Whole-lake experiments reveal the fate of terrestrial particulate organic carbon in benthic food webs of shallow lakes.

Lake ecosystems are strongly linked to their terrestrial surroundings by material and energy fluxes across ecosystem boundaries. However, the contribution of terrestrial particulate organic carbon (tPOC) from annual leaf fall to lake food webs has not yet been adequately traced and quantified. In this study, we conducted whole-lake experiments to trace artificially added tPOC through the food webs of two shallow lakes of similar eutrophic status, but featuring alternative stable regimes (macrophyte rich vs. phytoplankton dominated). Lakes were divided with a curtain, and maize (Zea mays) leaves were added, as an isotopically distinct tPOC source, into one half of each lake. To estimate the balance between autochthonous carbon fixation and allochthonous carbon input, primary production and tPOC and tDOC (terrestrial dissolved organic carbon) influx were calculated for the treatment sides. We measured the stable isotope ratios of carbon (delta13C) of about 800 samples from all trophic consumer levels and compared them between lake sides, lakes, and three seasons. Leaf litter bag experiments showed that added maize leaves were processed at rates similar to those observed for leaves from shoreline plants, supporting the suitability of maize leaves as a tracer. The lake-wide carbon influx estimates confirmed that autochthonous carbon fixation by primary production was the dominant carbon source for consumers in the lakes. Nevertheless, carbon isotope values of benthic macroinvertebrates were significantly higher with maize additions compared to the reference side of each lake. Carbon isotope values of omnivorous and piscivorous fish were significantly affected by maize additions only in the macrophyte-dominated lake and delta13C of zooplankton and planktivorous fish remained unaffected in both lakes. In summary, our results experimentally demonstrate that tPOC in form of autumnal litterfall is rapidly processed during the subsequent months in the food web of shallow lakes and is channeled to secondary and tertiary consumers predominantly via the benthic pathways. A more intense processing of tPOC seems to be connected to a higher structural complexity in littoral zones, and hence may differ between shallow lakes of alternative stable states.

The ability of an oligomeric human immunodeficiency virus type 1 (HIV-1) envelope antigen to elicit neutralizing antibodies against primary HIV-1 isolates is improved following partial deletion of the second hypervariable region.

Partial deletion of the second hypervariable region from the envelope of the primary-like SF162 virus increases the exposure of certain neutralization epitopes and renders the virus, SF162DeltaV2, highly susceptible to neutralization by clade B and non-clade B human immunodeficiency virus (HIV-positive) sera (L. Stamatatos and C. Cheng-Mayer, J. Virol. 78:7840-7845, 1998). This observation led us to propose that the modified, SF162DeltaV2-derived envelope may elicit higher titers of cross-reactive neutralizing antibodies than the unmodified SF162-derived envelope. To test this hypothesis, we immunized rabbits and rhesus macaques with the gp140 form of these two envelopes. In rabbits, both immunogens elicited similar titers of binding antibodies but the modified immunogen was more effective in eliciting neutralizing antibodies, not only against the SF162DeltaV2 and SF162 viruses but also against several heterologous primary HIV type 1 (HIV-1) isolates. In rhesus macaques both immunogens elicited potent binding antibodies, but again the modified immunogen was more effective in eliciting the generation of neutralizing antibodies against the SF162DeltaV2 and SF162 viruses. Antibodies capable of neutralizing several, but not all, heterologous primary HIV-1 isolates tested were elicited only in macaques immunized with the modified immunogen. The efficiency of neutralization of these heterologous isolates was lower than that recorded against the SF162 isolate. Our results strongly suggest that although soluble oligomeric envelope subunit vaccines may elicit neutralizing antibody responses against heterologous primary HIV-1 isolates, these responses will not be broad and potent unless specific modifications are introduced to increase the exposure of conserved neutralization epitopes.

Rapid discrimination among individual DNA hairpin molecules at single-nucleotide resolution using an ion channel.

RNA and DNA strands produce ionic current signatures when driven through an alpha-hemolysin channel by an applied voltage. Here we combine this nanopore detector with a support vector machine (SVM) to analyze DNA hairpin molecules on the millisecond time scale. Measurable properties include duplex stem length, base pair mismatches, and loop length. This nanopore instrument can discriminate between individual DNA hairpins that differ by one base pair or by one nucleotide.

IL-8 induces neutrophil chemotaxis predominantly via type I IL-8 receptors.

IL-8 is a potent proinflammatory cytokine that has a key role in the recruitment and activation of neutrophils during inflammation. IL-8 reacts with neutrophils via two distinct types of IL-8-R. Receptor-specific Abs were raised against peptides derived from the first extracellular domain of each IL-8-R. Anti-IL-8-R1 and anti-IL-8-R2 selectively block 125I-IL-8 binding to rIL-8-R type 1 or 2, respectively. The anti-peptide Abs were used to assess the role of each receptor in the chemotactic response of neutrophils to GRO alpha and to IL-8. Anti-IL-8-R2 blocks GRO alpha-induced chemotaxis of neutrophils. Chemotaxis to GRO alpha is not inhibited by anti-IL-8-R1. Thus GRO alpha stimulates chemotaxis exclusively through IL-8-R2 and independently of IL-8-R1. Surprisingly, anti-IL-8-R1 inhibits the majority (78 +/- 3%) of IL-8-induced neutrophil chemotaxis. Only a minor proportion of IL-8-induced chemotaxis (29 +/- 5%) is inhibited by anti-IL-8-R2. These findings indicate that chemotaxis to IL-8 is mediated predominantly by type 1 IL-8-Rs and suggest that IL-8-R1 is an appropriate target for therapeutic strategies to limit neutrophil influx in diseases where neutrophils contribute to pathophysiology.