Application of a new photocatalytic nanomaterial obtained by Pulse Laser Ablation for Polychrome Paintings Conservation: a feasibility study

This works aims to present a preliminary study about the application on painting of TiO2 nanoparticles for self-cleaning and protective purposes. We firstly assessed the photocatalytic activity of the TiO2 nanoparticles, obtained by Pulsed Laser Ablation, by the discoloration of dye. After, the colloidal dispersion is applied to painting samples prepared in laboratory, according to old recipes and using the most-used historical binders and pigments, in order to verify the cleaning efficiency by discoloration of the chromatic markers. The spectrophotometric analysis is performed studying the Spectral Reflectance Factor trend and the color coordinates

Sicilia—silicon carbide detectors for intense luminosity investigations and applications

Silicon carbide (SiC) is a compound semiconductor, which is considered as a possible alternative to silicon for particles and photons detection. Its characteristics make it very promising for the next generation of nuclear and particle physics experiments at high beam luminosity. Silicon Carbide detectors for Intense Luminosity Investigations and Applications (SiCILIA) is a project starting as a collaboration between the Italian National Institute of Nuclear Physics (INFN) and IMM-CNR, aiming at the realization of innovative detection systems based on SiC. In this paper, we discuss the main features of silicon carbide as a material and its potential application in the field of particles and photons detectors, the project structure and the strategies used for the prototype realization, and the first results concerning prototype production and their performance

The Role of Copper (II) on Kininogen Binding to Tropomyosin in the Presence of a Histidine–Proline-Rich Peptide

The antiangiogenic activity of the H/P domain of histidine–proline-rich glycoprotein is mediated by its binding with tropomyosin, a protein exposed on endothelial cell-surface during the angiogenic switch, in presence of zinc ions. Although it is known that copper ion serum concentration is significantly increased in cancer patients, its role in the interaction of H/P domain with tropomyosin, has not yet been studied. In this paper, by using ELISA assay, we determined the modulating effect of TetraHPRG peptide, a sequence of 20 aa belonging to H/P domain, on the binding of Kininogen (HKa) with tropomyosin, both in absence and presence of copper and zinc ions. A potentiometric study was carried out to characterize the binding mode adopted by metal ions with TetraHPRG, showing the formation of complex species involving imidazole amide nitrogen atoms in metal binding. Moreover, circular dichroism showed a conformational modification of ternary systems formed by TetraHPRG, HKa and copper or zinc. Interestingly, slight pH variation influenced the HKa-TetraHPRG-tropomyosin binding. All these results indicate that both metal ions are crucial in the interaction between TetraHPRG, tropomyosin and HKa

A Multifunctional Nanoplatform Made of Gold Nanoparticles and Peptides Mimicking the Vascular Endothelial Growth Factor

In this work, nanobiohybrids of plasmonic gold nanoparticles (AuNP, anti-angiogenic) and a peptide mimicking the vascular endothelial growth factor (VEGF, pro-angiogenic) were assembled and scrutinized in terms of physicochemical characterization, including optical properties, surface charge, surface chemical structure and morphology of the bioengineered metal nanoparticles, for their potential application as multifunctional theranostic (i.e., therapy + sensing) nanoplatform (AuNP/VEGF). Specifically, a peptide sequence encompassing the VEGF cellular receptor domain 73–101 (VEGF73–101) and its single point cysteine mutated were immobilized onto AuNP by physi- and chemi-sorption, respectively. The new hybrid systems were characterized by means of a multitechnique approach, including dynamic light scattering (DLS) analyses, zeta potential (ZP), spectroscopic (UV-Vis, FT-IR, XPS), spectrometric (TOF-SIMS) and microscopic (AFM, SEM) techniques. Proof-of-work cellular experiments in human umbilical vein endothelial cells (HUVEC) upon the treatment with AuNP/VEGF samples, demonstrated no toxicity up to 24 h (MTT assay) as well an effective internalization (laser confocal microscopy, LSM)

The Inorganic Perspective of VEGF: Interactions of Cu2 + with Peptides Encompassing a Recognition Domain of the VEGF Receptor

The vascular endothelial growth factor A (VEGF-A) is a potent angiogenic factor, its activity may be influenced by the presence of copper(II) ions. To mimic the interaction between copper(II) and VEGF (Vascular Endotelial Growth Factor), the N- and C-terminally blocked peptide fragments VEGF73-101 and VEGF84-101, owing to VEGF165 protein, have been synthesized. These protein domains represent a specific recognition site with the VEGF receptor (VEGFR). Copper(II) complexes with VEGF73-101 and VEGF84-101 were investigated by means of potentiometry and UV-Vis, ESI-MS, CD, EPR spectroscopic methods. Both peptides have three histidine residues and display a binding high affinity for copper(II) ions. The proliferative activity of the peptides in the absence and presence of copper(II) ions as well as of VEGF-165 protein was also tested on HUVEC cells (Human Umbilical Vein Endothelial Cells). The VEGF73-101 showed a dose-dependent anti-proliferative activity, while the shorter peptide VEGF84-101 did not affect HUVEC proliferation, both in the presence and in the absence of VEGF

Small Hexokinase 1 Peptide against Toxic SOD1 G93A Mitochondrial Accumulation in ALS Rescues the ATP-Related Respiration

Mutations in Cu/Zn Superoxide Dismutase (SOD1) gene represent one of the most common causes of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disorder that specifically affects motor neurons (MNs). The dismutase-active SOD1 G93A mutant is responsible for the formation of toxic aggregates onto the mitochondrial surface, using the Voltage-Dependent Anion Channel 1 (VDAC1) as an anchor point to the organelle. VDAC1 is the master regulator of cellular bioenergetics and by binding to hexokinases (HKs) it controls apoptosis. In ALS, however, SOD1 G93A impairs VDAC1 activity and displaces HK1 from mitochondria, promoting organelle dysfunction, and cell death. Using an ALS cell model, we demonstrate that a small synthetic peptide derived from the HK1 sequence (NHK1) recovers the cell viability in a dose–response manner and the defective mitochondrial respiration profile relative to the ADP phosphorylation. This correlates with an unexpected increase of VDAC1 expression and a reduction of SOD1 mutant accumulation at the mitochondrial level. Overall, our findings provide important new insights into the development of therapeutic molecules to fight ALS and help to better define the link between altered mitochondrial metabolism and MNs death in the disease

Adenosine receptors expression in cardiac fibroblasts of patients with left ventricular dysfunction due to valvular disease

Context: Adenosine restores tissue homeostasis through the interaction with its membrane receptors (AR) expressed on fibroblasts, endothelial cells, smooth muscle cells and leukocytes, but their modulation is still not fully understood. Objective: To evaluate whether changes in the transcriptomic profiling of adenosine receptors (AR) occur in cardiac fibroblasts (CF) of patients (pts) with LV dysfunction due to valvular disease (V). The secondary aim was to compare in the same pts the results obtained at cardiac level with those found in circulating leukocytes. Materials and methods: Auricle fragments were excised from 13 pts during prosthetic implantation while blood samples were collected from pts (n = 9) and from healthy subjects (C, n = 7). In 7 pts cardiac biopsy and blood samples were taken simultaneously. A human CF atrial cell line (cc) was used as control. Results: AR higher levels of mRNA expression were observed with real-time PCR in Vpts compared to C, both at cardiac (overexpression A1R:98%, A2AR:63%, A2BR:87%, A3R:85%, CD39:92%, CD73:93%) and at peripheral level (A1R vs C: p = .0056; A2AR vs C: p = .0173; A2BR vs C: p = .0272; A3R vs C: p = .855; CD39 vs C: p = .0001; CD73 vs C: p = .0091). Conclusion: All AR subtypes were overexpressed in CF of Vpts. The same trends in AR expression at cardiac level was assessed on circulating leukocytes, thus opening a new road to minimally invasive studies of the adenosinergic system in cardiac patients

The Ionophoric Activity of a Pro-Apoptotic VEGF165 Fragment on HUVEC Cells

Copper plays an important role as a regulator in many pathologies involving the angiogenesis process. In cancerogenesis, tumor progression, and angiogenic diseases, copper homeostasis is altered. Although many details in the pathways involved are still unknown, some copper-specific ligands have been successfully used as therapeutic agents. Copper-binding peptides able to modulate angiogenesis represent a possible way to value new drugs. We previously reported that a fragment (VEGF73-101) of vascular endothelial growth factor (VEGF165), a potent angiogenic, induced an apoptotic effect on human umbilical vein endothelial cells. The aim of this study was to investigate the putative copper ionophoric activity of VEGF73-101, as well as establish a relationship between the structure of the peptide fragment and the cytotoxic activity in the presence of copper(II) ions. Here, we studied the stoichiometry and the conformation of the VEGF73-101/Cu(II) complexes and some of its mutated peptides by electrospray ionization mass spectrometry and circular dichroism spectroscopy. Furthermore, we evaluated the effect of all peptides in the absence and presence of copper ions by cell viability and cytofuorimetric assays. The obtained results suggest that VEGF73-101 could be considered an interesting candidate in the development of new molecules with ionophoric properties as agents in antiangiogenic therapeutic approaches

Dataset seeding paper JAL.

Este trabajo se centra en el estudio de la propagación de la patología amiloidea en diferentes modelos animales para la Enfermedad de Alzheimer (EA). Los resultados sugieren que existen diversos factores que modulan este proceso de propagación, tales como, el origen de la semilla como los modelos empleados. En nuestro caso, empleamos dos modelos transgénicos de la EA que representan la forma familiar y otro la forma esporádica. Vemos que la propagación en ambos modelos es diferente, siendo mucho más lenta en el modelo esporádico. Así mismo, hemos evaluado en este trabajo como muestras cerebrales de distinto origen (humano y ratón) tienen capacidades diferentes de inducir y propagar la patología amiloidea. Vemos que las muestras humanas tienen mayor potencialidad de inducir la patología amiloidea, respecto a las muestras de roedores. Esto es debido a que el perfil molecular y conformaciones amiloideas es diferente en el extracto cerebral del paciente humano respecto al del modelo roedor. Así mismo, vemos que estos extractos afectan de forma diferencial a las células microgliales, encargadas de la compactación y formación de las placas amiloideas. Estudios de esta naturaleza son esenciales, para determinar que conformaciones amiloideas son las más patogénicas y como afectan y modulan la propagación patológica de la enfermedad. Para la realización de este trabajo se han empleado varios modelos transgénicos para la EA, los modelos 3xTg-AD y hAb-KI. Así mismo, se han empleado técnicas histológicas mediante el uso de inmunohistoquímica y microscopía tanto óptica como fluorescente de confocal, para determinar cambios patogénicos es estos modelos. Además, se han empleado técnicas moleculares como western-blot, dot-blot, proteómica para analizar las conformaciones y agregados amiloideos. Y finalmente, se han empleado cultivos celulares con células BV2 para ver la toxicidad de estos extractos.Proyecto del Ministerio de Ciencia e Innovación PID2019-108911RA-100 (D.B.V), proyecto de la Alzheimer Association AARG-22-928219 (D.B.V), programa Beatriz Galindo BAGAL18/00052 (D.B.V), proyecto Instituto de Salud Carlos III (ISCiii) PI21/00915 (A.G), cofinanciado por fondos FEDER de la Unión Europea; proyecto del National Institute of Health (NIH) U54-AG054349 (F.M.L); y proyecto de la Consejeria de Economia y Conocimiento de la Junta de Andalucia UMA18-FEDERJA-211 (A.G), y P18-RT-2233 (A.G)