Phylogenetic composition and structure of tree communities shed light on historical processes influencing tropical rainforest diversity

The Neotropics, Afrotropics and Madagascar have different histories which have influenced their respective patterns of diversity. Based on current knowledge of these histories, we developed the following predictions about the phylogenetic structure and composition of rainforest tree communities: (Hypothesis 1) isolation of Gondwanan biotas generated differences in phylogenetic composition among biogeographical regions; (H2) major Cenozoic extinction events led to lack of phylogenetic structure in Afrotropical and Malagasy communities; (H3) greater angiosperm diversification in the Neotropics led to greater phylogenetic clustering there than elsewhere; (H4) phylogenetic overdispersion is expected near the Andes due to the co‐occurrence of magnoliids tracking conserved habitat preferences and recently diversified eudicot lineages. Using abundance data of tropical rainforest tree species from 94 communities in the Neotropics, Afrotropics and Madagascar, we computed net relatedness index (NRI) to assess local phylogenetic structure, i.e. phylogenetic clustering vs. overdispersion relative to regional species pools, and principal coordinates of phylogenetic structure (PCPS) to assess variation in phylogenetic composition across communities. We observed significant differences in phylogenetic composition among biogeographical regions (agreement with H1). Overall phylogenetic structure did not differ among biogeographical regions, but results indicated variation from Andes to Amazon. We found widespread phylogenetic randomness in most Afrotropical and all Malagasy communities (agreement with H2). Most of central Amazonian communities were phylogenetically random, although some communities presented phylogenetic clustering (partial agreement with H3). We observed phylogenetic overdispersion near the Andes (agreement with H4). We were able to identify how differences in lineage composition are related to local phylogenetic co‐occurrences across biogeographical regions that have been undergoing different climatic and orographic histories during the past 100 Myr. We observed imprints of the history following Gondwana breakup on phylobetadiversity and local phylogenetic structure of rainforest tree communities in the Neotropics, Afrotropics and Madagascar.     

Increased glycated calmodulin in the submandibular salivary glands of streptozotocin‐induced diabetic rats

Non‐enzymatic glycosylation, a post translational protein modification may be implicated in the diabetes complications. Calmodulin is an important calcium binding protein that complexed with Ca²⁺ may be implicated in salivary gland secretory process. Glycated calmodulin has shown to be less effective in binding calcium. The aim of this study was to determine whether the concentration of glycated‐calmodulin may be elevated in the submandibular salivary glands of streptozotocin‐induced diabetic rats. Diabetes was induced by an intraperitoneal injection of spreptozotocin, and hyperglycemia was confirmed 72 h after injection using a glucosimeter. Thirty days after the induction of diabetes, submandibular salivary glands were used for the analysis of glycated and non‐glycated calmodulin, using a glycogel B columns for separation. Glycated and non‐glycated calmodulin were assayed by an enzymatic method and by ELISA. The overall concentration of CaM (non‐glycated + glycated) in induced diabetic rats was significantly lower than in controls (p < 0.05). The concentration of non‐glycated CaM in controls was significantly higher than in experimental group (p < 0.05), while the concentration of glycated calmodulin between these groups was statistically similar (p > 0.05). Copyright © 2009 John Wiley & Sons, Ltd.     

Monitoring Low Molecular Weight Heparins at Therapeutic Levels: Dose-Responses of,and Correlations and Differences between aPTT,Anti-Factor Xa and Thrombin Generation Assays

Background

Low molecular weight heparins (LMWH’s) are used to prevent and treat thrombosis. Tests for monitoring LMWH’s include anti-factor Xa (anti-FXa), activated partial thromboplastin time (aPTT) and thrombin generation. Anti-FXa is the current gold standard despite LMWH’s varying affinities for FXa and thrombin.

Aim

To examine the effects of two different LMWH’s on the results of 4 different aPTT-tests, anti-FXa activity and thrombin generation and to assess the tests’ concordance.

Method

Enoxaparin and tinzaparin were added ex-vivo in concentrations of 0.0, 0.5, 1.0 and 1.5 anti-FXa international units (IU)/mL, to blood from 10 volunteers. aPTT was measured using two whole blood methods (Free oscillation rheometry (FOR) and Hemochron Jr (HCJ)) and an optical plasma method using two different reagents (ActinFSL and PTT-Automat). Anti-FXa activity was quantified using a chromogenic assay. Thrombin generation (Endogenous Thrombin Potential, ETP) was measured on a Ceveron Alpha instrument using the TGA RB and more tissue-factor rich TGA RC reagents.

Results

Methods’ mean aPTT at 1.0 IU/mL LMWH varied between 54s (SD 11) and 69s (SD 14) for enoxaparin and between 101s (SD 21) and 140s (SD 28) for tinzaparin. ActinFSL gave significantly shorter aPTT results. aPTT and anti-FXa generally correlated well. ETP as measured with the TGA RC reagent but not the TGA RB reagent showed an inverse exponential relationship to the concentration of LMWH. The HCJ-aPTT results had the weakest correlation to anti-FXa and thrombin generation (R_s0.62–0.87), whereas the other aPTT methods had similar correlation coefficients (R_s0.80–0.92).

Conclusions

aPTT displays a linear dose-respone to LMWH. There is variation between aPTT assays. Tinzaparin increases aPTT and decreases thrombin generation more than enoxaparin at any given level of anti-FXa activity, casting doubt on anti-FXa’s present gold standard status. Thrombin generation with tissue factor-rich activator is a promising method for monitoring LMWH’s.     

Siaα2-3Galβ1- Receptor Genetic Variants Are Associated with Influenza A(H1N1)pdm09 Severity

Different host genetic variants may be related to the virulence and transmissibility of pandemic Influenza A(H1N1)pdm09, influencing events such as binding of the virus to the entry receptor on the cell of infected individuals and the host immune response. In the present study, two genetic variants of the ST3GAL1 gene, which encodes the Siaα2-3Galβ1- receptor to which influenza A(H1N1)pdm09 virus binds for entry into the host cell, were investigated in an admixed Brazilian population. First, the six exons encoding the ST3GAL1 gene were sequenced in 68 patients infected with strain A(H1N1)pdm09. In a second phase of the study, the rs113350588 and rs1048479 polymorphisms identified in this sample were genotyped in a sample of 356 subjects from the northern and northeastern regions of Brazil with a diagnosis of pandemic influenza. Functional analysis of the polymorphisms was performed in silico and the influence of these variants on the severity of infection was evaluated. The results suggest that rs113350588 and rs1048479 may alter the function of ST3GAL1 either directly through splicing regulation alteration and/or indirectly through LD with SNP with regulatory function. In the study the rs113350588 and rs1048479 polymorphisms were in linkage disequilibrium in the population studied (D’ = 0.65). The GC haplotype was associated with an increased risk of death in subjects with influenza (OR = 4.632, 95% CI = 2.10;1.21). The AT haplotype was associated with an increased risk of severe disease and death (OR = 1.993, 95% CI = 1.09;3.61 and OR 4.476, 95% CI = 2.37;8.44, respectively). This study demonstrated for the first time the association of ST3GAL1 gene haplotypes on the risk of more severe disease and death in patients infected with Influenza A(H1N1)pdm09 virus.     

Ontology Alignment Repair through Modularization and Confidence-Based Heuristics

Ontology Matching aims at identifying a set of semantic correspondences, called an alignment, between related ontologies. In recent years, there has been a growing interest in efficient and effective matching methods for large ontologies. However, alignments produced for large ontologies are often logically incoherent. It was only recently that the use of repair techniques to improve the coherence of ontology alignments began to be explored. This paper presents a novel modularization technique for ontology alignment repair which extracts fragments of the input ontologies that only contain the necessary classes and relations to resolve all detectable incoherences. The paper presents also an alignment repair algorithm that uses a global repair strategy to minimize both the degree of incoherence and the number of mappings removed from the alignment, while overcoming the scalability problem by employing the proposed modularization technique. Our evaluation shows that our modularization technique produces significantly small fragments of the ontologies and that our repair algorithm produces more complete alignments than other current alignment repair systems, while obtaining an equivalent degree of incoherence. Additionally, we also present a variant of our repair algorithm that makes use of the confidence values of the mappings to improve alignment repair. Our repair algorithm was implemented as part of AgreementMakerLight, a free and open-source ontology matching system.     

Characterization of iron-sulfur clusters in rat liver submitochondrial particles by electron paramagnetic resonance spectroscopy. Alterations produced by chronic ethanol consumption

Iron-sulfur clusters present in rat liver submitochondrial particles were characterized by ESR at temperatures between 30 and 5.5 K combined with potentiometric titrations. The spectral and thermodynamic characteristics of the iron-sulfur clusters were generally similar to those previously reported for pigeon or bovine heart submitochondrial particles. Clusters N-1a, N-1b, N-2, N-3 and N-4 of NADH dehydrogenase had midpoint oxidation-reduction potentials at pH 7.5 of ?425, ?265, ?85, ?240 and ?260 mV, respectively. Clusters S-1 and S-3 of succinate dehydrogenase had midpoint potentials of 0 and +65 mV, respectively. The iron-sulfur cluster of electron-transferring flavoprotein-ubiquinone oxidoreductase exhibited the g_z signal at g = 2.08 and had a midpoint potential of +30 mV. This signal was relatively prominent in rat liver compared to pigeon or bovine heart.Submitochondrial particles from rats chronically treated with ethanol (36% of total calories, 40 days) showed decreases of 20–30% in amplitudes of signals due to clusters N-2, N-3 and N-4 compared to those from pair-fed control rats. Signals from clusters N-1b, S-1, S-3 and electron-transferring flavoprotein-ubiquinone oxidoreductase were unaffected. Microwave power-saturation behavior was similar for both submitochondrial particle preparations, suggesting that the lower signal amplitudes reflected a lower content of these particular clusters. NADH dehydrogenase activity was significantly decreased (46%), whilst succinate dehydrogenase activity was elevated (25%), following chronic ethanol consumption. The results indicate that chronic ethanol treatment leads to an alteration of the structure and function of the NADH dehydrogenase segment of the electron transfer chain. This alteration is one of the factors contributing to the lower respiration rates observed following chronic ethanol administration.     

The role of cytologic NOR variants in the etiology of trisomy 21.

Silver-stained chromosomes from 29 couples with a trisomy 21 offspring and from 25 control couples were studied to determine whether there was an association of nucleolar-organizing-region variants in parents of children with trisomy 21. A reproducible scoring system for the analysis of silver-stained chromosomes was developed, and this was applied to the analysis of study participants in a blinded fashion. Seven of the 58 parents of children with trisomy 21 and seven of the 50 control parents were found to have variant NORs on silver staining. Therefore, we do not find a demonstrable risk for nondisjunction of chromosome 21 in individuals with silver-staining variants.