Heterogeneous pipelined square-root Kalman Filter algorithm for the MMSE-OSIC problem

The final publication is available at Springer via http://dx.doi.org/10.1007/s11227-009-0354-x[EN] This paper describes a pipelined parallel algorithm for the MMSE-OSIC decoding procedure proposed in V-BLAST wireless MIMO systems, for heterogeneous networks of processors. It is based on a block version of the square-root Kalman Filter algorithm that was initially devised to solve the RLS problem. It has been parallelized in a pipelined way obtaining a good efficiency and scalability. The optimum load balancing for this parallel algorithm is dynamic, but we derive a static load balancing scheme with good performance. © 2009 Springer Science+Business Media, LLC.This work has been supported by the Generalitat Valenciana, project 20080811, by the Universidad Politecnica de Valencia, project 20080009, by the Conserjería de Educacion de la Región de Murcia (Fundacion Séneca, 08763/PI/08), and by the Ministerio de Ciencia e Innovacion (TIN2008-06570-C04-02).Martínez Zaldívar, FJ.; Vidal Maciá, AM.; Giménez Cánovas, D. (2011). Heterogeneous pipelined square-root Kalman Filter algorithm for the MMSE-OSIC problem. Journal of Supercomputing. 58(2):235-243. https://doi.org/10.1007/s11227-009-0354-xS235243582Foschini GJ (1996) Layered space-time architecture for wireless communications in a fading environment when using multiple antennas. Bell Labs Techn J 1:41–59Hassibi B (2000) An efficient square-root algorithm for BLAST. In: IEEE international conference on acoustics, speech and signal processing 2000, vol 2, pp II737–II740Zhu H, Lei Z, Chin FPS (2004) An improved square-root algorithm for BLAST. IEEE Signal Process Lett 11(9)Choi Y-S, Voltz PJ, Cassara FA (2001) On channel estimation and detection for multicarrier signals in fast and selective Rayleigh fading channels. IEEE Trans Commun 49(8)Burg A, Haene S, Perels D, Luethi P, Felber N, Fichtner W (2006) Algorithm and VLSI architecture for linear MMSE detection in MIMO-OFDM systems. In: Proceedings of the IEEE int symp on circuits and systems, May 2006Martínez Zaldívar FJ (2007) Algoritmos paralelos segmentados para los problemas de Mínimos Cuadrados Recursivos (RLS) y de Detección por Cancelación Ordenada y Sucesiva de Interferencia (OSIC). PhD thesis, Facultad de Informática, Universidad Politécnica de Valencia, SpainSayed AH, Kailath T (1994) A state-space approach to adaptive RLS filtering. IEEE Signal Process Mag 11(3):18–60Kumar V, Gram A, Gupta A, Karypis G (2003) An introduction to parallel computing: design and analysis of algorithms, Chap 4, 2nd edn. Addison-Wesley, Harlow

Comisión de plan de estudios de la titulación de Ingeniería Técnica de Telecomunicaciones, especialidad en Sonido e Imagen de la EPS

La red docente de la Comisión de plan de estudios de la titulación de Ingeniería Técnica de Telecomunicación, especialidad en Sonido e Imagen de la EPS ha realizado durante el curso 2007/08 un estudio de los objetivos y competencias del futuro título de grado, así como el análisis y diseño de la posible estructura en bloques y asignaturas obligatorias en la que se podría distribuir dicho título. El estudio toma como base los resultados obtenidos en redes de cursos anteriores (ver memoria de redes 2005/06 y 2006/07), las cuales estaban orientadas al diseño curricular dentro del marco de los créditos ECTS para la convergencia al Espacio Europeo de Educación Superior, y sobre todo, se basa en la experiencia de los propios participantes en trabajos o redes previas. El objetivo principal de este proyecto es el diseño curricular del futuro título de grado en Ingeniería de Telecomunicación en Sonido e Imagen, directamente relacionada con la actual Ingeniería Técnica de Telecomunicación, especialidad en Sonido e Imagen, que se imparte en la Universidad de Alicante. Para ello se han seguido las pautas generales establecidas por el Real Decreto de ordenación de Enseñanzas Universitarias Oficiales (BOE, 30 de octubre de 2007), así como otros documentos elaborados por el Colegio Oficial de Ingenieros Técnicos de Telecomunicación y la Comisión de Universidades de Ingeniería Técnica de Telecomunicación

Multi-Omics Integration Highlights the Role of Ubiquitination in CCl4-Induced Liver Fibrosis

Liver fibrosis is the excessive accumulation of extracellular matrix proteins that occurs in chronic liver disease. Ubiquitination is a post-translational modification that is crucial for a plethora of physiological processes. Even though the ubiquitin system has been implicated in several human diseases, the role of ubiquitination in liver fibrosis remains poorly understood. Here, multi-omics approaches were used to address this. Untargeted metabolomics showed that carbon tetrachloride (CCl4)-induced liver fibrosis promotes changes in the hepatic metabolome, specifically in glycerophospholipids and sphingolipids. Gene ontology analysis of public deposited gene array-based data and validation in our mouse model showed that the biological process “protein polyubiquitination” is enriched after CCl4-induced liver fibrosis. Finally, by using transgenic mice expressing biotinylated ubiquitin (bioUb mice), the ubiquitinated proteome was isolated and characterized by mass spectrometry in order to unravel the hepatic ubiquitinated proteome fingerprint in CCl4-induced liver fibrosis. Under these conditions, ubiquitination appears to be involved in the regulation of cell death and survival, cell function, lipid metabolism, and DNA repair. Finally, ubiquitination of proliferating cell nuclear antigen (PCNA) is induced during CCl4-induced liver fibrosis and associated with the DNA damage response (DDR). Overall, hepatic ubiquitome profiling can highlight new therapeutic targets for the clinical management of liver fibrosis.This work was supported by grants from Gobierno Vasco-Departamento de Salud 2013111114 (to M.L.M.-C.), ELKARTEK 2016, Departamento de Industria del Gobierno Vasco (to M.L.M.-C.), Ministerio de Ciencia, Innovación y Universidades MICINN: SAF2017-87301-R, SAF2017-88041-R, RTI2018-096759-A-100 and SAF2016-76898-P integrado en el Plan Estatal de Investigación Cientifica y Técnica y Innovación, cofinanciado con Fondos FEDER (to M.L.M.-C., J.M.M., T.C.D. and U.M. respectively); AECC Bizkaia (M.S.-M.); Asociación Española contra el Cáncer (T.C.D.), Fundación Científica de la Asociación Española Contra el Cancer (AECC Scientific Foundation) Rare Tumor Calls 2017 (to M.L.M., J.M.B., M.A.A., J.J.G.M.), La Caixa Foundation Program (to M.L.M.), 2018 BBVA Foundation Grants for Scientific Research Teams (to M.L.M.-C.). This research was also funded by the CIBERehd (EHD15PI05/2016) and “Fondo de Investigaciones Sanitarias, Instituto de Salud Carlos III”, Spain (PI16/00598 and PI19/00819, co-funded by European Regional Development Fund/European Social Fund, “Investing in your future”); Spanish Ministry of Economy, Industry and Competitiveness (SAF2016-75197-R); “Junta de Castilla y Leon” (SA063P17); AECC Scientific Foundation (2017/2020), Spain; “Centro Internacional sobre el Envejecimiento” (OLD-HEPAMARKER, 0348_CIE_6_E), Spain; University of Salamanca Foundation, Spain (PC-TCUE18-20_051), and Fundació Marato TV3 (Ref. 201916-31), Spain (to J.J.G.M.). The UPV/EHU Lab and the Proteomics Platform are members of Proteored, PRB3 and is supported by grant PT17/0019, of the PE I + D + i 2013-2016, funded by ISCIII and ERDF. Ciberehd_ISCIII_MINECO is funded by the Instituto de Salud Carlos III. We thank MINECO for the Severo Ochoa Excellence Accreditation to CIC bioGUNE (SEV-2016-0644)

Restoring cellular magnesium balance through Cyclin M4 protects against acetaminophen-induced liver damage

Acetaminophen overdose is one of the leading causes of acute liver failure and liver transplantation in the Western world. Magnesium is essential in several cellular processess. The Cyclin M family is involved in magnesium transport across cell membranes. Herein, we identify that among all magnesium transporters, only Cyclin M4 expression is upregulated in the liver of patients with acetaminophen overdose, with disturbances in magnesium serum levels. In the liver, acetaminophen interferes with the mitochondrial magnesium reservoir via Cyclin M4, affecting ATP production and reactive oxygen species generation, further boosting endoplasmic reticulum stress. Importantly, Cyclin M4 mutant T495I, which impairs magnesium flux, shows no effect. Finally, an accumulation of Cyclin M4 in endoplasmic reticulum is shown under hepatoxicity. Based on our studies in mice, silencing hepatic Cyclin M4 within the window of 6 to 24 h following acetaminophen overdose ingestion may represent a therapeutic target for acetaminophen overdose induced liver injury

The outcome of boosting mitochondrial activity in alcohol-associated liver disease is organ-dependent.

BACKGROUND AND AIMS Alcohol-associated liver disease (ALD) accounts for 70% of liver-related deaths in Europe, with no effective approved therapies. Although mitochondrial dysfunction is one of the earliest manifestations of alcohol-induced injury, restoring mitochondrial activity remains a problematic strategy due to oxidative stress. Here, we identify methylation-controlled J protein (MCJ) as a mediator for ALD progression and hypothesize that targeting MCJ may help in recovering mitochondrial fitness without collateral oxidative damage. APPROACH AND RESULTS C57BL/6 mice [wild-type (Wt)] Mcj knockout and Mcj liver-specific silencing (MCJ-LSS) underwent the NIAAA dietary protocol (Lieber-DeCarli diet containing 5% (vol/vol) ethanol for 10 days, plus a single binge ethanol feeding at day 11). To evaluate the impact of a restored mitochondrial activity in ALD, the liver, gut, and pancreas were characterized, focusing on lipid metabolism, glucose homeostasis, intestinal permeability, and microbiota composition. MCJ, a protein acting as an endogenous negative regulator of mitochondrial respiration, is downregulated in the early stages of ALD and increases with the severity of the disease. Whole-body deficiency of MCJ is detrimental during ALD because it exacerbates the systemic effects of alcohol abuse through altered intestinal permeability, increased endotoxemia, and dysregulation of pancreatic function, which overall worsens liver injury. On the other hand, liver-specific Mcj silencing prevents main ALD hallmarks, that is, mitochondrial dysfunction, steatosis, inflammation, and oxidative stress, as it restores the NAD + /NADH ratio and SIRT1 function, hence preventing de novo lipogenesis and improving lipid oxidation. CONCLUSIONS Improving mitochondrial respiration by liver-specific Mcj silencing might become a novel therapeutic approach for treating ALD.This work was supported by grants from Ministerio de Ciencia e Innovación, Programa Retos-Colaboración RTC2019-007125-1 (for Jorge Simon and Maria Luz Martinez-Chantar); Ministerio de Economía, Industria y Competitividad, Retos a la Sociedad AGL2017- 86927R (for F.M.); Instituto de Salud Carlos III, Proyectos de Investigación en Salud DTS20/00138 and DTS21/00094 (for Jorge Simon and Maria Luz Martinez-Chantar, and Asis Palazon. respectively); Instituto de Salud Carlos III, Fondo de Investigaciones Sanitarias co-founded by European Regional Development Fund/European Social Fund, “Investing in your future” PI19/00819, “Una manera de hacer Europa” FIS PI20/00765, and PI21/01067 (for Jose J. G. Marin., Pau Sancho-Bru,. and Mario F. Fraga respectively); Departamento de Industria del Gobierno Vasco (for Maria Luz Martinez-Chantar); Asturias Government (PCTI) co-funding 2018-2023/ FEDER IDI/2021/000077 (for Mario F. Fraga.); Ministerio de Ciencia, Innovación y Universidades MICINN: PID2020-117116RB-I00, CEX2021-001136-S PID2020-117941RB-I00, PID2020-11827RB-I00 and PID2019-107956RA-100 integrado en el Plan Estatal de Investigación Científica y Técnica y Innovación, cofinanciado con Fondos FEDER (for Maria Luz Martinez-Chantar, Francisco J Cubero., Yulia A Nevzorova and Asis Palazon); Ayudas Ramón y Cajal de la Agencia Estatal de Investigación RY2013-13666 and RYC2018- 024183-I (for Leticia Abecia and Asis Palazon); European Research Council Starting Grant 804236 NEXTGEN-IO (for Asis Palazon); The German Research Foundation SFB/TRR57/P04, SFB1382-403224013/ A02 and DFG NE 2128/2-1 (for Francisco J Cubero and Yulia A Nevzorova); National Institute of Health (NIH)/National Institute of Alcohol Abuse and Alcoholism (NIAAA) 1U01AA026972-01 (For Pau Sancho-Bru); Junta de Castilla y León SA074P20 (for Jose J. G. Marin); Junta de Andalucía, Grupo PAIDI BIO311 (for Franz Martin); CIBERER Acciones Cooperativas y Complementarias Intramurales ACCI20-35 (for Mario F. Fraga); Ministerio de Educación, Cultura y Deporte FPU17/04992 (for Silvia Ariño); Fundació Marato TV3 201916-31 (for Jose J. G. Marin.); Ainize Pena-Cearra is a fellow of the University of the Basque Country (UPV/ EHU); BIOEF (Basque Foundation for Innovation and Health Research); Asociación Española contra el Cáncer (Maria Luz Martinez-Chantar and Teresa C. Delgado.); Fundación Científica de la Asociación Española Contra el Cáncer (AECC Scientific Foundation) Rare Tumor Calls 2017 (for Maria Luz Martinez-Chantar); La Caixa Foundation Program (for Maria Luz Martinez-Chantar); Proyecto Desarrollo Tecnologico CIBERehd (for Maria Luz Martinez-Chantar); Ciberehd_ISCIII_MINECO is funded by the Instituto de Salud Carlos III.S

One-year changes in fruit and vegetable variety intake and cardiometabolic risk factors changes in a middle-aged Mediterranean population at high cardiovascular risk

Background and aims Previous studies have shown beneficial associations between fruit and vegetable (FV) consumption and cardiometabolic risk factors. However, variety in FV, which may play an important role on cardiovascular health due to the different nutrient and phytochemical content among the different groups and subgroups of FV has been poorly investigated. We longitudinally investigated associations between 1-year changes in variety and quantity of FV and concurrent changes in cardiometabolic risk factors in elderly subjects with overweight/obesity and metabolic syndrome. Methods a one-year data longitudinal analysis of 6647 PREDIMED-plus study participants (48% women) was conducted. Data were collected at baseline, six months and 1-year of follow-up. Variety and quantity of FV were estimated using a food frequency questionnaire and continuous scores for variety were created based on items/month of FV. Linear mixed-models adjusted for potential confounders were performed to estimate associations (β-coefficients and 95% confidence interval) between 1-year changes in FV variety and/or quantity and concurrent changes in cardiometabolic risk factors. Results Two points increment in the FV variety score over one year was associated with a concurrent decrease in glucose (−0.33 mg/dL (0.58, −0.07)), body weight (−0.07 kg (−0.13, −0.02)) and waist circumference (WC) (−0.08 cm (−0.16, −10.01)). An increment of 100 g/d of FV over one year was associated with a concurrent decrease in triglycerides (−0.50 mg/dL (−0.93, −0.08)), glucose (−0.21 mg/dL (−0.32, −0.11)), body weight (−0.11 kg (−0.15, −0.07)) and WC (−0.10 cm (−0.14, −0.06)) over 1-year. Changes in FV consumption which led to higher quantity and variety over one year were associated with downward changes in glucose (−1.26 mg/dL (−2.09, −0.43)), body weight (−0.40 kg (−0.58, −0.23)) and WC (−0.50 cm (−0.73, −0.28)). Conclusion Greater variety, in combination with higher quantity of FV was significantly associated with a decrease in several cardiometabolic risk factors among elderly subjects at high cardiovascular risk

SUMOylation controls Hu antigen R posttranscriptional activity in liver cancer

© 2024 The Author(s). This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).The posttranslational modification of proteins critically influences many biological processes and is a key mechanism that regulates the function of the RNA-binding protein Hu antigen R (HuR), a hub in liver cancer. Here, we show that HuR is SUMOylated in the tumor sections of patients with hepatocellular carcinoma in contrast to the surrounding tissue, as well as in human cell line and mouse models of the disease. SUMOylation of HuR promotes major cancer hallmarks, namely proliferation and invasion, whereas the absence of HuR SUMOylation results in a senescent phenotype with dysfunctional mitochondria and endoplasmic reticulum. Mechanistically, SUMOylation induces a structural rearrangement of the RNA recognition motifs that modulates HuR binding affinity to its target RNAs, further modifying the transcriptomic profile toward hepatic tumor progression. Overall, SUMOylation constitutes a mechanism of HuR regulation that could be potentially exploited as a therapeutic strategy for liver cancer.This work was supported by grants to M.L.M.-C. from Departamento de Industria del Gobierno Vasco, Spain; Ministerio de Ciencia e Innovación, Spain (grant no. PID2020-117116RB-I00); European Regional Development Fund (ERDF), EU; and CIBERehd, which is funded by Instituto de Salud Carlos III (ISCIII), Spain. M.L.M.-C. and J.S. received funding from Ministerio de Ciencia e Innovación (grant no. RTC2019-007125-1) and ISCIII (grant no. DTS20/00138). M.L.M.-C. and R.M.L. acknowledge Ministerio de Ciencia e Innovación (grant no. RED2022-134397-T). M.L.M.-C. and J.M.B. were awarded with a grant from Fundación la Caixa, Spain (grant no. HR17-00601). M.L.M.-C., J.M.B., M.A.A., and J.J.G.M. acknowledge financial support from Fundación Científica de la Asociación Española Contra el Cáncer (AECC), Spain. M.S.R. recognizes funding from Fondo Sectorial de Investigación SRE - CONACYT, Mexico (grant no. 0280365); Horizon 2020 Research and Innovation Program funded under Marie Skłodowska-Curie Actions, EU (grant no. 765445); and REPÈRE and Programme de Prématuration from Région Occitanie, France. M.G., S.D., and K.M.-M. were supported by the National Institute on Aging (NIA), National Institutes of Health (NIH), US (grant no. Z01-AG000511-23). I.D.-M. is grateful for the grants received from Junta de Andalucía, Spain (grant no. BIO-198, US-1254317, P18-FR-3487, and P18-HO-4091); Ministerio de Ciencia, Innovación y Universidades, Spain (grant no. PGC2018-096049-BI00); and Fundación Ramón Areces, Spain. T.D. acknowledges Fondation ARC, France (grant no. 208084). J.J.G.M. was supported by Junta de Castilla y León, Spain (grant no. SA063P17); Fundación La Marató TV3, Spain (grant no. 201916-31); ISCIII (grant no. PI19/00819); CIBERehd; and ERDF (grant no. OLD-HEPAMARKER). M.A.A. recognizes Gobierno de Navarra, Spain (grant no. GºNa 42/21); Eurorregión Nueva Aquitania-Euskadi-Navarra, Spain; Ministerio de Ciencia e Innovación (grant no. PID2019-104878RB-I00); and CIBERehd. A.P. expresses gratitude to the European Research Council (ERC), EU (grant no. 804236) for their support. M.D.G. received financial support from Junta de Andalucía (grant no. PEMP-0036-2020 and BIO-0139); Ministerio de Universidades, Spain (grant no. FPU20/03957); ISCIII (grant no. PI20/01301), Fundación Sociedad Española de Endocrinología y Nutrición (FSEEN), Spain; CIBERehd; and CIBERobn, which is also funded by ISCIII. J.M.B. acknowledges Euskadi RIS3 (grant no. 2019222054, 2020333010, and 2021333003) and Elkartek programs from Gobierno Vasco (grant no. KK-2020/00008); ISCIII (grant no. PI18/01075, CPII19/00008, and PI21/00922); CIBERehd; PSC Support, UK; AMMF The Cholangiocarcinoma Charity, UK (grant no. EU/2019/AMMFt/001); Horizon 2020 Research and Innovation Program (grant no. 825510); ERDF; and PSC Partners Seeking a Cure, US. A.L. received financial support from the Damon Runyon-Rachleff Innovation Award, US (grant no. DR52-18) and the MERIT Award (R37) from the National Cancer Institute (NCI), NIH (grant no. R37CA230636). F.E. expresses his gratitude to ProteoRed from ISCIII (grant no. PT13/0001/0027) and CIBERehd. N.G.A.A. was funded by Ministerio de Ciencia, Innovación y Universidades (grant no. RTI2018-095700-B-I00). R.B. acknowledges financial support from Gobierno Vasco (grant no. IT1165-19); Ministerio de Economía, Industria y Competitividad, Spain (grant no. SAF2017-90900-REDT); Ministerio de Economía, Industria y Competitividad, ERDF (grant no. BFU2017-84653-P); Ministerio de Ciencia e Innovación (grant no. PID2020-114178GB-I00); and Horizon 2020 funded under Marie Skłodowska-Curie Actions (grant no. 765445-EU). A.M.A. acknowledges CIBERehd. L.A.M.-C. obtained grants from Ministerio de Economía y Competitividad (grant no. CSD2008-00005); Ministerio de Economía, Industria y Competitividad (grant no. BFU2016-77408-R); ISCIII; and EJP RD, EU (grant no. EJPRD19-040). I.G.-R. was supported by Ministerio de Economía, Industria y Competitividad (grant no. BES-2017-080435 ). M.S.-M. is grateful to the AECC, Sede de Bizkaia, Spain for the financial support. J.D.Z. was awarded with a grant from Ministerio de Economía, Industria y Competitividad (grant no. SEV-2016-0644-18-2). C.M. acknowledges Gobierno Vasco (grant no. IT-1264-19) and Ministerio de Ciencia e Innovación (grant no. PID2022-136788OB-I00). A.V.-C. was supported by Ministerio de Educación, Cultura y Deporte, Spain (grant no. FPU016/01513). C.F.-R. thanks Tekniker, Spain and CIC bioGUNE, Spain for financial support. A.G.-d.R. was funded by Bikaintek program from Gobierno Vasco (grant no. 48-AF-W1-2019-00012). N.G.-U. obtained a grant from Gobierno Vasco. T.C.D. expresses gratitude to AECC. J.S. received financial support from CIBERehd. C.M.R.-G. was supported by Ayudas a la Recualificación Margarita Salas from Universidad de Extremadura, Ministerio de Universidades financed by NextGenerationEU.Peer reviewe

Hepatic levels of S-adenosylmethionine regulate the adaptive response to fasting

26 p.-6 fig.-1 tab.-1 graph. abst.There has been an intense focus to uncover the molecular mechanisms by which fasting triggers the adaptive cellular responses in the major organs of the body. Here, we show that in mice, hepatic S-adenosylmethionine (SAMe)—the principal methyl donor—acts as a metabolic sensor of nutrition to fine-tune the catabolic-fasting response by modulating phosphatidylethanolamine N-methyltransferase (PEMT) activity, endoplasmic reticulum-mitochondria contacts, β-oxidation, and ATP production in the liver, together with FGF21-mediated lipolysis and thermogenesis in adipose tissues. Notably, we show that glucagon induces the expression of the hepatic SAMe-synthesizing enzyme methionine adenosyltransferase α1 (MAT1A), which translocates to mitochondria-associated membranes. This leads to the production of this metabolite at these sites, which acts as a brake to prevent excessive β-oxidation and mitochondrial ATP synthesis and thereby endoplasmic reticulum stress and liver injury. This work provides important insights into the previously undescribed function of SAMe as a new arm of the metabolic adaptation to fasting.M.V.-R. is supported by Proyecto PID2020-119486RB-100 (funded by MCIN/AEI/10.13039/501100011033), Gilead Sciences International Research Scholars Program in Liver Disease, Acción Estratégica Ciberehd Emergentes 2018 (ISCIII), Fundación BBVA, HORIZON-TMA-MSCA-Doctoral Networks 2021 (101073094), and Redes de Investigación 2022 (RED2022-134485-T). M.L.M.-C. is supported by La CAIXA Foundation (LCF/PR/HP17/52190004), Proyecto PID2020-117116RB-I00 (funded by MCIN/AEI/10.13039/501100011033), Ayudas Fundación BBVA a equipos de investigación científica (Umbrella 2018), and AECC Scientific Foundation (Rare Cancers 2017). A.W. is supported by RTI2018-097503-B-I00 and PID2021-127169OB-I00, (funded by MCIN/AEI/10.13039/501100011033) and by “ERDF A way of making Europe,” Xunta de Galicia (Ayudas PRO-ERC), Fundación Mutua Madrileña, and European Community’s H2020 Framework Programme (ERC Consolidator grant no. 865157 and MSCA Doctoral Networks 2021 no. 101073094). C.M. is supported by CIBERNED. P.A. is supported by Ayudas para apoyar grupos de investigación del sistema Universitario Vasco (IT1476-22), PID2021-124425OB-I00 (funded by MCIN/AEI/10.13039/501100011033 and “ERDF A way of making Europe,” MCI/UE/ISCiii [PMP21/00080], and UPV/EHU [COLAB20/01]). M.F. and M.G.B. are supported by PID2019-105739GB-I00 and PID2020-115472GB-I00, respectively (funded by MCIN/AEI/10.13039/501100011033). M.G.B. is supported by Xunta de Galicia (ED431C 2019/013). C.A., T.L.-D., and J.B.-V. are recipients of pre-doctoral fellowships from Xunta de Galicia (ED481A-2020/046, ED481A-2018/042, and ED481A 2021/244, respectively). T.C.D. is supported by Fundación Científica AECC. A.T.-R. is a recipient of a pre-doctoral fellowship from Fundación Científica AECC. S.V.A. and C.R. are recipients of Margarita Salas postdoc grants under the “Plan de Recuperación Transformación” program funded by the Spanish Ministry of Universities with European Union’s NextGeneration EU funds (2021/PER/00020 and MU-21-UP2021-03071902373A, respectively). T.C.D., A.S.-R., and M.T.-C. are recipients of Ayuda RYC2020-029316-I, PRE2019/088960, and BES-2016/078493, respectively, supported by MCIN/AEI/10.13039/501100011033 and by El FSE invierte en tu futuro. S.L.-O. is a recipient of a pre-doctoral fellowship from the Departamento de Educación del Gobierno Vasco (PRE_2018_1_0372). P.A.-G. is recipient of a FPU pre-doctoral fellowship from the Ministry of Education (FPU19/02704). CIC bioGUNE is supported by Ayuda CEX2021-001136-S financiada por MCIN/AEI/10.13039/501100011033. A.B.-C. was funded by predoctoral contract PFIS (FI19/00240) from Instituto de Salud Carlos III (ISCIII) co-funded by Fondo Social Europeo (FSE), and A.D.-L. was funded by contract Juan Rodés (JR17/00016) from ISCIII. A.B.-C. is a Miguel Servet researcher (CPII22/00008) from ISCIII.Peer reviewe

Impact of classical assumptions in modelling a microchannel gas cooler

[EN] Most of the current air-to-refrigerant heat exchanger models use the classic ¿-NTU approach, or some of its assumptions. These models do not account for longitudinal heat conduction in the tube and the fin, and the heat conduction between different tubes. This paper presents a more fundamental numerical approach to heat exchanger modelling which takes into account the 2D longitudinal heat conduction in any element, does not apply the fin theory, and captures a more detailed representation of air properties. Using the fundamental numerical approach, the paper assesses the impact of the traditional heat exchanger model assumptions when modelling a microchannel gas cooler working with CO 2. The study revealed significant differences in capacity predictions depending on the ¿-NTU relationship adopted. Large errors in capacity prediction of individual tubes occurred due to the adiabatic-fin-tip assumption when the neighbouring tubes were of different temperature. © 2011 Elsevier Ltd and IIR. All rights reserved.Santiago Martínez-Ballester’s work on this project was partially supported by Ministry for Education of Spain, under the training for university professors program (FPU).Martínez-Ballester, S.; Corberán, JM.; Gonzálvez-Maciá, J.; Domanski, PA. (2011). Impact of classical assumptions in modelling a microchannel gas cooler. International Journal of Refrigeration. 34(8):1898-1910. doi:10.1016/j.ijrefrig.2011.07.0051898191034