Lythraceae

Hierbas, sufrútices o arbustos de hojas opuestas, raro verticiladas o alternas, simples, enteras, sésiles o brevemente pecioladas. Flores solitarias o en cimas axilares o espigas apicales. Cíclicas, zigomorfas o actinomorfas, perfectas. Tálamo tubuloso o hipocraterimorfo, persistente a la fructificación. Cáliz 4-6-lobado, emplazado en el ápice del tálamo, simple o con apéndices intersepálicos. Pétalos 4-6, iguales o desiguales, a veces vestigiales o ausentes por aborto, libres, base angostada hasta pseudopecioliforme, nervios notorios, base soldada entre los lóbulos del cáliz en el ápice del tálamo. Estambres 4-12 (-22), heterodínamos, base de los filamentos soldadas a la cara interna del tálamo, desde muy cortos (doble o triple de la long. de las anteras) hasta muy largos; anteras dorsifijas, bitécicas, dehiscencia longitudinal. Disco glandular anular o dorsal asimétrico, raro ausente, en la base del ovario súpero, 2-carpelar, 1-2-locular, placentación central, axial o basal. Ovulos pocos a numerosos. Estilo corto o largo atenuándose hacia el ápice en un estigma esférico o agudo inconspicuo. Cápsula membranácea protegida por el tálamo persistente, 1-2-locular, indehiscente o de dehiscencia diversa. Semillas pequeñas, pocas a numerosas, orbicular-aplanadas hasta prismático-alargadas, veces aladas, exalbuminadas

The respiratory chain inhibitor rotenone affects peroxisomal dynamics via its microtubule-destabilizing activity

This is the author accepted manuscript. The final version is available from Springer Verlag via the DOI in this record.Peroxisomes and mitochondria in mammalian cells are closely linked subcellular organelles, which maintain a redox-sensitive relationship. Their interplay and role in ROS signalling is supposed to impact on age-related and degenerative disorders. Whereas the generation of peroxisome-derived oxidative stress can affect mitochondrial morphology and function, little is known about the impact of mitochondria-derived oxidative stress on peroxisomes. Here, we investigated the effect of the mitochondrial complex I inhibitor rotenone on peroxisomal and mitochondrial membrane dynamics. We show that rotenone treatment of COS-7 cells alters peroxisome morphology and distribution. However, this effect is related to its microtubule-destabilising activity rather than to the generation of oxidative stress. Rotenone also induced alterations in mitochondrial morphology, which – in contrast to its effect on peroxisomes - were dependent on the generation of ROS but independent of its microtubule-active properties. The importance of our findings for the peroxisome-mitochondria redox relationship and the interpretation of in cellulo and in vivo studies with rotenone, which is widely used to study Parkinson’s disease, are discussed.We would like to acknowledge the support of T. A. Schrader, N. A. Bonekamp and J. Jordan (University of Castilla-La Mancha, Albacete, Spain). This work was supported by the Biotechnology and Biological Sciences Research Council (BB/K006231/1, BB/N01541X/1 to M.S.), the Portuguese Foundation for Science and Technology and FEDER/COMPETE (SFRH/BPD/37725/2007 to M.G.L), the University of Aveiro, PT and CLES, University of Exeter, UK. M.S. is supported by a Marie Curie Initial Training Network (ITN) action PerFuMe (316723)

Evaluating the Sensitivity of Face Presentation Attack Detection Techniques to Images of Varying Resolutions

In the last decades, emerging techniques for face Presentation Attack Detection (PAD) have reported a remarkable performance to detect attack presentations whose attack type and capture conditions are known a priori. However, the generalisation capability of PAD approaches shows a considerable deterioration to detect unknown attacks. In order to tackle those generalisation issues, several PAD techniques have focused on the detection of homogeneous features from known attacks to detect unknown Presentation Attack Instruments without taking into account how some intrinsic image properties such as the image resolution or biometric quality could impact their detection performance. In this work, we carry out a thorough analysis of the sensitivity of several texture descriptors which shows how the use of images with varying resolutions for training leads to a high decrease on the attack detection performance

Barcelona, de las barracas a los polígonos

El barraquismo surge como respuesta a la incapacidad de ciertas clases sociales a acceder a una vivienda digna. Es una problemática que muchas ciudades sufren o han sufrido a lo largo de la historia y que en muchas de ellas han marcado su crecimiento y su configuración actual. Barcelona fue una de esas ciudades que sufrió el fenómeno del barraquismo y que actualmente vuelve a sufrirlo. Estos asentamientos empezaron a surgir a finales del s.XIX y perduraron durante gran parte del s.XX, llegando a su mayor auge entre 1920 -1950. Las grandes inmigraciones que sufrió la ciudad sumada a la escasez de vivienda, los elevados precios y la incapacidad de construcción de viviendas por falta de recursos, provocaron que empezaran a surgir asentamientos de barracas por varias zonas de la ciudad. La problemática de las barracas no se llegó a solucionar hasta los años 50-60, cuando se empezó una construcción masiva de polígonos residenciales que abastecían la demanda de vivienda. Sin embargo, la construcción rápida, sin urbanización y a bajo coste tuvo consecuencias en la calidad constructiva de las edificaciones y las condiciones de vida que ofrecían a sus residentes. Por estos motivos, el objetivo del trabajo consiste en mostrar el fenómeno del barraquismo en esta época de la ciudad de Barcelona y su posterior realojo en los polígonos de vivienda, para comparar la mejora de condiciones de vida que ofrecían y analizar si fue la mejor opción posible.The shantytown arises as a response to the inability of certain social classes to access decent housing. It is a problem that many cities suffer or have suffered throughout history and that in many of them have marked their growth and their current configuration. Barcelona was one of those cities that suffered from the phenomenon of squatting and is currently suffering again. These settlements emerged at the end of the 19th century and lasted for a large part of the 20th century, reaching their peak between 1920 and 1950. The large immigration that the city suffered, added to the shortage of housing, the high prices and the inability to build houses due to lack of resources, caused shanty towns to begin to emerge in various areas of the city. The problem of the shacks was not solved until the 1950s and 1960s, when the massive construction of residential estates that met the demand for housing began. However, rapid construction, without urbanization and at low cost, had consequences on the constructive quality of the buildings and the living conditions offered to its residents. For these reasons, the objective of the work is to show the phenomenon of shantytowns in this period of the city of Barcelona and its subsequent relocation to housing estates, to compare the improvement in living conditions that they offer and to analyze if it was the best option. possible

Gene deficiency in activating Fcγ receptors influences the macrophage phenotypic balance and reduces atherosclerosis in mice

Immunity contributes to arterial inflammation during atherosclerosis. Oxidized low-density lipoproteins induce an autoimmune response characterized by specific antibodies and immune complexes in atherosclerotic patients. We hypothesize that specific Fcγ receptors for IgG constant region participate in atherogenesis by regulating the inflammatory state of lesional macrophages. In vivo we examined the role of activating Fcγ receptors in atherosclerosis progression using bone marrow transplantation from mice deficient in γ-chain (the common signaling subunit of activating Fcγ receptors) to hyperlipidemic mice. Hematopoietic deficiency of Fcγ receptors significantly reduced atherosclerotic lesion size, which was associated with decreased number of macrophages and T lymphocytes, and increased T regulatory cell function. Lesions of Fcγ receptor deficient mice exhibited increased plaque stability, as evidenced by higher collagen and smooth muscle cell content and decreased apoptosis. These effects were independent of changes in serum lipids and antibody response to oxidized low-density lipoproteins. Activating Fcγ receptor deficiency reduced pro-inflammatory gene expression, nuclear factor-κB activity, and M1 macrophages at the lesion site, while increasing anti-inflammatory genes and M2 macrophages. The decreased inflammation in the lesions was mirrored by a reduced number of classical inflammatory monocytes in blood. In vitro, lack of activating Fcγ receptors attenuated foam cell formation, oxidative stress and pro-inflammatory gene expression, and increased M2-associated genes in murine macrophages. Our study demonstrates that activating Fcγ receptors influence the macrophage phenotypic balance in the artery wall of atherosclerotic mice and suggests that modulation of Fcγ receptor-mediated inflammatory responses could effectively suppress atherosclerosis

Biological implications of differential expression of mitochondrial-shaping proteins in Parkinson’s disease

It has long been accepted that mitochondrial function and morphology is affected in Parkinson’s disease, and that mitochondrial function can be directly related to its morphology. So far, mitochondrial morphological alterations studies, in the context of this neurodegenerative disease, have been performed through microscopic methodologies. The goal of the present work is to address if the modifications in the mitochondrial-shaping proteins occurring in this disorder have implications in other cellular pathways, which might constitute important pathways for the disease progression. To do so, we conducted a novel approach through a thorough exploration of the available proteomics-based studies in the context of Parkinson’s disease. The analysis provided insight into the altered biological pathways affected by changes in the expression of mitochondrial-shaping proteins via different bioinformatic tools. Unexpectedly, we observed that the mitochondrial-shaping proteins altered in the context of Parkinson’s disease are, in the vast majority, related to the organization of the mitochondrial cristae. Conversely, in the studies that have resorted to microscopy-based techniques, the most widely reported alteration in the context of this disorder is mitochondria fragmentation. Cristae membrane organization is pivotal for mitochondrial ATP production, and changes in their morphology have a direct impact on the organization and function of the oxidative phosphorylation (OXPHOS) complexes. To understand which biological processes are affected by the alteration of these proteins we analyzed the binding partners of the mitochondrial-shaping proteins that were found altered in Parkinson’s disease. We showed that the binding partners fall into seven different cellular components, which include mitochondria, proteasome, and endoplasmic reticulum (ER), amongst others. It is noteworthy that, by evaluating the biological process in which these modified proteins are involved, we showed that they are related to the production and metabolism of ATP, immune response, cytoskeleton alteration, and oxidative stress, amongst others. In summary, with our bioinformatics approach using the data on the modified proteins in Parkinson’s disease patients, we were able to relate the alteration of mitochondrial-shaping proteins to modifications of crucial cellular pathways affected in this disease.This work was financed by FEDER—Fundo Europeu de Desenvolvimento Regional funds through the COMPETE 2020—Operacional Programme for Competitiveness and Internationalisation (POCI), Portugal 2020, and by Portuguese funds through FCT—Fundação para a Ciência e a Tecnologia/ Ministério da Ciência, Tecnologia e Inovação in the framework of the projects “Institute for Research and Innovation in Health Sciences” (POCI-01-0145-FEDER-007274), iBiMED (UID/BIM/04501/2013) and UnIC (UID/IC/00051/2013) research units, the COST ACTION CA15203, and the Investigator Grant to Rui Vitorino (IF/00286/2015). Ana Freitas acknowledges FCT for her Ph.D. scholarship (SFRH/BD/111423/2015), as does Sofia C. Guimaraes (SFRH/BPD/122920/2016), and Miguel Aroso (SFRH/BPD/123261/2016). Sara Rocha was founded by the project Norte-01-0145-FEDER-000008 -Porto Neurosciences and Neurologic Disease Research Initiative at I3S, supported by Norte Portugal Regional Operational Programme (NORTE 2020), under the PORTUGAL 2020 Partnership Agreement, through the European Regional Development Fund (FEDER)”

Seeing is believing but quantifying is deciding

The work was financed by Portuguese funds through FCT – Fundação para a Ciência e a Tecnologia in the framework of project UID/BIM/04293/2013. CDF Lopes acknowledges FCT for her PhD scholarship (SFRH/BD/77933/2011). The authors have no other relevant affiliations or financial involvement with any organization or entity with a financial interest in or financial conflict with the subject matter or materials discussed in the manuscript apart from those disclosed. No writing assistance was utilized in the production of this manuscript

Data-Driven Modeling of the Cellular Pharmacokinetics of Degradable Chitosan-Based Nanoparticles

Nanoparticle drug delivery vehicles introduce multiple pharmacokinetic processes, with the delivery, accumulation, and stability of the therapeutic molecule influenced by nanoscale processes. Therefore, considering the complexity of the multiple interactions, the use of data-driven models has critical importance in understanding the interplay between controlling processes. We demonstrate data simulation techniques to reproduce the time-dependent dose of trimethyl chitosan nanoparticles in an ND7/23 neuronal cell line, used as an in vitro model of native peripheral sensory neurons. Derived analytical expressions of the mean dose per cell accurately capture the pharmacokinetics by including a declining delivery rate and an intracellular particle degradation process. Comparison with experiment indicates a supply time constant, τ = 2 h. and a degradation rate constant, b = 0.71 h−1. Modeling the dose heterogeneity uses simulated data distributions, with time dependence incorporated by transforming data-bin values. The simulations mimic the dynamic nature of cell-to-cell dose variation and explain the observed trend of increasing numbers of high-dose cells at early time points, followed by a shift in distribution peak to lower dose between 4 to 8 h and a static dose profile beyond 8 h