36 research outputs found

    Non-homotopicity of the linking set of algebraic plane curves

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    The linking set is an invariant of algebraic plane curves introduced by Meilhan and the first author. It has been successfully used to detect several examples of Zariski pairs, i.e. curves with the same combinatorics and different embedding in [Formula: see text]. Differentiating Shimada's [Formula: see text]-equivalent Zariski pair by the linking set, we prove, in the present paper, that this invariant is not determined by the fundamental group of the curve. </jats:p

    Multiplicativity of the I\mathcal{I}-invariant and topology of glued arrangements

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    The invariant I(A,ξ,γ)\mathcal{I}(\mathcal{A}, \xi, \gamma) was first introduced by E. Artal, V. Florens and the author. Inspired by the idea of G. Rybnikov, we obtain a multiplicativity theorem of this invariant under the gluing of two arrangements along a triangle. An application of this theorem is to prove that the extended Rybnikov arrangements form an ordered Zariski pair (i.e. two arrangements with the same combinatorial information and different ordered topologies). Finally, we extend this method to a family of arrangements and thus we obtain a method to construct new examples of Zariski pairs

    An arithmetic Zariski 4–tuple of twelve lines

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    Using the invariant developed by E Artal, V Florens and the author, we differentiate four arrangements with the same combinatorial information but in different deformation classes. From these arrangements, we construct four other arrangements such that there is no orientation-preserving homeomorphism between them. Furthermore, some pairs of arrangements among this 4-tuple form new arithmetic Zariski pairs, ie a pair of arrangements conjugate in a number field with the same combinatorial information but with different embedding topology in CP2

    On the nonconnectedness of moduli spaces of arrangements, II: construction of nonarithmetic pairs

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    Constructing lattice isomorphic line arrangements that are not lattice isotopic is a complex yet fundamental task. In this paper, we focus on such pairs but which are not Galois conjugated, referred to as nonarithmetic pairs. Splitting polygons have been introduced by the author to facilitate the construction of lattice isomorphic arrangements that are not lattice isotopic. Exploiting this structure, we develop two algorithms which produce nonarithmetic pairs: the first generates pairs over a number field, while the second yields pairs over the rationals. Moreover, explicit applications of these algorithms are presented, including one complex, one real, and one rational nonarithmetic pair

    Relationships between diet and gut microbiome in an Italian and Dutch cohort: does the dietary protein to fiber ratio play a role?

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    Purpose: To investigate the relationships between the habitual diet, the protein to fiber ratio (P/F), and the gut microbiome in one Italian and one Dutch cohort of healthy subjects consuming an omnivore diet. Methods: The Italian cohort included 19 males (M_IT, BMI 25.2 ± 0.72 kg/m2, age 25.4 ± 0.96 years) and 20 females (F_IT, BMI 23.9 ± 0.81 kg/m2, age 23.8 ± 0.54 years); the Dutch cohort included 30 females (F_NL, BMI: 23.9 ± 0.81 kg/m2, age: 23.8 ± 0.54 years). Individual diets were recorded through Food Frequency Questionnaires and analyzed to assess the nutrient composition. Gut microbiome was assessed in fecal samples. Results: M_IT consumed higher levels of proteins than F_NL and F_IT, whereas dietary fiber intake did not differ among groups. Data showed that consumption of plant protein to animal protein (PP/AP) and PP to total proteins ratio can determine a differentiation of F_NL more than the absolute amount of dietary fiber. Conversely, the protein to fiber (P/F) and AP to total proteins better characterized M_IT. M_IT harbored the highest abundance of proteolytic microorganisms and the lowest microbial gene richness. Conversely, F_NL had more fiber-degrading microorganisms like Bacteroides thetaiotaomicron, Bacteroides xylanisolvens, Roseburia sp., Coprococcus eutactus and Parabacteroides along with the highest number of genes encoding carbohydrate-active enzymes and gene richness. It was predicted that by each unit decrease in the P/F a 3% increase in gene richness occurred. Conclusion: Study findings suggested that dietary P/F, rather than the absolute amount of dietary fiber, could contribute to the shaping of the microbiome towards a more proteolytic or fiber-degrading gut ecosystem. Clinicaltrials: gov Identifier NCT04205045-01-10-2018, retrospectively registered. Dutch Trial Register NTR7531-05-10-2018

    The loop-linking number of line arrangements

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    In his Ph.D. thesis, Cadegan-Schlieper constructs an invariant of the embedded topology of a line arrangement which generalizes the I\mathcal{I}-invariant introduced by Artal, Florens and the author. This new invariant is called the loop-linking number in the present paper. We refine the result of Cadegan-Schlieper by proving that the loop-linking number is an invariant of the homeomorphism type of the arrangement complement. We give two effective methods to compute this invariant, both are based on the braid monodromy. As an application, we detect an arithmetic Zariski pair of arrangements with 11 lines whose coefficients are in the 5th cyclotomic field. Furthermore, we also prove that the fundamental groups of their complements are not isomorphic; it is the Zariski pair with the fewest number of lines which have this property. We also detect an arithmetic Zariski triple with 12 lines whose complements have non-isomorphic fundamental groups. In the appendix, we give 29 combinatorial types which lead to similar ordered arithmetic Zariski pairs of 11 lines. To conclude this paper, we give a additivity theorem for the union of arrangements. This first allows us to prove that the complements of Rybnikov’s arrangements are not homeomorphic, and then leads us to a generalization of Rybnikov’s result. Lastly, we use it to prove the existence of homotopy-equivalent lattice-isomorphic arrangements which have non-homeomorphic complements

    A topological invariant of line arrangements

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    We define a new topological invariant of line arrangements in the complex projective plane. This invariant is a root of unity defined under some combinatorial restrictions for arrangements endowed with some special torsion character on the fundamental group of their complement. It is derived from the peripheral structure on the group induced by the inclusion map of the boundary of a tubular neigborhood in the exterior of the arrangement. By similarity with knot theory, it can be viewed as an analogue of linking numbers. This is an orientation-preserving invariant for ordered arrangements. We give an explicit method to compute the invariant from the equations of the arrangement, using the wiring diagrams introduced by Arvola, that encode the braid monodromy. Moreover, this invariant is a crucial ingredient to compute the depth of a character satisfying some resonant conditions, and completes the existent methods by Libgober and the first author. Finally, we compute the invariant for extended MacLane arrangements with an additional line and observe that it takes different values for the deformation classes

    Axe intestin-cerveau et régulation de la satiété chez l'obèse : étude de l'origine de l'endotoxémie métabolique et de son rôle sur la physiologie du nerf vague dans un modèle d'obésité induite par un régime occidental chez le rat

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    A real public health issue, obesity and its associated metabolic and behavioral disorders are the consequences of a state of low grade chronic inflammation that might originate from the presence in host plasma of gut-derived bacteria components, lipopolysaccharides (LPS). This present state is called metabolic endotoxemia. The first aim of my thesis was to understand why, in diet-induced obesity (DIO), LPS initially contained in the gut lumen, are able to cross the intestine and enter into the circulatory system. My second aim was to investigate the effect of gut microbiota composition and LPS on the satiety regulation by the vagus nerve, the main communication pathway between the gut and the brain. To answer these questions, we have mainly used a DIO rat model.We showed that consumption of WD induced a loss of ileal barrier function characterized by a reduction in mucosal defenses associated to elevated LPS permeability. Obesity is also characterized by an alteration in feeding behavior including a decreased sensitivity to intestinal satiety signals. We showed that neither obesity nor the lipid percentage of the diet triggers loss of sensitivity to satiety signals but that gut microbiota alterations could rather be the main driver. Hence, metabolic endotoxemia could result from an increased transepithelial passage of LPS, which once spread in the blood could reach, among other things, the vagus nerve where they could disrupt intestinal signals of satiety.Véritable enjeu de santé publique, l’obésité et ses complications seraient la conséquence d’un état inflammatoire chronique de bas-grade qui pourrait résulter de la présence dans le sang de composés bactériens, les lipopolysaccharides (LPS), état appelé endotoxémie métabolique. Le premier objectif de cette thèse était de comprendre pourquoi les LPS, initialement contenus dans le microbiote, sont capables de traverser l’intestin et d’entrer dans le système sanguin. Mon second objectif était d’étudier l’impact de la composition du microbiote dans le contrôle de la satiété par le nerf vague, lien de communication entre l’intestin et le cerveau. Pour cela, un modèle de rats soumis à un régime obésogène a été utilisée.Mes travaux ont montré que la consommation d’un régime obésogène induisait une perte de la fonction de barrière intestinale au niveau de l’iléon caractérisée par une baisse des défenses mucosales et une augmentation de la perméabilité au LPS. L’obésité est également caractérisée par une altération du comportement alimentaire, avec notamment une réduction de la sensibilité aux signaux de satiété. Nous avons montré que ni l’obésité ni le pourcentage de lipides du régime n’étaient responsables de cette perte de sensibilité aux signaux de satiété mais que l’altération du microbiote en serait le contributeur principal. Ainsi, l’endotoxémie métabolique serait le résultat d’une augmentation du passage transepithelial de LPS, qui, une fois dans le sang, pourraient atteindre, entre autres, le nerf vague où ils perturberaient les signaux intestinaux de satiété

    Gut-brain axis and the regulation of satiey during obesity : Study of metabolic endotoxemia origin and its role on vagus nerve physiology in a rat model of diet-induced obesity.

    No full text
    Véritable enjeu de santé publique, l’obésité et ses complications seraient la conséquence d’un état inflammatoire chronique de bas-grade qui pourrait résulter de la présence dans le sang de composés bactériens, les lipopolysaccharides (LPS), état appelé endotoxémie métabolique. Le premier objectif de cette thèse était de comprendre pourquoi les LPS, initialement contenus dans le microbiote, sont capables de traverser l’intestin et d’entrer dans le système sanguin. Mon second objectif était d’étudier l’impact de la composition du microbiote dans le contrôle de la satiété par le nerf vague, lien de communication entre l’intestin et le cerveau. Pour cela, un modèle de rats soumis à un régime obésogène a été utilisée.Mes travaux ont montré que la consommation d’un régime obésogène induisait une perte de la fonction de barrière intestinale au niveau de l’iléon caractérisée par une baisse des défenses mucosales et une augmentation de la perméabilité au LPS. L’obésité est également caractérisée par une altération du comportement alimentaire, avec notamment une réduction de la sensibilité aux signaux de satiété. Nous avons montré que ni l’obésité ni le pourcentage de lipides du régime n’étaient responsables de cette perte de sensibilité aux signaux de satiété mais que l’altération du microbiote en serait le contributeur principal. Ainsi, l’endotoxémie métabolique serait le résultat d’une augmentation du passage transepithelial de LPS, qui, une fois dans le sang, pourraient atteindre, entre autres, le nerf vague où ils perturberaient les signaux intestinaux de satiété.A real public health issue, obesity and its associated metabolic and behavioral disorders are the consequences of a state of low grade chronic inflammation that might originate from the presence in host plasma of gut-derived bacteria components, lipopolysaccharides (LPS). This present state is called metabolic endotoxemia. The first aim of my thesis was to understand why, in diet-induced obesity (DIO), LPS initially contained in the gut lumen, are able to cross the intestine and enter into the circulatory system. My second aim was to investigate the effect of gut microbiota composition and LPS on the satiety regulation by the vagus nerve, the main communication pathway between the gut and the brain. To answer these questions, we have mainly used a DIO rat model.We showed that consumption of WD induced a loss of ileal barrier function characterized by a reduction in mucosal defenses associated to elevated LPS permeability. Obesity is also characterized by an alteration in feeding behavior including a decreased sensitivity to intestinal satiety signals. We showed that neither obesity nor the lipid percentage of the diet triggers loss of sensitivity to satiety signals but that gut microbiota alterations could rather be the main driver. Hence, metabolic endotoxemia could result from an increased transepithelial passage of LPS, which once spread in the blood could reach, among other things, the vagus nerve where they could disrupt intestinal signals of satiety

    Axe intestin-cerveau et régulation de la satiété chez l'obèse : étude de l'origine de l'endotoxémie métabolique et de son rôle sur la physiologie du nerf vague dans un modèle d'obésité induite par un régime occidental chez le rat

    No full text
    A real public health issue, obesity and its associated metabolic and behavioral disorders are the consequences of a state of low grade chronic inflammation that might originate from the presence in host plasma of gut-derived bacteria components, lipopolysaccharides (LPS). This present state is called metabolic endotoxemia. The first aim of my thesis was to understand why, in diet-induced obesity (DIO), LPS initially contained in the gut lumen, are able to cross the intestine and enter into the circulatory system. My second aim was to investigate the effect of gut microbiota composition and LPS on the satiety regulation by the vagus nerve, the main communication pathway between the gut and the brain. To answer these questions, we have mainly used a DIO rat model.We showed that consumption of WD induced a loss of ileal barrier function characterized by a reduction in mucosal defenses associated to elevated LPS permeability. Obesity is also characterized by an alteration in feeding behavior including a decreased sensitivity to intestinal satiety signals. We showed that neither obesity nor the lipid percentage of the diet triggers loss of sensitivity to satiety signals but that gut microbiota alterations could rather be the main driver. Hence, metabolic endotoxemia could result from an increased transepithelial passage of LPS, which once spread in the blood could reach, among other things, the vagus nerve where they could disrupt intestinal signals of satiety.Véritable enjeu de santé publique, l’obésité et ses complications seraient la conséquence d’un état inflammatoire chronique de bas-grade qui pourrait résulter de la présence dans le sang de composés bactériens, les lipopolysaccharides (LPS), état appelé endotoxémie métabolique. Le premier objectif de cette thèse était de comprendre pourquoi les LPS, initialement contenus dans le microbiote, sont capables de traverser l’intestin et d’entrer dans le système sanguin. Mon second objectif était d’étudier l’impact de la composition du microbiote dans le contrôle de la satiété par le nerf vague, lien de communication entre l’intestin et le cerveau. Pour cela, un modèle de rats soumis à un régime obésogène a été utilisée.Mes travaux ont montré que la consommation d’un régime obésogène induisait une perte de la fonction de barrière intestinale au niveau de l’iléon caractérisée par une baisse des défenses mucosales et une augmentation de la perméabilité au LPS. L’obésité est également caractérisée par une altération du comportement alimentaire, avec notamment une réduction de la sensibilité aux signaux de satiété. Nous avons montré que ni l’obésité ni le pourcentage de lipides du régime n’étaient responsables de cette perte de sensibilité aux signaux de satiété mais que l’altération du microbiote en serait le contributeur principal. Ainsi, l’endotoxémie métabolique serait le résultat d’une augmentation du passage transepithelial de LPS, qui, une fois dans le sang, pourraient atteindre, entre autres, le nerf vague où ils perturberaient les signaux intestinaux de satiété
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