Using complementary techniques to distinguish cryptic species: A new Erysimum (Brassicaceae) species from North Africa

• Premise of the study : Cryptic species are superfi cially morphologically indistinguishable and therefore erroneously classifi ed under one single name. The identifi cation and delimitation of these species is usually a diffi cult task. The main aim of this study is to provide an inclusive methodology that combines standard and new tools to allow accurate identifi cation of cryptic species. We used Erysimum nervosum s.l. as a model system. • Methods : Four populations belonging to E. nervosum s.l. were sampled at their two distribution ranges in Morocco (the Atlas Mountains and the Rif Mountains). Fifteen individuals per population were collected to assess standard taxonomic traits. Additionally, corolla color and shape were quantifi ed in 30 individuals per population using spectrophotometry and geometric morphometrics, respectively. Finally, we collected tissue samples from each population per species to study the phylogenetic relationships among them. • Key results : Using the standard taxonomic traits, we could not distinguish the four populations. Nonetheless, there were differences in corolla color and shape between plants from the two mountain ranges. The population differentiation based on quantitative morphological differences were confi rmed and supported by the phylogenetic relationships obtained for these populations and the rest of the Moroccan Erysimum species. • Conclusions : The joint use of the results obtained from standard taxonomic traits, quantitative analyses of plant phenotype, and molecular data suggests the occurrence of two species within E. nervosum s.l. in Morocco, one located in the Atlas Mountains ( E. nervosum s.s.) and the other in the Rif Mountains ( E. riphaeanum sp. nov.). Consequently, we suggest that combining quantitative and molecular approaches with standard taxonomy greatly benefi ts the identifi cation of cryptic species

Conservation assessments and Red Listing of the endemic Moroccan flora (monocotyledons)

Morocco constitutes an important centre of plant diversity and speciation in the Mediterranean Basin. However, numerous species are threatened by issues ranging from human activities to global climatic change. In this study, we present the conservation assessments and Red Listing of the endemic Moroccan monocotyledons according to International Union for Conservation of Nature (IUCN) criteria and categories. For each species, we include basic taxonomic information, local names and synonyms, uses, a distribution map, extent of occurrence, area of occupancy, population size and trend, a description of habitats and ecological requirements, and a discussion of the threats affecting the species and habitats. We assessed the threatened status of the endemic Moroccan monocotyledons at the species level (59 species) using the IUCN Red List criteria and categories (Version 3.1). This study shows the high extinction risk to the Moroccan monocotyledon flora, with 95% of threatened species (20% Critically Endangered, 50% Endangered, 25% Vulnerable) and only 5% not threatened (2% Near Threatened and 3% Least Concern). The flora is thus of conservation concern, which is poorly recognized, both nationally and internationally. The study presents the first part and so far the only national IUCN Red Data List for a large group of Moroccan plants, and thus provides an overview of the threatened Moroccan flora. This IUCN Red List is an important first step towards the recognition of the danger to Moroccan biodiversity hotspots, conservation of threatened species and the raising of public awareness at national and international levels

Biological flora of Central europe: Baldellia ranunculoides (Alismataceae)

Baldellia ranunculoides (L.) Parl. (Alismataceae) is a taxonomically problematic aquatic plant with an historically ill-defined distribution and global conservation status. This paper finds morphological, ecological and molecular evidence for two distinct taxa, probably best described as subspecies: (1) B. ranunculoides subsp. ranunculoides and (2) B. ranunculoides subsp. repens and provides detailed distribution data on their overlapping range, in different habitats, across the cool, high rainfall areas of western Europe and west Mediterranean. The two subspecies are amongst the relatively large number of threatened European and north Africa aquatic plants and this paper provides a systematic review of their relative conservation pressures and management needs, with particular emphasis on the status of both taxa in central Europe. Other observations indicate probable evolutionary relationships within B. ranunculoides s.l. and its associated taxa and the review points out where these and other research topics could potentially be pursued

Vieux arbres remarquables du Maroc

Jahandiez Émile. Vieux arbres remarquables du Maroc. In: La Terre et La Vie, Revue d'Histoire naturelle, tome 3, n°4, 1933. pp. 207-213

Caractères botaniques des Acacia dealbata, decurrens et mollissima.

Jahandiez Émile. Caractères botaniques des Acacia dealbata, decurrens et mollissima.. In: Revue de botanique appliquée et d'agriculture coloniale, 4ᵉ année, bulletin n°31, 31 mars 1924. pp. 179-181

Therapeutic hypothermia and mitochondrial permeability transition in the post-cardiac arrest syndrome

L’arrêt cardiaque (AC) est un problème de santé publique dont la mortalité reste très élevée malgré les progrès de la réanimation. La majorité des décès à distance de la réanimation cardio-pulmonaire (RCP) initiale est la conséquence du syndrome post‑AC provoqué par les lésions cellulaires d'ischémie-reperfusion (I/R) qui touchent principalement le cœur et le cerveau. L’ouverture du pore de transition de perméabilité mitochondrial (PTP), en lien avec la cyclophiline D (CypD), est un déterminant majeur des lésions d'I/R. L’hypothermie thérapeutique est le seul traitement adjuvant de la RCP qui a démontré un bénéfice sur la survie des patients en limitant le syndrome post-AC. Ses mécanismes d’action complexes ne sont que partiellement compris. Dans ce travail de thèse, nous avons, dans un premier temps, utilisé notre modèle d'AC chez le lapin pour étudier les mécanismes mitochondriaux de l’hypothermie thérapeutique. Notre modèle a d'abord permis de mettre en évidence le rôle important joué par la température dans la gravité du syndrome post‑AC et les effets protecteurs de l’hypothermie sur le cœur et le cerveau. Notre travail montre également que l'hypothermie inhibe l’ouverture du PTP par un mécanisme dépendant de la CypD et agit sur une voie de signalisation cellulaire. Nous avons, dans un second temps, mis au point un nouveau modèle d'AC chez la souris déficiente en CypD montrant que l'inhibition complète du mécanisme dépendant de la CypD d'ouverture du PTP améliore le succès de la RCP ainsi que le pronostic à long terme des animaux traités par hypothermie thérapeutique. Ainsi, nos travaux contribuent à identifier les mécanismes d'action mitochondriaux de l’hypothermie thérapeutique ainsi que des pistes pour améliorer le pronostic des patients après un AC réaniméDespite advances in resuscitation science, mortality after cardiac arrest (CA) remains very high. A substantial proportion of cardiac arrest deaths occur in patients following successful resuscitation and can be attributed to the development of post-CA syndrome caused by cellular ischemia-reperfusion (I/R) injury that primarily affect heart and brain cells. The opening of the mitochondrial permeability transition pore (PTP), promoted by cyclophilin D (CypD), is a major determinant of I/R injuries. Therapeutic hypothermia is the only adjuvant therapy to cardiopulmonary resuscitation (CPR) known to improve survival by limiting the post-AC syndrome. The mechanisms of action of therapeutic hypothermia are still poorly understood. In this present work, we used our model of CA in rabbit to study the role of the PTP in the mechanisms of action of therapeutic hypothermia. Our model first highlighted the important role played by temperature in the severity of post-AC syndrome and the protective effects of hypothermia on heart and brain injuries. Our work also determined that hypothermia inhibited PTP opening by a CypD-dependent mechanism and acted on a pro-survival signaling pathway. We then developed a new CA model using CypD-deficient mice showing that complete inhibition of the CypD-dependent mechanism of PTP opening improved success of CPR and long-term survival of hypothermia-treated animals. Thus, our work contributes to identifying the mitochondrial mechanisms of action of therapeutic hypothermia and ways to improve the prognosis of patients after C

Hypothermie thérapeutique et transition de perméabilité mitochondriale dans le syndrome post-arrêt cardiaque

Despite advances in resuscitation science, mortality after cardiac arrest (CA) remains very high. A substantial proportion of cardiac arrest deaths occur in patients following successful resuscitation and can be attributed to the development of post-CA syndrome caused by cellular ischemia-reperfusion (I/R) injury that primarily affect heart and brain cells. The opening of the mitochondrial permeability transition pore (PTP), promoted by cyclophilin D (CypD), is a major determinant of I/R injuries. Therapeutic hypothermia is the only adjuvant therapy to cardiopulmonary resuscitation (CPR) known to improve survival by limiting the post-AC syndrome. The mechanisms of action of therapeutic hypothermia are still poorly understood. In this present work, we used our model of CA in rabbit to study the role of the PTP in the mechanisms of action of therapeutic hypothermia. Our model first highlighted the important role played by temperature in the severity of post-AC syndrome and the protective effects of hypothermia on heart and brain injuries. Our work also determined that hypothermia inhibited PTP opening by a CypD-dependent mechanism and acted on a pro-survival signaling pathway. We then developed a new CA model using CypD-deficient mice showing that complete inhibition of the CypD-dependent mechanism of PTP opening improved success of CPR and long-term survival of hypothermia-treated animals. Thus, our work contributes to identifying the mitochondrial mechanisms of action of therapeutic hypothermia and ways to improve the prognosis of patients after CAL’arrêt cardiaque (AC) est un problème de santé publique dont la mortalité reste très élevée malgré les progrès de la réanimation. La majorité des décès à distance de la réanimation cardio-pulmonaire (RCP) initiale est la conséquence du syndrome post‑AC provoqué par les lésions cellulaires d'ischémie-reperfusion (I/R) qui touchent principalement le cœur et le cerveau. L’ouverture du pore de transition de perméabilité mitochondrial (PTP), en lien avec la cyclophiline D (CypD), est un déterminant majeur des lésions d'I/R. L’hypothermie thérapeutique est le seul traitement adjuvant de la RCP qui a démontré un bénéfice sur la survie des patients en limitant le syndrome post-AC. Ses mécanismes d’action complexes ne sont que partiellement compris. Dans ce travail de thèse, nous avons, dans un premier temps, utilisé notre modèle d'AC chez le lapin pour étudier les mécanismes mitochondriaux de l’hypothermie thérapeutique. Notre modèle a d'abord permis de mettre en évidence le rôle important joué par la température dans la gravité du syndrome post‑AC et les effets protecteurs de l’hypothermie sur le cœur et le cerveau. Notre travail montre également que l'hypothermie inhibe l’ouverture du PTP par un mécanisme dépendant de la CypD et agit sur une voie de signalisation cellulaire. Nous avons, dans un second temps, mis au point un nouveau modèle d'AC chez la souris déficiente en CypD montrant que l'inhibition complète du mécanisme dépendant de la CypD d'ouverture du PTP améliore le succès de la RCP ainsi que le pronostic à long terme des animaux traités par hypothermie thérapeutique. Ainsi, nos travaux contribuent à identifier les mécanismes d'action mitochondriaux de l’hypothermie thérapeutique ainsi que des pistes pour améliorer le pronostic des patients après un AC réanim

Notice sur Abel Albert

Volume: 56Start Page: 450End Page: 45