1beta-induced impairment of LTP and phosphorylation of JNK and c-Jun. We argued that, if a decrease in hippocampal IL-4 concentration significantly contributed to the age-related impairment in LTP, then restoration of IL-4 should restore LTP. To test this, we treated rats with VP015 (phospholipid microparticles-incorporating phosphatidylserine), which increases IL-4 concentration in hippocampus. The data indicate that the VP015-induced increase in IL-4 concentration in hippocampus of aged rats and lipopolysaccharide (LPS)-treated rats was accompanied by a reversal of the age-related and LPS-induced impairment in LTP in perforant path granule cell synapses. We propose that interplay between pro-inflammatory and anti-inflammatory responses impact significantly on synaptic function in the hippocampus of the aged rat.     

Nitroreductase-based therapy of prostate cancer, enhanced by raising expression of heat shock protein 70, acts through increased anti-tumour immunity

Gene-directed enzyme-prodrug therapy (GDEPT) using nitroreductase (NTR), with efficient adenoviral delivery, and CB1954 (CB), is an effective means of directly killing tumours. However, an immune-mediated bystander effect remains an important product of GDEPT since it is often critical to the elimination of untransduced tumour cells both locally and at distal metastatic sites through generation of tumour-specific immunity without the need for tumour antigen identification or the generation of a personalised vaccine. The mode of induced tumour cell death is thought to contribute to the immunisation process, together with the induction and release of stress proteins. Here, RM-9 murine prostate tumour cells were efficiently killed by adenovirally delivered NTR/CB treatment both in vitro and in vivo, and bystander effects were observed. Cells appeared to die by pathways that suggest necrosis more than that of classical apoptosis. NTR/CB-induced expression of a range of stress proteins was determined by proteomic analysis, revealing chiefly heat shock protein (HSP)25 and HSP70 upregulation, whilst immune responses in vivo were weak. In an attempt to enhance the anti-tumour effect, an adenoviral vector was constructed that co-expressed NTR and HSP70, the latter being a known immune stimulator and chaperone of antigen. This combination elicited significantly enhanced protection over NTR alone for both the treated tumour and a subsequent re-challenge. Protection was CD4⁺ and CD8⁺ T cell-dependent and was associated with tumour-specific CTL, IFNγ and IL-5 responses. The use of such a cytotoxic and immunomodulatory gene combination in cancer therapy warrants further pursuit.