Publications by authors named "Ursula WeiSS"

Studies in rodent models of acute and chronic neurodegenerative disorders have uncovered that glutamate-induced excitotoxic cell death is mediated primarily by extrasynaptic N-methyl-d-aspartate receptors (NMDARs). Rodent neurons can also build up in an activity-dependent manner a protective shield against excitotoxicity. This form of acquired neuroprotection is induced by preconditioning with low doses of NMDA or by activation of synaptic NMDARs triggered by bursts of action potentials.

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Carbon fiber reinforcement used in concrete has become a remarkable alternative to steel fibers. Admixing short fibers to fresh concrete and processing the material with a 3D printer leads to an orientation of fibers and a material with high uniaxial strength properties, which offers an economic use of fibers. To investigate its mechanical behavior, the material is subjected to flexural and tensional tests, combining several measuring techniques.

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In the adult brain, vascular endothelial growth factor D (VEGFD) is required for structural integrity of dendrites and cognitive abilities. Alterations of dendritic architectures are hallmarks of many neurologic disorders, including stroke-induced damage caused by toxic extrasynaptic NMDA receptor (eNMDAR) signaling. Here we show that stimulation of eNMDARs causes a rapid shutoff of expression, leading to a dramatic loss of dendritic structures.

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Synaptic NMDA receptors activating nuclear calcium-driven adaptogenomics control a potent body-own neuroprotective mechanism, referred to as acquired neuroprotection. Viral vector-mediated gene transfer in conjunction with stereotactic surgery has previously demonstrated the proficiency of several nuclear calcium-regulated genes to protect in vivo against brain damage caused by toxic extrasynaptic NMDA receptor signaling following seizures or stroke. Here we used noninvasive nose-to-brain administration of Activin A and SerpinB2, two secreted nuclear calcium-regulated neuroprotectants, for post-injury treatment of brain damage following middle cerebral artery occlusion (MCAO) in C57BL/6N mice.

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Objective: To evaluate whether the outcomes of minimally invasive aortic valve surgery were similar in younger versus older patient groups, as well as whether concomitant minimally invasive aortic valve replacement (AVR) surgeries added significant risks in these populations.

Methods: We performed a single-institution retrospective analysis of 1018 patients undergoing isolated AVR and 378 patients undergoing concomitant AVR procedures over a 6-year period. All surgeries were via a right minithoracotomy approach, and patients who underwent reoperation were excluded.

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Calcium-binding proteins (CaBPs) such as parvalbumin are part of the cellular calcium buffering system that determines intracellular calcium diffusion and influences the spatiotemporal dynamics of calcium signals. In neurons, CaBPs are primarily localized to the cytosol and function, for example, in nerve terminals in short-term synaptic plasticity. However, CaBPs are also expressed in the cell nucleus, suggesting that they modulate nuclear calcium signals, which are key regulators of neuronal gene expression.

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Background And Aim Of The Study: A significant number of patients aged > or =80 years are denied aortic valve surgery due to the assumption of poor outcomes with surgery. The study aim was to evaluate the outcomes of minimally invasive aortic valve replacement (AVR), performed via a right anterior thoracotomy approach, in octogenarians.

Methods: A retrospective review was conducted of all minimally invasive isolated AVRs in patients aged > or =80 years performed at the authors' institution between February 2009 and April 2014.

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Background: Subclinical cardiac damage has recently emerged as a potential predictor of adverse renal outcome. We therefore retrospectively evaluated the effect of left-ventricular hypertrophy (LVH), diagnosed electrocardiographically, on the renal outcome of hypertensive patients managed in primary care.

Methods: From a historical cohort of 39,525 hypertensive individuals evaluated in 2005, we retrieved 5-year data of the 18,510 surviving subjects for whom renal follow-up was available.

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The function of MeCP2, a methylated DNA-interacting protein that may act as a global chromatin modifier, is controlled by its phosphorylation on serine 421. Here we show that in hippocampal neurons, nuclear calcium signaling controls synaptic activity-induced phosphorylation of MeCP2 on serine 421. Pharmacological inhibition of calcium/calmodulin-dependent protein (CaM)kinases blocked activity-induced MeCP2 serine 421 phosphorylation.

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Article Synopsis
  • * ATF3 acts as a transcriptional repressor that protects hippocampal neurons from apoptosis and damage caused by either excessive NMDA receptor activation or oxygen-glucose deprivation.
  • * Modulating ATF3's function can either protect neurons or induce death, highlighting the importance of understanding nuclear calcium signaling and gene regulation in preventing neuronal loss related to age and disease.
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Background: Chronic kidney disease (CKD) is associated with poor renal and cardiovascular outcomes, and early identification largely depends on general practitioners' (GPs') awareness of it. To date, no study has evaluated CKD prevalence in patients with hypertension in primary care.

Study Design: Cross-sectional evaluation of the Italian GPs' database.

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