Numerical Evaluation in a Scaled Rotor-Less Nozzle Vaned Radial Turbine Model under Variable Geometry Conditions

[EN] The widespread trend of pursuing higher efficiencies in radial turbochargers led to the prompting of this work. A 3D-printed model of the static parts of a radial variable geometry turbine, the vaned nozzle, and the volute, was developed. This model was up-scaled from the actual reference turbine to place sensors and characterize the flow around the nozzle vanes, including the tip gap. In this study, a computational model of the scaled-up turbine was carried out to verify the results in two ways. For this model, firstly compared with an already validated CFD turbine model of the real device (which includes a rotor), its operating range was extended to different nozzle positions, and we checked the issues with rotor-stator interactions as well as the influence of elements such as the screws of the turbine stator. After showing results for different nozzle openings, another purpose of the study was to check the effect of varying the clearance over the tip of the stator vanes on the tip leakage flow since the 3D-printed model has variable gap height configurations.This research work was supported by Grant PDC2021-120821-I00, funded by MCIN/AEI/10.13039/501100011033 and by European Union NextGeneration EI/PRTR.Serrano, J.; Tiseira, A.; López-Carrillo, JA.; Hervás-Gómez, N. (2022). Numerical Evaluation in a Scaled Rotor-Less Nozzle Vaned Radial Turbine Model under Variable Geometry Conditions. Applied Sciences. 12(14):1-17. https://doi.org/10.3390/app12147254117121

Los ámbitos y límites de participación política en Colombia en la perspectiva del servidor público. Un problema jurídico.

Los constantes pronunciamientos diametralmente opuestos entre las Altas Cortes (Corte Constitucional y Consejo de Estado) y la Procuraduría General de la Nación, viene ocasionado una incertidumbre jurídica respecto al alcance y límites de la participación en política  por parte de los servidores públicos en Colombia. El presente artículo se propone dar claridad, respecto a que servidores públicos pueden intervenir en política, sin trasgredir el régimen de las prohibiciones establecidas en la constitución y la ley. De acuerdo al análisis realizado a la Constitución Política de 1991, jurisprudencia de las Altas Cortes y  normatividad que desarrolla el tema, se encontró que la prohibición para participar en política por parte de los servidores públicos no es una regla general, sino que por el contrario es una restricción que compromete a un grupo en particular. Se pudo concluir que la Constitución de 1991 estableció como principio la participación política de los servidores públicos, convirtiendo la participación en regla y  la restricción en la excepción, además de establecer que la prohibición de la participación en política se deriva del propósito estatal de neutralidad en la toma de decisiones, pues no es permitido utilizar el cargo para realizar proselitismo político. La prohibición de tomar parte en las controversias políticas no es general para todos los servidores del estado, sino que únicamente cobija a los enunciados expresamente en la norma

Genomic and proteomic analyses reveal a relationship between WNT pathway, genes, oxidative stress metabolism and vascular calcification

Comunicaciones a congreso

Aging-related hyperphosphatemia impairs myogenic differentiation and enhances fibrosis in skeletal muscle

14 p.Background Hyperphosphatemia has been related to the development of sarcopenia in aging mice. We describe the intracellular mechanisms involved in the impairment of the myogenic differentiation promoted by hyperphosphatemia and analyse these mechanisms in the muscle from older mice. Methods C2C12 cells were grown in 2% horse serum in order to promote myogenic differentiation, in the presence or absence of 10 mM beta-glycerophosphate (BGP) for 7 days. Troponin T, paired box 7 (Pax-7), myogenic factor 5 (Myf5), myogenic differentiation 1 (MyoD), myogenin (MyoG), myocyte enhancer factor 2 (MEF2C), P300/CBP-associated factor (PCAF), histone deacetylase 1 (HDAC1), fibronectin, vimentin, and collagen I were analysed at 48, 72, and 168 h, by western blotting or by immunofluorescence staining visualized by confocal microscopy. Studies in mice were performed in 5- and 24-month-old C57BL6 mice. Three months before sacrifice, 21-month-old mice were fed with a standard diet or a low phosphate diet, containing 0.6% or 0.2% phosphate, respectively. Serum phosphate concentration was assessed by a colorimetric method and forelimb strength by a grip test. Fibrosis was observed in the tibialis anterior muscle by Sirius Red staining. In gastrocnemius muscle, MyoG, MEF2C, and fibronectin expressions were analysed by western blotting. Results Cells differentiated in the presence of BGP showed near five times less expression of troponin T and kept higher levels of Pax-7 than control cells indicating a reduced myogenic differentiation. BGP reduced Myf5 about 50% and diminished MyoD transcriptional activity by increasing the expression of HDAC1 and reducing the expression of PCAF. Consequently, BGP reduced to 50% the expression of MyoG and MEF2C. A significant increase in the expression of fibrosis markers as collagen I, vimentin, and fibronectin was found in cells treated with BGP. In mice, serum phosphate (17.24 ± 0.77 mg/dL young; 23.23 ± 0.81 mg/dL old; 19.09 ± 0.75 mg/dL old with low phosphate diet) correlates negatively (r = 0.515, P = 0.001) with the muscular strength (3.13 ± 0.07 gf/g young; 1.70 ± 0.12 gf/ g old; 2.10 ± 0.09 gf/g old with low phosphate diet) and with the expression of MyoG (r = 0.535, P = 0.007) and positively with the expression of fibronectin (r = 0.503, P = 0.001) in gastrocnemius muscle. The tibialis anterior muscle from old mice showed muscular fibrosis. Older mice fed with a low phosphate diet showed improved muscular parameters relative to control mice of similar age. Conclusions Hyperphosphatemia impairs myogenic differentiation, by inhibiting the transcriptional activity of MyoD, and enhances the expression of fibrotic genes in cultured myoblasts. Experiments carried out in older mice demonstrate a close relationship between age-related hyperphosphatemia and the decrease in the expression of myogenic factors and the increase in factors related to muscle fibrosis.Instituto de Salud Carlos IIIPrincipado de AsturiasComunidad de Madri

Barley-ß-glucans reduce systemic inflammation, renal injury and aortic calcification through ADAM17 and neutral-sphingomyelinase2 inhibition

In chronic kidney disease (CKD), hyperphosphatemia-induced inflammation aggravates vascular calcification (VC) by increasing vascular smooth muscle cell (VSMC) osteogenic differentiation, ADAM17-induced renal and vascular injury, and TNFα-induction of neutral-sphingomyelinase2 (nSMase2) to release pro-calcifying exosomes. This study examined anti-inflammatory β-glucans efficacy at attenuating systemic inflammation in health, and renal and vascular injury favoring VC in hyperphosphatemic CKD. In healthy adults, dietary barley β-glucans (Bβglucans) reduced leukocyte superoxide production, inflammatory ADAM17, TNFα, nSMase2, and pro-aging/pro-inflammatory STING (Stimulator of interferon genes) gene expression without decreasing circulating inflammatory cytokines, except for γ-interferon. In hyperphosphatemic rat CKD, dietary Bβglucans reduced renal and aortic ADAM17-driven inflammation attenuating CKD-progression (higher GFR and lower serum creatinine, proteinuria, kidney inflammatory infiltration and nSMase2), and TNFα-driven increases in aortic nSMase2 and calcium deposition without improving mineral homeostasis. In VSMC, Bβglucans prevented LPS- or uremic serum-induced rapid increases in ADAM17, TNFα and nSMase2, and reduced the 13-fold higher calcium deposition induced by prolonged calcifying conditions by inhibiting osteogenic differentiation and increases in nSMase2 through Dectin1-independent actions involving Bβglucans internalization. Thus, dietary Bβglucans inhibit leukocyte superoxide production and leukocyte, renal and aortic ADAM17- and nSMase2 gene expression attenuating systemic inflammation in health, and renal injury and aortic calcification despite hyperphosphatemia in CKD.A grant to A.S.D. and M.J.M. from IRBLleida and Agrotecnio Research collaborative projects from the Consell Social at Lleida University supported initial work, Instituto de Salud Carlos III and co-funded by European Union (ERDF/FEDER) (FIS PI11/00259, PI14/01452, PI17/02181), Plan de Ciencia, Tecnología e Innovación 2013–2017 y 2018–2022 del Principado de Asturias (GRUPIN14-028, IDI-2018-000152), RedInRen from ISCIII (ISCIII-RETIC REDINREN RD16/0009). Investigator support included: NC-L by GRUPIN14-028 and IDI-2018-000152, LM-A by GRUPIN14-028, SP by FICYT; MVA and PV by Educational Grant 2 A/2015 from ERA-EDTA CKD-MBD Working Group; PV and AC by ERA-EDTA fellowships 2011 and 2012; JR-C by MINECO (“Juan de la Cierva” program, FJCI-2015-23849); A.S.D. by Asociación Investigación de Fisiología Aplicada. A.S.D. and M.J.M. are members of the Campus Iberus (Ebro Valley Campus of International Excellence)

Fibrosis in chronic kidney disease: Pathogenesis and consequences

Fibrosis is a process characterized by an excessive accumulation of the extracellular matrix as a response to different types of tissue injuries, which leads to organ dysfunction. The process can be initiated by multiple and different stimuli and pathogenic factors which trigger the cascade of reparation converging in molecular signals responsible of initiating and driving fibrosis. Though fibrosis can play a defensive role, in several circumstances at a certain stage, it can progressively become an uncontrolled irreversible and self-maintained process, named pathological fibrosis. Several systems, molecules and responses involved in the pathogenesis of the pathological fibrosis of chronic kidney disease (CKD) will be discussed in this review, putting special attention on inflammation, renin-angiotensin system (RAS), parathyroid hormone (PTH), fibroblast growth factor 23 (FGF23), Klotho, microRNAs (miRs), and the vitamin D hormonal system. All of them are key factors of the core and regulatory pathways which drive fibrosis, having a great negative kidney and cardiac impact in CKD

A subset of low density granulocytes is associated with vascular calcification in chronic kidney disease patients

Inflammation is central to chronic kidney disease (CKD) pathogenesis and vascular outcomes, but the exact players remain unidentified. Since low density granulocytes (LDGs) are emerging mediators in inflammatory conditions, we aimed to evaluate whether LDGs may be altered in CKD and related to clinical outcomes as biomarkers. To his end, LDGs subsets were measured in peripheral blood by flow cytometry and confocal microscopy in 33 CKD patients undergoing peritoneal dialysis and 15 healthy controls (HC). Analyses were replicated in an additional cohort. DEF3 (marker of early granulopoiesis) gene expression on PBMCs was quantified by qPCR. Total CD15+ LDGs and both CD14lowCD16+ and CD14−CD16− subsets were expanded in CKD. The relative frequency of the CD14−CD16− subpopulation was higher among the CD15+ pool in CKD. This alteration was stable over-time. The increased CD14−CD16−CD15+ paralleled Kauppila scores and DEF3 expression, whereas no association was found with CD14lowCD16+ CD15+. Both subsets differed in their CD11b, CD10, CD35, CD31, CD62L, IFNAR1 and CD68 expression, FSC/SSC features and nuclear morphology, pointing to different origins and maturation status. In conclusion, LDGs were expanded in CKD showing a skewed distribution towards a CD14−CD16−CD15+ enrichment, in association with vascular calcification. DEF3 expression in PBMC can be a marker of LDG expansion.Fil: Rodríguez Carrio, Javier. Hospital Universitario Central de Asturias. Instituto de Investigación Sanitaria del Principado de Asturias (ISPA). Bone and Mineral Research Unit; España. Universidad de Oviedo; EspañaFil: Carrillo López, Natalia. Hospital Universitario Central de Asturias; EspañaFil: Ulloa, Catalina. Hospital Universitario Central de Asturias; EspañaFil: Seijo, Mariana. Hospital Universitario Central de Asturias; España. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Inmunología, Genética y Metabolismo. Universidad de Buenos Aires. Facultad de Medicina. Instituto de Inmunología, Genética y Metabolismo; ArgentinaFil: Rodríguez García, Minerva. Hospital Universitario Central de Asturias; EspañaFil: Rodríguez Suárez, Carmen. Hospital Universitario Central de Asturias; EspañaFil: Díaz-Corte, Carmen. Hospital Universitario Central de Asturias; EspañaFil: Cannata Andía, Jorge B.. Universidad de Oviedo; España. Hospital Universitario Central de Asturias; EspañaFil: Suárez, Ana. Universidad de Oviedo; EspañaFil: Dusso, Adriana. Hospital Universitario Central de Asturias; Españ