44 research outputs found
Trauma e vulnerabilità nei migranti richiedenti protezione internazionale
INTRODUZIONE: I rifugiati richiedenti protezione internazionale mostrano un'alta vulnerabilità e Disturbo Post-Traumatico da Stress (PTSD). OBIETTIVI: abbiamo utilizzato un approccio integrato multidisciplinare per valutare la loro vulnerabilità e psicopatologia. METODI: sono stati valutati 180 rifugiati politici secondo i criteri del DSM-IV-TR. RISULTATI: in un'alta percentuale di rifugiati politici la diagnosi principale è stata di PTSD associata con disturbi di personalità e/o altri disturbi psichici. CONCLUSIONI: i rifugiati politici hanno più difficoltà nel gestire le proprie emozioni, questo probabilmente è dovuto alla propria storia personale intrisa di vissuti traumatici, tuttavia attraverso un lavoro sia psicoterapico che farmacologico è stato possibile migliorare le proprie condizioni
Predicting the Effects of Waning Vaccine Immunity Against COVID-19 through High-Resolution Agent-Based Modeling
The potential waning of the vaccination immunity to COVID-19 could pose
threats to public health, as it is tenable that the timing of such waning would
synchronize with the near-complete restoration of normalcy. Should also testing
be relaxed, we might witness a resurgent COVID-19 wave in winter 2021/2022. In
response to this risk, an additional vaccine dose, the booster shot, is being
administered worldwide. In a projected study with an outlook of six months, we
explore the interplay between the rate at which boosters are distributed and
the extent to which testing practices are implemented, using a highly granular
agent-based model tuned on a medium-sized U.S. town. Theoretical projections
indicate that the administration of boosters at the rate at which the vaccine
is currently administered could yield a severe resurgence of the pandemic.
Projections suggest that the peak levels of mid spring 2021 in the vaccination
rate may prevent such a scenario to occur, although exact agreement between
observations and projections should not be expected due to continuously
evolving nature of the pandemics. Our study highlights the importance of
testing, especially to detect asymptomatic individuals in the near future, as
the release of the booster reaches full speed.Comment: 56 pages; 15 figures; accepted for publication in Advanced Theory and
Simulation
Activity‑driven network modeling and control of the spread of two concurrent epidemic strains
The emergency generated by the current COVID-19 pandemic has claimed millions of lives worldwide. There have been multiple waves across the globe that emerged as a result of new variants, due to arising from unavoidable mutations. The existing network toolbox to study epidemic spreading cannot be readily adapted to the study of multiple, coexisting strains. In this context, particularly lacking are models that could elucidate re-infection with the same strain or a different strain—phenomena that we are seeing experiencing more and more with COVID-19. Here, we establish a novel mathematical model to study the simultaneous spreading of two strains over a class of temporal networks. We build on the classical susceptible–exposed–infectious–removed model, by incorporating additional states that account for infections and re-infections with multiple strains. The temporal network is based on the activity-driven network paradigm, which has emerged as a model of choice to study dynamic processes that unfold at a time scale comparable to the network evolution. We draw analytical insight from the dynamics of the stochastic network systems through a mean-field approach, which allows for characterizing the onset of different behavioral phenotypes (non-epidemic, epidemic, and endemic). To demonstrate the practical use of the model, we examine an intermittent stay-at-home containment strategy, in which a fraction of the population is randomly required to isolate for a fixed period of time
Designing the Safe Reopening of US Towns Through High-Resolution Agent-Based Modeling
As COVID‐19 vaccine is being rolled out in the US, public health authorities are gradually reopening the economy. To date, there is no consensus on a common approach among local authorities. Here, a high‐resolution agent‐based model is proposed to examine the interplay between the increased immunity afforded by the vaccine roll‐out and the transmission risks associated with reopening efforts. The model faithfully reproduces the demographics, spatial layout, and mobility patterns of the town of New Rochelle, NY — representative of the urban fabric of the US. Model predictions warrant caution in the reopening under the current rate at which people are being vaccinated, whereby increasing access to social gatherings in leisure locations and households at a 1% daily rate can lead to a 28% increase in the fatality rate within the next three months. The vaccine roll‐out plays a crucial role on the safety of reopening: doubling the current vaccination rate is predicted to be sufficient for safe, rapid reopening
High-Resolution Agent-Based Modeling of COVID-19 Spreading in a Small Town
Amid the ongoing COVID-19 pandemic, public health authorities and the general
population are striving to achieve a balance between safety and normalcy. Ever
changing conditions call for the development of theory and simulation tools to
finely describe multiple strata of society while supporting the evaluation of
"what-if" scenarios. Particularly important is to assess the effectiveness of
potential testing approaches and vaccination strategies. Here, an agent-based
modeling platform is proposed to simulate the spreading of COVID-19 in small
towns and cities, with a single-individual resolution. The platform is
validated on real data from New Rochelle, NY -- one of the first outbreaks
registered in the United States. Supported by expert knowledge and informed by
reported data, the model incorporates detailed elements of the spreading within
a statistically realistic population. Along with pertinent functionality such
as testing, treatment, and vaccination options, the model accounts for the
burden of other illnesses with symptoms similar to COVID-19. Unique to the
model is the possibility to explore different testing approaches -- in
hospitals or drive-through facilities -- and vaccination strategies that could
prioritize vulnerable groups. Decision making by public authorities could
benefit from the model, for its fine-grain resolution, open-source nature, and
wide range of features.Comment: 44 pages (including 16 of Supplementary Information). Published
online in Advanced Theory and Simulation
Unequal effects of the national lockdown on mental and social health in Italy
With the exception of a few countries that chose a different approach, the worldwide reaction to the COVID-19 pandemic was a (longer or shorter) period of national lockdown. While the economic consequences of shutting down national economies were immediately evident, the sociopsychiatric implications of the social confinement of the entire population remain hidden and not fully understood. Italy has been the first European country to be severely impacted by the COVID-19 pandemic, to which it responded through strict lockdown measurements. The results of a timely survey on mental and social health, carried out by students and teachers of a middle school in Rome, might help identify the most vulnerable groups of the population. This evidence could be crucial in conceiving and enacting targeted public health policies to mitigate the consequences of the pandemic on mental health and to prevent intolerance to containment measures in some population segments, which could hamper worldwide efforts in the fight against COVID-19
1000 Days: The “WeCare Generation” Program—The Ultimate Model for Improving Human Mental Health and Economics: The Study Protocol
Abstract
Introduction: The COVID-19 pandemic stressed the necessity of a new resilience of the human population and health system. The “WeCare Generation” program is a new proposal of territorial intervention, with a new paradigm, on the diseases of the human body and mind. Background: In recent decades, the independent strands of investigation on brain plasticity and early trauma consequences have demonstrated that traumatic experiences in the period from pregnancy to the age of 3 years have an enormous impact on an individual’s future development, and both physical and mental health. Research shows that adverse child experiences (ACEs) are associated with a strong risk of conditions such as: harmful alcohol use, smoking, illicit drug use, high body-mass index, depression, anxiety, interpersonal violence, cancer, type 2 diabetes, cardiovascular diseases, stroke respiratory diseases and, as a consequence, to a high financial cost in Italy and also across Europe (1–9% GDP) and the USA (total annual costs estimated to be USD 581 billion in Europe and USD 748 billion in North America). All this suggests that an early intervention on that traumatized-slice of population leads to multiplied savings. Methods: A multi-center, randomized, controlled trial was designed. The parents of the future neonatal population (from pregnancy to delivery) with trauma will be enrolled, and randomized to treatment, or control arm. The article describes in detail how the primary outpoint (cost to the national health system), and some secondary outpoints, will be collected. Discussion: An overall rate of return on investment (ROI) statistically significant 13.0% per annum with an associated benefit/cost ratio (BCR) of 6.3 is expected as the primary outcome of the “WeCare Generation” program. Our proposed model predicts a new medical paradigm aiming to empower new generations, with a strong return on economy and health
PMCA-based detection of prions in the olfactory mucosa of patients with Sporadic Creutzfeldt-Jakob Disease
Sporadic Creutzfeldt-Jakob disease (sCJD) is a rare neurodegenerative disorder caused by the conformational conversion of the prion protein (PrPC) into an abnormally folded form, named prion (or PrPSc). The combination of the polymorphism at codon 129 of the PrP gene (coding either methionine or valine) with the biochemical feature of the proteinase-K resistant PrP (generating either PrPSc type 1 or 2) gives rise to different PrPSc strains, which cause variable phenotypes of sCJD. The definitive diagnosis of sCJD and its classification can be achieved only post-mortem after PrPSc identification and characterization in the brain. By exploiting the Real-Time Quaking-Induced Conversion (RT-QuIC) assay, traces of PrPSc were found in the olfactory mucosa (OM) of sCJD patients, thus demonstrating that PrPSc is not confined to the brain. Here, we have optimized another technique, named protein misfolding cyclic amplification (PMCA) for detecting PrPSc in OM samples of sCJD patients. OM samples were collected from 27 sCJD and 2 genetic CJD patients (E200K). Samples from 34 patients with other neurodegenerative disorders were included as controls. Brains were collected from 26 sCJD patients and 16 of them underwent OM collection. Brain and OM samples were subjected to PMCA using the brains of transgenic mice expressing human PrPC with methionine at codon 129 as reaction substrates. The amplified products were analyzed by Western blot after proteinase K digestion. Quantitative PMCA was performed to estimate PrPSc concentration in OM. PMCA enabled the detection of prions in OM samples with 79.3% sensitivity and 100% specificity. Except for a few cases, a predominant type 1 PrPSc was generated, regardless of the tissues analyzed. Notably, all amplified PrPSc were less resistant to PK compared to the original strain. In conclusion, although the optimized PMCA did not consent to recognize sCJD subtypes from the analysis of OM collected from living patients, it enabled us to estimate for the first time the amount of prions accumulating in this biological tissue. Further assay optimizations are needed to faithfully amplify peripheral prions whose recognition could lead to a better diagnosis and selection of patients for future clinical trials
Altered plasma protein profiles in genetic FTD – a GENFI study
© The Author(s) 2023. Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.Background: Plasma biomarkers reflecting the pathology of frontotemporal dementia would add significant value to clinical practice, to the design and implementation of treatment trials as well as our understanding of disease mechanisms. The aim of this study was to explore the levels of multiple plasma proteins in individuals from families with genetic frontotemporal dementia.
Methods: Blood samples from 693 participants in the GENetic Frontotemporal Dementia Initiative study were analysed using a multiplexed antibody array targeting 158 proteins.
Results: We found 13 elevated proteins in symptomatic mutation carriers, when comparing plasma levels from people diagnosed with genetic FTD to healthy non-mutation controls and 10 proteins that were elevated compared to presymptomatic mutation carriers.
Conclusion: We identified plasma proteins with altered levels in symptomatic mutation carriers compared to non-carrier controls as well as to presymptomatic mutation carriers. Further investigations are needed to elucidate their potential as fluid biomarkers of the disease process.Open access funding provided by Karolinska Institute. C.G. received funding from EU Joint Programme—Neurodegenerative Disease Research -Prefrontals Vetenskapsrådet Dnr 529–2014-7504, Vetenskapsrådet 2015–02926, Vetenskapsrådet 2018–02754, the Swedish FTD Inititative-Schörling Foundation, Alzheimer Foundation, Brain Foundation, Dementia Foundation and Region Stockholm ALF-project. PN received funding from KTH Center for Applied Precision Medicine (KCAP) funded by the Erling-Persson Family Foundation, the Swedish FTD Inititative-Schörling Foundation and Åhlén foundation. D.G. received support from the EU Joint Programme—Neurodegenerative Disease Research and the Italian Ministry of Health (PreFrontALS) grant 733051042. E.F. has received funding from a Canadian Institute of Health Research grant #327387. F.M. received funding from the Tau Consortium and the Center for Networked Biomedical Research on Neurodegenerative Disease. J.B.R. has received funding from the Welcome Trust (103838) and is supported by the Cambridge University Centre for Frontotemporal Dementia, the Medical Research Council (SUAG/051 G101400) and the National Institute for Health Research Cambridge Biomedical Research Centre (BRC-1215–20014). J.C.V.S. was supported by the Dioraphte Foundation grant 09–02-03–00, Association for Frontotemporal Dementias Research Grant 2009, Netherlands Organization for Scientific Research grant HCMI 056–13-018, ZonMw Memorabel (Deltaplan Dementie, project number 733 051 042), Alzheimer Nederland and the Bluefield Project. J.D.R. is supported by the Bluefield Project and the National Institute for Health and Care Research University College London Hospitals Biomedical Research Centre, and has received funding from an MRC Clinician Scientist Fellowship (MR/M008525/1) and a Miriam Marks Brain Research UK Senior Fellowship. M.M. has received funding from a Canadian Institute of Health Research operating grant and the Weston Brain Institute and Ontario Brain Institute. M.O. has received funding from Germany’s Federal Ministry of Education and Research (BMBF). R.S-V. is supported by Alzheimer’s Research UK Clinical Research Training Fellowship (ARUK-CRF2017B-2) and has received funding from Fundació Marató de TV3, Spain (grant no. 20143810). R.V. has received funding from the Mady Browaeys Fund for Research into Frontotemporal Dementia. This work was also supported by the EU Joint Programme—Neurodegenerative Disease Research GENFI-PROX grant [2019–02248; to J.D.R., M.O., B.B., C.G., J.C.V.S. and M.S.info:eu-repo/semantics/publishedVersio