Endosymbiosis before eukaryotes: mitochondrial establishment in protoeukaryotes

Endosymbiosis and organellogenesis are virtually unknown among prokaryotes. The single presumed example is the endosymbiogenetic origin of mitochondria, which is hidden behind the event horizon of the last eukaryotic common ancestor. While eukaryotes are monophyletic, it is unlikely that during billions of years, there were no other prokaryote–prokaryote endosymbioses as symbiosis is extremely common among prokaryotes, e.g., in biofilms. Therefore, it is even more precarious to draw conclusions about potentially existing (or once existing) prokaryotic endosymbioses based on a single example. It is yet unknown if the bacterial endosymbiont was captured by a prokaryote or by a (proto-)eukaryote, and if the process of internalization was parasitic infection, slow engulfment, or phagocytosis. In this review, we accordingly explore multiple mechanisms and processes that could drive the evolution of unicellular microbial symbioses with a special attention to prokaryote–prokaryote interactions and to the mitochondrion, possibly the single prokaryotic endosymbiosis that turned out to be a major evolutionary transition. We investigate the ecology and evolutionary stability of inter-species microbial interactions based on dependence, physical proximity, cost–benefit budget, and the types of benefits, investments, and controls. We identify challenges that had to be conquered for the mitochondrial host to establish a stable eukaryotic lineage. Any assumption about the initial interaction of the mitochondrial ancestor and its contemporary host based solely on their modern relationship is rather perilous. As a result, we warn against assuming an initial mutually beneficial interaction based on modern mitochondria–host cooperation. This assumption is twice fallacious: (i) endosymbioses are known to evolve from exploitative interactions and (ii) cooperativity does not necessarily lead to stable mutualism. We point out that the lack of evidence so far on the evolution of endosymbiosis from mutual syntrophy supports the idea that mitochondria emerged from an exploitative (parasitic or phagotrophic) interaction rather than from syntrophy

The Evolution of Microbial Facilitation: Sociogenesis, Symbiogenesis, and Transition in Individuality

Metabolic cooperation is widespread, and it seems to be a ubiquitous and easily evolvable interaction in the microbial domain. Mutual metabolic cooperation, like syntrophy, is thought to have a crucial role in stabilizing interactions and communities, for example biofilms. Furthermore, cooperation is expected to feed back positively to the community under higher-level selection. In certain cases, cooperation can lead to a transition in individuality, when freely reproducing, unrelated entities (genes, microbes, etc.) irreversibly integrate to form a new evolutionary unit. The textbook example is endosymbiosis, prevalent among eukaryotes but virtually lacking among prokaryotes. Concerning the ubiquity of syntrophic microbial communities, it is intriguing why evolution has not lead to more transitions in individuality in the microbial domain. We set out to distinguish syntrophy-specific aspects of major transitions, to investigate why a transition in individuality within a syntrophic pair or community is so rare. We review the field of metabolic communities to identify potential evolutionary trajectories that may lead to a transition. Community properties, like joint metabolic capacity, functional profile, guild composition, assembly and interaction patterns are important concepts that may not only persist stably but according to thought-provoking theories, may provide the heritable information at a higher level of selection. We explore these ideas, relating to concepts of multilevel selection and of informational replication, to assess their relevance in the debate whether microbial communities may inherit community-level information or not

Orthodontic-logaoedic treatment using a modified Hawley device.

Introduction: According to the World Health Organization, malocclusion ia a higly risky entity that is placed in the 3rd position worldwide within oral diseases. There is a great relation among dento-maxillofacial disorders, dental vestibulo version, open bite and speaking disorders. Occlusion disorders can be more or less severe and can involve almost all the structures of the oral cavity. Objective: To check the usefulness of the modified Hawley´s device in patients with dental malocclusion produced by deforming habits and carriers of dyslalia. Method: Observational, analytico-comparative study carried out at the elementary school ¨Guerrillero Heroico¨ from Cienfuegos Municipality . A non-probabilistic sample of 32 patients was taken for this study; patients to whom 2 measurements were made. The variables under study were: Number of the Clinical record, Files, Dentomaxilofacial anomalies, sucking of the thomb, atypical deglussion, analysis of the pronunciation and levels of articulation. Hawley´s device was placed with an oval perforation at the level of the palatal folds changing the traditional form of the device. Result: There is a prevalence of malocclusion Class I. The most common maxillofacial disorders are: vestibulo version (87,5%), increased enhancement (84,4 %) and abnormal bilabial closure (68,8 %). Dyslalias were reduced during treatment from 81,2 % to 28,1 % at the end of treatment

Galectin-3 shapes toxic alpha-synuclein strains in Parkinson's disease.

Parkinson's Disease (PD) is a neurodegenerative and progressive disorder characterised by intracytoplasmic inclusions called Lewy bodies (LB) and degeneration of dopaminergic neurons in the substantia nigra (SN). Aggregated α-synuclein (αSYN) is known to be the main component of the LB. It has also been reported to interact with several proteins and organelles. Galectin-3 (GAL3) is known to have a detrimental function in neurodegenerative diseases. It is a galactose-binding protein without known catalytic activity and is expressed mainly by activated microglial cells in the central nervous system (CNS). GAL3 has been previously found in the outer layer of the LB in post-mortem brains. However, the role of GAL3 in PD is yet to be elucidated. In post-mortem samples, we identified an association between GAL3 and LB in all the PD subjects studied. GAL3 was linked to less αSYN in the LB outer layer and other αSYN deposits, including pale bodies. GAL3 was also associated with disrupted lysosomes. In vitro studies demonstrate that exogenous recombinant Gal3 is internalised by neuronal cell lines and primary neurons where it interacts with endogenous αSyn fibrils. In addition, aggregation experiments show that Gal3 affects spatial propagation and the stability of pre-formed αSyn fibrils resulting in short, amorphous toxic strains. To further investigate these observations in vivo, we take advantage of WT and Gal3KO mice subjected to intranigral injection of adenovirus overexpressing human αSyn as a PD model. In line with our in vitro studies, under these conditions, genetic deletion of GAL3 leads to increased intracellular αSyn accumulation within dopaminergic neurons and remarkably preserved dopaminergic integrity and motor function. Overall, our data suggest a prominent role for GAL3 in the aggregation process of αSYN and LB formation, leading to the production of short species to the detriment of larger strains which triggers neuronal degeneration in a mouse model of PD

Ups and Downs in Finance, Ups without Downs in Inequality

The upswing in finance over the past several decades has led to rising inequality, but do downswings in finance lead to a symmetric decline in inequality? In this paper, we analyze the asymmetry of the effect of ups and downs in financial markets, as well as the effect of increased capital requirements and the bonus cap on national earnings in- equality. We use administrative employer–employee linked data on earnings from 1990 to 2017 for twelve countries. Additionally, we use data on earnings from bank reports, from 2009 to 2017 in thirteen European countries. We find a strong asymmetry in the effects of financial ups and downs on earnings inequality, a mitigating effect of rising capital requirements on the contribution of finance to inequality, and a restructuring ef- fect of the bonus cap for the earnings of financiers, while neither policy affects absolute levels of earnings inequality.La hausse de la finance au cours des dernières décennies a entraîné une hausse des inégalités, mais les ralentissements de la finance entraînent-ils une baisse symétrique des inégalités? Dans cet article, nous examinons l'asymétrie de l'effet des hausses et des ralentissements des marchés financiers, ainsi que l'effet de l'augmentation des exi- gences en matière de capital et du plafonnement des primes sur l'inégalité des salaires nationaux. Nous utilisons des données administratives couplées employeur-employé sur les salaires de 1990 à 2017 pour douze pays. De plus, nous employons des données sur les salaires provenant des rapports bancaires, de 2009 à 2017, dans 13 pays euro- péens. Nous constatons une forte asymétrie dans les effets des hausses et des ralentis- sements financières sur l'inégalité des salaires, un effet de mitigation de l'augmentation des exigences de capitalisation sur la contribution de la finance à l'inégalité, et un effet de restructuration du plafonnement des primes pour les salaires des financiers, alors qu'aucune des deux mesures n'affecte les niveaux absolus d'inégalité des salaires.iv MaxPo Discussion Paper 21/2 1 Introduction 2 Data Administrative employer–employee linked data World Bank GFDD database European bank reports 3 The contribution of financiers’ earnings to inequality and its asymmetry in upswings and downswings Less finance, less inequality? The asymmetry of the redistribution of earnings through financialization 4 Finance, regulation, and inequality Capital requirements and inequality The bonus cap 5 Conclusion Appendices A1 Data description A2 Supplementary tables and figures Reference

The Great Separation: Top Earner Segregation at Work in High-Income Countries

Analyzing linked employer-employee panel administrative databases, we study the evolving isolation of higher earners from other employees in eleven countries: Canada, Czechia, Denmark, France, Germany, Hungary, Japan, Norway, Spain, South Korea, and Sweden. We find in almost all countries a growing workplace isolation of top earners and dramatically declining exposure of top earners to bottom earners. We compare these trends to segregation based on occupational class, education, age, gender, and nativity, finding that the rise in top earner isolation is much more dramatic and general across countries. We find that residential segregation is also growing, although more slowly than segregation at work, with top earners and bottom earners increasingly living in different distinct municipalities. While work and residential segregation are correlated, statistical modeling suggests that the primary causal effect is from work to residential segregation. These findings open up a future research program on the causes and consequences of top earner segregation.En nous appuyant sur des données administratives longitudinales employeur–employés, nous analysons l’évolution de la ségrégation sociale des salariés à hauts salaires dans onze pays: Allemagne, Canada, Corée du Sud, Danemark, Espagne, France, Hongrie, Japon, Norvège, République tchèque et Suède. Nous constatons dans presque tous les pays une forte augmentation de l’entre soi des salariés bien payés sur le lieu de travail et une diminution spectaculaire de leur exposition aux bas salaires. Nous comparons ces tendances à l’évolution de la ségrégation fondée sur la catégorie sociale, l’éducation, l’âge, le sexe et le statut migratoire, et nous constatons que l’augmentation de l’entre soi des hauts salaires est celle qui est la plus prononcée et la plus générale. Nous montrons que la ségrégation résidentielle se développe aussi, bien que plus lentement que la ségrégation au travail, avec les hauts et les bas salaires vivant de plus en plus dans des municipalités distinctes. Ségrégation au travail et ségrégation résidentielle sont corrélées. Mais nos modèles statistiques suggèrent aussi que la principale relation de causalité va de la ségrégation au travail vers la ségrégation résidentielle. Ces résultats ouvrent la voie à un futur programme de recherche sur les causes et les conséquences de la ségrégation des hauts salaires.1 Introduction 2 From ethnic residential segregation to earnings segregation at work 3 Administrative data for estimating exposure measures 4 A strong increase in earnings segregation at work 5 A robust trend 17 French robustness tests 6 A specific trend 7 The link between work and residential segregation 8 Elements for a research program on the causes and consequences of increasing segregation at work The roots of growing earnings segregation at work The consequences of growing earnings segregation at work Appendices A1 Data sources and sample definition A2 Demonstration of the symmetry of relative exposure gRh = hRg A3 Figure construction A4 French robustness checks Supplementary figures and tables Reference

Length of carotid stenosis predicts peri-procedural stroke or death and restenosis in patients randomized to endovascular treatment or endarterectomy.

BACKGROUND: The anatomy of carotid stenosis may influence the outcome of endovascular treatment or carotid endarterectomy. Whether anatomy favors one treatment over the other in terms of safety or efficacy has not been investigated in randomized trials. METHODS: In 414 patients with mostly symptomatic carotid stenosis randomized to endovascular treatment (angioplasty or stenting; n = 213) or carotid endarterectomy (n = 211) in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS), the degree and length of stenosis and plaque surface irregularity were assessed on baseline intraarterial angiography. Outcome measures were stroke or death occurring between randomization and 30 days after treatment, and ipsilateral stroke and restenosis ≥50% during follow-up. RESULTS: Carotid stenosis longer than 0.65 times the common carotid artery diameter was associated with increased risk of peri-procedural stroke or death after both endovascular treatment [odds ratio 2.79 (1.17-6.65), P = 0.02] and carotid endarterectomy [2.43 (1.03-5.73), P = 0.04], and with increased long-term risk of restenosis in endovascular treatment [hazard ratio 1.68 (1.12-2.53), P = 0.01]. The excess in restenosis after endovascular treatment compared with carotid endarterectomy was significantly greater in patients with long stenosis than with short stenosis at baseline (interaction P = 0.003). Results remained significant after multivariate adjustment. No associations were found for degree of stenosis and plaque surface. CONCLUSIONS: Increasing stenosis length is an independent risk factor for peri-procedural stroke or death in endovascular treatment and carotid endarterectomy, without favoring one treatment over the other. However, the excess restenosis rate after endovascular treatment compared with carotid endarterectomy increases with longer stenosis at baseline. Stenosis length merits further investigation in carotid revascularisation trials