Time Series on Functional Service Life of Buildings using Fuzzy Delphi Method

The functional service life of heritage buildings, defined as the time period during which the building fulfils the requirements for which it was designed, is a complex system that has still not been fully resolved and continues to be the object of research regarding its social, economic and cultural importance. This paper presents an application for analysing time series that reflect the state of building performance over time. To this end, historical time records are used that provided data that could be interpreted by experts in the field. The latter can then evaluate the input variables (vulnerability and risk) using the expert system for predicting the service life of buildings, Fuzzy Building Service Life (FBSL), this methodology put together the fuzzy logic tools and Delphi method. This model provides output data on the state of functionality or performance of each buildings at each moment in time whenever information records are available. The Delphi Method is used to eliminate expert subjectivity, establishing an FDM-type assessment methodology that effectively quantifies the service life of buildings over time. The application is able to provide significant data when generating future preventive maintenance programmes in architectural-cultural heritage buildings. It can also be used to optimise the resources invested in the conservation of heritage buildings. In order to validate this system, the FDM methodology is applied to some specific building examples.Ministerio de Economía y Competitividad de España, Project ART-RISK - BIA2015-64878-RMinisterio de Economía y Competitividad de España MTM 2015-65397-

Fish- and Shellmiddens from Galicia (Northwest Spain): Reflections upon a Neglected Coastal Cultural Heritage from the Iberian Peninsula

[EN] The physiographical features of the Galician sea, in particular its temperature, marine currents and plankton richness, have turned its waters into one of the most biologically diversified marine regions of the planet. The 1500 km of shorelines from this Northwest Iberian region are dotted with rías (Galician fjords) where settlements devoted to fishing and trade have existed since prehistoric times. These activities left abundant testimonies in terms of archaeological deposits. In recent decades, urban/industrial development, as well as a number of natural agents (e.g., storms, sea level rise, climate change), is rapidly erasing the evidences of this rich cultural heritage. Loss of fish and shellmiddens in particular will hamper our ability to infer traditional lifeways, doing away with evidence that is crucial to monitoring past climatic changes and to inferring those biological conditions under which marine species and coastal populations thrived in the past. This paper surveys some issues dealing with the coastal bio-archaeological heritage of Galicia, and the risks these deposits face. It concludes with a proposal to save this increasingly threatened marine heritage.S

Preventive Conservation and Restoration Monitoring of Heritage Buildings Based on Fuzzy Logic

This article discusses the usability of the Art-Risk 3.0 software for research on the conservation of heritage buildings. It is a new and free software based on fuzzy logic, which enables the assessment of preventive conservation and surveillance of the restoration of heritage buildings over a period of time. This artificial intelligence-based tool considers the vulnerability of buildings, their environ ments, and their management to evaluate the necessity of their restoration or preventive con servation. To validate the Art-Risk 3.0, 500 theoretical case studies were analyzed, and a 14th century Mudejar-Gothic-style Church in Seville, Spain was studied both before and after its restora tion to identify post-restoration changes. This proof of concept demonstrates the capability of the Art-Risk 3.0 software to analyze environmental impacts on the vulnerability, risk, and functional service life of buildings, and assess the effectiveness of restoration activities. Additionally, this software identifies the most problematic factors and the necessity of restoration.Ministerio de Economía y Competitividad BIA2015- 64878-R (RETOS)Ministerio de Ciencia e Innovación PID2019-107257RB-I00 (FENIX)Ministerio de Ciencia, Innovación y Universidades EQC2019-005780-P (Ambulab-LAB)Junta de Andalucía PYC20 RE 034 UPO RESILIENT-TOURISMMinisterio de Ciencia e Innovación PTA2019-01688

Analysis of variants in the HCN4 gene and in three single nucleotide polymorphisms of the CYP3A4 gene for association with ivabradine reduction in heart rate: a preliminary report

[Abstract] Background: Ivabradine, a selective bradycardic drug, inhibits the If. In patients with heart failure (HF), ivabradine reduces the risk of rehospitalization and mortality. The average heart rate (HR) reduction is 8–10 beats, although clinical trials reveal interindividual variability. The aim of the study is to identify variants associated with HR reduction produced by ivabradine in genes involved in the drug metabolism (CYP3A4) or related to the drug target (HCN4). Methods: In an exploratory cohort (n = 11), patients started on ivabradine were genotyped and the HR reduction was studied. Results: The mean HR reduction after the treatment was 18.10 ± 12.26 bpm. The HR reduction was ≥ 15 bpm in 3 patients and > 5 and < 15 bpm in 7 patients. Four synonymous variants, L12L, L520L, P852P, and P1200P, were detected in the HCN4 gene (frequency = 0.045, 0.045, and 0.681, respectively). Moreover, the CYP3A4*1F and CYP3A4*1B were found in one patient each and CYP3A4*1G was presented in 3 patients. Conclusions: This is the first study using an exploratory pharmacogenetic approach that attempts to explain interindividual variability in ivabradine HR reduction. However, more research must be undertaken in order to determine the role of variants in HCN4 and CYP3A4 genes in response to ivabradine.Instituto de Salud Carlos III; RD12/004

Familial Dilated Cardiomyopathy and Isolated Left Ventricular Noncompaction Associated With Lamin A/C Gene Mutations

[Abstract] LMNA mutations have been associated with familial or sporadic dilated cardiomyopathy (DC), with or without conduction system disease. We studied the LMNA gene in 67 consecutive patients with DC (18 had familial DC, 17 had possible familial DC, and 32 sporadic DC). From genomic DNA, coding regions of the LMNA gene were amplified by polymerase chain reaction, studied by single-strand conformation polymorphism, and cycle sequenced. Mutations were confirmed by restriction fragment length polymorphism. Two disease-causing mutations were found in families A and B. In family A, a novel R349L mutation was present in the mother and her identical twin daughters. They required cardiac transplantation at 36, 18, and 20 years of age. In family B, the R190W mutation was present in 2 cousins with DC and without conduction system disease (1 had cardiac transplantation at 45 years of age and 1 died suddenly at 46 years of age) and in 2 of their sons. The mothers of the 2 affected patients died due to cardiac causes in their 40s (1 died suddenly). One of the carriers fulfilled diagnostic criteria for isolated left ventricular noncompaction. Our data associated the R349L and R190W mutations in LMNA with severe forms of familial DC. LMNA mutations should be considered in the genetic screening of patients with familial DC without conduction system disease. Isolated left ventricular noncompaction may be part of the phenotypic spectrum of the laminopathies.Xunta de Galicia; PGIDT00PXI13401P

Analysis of variants in the HCN4 gene and in three single nucleotide polymorphisms of the CYP3A4 gene for association with ivabradine reduction in heart rate: A preliminary report

Background: Ivabradine, a selective bradycardic drug, inhibits the If. In patients with heart failure (HF), ivabradine reduces the risk of rehospitalization and mortality. The average heart rate (HR) reduction is 8–10 beats, although clinical trials reveal interindividual variability. The aim of the study is to identify variants associated with HR reduction produced by ivabradine in genes involved in the drug metabolism (CYP3A4) or related to the drug target (HCN4). Methods: In an exploratory cohort (n = 11), patients started on ivabradine were genotyped and the HR reduction was studied. Results: The mean HR reduction after the treatment was 18.10 ± 12.26 bpm. The HR reduction was ≥ 15 bpm in 3 patients and &gt; 5 and &lt; 15 bpm in 7 patients. Four synonymous variants, L12L, L520L, P852P, and P1200P, were detected in the HCN4 gene (frequency = 0.045, 0.045, and 0.681, respectively). Moreover, the CYP3A4*1F and CYP3A4*1B were found in one patient each and CYP3A4*1G was presented in 3 patients. Conclusions: This is the first study using an exploratory pharmacogenetic approach that attempts to explain interindividual variability in ivabradine HR reduction. However, more research must be undertaken in order to determine the role of variants in HCN4 and CYP3A4 genes in response to ivabradine

Polymorphisms in genes related to the complement system and antibody-mediated cardiac allograft rejection

[Abstract] Background. Heart transplantation (HT) is a life-saving treatment for patients with end-stage heart failure. One of the main problems after HT is the humoral response termed antibody-mediated rejection (AMR). Complement activation plays a key role in AMR contributing to graft damage. The aim of this study was to analyze genetic variants in genes related to the complement pathways that could be associated with the development of AMR. Methods. Analysis of 51 genes related to the complement pathway was performed by next-generation sequencing in 46 HT recipients, 23 with and 23 without AMR. Statistical analysis was performed with SNPstats and R. Results. We identified 2 single nucleotide polymorphisms, 1 in the mannose-binding lectin 2 gene (p.Gly54Asp-MBL2) and 1 in the complement factor properdin gene (p.Asn428(p=)-CFP), that showed significant association with the absence and development of AMR, respectively. Moreover, the presence of the rare allele in p.Gly54Asp-MBL2 control patients correlated with an immunodeficiency of mannose-binding lectin (6.24 ng/ml vs 207.50 ng/ml, p < 0.01), whereas the presence of the rare allele p.Asn428(p=)-CFP in patients with AMR correlated with higher levels of properdin protein (14.65 μg/ml vs 10.77 μg/ml, p < 0.05). Conclusions. AMR is a complex phenotype affected by many recipient factors. Variants in p.Gly54Asp-MBL2 and p.Asn428(p=)-CFP genes, encoding mannose-binding lectin 2 and properdin, may influence the risk of AMR.Instituto de Salud Carlos III; PI13/0217

Efecto de las variantes genéticas en apoa5 en la activación de la lipoproteina lipasa y su asociación al síndrome de quilomicronemia familiar

La lipoproteína Lipasa (LPL) tiene entre sus activadores a la APO-AV, aunque existe controversia sobre si esta resulta esencial en la activación de la enzima. Nuestro objetivo fue estudiar el efecto de determinadas variantes genéticas en APOA5 presentes en 4 pacientes con historia de Hipertrigliceridemia Grave (HTG) sobre la actividad de la Lipoproteína Lipasa post-heparina in vitro y su asociación con las manifestaciones clínicas del Síndrome de Quilomicronemia Familiar (SQF). Material y métodos: Para estudiar la capacidad de activación del suero cada paciente sobre la actividad Lipoproteína Lipasa, se añadieron cantidades crecientes del suero pre-heparina de cada paciente, como fuente de APO-AV, a la mezcla de reacción (10, 20 y 40 µL; pre-calentados a 56 °C durante 60 minutos con PMSF al 0.1% (m/v)). En cada ensayo enzimático a punto final se empleó LPL de un plasma post-heparina (100 U/Kg) procedente de un individuo sano. Por otro lado, se estableció el perfil apolipoproteico mediante turbidimetría, ELISA y ultracentrifugación secuencial, se estableció la presencia de HPLI mediante el cálculo del cociente de triglicéridos en quilomicrones entre triglicéridos en VLDL y se recogieron datos clínicos y antropométricos. Resultados: PACIENTE RESUMEN DE VARIANTES GENÉTICAS EN APOA5 1 Hom c.758T>C 2 het c.758T>C & c.326_327insC 3 Het c.990_993delAACA & c.289C>T 4 het c.289C>T & c.50-2ª>G Los pacientes 1, 2 y 3, presentaron HPLI, y hospitalizaciones por episodios de pancreatitis. Además, los sueros pre-heparina de estos pacientes no activaron significativamente la actividad LPL (p<0.05). En cambio, el paciente 4 no presentó HPLI, no tuvo episodios de pancreatitis y su plasma pre-heparina sí activó significativamente la actividad LPL (p<0.05). Conclusiones: En pacientes con historia clínica de HTG, determinadas variantes genéticas en APOA5 no activan a la LPL, asociándose además a la presencia de HPLI y a una clínica compatible con SQF.Universidad de Málaga. Campus de Excelencia Internacional Andalucía Tech

La extrabuc: una colección extramuros, extravagante, extraordinaria

Comunicación presentada en las I Jornadas de Bibliotecas G9 sobre buenas prácticas en atención a espacios y usuarios, organizada por el Servicio de Bibliotecas de la UEx en Jarandilla de la Vera (Cáceres) los días 29 y 30 de septiembre de 2016Presentación de las acciones realizadas por la Biblioteca de la Universidad de Cantabria para fomentar la lectura.Presentation of the actions taken by the Library of the University of Cantabria to promote reading