Effects of impurities on the ice microstructure of Monte Perdido Glacier, Central Pyrenees, NE Spain

Monte Perdido Glacier, located in the central Pyrenees, is one of the southernmost glaciers in Europe. Due to climate change, this glacier is suffering an accelerated mass loss, especially in the last decades. If the current trends persist, this glacier is expected to disappear in the next 50 years. As part of the efforts of the scientific community to increase the knowledge about this glacier, this research presents the first microstructural characterization of the Monte Perdido Glacier, focused on a high-impurity concentration segment that belongs to an ice core drilled in 2017. The results reveal the ice has a layering defined by air bubbles and non-soluble impurities. The bubble-defined layering exhibits features of both a primary (sedimentary) and a secondary (strain-induced) origin. We found a clear inverse correspondence between the particle concentration and the grains' size and roundness index. A preliminary micro-Raman characterization of the particles shows the occurrence of atacamite, anatase (likely related to ancient mining activities in the vicinity of the glacier) and quartz. The latter could be an indicator of mineral dust, probably suggesting the arrival of dust-laden air masses from the north of the African continent.This research was supported by the Spanish Government through the María de Maeztu excellence accreditation 2018–2022 (MDM-2017-0714) and by the Spanish Agencia Estatal de Investigación (AEI Spain) through the projects PaleoICE EXPLORA (CGL2015-72167-EXP) and iMechPro (RTI2018-100696-B-I00). NGS acknowledges a PhD grant from the Basque Government (PRE-2018-1-0116). We thank the directorate of the Parque Nacional de Ordesa y Monte Perdido (Spain) for permission to investigate the Monte Perdido glacier. We also thank Ibai Rico ( https://basquemountainguides.com/ , UPV/EHU), Maria Leunda (UPV/EHU), and Juan Ignacio López-Moreno (IPE-CSIC) for their help during the sampling of the MP1 ice core, and Pedro Sanchez Navarrete (IPE-CSIC) for transporting the ice samples. Finally, we would like to extend our appreciation to the anonymous reviewers, the Scientific Editor, Christine Hvidberg, and the Chief Editor, Hester Jiskoot, for their valuable comments on this manuscript

Application of a new protocol for providing obstetric care in an outpatient service during the COVID-19 pandemic in a public hospital in Madrid, Spain.

Objective: To evaluate the clinical implementation of a preventive COVID-19 protocol regarding re-organization of appointments and documented infections among health workers in an obstetric outpatient service. Methods: Descriptive analysis of the antenatal care at our obstetric outpatient service and infection rates among health care providers from March 19th to May 22nd, 2020. Appointments were divided into telephone calls or face-to-face examinations. A pre-consultation triage was implemented to identify suspected SARS-CoV2 infected women to reschedule them 14 days later or, if the consultation was non-delayable, to use complete Personal Protective Equipment (PPE). Firstly, the number of face-to-face appointments, telephone appointments, and COVID-19 diagnoses in pregnant women were analyzed. Secondly, the number of obstetricians and nurses diagnosed with SARS-CoV2 infection and their serologic status during universal screening in May 2020 were recorded. Results: One thousand eight hundred forty-two obstetric appointments were scheduled during this period, including 432 (23.5%) telephone appointments (96.53% according to clinical protocol, 1.62% symptomatic patients advised to stay at home, and 1.85% COVID-19 confirmed cases), and 1,410 (76.5%) face-to-face appointments (9.7% did not attend due to fear of getting the infection, 3.1% were lost-to-follow-up, 0.5% were rescheduled due to COVID-19 symptoms and 86.7% who did attend). Of the 1,223 women attending their hospital appointment, 3.6% screened positive at the triage (72.7% rescheduled and 27.3% seen with PPE). 43 rRT-PCR-SARS-CoV2 tests were performed, and two tested positive. No COVID-19 symptoms were reported among health workers at the outpatient obstetric service, and only one nurse presented immunoglobulin (Ig)G anti-SARS-CoV2. Conclusion: A prompt implementation of a preventive protocol in a hospital obstetric outpatient service, including triage, hygienic and preventive measurements, and rescheduling pregnancy appointments, reduces the percentage of health workers affected by SARS-CoV2.post-print369 K

Vectorcardiography-derived index allows a robust quantification of ventricular electrical synchrony

Alteration of muscle activation sequence is a key mechanism in heart failure with reduced ejection fraction. Successful cardiac resynchronization therapy (CRT), which has become standard therapy in these patients, is limited by the lack of precise dyssynchrony quantification. We implemented a computational pipeline that allows assessment of ventricular dyssynchrony by vectorcardiogram reconstruction from the patient’s electrocardiogram. We defined a ventricular dyssynchrony index as the distance between the voltage and speed time integrals of an individual observation and the linear fit of these variables obtained from a healthy population. The pipeline was tested in a 1914-patient population. The dyssynchrony index showed minimum values in heathy controls and maximum values in patients with left bundle branch block (LBBB) or with a pacemaker (PM). We established a critical dyssynchrony index value that discriminates electrical dyssynchronous patterns (LBBB and PM) from ventricular synchrony. In 10 patients with PM or CRT devices, dyssynchrony indexes above the critical value were associated with high time to peak strain standard deviation, an echocardiographic measure of mechanical dyssynchrony. Our index proves to be a promising tool to evaluate ventricular activation dyssynchrony, potentially enhancing the selection of candidates for CRT, device configuration during implantation, and post-implant optimization.Fil: Fernández, Juan Manuel Francisco. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Física de Líquidos y Sistemas Biológicos. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Instituto de Física de Líquidos y Sistemas Biológicos; ArgentinaFil: Spagnuolo, Damián N.. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Física de Líquidos y Sistemas Biológicos. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Instituto de Física de Líquidos y Sistemas Biológicos; ArgentinaFil: Politi, María T.. Universidad de Buenos Aires; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Fisiología y Biofísica Bernardo Houssay. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Fisiología y Biofísica Bernardo Houssay; ArgentinaFil: Tello Santacruz, Iván A.. Hospital Británico de Buenos Aires; ArgentinaFil: Schiavone, Miguel. Hospital Británico de Buenos Aires; ArgentinaFil: Cáceres Monié, César. Hospital Británico de Buenos Aires; ArgentinaFil: Avaca, Horacio A.. Hospital Británico de Buenos Aires; ArgentinaFil: Chara, Osvaldo. Universidad Argentina de la Empresa; Argentina. Consejo Nacional de Investigaciones Científicas y Técnicas. Centro Científico Tecnológico Conicet - La Plata. Instituto de Física de Líquidos y Sistemas Biológicos. Universidad Nacional de La Plata. Facultad de Ciencias Exactas. Instituto de Física de Líquidos y Sistemas Biológicos; Argentina. Technische Universität Dresden; Alemani

Risk of miscarriage after chorionic villus sampling.

OBJECTIVE: To estimate the risk of miscarriage associated to chorionic villus sampling (CVS). METHODS: This was a retrospective cohort study performed in eight fetal-medicine units in Spain, Belgium and Bulgaria. Two populations were included: first, all singleton pregnancies attending to their first-trimester assessment in Murcia, Spain, and second, all singleton pregnancies having a CVS following first-trimester assessment at any of the participating centers. We used propensity score matching analysis to estimate the association between CVS and miscarriage. We compared risks of miscarriage of CVS and non-CVS groups after propensity score matching (1:1 ratio). This procedure creates two comparable groups balancing the maternal and pregnancy characteristics that lead to CVS, in a similar way in which randomization operates in a randomized clinical trial. RESULTS: The study population consisted of 22,250 participants in the non-CVS group and 3,613 in the CVS group. The incidence of miscarriage in the CVS group was 2.1% (77/3,613), which was significantly higher than the 0.9% (207/22,250) in the non-CVS group (p <0.001). The propensity score algorithm matched 2,122 CVS cases with 2,122 non-CVS cases including 40 (1.9%) and 55 (2.6%) miscarriages in the CVS and non-CVS groups, respectively (OR 0.72 [95% CI 0.48 to 1.10]; p = 0.146). However, we found a significant interaction between the CVS risk of miscarriage and the risk of aneuploidies, suggesting a different effect of the CVS for different baseline characteristics in such a way that, when the risk of aneuploidies is low, the risk after CVS increases (OR 2.87 [95% CI 1.13 to 7.30]) but when the risk is high, the risk after CVS is paradoxically reduced (OR 0.47 [95% CI 0.28 to 0.76]), presumably due to prenatal diagnosis and termination of major aneuploidies that would have otherwise resulted in spontaneous miscarriage. CONCLUSIONS: The risk of miscarriage in women having a CVS is about 1% higher than in women without CVS, although this excess risk is not entirely due to the invasive procedure but to some extent the demographic and pregnancy characteristics of the patient undergoing CVS. After accounting for these risk factors and confining the analysis to low-risk pregnancies, CVS seems to increase the risk of miscarriage about three times above the patient's background-risk. Although this is a substantial increase in relative terms, in pregnancies without risk factors, the risk of miscarriage after CVS will still remain low and similar to or slightly higher than that of the general population. For example, if her risk of aneuploidy is 1 in a 1,000 (0.1%), her risk of miscarriage after CVS will increase to 0.3% (0.2% higher)

Specific patterns of brain alterations underlie distinct clinical profiles in Huntington's disease

Huntington's disease (HD) is a genetic neurodegenerative disease which involves a triad of motor, cognitive and psychiatric disturbances. However, there is great variability in the prominence of each type of symptom across individuals. The neurobiological basis of such variability remains poorly understood but would be crucial for better tailored treatments. Multivariate multimodal neuroimaging approaches have been successful in disentangling these profiles in other disorders. Thus we applied for the first time such approach to HD. We studied the relationship between HD symptom domains and multimodal measures sensitive to grey and white matter structural alterations. Forty-three HD gene carriers (23 manifest and 20 premanifest individuals) were scanned and underwent behavioural assessments evaluating motor, cognitive and psychiatric domains. We conducted a multimodal analysis integrating different structural neuroimaging modalities measuring grey matter volume, cortical thickness and white matter diffusion indices - fractional anisotropy and radial diffusivity. All neuroimaging measures were entered into a linked independent component analysis in order to obtain multimodal components reflecting common inter-subject variation across imaging modalities. The relationship between multimodal neuroimaging independent components and behavioural measures was analysed using multiple linear regression. We found that cognitive and motor symptoms shared a common neurobiological basis, whereas the psychiatric domain presented a differentiated neural signature. Behavioural measures of different symptom domains correlated with different neuroimaging components, both the brain regions involved and the neuroimaging modalities most prominently associated with each type of symptom showing differences. More severe cognitive and motor signs together were associated with a multimodal component consisting in a pattern of reduced grey matter, cortical thickness and white matter integrity in cognitive and motor related networks. In contrast, depressive symptoms were associated with a component mainly characterised by reduced cortical thickness pattern in limbic and paralimbic regions. In conclusion, using a multivariate multimodal approach we were able to disentangle the neurobiological substrates of two distinct symptom profiles in HD: one characterised by cognitive and motor features dissociated from a psychiatric profile. These results open a new view on a disease classically considered as a uniform entity and initiates a new avenue for further research considering these qualitative individual differences

Specific patterns of brain alterations underlie distinct clinical profiles in Huntington's disease

Huntington's disease (HD) is a genetic neurodegenerative disease which involves a triad of motor, cognitive and psychiatric disturbances. However, there is great variability in the prominence of each type of symptom across individuals. The neurobiological basis of such variability remains poorly understood but would be crucial for better tailored treatments. Multivariate multimodal neuroimaging approaches have been successful in disentangling these profiles in other disorders. Thus we applied for the first time such approach to HD. We studied the relationship between HD symptom domains and multimodal measures sensitive to grey and white matter structural alterations. Forty-three HD gene carriers (23 manifest and 20 premanifest individuals) were scanned and underwent behavioural assessments evaluating motor, cognitive and psychiatric domains. We conducted a multimodal analysis integrating different structural neuroimaging modalities measuring grey matter volume, cortical thickness and white matter diffusion indices - fractional anisotropy and radial diffusivity. All neuroimaging measures were entered into a linked independent component analysis in order to obtain multimodal components reflecting common inter-subject variation across imaging modalities. The relationship between multimodal neuroimaging independent components and behavioural measures was analysed using multiple linear regression. We found that cognitive and motor symptoms shared a common neurobiological basis, whereas the psychiatric domain presented a differentiated neural signature. Behavioural measures of different symptom domains correlated with different neuroimaging components, both the brain regions involved and the neuroimaging modalities most prominently associated with each type of symptom showing differences. More severe cognitive and motor signs together were associated with a multimodal component consisting in a pattern of reduced grey matter, cortical thickness and white matter integrity in cognitive and motor related networks. In contrast, depressive symptoms were associated with a component mainly characterised by reduced cortical thickness pattern in limbic and paralimbic regions. In conclusion, using a multivariate multimodal approach we were able to disentangle the neurobiological substrates of two distinct symptom profiles in HD: one characterised by cognitive and motor features dissociated from a psychiatric profile. These results open a new view on a disease classically considered as a uniform entity and initiates a new avenue for further research considering these qualitative individual differences

White matter cortico-striatal tracts predict apathy subtypes in Huntington's disease

BACKGROUND: Apathy is the neuropsychiatric syndrome that correlates most highly with Huntington's disease progression, and, like early patterns of neurodegeneration, is associated with lesions to cortico-striatal connections. However, due to its multidimensional nature and elusive etiology, treatment options are limited. OBJECTIVES: To disentangle underlying white matter microstructural correlates across the apathy spectrum in Huntington's disease. METHODS: Forty-six Huntington's disease individuals (premanifest (N = 22) and manifest (N = 24)) and 35 healthy controls were scanned at 3-tesla and underwent apathy evaluation using the short-Problem Behavior Assessment and short-Lille Apathy Rating Scale, with the latter being characterized into three apathy domains, namely emotional, cognitive, and auto-activation deficit. Diffusion tensor imaging was used to study whether individual differences in specific cortico-striatal tracts predicted global apathy and its subdomains. RESULTS: We elucidate that apathy profiles may develop along differential timelines, with the auto-activation deficit domain manifesting prior to motor onset. Furthermore, diffusion tensor imaging revealed that inter-individual variability in the disruption of discrete cortico-striatal tracts might explain the heterogeneous severity of apathy profiles. Specifically, higher levels of auto-activation deficit symptoms significantly correlated with increased mean diffusivity in the right uncinate fasciculus. Conversely, those with severe cognitive apathy demonstrated increased mean diffusivity in the right frontostriatal tract and left dorsolateral prefrontal cortex to caudate nucleus tract. CONCLUSIONS: The current study provides evidence that white matter correlates associated with emotional, cognitive, and auto-activation subtypes may elucidate the heterogeneous nature of apathy in Huntington's disease, as such opening a door for individualized pharmacological management of apathy as a multidimensional syndrome in other neurodegenerative disorders

Clinical and Biomarker Changes in Dominantly Inherited Alzheimer's Disease

BACKGROUND: The order and magnitude of pathologic processes in Alzheimer's disease are not well understood, partly because the disease develops over many years. Autosomal dominant Alzheimer's disease has a predictable age at onset and provides an opportunity to determine the sequence and magnitude of pathologic changes that culminate in symptomatic disease. METHODS: In this prospective, longitudinal study, we analyzed data from 128 participants who underwent baseline clinical and cognitive assessments, brain imaging, and cerebrospinal fluid (CSF) and blood tests. We used the participant's age at baseline assessment and the parent's age at the onset of symptoms of Alzheimer's disease to calculate the estimated years from expected symptom onset (age of the participant minus parent's age at symptom onset). We conducted cross-sectional analyses of baseline data in relation to estimated years from expected symptom onset in order to determine the relative order and magnitude of pathophysiological changes. RESULTS: Concentrations of amyloid-beta (Aβ)(42) in the CSF appeared to decline 25 years before expected symptom onset. Aβ deposition, as measured by positron-emission tomography with the use of Pittsburgh compound B, was detected 15 years before expected symptom onset. Increased concentrations of tau protein in the CSF and an increase in brain atrophy were detected 15 years before expected symptom onset. Cerebral hypometabolism and impaired episodic memory were observed 10 years before expected symptom onset. Global cognitive impairment, as measured by the Mini-Mental State Examination and the Clinical Dementia Rating scale, was detected 5 years before expected symptom onset, and patients met diagnostic criteria for dementia at an average of 3 years after expected symptom onset. CONCLUSIONS: We found that autosomal dominant Alzheimer's disease was associated with a series of pathophysiological changes over decades in CSF biochemical markers of Alzheimer's disease, brain amyloid deposition, and brain metabolism as well as progressive cognitive impairment. Our results require confirmation with the use of longitudinal data and may not apply to patients with sporadic Alzheimer's disease. (Funded by the National Institute on Aging and others; DIAN ClinicalTrials.gov number, NCT00869817.)