University of Modena and Reggio Emilia
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A conceptual data modeling framework with four levels of abstraction for environmental information
Get PDFLate-onset temporal lobe epilepsy: insights from brain atrophy and Alzheimer's disease biomarkers
No full text: Considering the growing age of the world population, the incidence of epilepsy in older adults is expected to increase significantly. It has been suggested that late-onset temporal lobe epilepsy (LO-TLE) may be neurodegenerative in origin and overlap with Alzheimer's Disease (AD). Herein, we aimed to characterize the pattern of cortical atrophy and cerebrospinal fluid (CSF) biomarkers of AD (total and phosphorylated tau, and β-amyloid) in a selected population of LO-TLE of unknown origin. We prospectively enrolled individuals with temporal lobe epilepsy onset after the age of 50 and no cognitive impairment. They underwent a structural MRI scan and CSF biomarkers measurement. Imaging and biomarkers data were compared to three retrospectively collected groups: (i) age-sex-matched healthy controls, (ii) patients with Mild Cognitive Impairment (MCI) and abnormal CSF AD biomarkers (MCI-AD), and (iii) patients with MCI and normal CSF AD biomarkers (MCI-noAD). From a pool of 52 patients, twenty consecutive eligible LO-TLE patients with a mean disease duration of 1.8 years were recruited. As control populations, 25 patients with MCI-AD, 25 patients with MCI-noAD, and 25 healthy controls were enrolled. CSF biomarkers returned normal values in LO-TLE, significantly different from patients with MCI due to AD. There were no differences in cortico-subcortical atrophy between epilepsy patients and healthy controls, while patients with MCI demonstrated widespread injuries of cortico-subcortical structures. Individuals with a late-onset form of temporal lobe epilepsy, characterized by short disease duration and normal CSF β-amyloid and tau protein levels, showed patterns of cortical thickness and subcortical volumes not significantly different from healthy controls, but highly different from patients with MCI, either due to Alzheimer's Disease or not.Considering the growing age of the world population, the incidence of epilepsy in older adults is expected to increase significantly. It has been suggested that late-onset temporal lobe epilepsy (LO-TLE) may be neurodegenerative in origin and overlap with Alzheimer's disease (AD). Herein, we aimed to characterize the pattern of cortical atrophy and CSF biomarkers of AD (total and phosphorylated tau and amyloid-β) in a selected population of LO-TLE of unknown origin. We prospectively enrolled individuals with temporal lobe epilepsy onset after the age of 50 and no cognitive impairment. They underwent a structural MRI scan and CSF biomarkers measurement. Imaging and biomarkers data were compared to three retrospectively collected groups: (i) age-sex-matched healthy controls; (ii) patients with mild cognitive impairment (MCI) and abnormal CSF AD biomarkers (MCI-AD); and (iii) patients with MCI and normal CSF AD biomarkers (MCI-noAD). From a pool of 52 patients, 20 consecutive eligible LO-TLE patients with a mean disease duration of 1.8 years were recruited. As control populations, 25 patients with MCI-AD, 25 patients with MCI-noAD and 25 healthy controls were enrolled. CSF biomarkers returned normal values in LO-TLE, significantly different from patients with MCI due to AD. There were no differences in cortico-subcortical atrophy between epilepsy patients and healthy controls, while patients with MCI demonstrated widespread injuries of cortico-subcortical structures. Individuals with LO-TLE, characterized by short disease duration and normal CSF amyloid-β and tau protein levels, showed patterns of cortical thickness and subcortical volumes not significantly different from healthy controls, but highly different from patients with MCI, either due to AD or not
Timing and adequacy of intrapartum antibiotic prophylaxis: new insights for future guidelines
No full textWhy do women develop lower levels of political interest? Examining the influence of education, family socialisation and adult roles
Get PDFThe political interest of men rises faster than that of women during late adolescence and early adulthood in Britain (Fraile and Sánchez-Vítores in Polit Psychol 41(1):89–106, 2020). This paper analyses whether factors relating to education, the assumption of adult roles and family background can explain this growing disparity. We use panel data of the British Household Panel Study (BHPS) and Understanding Society (USoc) to examine these factors. Education turns out to be the only factor that is related to different growth trajectories of political interest between men and women. Women with lower levels of education or vocational qualifications show stable or declining levels of political interest while all other categories show rising levels of interest between ages 16 and 30. Education can, however, only partially account for the rising gender gap. Variables representing the attainment of adult roles, such as occupational status, marital status and household composition, and variables capturing family socialisation are not linked to the growing disparity of political interest between men and women. Most of this gap thus remains unexplained
Remobilization of inverted normal faults drives active extension in the axial zone of the southern Apennine mountain belt (Italy)
Get PDFThe Irpinia region is one of the most seismically active areas of Italy owing to ongoing, late-orogenic extension in the axial zone of the Apennine mountain belt. However, the 3D architecture and the nature of the faults that drive this extension are still uncertain, posing challenges to seismic hazard assessment. Here, we address these uncertainties by integrating a new catalogue of high-resolution micro-seismicity (ML < 3.5) complemented by earthquake focal mechanisms, with existing 3D seismic velocity models and geological data. We found that micro-seismicity is primarily taking place along a segmented, approximately 60 km long, deep-seated, Mesozoic normal fault that was inverted during the shortening stages of the Apennine orogeny and then extensionally reactivated during the Quaternary. These findings suggest that multiple events of reactivation of long-lived faults can weaken their strength, making them prone to co-seismic remobilization under newly imposed strain fields in active mountain belts
Clinical, etiological, and therapeutic profile of early-onset absence seizures: A case series analysis
No full text: Typical absence seizures represent a distinctive form of epileptic activity typically observed in pediatric populations, predominantly manifesting between the ages of 4 and 10, constituting Childhood Absence Epilepsy (CAE). However, a subset of patients presents with Early-onset Absence Epilepsy (EOAE), characterized by seizure onset before the fourth year of life, often displaying favorable outcomes with antiseizure medication. Conversely, atypical absence seizures exhibit prolonged duration and frequently entail tonic, atonic, or myoclonic motor elements, suggesting a more severe clinical course, commonly associated with epileptic encephalopathies of childhood onset. Recent genetic investigations have highlighted the involvement of specific genes, notably the SLC1A2 mutation, identified in 10 % of EOAE cases, underlying the GLUT1 deficiency syndrome. Timely recognition of such genetic anomalies facilitates tailored interventions, including ketogenic dietary regimes, shown to ameliorate epileptic symptomatology and neurocognitive sequelae. This retrospective study aimed to delineate the distinct features of EOAE and early-onset atypical absence seizures, facilitating prompt diagnosis, particularly emphasizing genetic aberrations, and initiating precision therapeutic approaches to optimize patient outcomes. Evaluation of 23 patients with absence epilepsy onset within the first four years of life, conducted at the Neuropediatrics Outpatient Clinic of the Policlinico of Modena, revealed that children with atypical absences often exhibit a complex clinical and electroencephalographic phenotype, frequently associated with genetic abnormalities. Notably, neurocognitive prognosis appears less favorable in this subgroup, with half of the patients displaying pharmacoresistance. In contrast, all EOAE cases demonstrated seizure freedom, corroborating previous literature suggesting a relatively benign clinical course in these individuals
Multi objective design optimization of self-expandable nitinol braided stents
No full textCardiovascular stents are indispensable medical devices used to treat vessel-related issues such as atherosclerotic plaque. In the past, stents were mainly made of materials like stainless steel or cobalt-chromium alloy. However, over the last two decades, research has focused on the use of Nitinol (NiTi) due to its superior properties such as super-elasticity, biocompatibility, and strength. The aim of this paper is to optimize the design of an open-ended braided stent, subjected to radial compression, with enhanced performance. The optimization process uses Multi-Objective Particle Swarm Optimization (MOPSO), which explores three design variables, namely wire diameter, number of coils, and braided angle, to determine the optimal shape that maximizes radial pressure stiffness and radial force exerted on the vessel walls while minimizing foreshortening. The analytical model developed is compared against literature findings, and the optimization results are implemented in a finite element analysis solver and compared with existing references. The results show that the optimized design using MOPSO enhances the stent’s average radial force and radial pressure stiffness by 28% and 40% respectively, while decreasing foreshortening by nearly 5%. The results demonstrate the feasibility of MOPSO for optimizing braided NiTi stents and the use of FEM for validating optimized designs
Real-Time Flood Inundation Modeling With Flow Resistance Parameter Learning
Get PDFEmergency response to flood plain inundations requires real-time forecasts of flow depth, velocity, and arrival time. Detailed and rapid flood inundation forecasts can be obtained from numerical solution of 2D unsteady flow equations based on high-resolution topographic data and geomorphologically informed unstructured meshes. However, flow resistance parameters representing the effects of land surface topography unresolved by digital terrain model data remain uncertain. In the present study, flow resistance parameters representing the effects of roughness, vegetation, and buildings are determined hydraulically in real-time using flow depth observations. A detailed numerical reproduction of a real flood has been largely corroborated by observations and subsequently used as a surrogate of the ground truth target. In synthetic numerical experiments, flow depth observations are obtained from a network of in-situ flow depth sensors assigned to hydraulically relevant locations in the flood plain. Starting from a generic resistance parameter set, the capability of a tandem 2D surface flow model and Bayesian optimization technique to achieve convergence to the target resistance parameter set is tested. Convergence to the target resistance parameter set was obtained with 50 or fewer tandem flow + optimization iterations for each forecasting cycle in which the difference between simulated and observed flow depths is minimized. The flood arrival time errors across a 52 km2 flood plain inundation area were reduced by 3.13 hr with respect to results obtained without optimization from a fixed range of flow resistance parameters. Performance metrics like critical success index and probability of detection reach values above 90% across the flood plain
Critical role of protein kinase CK2 in chronic myeloid leukemia cells harboring the T315I BCR::ABL1 mutation
Get PDFChronic myeloid leukemia (CML) is characterized by the fusion protein BCR::ABL1, a constitutively active tyrosine kinase. The frontline treatment, represented by tyrosine kinase inhibitors (TKIs), has dramatically improved the clinical outcomes of patients. However, TKI resistance through various mechanisms has been reported. In particular, the BCR::ABL11 T315I mutation is associated with resistance to first- and secondgeneration TKIs and poor survival outcomes. For patients harboring this mutation, treatments with third generation TKIs are indicated, which are however accompanied by adverse events. Protein kinase CK2 is implicated in several human diseases. Although its role in CML has already been proven, its essentialness in T315I-mediated TKI resistance has yet to be investigated. Here we show that CK2 contributes to the aberrantly high signaling pathways in T315I-cells, and that its pharmacological or genetic targeting diminishes those signals, induces apoptosis, and reduces the proliferation and clonogenic potential of T315I-cells. The effects of CK2 inhibition are also observed in the presence of bone marrow stromal cells and under hypoxic conditions, and, remarkably, in patient-derived cells. Moreover, CK2 inhibition or genetic ablation of the CK2 alpha catalytic subunit sensitizes T315I-cells towards TKIs . Collectively, our results suggest the potential benefit of inhibiting CK2 in CML characterized by T315Idependent resistance