Alberto Sols Biomedical Research Institute
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Abordaje bioinformático global para la caracterización del papel de CAV1 y su regulación en condiciones fisiológicas y patológicas
No full textTesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Medicina, Departamento de Bioquímica. Fecha de Lectura: 07-11-2023Esta tesis tiene embargado el acceso al texto completo hasta el 07-05-2025This thesis aims at contributing to a better understanding of the multifaceted roles of caveolin-1 (CAV1), a highly pleiotropic protein with cell-type-specific functions that broadly impacts on organismal homeostasis despite its restricted expression to certain cell types and states. The primary objective of this thesis is to unravel the intricate roles of CAV1 across various tissues, to identify upstream modulating stimuli, and to infer regulators responsible for changes in CAV1 expression in these tissues, as well as the transcriptional changes that arise when CAV1 is deleted or modulated in pathophysiological conditions such as cancer, cardiovascular disease, or epithelial-to-mesenchymal transition (EMT).
An unbiased, data-driven strategy was employed to infer CAV1 correlation networks that are tissue and condition-specific. Bulk RNA-seq data from 52 tissues and 948 individuals, and scRNA-seq data from 8 tissues and 16 individuals from the GTEx project were reanalyzed. Additionally, 33 datasets of microarrays and RNA-seq with CAV1 deletion in different tissues and conditions were examined. The role of CAV1 in pathophysiological conditions was further investigated through the reanalysis of FANTOM5 data in carcinoma samples and during EMT induction in ARPE-19 epithelial cells.
The analysis of human donor data from the GTEx project revealed that CAV1 regulation exhibits cell-type specificity, and that its transcriptional levels are influenced by various factors, such as the proportion of cell types in the sample and other donor-dependent variables such as their Terminal Phase Context and underlying diseases. Contrary to our initial hypothesis, our unbiased analysis of GTEX data did not identify CAV1 transcriptional regulatory programs specific for caveolae-dense and caveolae-depleted tissues that might explain the different roles and expression of this gene in these different scenarios. The results of the analysis showed that CAV1 might act as a mediator of cell communication or as an inflammation marker, depending on the context. In general, genes correlating with CAV1 in a tissue-specific manner were significantly associated with three functional categories: mechanobiology, immunity, and metabolism. Upon CAV1 gene deletion, compensation mechanisms varied across tissues and conditions, primarily affecting the aforementioned functional categories: mechanobiology, immunity, and metabolism. The main upstream regulators associated with CAV1 are chromatin modifiers, displaying universal associations like SMARCA2 or condition-specific ones like PRC2 members, and transcription factors regulating the previously mentioned functional categories such as TEAD4, RELA, STAT3, and MYC.
A Bayesian differential gene expression model was developed to infer changes in cell-type proportions concurrently with alterations in cell-type-specific transcriptomes in the heart transcriptomes of CAV1KO
CAV3KO mice. This analysis unravelled that the absence of CAV1 in the heart leads to an increase in fibroblast, endothelial, and immune cell content, supporting a role for CAV1 in inflammation modulation through cell communication mechanisms, as previously observed from the GTEx data.
Finally, we investigated the role and regulation of CAV1 in pathological scenarios. CAV1 and caveolar components were found differentially expressed between small cell carcinoma and non-small cell carcinoma, correlating with distinct transcriptional programs. In fact, high levels of CAV1 were found to be associated with mechanoresponsive, inflammatory, and EMT-related pathways, while low levels corresponded to neuroendocrine differentiation signatures. The transcriptional levels of CAV1 dynamically respond to EMT induction in ARPE-19 cells, concurrently regulating cellular metabolism and proliferation during the process.
In conclusion, this thesis provides a comprehensive understanding of CAV1 involvement in cellular physiology through a comprehensive approach. The study highlights CAV1’s potential as a promising therapeutic target, particularly in the context of carcinoma and EMT. By identifying upstream regulators of CAV1 and uncovering its multifaceted roles, this research offers valuable insights for future investigations and the development of more effective treatments targeting key CAV1 modulators and related signaling pathway
Dinámica de la reparación de las roturas exógenas generadas en el DNA con radiación ionizante durante la profase-I meiótica de ratón
No full textTesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología. Fecha de Lectura: 12-12-2023Esta Tesis tiene embargado el acceso al texto completo hasta el 12-06-2025Esta Tesis ha sido financiada por el Ministerio de Economía y Competitividad y el Departamento de Biología de la Facultad de Ciencias de la Universidad Autónoma de Madrid, mediante los proyectos: “La meiosis y la evolución de los cromosomas sexuales en mamíferos” (CGL2014-53106) y “Estudio de la reparación del DNA durante la meiosis de ratón en poblaciones de espermatocitos purificadas por citometría de flujo” (BIOUAM02-2020
Identificación de genes reguladores implicados en la percepción de arsénico en Arabidopsis thaliana
No full textTesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología Molecular. Fecha de Lectura: 14-12-2023Esta tesis tiene embargado el acceso al texto completo hasta el 14-06-2025Arsenic is a toxic metalloid naturally present in the biosphere. Agricultural soils and
drinking waters are under threat of toxic metalloid contamination due to natural weathering
processes —further exacerbated by climate change—, posing a significant risk to
humans. This serious situation has sparked interest in the design of novel sustainable
strategies to deal with arsenic contamination. In this sense, understanding how plants
sense and tolerate arsenic would be of outmost importance for phytoremediation applications,
as well as for the generation of crops that limit the accumulation of the metalloid
in edible plants, enabling safe agriculture in contaminated areas. In recent years, we
have gained understanding of the mechanisms of arsenic uptake and detoxification in
plants. However, the components of arsenic signaling triggering the arsenic response in
plants remain to be discovered. Arsenic tolerance comprises a compendium of responses
that include uptake restriction, sequestering and extrusion of the metalloid. In response
to arsenic, a number of genes and biological pathways exhibit transcriptional regulation,
indicating the existence of an arsenic-specific signaling pathway and suggesting
that transcriptional regulation is a major factor in the arsenic response in plants. In
this thesis, we aimed at the identification of transcriptional regulators of the arsenic
response in Arabidopsis thaliana by means of a high-throughput Y1H, using as baits
arsenic responsive promoters in combination with an in silico analysis of binding sites of
gene clusters derived from an RNA-seq of roots exposed to the metalloid. Among all
the selected transcription factors , we focused on PLETHORA3/5/7 and GLABRA2
as central regulators of arsenic detoxification mechanisms in tight coordination with
the modulation root development under arsenic stress. In this work we have made a
significant contribution to the identification and characterization of master regulators
involved in arsenic sensing in Arabidopsis and we provide the first insights into how
plants effectively adapt their root shape and growth and recover from the arsenic stres
Estructura cerebral y perfil fenotípico de los superagers
No full textTesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Medicina, Departamento de Anatomía, Histología y Neurociencia. Fecha de Lectura: 26-01-2024Esta tesis tiene embargado el acceso al texto completo hasta el 26-07-2025Reaching old age with an episodic memory comparable to that of a person 30 years younger is possible, and this ability to remember past experiences as if we were younger has been conceptualised as superageing. The study of the superager phenotype is an alternative strategy to the numerous efforts devoted to curbing the pathological deterioration of episodic memory that characterises Alzheimer's disease. In this thesis, four complementary studies have been carried out on a large sample of superagers and typical older adults of the same age selected from the longitudinal cohort of the Vallecas Project. In the first study, a cross-sectional and longitudinal examination of the grey matter reveals a larger volume in the medial temporal lobe, the basal forebrain and the motor thalamus, as well as a slower rate of atrophy in superagers. A machine learning approach shows that higher movement speed and better mental health are the most differentiating factors in superagers. The second study replicates the cross-sectional and longitudinal examination for white matter microstructure using diffusion measures and reveals that age-related changes in the brains of superagers occur at a slower rate than in typical older adults. In the third study, telomere length was measured in blood cells and superagers show shorter telomere length compared to typical older adults. The fourth study correlates brain structure with episodic learning rate in the cognitively healthy sample from the first visit of the Vallecas Project and extends this analysis by showing that superagers have a faster learning rate relative to typical older adults. This thesis advances the field of episodic memory ageing by identifying a large sample of superagers who had neuroimaging data with up to 5 years of annual follow-up and a wide range of demographic, clinical and lifestyle variables. Overall, this thesis provides valuable insights into the brain structure of superagers and their ageing mechanism, as well as the factors associated with this phenotype, offering new perspectives on how to preserve episodic memory function at advanced age
Who wrote the replies to al-Īsī? Islamization in the Sahel and trans-saharan slavery in Early Modern Mālikī Fatāwā
No full textThis article analyzes how the currently known West African fatāwā up to the 11th/17th-century, namely the rulings by Maḥmud b. ʿUmar b. Muḥammad Aqīt, Maḫlūf al-Balbālī and Aḥmad Bābā al-Tinbutkī, portray the sale of free Muslims (bīʿ al-aḥrār) in the premodern Sahel. It argues that the strong contradictions between Aḥmad Bābā al-Tinbuktī’s Miʿrāǧ al-ṣuʿūd and his previous legal replies to Yūsuf al-Īsī may justify to affirm that these Aǧwiba were not authored by the Timbuktu scholar, and suggests that the reasons for their elaboration and their attribution to him may be related to the interests of traders from the Maghreb, where the manuscripts of the Aǧwiba were found and the Replies supposedly emitted. This study brings forward the hypothesis that the aim of the text may have been to reduce the impact that the extraordinary measure of accepting the enslaved person’s qawl when declaring to have been illicitly captured at times and places where the sale of unenslaveable persons is attested, found in the Sahelian rulings but also in preceding Andalusi and Maghrebian rulings, could have probably caused in putting the indiscriminate sale of West African captives into question. This would also imply the existence of voices against their sale, probably because the adherence to Islam of the enslaved persons must have been clearly manifestThis article is part of the results of the Research Group (GIF) MASYG (Universidad de Alcalá, UAH) and the Research Sub-Project “Transits and Migrations in North Africa: Diachronic Analysis of the Population and its Environment (DIANA)” (HAR2017-82152-C2-2-P; P.I. Helena de Felipe, Universidad de Alcalá), which, together with the Research Sub-Project “Transformations in Maghrebian Space through a Historic Perspective (TRAMAGHIS)” (HAR2017-82152-C2-1-P; P.I. Miguel Ángel Manzano, IEMYRhd, Universidad de Salamanca), is integrated in the Coordinated Research Project “Transits and Transformations in Maghrebian Space and Population (MAGNA II)” (MICIN/AEI/10.13039/501100011033 y FEDER Una manera de hacer Europa, coord. Miguel Ángel Manzano
Nuevos mecanismos de aterosclerosis y disfunción de células inmunes ligados al envejecimiento: el papel de LMNA y PPM1D
No full textTesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Medicina, Departamento de Bioquímica. Fecha de Lectura: 01-02-2024Esta tesis tiene embargado el acceso al texto completo hasta el 01-08-2025Aging is the major risk factor for cardiovascular and cerebrovascular disease (CVD), in part due to the cumulative exposure to traditional cardiovascular risk factors such as hypercholesterolemia. However, clinical and epidemiological evidence suggest the existence of yet unidentified risk factors that contribute to age-dependent CVD. Previous research from our laboratory demonstrates that the levels of Lamin A/C, one of the main components of the nuclear envelope, decrease in circulating leukocytes during aging in both humans and mice, and that Lamin A/C deficiency in immune cells leads to accelerated atherosclerosis in mice. Our laboratory has also provided extensive experimental data supporting that clonal hematopoiesis (CH) driven by somatic mutations is a new risk factor for CVD. PPM1D encodes for a protein phosphatase that negatively regulates the DNA damage repair pathway and is among the most commonly mutated genes in CH. Truncating PPM1D gain-of-function mutations are relatively frequent in elderly individuals, and are particularly enriched in cancer survivors, a phenomenon termed therapy-related CH (t-CH). Our previous sequencing studies in humans demonstrate an association between PPM1D mutations and an increased risk of coronary and peripheral artery disease, but the mechanism underlying this association remains unexplored. Based on these previous findings, we hypothesized that age-related downregulation of Lamin A/C in immune cells, and CH driven by somatic PPM1D mutations constitute two emerging age-dependent CVD risk factors. To test this hypothesis, we used in this doctoral thesis different mouse models and bone marrow transplant strategies to specifically modify the hematopoietic cell compartment. To study the role of Lamin A in atherosclerosis, we have generated a new transgenic mouse model with inducible Lamin A overexpression and demonstrated that hematopoietic cell-specific Lamin A overexpression is associated with decreased atherosclerosis development in Ldlr-/- mice, mainly due to decreased leukocyte infiltration within the artery wall. These results were further validated by sc-RNAseq analysis of atherosclerotic aortas from mice with hematopoietic Lamin A deficiency and overexpression, highlighting an important role of Lamin A/C in atherosclerosis development, mediated at least in part through regulation of leukocyte extravasation. To address the role of CH-driven by PPM1D mutations in atherosclerosis, we have generated a novel mouse model of radiation therapy-related CH driven by Ppm1d mutations by using a non-invasive adoptive transfer strategy to generate chimeric Ldlr-/- mice carrying hematopoietic cells with the truncating Ppm1d(R451X) mutation. Notably, Ppm1d mutant cells expanded in blood and bone marrow (BM) to outcompete normal cells after exposure to radiation therapy, reaching approximately 20% chimerism in blood, comparable to the human scenario. Nevertheless, no effect on hypercholesterolemia-induced atherosclerosis development was observed regardless of BM genotype or treatment. These results were corroborated by using conventional bone marrow transplant strategies to generate chimeric Ldlr-/- mice carrying heterozygous and homozygous Ppm1d(R451X) mutations. In contrast, in a mouse model of atherosclerosis regression based on adenovirus-mediated LDLR recue we found that carrying heterozygous Ppm1d(R451X) mutations impairs the beneficial atherosclerotic plaque remodeling induced by cholesterol lowering. Collectively, our results support the notion that the age-dependent downregulation of Lamin A/C in immune cells and CH-driven by PPM1D mutations are new age-related mechanisms that contribute to atherosclerosis and immune cell dysfunctio
Nanosondas que contienen esfingomielina como agentes teranósticos para la aterosclerosis
No full textTesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología Molecular. Fecha de Lectura: 15-09-2023Esta tesis tiene embargado el acceso al texto completo hasta el 15-03-2025Objective: The clinical complications of atherosclerosis constitute the leading cause of death
worldwide. Current imaging techniques for the diagnosis of atherosclerosis have not shown to
be very effective in detecting early-stage progressive lesions or identifying high-risk plaques.
Nanoparticles have emerged as promising tools for the non-invasive molecular imaging and
treatment of atherosclerosis. It has been demonstrated that enzymes that aggregate LDL are
particularly important for disease activity in established plaques. Among the different arterial
enzymes, SMase has been shown to be of high importance in atherosclerosis progression.
Therefore, during this work we hypothesised that SMase could be used as a biomarker to
develop atherosclerosis-targeted theranostic nanoprobes, expanding the library of markers
that can be used for the in vivo characterisation of the disease.
Approaches: In this thesis, we synthesised and comprehensively characterised two different
nanoprobes based on: sphingomyelin nanomicelles with a core of iron oxide nanoparticles
(SPHIONMs) and sphingomyelin solid lipid nanoparticles (SPH-SLNPs). We investigated if
the nanoprobes were able to accumulate in established murine atherosclerotic plaque using
ex vivo confocal microscopy and TEM imaging. We also studied the role of SMase in the
accumulation process by a colocalisation analysis. The developed nanoparticles were tested
as molecular imaging probes for atherosclerosis visualisation. SPHIONMs were used in T2-
weighted MRI, and SPH-SLNPs were used for PET imaging. In addition, SPH-SLNPs were
loaded with everolimus, to act as drug delivery agents for the targeted delivery of this drug
into atherosclerosis lesions. The effect of the everolimus-loaded SPH-SLNPs was compared
to that of the free drug. Aortic roots from treated mice were analysed for plaque size, and
cellular composition.
Results and Conclusions: We demonstrated that both the synthesis of SPHIONMs and
SPH-SLNPs yielded colloidally stable nanoparticles in a reproducible manner. Confocal
microscopy images showed that both nanoprobes accumulated in the atherosclerotic plaque,
and that the accumulation pattern colocalised with that of SMase. T2-weighted MRI suggested
the presence of SPHIONMs in atherosclerotic plaques, which was confirmed by TEM imaging.
SPH-SLNPs were used as biological vectors targeting atherosclerosis which we used to
develop a pretargeting approach with 68Ga-IONPs as the nanoradiotracer. Atherosclerosis
visualisation with PET imaging using this method was successful. SPH-SLNPs were efficiently
loaded with everolimus. Plasma lipid measurements showed that the loaded SPH-SLNPs
decreased the hypercholesterolemia and hypertriglyceridemia produced by the free drug.
Results from the analysed plaque features showed that empty SPH-SLNPs produced proatherogenic
effects, which everolimus-loaded SPH-SLNPs trended to reduc
Los procesos de conversión al islam en la España contemporánea: de la traición a España a la inserción comunitaria
Get PDFTesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Filosofía y Letras, Departamento de Estudios Árabes e Islámicos y Estudios Orientales. Fecha de Lectura: 21-09-2023Esta tesis tiene embargado el acceso al texto completo hasta el 21-03-202
Generación de una plataforma de análisis funcional de variantes en PMM2 con fines diagnósticos y terapéuticos
Get PDFTesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Biología Molecular. Fecha de Lectura: 04-09-2023Esta Tesis tiene embargado el acceso al texto completo hasta el 04-03-2025La deficiencia de fosfomanomutasa 2 o PMM2-CDG, el defecto congénito de glicosilación (CDG) más frecuente, es una patología severa multisistémica considerada una enfermedad conformacional para la que no existe tratamiento. La identificación de la farmacochaperona (PC) 1-(3-clorofenil)-3,3-bis(piridin-2-il)urea (CVIII) abre el camino a una potencial terapia farmacológica para esta enfermedad huérfana. Con este fin, este trabajo se ha centrado en avanzar en el desarrollo de una terapia con PCs mediante la generación de una plataforma de evaluación de variantes clínicas y de moléculas pequeñas.
Las variantes clínicas seleccionadas, identificadas en pacientes con PMM2-CDG, fueron analizadas en la estructura de PMM2, en un modelo de expresión procariota y en un modelo de expresión eucariota generado por CRISPR-Cas9.
En el sistema procariota se expresaron 13 variantes de las cuales 5 no habían sido descritas anteriormente, entre ellas p.Glu146Lys y p.Asn216Asp, que fueron identificadas en un proceso de asesoramiento reproductivo. Todas las variantes, excepto p.Asp65Gly y p.Thr237Lys, se expresaron en el sistema procariota mostrando todas ellas una actividad enzimática reducida entre el 10-65 % comparada con la proteína wild-type, a excepción de p.Thr18Ser que reveló una actividad del 99 %. Los resultados obtenidos del estudio de las proteínas mutantes (oligomerización, actividad y estabilidad), junto con la predicción del efecto a partir de su análisis estructural, han permitido identificar variantes hipomórficas.
En el modelo eucariota basado en la expresión constitutiva de los mutantes en la línea knockout de PMM2 en HepG2 se estudiaron las variantes p.Thr18Ser, p.Asp65Gly y p.Thr237Lys. Los resultados obtenidos en este sistema confirmaron el efecto severo sobre la estabilidad observado para p.Asp65Gly y p.Thr237Lys, así como la elevada actividad del mutante p.Thr18Ser, evidenciando su suavidad. Esta plataforma se ha utilizado para evaluar el efecto del CVIII y sus derivados obtenidos por química médica. La evaluación del efecto del CVIII sobre la estabilidad de las proteínas recombinantes reveló la recuperación de la estabilidad térmica de los 9 mutantes ensayados, confirmando su efecto estabilizante y la posibilidad de recuperar la actividad de la proteína PMM2 portadora de estas variantes ampliando el espectro de pacientes que se beneficiarían de una terapia con PCs.
La evaluación en el modelo celular eucariota ha supuesto la generación de un sistema de análisis de farmacochaperonas para analizar la mejora de la estabilidad de PMM2 y, en consecuencia, de su actividad. Los resultados preliminares revelan la existencia de un grupo de compuestos que superaría el potencial farmacológico del CVIII, abriendo una ventana de oportunidad a la mejora de la eficacia de esta P
Desarrollo de sensores cuánticos en diamánte sintético: Hacia un magnetoencefalógrafo portable
No full textTesis Doctoral inédita leída en la Universidad Autónoma de Madrid, Facultad de Ciencias, Departamento de Física Aplicada. Fecha de Lectura: 17-10-2023Esta tesis tiene embargado el acceso al texto completo hasta el 17-04-2025A high-performance wearable sensor for measuring the electromagnetic activity
generated by the human body could be very useful for certain fields of medicine,
such as neurology or cardiology, by allowing its use in the natural environment
of the subject. Furthermore, its applications outside of the medical field could
also be impressive. Such a device does not currently exist since none of the
technologies meets all the required characteristics. However, properly doped
diamond crystals could offer us a new possibility.
The physical properties of diamond crystals, such as color or electrical conductivity,
can be controlled by impurities. In particular, when a diamond is
doped with nitrogen and, under certain conditions, optically active nitrogenvacancy
(NV ) centers can be induced.
The center is a quantum spin system that enables, at room temperature,
optical initialization and readout, and microwave coherent control, with applications
in quantum information, quantum imaging and quantum sensing. Given
the unprecedented multiple capabilities, brought together by these centers, in
aspects such as their sensitivity, temporal and spatial resolution, miniaturization
tolerance, operation in a wide range of temperatures, long spin coherence time,
wide bandwidth and dynamic range, make it a perfect physical phenomenon for
its application as a sensor.
Specifically, and this is the main object of this doctoral thesis, as a sensor
that allows wearable magnetoencephalography.
In addition, the development of the material itself has been studied, creating
color centers by ion irradiation and subsequent annealing from diamond
samples. Irradiation causes damage to the crystalline structure of the diamond,
generating vacancies, subsequent annealing allows its mobility so that, when
combined with nitrogen atoms, they form nitrogen-vacancy couples that give
the material the desired properties. This entire process has been studied in
search of optimum the material.
Finally, and to deepen the understanding of the properties of NV centers
and how they are affected by their environment, like other centers or atoms in
the lattice, the center has been studied using computational chemistry and its
implementation using quantum computingUn sensor portátil de alto rendimiento para medir la actividad electromagnética generada por el cuerpo humano podría ser de gran utilidad para determinados
campos de la medicina, como la neurología o la cardiología, al permitir su uso en
el entorno natural del sujeto. Además, sus aplicaciones fuera del campo médico
podrían ser impresionantes.
Tal dispositivo no existe actualmente ya que ninguna de las tecnologías
cumple con todas las características requeridas. Sin embargo, los cristales de
diamante debidamente dopados, podrían ofrecernos una nueva posibilidad.
Las propiedades físicas de los cristales de diamante, como el color o la conductividad
eléctrica, pueden controlarse mediante impurezas. En particular,
cuando un diamante está dopado con nitrógeno bajo ciertas condiciones, pueden
inducirse centros de color (centro NV o centro nitrógeno-vacante) ópticamente
activos.
El centro es un sistema de espín cuántico que permite, a temperatura ambiente,
inicialización y lectura ópticas, así como un control coherente mediante
microondas, con aplicaciones en información cuántica, imagen y sensórica cuánticas.
Dadas las múltiples capacidades sin precedentes que reúnen estos centros, en
aspectos como sensibilidad, resolución temporal, resolución espacial, tolerancia
a la miniaturización, operación en un amplio rango de temperaturas, tiempo de
coherencia, ancho de banda y rango dinámico, lo convierten en un fenómeno
físico perfecto para su aplicación como sensor.
En concreto, y este es el objeto principal de esta tesis doctoral, como un
sensor que permite la magnetoencefalografía portatil.
Además de la magnetometría, se ha estudiado el desarrollo del propio material,
creando centros de color mediante irradiación con iones y posterior recocido
a partir de muestras de diamantes. La irradiación produce daños en la estructura
cristalina del diamante, generando vacantes, el recocido posterior permite
la difusión de las vacantes que, al combinarse con átomos de nitrógeno, forman
las parejas nitrógeno-vacante que otorgan al material las propiedades deseadas.
Todo este proceso ha sido estudiado en busca de optimizar el material.
Finalmente, y para profundizar en la comprensión de las propiedades de los
centros NV y cómo se ven afectados por su entorno, al igual que otros centros
o átomos en la red, se ha estudiado el centro mediante química computacional
y su implementación mediante computación cuántic