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Institution

Hospital General Universitario Gregorio Marañón

HealthcareMadrid, Spain
About: Hospital General Universitario Gregorio Marañón is a healthcare organization based out in Madrid, Spain. It is known for research contribution in the topics: Population & Transplantation. The organization has 11975 authors who have published 12386 publications receiving 244847 citations.


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Journal ArticleDOI
TL;DR: It is suggested that the affinity of cilastatin for renal dipeptidase makes this effect specific for proximal tubular cells and may be related to a reduction in intracellular drug accumulation.
Abstract: A major area in cancer therapy is the search for protective strategies against cisplatin-induced nephrotoxicity. We investigated the protective effect of cilastatin on cisplatin-induced injury to renal proximal tubular cells. Cilastatin is a specific inhibitor of renal dehydrodipeptidase I (DHP-I), which prevents hydrolysis of imipenem and its accumulation in the proximal tubule. Primary cultures of proximal cells were treated with cisplatin (1-30 microM) in the presence or absence of cilastatin (200 microg/ml). Apoptosis and mitochondrial injury were assessed by different techniques. Cisplatin uptake and DNA binding were measured by inductively coupled plasma spectrometry. HeLa cells were used to control the effect of cilastatin on the tumoricidal activity of cisplatin. Cisplatin increased cell death, apoptotic-like morphology, caspase activation, and mitochondrial injury in proximal tubular cells in a dose- and time-dependent way. Concomitant treatment with cilastatin reduced cisplatin-induced changes. Cilastatin also reduced the DNA-bound platinum but did not modify cisplatin-dependent up-regulation of death receptors (Fas) or ligands (tumor necrosis factor alpha, Fas ligand). In contrast, cilastatin did not show any effects on cisplatin-treated HeLa cells. Renal DHP-I was virtually absent in HeLa cells. Cilastatin attenuates cisplatin-induced cell death in proximal tubular cells without reducing the cytotoxic activity of cisplatin in tumor cells. Our findings suggest that the affinity of cilastatin for renal dipeptidase makes this effect specific for proximal tubular cells and may be related to a reduction in intracellular drug accumulation. Therefore, cilastatin administration might represent a novel strategy in the prevention of cisplatin-induced acute renal injury.

70 citations

Journal ArticleDOI
TL;DR: It is observed that HAART produces a decrease in adverse clinical outcomes (i.e., hospital admission, AIDS, and death) in children with vertical HIV-1 infection in Madrid, Spain.
Abstract: Background Use of antiretroviral therapy has resulted in a decrease in morbidity and mortality rates in human immunodeficiency virus type 1 (HIV-1)-infected childrenMethods We performed a retrospective study involving 427 children to determine the effectiveness of different antiretroviral therapy protocols on clinical outcome The follow-up period was divided into 5 calendar periods (CPs): CP1 (1980-1989), before antiretroviral therapy was administered; CP2 (1990-1993), when monotherapy was administered; CP3 (1994-1996), when combined therapy was administered; CP4 (1997-1998), when /=60% of children were receiving HAARTResults Children experienced a progressive increase in the CD4(+) cell count and decrease in the viral load from 1997 onwards A lower number of AIDS cases and deaths occurred during CP5 than during the other CPs (P 20 and a relative risk of survival of >30 The AIDS rate was >50% in CP1; we observed a very strong decrease to 14% in CP2, to 16% in CP3, to 7% in CP4, and to 2% in CP5 The mortality rates in CP2 and CP3 were >6% and thereafter decreased to 05% in CP5 The relative risks for no hospital admission in CP4 and CP5 were >35 The total rates of hospital admission in CP1, CP2, and CP3 were >30%; we observed a decrease in CP4 and CP5 The duration of hospitalization decreased during the follow-up period, and it was higher in CP1 (~30 days) than in the other periodsConclusions We observed that HAART produces a decrease in adverse clinical outcomes (ie, hospital admission, AIDS, and death) in children with vertical HIV-1 infection in Madrid, Spain

70 citations

Journal ArticleDOI
TL;DR: An association between several proteins involved in hypoxia and sunitinib efficacy is found, and low VEGFR3 expression was associated with worse outcome and with VEG FR3 rs307826 variant allele, reinforcing VEGfr3 as a marker of sunit inib resistance.

70 citations

Journal ArticleDOI
TL;DR: This paper summarizes the conclusions of a consensus conference focused on the potential pathogenetic role of environmental factors and on their interactions with genetics and offers new opportunities to disentangle the gene–environment interplay that can lead to the development of ASD.
Abstract: Autism Spectrum Disorder (ASD) is a complex condition with early childhood onset, characterized by a set of common behavioral features. The etiology of ASD is not yet fully understood; however, it reflects the interaction between genetics and environment. While genetics is now a well-established risk factor, several data support a contribution of the environment as well. This paper summarizes the conclusions of a consensus conference focused on the potential pathogenetic role of environmental factors and on their interactions with genetics. Several environmental factors have been discussed in terms of ASD risk, namely advanced parental age, assisted reproductive technologies, nutritional factors, maternal infections and diseases, environmental chemicals and toxicants, and medications, as well as some other conditions. The analysis focused on their specific impact on three biologically relevant time windows for brain development: the periconception, prenatal, and early postnatal periods. Possible protective factors that might prevent or modify an ASD trajectory have been explored as well. Recommendations for clinicians to reduce ASD risk or its severity have been proposed. Developments in molecular biology and big data approaches, which are able to assess a large number of coexisting factors, are offering new opportunities to disentangle the gene⁻environment interplay that can lead to the development of ASD.

70 citations

Journal ArticleDOI
TL;DR: The clinical characteristics and outcomes of patients with COVID-19 in BIOBADASER are described, including 41 patients with RMDs treated with bDMARD and …
Abstract: From the beginning of the COVID-19 pandemic, more than 4.7 million cases have been detected in the world, Spain being one of the countries hardest hit by the SARS-CoV-2.1 The role of the immune system and immunomodulatory therapies in the evolution of this infection is still controversial.2 The study of patients with rheumatic and musculoskeletal diseases (RMDs) such as rheumatoid arthritis (RA), spondyloarthropathies (SpA) or systemic lupus erythematosus, treated with immunomodulatory therapies is essential to understand the prognosis of COVID-19 in this specific population and to the management of these patients. BIOBADASER is a multicentre prospective observational registry promoted by the Spanish Society of Rheumatology (SER) and supported by the Spanish Agency of Drugs and Medical Devices. It is aimed at assessing safety in patients with RMDs starting treatment with any biological (bDMARD) or targeted synthetic disease-modifying antirheumatic drug (tsDMARD). More than 6600 patients are prospectively followed up in BIOBADASER 3.0. This report describes the clinical characteristics and outcomes of patients with COVID-19 in BIOBADASER. We have identified 41 patients with RMDs treated with bDMARD and …

70 citations


Authors

Showing all 12014 results

NameH-indexPapersCitations
David H. Adams1551613117783
Stefanie Dimmeler14757481658
Stuart J. Pocock145684143547
M. I. Martínez134125179885
Guy A. Rouleau12988465892
Jose L. Jimenez12465464226
Antoni Torres120123865049
Paul P. Tak11259157689
Luis A. Diaz11159675036
Frans Van de Werf10974763537
José Luis Zamorano105695133396
Francisco Sánchez-Madrid10252743418
Francesco Locatelli9982042454
Roberto M. Lang9682356638
Carlos Simón9558931147
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
202317
202246
20211,186
20201,045
2019898
2018637