Seamless Fusion: Multi-Modal Localization for First Responders in Challenging Environments.

In dynamic and unpredictable environments, the precise localization of first responders and rescuers is crucial for effective incident response. This paper introduces a novel approach leveraging three complementary localization modalities: visual-based, Galileo-based, and inertial-based. Each modality contributes uniquely to the final Fusion tool, facilitating seamless indoor and outdoor localization, offering a robust and accurate localization solution without reliance on pre-existing infrastructure, essential for maintaining responder safety and optimizing operational effectiveness. The visual-based localization method utilizes an RGB camera coupled with a modified implementation of the ORB-SLAM2 method, enabling operation with or without prior area scanning. The Galileo-based localization method employs a lightweight prototype equipped with a high-accuracy GNSS receiver board, tailored to meet the specific needs of first responders. The inertial-based localization method utilizes sensor fusion, primarily leveraging smartphone inertial measurement units, to predict and adjust first responders' positions incrementally, compensating for the GPS signal attenuation indoors. A comprehensive validation test involving various environmental conditions was carried out to demonstrate the efficacy of the proposed fused localization tool. Our results show that our proposed solution always provides a location regardless of the conditions (indoors, outdoors, etc.), with an overall mean error of 1.73 m.

Short- and long-term outcomes after distal pancreatectomy with radiologic infiltration of splenic vessels for pancreatic ductal adenocarcinoma.

BACKGROUND: The effect of radiologic splenic vessels involvement (RSVI) on the survival of patients with pancreatic adenocarcinoma (PAC) located in the body and tail of the pancreas is controversial, and its influence on postoperative morbidity after distal pancreatectomy (DP) is unknown. This study aimed to determine the influence of RSVI on postoperative complications, overall survival (OS), and disease-free survival (DFS) in patients undergoing DP for PAC. METHODS: A multicenter retrospective study of DP was conducted at 7 hepatopancreatobiliary units between January 2008 and December 2018. Patients were classified according to the presence of RSVI. A Clavien-Dindo grade of >II was considered to represent a major complication. RESULTS: A total of 95 patients were included in the analysis. Moreover, 47 patients had vascular infiltration: 4 had arterial involvement, 10 had venous involvement, and 33 had both arterial and venous involvements. The rates of major complications were 20.8% in patients without RSVI, 40.0% in those with venous RSVI, 25.0% in those with arterial RSVI, and 30.3% in those with both arterial and venous RSVIs (P = .024). The DFS rates at 3 years were 56% in the group without RSVI, 50% in the group with arterial RSVI, and 16% in the group with both arterial and venous RSVIs (P = .003). The OS rates at 3 years were 66% in the group without RSVI, 50% in the group with arterial RSVI, and 29% in the group with both arterial and venous RSVIs (P < .0001). CONCLUSION: RSVI increased the major complication rates after DP and reduced the OS and DFS. Therefore, it may be a useful prognostic marker in patients with PAC scheduled to undergo DP and may help to select patients likely to benefit from neoadjuvant treatment.

Enhancing Kidney Transplant Outcomes: The Impact of Living Donor Programs.

INTRODUCTION: The protocol for deceased donor kidney transplants has been standardised. The procedure for a living donor has peculiarities derived from the differences in the graft. When a living kidney donor program is implemented, changes occur in both the profile of the kidney transplant candidate and in the postoperative treatments. AIMS: To discover whether a living donor program influences the functional outcomes of kidney grafts in a longstanding classical deceased donor kidney transplant program and to identify the factors associated with transplant outcomes. METHODS: Retrospective observational multicentre study. SAMPLE: Kidney transplant patients in two urology referral centres for renal transplant in Spain between 1994 and 2019. Groups: TV (living transplant): patients given kidney transplants from living donors (n = 150); TCpre11 (deceased transplant previous to 2011): patients given kidney transplants from deceased donors before the living donor program was implemented (n = 650); and TCpost11 (deceased transplant after 2011): patients given kidney transplants from deceased donors after the living donor program was implemented (n = 500). RESULTS: Mean age was 55.75 years (18-80 years), higher in TCpre11. There were 493 female patients (37.92%) and 1007 male patients (62.08%). Mean body mass index (BMI) was 26.69 kg/m2 (17.50-42.78 kg/m2), higher in TCpre11. Mean ischemia time was 17.97 h (6-29 h), higher in TCpost11. Median duration of urethral catheter: 8 days (6-98 days), higher in TCpost11. Median duration of double-J ureteral stent: 58 days (24-180 days), higher in TCpost11. Pretransplant UTIs: 17.77%, higher in TCpre11 (25.69%) than in TV (12%), higher in TV (12%) than TCpost11 (9.2%), and higher in TCpre11 (25.69%) than TCpost11 (9.2%). Acute renal rejection in 9.33% of TV, 14.77% of TCpre11, and 9.8% of TCpost11. Multivariate analysis: TCpost11 featured higher BMI, more smoking, and chronic renal failure progression time. Lower use of nonantibiotic prophylaxis to prevent recurrent urinary tract infections, increased duration of urethral catheters due to obstructive problems, and favoured deterioration of kidney function was observed in the deceased donor program. The living donor (LD) program had a strong influence on deceased donor transplants in the prelysis phase. Implementation of a LD program was associated with a decrease in the likelihood of acute rejection in TCpost11 and an increase in the tendency towards normal kidney function. CONCLUSIONS: Implementing living donor transplant programs affects functional outcomes in deceased donor transplants, reducing the probability of acute rejection and increasing the tendency towards normal kidney function. Preventing recurrent urinary tract infections with measures other than antibiotics, smoking cessation, delaying the removal of the double-J stent from the graft, and pre-emptive transplant (transplant prior to dialysis) are associated with improved renal function of the graft.

Hereditary Transthyretin Amyloidosis and the Impact of Classic and New Treatments on Kidney Function: A Review.

Hereditary transthyretin amyloidosis (ATTRv) is a rare, progressive, and life-threatening disease caused by misfolded transthyretin (TTR) proteins that aggregate as abnormal amyloid fibrils and accumulate throughout the body. The kidney is one of the main organs affected in amyloid light chain (AL) amyloidosis and ATTRv amyloidosis. The most common clinical presentation is proteinuria, which consists mainly of albumin; this is the first step in the natural history of ATTRv nephropathy. Not all TTR mutations are equal in terms of ATTRv kidney involvement. Kidney involvement in ATTRv itself is difficult to define, given the numerous associated confounding factors. There are several treatments available to treat ATTRv, including orthotopic liver transplant (OLT), which is the classic treatment for ATTRv. However, we should be careful regarding the use of calcineurin inhibitors in the setting of OLT because these can be nephrotoxic. New treatments for amyloidosis may have an impact on kidney function, including drugs that target specific pathways involved in the disease. Tafamidis and diflunisal, which are TTR stabilizers, patisiran (RNA interference agent), and inotersen (antisense oligonucleotide inhibitor) have been shown to reduce TTR amyloid. Tafamidis and patisiran are medications that have reduced the progression of kidney disease in amyloidosis, but inotersen and diflunisal may damage kidney function.

Profiling the proximal proteome of the activated µ-opioid receptor.

The µ-opioid receptor (µOR) represents an important target of therapeutic and abused drugs. So far, most understanding of µOR activity has focused on a subset of known signal transducers and regulatory molecules. Yet µOR signaling is coordinated by additional proteins in the interaction network of the activated receptor, which have largely remained invisible given the lack of technologies to interrogate these networks systematically. Here we describe a proteomics and computational approach to map the proximal proteome of the activated µOR and to extract subcellular location, trafficking and functional partners of G-protein-coupled receptor (GPCR) activity. We demonstrate that distinct opioid agonists exert differences in the µOR proximal proteome mediated by endocytosis and endosomal sorting. Moreover, we identify two new µOR network components, EYA4 and KCTD12, which are recruited on the basis of receptor-triggered G-protein activation and might form a previously unrecognized buffering system for G-protein activity broadly modulating cellular GPCR signaling.

Fourier phase index for extracting signatures of determinism and nonlinear features in time series.

Detecting determinism and nonlinear properties from empirical time series is highly nontrivial. Traditionally, nonlinear time series analysis is based on an error-prone phase space reconstruction that is only applicable for stationary, largely noise-free data from a low-dimensional system and requires the nontrivial adjustment of various parameters. We present a data-driven index based on Fourier phases that detects determinism at a well-defined significance level, without using Fourier transform surrogate data. It extracts nonlinear features, is robust to noise, provides time-frequency resolution by a double running window approach, and potentially distinguishes regular and chaotic dynamics. We test this method on data derived from dynamical models as well as on real-world data, namely, intracranial recordings of an epileptic patient and a series of density related variations of sediments of a paleolake in Tlaxcala, Mexico.

An epigenetic barrier sets the timing of human neuronal maturation.

The pace of human brain development is highly protracted compared with most other species1-7. The maturation of cortical neurons is particularly slow, taking months to years to develop adult functions3-5. Remarkably, such protracted timing is retained in cortical neurons derived from human pluripotent stem cells (hPSCs) during in vitro differentiation or upon transplantation into the mouse brain4,8,9. Those findings suggest the presence of a cell-intrinsic clock setting the pace of neuronal maturation, although the molecular nature of this clock remains unknown. Here we identify an epigenetic developmental programme that sets the timing of human neuronal maturation. First, we developed a hPSC-based approach to synchronize the birth of cortical neurons in vitro which enabled us to define an atlas of morphological, functional and molecular maturation. We observed a slow unfolding of maturation programmes, limited by the retention of specific epigenetic factors. Loss of function of several of those factors in cortical neurons enables precocious maturation. Transient inhibition of EZH2, EHMT1 and EHMT2 or DOT1L, at progenitor stage primes newly born neurons to rapidly acquire mature properties upon differentiation. Thus our findings reveal that the rate at which human neurons mature is set well before neurogenesis through the establishment of an epigenetic barrier in progenitor cells. Mechanistically, this barrier holds transcriptional maturation programmes in a poised state that is gradually released to ensure the prolonged timeline of human cortical neuron maturation.

An illness-death multistate model to implement delta adjustment and reference-based imputation with time-to-event endpoints.

With a treatment policy strategy, therapies are evaluated regardless of the disturbance caused by intercurrent events (ICEs). Implementing this estimand is challenging if subjects are not followed up after the ICE. This circumstance can be dealt with using delta adjustment (DA) or reference-based (RB) imputation. In the survival field, DA and RB imputation have been researched so far using multiple imputation (MI). Here, we present a fully analytical solution. We use the illness-death multistate model with the following transitions: (a) from the initial state to the event of interest, (b) from the initial state to the ICE, and (c) from the ICE to the event. We estimate the intensity function of transitions (a) and (b) using flexible parametric survival models. Transition (c) is assumed unobserved but identifiable using DA or RB imputation assumptions. Various rules have been considered: no ICE effect, DA under proportional hazards (PH) or additive hazards (AH), jump to reference (J2R), and (either PH or AH) copy increment from reference. We obtain the marginal survival curve of interest by calculating, via numerical integration, the probability of transitioning from the initial state to the event of interest regardless of having passed or not by the ICE state. We use the delta method to obtain standard errors (SEs). Finally, we quantify the performance of the proposed estimator through simulations and compare it against MI. Our analytical solution is more efficient than MI and avoids SE misestimation-a known phenomenon associated with Rubin's variance equation.

Dissecting the molecular basis for the modulation of neurotransmitter GPCR signaling by GINIP.

It is well established that G-protein-coupled receptors (GPCRs) stimulated by neurotransmitters are critical for neuromodulation. Much less is known about how heterotrimeric G-protein (Gαßγ) regulation after receptor-mediated activation contributes to neuromodulation. Recent evidence indicates that the neuronal protein GINIP shapes GPCR inhibitory neuromodulation via a unique mechanism of G-protein regulation that controls pain and seizure susceptibility. However, the molecular basis of this mechanism remains ill-defined because the structural determinants of GINIP responsible for binding and regulating G proteins are not known. Here, we combined hydrogen-deuterium exchange mass spectrometry, computational structure predictions, biochemistry, and cell-based biophysical assays to demonstrate an effector-like binding mode of GINIP to Gαi. Specific amino acids of GINIP's PHD domain first loop are essential for G-protein binding and subsequent regulation of Gαi-GTP and Gßγ signaling upon neurotransmitter GPCR stimulation. In summary, these findings shed light onto the molecular basis for a post-receptor mechanism of G-protein regulation that fine-tunes inhibitory neuromodulation.

Descontrol glucémico: desafío de salud pública en prepandemia y pandemia.

OBJETIVO: Comparar el control glucémico entre pacientes con diabetes mellitus tipo 2 prepandemia vs pandemia de Covid-19 que acudieron a unidades de salud de primer nivel de atención de la Ciudad de México. Material y métodos. Se analizaron los registros de 23 912 pacientes con diabetes; 78.7% fueron del grupo prepandemia (2016 a 2020) y 21.3% del grupo pandemia (marzo 2020 a julio 2021). Se calcularon medidas de tendencia central y de dispersión, pruebas t de Student y se ajustó un modelo de regresión logística múltiple. RESULTADOS: La mayoría de los pacientes con diabetes fueron mujeres (66.6 y 62.6%) con edad promedio de 59 y 58 años, respectivamente, y con hemoglobina glucosilada (HbA1) final de 7.7 vs el grupo pandemia (8.0). Las variables asociadas con el descontrol glucémico incluyeron periodo, nivel de HbA1, sobrepeso, obesidad, antecedente de padres con diabetes, número de medicamentos y tipo de insulina. CONCLUSIONES: La mayoría de los pacientes con diabetes en ambos grupos tuvieron descontrol glucémico. Los pacientes del grupo pandemia tuvieron mayor descontrol glucémico de HbA1 comparados con los del grupo prepandemia. Después de recibir atención médica en ambos grupos, los pacientes mejoraron su control glucémico.

Distinct beta-arrestin coupling and intracellular trafficking of metabotropic glutamate receptor homo- and heterodimers.

The metabotropic glutamate receptors (mGluRs) are family C, dimeric G protein-coupled receptors (GPCRs), which play critical roles in synaptic transmission. Despite an increasing appreciation of the molecular diversity of this family, how distinct mGluR subtypes are regulated remains poorly understood. We reveal that different group II/III mGluR subtypes show markedly different beta-arrestin (ß-arr) coupling and endocytic trafficking. While mGluR2 is resistant to internalization and mGluR3 shows transient ß-arr coupling, which enables endocytosis and recycling, mGluR8 and ß-arr form stable complexes, which leads to efficient lysosomal targeting and degradation. Using chimeras and mutagenesis, we pinpoint carboxyl-terminal domain regions that control ß-arr coupling and trafficking, including the identification of an mGluR8 splice variant with impaired internalization. We then use a battery of high-resolution fluorescence assays to find that heterodimerization further expands the diversity of mGluR regulation. Together, this work provides insight into the relationship between GPCR/ß-arr complex formation and trafficking while revealing diversity and intricacy in the regulation of mGluRs.

Improving the performance of the Cleveland Clinic Score for predicting acute kidney injury after cardiac surgery: a prospective multicenter cohort study.

BACKGROUND: Cardiac surgery-associated acute kidney injury (CSA-AKI) is associated with high short- and long-term mortality rates. The prediction of CSA-AKI is crucial for early detection and treatment. Current predictive models may be improved by potentially useful preoperative and intraoperative information. METHODS: This multicenter prospective cohort study recruited 261 consecutive patients at high risk for developing CSA-AKI, based on a Cleveland Clinical Score (CCS) of ≥4 points from July to December 2017 in 14 hospitals in Spain and the UK. Postoperative AKI occurred in 145 (55.5%) patients. The receiver operating characteristics curve (AUC) of a base model including only the CCS was compared with models including additional preoperative and intraoperative variables such as the estimated glomerular filtration rate (eGFR) instead of plasmatic creatinine, intraoperative urine output, baseline hemoglobin, nadir hemoglobin, and glycosylated hemoglobin (HbA1c) instead of diabetes mellitus. The performance of each model for AKI was compared. RESULTS: The CCS alone gave an AUC of 0.67 (95% CI, 0.56-0.78) for postoperative AKI. None of the single variables added to the base model CCS improve discrimination. The AUC for postoperative AKI was improved when baseline hemoglobin, eGFR instead of plasmatic creatinine, HbA1c, and nadir hemoglobin were added to the CCS (AUC=0.77; 95% CI, 0.67-0.87; P=0.02). CONCLUSIONS: The addition of baseline hemoglobin, eGFR, HbA1c, and nadir intraoperative hemoglobin may be useful for improving the discrimination of the clinical predictive risk scores for AKI.

Prognostic Significance of Amino Acid and Biogenic Amines Profiling in Chronic Kidney Disease.

There is a pressing need for more precise biomarkers of chronic kidney disease (CKD). Plasma samples from 820 subjects [231 with CKD, 325 with end-stage kidney disease (ESKD) and 264 controls] were analyzed by liquid chromatography with tandem mass spectrometry (LC-MS/MS) to determine a metabolic profile of 28 amino acids (AAs) and biogenic amines to test their value as markers of CKD risk and progression. The kynurenine/tryptophan ratio showed the strongest correlation with estimated glomerular filtration rate values (coefficient = -0.731, p < 0.0001). Models created with orthogonal partial least squares-discriminant analysis (OPLS-DA) containing the metabolic signature showed a high goodness of fit and predictability for controls/CKD (R2X:0.73:R2Y:0.92:Q2:0.92, p < 0.0001) and lower values for CKD/ESKD (R2X:0.56:R2Y:0.59:Q2:0.55, p < 0.0001). Based on generated VIP scores, the most relevant markers for segregating samples into control/CKD and CKD/ESKD groups were citrulline (1.63) and tryptophan (1.47), respectively. ROC analysis showed that the addition of the metabolic profile to a model including CKD classic risk factors improved the AUC from 86.7% (83.6-89.9) to 100% (100-100) for CKD risk (p < 0.0001) and from 63.0% (58.2-67.8) to 96.5% (95.3-97.8) for the risk of progression from CKD to ESKD (p < 0.0001). Plasma concentrations of AAs and related amines may be useful as diagnostic biomarkers of kidney disease, both for CKD risk and for progression of CKD patients to ESKD.

Influence of phylogenetic, environmental, and behavioral factors on the gut bacterial community structure of dung beetles (Scarabaeidae: Scarabaeinae) in a Neotropical Biosphere Reserve.

Gut bacteria help dung beetles metabolize nutrients contained and synthesize those unavailable in their food, depending on the ecological scenario in which they develop. However, less is known about the influence of environmental and behavioral factors on the taxonomic composition of bacterial gut communities in Scarabaeinae beetles. To address this research topic, we analyzed 13 tropical dung beetle species in the Los Tuxtlas Biosphere Reserve, Mexico, to understand how the beetle tribe, habitat, food preference, food relocation, and parental care influence the composition of gut bacterial communities. We found that the beetle tribe is the primary factor impacting the taxonomic composition of gut bacterial communities. Among them, Deltochilini displayed the highest variability in diversity due to the different combinations of habitat and food preferences among its species. On the other hand, the other tribes studied did not exhibit such variable combinations. Habitat emerged as the second most influential factor, with forest-dwelling beetles displaying higher diversity. This can be attributed to the heterogeneous environments within tropical forests, which offer a greater diversity of food resources. In contrast, grassland beetles, living in more homogeneous environments and relying on cow feces as their main food source, exhibited lower diversity. Our findings suggest a correlation between bacterial diversity and food resource availability in complex habitats, such as tropical forests, which offer a wider array of food sources compared to simpler environments like grasslands.

Structural basis of allosteric modulation of metabotropic glutamate receptor activation and desensitization.

The metabotropic glutamate receptors (mGluRs) are neuromodulatory family C G protein coupled receptors which assemble as dimers and allosterically couple extracellular ligand binding domains (LBDs) to transmembrane domains (TMDs) to drive intracellular signaling. Pharmacologically, mGluRs can be targeted either at the LBDs by glutamate and synthetic orthosteric compounds or at the TMDs by allosteric modulators. Despite the potential of allosteric TMD-targeting compounds as therapeutics, an understanding of the functional and structural basis of their effects on mGluRs is limited. Here we use a battery of approaches to dissect the distinct functional and structural effects of orthosteric versus allosteric ligands. We find using electrophysiological and live cell imaging assays that both agonists and positive allosteric modulators (PAMs) can drive activation and desensitization of mGluRs. The effects of PAMs are pleiotropic, including both the ability to boost the maximal response to orthosteric agonists and to serve independently as desensitization-biased agonists across mGluR subtypes. Conformational sensors reveal PAM-driven inter-subunit re-arrangements at both the LBD and TMD. Motivated by this, we determine cryo-electron microscopy structures of mGluR3 in the presence of either an agonist or antagonist alone or in combination with a PAM. These structures reveal PAM-driven re-shaping of intra- and inter-subunit conformations and provide evidence for a rolling TMD dimer interface activation pathway that controls G protein and beta-arrestin coupling. Highlights: -Agonists and PAMs drive mGluR activation, desensitization, and endocytosis-PAMs are desensitization-biased and synergistic with agonists-Four combinatorial ligand conditions reveal an ensemble of full-length mGluR structures with novel interfaces-Activation and desensitization involve rolling TMD interfaces which are re-shaped by PAM.

Control of G protein-coupled receptor function via membrane-interacting intrinsically disordered C-terminal domains.

G protein-coupled receptors (GPCRs) control intracellular signaling cascades via agonist-dependent coupling to intracellular transducers including heterotrimeric G proteins, GPCR kinases (GRKs), and arrestins. In addition to their critical interactions with the transmembrane core of active GPCRs, all three classes of transducers have also been reported to interact with receptor C-terminal domains (CTDs). An underexplored aspect of GPCR CTDs is their possible role as lipid sensors given their proximity to the membrane. CTD-membrane interactions have the potential to control the accessibility of key regulatory CTD residues to downstream effectors and transducers. Here we report that the CTDs of two closely related family C GPCRs, metabotropic glutamate receptor 2 (mGluR2) and mGluR3, bind to membranes and that this interaction controls receptor function. We first characterize CTD structure with NMR spectroscopy, revealing lipid composition-dependent modes of membrane binding. Using molecular dynamics simulations and structure-guided mutagenesis, we identify key conserved residues and cancer-associated mutations that control CTD-membrane binding. Finally, we provide evidence that mGluR3 transducer coupling is controlled by CTD-membrane interactions in live cells which can be modulated by disease-associated mutations or CTD phosphorylation. This work reveals a novel mechanism of GPCR modulation, suggesting that CTD-membrane binding may be a general regulatory mode throughout the broad GPCR superfamily.

Clinical factors for predicting cardiovascular risk, need for renal replacement therapy, and mortality in patients with non-dialysis-dependent stage 3-5 chronic kidney disease from the Salford Kidney Study.

BACKGROUND: Established cardiovascular risk assessment tools lack chronic kidney disease-specific clinical factors and may underestimate cardiovascular risk in non-dialysis-dependent chronic kidney disease (CKD) patients. METHODS: A retrospective analysis of a cohort of patients with stage 3-5 non-dialysis-dependent chronic kidney disease in the Salford Kidney Study (UK, 2002-2016) was performed. Multivariable Cox regression models with backward selection and repeated measures joint models were used to evaluate clinical risk factors associated with cardiovascular events (individual and composite cardiovascular major adverse cardiovascular events), mortality (all-cause and cardiovascular-specific), and need for renal replacement therapy. Models were established using 70% of the cohort and validated on the remaining 30%. Hazard ratios ([95% CIs]) were reported. RESULTS: Among 2192 patients, mean follow-up was 5.6 years. Cardiovascular major adverse cardiovascular events occurred in 422 (19.3%) patients; predictors included prior history of diabetes (1.39 [1.13-1.71]; P = 0.002) and serum albumin reduction of 5 g/L (1.20 [1.05-1.36]; P = 0.006). All-cause mortality occurred in 740 (33.4%) patients, median time to death was 3.8 years; predictors included reduction of estimated glomerular filtration of 5 mL/min/1.73 m2 (1.05 [1.01-1.08]; P = 0.011) and increase of phosphate of 0.1 mmol/L (1.04 [1.01-1.08]; P = 0.021), whereas a 10 g/L hemoglobin increase was protective (0.90 [0.85-0.95]; P < 0.001). In 394 (18.0%) patients who received renal replacement therapy, median time to event was 2.3 years; predictors included halving of estimated glomerular filtration rate (3.40 [2.65-4.35]; P < 0.001) and antihypertensive use (1.23 [1.12-1.34]; P < 0.001). Increasing age, albumin reduction, and prior history of diabetes or cardiovascular disease were risk factors for all outcomes except renal replacement therapy. CONCLUSIONS: Several chronic kidney disease-specific cardiovascular risk factors were associated with increased mortality and cardiovascular event risk in patients with non-dialysis-dependent chronic kidney disease.

A database of low-energy atomically precise nanoclusters.

The chemical and structural properties of atomically precise nanoclusters are of great interest in numerous applications, but the structures of the clusters can be computationally expensive to predict. In this work, we present the largest database of cluster structures and properties determined using ab-initio methods to date. We report the methodologies used to discover low-energy clusters as well as the energies, relaxed structures, and physical properties (such as relative stability, HOMO-LUMO gap among others) for 63,015 clusters across 55 elements. We have identified clusters for 593 out of 1595 cluster systems (element-size pairs) explored by literature that have energies lower than those reported in literature by at least 1 meV/atom. We have also identified clusters for 1320 systems for which we were unable to find previous low-energy structures in the literature. Patterns in the data reveal insights into the chemical and structural relationships among the elements at the nanoscale. We describe how the database can be accessed for future studies and the development of nanocluster-based technologies.

Uso de móviles, problemas de sueño y obesidad en una zona de exclusión social / Mobile phone use, sleep disorders and obesity in a social exclusion zone

Introducción: Existe poca información del impacto del abuso del teléfono móvil (AM) en zonas con necesidad de transformación social (ZNTS). Nuestro objetivo es estimar la prevalencia de AM en ZNTS, y su asociación con problemas de sueño, rendimiento escolar y obesidad. Pacientes y métodos: Muestreo consecutivo de sujetos entre 10 y 17 años que acuden a consulta de atención primaria en ZNTS entre octubre 2019 y marzo de 2020. Realización de entrevista clínica, antropometría, datos sociodemográficos, de uso de móvil y sueño. Resultados: Se estudiaron 214 sujetos. El AM durante la semana (más de dos horas diarias) fue de 37,5% en el grupo de 10-12 años y de 65,2% en el grupo de 13 a 17 años; durante el fin de semana, las prevalencias fueron de 66,6 y 81,3%, respectivamente. El AM durante la semana se asoció a más obesidad; menor nivel de estudios maternos, mayor dificultad para despertarse, somnolencia diurna y mayor frecuencia de suspensos. El riesgo ajustado se duplica para sobrepeso u obesidad (odds ratio [OR] 1,90; intervalo de confianza del 95% [IC 95%] 1,04 a 3,47), obesidad (OR 2,45; IC 95% 1,23 a 4,89) y problemas de sueño o duración de sueño menor de siete horas (OR 2,26; IC 95% 1,31 a 3,92). El AM durante el fin de semana se asoció a problemas de sueño o duración menor de siete horas (OR 2,68; IC 95% 1,40 a 5,11). Conclusiones: Existe una alta prevalencia de AM en zonas de exclusión social, que se asocia con problemas del sueño, suspensos escolares y obesidad. (AU)

Introduction: There is little information on the impact of mobile phone overuse (MPO) in areas in need of social transformation (ANST). Our objective was to estimate the prevalence of MPO in an ANST and its association with sleep disorders, academic performance and obesity. Patients and methods: Consecutive sampling of patients aged 10–17 years who visited a primary care centre in an ARST between October 2019 and March 2020. The study involved performance of a clinical interview with collection of anthropometric, sociodemographic, mobile phone use and sleep data. Results: The analysis included 214 participants. The prevalence of MPO during weekdays (more than 2 h a day) was 37.5% in children aged 10–12 years and 65.2% in 13- to 17-year-olds; in the weekend, the prevalence increased to 66.6% and 81.3%, respectively. In weekdays, MPO was associated with an increased prevalence of obesity, lower maternal educational attainment, greater difficulty waking up, daytime sleepiness and higher frequency of school failure. The adjusted risk was double for excess weight (odds ratio [OR] 1.90, 95% confidence interval [95% CI] 1.04–3.47), obesity (OR 2.45, 95% CI 1.23–4.89) and sleep disorders or sleep duration of less than 7 h (OR 2.26; 95% CI 1.31–3.92). Weekend MPO was associated with sleep disorders or sleep duration of less than 7 h (OR 2.68; 95% CI 1.40–5.11). Conclusions: The prevalence of mobile phone overuse is high in areas of social exclusion and is associated with sleep disorders, school failure, and obesity. (AU)

A New Species of the Pythonomorph Carentonosaurus from the Cenomanian of Algora (Guadalajara, Central Spain).

The Cenomanian (lowermost Upper Cretaceous) faunal assemblages are of high interest in understanding the turnovers that took place between the Early and the Late Cretaceous, resulting in significant differences. In this context, the analysis of the association of reptiles found in the Algora fossil site (Guadalajara Province, Central Spain) is of great interest since it represents the first European Cenomanian site with a high concentration of macrovertebrate remains. A new pythonomorph 'lizard' from Algora, Carentonosaurus algorensis sp. nov., is described here. It is the second representative of this European genus. Its microanatomical study reveals that an extreme pachyosteosclerosis affected at least its dorsal vertebrae, suggesting adaptations for slow-swimming habits in shallow-water environments. Consequently, this new taxon is interpreted as a slow swimmer, hovering near the bottom of near-shore marine environments of the Late Cretaceous European Archipelago and, more specifically, along the shores of the larger Iberian Island for that period. This is in concordance with the high diversification of 'pachyostotic' pythonomorphs recorded during the Cenomanian, allowing the subsequent adaptation of this lineage to open marine environments.