Oribatid mites show how climate and latitudinal gradients in organic matter can drive large-scale biodiversity patterns of soil communities

Aim: The factors determining spatial distributions and diversity of terrestrial invertebrates are typically investigated at small scales. Large‐scale studies are lacking for soil animals, which control microbial communities and represent one of the most diverse yet poorly known animal assemblages. Here, we analyzed a major group (Oribatida) to test whether belowground macroecological patterns can be predicted by climatic variables, vegetation and large‐scale variation in key soil properties. Location: We modelled the multivariate distribution of more than 100 species using biodiversity data collected across Great Britain in the framework of the Countryside Survey (http://www.countrysidesurvey.org.uk). Methods: We analyzed species‐level data from 582 samples collected across 162 hectads (10 × 10 km) covering the largest possible range of vegetation types, soil properties and climatic conditions within GB. We created the first large‐scale maps of soil animal diversity metrics at the GB scale, including novel estimates of metrics of phylogenetic diversity (PD). Using structural equation modelling, we quantified the direct and indirect effects of location (latitude, longitude), plant community structure and abiotic factors such as precipitation on species composition, richness and PD. Results: We found that variation in species composition follows a latitudinal gradient with diversity generally increasing northward. The latitudinal variation in species composition drives PD via changes in both species richness and phylogenetic distance between species. This gradient is mostly determined by latitudinal variation in precipitation and organic matter, which were very good predictors of species composition. Precipitation and organic matter were, however, relatively weak while statistically significant predictors of diversity metrics. Conclusions: Past studies have emphasized the unpredictability of species distributions and variation in species composition in hyper diverse soil animal communities. However, past studies were conducted at small scales, where stochastic factors may weaken the signal of deterministic factors. Oribatid mites in our study show for the first time that the large scale latitudinal gradients in climate and organic matter predict not only variation in species composition but also taxonomic and PD of soil animal communities

The transcription factor NFATc2 controls IL-6-dependent T cell activation in experimental colitis.

The nuclear factor of activated T cells (NFAT) family of transcription factors controls calcium signaling in T lymphocytes. In this study, we have identified a crucial regulatory role of the transcription factor NFATc2 in T cell-dependent experimental colitis. Similar to ulcerative colitis in humans, the expression of NFATc2 was up-regulated in oxazolone-induced chronic intestinal inflammation. Furthermore, NFATc2 deficiency suppressed colitis induced by oxazolone administration. This finding was associated with enhanced T cell apoptosis in the lamina propria and strikingly reduced production of IL-6, -13, and -17 by mucosal T lymphocytes. Further studies using knockout mice showed that IL-6, rather than IL-23 and -17, are essential for oxazolone colitis induction. Administration of hyper-IL-6 blocked the protective effects of NFATc2 deficiency in experimental colitis, suggesting that IL-6 signal transduction plays a major pathogenic role in vivo. Finally, adoptive transfer of IL-6 and wild-type T cells demonstrated that oxazolone colitis is critically dependent on IL-6 production by T cells. Collectively, these results define a unique regulatory role for NFATc2 in colitis by controlling mucosal T cell activation in an IL-6-dependent manner. NFATc2 in T cells thus emerges as a potentially new therapeutic target for inflammatory bowel diseases

Composite quasiparticle formation and the low-energy effective Hamiltonians of the one- and two-dimensional Hubbard Model

We investigate the effect of hole doping on the strong-coupling Hubbard model at half-filling in spatial dimensions $D\ge 1$. We start with an antiferromagnetic mean-field description of the insulating state, and show that doping creates solitons in the antiferromagnetic background. In one dimension, the soliton is topological, spinless, and decoupled from the background antiferromagnetic fluctuations at low energies. In two dimensions and above, the soliton is non-topological, has spin quantum number 1/2, and is strongly coupled to the antiferromagnetic fluctuations. We derive the effective action governing the quasiparticle motion, study the properties of a single carrier, and comment on a possible description at finite concentration.Comment: REVTEX 3.0, 22 pages with 14 figures in the PostScript format compressed using uufile. Submitted to Phys. Rev. B. The complete PostScript file including figures can be obtained via ftp at ftp://serval.berkeley.edu/hubbard.ps . It is also available via www at http://roemer.fys.ku.dk/recent.ht

Live Imaging at the Onset of Cortical Neurogenesis Reveals Differential Appearance of the Neuronal Phenotype in Apical versus Basal Progenitor Progeny

The neurons of the mammalian brain are generated by progenitors dividing either at the apical surface of the ventricular zone (neuroepithelial and radial glial cells, collectively referred to as apical progenitors) or at its basal side (basal progenitors, also called intermediate progenitors). For apical progenitors, the orientation of the cleavage plane relative to their apical-basal axis is thought to be of critical importance for the fate of the daughter cells. For basal progenitors, the relationship between cell polarity, cleavage plane orientation and the fate of daughter cells is unknown. Here, we have investigated these issues at the very onset of cortical neurogenesis. To directly observe the generation of neurons from apical and basal progenitors, we established a novel transgenic mouse line in which membrane GFP is expressed from the beta-III-tubulin promoter, an early pan-neuronal marker, and crossed this line with a previously described knock-in line in which nuclear GFP is expressed from the Tis21 promoter, a pan-neurogenic progenitor marker. Mitotic Tis21-positive basal progenitors nearly always divided symmetrically, generating two neurons, but, in contrast to symmetrically dividing apical progenitors, lacked apical-basal polarity and showed a nearly randomized cleavage plane orientation. Moreover, the appearance of beta-III-tubulin–driven GFP fluorescence in basal progenitor-derived neurons, in contrast to that in apical progenitor-derived neurons, was so rapid that it suggested the initiation of the neuronal phenotype already in the progenitor. Our observations imply that (i) the loss of apical-basal polarity restricts neuronal progenitors to the symmetric mode of cell division, and that (ii) basal progenitors initiate the expression of neuronal phenotype already before mitosis, in contrast to apical progenitors

The nucleosynthesis of heavy elements in Stars : The key isotope 25Mg

This is an Open Access article distributed under the terms of the Creative Commons Attribution License 2.0, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly citedWe have measured the radiative neutron-capture cross section and the total neutron-induced cross section of one of the most important isotopes for the s process, the 25Mg. The measurements have been carried out at the neutron time-of-flight facilities n-TOF at CERN (Switzerland) and GELINA installed at the EC-JRC-IRMM (Belgium). The cross sections as a function of neutron energy have been measured up to approximately 300 keV, covering the energy region of interest to the s process. The data analysis is ongoing and preliminary results show the potential relevance for the s process.Peer reviewe

Interlayer tunneling in a non-Fermi-liquid metal

We study the effect of interlayer tunneling in the gauge theory describing a quasi-two-dimensional paramagnetic metal close to a second-order or weakly first-order antiferromagnetic phase boundary. In that theory, two species of fermions have opposite (rather than equal) charges with respect to the gauge field. We find that single-particle interlayer tunneling is suppressed at low energies. The effect of pair tunneling is analyzed within the $(3-d)$ expansion. The resulting phase diagram has superconducting and non-Fermi-liquid normal phases, and so is compatible with that of the copper-oxide superconductors.Comment: 13 pages, latex, one uuencoded postscript figur

Drug-induced activation of SREBP-controlled lipogenic gene expression in CNS-related cell lines: Marked differences between various antipsychotic drugs

BACKGROUND: The etiology of schizophrenia is unknown, but neurodevelopmental disturbances, myelin- and oligodendrocyte abnormalities and synaptic dysfunction have been suggested as pathophysiological factors in this severe psychiatric disorder. Cholesterol is an essential component of myelin and has proved important for synapse formation. Recently, we demonstrated that the antipsychotic drugs clozapine and haloperidol stimulate lipogenic gene expression in cultured glioma cells through activation of the sterol regulatory element-binding protein (SREBP) transcription factors. We here compare the action of chlorpromazine, haloperidol, clozapine, olanzapine, risperidone and ziprasidone on SREBP activation and SREBP-controlled gene expression (ACAT2, HMGCR, HMGCS1, FDPS, SC5DL, DHCR7, LDLR, FASN and SCD1) in four CNS-relevant human cell lines. RESULTS: There were marked differences in the ability of the antipsychotic drugs to activate the expression of SREBP target genes, with clozapine and chlorpromazine as the most potent stimulators in a context of therapeutically relevant concentrations. Glial-like cells (GaMg glioma and CCF-STTG1 astrocytoma cell lines) displayed more pronounced drug-induced SREBP activation compared to the response in HCN2 human cortical neurons and SH-SY5Y neuroblastoma cells, indicating that antipsychotic-induced activation of lipogenesis is most prominent in glial cells. CONCLUSION: Our present data show a marked variation in the ability of different antipsychotics to induce SREBP-controlled transcriptional activation of lipogenesis in cultured human CNS-relevant cells. We propose that this effect could be relevant for the therapeutic efficacy of some antipsychotic drugs

Circulating hematopoietic stem cells and putative intestinal stem cells in coeliac disease

Background: The intestinal stem cells (ISC) modulation and the role of circulating hematopoietic stem cells (HSC) in coeliac disease (CD) are poorly understood. Our aim was to investigate the longitudinal modifications in peripheral blood HSC traffic and putative ISC density induced by gluten-free diet (GFD) in CD. Methods: Thirty-one CD patients and 7 controls were enrolled. Circulating CD133+ and CD34+ HSC were measured by flow cytometry, at enrolment and after 7 days and 1, 3, 6, 12, and 24 months of GFD. Endoscopy was performed at diagnosis and repeated at 6, 12, and 24 months following GFD. We used the Marsh-Oberhuber score to evaluate the histological severity of duodenal damage; immunohistochemistry was employed to measure the intraepithelial lymphoid infiltrate (IEL, CD3+ lymphoid cells) and the putative ISC compartment (CD133+ and Lgr5+ epithelial cells). Results: At enrolment, circulating HSCs were significantly increased in CD patients and they further augmented during the first week of GFD, but progressively decreased afterwards. CD patients presented with villous atrophy, abundant IEL and rare ISC residing at the crypt base. Upon GFD, IEL progressively decreased, while ISC density increased, peaking at 12 months. After 24 months of GFD, all patients were asymptomatic and their duodenal mucosa was macroscopically and histologically normal. Conclusions: In active CD patients, the ISC niche is depleted and there is an increased traffic of circulating HSC versus non-coeliac subjects. GFD induces a precocious mobilization of circulating HSC, which is followed by the expansion of the local ISC compartment, leading to mucosal healing and clinical remission

A multi-targeted approach to suppress tumor-promoting inflammation

Cancers harbor significant genetic heterogeneity and patterns of relapse following many therapies are due to evolved resistance to treatment. While efforts have been made to combine targeted therapies, significant levels of toxicity have stymied efforts to effectively treat cancer with multi-drug combinations using currently approved therapeutics. We discuss the relationship between tumor-promoting inflammation and cancer as part of a larger effort to develop a broad-spectrum therapeutic approach aimed at a wide range of targets to address this heterogeneity. Specifically, macrophage migration inhibitory factor, cyclooxygenase-2, transcription factor nuclear factor-κB, tumor necrosis factor alpha, inducible nitric oxide synthase, protein kinase B, and CXC chemokines are reviewed as important antiinflammatory targets while curcumin, resveratrol, epigallocatechin gallate, genistein, lycopene, and anthocyanins are reviewed as low-cost, low toxicity means by which these targets might all be reached simultaneously. Future translational work will need to assess the resulting synergies of rationally designed antiinflammatory mixtures (employing low-toxicity constituents), and then combine this with similar approaches targeting the most important pathways across the range of cancer hallmark phenotypes