Efecto de la urea sobre la cristalización de carbonatos de calcio y magnesio

La dolomita (CaMg(CO3)2) es, tras la calcita (CaCO3), el segundo mineral carbonático más abundante en la corteza terrestre. La formación de este mineral en condiciones características del ciclo sedimentario ha sido un misterio conocido como el “problema de la dolomita”. Recientemente, se han aportado nuevas evidencias de que la formación de dolomita requiere de largos tiempos de maduración que no pueden simularse en el laboratorio (Pina et al., 2022 y referencias contenidas en este artículo), aunque aún quedan muchos interrogantes que deben ser resueltos. En el laboratorio, la formación de dolomita puede acelerarse: (i) a temperaturas superiores a 100 ºC (Rodríguez-Blanco et al., 2015); (ii) promoviendo oscilaciones fisicoquímicas (Deelman, 1999) o (iii) añadiendo a las soluciones compuestos orgánicos, como los EPS (Diloreto et al., 2021) o la urea (Deelman, 1999). Estos dos últimos métodos son los que presentan un mayor interés para tratar de estudiar los mecanismos que pueden favorecer la formación de dolomita y otros carbonatos de calcio y magnesio en condiciones naturales, así como para proponer vías más rápidas y eficientes de formación de este mineral con aplicaciones de interés industrial (p. ej., captura de CO2). En este trabajo presentamos resultados preliminares sobre el efecto de la urea en la cristalización de carbonatos de calcio y magnesio.Depto. de Mineralogía y PetrologíaFac. de Ciencias GeológicasTRUEpu

Pseudomorphic Replacement of Mg–Ca Carbonates after Gypsum and Anhydrite

In this paper, we present a comparative study of the pseudomorphic carbonatation of gypsum and anhydrite single crystals in Mg-bearing aqueous solutions at room temperature. We have found that carbonatation of gypsum an anhydrite occurs via a similar coupled dissolution–crystallization mechanism. However, whereas pseudomorphization of anhydrite precisely preserves the external form and dimension of the initial crystals, pseudomorphs after gypsum are less perfect and the shape and volume of the original crystals are partially lost. Furthermore, the mineralogical compositions of the pseudomorphs after anhydrite and gypsum are different, because gypsum is replaced by relatively large calcite crystals, while anhydrite pseudomorphs consist of aggregates of calcite and aragonite. Such textural and compositional differences can be clearly related to the length scale of the coupling between dissolution and crystallization at the replacement fronts. In situ atomic force microscopy observations of the early stages of carbonatation have shown that dissolution and crystallization are very tightly coupled on anhydrite rather than on gypsum surfaces. This clearly indicates that during the replacement of anhydrite and gypsum, dissolution and precipitation, respectively, are the rate-limiting steps. On the other hand, the higher supersaturation levels reached during the replacement of anhydrite lead to a competition between calcite and aragonite crystallization. This explains the fact that calcite and aragonite coexist within the replacement layers after anhydrite. Finally, we have found that dissolved magnesium in the reacting solutions is almost equally incorporated into the pseudomorphs, regardless of both the precursor phase and the mineralogical composition of the replacements. Our calculations and chemical analyses have shown that the compositions of the MgxCa1–xCO3 solid solution for which supersaturations reach maximum values correspond quite well with maximum Mg/Ca ratios in the replacement layers.This work was supported by the Spanish Government (MAT2012-38810 and CGL2013-48247-P). AFM and SEM images, and EDX analyses were obtained at the ICTS Centro Nacional de Microscopia Electrónica-UCM. We thank Ana Vicente for assistance with the SEM. GIXRD patterns were recorded at the X-ray Diffraction Central Service-UCM. We also thank Ignacio Carabias for technical support and valuable help in GIXRD interpretation. C.P. is grateful to the Spanish Government for a FPU Fellowship.Peer reviewe

Implication of miR-155-5p and miR-143-3p in the Vascular Insulin Resistance and Instability of Human and Experimental Atherosclerotic Plaque

(1) Background: Cardiovascular diseases (CVDs) are the main cause of death in developed countries, being atherosclerosis, a recurring process underlying their apparition. MicroRNAs (miRNAs) modulate the expression of their targets and have emerged as key players in CVDs; (2) Methods: 18 miRNAs were selected (Pubmed and GEO database) for their possible role in promoting atherosclerosis and were analysed by RT-qPCR in the aorta from apolipoprotein E-deficient (ApoE−/−) mice. Afterwards, the altered miRNAs in the aorta from 18 weeks-ApoE−/− mice were studied in human aortic and carotid samples; (3) Results: miR-155-5p was overexpressed and miR-143-3p was downregulated in mouse and human atherosclerotic lesions. In addition, a significant decrease in protein kinase B (AKT), target of miR-155-5p, and an increase in insulin-like growth factor type II receptor (IGF-IIR), target of miR-143-3p, were noted in aortic roots from ApoE−/− mice and in carotid plaques from patients with advanced carotid atherosclerosis (ACA). Finally, the overexpression of miR-155-5p reduced AKT levels and its phosphorylation in vascular smooth muscle cells, while miR-143-3p overexpression decreased IGF-IIR reducing apoptosis in vascular cells; (4) Conclusions: Our results suggest that miR-155-5p and miR-143-3p may be implicated in insulin resistance and plaque instability by the modulation of their targets AKT and IGF-IIR, contributing to the progression of atherosclerosis.Ministerio de Ciencia e Innovación y UniversidadesBanco SantanderUniversidad Complutense de MadridDepto. de Bioquímica y Biología MolecularFac. de FarmaciaTRUEpu

Increased let‐7d‐5p in non‐alcoholic fatty liver promotes insulin resistance and is a potential blood biomarker for diagnosis

Background and Aims: The molecular mechanisms driving non-alcoholic fatty liver disease (NAFLD) are poorly understood; however, microRNAs might play a key role in these processes. We hypothesize that let-7d- 5p could contribute to the pathophysiol-ogy of NAFLD and serve as a potential diagnostic biomarker.Methods: We evaluated let-7d- 5p levels and its targets in liver biopsies from a cross- sectional study including patients with NAFLD and healthy donors, and from a mouse model of NAFLD. Moreover, the induction of let-7d- 5p expression by fatty acids was evaluated in vitro. Further, we overexpressed let-7d- 5p in vitro to corroborate the results observed in vivo. Circulating let-7d- 5p and its potential as a NAFLD biomarker was determined in isolated extracellular vesicles from human plasma by RT-qPCR.Results: Our results demonstrate that hepatic let-7d- 5p was significantly up- regulated in patients with steatosis, and this increase correlated with obesity and a decreased expression of AKT serine/threonine kinase (AKT), insulin- like growth factor 1 (IGF1), IGF- I receptor (IGF1R) and insulin receptor (INSR). These alterations were corrobo-rated in a NAFLD mouse model. In vitro, fatty acids increased let-7d- 5p expression, and its overexpression decreased AKT, IGF-IR and IR protein expression. Furthermore, let- 7d- 5p hindered AKT phosphorylation in vitro after insulin stimulation. Finally, cir-culating let-7d- 5p significantly decreased in steatosis patients and receiver operating characteristic (ROC) analyses confirmed its utility as a diagnostic biomarker.Ministerio de Ciencia, Innovación y UniversidadesSantander-UCMUCMInstituto de Salud Carlos IIIFondo Europeo para el Desarrollo Regional (FEDER)American Heart AssociationDOD CDMRPNational Institutes of HealthDepto. de Bioquímica y Biología MolecularFac. de FarmaciaTRUEpu

Severe Hepatic Insulin Resistance Induces Vascular Dysfunction: Improvement by Liver-Specific Insulin Receptor Isoform A Gene Therapy in a Murine Diabetic Model

Background: Cardiovascular dysfunction is linked to insulin-resistant states. In this paper, we analyzed whether the severe hepatic insulin resistance of an inducible liver-specific insulin receptor knockout (iLIRKO) might generate vascular insulin resistance and dysfunction, and whether insulin receptor (IR) isoforms gene therapy might revert it. Methods: We studied in vivo insulin signaling in aorta artery and heart from iLIRKO. Vascular reactivity and the mRNA levels of genes involved in vascular dysfunction were analyzed in thoracic aorta rings by qRT-PCR. Finally, iLIRKO mice were treated with hepatic-specific gene therapy to analyze vascular dysfunction improvement. Results: Our results suggest that severe hepatic insulin resistance was expanded to cardiovascular tissues. This vascular insulin resistance observed in aorta artery from iLIRKO mice correlated with a reduction in both PI3K/AKT/eNOS and p42/44 MAPK pathways, and it might be implicated in their vascular alterations characterized by endothelial dysfunction, hypercontractility and eNOS/iNOS levels’ imbalance. Finally, regarding long-term hepatic expression of IR isoforms, IRA was more efficient than IRB in the improvement of vascular dysfunction observed in iLIRKO mice. Conclusion: Severe hepatic insulin resistance is sufficient to produce cardiovascular insulin resistance and dysfunction. Long-term hepatic expression of IRA restored the vascular damage observed in iLIRKO mice.Ministerio de Ciencia, Innovación y UniversidadesSantander-UCMISCIIICIBER de Diabetes y Enfermedades Metabólicas AsociadasDepto. de Bioquímica y Biología MolecularFac. de FarmaciaTRUEpu

New Mediators in the Crosstalk between Different Adipose Tissues

Adipose tissue is a multifunctional organ that regulates many physiological processes such as energy homeostasis, nutrition, the regulation of insulin sensitivity, body temperature, and immune response. In this review, we highlight the relevance of the different mediators that control adipose tissue activity through a systematic review of the main players present in white and brown adipose tissues. Among them, inflammatory mediators secreted by the adipose tissue, such as classical adipokines and more recent ones, elements of the immune system infiltrated into the adipose tissue (certain cell types and interleukins), as well as the role of intestinal microbiota and derived metabolites, have been reviewed. Furthermore, anti-obesity mediators that promote the activation of beige adipose tissue, e.g., myokines, thyroid hormones, amino acids, and both long and micro RNAs, are exhaustively examined. Finally, we also analyze therapeutic strategies based on those mediators that have been described to date. In conclusion, novel regulators of obesity, such as microRNAs or microbiota, are being characterized and are promising tools to treat obesity in the future.European Commission-ERCMinisterio de Ciencia e Innovación (España)Depto. de Bioquímica y Biología MolecularFac. de FarmaciaTRUEpubDescuento UC

Modelos bidimensionales y tridimensionales para la enseñanza de la Cristalografía y la Mineralogía

Depto. de Mineralogía y PetrologíaFac. de Ciencias GeológicasFALSEsubmitte