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En la actualidad, existe un déficit de herramientas computacionales de bajo costo para modelar y simular distintas condiciones de operación de las microrredes con fuentes de generación no convencionales. Por está razón, nuestro proyecto desarrolló la herramienta SEM ( Simulación - Eventos - Microrredes ) en ATP-EMTP con interfaz en PyQt de Python, que simula automáticamente eventos en escenario de operación normal y fallas de baja impedancia en sistemas de distribución que incluyen fuentes no convencionales. Durante el desarrollo de este proyecto, fuimos cuidadosos del cumplimiento de las normas (IEC 60909, ANSI/IEEE 141-4, IEEE 399) y además contemplamos restricciones de ingeniería. Por ejemplo, restricciones económicas garantizando que el proyecto fuera de bajo presupuesto; restricciones ambientales contemplando que este proyecto contribuya en la reducción de gases de efecto invernadero y tecnológicas mediante la implementación de tecnologías informáticas. El proceso de validación experimental de funcionamiento de la herramienta se realizó mediante la implementación de los sistemas IEEE 34 nodos e IEEE 123 nodos. Se desarrollaron casos de estudios en ambos sistemas que fueron solucionados de forma manual y automática. En conclusión, se demostró que la herramienta SEM cumplió con el objetivo de simular y enriquecer la base de datos de escenarios de operación normal y bajo condiciones de falla para el estudio de microrredes. Los impactos de la herramienta son : tecnológico debido a que es una herramienta muy importante para el diseño de las protecciones de microrredes, específicamente aquellas que cuentan con fuentes no convencionales de energía; económico porque el costo de producción del prototipo es inferior que el de otro software con las mismas características. Nowadays, there is a deficit of low-cost computational tools for the simulation of different operating conditions in microgrids with unconventional generation sources. For this reason, we developed SEM computational tool (Simulation - Events - Microgrids) in ATP-EMTP with a Python PyQt5 interface, which automatically simulates events in a normal operating scenario and low impedance faults in distribution systems that include unconventional renewable sources. During the development of this project, we were careful to comply with the standards (IEC 60909, ANSI / IEEE 141-4, IEEE 399) and contemplated engineering restrictions. For example, economic constraints ensuring the project was low budget; environmental restrictions considering that this project contributes to the reduction of greenhouse gases and technology through the implementation of information technology. The process of experimental validation of the operation of the tool was carried out by implementing the IEEE 34 nodes and IEEE 123 nodes systems. Case studies were developed in both systems by creating an event and comparing the manual results with the computational tool results. In conclusion, it was shown that the SEM tool fulfilled the objective of simulating and enriching the database of normal operation scenarios and under fault conditions for the study of microgrids. The impacts of the tool are technological because it is a very important tool for the design of microgrid protections, specifically those that have unconventional energy sources; economic because the production cost of the prototype is lower than that of other software with the same characteristics.

The third edition of Flow Cytometry Guidelines provides the key aspects to consider when performing flow cytometry experiments and includes comprehensive sections describing phenotypes and functional assays of all major human and murine immune cell subsets. Notably, the Guidelines contain helpful tables highlighting phenotypes and key differences between human and murine cells. Another useful feature of this edition is the flow cytometry analysis of clinical samples with examples of flow cytometry applications in the context of autoimmune diseases, cancers as well as acute and chronic infectious diseases. Furthermore, there are sections detailing tips, tricks and pitfalls to avoid. All sections are written and peer-reviewed by leading flow cytometry experts and immunologists, making this edition an essential and state-of-the-art handbook for basic and clinical researchers., European Journal of Immunology, 51 (12), ISSN:0014-2980, ISSN:1521-4141

Automated cell counting in in-vivo specular microscopy images is challenging, especially in situations where single-cell segmentation methods fail due to pathological conditions. This work aims to obtain reliable cell segmentation from specular microscopy images of both healthy and pathological corneas. We cast the problem of cell segmentation as a supervised multi-class segmentation problem. The goal is to learn a mapping relation between an input specular microscopy image and its labeled counterpart, indicating healthy (cells) and pathological regions (e.g., guttae). We trained a U-net model by extracting 96 96 pixel patches from corneal endothelial cell images and the corresponding manual segmentation by a physician. Encouraging results show that the proposed method can deliver reliable feature segmentation enabling more accurate cell density estimations for assessing the state of the cornea. This work has been partly funded by the Centre de Cooperació i Desenvolupament (CCD) at the Universitat Politècnica de Catalunya under project ref. CCD 2020-B014.

Human inborn errors of immunity mediated by the cytokines interleukin 17A and interleukin 17F (IL 17A/F) underlie mucocutaneous candidiasis whereas inborn errors of interferon ? (IFN ?) immunity underlie mycobacterial disease. We report the discovery of bi allelic RORC loss of function mutations in seven individuals from three kindreds of different ethnic origins with both candidiasis and mycobacteriosis. The lack of functional ROR? and ROR?T isoforms resulted in the absence of IL 17A/F producing T cells in these individuals probably accounting for their chronic candidiasis. Unexpectedly leukocytes from ROR? and ROR?T deficient individuals also displayed an impaired IFN ? response to Mycobacterium. This principally reflected profoundly defective IFN ? production by circulating ?d T cells and CD4(+)CCR6(+)CXCR3(+) aß T cells. In humans both mucocutaneous immunity to Candida and systemic immunity to Mycobacterium require ROR? ROR?T or both.

Distinct types of CD4(+) T cells protect the host against different classes of pathogens. However, it is unclear whether a given pathogen induces a single type of polarized T cell. By combining antigenic stimulation and T cell receptor deep sequencing, we found that human pathogen- and vaccine-specific T helper 1 (T(H)1), T(H)2, and T(H)17 memory cells have different frequencies but comparable diversity and comprise not only clones polarized toward a single fate, but also clones whose progeny have acquired multiple fates. Single naïve T cells primed by a pathogen in vitro could also give rise to multiple fates. Our results unravel an unexpected degree of interclonal and intraclonal functional heterogeneity of the human T cell response and suggest that polarized responses result from preferential expansion rather than priming.

Sea G un grupo finito de automorfismos de una curva proyectiva suave X, sobre elcuerpo de los números complejos, y D un divisor no especial de X invariante bajola acción de G. En este trabajo estudiaremos el problema de descomposición de larepresentación natural del grupo G en el espacio de Riemann-Roch L(D), asociadoal divisor D. Presentaremos fórmulas explícitas para la multiplicidad de cada factor irreducible, en términos de la multiplicidad de estos factores en la descomposición de la acción de G, en el espacio dual de las 1-formas diferenciales holomorfas sobre X.Generalizando de esta forma las fórmulas conocidas para la multiplicidad de los factores irreducibles para el caso racional. Doctor en Ciencias Mención Matemáticas TERMINADA PFCHA-Becas 114p. PFCHA-Becas

MAGISTER EN CIENCIAS EXACTAS FONDECYT FONDECYT

Background The brain barriers establish compartments in the central nervous system (CNS) that significantly differ in their communication with the peripheral immune system. In this function they strictly control T-cell entry into the CNS. T cells can reach the CNS by either crossing the endothelial blood–brain barrier (BBB) or the epithelial blood-cerebrospinal fluid barrier (BCSFB) of the choroid plexus (ChP). Objective Analysis of the cellular and molecular mechanisms involved in the migration of different human CD4+ T-cell subsets across the BBB versus the BCSFB. Methods Human in vitro models of the BBB and BCSFB were employed to study the migration of circulating and CNS-entry experienced CD4+ T helper cell subsets (Th1, Th1*, Th2, Th17) across the BBB and BCSFB under inflammatory and non-inflammatory conditions in vitro. Results While under non-inflammatory conditions Th1* and Th1 cells preferentially crossed the BBB, under inflammatory conditions the migration rate of all Th subsets across the BBB was comparable. The migration of all Th subsets across the BCSFB from the same donor was 10- to 20-fold lower when compared to their migration across the BBB. Interestingly, Th17 cells preferentially crossed the BCSFB under both, non-inflamed and inflamed conditions. Barrier-crossing experienced Th cells sorted from CSF of MS patients showed migratory characteristics indistinguishable from those of circulating Th cells of healthy donors. All Th cell subsets could additionally cross the BCSFB from the CSF to ChP stroma side. T-cell migration across the BCSFB involved epithelial ICAM-1 irrespective of the direction of migration. Conclusions Our observations underscore that different Th subsets may use different anatomical routes to enter the CNS during immune surveillance versus neuroinflammation with the BCSFB establishing a tighter barrier for T-cell entry into the CNS compared to the BBB. In addition, CNS-entry experienced Th cell subsets isolated from the CSF of MS patients do not show an increased ability to cross the brain barriers when compared to circulating Th cell subsets from healthy donors underscoring the active role of the brain barriers in controlling T-cell entry into the CNS. Also we identify ICAM-1 to mediate T cell migration across the BCSFB., Fluids and Barriers of the CNS, 17 (1), ISSN:2045-8118

Narcolepsy type 1 (NT1) is a disorder with well-established markers and a suspected autoimmune aetiology. Conversely, the narcoleptic borderland (NBL) disorders, including narcolepsy type 2, idiopathic hypersomnia, insufficient sleep syndrome and hypersomnia associated with a psychiatric disorder, lack well-defined markers and remain controversial in terms of aetiology, diagnosis and management. The Swiss Primary Hypersomnolence and Narcolepsy Cohort Study (SPHYNCS) is a comprehensive multicentre cohort study, which will investigate the clinical picture, pathophysiology and long-term course of NT1 and the NBL. The primary aim is to validate new and reappraise well-known markers for the characterization of the NBL, facilitating the diagnostic process. Seven Swiss sleep centres, belonging to the Swiss Narcolepsy Network (SNaNe), joined the study and will prospectively enrol over 500 patients with recent onset of excessive daytime sleepiness (EDS), hypersomnia or a suspected central disorder of hypersomnolence (CDH) during a 3-year recruitment phase. Healthy controls and patients with EDS due to severe sleep-disordered breathing, improving after therapy, will represent two control groups of over 50 patients each. Clinical and electrophysiological (polysomnography, multiple sleep latency test, maintenance of wakefulness test) information, and information on psychomotor vigilance and a sustained attention to response task, actigraphy and wearable devices (long-term monitoring), and responses to questionnaires will be collected at baseline and after 6, 12, 24 and 36 months. Potential disease markers will be searched for in blood, cerebrospinal fluid and stool. Analyses will include quantitative hypocretin measurements, proteomics/peptidomics, and immunological, genetic and microbiota studies. SPHYNCS will increase our understanding of CDH and the relationship between NT1 and the NBL. The identification of new disease markers is expected to lead to better and earlier diagnosis, better prognosis and personalized management of CDH.

Background Echovirus 30 (E-30) is one of the most frequently isolated pathogens in aseptic meningitis worldwide. To gain access to the central nervous system (CNS), E-30 and immune cells have to cross one of the two main barriers of the CNS, the epithelial blood–cerebrospinal fluid barrier (BCSFB) or the endothelial blood–brain barrier (BBB). In an in vitro model of the BCSFB, it has been shown that E-30 can infect human immortalized brain choroid plexus papilloma (HIBCPP) cells. Methods In this study we investigated the migration of different T cell subpopulations, naive and effector T cells, through HIBCPP cells during E-30 infection. Effects of E-30 infection and the migration process were evaluated via immunofluorescence and flow cytometry analysis, as well as transepithelial resistance and dextran flux measurement. Results Th1 effector cells and enterovirus-specific effector T cells migrated through HIBCPP cells more efficiently than naive CD4+ T cells following E-30 infection of HIBCPP cells. Among the different naive T cell populations, CD8+ T cells crossed the E-30-infected HIBCPP cell layer in a significantly higher number than CD4+ T cells. A large amount of effector T cells also remained attached to the basolateral side of the HIBCPP cells compared with naive T cells. Analysis of HIBCPP barrier function showed significant alteration after E-30 infection and trans- as well as paracellular migration of T cells independent of the respective subpopulation. Morphologic analysis of migrating T cells revealed that a polarized phenotype was induced by the chemokine CXCL12, but reversed to a round phenotype after E-30 infection. Further characterization of migrating Th1 effector cells revealed a downregulation of surface adhesion proteins such as LFA-1 PSGL-1, CD44, and CD49d. Conclusion Taken together these results suggest that naive CD8+ and Th1 effector cells are highly efficient to migrate through the BCSFB in an inflammatory environment. The T cell phenotype is modified during the migration process through HIBCPP cells., Journal of Neuroinflammation, 16 (1), ISSN:1742-2094

BACKGROUND The brain barriers establish compartments in the central nervous system (CNS) that significantly differ in their communication with the peripheral immune system. In this function they strictly control T-cell entry into the CNS. T cells can reach the CNS by either crossing the endothelial blood-brain barrier (BBB) or the epithelial blood-cerebrospinal fluid barrier (BCSFB) of the choroid plexus (ChP). OBJECTIVE Analysis of the cellular and molecular mechanisms involved in the migration of different human CD4+ T-cell subsets across the BBB versus the BCSFB. METHODS Human in vitro models of the BBB and BCSFB were employed to study the migration of circulating and CNS-entry experienced CD4+ T helper cell subsets (Th1, Th1*, Th2, Th17) across the BBB and BCSFB under inflammatory and non-inflammatory conditions in vitro. RESULTS While under non-inflammatory conditions Th1* and Th1 cells preferentially crossed the BBB, under inflammatory conditions the migration rate of all Th subsets across the BBB was comparable. The migration of all Th subsets across the BCSFB from the same donor was 10- to 20-fold lower when compared to their migration across the BBB. Interestingly, Th17 cells preferentially crossed the BCSFB under both, non-inflamed and inflamed conditions. Barrier-crossing experienced Th cells sorted from CSF of MS patients showed migratory characteristics indistinguishable from those of circulating Th cells of healthy donors. All Th cell subsets could additionally cross the BCSFB from the CSF to ChP stroma side. T-cell migration across the BCSFB involved epithelial ICAM-1 irrespective of the direction of migration. CONCLUSIONS Our observations underscore that different Th subsets may use different anatomical routes to enter the CNS during immune surveillance versus neuroinflammation with the BCSFB establishing a tighter barrier for T-cell entry into the CNS compared to the BBB. In addition, CNS-entry experienced Th cell subsets isolated from the CSF of MS patients do not show an increased ability to cross the brain barriers when compared to circulating Th cell subsets from healthy donors underscoring the active role of the brain barriers in controlling T-cell entry into the CNS. Also we identify ICAM-1 to mediate T cell migration across the BCSFB.