L’Évolution biologique, un superbe bricolage

Quand François Jacob (prix Nobel de médecine 1965) s’inspire pour la biologie de la notion de « bricolage » développée par Claude Lévi-Strauss en anthropologie dans La Pensée sauvage (1962) … ou la rencontre de deux géants. Dans ce texte mêlant épistémologie et théorie de l’évolution, F. Jacob émet l’idée que la connaissance scientifique est faite de milliers d’observations parcellaires qui convergent pour être à l’origine d’une découverte ou d’une innovation, tout comme le fait l’évolution biologique pour aboutir à un nouveau trait ou à une nouvelle espèce vivante. Il donne à cet égard l’exemple tout à fait éclairant de la formation progressive (et bricolée ?) du globe oculaire chez les animaux

Le désastre écologique selon… Saint François d’Assise

Ce texte de 1967 du médiéviste américain, volontiers provocateur, rend la civilisation chrétienne responsable du désastre écologique actuel (déjà perceptible… il y a 50 ans). Il nous paraît important de le présenter ici, sous la plume elle aussi acérée du biologiste B. Swynghedauw

Genomics in cardiac metabolism

Cell biology is in transition from reductionism to a more integrated science. Large-scale analysis of genome structure, gene expression, and metabolites are new technologies available for studying cardiac metabolism in diseases known to modify cardiac function. These technologies have several limitations and this review aims both to assess and take a critical look at some important results obtained in genomics restricted to molecular genetics, transcriptomics and metabolomics of cardiac metabolism in pathophysiological processes known to alter myocardial function. Therefore, our goal was to delineate new signalling pathways and new areas of research from the vast amount of data already published on genomics as applied to cardiac metabolism in diseases such as coronary heart disease, heart failure, and ischaemic reperfusio

Statistical Modelling of Cardiovascular Data. An Introduction to Linear Mixed Models

Most of statistical approaches in cardiovascular research were based on variance analysis (ANOVA). However, most of the time, the assumption that data are independent is violated since several measures are performed on the same subject (repeated measures). In addition, the presence of intra- and inter-observers variability can potentially obscure significant differences. The linear mixed model (LMM) is an extended multivariate linear regression method of analysis that accounts for both fixed and random effects. LMM allows for addressing incomplete design cases. In this paper, LMM was applied to two sets of cardiovascular research data and compared to ANOVA. The first example is an analysis of heart rate in mice after atropine and propranolol injections. LMM shows an important mouse random effects that depends on pharmacological treatment and provides with accurate estimates for each significant experimental factors. When randomly suppressing observations from the data sets (20-30%) the time factor of Anova model becomes non significant while LMM still remains significant. The second example is the analysis of isolated coronary-perfused pressure of transgenic mice hearts. LMM evidenced a significant transgenic effect in both male and female animals, while, with ANOVA, the transgenic effects was limited to male mice only. In both cases, as compared to ANOVA, the LMM separately accounts for fixed and random effects, allowing thus for studying more adequately incomplete designs on repeated measures

Le myocyte cardiaque adulte peut-il encore proliférer ?

À l’inverse des cellules non musculaires (cellules vasculaires, endothéliales et musculaires lisses, présentes dans la circulation coronaire, fibroblastes en charge du réseau de collagène assurant un rôle de soutien majeur pour coordonner les éléments contractiles), les cellules musculaires cardiaques adultes sont dans un stade postmitotique. En dépit de différentes annonces, ce « dogme », ancien, ne semble pas sérieusement ébranlé. Mais on peut noter au stade terminal de l’insuffisance cardiaque l’apparition de nouvelles cellules aussi bien de type endothélial que myocytaire. Cette régénération trouve son origine soit dans des cellules souches préexistantes, soit dans des cellules progénitrices circulantes provenant de la moelle osseuse ou de l’endothélium vasculaire. Ces dernières colonisent les organes transplantés, au sein desquels on peut les voir former des chimères. Ce processus adaptatif peut être complété en injectant dans le myocarde, ou dans la circulation coronaire, divers types de cellules. Deux types sont surtout utilisés, les cellules de la moelle osseuse et les myoblastes (ou cellules satellites) du muscle squelettique. Les premières applications cliniques après infarctus du myocarde ont montré la faisabilité de la technique et les possibilités d’amélioration de la fonction contractile cardiaque.Adult cardiac myocytes do not divide anymore. Mechanically overloaded hearts undergo hypertrophy and then fail. Cardiac hypertrophy is mainly caused by myocyte hypertrophy without myocyte proliferation, except during end-stage heart failure. By contrast, non muscular myocardial cells, such as the endothelial cells of the vessels, not only hypertrophy but are also able to proliferate. Recent works have suggested that these new cells are likely to be progenitor cells originating from bone marrow or vascular endothelium. These cells may form chimeras in the donor heart following heart transplantation. It is possible to mimic such an adaptative process by injecting progenitor cells either within the myocardium, or through the coronary circulation. Two type of cells have been utilised so far, namely bone marrow cells and myoblasts (or satellite cells) from skeletal muscles. The first clinical applications after myocardial infarction have been recently reported and showed the safety of the procedure and the possibility of improving myocardial function

Heart Failure Reviews Darwinian evolution and cardiovascular remodeling

International audienceMechanotransduction, MT, is an ancient evolutionary legacy existing in every living species and involving complex rearrangements of multiple proteins in response to a mechanical stress. MT includes three different interrelated processes: mechanosensation, mechanotransmission, and mechanoresponse. Each process is specifically adapted to a given tissue and stress. Both cardiac and arterial remodeling involve MT. Physiological or pathological cardiac remodeling, CR, is firstly a beneficial mechanoresponse, MR, which allows the heart to recover to a normal economy, better adapted to the new working conditions. Nevertheless, exercise-induced cardiac remodeling is more a coming-back to normal conditions than a superimposed event. On the longer term, the MR creates fibrosis which accounts, in part, for the reduced cardiac output in the CR. In the hypertension-induced arterial remodeling, arterial MR allows the vessels to maintain a normal circumferential constraint before an augmented arterial pressure. In atherogenesis: (i) The presence of atheroma in several animal species and atherosclerosis in ancient civilizations suggests more basic predispositions. (ii) The atherosclerotic plaques preferably develop at predictable arterial sites of disturbed blood flow showing that MT is involved in the initial steps of atherogenesis