L'article propose une première approche systématique de la tradition manuscrite du Liber de causis, en étudiant à la fois les variantes manuscrites et les difficultés doctrinales suscitées par la translittération de l'arabe al-ʿaql conservée dans la traduction latine. Certains médiévaux (tel Albert le Grand) l'entendent comme un concept sans équivalent en latin, forgé par des philosophes arabes dont on ignore tout. D'autres médiévaux (tels Thomas d'Aquin et Gilles de Rome), qui ont probablement connu une branche différente de la tradition manuscrite du Liber de causis, n'en font aucune mention. En examinant cent dix manuscrits latins du Liber de causis (sur deux cent soixantecinq actuellement connus), on constate de nombreuses variations tant pour la présence de cette translittération dans les propositions du texte que pour les formes et les graphies (alatyr, alachili, adlahic, etc.). Cette analyse permet de comprendre tant la position d'Albert que la grande diversité, jusqu’à présent insoupçonnée, de la transmission du Liber de causis dans le monde latin.

We prove a quantitative partial result in support of the dynamical Mordell–Lang conjecture (also known as the DML conjecture) in positive characteristic. More precisely, we show the following: given a field K of characteristic p, a semiabelian variety X defined over a finite subfield of K and endowed with a regular self-map $\Phi :X{\longrightarrow } X$ defined over K, a point $\alpha \in X(K)$ and a subvariety $V\subseteq X$, then the set of all nonnegative integers n such that $\Phi ^n(\alpha )\in V(K)$ is a union of finitely many arithmetic progressions along with a subset S with the property that there exists a positive real number A (depending only on X, $\Phi $, $\alpha $ and V) such that for each positive integer M,

$$\begin{align*}\scriptsize\#\{n\in S\colon n\le M\}\le A\cdot (1+\log M)^{\dim V}.\end{align*}$$

The field of electrophysiology (EP) in paediatric cardiology patients and adults with congenital heart disease is complex and rapidly growing. The current recommendations for diagnostic and invasive electrophysiology of the working group for Cardiac Dysrhythmias and Electrophysiology of the Association for European Paediatric and Congenital Cardiology acknowledges the diveristy of European countries and centers. These training recommendations can be fulfilled in a manageable period of time, without compromising the quality of training required to become an expert in the field of paediatric and congenital EP and are for trainees undergoing or having completed accredited paediatric cardiologist fellowship. Three levels of expertise, the training for General paediatric cardiology EP, for non-invasive EP and invasive EP have been defined. This Association for European EP curriculum describes the theoretical and practicsal knowledge in clinical EP; catheter ablation, cardiac implantable electronic devices, inherited arrhythmias and arrhythmias in adults with congenital heart defects for the 3 levels of expertise.

We provide a direct proof of a Bogomolov-type statement for affine varieties V defined over function fields K of finite transcendence degree over an arbitrary field k, generalising a previous result (obtained through a different approach) of the first author in the special case when K is a function field of transcendence degree $1$ . Furthermore, we obtain sharp lower bounds for the Weil height of the points in $V(\overline {K})$ , which are not contained in the largest subvariety $W\subseteq V$ defined over the constant field $\overline {k}$ .

We formulate a general question regarding the size of the iterated Galois groups associated with an algebraic dynamical system and then we discuss some special cases of our question. Our main result answers this question for certain split polynomial maps whose coordinates are unicritical polynomials.

We advance a new conjecture in the spirit of the dynamical Manin–Mumford conjecture. We show that our conjecture holds for all polarisable endomorphisms of abelian varieties and for all polarisable endomorphisms of $(\mathbb{P}^{1})^{N}$. Furthermore, we show various examples which highlight the restrictions one would need to consider in formulating any general conclusion in the dynamical Manin–Mumford conjecture.

We recently reported an association between TAAR6 (trace amine associated receptor 6 gene) variations and schizophrenia (SZ). We now report an association of a set of TAAR6 variations and clinical presentation and outcome in a sample of 240 SZ Korean patients. Patients were selected by a Structured Clinical Interview, DSM-IV Axis I disorders – Clinical Version (SCID-CV). Other psychiatric or neurologic disorders, as well as medical diseases, were exclusion criteria. To assess symptom severity, patients were administered the CGI scale and the PANSS at baseline and at the moment of discharge, 1 month later on average. TAAR6 variations rs6903874, rs7452939, rs8192625 and rs4305745 were investigated; rs6903874, rs7452939 and rs8192625 entered the statistical investigation after LD analysis. Rs8192625 G/G homozygosis was found to be significantly associated both with a worse clinical presentation at PANSS total and positive scores and with a shorter period of illness before hospitalization. No haplotype significant findings were found. The present study stands for a role of the TAAR6 in the clinical presentation of SZ. Moreover, our results show that this genetic effect may be counteracted by a correct treatment. Haplotype analysis was not informative in our sample, probably also because of the incomplete SNPs' coverage of the gene we performed. Further studies in this direction are warranted.

We previously reported an association of Dysbindin gene (DTNBP1) variants with Bipolar Disorder I (BPI) patients (Pae, C. U., A. Serretti, et al. (2006)). This paper extends previous results investigating the possible role of DTNBP1 variants on response to acute mood stabilizer treatment. Moreover, we recently reported positive association results of heat-shock -70 family proteins (HSP70) and genetic variations and antidepressant response (Pae, C. U., A. Serretti, et al. (2007)). Since evidence stands for a possible involvement of chaperone activity in Bipolar Disorder pathophysiology, a pharmacogenetic approach was used to investigate the role of HSP70 on acute antimanic effect. A sample of 45 BPI were treated for an average of 36.52 (±19.87) days with mood stabilizers (lithium, valproate, carbamazepine), evaluated using the Clinical Global Impression (CGI) scale and the Young Mania Rating Scale (YMRS) and genotyped for their DTNBP1 variants (rs3213207 A/G, rs1011313 C/T, rs2005976 G/A, rs760761 C/T and rs2619522 A/C) and HSP70 variants (rs2227956 C/T, rs2075799 A/G, rs1043618 C/G, rs562047 C/G, rs539689 C/G). No association was found between the investigated variations and response to mood stabilizer treatment even considering possible stratification factors. The small number of subjects is an important limitation to our study, nonetheless, Dysbindin and HSP 70 seem not to be involved in acute antimanic efficacy.

In the last few years, we conducted a number of molecular pathway analyses on the genetic samples provided by the NIMH. The molecular pathway approach accounts for the polygenic nature of the most part of psychiatric disorders. Nevertheless, the limits of this approach including the limited knowledge about the function of the genes, the fact that longer genes have higher probability to harbour variations significantly associated with the phenotype under analysis and the false positive associations for single variations, demand statistical control and bio-statistical knowledge. Permutations are a methodology to control for false positive associations, but their implementation requires that a number of criteria are taken into account: 1) the same number of genes and the same number of variations of the index pathway must be simulated in order to limit the bias of selecting significantly longer or shorter genes; 2) a sufficient number of permutated pathways is created (10E5 to 10E6 depending on computational resources) which demands higher computational power; 3) the correct statistical thresholds are identified and discussed; 4) some pathways might be over-represented and the source of information must be constantly updated. The tools for running a molecular pathway analysis (R Foundation for Statistical Computing, 2013) when interacting with a supercluster PC and the international bioinformatic datasets (Embase, NIMH and others), together with the critical steps of bioinformatics scripting (bash language) are described and discussed.