Registro de actividades de la Sociedad Española de Angiología y Cirugía Vascular, año 2019 / Registry of activities of the Spanish Society of Angiology and Vascular Surgery, year 2019

Objetivo: describir la actividad asistencial del año 2019 de los servicios/unidades de angiología y cirugía vascular en España. Pacientes y métodos: estudio transversal con encuesta a 107 centros sobre procedimientos quirúrgicos y exploraciones vasculares realizados en 2019. Análisis descriptivo de resultados y comparación de la ratio de actividad /100 000 habitantes con 2018. Resultados: respondieron 44 servicios (41,1 %), 4 de ámbito privado. De los 42 servicios docentes, respondieron 29 (65,9 %), un 65,9 %. En los servicios que respondieron se produjeron 26 960 ingresos, el 46,4 % urgentes y el 53,5 % programados (estancia media: 6,8 días). En la mayoría de sectores no hubo cambios significativos en la ratio/100 000 habitantes, salvo un aumento moderado (10,7 frente a 9,4) en el sector distal, tanto en procedimientos quirúrgicos (3,3 frente a 2,8) como en endovasculares (7,3 frente a 6,6). Descenso moderado de procedimientos endovasculares en los troncos supraaórticos (1,4 frente a 1,6). Hubo una disminución moderada de procedimientos quirúrgicos en aorta torácica (0,17 frente a 0,20) y abdominal (2,38 frente a 2,78), que contrastó con un aumento moderado en procedimientos endovasculares abdominotorácicos (0,40 frente a 0,35). En las arterias viscerales se encontró una disminución relevante de procedimientos endovasculares (0,89 frente a 1,16) y un aumento moderado de los quirúrgicos (0,99 frente a 0,89). En el sector aortoilíaco hubo un aumento moderado de procedimientos endovasculares (6,8 frente a 5,8). En 2019 también se encontró una disminución relevante en el número de procedimientos endovasculares relacionados con los accesos de hemodiálisis (1,2 frente a 1,5), un descenso moderado en el número de amputaciones mayores (6,9 frente a 7,8) y un descenso relevante de actividad sobre las malformaciones (0,32 frente a 0,59). Se encontró un aumento moderado en la actividad global sobre el sector venoso con respecto a la de 2018 (93,3 vs. 80,3)...(AU)

Introduction and objective: to describe the healthcare activity of the Angiology and Vascular Surgery services/units in Spain in 2019.Patients and methods: cross-sectional study with a survey of 107 centers on surgical procedures and vascularexplorations performed in 2019. Descriptive analysis of results and comparison of the activity ratio / 100,000inhabitants with 2018.Results: 44 services responded (41.1 %), with only 4 being private. Of the 42 teaching services, 29 (65.9 %) respon-ded, representing 65.9 % of the total. In the services that responded, there were 26,960 admissions, 46.4 % urgentand 53.5% scheduled, with an average stay of 6.8 days. Global surgical activity in arterial surgery in 2019 was similarto that of 2018. In most sectors there were no significant changes in the ratio / 100,000 inhabitants, except for amoderate increase (10.7 vs. 9.4) in the distal sector , finding the increase in both surgical procedures (3.3 vs. 2.8) andendovascular procedures (7.3 vs. 6.6). Furthermore, a moderate decrease in endovascular procedures was foundin the supra-aortic trunks (1.4 vs. 1.6). There was a moderate decrease in surgical procedures in the thoracic aorta(0.17 vs. 0.20) and abdominal (2.38 vs. 2.78), which contrasted with a moderate increase in thoraco-abdominalendovascular procedures (0.40 vs. to 0.35). In visceral arteries, a relevant decrease in endovascular procedures wasfound (0.89 vs. 1.16) and a moderate increase in surgical procedures (0.99 vs. 0.89). In the aorto-iliac sector therewas a moderate increase in endovascular procedures (6.8 vs. 5.8). In 2019, a relevant decrease was also found inthe number of endovascular procedures related to hemodialysis accesses (1.2 vs. 1.5), and a moderate decreasein the number of major amputations (6.9 vs. 7.8)...(AU)

Beyond Quiescent and Active: Intermediate Microglial Transcriptomic States in a Mouse Model of Down Syndrome.

Research on microglia in Down syndrome (DS) has shown that microglial activation, increased inflammatory gene expression, and oxidative stress occur at different ages in DS brains. However, most studies resulted in simplistic definitions of microglia as quiescent or active, ignoring potential intermediate states. Indeed, recent work on microglial cells in young DS brains indicated that those evolve through different intermediate activation phenotypes before reaching a fully activated state. Here we used single nucleus RNA sequencing, to examine how trisomy affects microglial states in the Ts65Dn mouse model of DS. Despite no substantial changes in the proportion of glial populations, differential expression analysis revealed cell type-specific gene expression changes, most notably in astroglia, microglia, and oligodendroglia. Focusing on microglia, we identified differential expression of genes associated with different microglial states, including disease-associated microglia (DAMs), activated response microglia (ARMs), and human Alzheimer's disease microglia (HAMs), in trisomic microglia. Furthermore, pseudotime analysis reveals a unique reactivity profile in Ts65Dn microglia, with fewer in a homeostatic state and more in an intermediate aberrantly reactive state than in euploid microglia. This comprehensive understanding of microglial transcriptional dynamics sheds light on potential pathogenetic mechanisms but also possible avenues for therapy for neurodevelopmental disorders.

The lncRNA Snhg11, a new candidate contributing to neurogenesis, plasticity, and memory deficits in Down syndrome.

Down syndrome (DS) stands as the prevalent genetic cause of intellectual disability, yet comprehensive understanding of its cellular and molecular underpinnings remains limited. In this study, we explore the cellular landscape of the hippocampus in a DS mouse model, the Ts65Dn, through single-nuclei transcriptional profiling. Our findings demonstrate that trisomy manifests as a highly specific modification of the transcriptome within distinct cell types. Remarkably, we observed a significant shift in the transcriptomic profile of granule cells in the dentate gyrus (DG) associated with trisomy. We identified the downregulation of a specific small nucleolar RNA host gene, Snhg11, as the primary driver behind this observed shift in the trisomic DG. Notably, reduced levels of Snhg11 in this region were also observed in a distinct DS mouse model, the Dp(16)1Yey, as well as in human postmortem brain tissue, indicating its relevance in Down syndrome. To elucidate the function of this long non-coding RNA (lncRNA), we knocked down Snhg11 in the DG of wild-type mice. Intriguingly, this intervention alone was sufficient to impair synaptic plasticity and adult neurogenesis, resembling the cognitive phenotypes associated with trisomy in the hippocampus. Our study uncovers the functional role of Snhg11 in the DG and underscores the significance of this lncRNA in intellectual disability. Furthermore, our findings highlight the importance of DG in the memory deficits observed in Down syndrome.

Readaptación funcional basada en ejercicio físico terapéutico en pacientes con COVID persistente (RECOVER) / Functional rehabilitation based on therapeutic exercise training in patients with postacute COVID syndrome (RECOVER)

Introduction and objectives Postacute COVID syndrome (PACS) is common after acute SARS-CoV-2 infection. One of the most frequent and disabling symptoms is exercise intolerance (EI). Recent evidence suggests that EI in PACS has a peripheral (metabolic-neuromuscular) origin, suggesting that exercise training may be an effective treatment. The aim of this study was to assess the role a therapeutic physical exercise program (TPEP) in PACS with EI. Method This single-center, open-label, randomized clinical trial compared an exercise training program (intervention group) with regular physical activity recommendations (control group) in patients with PACS and EI. The intervention group underwent an 8-week TPEP. The primary endpoint was improvement in functional capacity, assessed as the change in peak VO2. Results We included 50 participants with PACS (73% women, mean age 47±7.1 years). The intervention group showed a 15% improvement in peak VO2 (peak VO2 pre- and postintervention: 25.5±7.7mL/kg/min and 29.3±4.7 mL/kg/min; P <.001) and a 13.2% improvement in predicted values (92.1±14.3% and 108.4±13.4%; P <.001). No significant changes in VO2 values were observed in the control group. Unlike the control group, the intervention group also showed improvements in all secondary outcomes: quality of life scales, muscle power, maximum inspiratory power, metabolic flexibility, and body fat percentage. Conclusions The program improved functional capacity in patients with PACS and EI (AU)

Introducción y objetivos El síndrome de COVID persistente (SCP) es frecuente tras la infección aguda por SARS-CoV-2, y la intolerancia al ejercicio (IE) uno de los síntomas más frecuentes y limitantes. La evidencia reciente indica que el origen de los síntomas es periférico (muscular), por lo que el ejercicio físico podría ser un tratamiento eficaz. Este estudio evalúa la eficacia de un programa de ejercicio físico terapéutico (PEFT) en la mejora de la capacidad funcional de los pacientes con SCP e IE. Métodos Estudio aleatorizado, unicéntrico, controlado y abierto que compara un PEFT (grupo de intervención) con recomendaciones de actividad física estándar (grupo de control) en pacientes con SCP con IE. El grupo de intervención recibió 8 semanas de PEFT. El objetivo principal fue el cambio en la capacidad funcional medido mediante el consumo pico de oxígeno (VO2 pico). Resultados Se incluyó a un total de 50 pacientes con SCP (el 73% mujeres; media de edad, 47±7,1 años). El grupo de intervención presentó una mejora en el VO2 pico del 15% (VO2 pico inicial y final: 25,5±7,7 y 29,3±4,7ml/kg/min; p <0,001) y del 13,2% en valores del %VO2 máximo predicho (el 92,1±14,3% y el 108,4±13,4%; p <0,001), sin cambios significativos en el grupo de control. Todos los objetivos secundarios también mejoraron exclusivamente en el grupo de intervención: escalas de calidad de vida, potencia muscular desarrollada, potencia inspiratoria máxima, flexibilidad metabólica y porcentaje de grasa corporal. Conclusiones El PEFT mejora la capacidad funcional de los pacientes con SCP e IE (AU)

Functional rehabilitation based on therapeutic exercise training in patients with postacute COVID syndrome (RECOVER).

INTRODUCTION AND OBJECTIVES: Postacute COVID syndrome (PACS) is common after acute SARS-CoV-2 infection. One of the most frequent and disabling symptoms is exercise intolerance (EI). Recent evidence suggests that EI in PACS has a peripheral (metabolic-neuromuscular) origin, suggesting that exercise training may be an effective treatment. The aim of this study was to assess the role a therapeutic physical exercise program (TPEP) in PACS with EI. METHODS: This single-center, open-label, randomized clinical trial compared an exercise training program (intervention group) with regular physical activity recommendations (control group) in patients with PACS and EI. The intervention group underwent an 8-week TPEP. The primary endpoint was improvement in functional capacity, assessed as the change in peak VO2. RESULTS: We included 50 participants with PACS (73% women, mean age 47±7.1 years). The intervention group showed a 15% improvement in peak VO2 (peak VO2 pre- and postintervention: 25.5±7.7mL/kg/min and 29.3±4.7 mL/kg/min; P <.001) and a 13.2% improvement in predicted values (92.1±14.3% and 108.4±13.4%; P <.001). No significant changes in VO2 values were observed in the control group. Unlike the control group, the intervention group also showed improvements in all secondary outcomes: quality of life scales, muscle power, maximum inspiratory power, metabolic flexibility, and body fat percentage. CONCLUSIONS: The program improved functional capacity in patients with PACS and EI.

Chemical, Biochemical, Cellular, and Physiological Characterization of Leucettinib-21, a Down Syndrome and Alzheimer's Disease Drug Candidate.

Leucettinibs are substituted 2-aminoimidazolin-4-ones (inspired by the marine sponge natural product Leucettamine B) developed as pharmacological inhibitors of DYRK1A (dual-specificity, tyrosine phosphorylation-regulated kinase 1A), a therapeutic target for indications such as Down syndrome and Alzheimer's disease. Leucettinib-21 was selected as a drug candidate following extensive structure/activity studies and multiparametric evaluations. We here report its physicochemical properties (X-ray powder diffraction, differential scanning calorimetry, stability, solubility, crystal structure) and drug-like profile. Leucettinib-21's selectivity (analyzed by radiometric, fluorescence, interaction, thermal shift, residence time assays) reveals DYRK1A as the first target but also some "off-targets" which may contribute to the drug's biological effects. Leucettinib-21 was cocrystallized with CLK1 and modeled in the DYRK1A structure. Leucettinib-21 inhibits DYRK1A in cells (demonstrated by direct catalytic activity and phosphorylation levels of Thr286-cyclin D1 or Thr212-Tau). Leucettinib-21 corrects memory disorders in the Down syndrome mouse model Ts65Dn and is now entering safety/tolerance phase 1 clinical trials.

Exploring the link between hedonic overeating and prefrontal cortex dysfunction in the Ts65Dn trisomic mouse model.

Individuals with Down syndrome (DS) have a higher prevalence of obesity compared to the general population. Conventionally, this has been attributed to endocrine issues and lack of exercise. However, deficits in neural reward responses and dopaminergic disturbances in DS may be contributing factors. To investigate this, we focused on a mouse model (Ts65Dn) bearing some triplicated genes homologous to trisomy 21. Through detailed meal pattern analysis in male Ts65Dn mice, we observed an increased preference for energy-dense food, pointing towards a potential "hedonic" overeating behavior. Moreover, trisomic mice exhibited higher scores in compulsivity and inflexibility tests when limited access to energy-dense food and quinine hydrochloride adulteration were introduced, compared to euploid controls. Interestingly, when we activated prelimbic-to-nucleus accumbens projections in Ts65Dn male mice using a chemogenetic approach, impulsive and compulsive behaviors significantly decreased, shedding light on a promising intervention avenue. Our findings uncover a novel mechanism behind the vulnerability to overeating and offer potential new pathways for tackling obesity through innovative interventions.

The lncRNA Snhg11, a new candidate contributing to neurogenesis, plasticity and memory deficits in Down syndrome.

Down syndrome (DS) stands as the prevalent genetic cause of intellectual disability, yet comprehensive understanding of its cellular and molecular underpinnings remains limited. In this study, we explore the cellular landscape of the hippocampus in a DS mouse model through single-nuclei transcriptional profiling. Our findings demonstrate that trisomy manifests as a highly specific modification of the transcriptome within distinct cell types. Remarkably, we observed a significant shift in the transcriptomic profile of granule cells in the dentate gyrus (DG) associated with trisomy. We identified the downregulation of a specific small nucleolar RNA host gene, Snhg11, as the primary driver behind this observed shift in the trisomic DG. Notably, reduced levels of Snhg11 in this region were also observed in a distinct DS mouse model, the Dp(16)1Yey, as well as in human postmortem tissue, indicating its relevance in Down syndrome. To elucidate the function of this long non-coding RNA (lncRNA), we knocked down Snhg11 in the DG of wild-type mice. Intriguingly, this intervention alone was sufficient to impair synaptic plasticity and adult neurogenesis, resembling the cognitive phenotypes associated with trisomy in the hippocampus. Our study uncovers the functional role of Snhg11 in the DG and underscores the significance of this lncRNA in intellectual disability. Furthermore, our findings highlight the importance of the DG in the memory deficits observed in Down syndrome.

Fano-Like Resonance from Disorder Correlation in Vacancy-Doped Photonic Crystals.

By preparing colloidal crystals with random missing scatterers, crystals are created where disorder is embodied as vacancies in an otherwise perfect lattice. In this special system, there is a critical defect concentration where light propagation undergoes a transition from an all but perfect reflector (for the spectral range defined by the Bragg condition), to a metamaterial exhibiting an enhanced transmission phenomenon. It is shown that this behavior can be phenomenologically described in terms of Fano-like resonances. The results show that the Fano's parameter q experiences a sign change signaling the transition from a perfect crystal exhibiting a reflectance Bragg peak, through a state where background scattering is maximum and Bragg reflectance reaches a minimum to a point where the system reenters a low scattering state recovering ordinary Bragg diffraction. A simple dipolar model considering the correlation between scatterers and vacancies is proposed and the reported evolution of the Fano-like scattering is explained in terms of the emerging covariance between the optical paths and polarizabilities and the effect of field enhancement in photonic crystal (PhC) defects.

The method behind the unprecedented production of indicators of the presence of languages in the Internet.

Reliable and updated indicators of the presence of languages in the Internet are required to drive efficiently policies for languages, to forecast e-commerce market or to support further researches on the field of digital support of languages. This article presents a complete description of the methodological elements involved in the production of an unprecedented set of indicators of the presence in the Internet of the 329 languages with more than 1 million L1 speakers. A special emphasis is given to the treatment of the comprehensive set of biases involved in the process, either from the method or the various sources used in the modeling process. The biases related to other sources providing similar data are also discussed, and in particular, it is shown how the lack of consideration of the high level of multilingualism of the Web leads to a huge overestimation of the presence of English. The detailed list of sources is presented in the various annexes. For the first time in the history of the Internet, the production of indicators about virtual presence of a large set of languages could allow progress in the fields of economy of languages, cyber-geography of languages and language policies for multilingualism.

Defective engram allocation contributes to impaired fear memory performance in Down syndrome.

Down syndrome (DS) is the most common genetic form of intellectual disability (ID). The cellular and molecular mechanisms contributing to ID in DS are not completely understood. Recent evidence indicates that a given memory is encoded by sparsely distributed neurons, highly activated during learning, the engram cells. Intriguingly, mechanisms that are of paramount importance for engram formation are impaired in DS. Here we explored engram formation in a DS mouse model, the Ts65Dn and we found a reduced number of engram cells in the dentate gyrus (DG), suggesting reduced neuronal allocation to engrams. We also show that trisomic engram cells present reduced number of mature spines than WT engram cells and their excitability is not enhanced during memory recall. In fact, activation of engram cells using a chemogenetic approach does not recover memory deficits in Ts65Dn. Altogether, our findings suggest that perturbations in engram neurons may play a significant role in memory alterations in DS.

Extrathoracic Aneurysms in Marfan Syndrome: A Systematic Review of the Literature.

BACKGROUND: Marfan syndrome (MS) most often shows as thoracic aortic aneurysm (TAA) or aortic dissection, but it may also involve other vascular territories. This study aimed to identify those extrathoracic vascular manifestations most frequently associated with MS. METHODS: A systematic review of the literature with Preferred Reporting Items for Systematic Reviews and Meta-Analyses criteria was carried out. The following databases were included: MEDLINE, Embase, Web of Science, Cumulative Index of Nursing and Health Sciences Literature (CINHAL); Spanish database MEDESY Cochrane Central Register of Controlled Trials (CENTRAL). RESULTS: A total of 10,008 articles were identified, leaving 155 for the first stage of data analysis (total incidence of aneurysms) and 83 for the second (descriptive data analysis). Overall, 518 aneurysms were identified: 149 in the head and neck, 94 in the extremities, and 275 in the aortic, iliac, and visceral sectors. Mostly, they were simultaneously discovered during studies of the TAA. In the abdominal aorta, the presentation with rupture in 11 of 32 patients stands out. Resection and bypass were the most frequently used methods for repair in the treated cases. CONCLUSIONS: Although its frequency in the general population is unknown, this systematic review suggests that extrathoracic aneurysmal arterial involvement in the MS may be more frequent than expected. We believe screening for aneurysms in other vascular sectors may be advisable, especially in patients with MS and TAA.

Müller glia fused with adult stem cells undergo neural differentiation in human retinal models.

BACKGROUND: Visual impairments are a critical medical hurdle to be addressed in modern society. Müller glia (MG) have regenerative potential in the retina in lower vertebrates, but not in mammals. However, in mice, in vivo cell fusion between MG and adult stem cells forms hybrids that can partially regenerate ablated neurons. METHODS: We used organotypic cultures of human retina and preparations of dissociated cells to test the hypothesis that cell fusion between human MG and adult stem cells can induce neuronal regeneration in human systems. Moreover, we established a microinjection system for transplanting human retinal organoids to demonstrate hybrid differentiation. FINDINGS: We first found that cell fusion occurs between MG and adult stem cells, in organotypic cultures of human retina as well as in cell cultures. Next, we showed that the resulting hybrids can differentiate and acquire a proto-neural electrophysiology profile when the Wnt/beta-catenin pathway is activated in the adult stem cells prior fusion. Finally, we demonstrated the engraftment and differentiation of these hybrids into human retinal organoids. INTERPRETATION: We show fusion between human MG and adult stem cells, and demonstrate that the resulting hybrid cells can differentiate towards neural fate in human model systems. Our results suggest that cell fusion-mediated therapy is a potential regenerative approach for treating human retinal dystrophies. FUNDING: This work was supported by La Caixa Health (HR17-00231), Velux Stiftung (976a) and the Ministerio de Ciencia e Innovación, (BFU2017-86760-P) (AEI/FEDER, UE), AGAUR (2017 SGR 689, 2017 SGR 926).

Proteomic profiling reveals mitochondrial dysfunction in the cerebellum of transgenic mice overexpressing DYRK1A, a Down syndrome candidate gene.

Introduction: DYRK1A is a dual-specificity kinase that is overexpressed in Down syndrome (DS) and plays a key role in neurogenesis, neuronal differentiation and function, cognitive phenotypes, and aging. Dyrk1A has also been implicated in cerebellar abnormalities observed in association with DS, and normalization of Dyrk1A dosage rescues granular and Purkinje cell densities in a trisomic DS mouse model. However, the underlying molecular mechanisms governing these processes are unknown. Methods: To shed light on the effects of Dyrk1A overexpression in the cerebellum, here we investigated the cerebellar proteome in transgenic Dyrk1A overexpressing mice in basal conditions and after treatment with green tea extract containing epigallocatechin-3-gallate (EGCG), a DYRK1A inhibitor. Results and Discussion: Our results showed that Dyrk1A overexpression alters oxidative phosphorylation and mitochondrial function in the cerebellum of transgenic mice. These alterations are significantly rescued upon EGCG-containing green tea extract treatment, suggesting that its effects in DS could depend in part on targeting mitochondria, as shown by the partially restoration by the treatment of the increased mtDNA copy number in TG non-treated mice.

Neurodevelopmental disorders: 2022 update.

With a prevalence of 2-4% of the worldwide population, neurodevelopmental disorders (NDDs) comprise a heterogeneous group of disorders associated with neurodevelopmental dysfunction, including intellectual disability (ID), autism spectrum disorder (ASD), Down syndrome (DS) and attention-deficit/hyperactivity disorder (ADHD) among others. However, due to their heterogeneity and overlapping clinical features, NDDs such as ASD are often misdiagnosed, while for others with more distinct symptoms, such as Rett syndrome or DS, the mechanisms underlying their pathogenesis remain elusive. Last year, important steps in the mechanistic understanding of several NDDs have been achieved. New preclinical models demonstrated causality between PAK3 mutations and disorders associated with social deficiencies. ARID1B mutations have been linked to neuroectoderm specification in Coffin-Siris syndrome and DNA damage was established as an important pathologic mechanism in Aicardi-Goutières syndrome. Moreover, alterations in basic molecular processes including translation and histone acetylation have been established as major traits in the pathology of X-linked ID and Rett syndrome, revealing new pathogenetic mechanisms. Last year, advances in bioinformatics have begun to shed light on the human repeatome, a largely unexplored part of our genome, and how alterations in these sequences have a central role in ASD. The role of mitochondria in neuropathology was clarified last year with the discovery of previously unknown vesicles derived from mitochondria with a putative role in DS. An interesting discovery in the field of basic neurodevelopment showed that during postnatal brain development, changes in genome architecture and transcriptional dynamics progress independently of sensory experience. Finally, our neurocentric views of NDDs are changing as new players such as astrocytes are revealed to be crucial in neuropathology. The role of astrocytes has been clarified for some pathologies such as ASD and DS, linking well-known genetic mutations to impaired astrocyte function.

Conservative Surgical Management of Late Carotid Patch Infection in a Patient with Subsequent Stenting for Restenosis.

Carotid patch infection is a rare but dreaded complication after endarterectomy. About 160 cases can be found in literature, but presentation in a patient with post-endarterectomy stenting has not been reported. Most frequent clinical manifestations include the occurrence of a sinus, a pseudoaneurysm, or neck swelling, but in severe cases it may present anastomosis dehiscence with hematoma or hemorrhage. Usually, patch removal and reconstruction is recommended, but there is not a standard protocol for management. Conservative surgical management with patch preservation has only been reported in a minority of cases. We report a patient with a history of carotid endarterectomy and subsequent carotid stenting 21 months later because of >80% restenosis. He presented a sinus in the scar 81 months after the former intervention. The patient underwent surgery, and during the procedure, a detachment of a small segment of the Dacron patch from the surrounding tissue was found. The sinus tract was resected, and after verifying the integrity of the patch, it was irrigated with rifampicin and preserved in situ. S. epidermidis was isolated from tissue cultures. Twenty-four months later, the patient remains asymptomatic and duplex ultrasound shows no signs of infection. Conservative surgical approach can be a valid option for treatment and may be considered in selected patients with limited infection.

Endotension: twenty years of a controversial term.

Use of the term endotension in the treatment of aortic aneurysm is currently controversial. Initially it was proposed to define the circumstance in which there is an enlargement of the aneurysm sac after endovascular repair without a demonstrable endoleak. The term was established with the aim of transmitting the possibility of causes other than pressure applying stress to the aneurysm wall. Twenty years have passed since the proposal of this terminology was published. The literature is reviewed with the purpose of providing an update on advances in the knowledge of the possible etiological mechanisms. The experimental studies call into question that causes other than pressure determine the increase of the aneurysm. On the basis of this review, the term `Sac Expansion Without Evident Leak´ (SEWEL) is proposed as a more accurate and precise denomination for what is aimed to be defined. Evidence suggests that the more likely mechanisms of persistent pressurization of the aneurysm sac are an unidentified endoleak (likely type I or low-flow Type II) or thrombus occluding wide and short channels that connects with the excluded aneurysm sac (at the attachment sites of the stent-graft or at the branch vessels orifices).

Rethinking Intellectual Disability from Neuro- to Astro-Pathology.

Neurodevelopmental disorders arise from genetic and/or from environmental factors and are characterized by different degrees of intellectual disability. The mechanisms that govern important processes sustaining learning and memory, which are severely affected in intellectual disability, have classically been thought to be exclusively under neuronal control. However, this vision has recently evolved into a more integrative conception in which astroglia, rather than just acting as metabolic supply and structural anchoring for neurons, interact at distinct levels modulating neuronal communication and possibly also cognitive processes. Recently, genetic tools have made it possible to specifically manipulate astrocyte activity unraveling novel functions that involve astrocytes in memory function in the healthy brain. However, astrocyte manipulation has also underscored potential mechanisms by which dysfunctional astrocytes could contribute to memory deficits in several neurodevelopmental disorders revealing new pathogenic mechanisms in intellectual disability. Here, we review the current knowledge about astrocyte dysfunction that might contribute to learning and memory impairment in neurodevelopmental disorders, with special focus on Fragile X syndrome and Down syndrome.

Vacancies in Self-Assembled Crystals: An Archetype for Clusters Statistics at the Nanoscale.

Complex systems involving networks have attracted strong multidisciplinary attention since they are predicted to sustain fascinating phase transitions in the proximity of the percolation threshold. Developing stable and compact archetypes that allow one to experimentally study physical properties around the percolation threshold remains a major challenge. In nanoscale systems, this achievement is rare since it is tied to the ability to control the intentional disorder and perform a vast statistical analysis of cluster configurations. Here, a self-assembly method to fabricate perfectly ordered structures where random defects can be introduced is presented. Building binary crystals from two types of dielectric nanospheres and selectively removing one of them creates vacancies at random lattice positions that form a complex network of clusters. Vacancy content can be easily controlled and raised even beyond the percolation threshold. In these structures, the distribution of cluster sizes as a function of vacancy density is analyzed. For moderate concentrations, it is found to be homogeneous throughout the structure and in good agreement with the assumption of a random vacancy distribution.