Collembola,the biological species concept and the underestimation of global species richness

Despite its ancient origin, global distribution and abundance in nearly all habitats, the class Collembola is comprised of only 8000 described species and is estimated to number no more than 50 000. Many morphologically defined species have broad geographical ranges that span continents, and recent molecular work has revealed high genetic diversity within species. However, the evolutionary significance of this genetic diversity is unknown. In this study, we sample five morphological species of the globally distributed genus Lepidocyrtus from 14 Panamanian sampling sites to characterize genetic diversity and test morphospecies against the biological species concept. Mitochondrial and nuclear DNA sequence data were analysed and a total of 58 molecular lineages revealed. Deep lineage diversification was recovered, with 30 molecular lineages estimated to have established more than 10 million years ago, and the origin almost all contemporary lineages preceding the onset of the Pleistocene (~2 Mya). Thirty‐four lineages were sampled in sympatry revealing unambiguous cosegregation of mitochondrial and nuclear DNA sequence variation, consistent with biological species. Species richness within the class Collembola and the geographical structure of this diversity are substantially misrepresented components of terrestrial animal biodiversity. We speculate that global species richness of Collembola could be at least an order of magnitude greater than a previous estimate of 50 000 species.     

Where Do We Go from Here? Prevalence of Trachoma Three Years after Stopping Mass Distribution of Antibiotics in the Regions of Kayes and Koulikoro,Mali

Objectives

A national survey in 1997 demonstrated that trachoma was endemic in Mali. Interventions to control trachoma including mass drug administration (MDA) with azithromycin were launched in the regions of Kayes and Koulikoro in 2003. MDA was discontinued after three annual rounds in 2006, and an impact survey conducted. We resurveyed all districts in Kayes and Koulikoro in 2009 to reassess trachoma prevalence and determine intervention objectives for the future. In this paper we present findings from both the 2006 and 2009 surveys.

Methods

Population-based cluster surveys were conducted in each of the nine districts in Koulikoro in 2006 and 2009, whilst in Kayes, four of seven districts in 2006 and all seven districts in 2009 were surveyed. Household members present were examined for clinical signs of trachoma.

Results

Overall, 29,179 persons from 2,528 compounds, in 260 clusters were examined in 2006 and 32,918 from 7,533 households in 320 clusters in 2009. The prevalence of TF in children aged 1–9 years in Kayes and Koulikoro was 3.9% (95%CI 2.9–5.0%, range by district 1.2–5.4%) and 2.7% (95%CI 2.3–3.1%, range by district 0.1–5.0%) respectively in 2006. In 2009 TF prevalence was 7.26% (95%CI 6.2–8.2%, range by district 2.5–15.4%) in Kayes and 8.19% (95%CI 7.3–9.1%, range by district 1.7–17.2%) in Koulikoro among children of the same age group. TT in adults 15 years of age and older was 2.37% (95%CI 1.66–3.07%, range by district 0.30–3.54%) in 2006 and 1.37% (95%CI 1.02–1.72%, range by district 0.37–1.87%) in 2009 in Kayes and 1.75% (95%CI 1.31–2.23%, range by district 1.06–2.49%) in 2006 and 1.08% (95%CI 0.86–1.30%, range by district 0.34–1.78%) in 2009 in Koulikoro.

Conclusions

Using WHO guidelines for decision making, four districts, Bafoulabe in Kayes Region; and Banamba, Kolokani and Koulikoro in Koulikoro Region, still meet criteria for district-wide implementation of the full SAFE strategy as TF in children exceeds 10%. A community-by-community approach to trachoma control may now be required in the other twelve districts. Trichiasis surgery provision remains a need in all districts and should be enhanced in six districts in Kayes and five in Koulikoro where the prevalence exceeded 1.0% in adults. Since 1997 great progress has been observed in the fight against blinding trachoma; however, greater effort is required to meet the elimination target of 2015.     

Structural Evidence of Glycoprotein Assembly in Cellular Membrane Compartments prior to Alphavirus Budding

Membrane glycoproteins of alphavirus play a critical role in the assembly and budding of progeny virions. However, knowledge regarding transport of viral glycoproteins to the plasma membrane is obscure. In this study, we investigated the role of cytopathic vacuole type II (CPV-II) through in situ electron tomography of alphavirus-infected cells. The results revealed that CPV-II contains viral glycoproteins arranged in helical tubular arrays resembling the basic organization of glycoprotein trimers on the envelope of the mature virions. The location of CPV-II adjacent to the site of viral budding suggests a model for the transport of structural components to the site of budding. Thus, the structural characteristics of CPV-II can be used in evaluating the design of a packaging cell line for replicon production.Semliki Forest virus (SFV) is an enveloped alphavirus belonging to the family Togaviridae. This T=4 icosahedral virus particle is approximately 70 nm in diameter (30) and consists of 240 copies of E1/E2 glycoprotein dimers (3, 8, 24). The glycoproteins are anchored in a host-derived lipid envelope that encloses a nucleocapsid, made of a matching number of capsid proteins and a positive single-stranded RNA molecule. After entry of the virus via receptor-mediated endocytosis, a low-pH-induced fusion of the viral envelope with the endosomal membrane delivers the nucleocapsid into the cytoplasm, where the replication events of SFV occur (8, 19, 30). Replication of the viral genome and subsequent translation into structural and nonstructural proteins followed by assembly of the structural proteins and genome (7) lead to budding of progeny virions at the plasma membrane (18, 20). The synthesis of viral proteins shuts off host cell macromolecule synthesis, which allows for efficient intracellular replication of progeny virus (7). The expression of viral proteins leads to the formation of cytopathic vacuolar compartments as the result of the reorganization of cellular membrane in the cytoplasm of an infected cell (1, 7, 14).Early studies using electron microscopy (EM) have characterized the cytopathic vacuoles (CPVs) in SFV-infected cells (6, 13, 14) and identified two types of CPV, namely, CPV type I (CPV-I) and CPV-II. It was found that CPV-I is derived from modified endosomes and lysosomes (18), while CPV-II is derived from the trans-Golgi network (TGN) (10, 11). Significantly, the TGN and CPV-II vesicles are the major membrane compartments marked with E1/E2 glycoproteins (9, 11, 12). Inhibition by monensin results in the accumulation of E1/E2 glycoproteins in the TGN (12, 26), thereby indicating the origin of CPV-II. While CPV-II is identified as the predominant vacuolar structure at the late stage of SFV infection, the exact function of this particular cytopathic vacuole is less well characterized than that of CPV-I (2, 18), although previous observations have pointed to the involvement of CPV-II in budding, because an associated loss of viral budding was observed when CPV-II was absent (9, 36).In this study, we characterized the structure and composition of CPV-II in SFV-infected cells in situ with the aid of electron tomography and immuno-electron microscopy after physical fixation of SFV-infected cells by high-pressure freezing and freeze substitution (21, 22, 33). The results revealed a helical array of E1/E2 glycoproteins within CPV-II and indicate that CPV-II plays an important role in intracellular transport of glycoproteins prior to SFV budding.     

Maximal lactate steady-state prediction through quadratic modeling of selected stages of the lactate minimum test

In this study, we compared the maximal lactate steady state (MLSS) with lactate minimal (LM) intensities determined visually and through a quadratic polynomial function of selected stages of LM test. Eleven male recreational cyclists (27.7 +/- 4.5 years, 175.7 +/- 5.6 cm, 69.5 +/- 10.8 kg, and 12.0 +/- 5.5% body fat) performed one LM test under previous induction of hyperlactaemia with an initial intensity of 75 W with 30-W increments every 3 minutes with blood lactate concentration (HLa) and rating of perceived exertion (RPE) measurements. The LM intensity was determined visually (VLM) and by modeling the lactate response through polynomial function by using: 1) all stages (LMP); 2) the first stage, the stage corresponding to RPE-13 and the last stage/exhaustion (LMP3max); 3) the three lowest lactate concentration stages (LMP3adj); and 4) the initial, RPE-13, and RPE-16 stages (LMP3sub). The MLSS was determined as the highest intensity at a variation not greater than 0.05 mmol.l.min of HLa during the last 20 minutes of a 30-minute exercise session. The MLSS (204.0 +/- 16.0 W), VLM (198.6 +/- 15.2 W), LMP3adj (190.4 +/- 12.9 W), and LMP3sub (192.1 +/- 27.2 W) were not different, well correlated, and in agreement to each other. In conclusion, the polynomial modeling of HLa response to three submaximal stages produced exercise intensities that did not differ from MLSS.     

Further reading in geomicrobiology

In the wetland rhizosphere, high densities of lithotrophic Fe(II)-oxidizing bacteria (FeOB) and a favorable environment (i.e., high Fe(II) availability and microaerobic conditions) suggest that these organisms are actively contributing to the formation of Fe plaque on plant roots. We manipulated the presence/absence of an Fe(II)-oxidizing bacterium (Sideroxydans paludicola, strain BrT) in axenic hydroponic microcosms containing the roots of intact Juncus effusus (soft rush) plants to determine if FeOB affected total rates of rhizosphere Fe(II) oxidation and Fe plaque accumulation. Our experimental data highlight the importance of both FeOB and plants in influencing short-term rates of rhizosphere Fe oxidation. Over time scales ca. 1 wk, the FeOB increased Fe(II) oxidation rates by 1.3 to 1.7 times relative to FeOB-free microcosms. Across multiple experimental trials, Fe(II) oxidation rates were significantly correlated with root biomass, reflecting the importance of radial O ₂ loss in supporting rhizosphere Fe(II) oxidation. Rates of root Fe(III) plaque accumulation (time scales: 3 to 6 wk) were ～ 70 to 83% lower than expected based on the short-term Fe(II) oxidation rates and were unaffected by the presence/absence of FeOB. Decreasing rates of Fe(II) oxidation and Fe(III) plaque accumulation with increasing time scales indicate changes in rates of Fe(II) diffusion and radial O ₂ loss, shifts in the location of Fe oxide accumulation, or temporal changes in the microbial community within the microcosms. The microcosms used herein replicated many of the environmental characteristics of wetland systems and allowed us to demonstrate that FeOB can stimulate rates of Fe(II) oxidation in the wetland rhizosphere, a finding that has implications for the biogeochemical cycling of carbon, metals, and nutrients in wetland ecosystems.     

Isolation of a human stromal cell strain secreting hemopoietic growth factors

A diploid fibroblastoid cell strain, termed "ST-1," has been established from a long-term liquid culture of human fetal liver cells. ST-1 cells are nonphagocytic, nonspecific esterase negative and do not possess factor VIII-related antigen but stain with antibodies specific for fibronectin and type I collagen. The ST-1 cells produce nondialyzable hemopoietic growth factors capable of stimulating the development of erythroid bursts, mixed granulocyte-macrophage colonies, pure granulocyte colonies, and pure macrophage colonies. These factors are active on both human fetal liver and human adult bone marrow progenitors. When liquid cultures of human fetal liver hemopoietic progenitors are established with a preformed monolayer of ST-1 cells, the yields of nonadherent cells, erythroid progenitors, and myeloid progenitors are greatly increased. These studies demonstrate that the fibroblastoid ST-1 cells support hemopoiesis in vitro and may be a critical element in the stromal microenviroment in vivo.     

Thrombosis is reduced by inhibition of COX-1, but unaffected by inhibition of COX-2, in an acute model of platelet activation in the mouse

Background

Clinical use of selective inhibitors of cyclooxygenase (COX)-2 appears associated with increased risk of thrombotic events. This is often hypothesised to reflect reduction in anti-thrombotic prostanoids, notably PGI₂, formed by COX-2 present within endothelial cells. However, whether COX-2 is actually expressed to any significant extent within endothelial cells is controversial. Here we have tested the effects of acute inhibition of COX on platelet reactivity using a functional in vivo approach in mice.

Methodology/Principal Findings

A non-lethal model of platelet-driven thromboembolism in the mouse was used to assess the effects of aspirin (7 days orally as control) diclofenac (1 mg.kg⁻¹, i.v.) and parecoxib (0.5 mg.kg⁻¹, i.v.) on thrombus formation induced by collagen or the thromboxane (TX) A₂-mimetic, U46619. The COX inhibitory profiles of the drugs were confirmed in mouse tissues ex vivo. Collagen and U46619 caused in vivo thrombus formation with the former, but not latter, sensitive to oral dosing with aspirin. Diclofenac inhibited COX-1 and COX-2 ex vivo and reduced thrombus formation in response to collagen, but not U46619. Parecoxib inhibited only COX-2 and had no effect upon thrombus formation caused by either agonist.

Conclusions/Significance

Inhibition of COX-1 by diclofenac or aspirin reduced thrombus formation induced by collagen, which is partly dependent upon platelet-derived TXA₂, but not that induced by U46619, which is independent of platelet TXA₂. These results are consistent with the model demonstrating the effects of COX-1 inhibition in platelets, but provide no support for the hypothesis that acute inhibition of COX-2 in the circulation increases thrombosis.