Interact J Med Res. 2022 Jun 9;11(1):e35698. doi: 10.2196/35698. PMID: 35485280
Publicaciones
DNA Methylation and Ischemic Stroke Risk: An Epigenome-Wide Association Study
Thromb Haemost. 2022 Jun 19. doi: 10.1055/s-0042-1749328. Online ahead of print.PMID: 35717949
Preclinical Characterization of Antioxidant Quinolyl Nitrone QN23 as a New Candidate for the Treatment of Ischemic Stroke
Antioxidants (Basel). 2022 Jun 16;11(6):1186. doi: 10.3390/antiox11061186. PMID: 35740081
https://pubmed.ncbi.nlm.nih.gov/35740081/
Abstract: Nitrones are encouraging drug candidates for the treatment of oxidative stress-driven diseases such as acute ischemic stroke (AIS). In a previous study, we found a promising quinolylnitrone, QN23, which exerted a neuroprotective effect in neuronal cell cultures subjected to oxygen–glucose deprivation and in experimental models of cerebral ischemia. In this paper, we update the biological and pharmacological characterization of QN23. We describe the suitability of intravenous administration of QN23 to induce neuroprotection in transitory four-vessel occlusion (4VO) and middle cerebral artery occlusion (tMCAO) experimental models of brain ischemia by assessing neuronal
death, apoptosis induction, and infarct area, as well as neurofunctional outcomes. QN23 significantly decreased the neuronal death and apoptosis induced by the ischemic episode in a dose-dependent manner and showed a therapeutic effect when administered up to 3 h after post-ischemic reperfusion onset, effects that remained 11 weeks after the ischemic episode. In addition, QN23 significantly reduced infarct volume, thus recovering the motor function in a tMCAO model. Remarkably, we assessed the antioxidant activity of QN23 in vivo using dihydroethidium as a molecular probe for radical species. Finally, we describe QN23 pharmacokinetic parameters. All these resul
Funding: This work was supported by the Instituto de Salud Carlos III and co-financed by the European Development Regional Fund (FEDER) through grants PI18/00255, RD16/0019/0006,and RD21/0006/0019 to J.M. and A.A., and RD16/0019/0008 and RD21/0 006/0014 to J.B.S.; the MINECO grant SAF2015-65586-R to J.M.-C.; and the Comunidad de Madrid Neurocentro project B2017/BMD-3760 to D.G.-N.
Study protocol for a randomized controlled trial of the NEIVATECH virtual reality system to improve visual function in children with anisometropic amblyopia
BMC Ophthalmol. 2022 Jun 7;22(1):253. doi: 10.1186/s12886-022-02466-z. PMID: 35672688
First-in-human phase I clinical trial of a TLR4-binding DNA aptamer, ApTOLL: Safety and pharmacokinetics in healthy volunteers
Mol Ther Nucleic Acids. 2022 Mar 9;28:124-135. doi: 10.1016/j.omtn.2022.03.005. eCollection 2022 Jun 14. PMID: 35402075
Neuroimaging in small vessel disease
Editorial: Remote Ischemic Conditioning (Pre, Per, and Post) as an Emerging Strategy of Neuroprotection in Ischemic Stroke
Grant 2014 AOR13032 to FP, TE is the Chief Investigator for the Remote ischaemic conditioning after stroke trial (RECAST), RECAST-2, and RECAST-3 funded through the NIHR Efficacy and Mechanism Evaluation (EME) Programme, Award ID NIHR128240.
Machine Learning-Based Identification of Target Groups for Thrombectomy in Acute Stroke
Genetics and Epigenetics of Spontaneous Intracerebral Hemorrhage
and nonlobar (hypertension-related vasculopathy) ICH. Accurate phenotyping aims to reflect these biological differences in the underlying mechanisms and has been demonstrated to be crucial to the success of genetic studies in this field. This review summarizes how current knowledge on genetics
and epigenetics of this devastating stroke subtype are contributing to improve the understanding of ICH pathophysiology and their potential role in developing therapeutic strategies.
Matrix Metalloproteinase 10 Contributes to Choroidal Neovascularisation
in several steps of the pathophysiology of AMD, especially in its neovascular form; therefore, there is of great interest in understanding their role in choroidal neovascularisation. This study aimed to elucidate the role of MMP10 in the development of choroidal neovascularisation (CNV). We have
demonstrated that MMP10 was expressed by retinal pigment epithelium cells and endothelial cells of the neovascular membrane, in cell culture, mouse and human retina. MMP10 expression and activity increased under oxidative stress conditions in ARPE-19 cells. MMP10-/- mice developed smaller
laser-induced areas of CNV. Furthermore, to exclude a systemic MMP10 imbalance in these patients, plasma MMP10 concentrations were assessed in an age- and sex-matched sample of 52 control patients and 52 patients with neovascular AMD and no significant differences were found between the groups, demonstrating that MMP10 induction is a local phenomenon. Our findings suggest that MMP10 participates in the development of choroidal neovascularisation and promotes MMP10 as a possible new therapeutic target.