55 research outputs found

    Modern Heritage, organic space, material permanence: Torres Posse House in Tafí del Valle

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    The Torres Posse House (1957-1958) is a testimony to the particular forms that the modern house took in the context of northern Argentina, and at the same time shows how the conservation and sustainability of modern heritage come in large part from the quality of its original project. Built to enjoy the holidays, it was rationally organized, according to the demands of economy, topography of the site, climate, and orientation. The gallery, the most memorable space, is a typological approach that remains in good condition. The project established a stone box within which to arrange a demanding interior program with total freedom. The durability of the material proposed it as a modern architecture, capable of transcending the obsolescence of the modern image to resist the passage of time and aging without conflict

    Cognitive awareness after treatment for high-grade glioma

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    Objective: In patients with brain lesion, awareness of cognitive deficits is an important aspect of disease awareness. Glioblastoma (GBM) and anaplastic astrocytoma (AA) can cause cognitive deficits, but, to date, awareness of these deficits has not been documented. This study aimed to test cognitive awareness in these patients after the end of treatment. Methods: Fifty patients with GBM or AA were assessed using the Multiple Ability Self-Report Questionnaire (MASQ), State-Trait Anxiety Inventory (STAI), Self Rating Depression Scale (SRDS), and memory, attention, mental speed, abstract reasoning, and flexibility neuropsychological tests. Cognitive awareness was calculated as the concordance between the composite score of neuropsychological performance (PEC) and the total MASQ score. The controls were 48 healthy subjects. Analysis of variance and regression analysis compared subject groups and explored variables predicting perceived abilities. Results: Patients with GBM or AA showed similar attention, memory, and executive deficits compared with controls. Cognitive awareness was fair/full in 64% of patients. In the entire patients group, the worst MASQ scores were associated with neuropsychological deficits, anxiety, depression, and glioma location in the right hemisphere . In patients with fair/full awareness, MASQ scores were related to affective status and neuropsychological performance, whereas, in those with scarce/no awareness, they were related only to affective status. Conclusions: After treatment, many patients with GBM or AA are aware of their cognitive deficits. Anxiety, depression, and right hemisphere tumour exacerbate the perceived difficulties. This neurocognitive approach expands the behavioural phenotypes of high-grade gliomas and may have therapeutic implications over the course of the disease.info:eu-repo/semantics/publishedVersio

    A Window into the Heterogeneity of Human Cerebrospinal Fluid Aβ Peptides

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    The initiating event in Alzheimer's disease (AD) is an imbalance in the production and clearance of amyloid beta (Aβ) peptides leading to the formation of neurotoxic brain Aβ assemblies. Cerebrospinal Fluid (CSF), which is a continuum of the brain, is an obvious source of markers reflecting central neuropathologic features of brain diseases. In this review, we provide an overview and update on our current understanding of the pathobiology of human CSF Aβ peptides. Specifically, we focused our attention on the heterogeneity of the CSF Aβ world discussing (1) basic research studies and what has been translated to clinical practice, (2) monomers and other soluble circulating Aβ assemblies, and (3) communication modes for Aβ peptides and their microenvironment targets. Finally, we suggest that Aβ peptides as well as other key signals in the central nervous system (CNS), mainly involved in learning and hence plasticity, may have a double-edged sword action on neuron survival and function

    Placental pathology in perinatal asphyxia: a case–control study

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    IntroductionPlacentas of term infants with birth asphyxia are reported to have more lesion such as maternal vascular malperfusion (MVM), fetal vascular malperfusion (FVM) and chorioamnionitis with fetal response (FIR) than those of term infants without birth asphyxia. We compared the placental pathology of asphyxiated newborns, including those who developed hypoxic-ischemic encephalopathy (HIE), with non-asphyxiated controls.MethodsWe conducted a retrospective case–control study of placentas from neonates with a gestational age ≥ 35 weeks, a birthweight ≥ 1,800 g, and no malformations. Cases were asphyxiated newborns (defined as those with an umbilical artery pH ≤ 7.0 or base excess ≤ −12 mMol, 10-minute Apgar score ≤ 5, or the need for resuscitation lasting >10 min) from a previous cohort, with (n=32) and without (n=173) diagnosis of HIE. Controls were non-asphyxiated newborns from low-risk l (n= 50) or high-risk (n= 68) pregnancies. Placentas were analyzed according to the Amsterdam Placental Workshop Group Consensus Statement 2014.ResultsCases had a higher prevalence of nulliparity, BMI>25, thick meconium, abnormal fetal heart monitoring, and acute intrapartum events than controls (p<0.001). MVM and FVM were more frequent among non-asphyxiated than asphyxiated newborns (p<0.001). There was no significant difference in inflammatory lesions or abnormal umbilical insertion site. Histologic meconium-associated changes (MAC) were observed in asphyxiated newborns only (p= 0.039).DiscussionOur results confirm the role of antepartum and intrapartum risk factors in neonatal asphyxia and HIE. No association between neonatal asphyxia and placental lesions was found, except for in the case of MAC. The association between clinical and placental data is crucial to understanding and possibly preventing perinatal asphyxia in subsequent pregnancies

    A multi-element psychosocial intervention for early psychosis (GET UP PIANO TRIAL) conducted in a catchment area of 10 million inhabitants: study protocol for a pragmatic cluster randomized controlled trial

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    Multi-element interventions for first-episode psychosis (FEP) are promising, but have mostly been conducted in non-epidemiologically representative samples, thereby raising the risk of underestimating the complexities involved in treating FEP in 'real-world' services

    Indagine sull'infezione da virus del cimurro e da toxoplasma gondii in volpi cacciate in Valle d'Aosta

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    La volpe è uno dei carnivori selvatici più diffusi nella nostra penisola e nel resto d'europa. Avendo a disposizione volpi cacciate in un'area ristretta come quella della Valle d'Aosta, si è deciso di ricercare due patogeni, mai ricercati finora in qust'area, che possono colpire la volpe e che sono entrambi importanti, seppur per aspetti diversi: Canine distemper virus e Toxoplasma gondi

    Proposte di Unità di apprendimento inclusive

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    Le Unità di Apprendimento rappresentano la concretizzazione del pensiero progettuale dell'insegnante nonché la filosofia inclusiva che ne guida l'azione didattica ed educativa

    Rac1 activation links tau hyperphosphorylation and Aβ dysmetabolism in Alzheimer’s disease

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    Abstract One of the earliest pathological features characterizing Alzheimer’s disease (AD) is the loss of dendritic spines. Among the many factors potentially mediating this loss of neuronal connectivity, the contribution of Rho-GTPases is of particular interest. This family of proteins has been known for years as a key regulator of actin cytoskeleton remodeling. More recent insights have indicated how its complex signaling might be triggered also in pathological conditions. Here, we showed that the Rho-GTPase family member Rac1 levels decreased in the frontal cortex of AD patients compared to non-demented controls. Also, Rac1 increased in plasma samples of AD patients with Mini-Mental State Examination < 18 compared to age-matched non demented controls. The use of different constitutively active peptides allowed us to investigate in vitro Rac1 specific signaling. Its activation increased the processing of amyloid precursor protein and induced the translocation of SET from the nucleus to the cytoplasm, resulting in tau hyperphosphorylation at residue pT181. Notably, Rac1 was abnormally activated in the hippocampus of 6-week-old 3xTg-AD mice. However, the total protein levels decreased at 7-months. A rescue strategy based on the intranasal administration of Rac1 active peptide at 6.5 months prevented dendritic spine loss. This data suggests the intriguing possibility of a dual role of Rac1 according to the different stages of the pathology. In an initial stage, Rac1 deregulation might represent a triggering co-factor due to the direct effect on Aβ and tau. However, at a later stage of the pathology, it might represent a potential therapeutic target due to the beneficial effect on spine dynamics
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