Ultrafast Delamination of Graphite into High-Quality Graphene Using Alternating Currents

To bridge the gap between laboratory‐scale studies and commercial applications, mass production of high quality graphene is essential. A scalable exfoliation strategy towards the production of graphene sheets is presented that has excellent yield (ca. 75 %, 1–3 layers), low defect density (a C/O ratio of 21.2), great solution‐processability, and outstanding electronic properties (a hole mobility of 430 cm2 V−1 s−1). By applying alternating currents, dual exfoliation at both graphite electrodes enables a high production rate exceeding 20 g h−1 in laboratory tests. As a cathode material for lithium storage, graphene‐wrapped LiFePO4 particles deliver a high capacity of 167 mAh g−1 at 1 C rate after 500 cycles

Ecophysiology of syntrophic communities that degrade saturated and unsaturated long-chain fatty acids

Syntrophic relationships are the key for biodegradation in methanogenic environments. We review the ecological and physiological features of syntrophic communities involved in the degradation of saturated and unsaturated long-chain fatty acids (LCFA), as well as their potential application to convert lipids/fats containing waste to biogas. Presently, about 14 species have been described with the ability to grow on fatty acids in syntrophy with methanogens, all belonging to the families Syntrophomonadaceae and Syntrophaceae. The principle pathway of LCFA degradation is through β-oxidation, but the initial steps in the conversion of unsaturated LCFA are unclear. Communities enriched on unsaturated LCFA also degrade saturated LCFA, but the opposite generally is not the case. For efficient methane formation, the physical and inhibitory effects of LCFA on methanogenesis need to be considered. LCFA adsorbs strongly to biomass, which causes encapsulation of active syntrophic communities and hampers diffusion of substrate and products in and out of the biomass. Quantification of archaea by real-time PCR analysis suggests that potential LCFA inhibitory effect towards methanogens might be reversible. Rather, the conversion of adsorbed LCFA in batch assays was shown to result in a significant increase of archaeal cell numbers in anaerobic sludge samples.The authors thank J. Prosser for the invitation to write this minireview. We appreciated the critical reading of I.M. Head and of the anonymous reviewers, and we thank them for their constructive comments and suggestions. This work was possible through the financial support provided by the Portuguese Science Foundation (FCT) and European Social Fund (ESF) (grant SFRH/BD/8726/2002), and by the Wageningen Institute for Environmental and Climate Research (WIMEK)

Protocol of a prospective study on the diagnostic value of transcranial duplex scanning of the substantia nigra in patients with parkinsonian symptoms

<p>Abstract</p> <p>Background</p> <p>Parkinson's disease (PD) is the second most common neurodegenerative disorder. As there is no definitive diagnostic test, its diagnosis is based on clinical criteria. Recently transcranial duplex scanning (TCD) of the substantia nigra in the brainstem has been proposed as an instrument to diagnose PD. We and others have found that TCD scanning of substantia nigra duplex is a relatively accurate diagnostic instrument in patients with parkinsonian symptoms. However, all studies on TCD so far have involved well-defined, later-stage PD patients, which will obviously lead to an overestimate of the diagnostic accuracy of TCD.</p> <p>We have therefore set out to conduct a prospective study testing the diagnostic accuracy of TCD in patients with a parkinsonism of unclear origin.</p> <p>Methods/Design</p> <p>We will enrol 250 consecutive patients, who are referred to neurology outpatient clinics of two teaching hospitals, for analysis of clinically unclear parkinsonism. Patients, whose parkinsonism is clearly diagnosable at the first visit, will be excluded from the study. All patients will undergo a TCD of the substantia nigra. As a surrogate gold standard we will use the consensus clinical diagnosis reached by two independent, blinded, movement disorder specialist neurologists after 2 years follow-up. At the time of TCD, patients will also undergo a SPECT scan of the brain.</p> <p>Discussion</p> <p>As this prospective trial enrols only patients with an early-stage parkinsonism, it will yield data on the diagnostic accuracy of TCD that is relevant to daily clinical practice: The neurologist needs a diagnostic tool that provides additional information in patients with a clinically indefinable parkinsonian syndrome. The above described observational longitudinal study was designed to explicitly study this aspect in the diagnostic process.</p> <p>Trial registration</p> <p><b>(ITRSCC) NCT00368199</b></p

Human Bone Marrow Mesenchymal Stem Cells Display Anti-Cancer Activity in SCID Mice Bearing Disseminated Non-Hodgkin's Lymphoma Xenografts

Abstract BACKGROUND: Although multimodality treatment can induce high rate of remission in many subtypes of non-Hodgkin's lymphoma (NHL), significant proportions of patients relapse with incurable disease. The effect of human bone marrow (BM) mesenchymal stem cells (MSC) on tumor cell growth is controversial, and no specific information is available on the effect of BM-MSC on NHL. METHODOLOGY/PRINCIPAL FINDINGS: The effect of BM-MSC was analyzed in two in vivo models of disseminated non-Hodgkin's lymphomas with an indolent (EBV(-) Burkitt-type BJAB, median survival = 46 days) and an aggressive (EBV(+) B lymphoblastoid SKW6.4, median survival = 27 days) behavior in nude-SCID mice. Intra-peritoneal (i.p.) injection of MSC (4 days after i.p. injection of lymphoma cells) significantly increased the overall survival at an optimal MSC:lymphoma ratio of 1:10 in both xenograft models (BJAB+MSC, median survival = 58.5 days; SKW6.4+MSC, median survival = 40 days). Upon MSC injection, i.p. tumor masses developed more slowly and, at the histopathological observation, exhibited a massive stromal infiltration coupled to extensive intra-tumor necrosis. In in vitro experiments, we found that: i) MSC/lymphoma co-cultures modestly affected lymphoma cell survival and were characterized by increased release of pro-angiogenic cytokines with respect to the MSC, or lymphoma, cultures; ii) MSC induce the migration of endothelial cells in transwell assays, but promoted endothelial cell apoptosis in direct MSC/endothelial cell co-cultures. CONCLUSIONS/SIGNIFICANCE: Our data demonstrate that BM-MSC exhibit anti-lymphoma activity in two distinct xenograft SCID mouse models of disseminated NHL

Analysis of shared heritability in common disorders of the brain

ience, this issue p. eaap8757 Structured Abstract INTRODUCTION Brain disorders may exhibit shared symptoms and substantial epidemiological comorbidity, inciting debate about their etiologic overlap. However, detailed study of phenotypes with different ages of onset, severity, and presentation poses a considerable challenge. Recently developed heritability methods allow us to accurately measure correlation of genome-wide common variant risk between two phenotypes from pools of different individuals and assess how connected they, or at least their genetic risks, are on the genomic level. We used genome-wide association data for 265,218 patients and 784,643 control participants, as well as 17 phenotypes from a total of 1,191,588 individuals, to quantify the degree of overlap for genetic risk factors of 25 common brain disorders. RATIONALE Over the past century, the classification of brain disorders has evolved to reflect the medical and scientific communities' assessments of the presumed root causes of clinical phenomena such as behavioral change, loss of motor function, or alterations of consciousness. Directly observable phenomena (such as the presence of emboli, protein tangles, or unusual electrical activity patterns) generally define and separate neurological disorders from psychiatric disorders. Understanding the genetic underpinnings and categorical distinctions for brain disorders and related phenotypes may inform the search for their biological mechanisms. RESULTS Common variant risk for psychiatric disorders was shown to correlate significantly, especially among attention deficit hyperactivity disorder (ADHD), bipolar disorder, major depressive disorder (MDD), and schizophrenia. By contrast, neurological disorders appear more distinct from one another and from the psychiatric disorders, except for migraine, which was significantly correlated to ADHD, MDD, and Tourette syndrome. We demonstrate that, in the general population, the personality trait neuroticism is significantly correlated with almost every psychiatric disorder and migraine. We also identify significant genetic sharing between disorders and early life cognitive measures (e.g., years of education and college attainment) in the general population, demonstrating positive correlation with several psychiatric disorders (e.g., anorexia nervosa and bipolar disorder) and negative correlation with several neurological phenotypes (e.g., Alzheimer's disease and ischemic stroke), even though the latter are considered to result from specific processes that occur later in life. Extensive simulations were also performed to inform how statistical power, diagnostic misclassification, and phenotypic heterogeneity influence genetic correlations. CONCLUSION The high degree of genetic correlation among many of the psychiatric disorders adds further evidence that their current clinical boundaries do not reflect distinct underlying pathogenic processes, at least on the genetic level. This suggests a deeply interconnected nature for psychiatric disorders, in contrast to neurological disorders, and underscores the need to refine psychiatric diagnostics. Genetically informed analyses may provide important "scaffolding" to support such restructuring of psychiatric nosology, which likely requires incorporating many levels of information. By contrast, we find limited evidence for widespread common genetic risk sharing among neurological disorders or across neurological and psychiatric disorders. We show that both psychiatric and neurological disorders have robust correlations with cognitive and personality measures. Further study is needed to evaluate whether overlapping genetic contributions to psychiatric pathology may influence treatment choices. Ultimately, such developments may pave the way toward reduced heterogeneity and improved diagnosis and treatment of psychiatric disorders

Le voyage d'Urbain II en France

Se rendant en France en août 1095, Urbain II voulut certes y déclencher une entreprise militaire de grande envergure pour la libération des chrétiens d'Orient et de la Terre sainte. Mais ce qui devint, depuis le concile de Clermont (en nov. 1095), la croisade, ne fut pas le seul but du voyage pontifical, comme le prouvent itinéraire et activités du pape en France pendant toute une année (août 1095-août 1096). Accompagné d'une suite considérable, dont une curie et une chancellerie réduites mais efficaces, il parcourt une vaste partie du royaume (Midi, Centre, Ouest), -à l'exception du domaine royal. Il préside des conciles (Clermont, Tours, Nîmes), consacre cathédrales, basiliques et autels, et bénit prieurés et chantiers de construction ; il rend la justice, accorde des privilèges, représente l'Église romaine à l'occasion de grandes manifesta¬ tions religieuses et se fait entendre (souvent sans doute en langue fran¬ çaise) par ses prédications publiques. Il rend aussi visibles, et fait accepter dans une large mesure, l'autorité pontificale et la direction de la chrétienté par le pape, il fait progresser la réforme grégorienne, gagne l'obédience définitive de l'Église et du royaume de France à la papauté de la réforme et unit autour de cette pa¬ pauté les forces de la Romania chrétienne pour la croisade.Becker Alfons. Le voyage d'Urbain II en France. In: Le concile de Clermont de 1095 et l’appel à la croisade. Actes du Colloque Universitaire International de Clermont-Ferrand (23-25 juin 1995) Rome : École Française de Rome, 1997. pp. 127-140. (Publications de l'École française de Rome, 236