84 research outputs found
The black pedagogy scale: A new task to explore educational practices for children's well-being
The present contribute focuses on the concept of "Black Pedagogy" (Rutschky, 1977; ISBN: 3548356702), meant as a set of educational practices assimilable into those that nowadays are included in the frame of physical and psychological maltreatment (e.g., corporal punishment, frightening children, etc.). The purpose of this work is to present our operationalization proposal of the concept and the results deriving from a first validation of the "Black Pedagogy Scale". The questionnaire was administered to 374 Italian university students in their university classrooms (pilot study with double administration) and to 830 Italian adults, parents of primary school-aged children, through an online survey platform (main study). In the pilot study, explorative analyses, paired-samples t-test and ML EFA (with Varimax rotation) were performed. In the main study, proprieties of the refined instrument and relations between the construct of Black Pedagogy and demographics were explored. The Black Pedagogy Scale (α > .8) resulted composed by three factors, consistently with what was initially hypothesized: "Values of Black Pedagogy" (var. 18.7%), "Education of children over time" (var. 10.6%) "Methods of Black Pedagogy" (var. 8.6%). Participants resulted more in agreement with Black Pedagogy's values rather than with its methods, and those with higher educational qualification showed less agreement with the construct, F(2, 813) = 28.22, p < .001, η² = .065. The possible legacy of a Black Pedagogy's forma mentis can contribute to explain why some detrimental disciplinary practices are culturally deemed as acceptable. Results suggest designing interventions focused on educational values to discourage such practices
Regulation of the microtubular cytoskeleton by Polycystin-1 favors focal adhesions turnover to modulate cell adhesion and migration.
BACKGROUND: Polycystin-1 (PC-1) is a large plasma membrane receptor, encoded by the PKD1 gene, which is mutated in most cases of Autosomal Dominant Polycystic Kidney Disease (ADPKD). The disease is characterized by renal cysts. The precise function of PC-1 remains elusive, although several studies suggest that it can regulate the cellular shape in response to external stimuli. We and others reported that PC-1 regulates the actin cytoskeleton and cell migration. RESULTS: Here we show that cells over-expressing PC-1 display enhanced adhesion rates to the substrate, while cells lacking PC-1 have a reduced capability to adhere. In search for the mechanism responsible for this new property of PC-1 we found that this receptor is able to regulate the stability of the microtubules, in addition to its capability to regulate the actin cytoskeleton. The two cytoskeletal components are acting in a coordinated fashion. Notably, we uncovered that PC-1 regulation of the microtubule cytoskeleton impacts on the turnover rates of focal adhesions in migrating cells and we link all these properties to the capability of PC-1 to regulate the activation state of Focal Adhesion Kinase (FAK). CONCLUSIONS: In this study we show several new features of the PC-1 receptor in modulating microtubules and adhesion dynamics, which are essential for its capability to regulate migration. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12860-015-0059-3) contains supplementary material, which is available to authorized users
'Candidatus Sarmatiella mevalonica' endosymbiont of the ciliate Paramecium provides insights on evolutionary plasticity among Rickettsiales
Members of the bacterial order Rickettsiales are obligatorily associated with a wide range of eukaryotic hosts. Their evolutionary trajectories, in particular concerning the origin of shared or differential traits among distant sub-lineages, are still poorly understood. Here, we characterized a novel Rickettsiales bacterium associated with the ciliate Paramecium tredecaurelia and phylogenetically related to the Rickettsia genus. Its genome encodes significant lineage-specific features, chiefly the mevalonate pathway gene repertoire, involved in isoprenoid precursor biosynthesis. Not only this pathway has never been described in Rickettsiales, it also is very rare among bacteria, though typical in eukaryotes, thus likely representing a horizontally acquired trait. The presence of these genes could enable an efficient exploitation of host-derived intermediates for isoprenoid synthesis. Moreover, we hypothesize the reversed reactions could have replaced canonical pathways for producing acetyl-CoA, essential for phospholipid biosynthesis. Additionally, we detected phylogenetically unrelated mevalonate pathway genes in metagenome-derived Rickettsiales sequences, likely indicating evolutionary convergent effects of independent horizontal gene transfer events. Accordingly, convergence, involving both gene acquisitions and losses, is highlighted as a relevant evolutionary phenomenon in Rickettsiales, possibly favoured by plasticity and comparable lifestyles, representing a potentially hidden origin of other more nuanced similarities among sub-lineages.Peer reviewe
The role of nutritional supplement on post-stroke fatigue: a pilot randomized controlled trial
Objectives: Post-stroke fatigue (PSF) is an experience characterized by an early feeling of exhaustion with fatigue, a
lack of energy, and difficulty in exertion, both motor and cognitive. To counteract fatigue and limit its effects on
activities of daily living, the use of vitamins and minerals is known in addition to the pharmacological approach.
However, few studies have evaluated the effect of vitamin and mineral supplementation on fatigue management.
SiderAL Med is a food for special medical purposes with a complete formulation containing vitamins, sucrosomal
minerals, copper and algal calcium. The aim of the study is to evaluate whether nutritional supplementation with
SiderAL Med improves the symptom of fatigue and motor and cognitive function in stroke patients.
Design: This is a pilot, randomized study with a control group.
Setting: Post-Acute Rehabilitation Unit of the Fondazione Policlinico “A. Gemelli” IRCCS.
Participants: Twenty-four patients with stroke outcomes, admitted to rehabilitation, were recruited and randomized
into the experimental group (Sid-G) and the control group (CG).
Intervention: The Sid-G patients, in association with the pharmacological and rehabilitation therapy foreseen during
hospitalization, took SiderAL1 Med, one sachet per day for 8 weeks, while the CG patients underwent only the
pharmacological and rehabilitation therapy foreseen in the daily routine.
Measurements: All patients were assessed at baseline (T0), after 4 weeks (T1), after 8 weeks (T2) and after 12 weeks
(T3) for motor and cognitive fatigue, balance, walking, functional capacity, cognitive performance, autonomy,
quality of life and body composition.
Results: Both Sid-G and CG patients showed significant improvement on most rating scales between T0-T1-T2-T3 (p=0.0001). When comparing the two groups, a statistically significant difference emerged in favor of Sid-G with
regard to motor fatigue (p=0.007), cognitive fatigue (p=0.009) and total fatigue (p=0.034); balance (p<0.001), functional capacity (p<0.001); cognitive performance (p=0.004); bone mineral content (p=0.005), lean
mass (p=0.005), total mass (p<0.001) and percentage of fat mass (p=0.039).
Conclusion: Nutritional supplementation with SiderAL Med, in concert with intensive rehabilitation treatment,
appears to be effective in managing fatigue and improving motor and cognitive performance and body composition,
representing a valuable tool to associate with rehabilitation treatment in stroke patients
Corrigendum: Sleep behavior and daily activity levels in people with metabolic syndrome: effect of 1 year of metformin treatment
Sleep behavior and daily activity levels in people with metabolic syndrome: effect of 1 year of metformin treatment
Impaired sleep and low daily activity levels increase the risk of developing metabolic syndrome (MS). Metformin (MET), an insulin sensitizer drug, is effective in regressing MS and has been recently studied as an adjuvant agent for managing sleep disorders. The present study aimed to assess whether 1,700 mg/day of MET treatment modifies sleep and daily activity levels in people with MS evaluated by Rest-Activity circadian Rhythm (RAR), which is the expression of 24 h of spontaneous activity parameters. A total of 133 subjects with MS, randomized into the MET (n = 65) or placebo (PLA, n = 68) group, underwent a clinical/anthropometric examination and carried out a continuous 7-day actigraphic monitoring to investigate sleep and RAR parameters at baseline and after 1 year of intervention. After 1 year of intervention, 105 subjects were analyzed. The MET group showed greater anthropometric and metabolic improvements compared with placebo, with a significant reduction in weight (p = 0.01), body mass index (p = 0.01), waist circumference (p = 0.03), and glucose (p < 0.001). With regard to sleep parameters, the MET group showed a significant increase in actual sleep time (p = 0.01) and sleep efficiency (p = 0.04) compared with placebo. There were no significant changes reported in the RAR parameters. Our study suggests that MET might be used as an adjuvant treatment for sleep disorders in people with MS
An explainable model of host genetic interactions linked to COVID-19 severity
We employed a multifaceted computational strategy to identify the genetic factors contributing to increased risk of severe COVID-19 infection from a Whole Exome Sequencing (WES) dataset of a cohort of 2000 Italian patients. We coupled a stratified k-fold screening, to rank variants more associated with severity, with the training of multiple supervised classifiers, to predict severity based on screened features. Feature importance analysis from tree-based models allowed us to identify 16 variants with the highest support which, together with age and gender covariates, were found to be most predictive of COVID-19 severity. When tested on a follow-up cohort, our ensemble of models predicted severity with high accuracy (ACC = 81.88%; AUCROC = 96%; MCC = 61.55%). Our model recapitulated a vast literature of emerging molecular mechanisms and genetic factors linked to COVID-19 response and extends previous landmark Genome-Wide Association Studies (GWAS). It revealed a network of interplaying genetic signatures converging on established immune system and inflammatory processes linked to viral infection response. It also identified additional processes cross-talking with immune pathways, such as GPCR signaling, which might offer additional opportunities for therapeutic intervention and patient stratification. Publicly available PheWAS datasets revealed that several variants were significantly associated with phenotypic traits such as "Respiratory or thoracic disease", supporting their link with COVID-19 severity outcome.A multifaceted computational strategy identifies 16 genetic variants contributing to increased risk of severe COVID-19 infection from a Whole Exome Sequencing dataset of a cohort of Italian patients
Carriers of ADAMTS13 Rare Variants Are at High Risk of Life-Threatening COVID-19
Thrombosis of small and large vessels is reported as a key player in COVID-19 severity. However, host genetic determinants of this susceptibility are still unclear. Congenital Thrombotic Thrombocytopenic Purpura is a severe autosomal recessive disorder characterized by uncleaved ultra-large vWF and thrombotic microangiopathy, frequently triggered by infections. Carriers are reported to be asymptomatic. Exome analysis of about 3000 SARS-CoV-2 infected subjects of different severities, belonging to the GEN-COVID cohort, revealed the specific role of vWF cleaving enzyme ADAMTS13 (A disintegrin-like and metalloprotease with thrombospondin type 1 motif, 13). We report here that ultra-rare variants in a heterozygous state lead to a rare form of COVID-19 characterized by hyper-inflammation signs, which segregates in families as an autosomal dominant disorder conditioned by SARS-CoV-2 infection, sex, and age. This has clinical relevance due to the availability of drugs such as Caplacizumab, which inhibits vWF-platelet interaction, and Crizanlizumab, which, by inhibiting P-selectin binding to its ligands, prevents leukocyte recruitment and platelet aggregation at the site of vascular damage
Gain- and Loss-of-Function CFTR Alleles Are Associated with COVID-19 Clinical Outcomes
Carriers of single pathogenic variants of the CFTR (cystic fibrosis transmembrane conductance regulator) gene have a higher risk of severe COVID-19 and 14-day death. The machine learning post-Mendelian model pinpointed CFTR as a bidirectional modulator of COVID-19 outcomes. Here, we demonstrate that the rare complex allele [G576V;R668C] is associated with a milder disease via a gain-of-function mechanism. Conversely, CFTR ultra-rare alleles with reduced function are associated with disease severity either alone (dominant disorder) or with another hypomorphic allele in the second chromosome (recessive disorder) with a global residual CFTR activity between 50 to 91%. Furthermore, we characterized novel CFTR complex alleles, including [A238V;F508del], [R74W;D1270N;V201M], [I1027T;F508del], [I506V;D1168G], and simple alleles, including R347C, F1052V, Y625N, I328V, K68E, A309D, A252T, G542*, V562I, R1066H, I506V, I807M, which lead to a reduced CFTR function and thus, to more severe COVID-19. In conclusion, CFTR genetic analysis is an important tool in identifying patients at risk of severe COVID-19
The polymorphism L412F in TLR3 inhibits autophagy and is a marker of severe COVID-19 in males
The polymorphism L412F in TLR3 has been associated with several infectious diseases. However, the mechanism underlying this association is still unexplored. Here, we show that the L412F polymorphism in TLR3 is a marker of severity in COVID-19. This association increases in the sub-cohort of males. Impaired macroautophagy/autophagy and reduced TNF/TNFα production was demonstrated in HEK293 cells transfected with TLR3L412F-encoding plasmid and stimulated with specific agonist poly(I:C). A statistically significant reduced survival at 28 days was shown in L412F COVID-19 patients treated with the autophagy-inhibitor hydroxychloroquine (p = 0.038). An increased frequency of autoimmune disorders such as co-morbidity was found in L412F COVID-19 males with specific class II HLA haplotypes prone to autoantigen presentation. Our analyses indicate that L412F polymorphism makes males at risk of severe COVID-19 and provides a rationale for reinterpreting clinical trials considering autophagy pathways. Abbreviations: AP: autophagosome; AUC: area under the curve; BafA1: bafilomycin A1; COVID-19: coronavirus disease-2019; HCQ: hydroxychloroquine; RAP: rapamycin; ROC: receiver operating characteristic; SARS-CoV-2: severe acute respiratory syndrome coronavirus 2; TLR: toll like receptor; TNF/TNF-α: tumor necrosis factor
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