Fotocatálisis y seguridad alimentaria

Ponencia invitada a Congres

Geometric biplane graphs I: maximal graphs

We study biplane graphs drawn on a finite planar point set in general position. This is the family of geometric graphs whose vertex set is and can be decomposed into two plane graphs. We show that two maximal biplane graphs-in the sense that no edge can be added while staying biplane-may differ in the number of edges, and we provide an efficient algorithm for adding edges to a biplane graph to make it maximal. We also study extremal properties of maximal biplane graphs such as the maximum number of edges and the largest maximum connectivity over -element point sets.Peer ReviewedPostprint (author's final draft

Geometric biplane graphs II: graph augmentation

We study biplane graphs drawn on a finite point set in the plane in general position. This is the family of geometric graphs whose vertex set is and which can be decomposed into two plane graphs. We show that every sufficiently large point set admits a 5-connected biplane graph and that there are arbitrarily large point sets that do not admit any 6-connected biplane graph. Furthermore, we show that every plane graph (other than a wheel or a fan) can be augmented into a 4-connected biplane graph. However, there are arbitrarily large plane graphs that cannot be augmented to a 5-connected biplane graph by adding pairwise noncrossing edges.Peer ReviewedPostprint (author's final draft

Geometric biplane graphs I: maximal graphs

Postprint (author’s final draft

Geometric Biplane Graphs II: Graph Augmentation

We study biplane graphs drawn on a nite point set S in the plane in general position. This is the family of geometric graphs whose vertex set is S and which can be decomposed into two plane graphs. We show that every su ciently large point set admits a 5-connected biplane graph and that there are arbitrarily large point sets that do not admit any 6- connected biplane graph. Furthermore, we show that every plane graph (other than a wheel or a fan) can be augmented into a 4-connected biplane graph. However, there are arbitrarily large plane graphs that cannot be augmented to a 5-connected biplane graph by adding pairwise noncrossing edges.Peer ReviewedPostprint (author’s final draft

Salivary PYY: A Putative Bypass to Satiety

Peptide YY3-36 is a satiation hormone released postprandially into the bloodstream from L-endocrine cells in the gut epithelia. In the current report, we demonstrate PYY3-36 is also present in murine as well as in human saliva. In mice, salivary PYY3-36 derives from plasma and is also synthesized in the taste cells in taste buds of the tongue. Moreover, the cognate receptor Y2R is abundantly expressed in the basal layer of the progenitor cells of the tongue epithelia and von Ebner's gland. The acute augmentation of salivary PYY3-36 induced stronger satiation as demonstrated in feeding behavioral studies. The effect is mediated through the activation of the specific Y2 receptor expressed in the lingual epithelial cells. In a long-term study involving diet-induced obese (DIO) mice, a sustained increase in PYY3-36 was achieved using viral vector-mediated gene delivery targeting salivary glands. The chronic increase in salivary PYY3-36 resulted in a significant long-term reduction in food intake (FI) and body weight (BW). Thus this study provides evidence for new functions of the previously characterized gut peptide PYY3-36 suggesting a potential simple and efficient alternative therapeutic approach for the treatment of obesity

Damaging variants in FOXI3 cause microtia and craniofacial microsomia

Q1Q1Pacientes con Microtia y Microsomía craneofacialPurpose: Craniofacial microsomia (CFM) represents a spectrum of craniofacial malformations, ranging from isolated microtia with or without aural atresia to underdevelopment of the mandible, maxilla, orbit, facial soft tissue, and/or facial nerve. The genetic causes of CFM remain largely unknown. Methods: We performed genome sequencing and linkage analysis in patients and families with microtia and CFM of unknown genetic etiology. The functional consequences of damaging missense variants were evaluated through expression of wild-type and mutant proteins in vitro. Results: We studied a 5-generation kindred with microtia, identifying a missense variant in FOXI3 (p.Arg236Trp) as the cause of disease (logarithm of the odds = 3.33). We subsequently identified 6 individuals from 3 additional kindreds with microtia-CFM spectrum phenotypes harboring damaging variants in FOXI3, a regulator of ectodermal and neural crest development. Missense variants in the nuclear localization sequence were identified in cases with isolated microtia with aural atresia and found to affect subcellular localization of FOXI3. Loss of function variants were found in patients with microtia and mandibular hypoplasia (CFM), suggesting dosage sensitivity of FOXI3. Conclusion: Damaging variants in FOXI3 are the second most frequent genetic cause of CFM, causing 1% of all cases, including 13% of familial cases in our cohort.https://orcid.org/0000-0003-3822-7780https://orcid.org/0000-0002-0729-6866Revista Internacional - IndexadaA1N