Disturbance, neutral theory and patterns of beta diversity in soil communities

Beta diversity describes how local communities within an area or region differ in species composition/abundance. There have been attempts to use changes in beta diversity as a biotic indicator of disturbance, but lack of theory and methodological caveats have hampered progress. We here propose that the neutral theory of biodiversity plus the definition of beta diversity as the total variance of a community matrix provide a suitable, novel, starting point for ecological applications. Observed levels of beta diversity (BD) can be compared to neutral predictions with three possible outcomes: Observed BD equals neutral prediction or is larger (divergence) or smaller (convergence) than the neutral prediction. Disturbance might lead to either divergence or convergence, depending on type and strength. We here apply these ideas to datasets collected on oribatid mites (a key, very diverse soil taxon) under several regimes of disturbances. When disturbance is expected to increase the heterogeneity of soil spatial properties or the sampling strategy encompassed a range of diverging environmental conditions, we observed diverging assemblages. On the contrary, we observed patterns consistent with neutrality when disturbance could determine homogenization of soil properties in space or the sampling strategy encompassed fairly homogeneous areas. With our method, spatial and temporal changes in beta diversity can be directly and easily monitored to detect significant changes in community dynamics, although the method itself cannot inform on underlying mechanisms. However, human-driven disturbances and the spatial scales at which they operate are usually known. In this case, our approach allows the formulation of testable predictions in terms of expected changes in beta diversity, thereby offering a promising monitoring tool.

CHROMIUM(II)-MEDIATED CONVERSION OF ALPHA,BETA-UNSATURATED ALDEHYDES TO CYCLOPROPANOLS

Chromium(II) chloride converts alpha,beta-unsaturated aldehydes to the corresponding cyclopropanols.

A multivariate analysis of beta diversity across organisms and environments

We examined variability in hierarchical beta diversity across ecosystems, geographical gradients, and organism groups using multivariate spatial mixed modeling analysis of two independent data sets. The larger data set comprised reported ratios of regional species richness (RSR) to local species richness (LSR) and the second data set consisted of RSR: LSR ratios derived from nested species-area relationships. There was a negative, albeit relatively weak, relationship between beta diversity and latitude. We found only relatively subtle differences in beta diversity among the realms, yet beta diversity was lower in marine systems than in terrestrial or freshwater realms. Beta diversity varied significantly among organisms' major characteristics such as body mass, trophic position, and dispersal type in the larger data set. Organisms that disperse via seeds had highest beta diversity, and passively dispersed organisms showed the lowest beta diversity. Furthermore, autotrophs had lower beta diversity than organisms higher up the food web; omnivores and carnivores had consistently higher beta diversity. This is evidence that beta diversity is simultaneously controlled by extrinsic factors related to geography and environment, and by intrinsic factors related to organism characteristics.

Measuring beta diversity for presence-absence data

1. Little consensus has been reached as to general features of spatial variation in beta diversity, a fundamental component of species diversity. This could reflect a genuine lack of simple gradients in beta diversity, or a lack of agreement as to just what constitutes beta diversity. Unfortunately, a large number of approaches have been applied to the investigation of variation in beta diversity, which potentially makes comparisons of the findings difficult.

2. We review 24 measures of beta diversity for presence/absence data (the most frequent form of data to which such measures are applied) that have been employed in the literature, express many of them for the first time in common terms, and compare some of their basic properties.

3. Four groups of measures are distinguished, with a fundamental distinction arising between 'broad sense' measures incorporating differences in composition attributable to species richness gradients, and 'narrow sense' measures that focus on compositional differences independent of such gradients. On a number of occasions on which the former have been employed in the literature the latter may have been more appropriate, and there are many situations in which consideration of both kinds of measures would be valuable.

4. We particularly recommend (i) considering beta diversity measures in terms of matching/mismatching components (usually denoted a , b and c) and thereby identifying the contribution of different sources of variation in species composition, and (ii) the use of ternary plots to express the relationship between the values of these measures and of the components, and as a way of understanding patterns in beta diversity.

Transforming Growth Factor-beta superfamily:evaluation as breast cancer biomarkers and preventive agents

The Transforming Growth Factor-beta (TGFbeta) superfamily of cytokines is comprised of a number of structurally-related, secreted polypeptides that regulate a multitude of cellular processes including proliferation, differentiation and neoplastic transformation. These growth regulatory molecules induce ligand-mediated hetero-oligomerization of distinct type II and type I serine/threonine kinase receptors that transmit signals predominantly through receptor-activated Smad proteins but also induce Smad-independent pathways. Ligands, receptors and intracellular mediators of signaling initiated by members of the TGFbeta family are expressed in the mammary gland and disruption of these pathways may contribute to the development and progression of human breast cancer. Since many facets of TGFbeta and breast cancer have been recently reviewed in several articles, except for discussion of recent developments on some aspects of TGFbeta, the major focus of this review will be on the role of activins, inhibins, BMPs, nodal and MIS-signaling in breast cancer with emphasis on their utility as potential diagnostic, prognostic and therapeutic targets.

The vascular targeting agent combretastatin-A4 and a novel cis-Restricted {beta}-Lactam Analogue, CA-432, induce apoptosis in human chronic myeloid leukemia cells and ex vivo patient samples including those displaying multidrug resistance

Combretastatin-A4 (CA-4) is a natural derivative of the African willow tree Combretum caffrum. CA-4 is one of the most potent antimitotic components of natural origin, but it is, however, intrinsically unstable. A novel series of CA-4 analogs incorporating a 3,4-diaryl-2-azetidinone (β-lactam) ring were designed and synthesized with the objective to prevent cis -trans isomerization and improve the intrinsic stability without altering the biological activity of CA-4. Evaluation of selected β-lactam CA-4 analogs demonstrated potent antitubulin, antiproliferative, and antimitotic effects in human leukemia cells. A lead β-lactam analog, CA-432, displayed comparable antiproliferative activities with CA-4. CA-432 induced rapid apoptosis in HL-60 acute myeloid leukemia cells, which was accompanied by depolymerization of the microtubular network, poly(ADP-ribose) polymerase cleavage, caspase-3 activation, and Bcl-2 cleavage. A prolonged G(2)M cell cycle arrest accompanied by a sustained phosphorylation of mitotic spindle checkpoint protein, BubR1, and the antiapoptotic proteins Bcl-2 and Bcl-x(L) preceded apoptotic events in K562 chronic myeloid leukemia (CML) cells. Molecular docking studies in conjunction with comprehensive cell line data rule out CA-4 and β-lactam derivatives as P-glycoprotein substrates. Furthermore, both CA-4 and CA-432 induced significantly more apoptosis compared with imatinib mesylate in ex vivo samples from patients with CML, including those positive for the T315I mutation displaying resistance to imatinib mesylate and dasatinib. In summary, synthetic intrinsically stable analogs of CA-4 that display significant clinical potential as antileukemic agents have been designed and synthesized.

Alterations in beta-catenin expression and localization in prostate cancer

BACKGROUND: Wnt signaling is thought to be important in prostate cancer, in part because proteins such as beta-catenin can also affect androgen receptor signaling. beta-Catenin forms a cell adhesion complex with E-cadherin raising the possibility that loss of expression or a change in beta-catenin distribution in the cell could also alter downstream signaling, decreased inter-cellular adhesion and the promotion of metastasis. A number of studies have reported the altered expression and/or localization of beta-catenin as a biomarker in prostate cancer.

METHODS: Tissue microarrays comprised of BPH and low, moderate and high-grade prostate cancer (n=77) were assessed for beta-catenin expression and distribution using immunohistochemistry. Staining was also performed on a tissue microarray containing tissue from patients before and after hormone manipulation. The effects of fixation and different antibodies was assessed on fixed LNCaP cell pellets and small prostate tissue microarrays.

RESULTS: We have observed increased beta-catenin expression in only high Gleason score (>7) prostate cancer. A nuclear re-distribution of beta-catenin has previously been reported. We noted nuclear beta-catenin in benign prostatic hyperplasia and a gradual loss in nuclear distribution with increasing Gleason grade. We found no evidence for an alteration in beta-catenin expression or re-distribution with hormone ablation. Altered fixation, antibodies and antibody concentration did affect the intensity and specificity of staining.

CONCLUSIONS: A loss of nuclear beta-catenin is the most consistent feature in prostate cancer rather than absolute levels of expression. We also suggest that variation in immunohistochemical protocols may explain variations in the reported literature.