Progressive and self-limiting neurodegenerative disorders in Africa: a new prominent field of research led by South Africa but without strong health policy

Introduction: Neurodegenerative disorders are involved in mortality and morbidity of every country. A high prevalence is estimated in Africa. Neurodegenerative disorders are defined by a progressive or self-limiting alteration of neurons implied in specific functional and anatomical functions. It encompasses a various range of clinical disorders from self-limiting to progressive. Focus on public health policies and scientific research is needed to understand the mechanisms to reduce this high prevalence. We use bibliometrics and mapping tools to explore the area studies and countries involved in scientific research on neurodegenerative disorders in Africa. Methods: We used two databases: Web of Science and Pubmed. We analyzed the journals, most cited articles, authors, publication years, organizations, funding agencies, countries and keywords in Web of Science Core collection database and publication years and Medical Subject Headings in Pubmed database. We mapped the data using VOSviewer. Results: We accessed 44 articles published between 1975 and 2014 in Web of Science Core collection Database and 669 from Pubmed database. The majority of which were after 2006. The main countries involved in research on neurodegenerative disorders in Africa the USA, the United Kingdom, France and South Africa representing the main network collaboration. Clinical neurology and Genetics hereditary are the main Web of Science categories whereas Neurosciences and Biochemistry and Molecular Biology are the main Web of Science categories for the general search "neurodegenerative disorders" not restrained to Africa. This is confirmed by Medical Subject Headings analysis from Pubmed with one more area study: Treatment. Conclusion: Neurodegenerative disorders research is leaded by South Africa with a network involving the USA, the UK, as well as African countries such Zambia. The chief field that emerged was on patient and hereditary as well as treatment. Public health policies were lacking fields in research whereas prevalence is estimated to be important in every country. New 17 sustainable development goals of the United Nations could help in this way.Pan African Medical Journal 2016; 2

Mapping South African public health research (1975 - 2014)

Background. Since 1994, South Africa (SA) has faced up to the challenge of building a strong economy, to which public health provides an important underpinning. Objectives. To map the scientific research in public health in SA after the end of apartheid and to present the links between the different financing/funding systems.Methods. Bibliographic analyses utilising the Web of Science of papers published during the period 1975 - 2014, analyses of journals, most cited articles, authors, publication years, organisations, funding agencies, countries and keywords, and mapping of the relations between countries involved in public health research and of the Web of Science Categories using VOSviewer.Results. I accessed 2 246 articles published between 1975 and 2014, the majority of which were published after 2007. The main countries of research were the USA, SA, Switzerland and the UK, representing the main network collaborations. The relevant keywords were HIV, woman, child, program/programme, rural, tuberculosis, district and sex.Conclusions. Public health research in SA reached a high level 16 years after the end of apartheid. The chief field that emerged was the spread of HIV, including mother-to-child transmission, and the policies applied to all districts of SA, through a network of institutions between the USA and SA

Simondon, philosophe du vivant ?

Philosophe de la technique, Gilbert Simondon (1924-1989) a également développé une théorie de l'individuation où le vivant tient une place à part. Le présent ouvrage expose une vision historique et philosophique de la pensée biologique de Simondon. La démonstration est faite qu'un biologiste du vingtième siècle, Etienne Rabaud est la source principale du philosophe. Quelles sont les conséquences sur sa théorie de l'individuation produite durant la seconde moitié du vingtième siècle ? Simondon est-il donc aussi un philosophe du vivant

La portée des travaux de Pierre-Joseph Van Beneden sur le commensalisme : enjeux et perspectives

International audienceCommensalism is a kind of biological association between two different species. One species gets an advantage whereas the other one gets no advantage neither disadvantage. Interpreting observations in marine zoology, Pierre-Joseph Van Beneden (1809-1894) will theorize this concept at the end of the 1860's. The impact of the works of Van Beneden on commensalism will be amazing, not only in his proper career, but also according to his peers. This historical argument is clearly a deciding factor. It will make durable the concept of commensalism during the following century. Also this concept will be spread to other fields than zoology, particularly ecology. This article puts forward the arguments of the impact of the works of Van Beneden on commensalism in order to deduce the outlook.Le commensalisme est une association biologique entre deux espèces différentes où l'une des deux, le commensal obtient un bénéfice, alors que l'autre, l'hôte, n'obtient ni bénéfice, ni désavantage. Issu d'observations en zoologie marine, Pierre-Joseph Van Beneden (1809-1894) va théoriser ce concept dès la fin des années 1860. La portée de ses travaux sur le commensalisme sera considérable, non seulement au sein de sa propre carrière scientifique, mais aussi selon ses pairs. Cet argument historique est l'un des arguments majeurs qui va permettre de pérenniser le concept de commensalisme durant le siècle suivant. De même, l'emploi de ce concept sera étendu au-delà de la discipline initiale, en particulier en écologie. Cet article se propose d'argumenter la portée des travaux de Van Beneden sur le commensalisme afin d'en déduire les enjeux et les perspectives en prenant un exemple précis

Editorial

International audienc

Commensalisme, mutualisme, parasitisme, une preuve de l'Evolution pour Etienne Rabaud

International audienc

Rôle de la huntingtine dans le muscle

Huntington Disease (HD) is a rare multisystemic neurodegenerative genetic disorder, which combines psychiatric, cognitive and motor alterations. It is caused by an increase in CAG repeats in the huntingtin gene, resulting in an expansion of polyglutamine stretch in the protein. This induced a loss of the huntingtin protein (HTT) normal function associated with production of a mutant protein. HTT is an ubiquitous microtubules associated protein, with numerous functions among which vesicles and organelles traffic along microtubules. Along this line, one of its functions could be the traffic of reticulum vesicles to form contact point with the plasma membrane in neurons. Moreover, a phenocopy named Huntington’s disease like 2 is due to junctophilin-3 loss of function. Junctophilin 3 is involved in contact points between endoplasmic reticulum and plasma membrane in neurons. These studies are dedicated to the validation of the hypothesis of the role of HTT in contact points between endoplasmic reticulum and plasma membrane in another model, in which contacts between reticulum and plasma membrane are of major importance: the skeletal muscle cell. Indeed, the contact points between sarcoplasmic reticulum and plasma membrane (T-Tubule), called the triads, are the basis of excitation-contraction coupling in muscle. In these studies, we develop cellular and animals models with a loss of expression of HTT in skeletal muscle specifically. Theses studies show that calcium release is altered at the cellular level and muscle force is altered at animal model level. Theses alterations are correlated with loss of expression of the main receptors of the triad. Finally, fragment of the normal protein can restore calcium defects. Theses studies put forward the role of huntingtine in skeletal muscle.La maladie de Huntington (HD) est une pathologie génétique multisystémique neurodégénérative rare caractérisée par des atteintes motrices, cognitives et psychiatriques. Elle est due à une augmentation de la répétition de triplet CAG dans l'exon 1 du gène HTT, dont la taille normale est de 6 à 35 répétitions. Cette expansion de triplets conduit à la présence d'une répétition de glutamine de taille anormale dans l'extrémité N-terminale de la protéine huntingtine (HTT). Les conséquences de la mutation sont d’une part la diminution de l’expression de la protéine non mutée et d’autre part l’expression d’une protéine mutée. L’une des fonctions de la HTT est le transport intracellulaire de vésicules le long des microtubules dans les neurones. Par ailleurs, une phénocopie : Huntington disease like 2 maladie ayant un phénotype similaire, est due à une perte de fonction de la junctophilin-3 ayant pour rôle l’établissement de points de contact entre la membrane plasmique et le reticulum endoplasmique au niveau neuronal. Les présents travaux visent à découvrir les mécanismes au sein desquels la HTT est impliquée dans un modèle différent de la cellule neuronale : la cellule musculaire. En effet, les points de contact nommées triades sont le cœur du couplage excitation-contraction. Les travaux ont permis de montrer, après avoir créé des modèles cellulaires et in vivo avec baisse d’expression de la protéine, un défaut de la fonction musculaire au niveau cellulaire comme au niveau physiologique. Les relâchements calciques sont altérés. La force est diminuée. De plus, ces altérations de fonctionnement sont corrélées à une baisse d’expression des principaux récepteurs de la triade. Enfin, une fraction exogène de la partie N-terminale de la protéine non mutée restaure les défauts calciques observés. La huntingtine a donc un rôle prépondérant dans la fonction princeps du muscle : la contraction