Parenting during the COVID-19 lockdown in Portugal: changes in daily routines, co-parenting relationships, emotional experiences, and support networks

The COVID-19 pandemic challenged parental resources pertinent to coping with lockdowns. The main objective of this work was to study parenting during the COVID-19 lockdown. Specifically at focus were parental behaviors concerning key domains for the family (daily routine, co-parenting, emotional experience, and support network) and changes related to the pandemic and associated with the parents’ employment statuses. An online survey was carried out through an ad hoc questionnaire where participants completed questions about their sociodemographic data and rated how much their family routines, their co-parenting relationship, their emotional experiences, and the support available in the family network varied on a 5-point scale. The participants included 1384 parents, of which 286 responded to open questions regarding impactful experiences during the lockdown. The results showed differences in daily routine, co-parenting, emotional experience, and support network according to the parents’ employment statuses. Between-group comparisons showed that at-home parents caring for children with governmental aids generally revealed more positive parenting behavior changes, while at-home parents who were teleworking reported more difficulties in parent-child activities and co-parenting. Furthermore, the content analysis of the data confirmed how important themes such as family dynamics, professional activities, and the relationship with the school community were throughout the participants’ accounts of gains and losses. Overall, parents’ employment statuses are associated with diverse experiences during lockdown. The COVID-19 pandemic highlighted the importance of family resources and parental resilience, particularly during circumstances jeopardizing the ever-sensitive work-family balance.info:eu-repo/semantics/publishedVersio

Caffeine and adenosine A 2A receptor inactivation decrease striatal neuropathology in a lentiviral-based model of Machado–Joseph disease

Objective: Machado–Joseph disease (MJD) is a neurodegenerative disorder associated with an abnormal CAG expansion, which translates into an expanded polyglutamine tract within ataxin-3. There is no therapy to prevent or modify disease progression. Because caffeine (a nonselective adenosine receptor antagonist) and selective adenosine A2A receptor (A2A R) blockade alleviate neurodegeneration in different brain diseases, namely at early stages of another polyglutamine-related disorder such as Huntington’s disease, we now tested their ability to control MJD-associated neurodegeneration. Methods: MJD was modeled by transducing the striatum of male adult C57Bl/6 mice with lentiviral vectors encoding mutant ataxin-3 in one hemisphere and wild-type ataxin-3 in the other hemisphere (as internal control). Caffeine (1g/L) was applied through the drinking water. Mice were killed at different time points (from 2 to 12 weeks) to probe for the appearance of different morphological changes using immunohistochemical analysis. Results: Mutant ataxin-3 caused an evolving neuronal dysfunction (loss of DARPP-32 staining) leading to neurodegeneration (cresyl violet and neuronal nuclei staining) associated with increased number of mutant ataxin-3 inclusions in the basal ganglia. Notably, mutant ataxin-3 triggered early synaptotoxicity (decreased synaptophysin and microtubule-associated protein-2 staining) and reactive gliosis (glial fibrillary acidic protein and CD11b staining), which predated neuronal dysfunction and damage. Caffeine reduced the appearance of all these morphological modifications, which were also abrogated in mice with a global A2A R inactivation (knockout). Interpretation: Our findings provide a demonstration that synaptotoxicity and gliosis are precocious events in MJD and that caffeine and A2A R inactivation decrease MJD-associated striatal pathology, which paves the way to consider A2A Rs as novel therapeutic targets to manage MJD

Magnetic micellar nanovehicles: prospects of multifunctional hybrid systems for precision theranostics

Hybrid nanoarchitectures such as magnetic polymeric micelles (MPMs) are among the most promising nanotechnology-enabled materials for biomedical applications combining the benefits of polymeric micelles and magnetic nanoparticles within a single bioinstructive system. MPMs are formed by the self-assembly of polymer amphiphiles above the critical micelle concentration, generating a colloidal structure with a hydrophobic core and a hydrophilic shell incorporating magnetic particles (MNPs) in one of the segments. MPMs have been investigated most prominently as contrast agents for magnetic resonance imaging (MRI), as heat generators in hyperthermia treatments, and as magnetic-susceptible nanocarriers for the delivery and release of therapeutic agents. The versatility of MPMs constitutes a powerful route to ultrasensitive, precise, and multifunctional diagnostic and therapeutic vehicles for the treatment of a wide range of pathologies. Although MPMs have been significantly explored for MRI and cancer therapy, MPMs are multipurpose functional units, widening their applicability into less expected fields of research such as bioengineering and regenerative medicine. Herein, we aim to review published reports of the last five years about MPMs concerning their structure and fabrication methods as well as their current and foreseen expectations for advanced biomedical applications.This research was funded by European Research Council, Consolidator Grant, grant number 772817. European Union’s Horizon 2020 Research and Innovation programme, grant number 810850. Fundação para a Ciência e a Tecnologia, grant number SFRD/BD/144816/2019

Prevalência do consumo de substâncias ilícitas em estudantes universitários portugueses

Publicado em "Gaceta sanitaria", vol. 29 (Espec. Congr.), p. 145-146O uso de substâncias psicoativas lícitas (bebidas alcoólicas, tabaco e medicamentos) e ilícitas (canábis, cocaí-na, ectasy, entre outras) (SPAs) está atualmente entre as principais preocupações em saúde, na sociedade. Os estudos sobre a prevalência de consumo na população universitária são escassos e sem representatividade nacional. Além disso, para se conhecer a dimensão do problema e delinear medidas preventivas para uma população é essencial conhecer a prevalência e fatores associados nesse público-alvo. Este estudo teve como objetivo descrever a prevalência do consumo de drogas ilícitas, nos últimos 30 dias e nos últimos 12 meses, em estudantes universitários, em função do sexo e tipo de drogas.CIEC - Centro de Investigação em Estudos da Criança, IE, UMinho (UI 317 da FCT

Essencial oil components of Hypericum androsaemum infusions and their nematotoxic effects against Meloidogyne javanica (Treub) Chitwood.

Real Sociedad Española de Química, CITAB -UM, CBMA - UM, FCTUniversidade do Minho - CITAB -UM, CBMA - UMFundação para a Ciência e a Tecnologia (FCT

Magnetic stimulation drives macrophage polarization in cell to–cell communication with IL-1β primed tendon cells

Inflammation is part of the natural healing response, but it has been simultaneously associated with tendon disorders, as persistent inflammatory events contribute to physiological changes that compromise tendon functions. The cellular interactions within a niche are extremely important for healing. While human tendon cells (hTDCs) are responsible for the maintenance of tendon matrix and turnover, macrophages regulate healing switching their functional phenotype to environmental stimuli. Thus, insights on the hTDCs and macrophages interactions can provide fundamental contributions on tendon repair mechanisms and on the inflammatory inputs in tendon disorders. We explored the crosstalk between macrophages and hTDCs using co-culture approaches in which hTDCs were previously stimulated with IL-1β. The potential modulatory effect of the pulsed electromagnetic field (PEMF) in macrophage-hTDCs communication was also investigated using the magnetic parameters identified in a previous work. The PEMF influences a macrophage pro-regenerative phenotype and favors the synthesis of anti-inflammatory mediators. These outcomes observed in cell contact co-cultures may be mediated by FAK signaling. The impact of the PEMF overcomes the effect of IL-1β-treated-hTDCs, supporting PEMF immunomodulatory actions on macrophages. This work highlights the relevance of intercellular communication in tendon healing and the beneficial role of the PEMF in guiding inflammatory responses toward regenerative strategies.This research was funded by the ERC CoG grant MagTendon (No. 772817), FCT Project Mag TT PTDC/CTM-CTM/29930/2017, and project NORTE-01-0145-FEDER-000021 supported by Norte Portugal Regional Operational Programme (NORTE 2020). A. Vinhas is funded by Fundação para a Ciência e Tecnologia (FCT)-doctoral grant PD/BD/128089/2016

Contactless resolution of inflammatory signals in tailored macrophage-based cell therapeutics

In recent years, nanotechnology-based microRNA (miR) therapeutic platforms have shown great promise for immunotherapy and tissue regeneration, despite the unmet challenge of achieving efficient and safe delivery of miRs. The transport of miRs offers precision and regulatory value for a myriad of biological processes and pathways, including the control of macrophage (MÏ ) functions and, consequently, the inflammatory cascades MÏ are involved in. Thus, enforcement of MÏ can boost the regenerative process and provide new solutions for diverse chronic pathologies. In this study, we sought to develop a magnetically guided transporter to deliver an miR-155 antagonist to M1-primed MÏ . Furthermore, we determined its modulatory effect in reprogramming MÏ from inflammatory to pro-regenerative phenotypes, with the aim of tissue healing and regenerative medicine approaches. This strategy combines contactless and high-precision control of MÏ , anticipating new functional miR carriers for targeted strategies controlled by extracorporeal action. The magnetoplexes SPION@PEI-miR were efficiently delivered into MÏ without compromising cell viability and successfully induced miR-mediated gene silencing by enhancing the expression of anti-inflammatory markers (IL4 and IL10) and the production of M2Ï -related markers (CD206 and IL4). Given its multimodal features, SPION@PEI-miR represents a simple, safe, and nonviral theranostic platform that enables imaging, tracking, and miR delivery with modulatory effects on immune cells.This research was funded by the European Research Council, Consolidator Grant MagTendon, grant number 772817 and by the FCT - Fundação para a Ciência e a Tecnologia, scholarship number SFRD/BD/144816/2019

Atypical form of acute myocardial infarction with tamponade

Published on behalf of the European Society of Cardiology. All rights reserved. © The Author 2019.Background: Nowadays it is well recognized that the absence of obstructive coronary artery disease in a patient presenting with symptoms suggestive of ischemia and ST-segment alterations does not preclude an atherothrombotic etiology. CMR is an essential method for the investigation of Myocardial infarction (MI) with non obstructive coronary artery disease (MINOCA). Clinical Case: A 66 years-old female patient was referred after an episode of acute oppressive chest pain, nausea and hypersudorese, followed by syncope. She had a previous medical history of rheumatoid arthritis, under immunosuppression, occlusion of the cilioretinal artery, hypertension and dyslipidemia. On admission she was hypotensive (80/60mmHg). The ECG showed sinus rhythm and mild ST depression in V2-V3 leads, and the echocardiogram a small circumferential pericardial effusion (10mm) with signs of hemodynamic compromise. The blood tests documented a slight leukocytosis and an elevated troponin (hs-TnT 619ng/L).info:eu-repo/semantics/publishedVersio

Calpastatin-mediated inhibition of calpains in the mouse brain prevents mutant ataxin 3 proteolysis, nuclear localization and aggregation, relieving Machado-Joseph disease

Machado-Joseph disease is the most frequently found dominantly-inherited cerebellar ataxia. Over-repetition of a CAG trinucleotide in the MJD1 gene translates into a polyglutamine tract within the ataxin 3 protein, which upon proteolysis may trigger Machado-Joseph disease. We investigated the role of calpains in the generation of toxic ataxin 3 fragments and pathogenesis of Machado-Joseph disease. For this purpose, we inhibited calpain activity in mouse models of Machado-Joseph disease by overexpressing the endogenous calpain-inhibitor calpastatin. Calpain blockage reduced the size and number of mutant ataxin 3 inclusions, neuronal dysfunction and neurodegeneration. By reducing fragmentation of ataxin 3, calpastatin overexpression modified the subcellular localization of mutant ataxin 3 restraining the protein in the cytoplasm, reducing aggregation and nuclear toxicity and overcoming calpastatin depletion observed upon mutant ataxin 3 expression. Our findings are the first in vivo proof that mutant ataxin 3 proteolysis by calpains mediates its translocation to the nucleus, aggregation and toxicity and that inhibition of calpains may provide an effective therapy for Machado-Joseph diseas