Landecho, M.F. (Manuel F.)

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    Does the metabolic syndrome need more descriptive studies or more evidence of its involvement in secondary prevention? Response
    (2011) Landecho, M.F. (Manuel F.); Beloqui, O. (Óscar); Fortuño, A. (Ana); Zalba, G. (Guillermo)
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    Spatial transcriptomic characterization of COVID-19 pneumonitis identifies immune circuits related to tissue injury
    (2023) Landecho, M.F. (Manuel F.); Weeratunga, P. (Praveen); Klenerman, P. (Paul); Issa, F. (Fadi); Etherington, R.E. (Rachel E.); Denney, L. (Laura); Roberts, I.S.D. (Ian S. D.); Hester, J. (Joanna); Villalba-Esparza, M. (María); Sansom, S.N. (Stephen N.); Melero, I. (Ignacio); Cerundolo, L. (Lucia); Ogg, G. (Graham); Cross, A.R. (Amy R.); Ho, L.P. (Ling-Pei); Andrea, C.E. (Carlos Eduardo) de
    Severe lung damage resulting from COVID-19 involves complex interactions between diverse populations of immune and stromal cells. In this study, we used a spatial transcriptomics approach to delineate the cells, pathways, and genes present across the spectrum of histopathological damage in COVID-19-affected lung tissue. We applied correlation network-based approaches to deconvolve gene expression data from 46 areas of interest covering more than 62,000 cells within well-preserved lung samples from 3 patients. Despite substantial interpatient heterogeneity, we discovered evidence for a common immune-cell signaling circuit in areas of severe tissue that involves crosstalk between cytotoxic lymphocytes and pro-inflammatory macrophages. Expression of IFNG by cytotoxic lymphocytes was associated with induction of chemokines, including CXCL9, CXCL10, and CXCL11, which are known to promote the recruitment of CXCR3+ immune cells. The TNF superfamily members BAFF (TNFSF13B) and TRAIL (TNFSF10) were consistently upregulated in the areas with severe tissue damage. We used published spatial and single-cell SARS-CoV-2 data sets to validate our findings in the lung tissue from additional cohorts of patients with COVID-19. The resulting model of severe COVID-19 immune-mediated tissue pathology may inform future therapeutic strategies.
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    Tiempo de demora prehospitalaria, la cara oculta de la isquemia coronaria
    (2016) Landecho, M.F. (Manuel F.); Artaiz, M. (Miguel)
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    Relevance of leptin and other adipokines in obesity-associated cardiovascular risk
    (MDPI AG, 2019) Landecho, M.F. (Manuel F.); Valenti, V. (Víctor); Frühbeck, G. (Gema); Higuera, M. (Magdalena) de la; Tuero, C. (Carlota); Bilbao, I. (Idoia)
    Obesity, which is a worldwide epidemic, confers increased risk for multiple serious conditions including type 2 diabetes, nonalcoholic fatty liver disease, and cardiovascular diseases. Adipose tissue is considered one of the largest endocrine organs in the body as well as an active tissue for cellular reactions and metabolic homeostasis rather than an inert tissue only for energy storage. The functional pleiotropism of adipose tissue relies on its ability to synthesize and release a large number of hormones, cytokines, extracellular matrix proteins, and growth and vasoactive factors, which are collectively called adipokines known to influence a variety of physiological and pathophysiological processes. In the obese state, excessive visceral fat accumulation causes adipose tissue dysfunctionality that strongly contributes to the onset of obesity-related comorbidities. The mechanisms underlying adipose tissue dysfunction include adipocyte hypertrophy and hyperplasia, increased inflammation, impaired extracellular matrix remodeling, and fibrosis together with an altered secretion of adipokines. This review describes the relevance of specific adipokines in the obesity-associated cardiovascular disease.
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    Design and Performance of a New Severity Score for Intermediate Care
    (San Francisco CA: Public Library of Science, 2015) Landecho, M.F. (Manuel F.); Lucena-Ramírez, J.F. (Juan Felipe); Huerta, A. (Ana); Alegre, F. (Félix); Fernandez-Ros, N. (Nerea); Martinez-Urbistondo, D. (Diego); Garcia, N. (Nicolás)
    Background Application of illness-severity scores in Intermediate Care Units (ImCU) shows conflicting results. The aim of the study is to design a severity-of-illness score for patients admitted to an ImCU. Methods We performed a retrospective observational study in a single academic medical centre in Pamplona, Spain. Demographics, past medical history, reasons for admission, physiologi- cal parameters at admission and during the first 24 hours of ImCU stay, laboratory variables and survival to hospital discharge were recorded. Logistic regression analysis was per- formed to identify variables for mortality prediction. Results A total of 743 patients were included. The final multivariable model (derivation cohort = 554 patients) contained only 9 variables obtained at admission to the ImCU: previous length of stay 7 days (6 points), health-care related infection (11), metastatic cancer (9), immunosup- pressive therapy (6), Glasgow comma scale 12 (10), need of non-invasive ventilation (14), platelets 50000/mcL (9), urea 0.6 g/L (10) and bilirubin 4 mg/dL (9). The ImCU severity score (ImCUSS) is generated by summing the individual point values, and the formula for determining the expected in-hospital mortality risk is: eImCUSS points*0.099 – 4,111 / (1 + eImCUSS points*0.099 – 4,111). The model showed adequate calibration and discrimination. Performance of ImCUSS (validation cohort = 189 patients) was comparable to that of SAPS II and 3. Hos- mer-Lemeshow goodness-of-fit C test was χ2 8.078 (p=0.326) and the area under receiver operating curve 0.802. Conclusions ImCUSS, specially designed for intermediate care, is based on easy to obtain variables at admission to ImCU. Additionally, it shows a notable performance in terms of calibration and mortality discrimination.
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    Obesity as an adipose tissue dysfunction disease and a risk factor for infections – Covid-19 as a case study
    (Elsevier, 2021) Landecho, M.F. (Manuel F.); Marín-Oto, M. (Marta); Frühbeck, G. (Gema); Recalde-Zamacona, B. (Borja); Bilbao, I. (Idoia)
    Severe Acute Respiratory Syndrome Coronavirus 2 (SARS CoV2) disease (COVID-19) is a novel threat that hampers life expectancy especially in obese individuals. Though this association is clinically relevant, the underlying mechanisms are not fully elucidated. SARS CoV2 enters host cells via the Angiotensin Converting Enzyme 2 receptor, that is also expressed in adipose tissue. Moreover, adipose tissue is also a source of many proinflammatory mediators and adipokines that might enhance the characteristic COVID-19 cytokine storm due to a chronic low-grade inflammatory preconditioning. Further obesity-dependent thoracic mechanical constraints may also incise negatively into the prognosis of obese subjects with COVID-19. This review summarizes the current body of knowledge on the obesity-dependent circumstances triggering an increased risk for COVID-19 severity, and their clinical relevance
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    Does chronic kidney disease facilitate malignant myocardial fibrosis in heart failure with preserved ejection fraction of hypertensive origin?
    (MDPI AG, 2020) Landecho, M.F. (Manuel F.); Eiros-Bachiller, R. (Rocío); Beloqui, O. (Óscar); Colina, I. (Inmaculada); Gavira, J.J. (Juan José); Ravassa, S. (Susana); Romero-González, G. (Gregorio); Gonzalez, A. (Arantxa); López, B. (Begoña); Diez, J. (Javier)
    In hypertensive patients with heart failure (HF) a serum biomarker combination of high carboxy-terminal propeptide of procollagen type-I (PICP) and low carboxy-terminal telopeptide of collagen type-I to matrix metalloproteinase-1 (CITP:MMP-1) ratio identifies a histomolecular phenotype of malignant myocardial fibrosis (mMF) associated with severe diastolic dysfunction (DD) and poor outcomes. As chronic kidney disease (CKD) facilitates MF and DD, we investigated the influence of CKD on the mMF biomarker combination in HF patients with preserved ejection fraction (HFpEF). Hypertensives (n = 365), 232 non-HF and 133 HFpEF, were studied, and 35% non-HF and 46% HFpEF patients had CKD (estimated glomerular filtration rate < 60 mL/min/1.73 m2 or urine albumin-to-creatinine ratio ≥ 30 mg/g). Specific immunoassays were performed to determine biomarkers. Medians were used to establish the high PICP and low CITP:MMP-1 combination. A comparison with non-HF showed that the biomarker combination presence was increased in HFpEF patients, being associated with CKD in all patients. CKD influenced the association of the biomarker combination and HFpEF (p for interaction ≤ 0.019). The E:e’ ratio was associated with the biomarker combination in CKD patients. Among CKD patients with HFpEF, those with the biomarker combination exhibited higher (p = 0.016) E:e’ ratio than those without the pattern. These findings suggest that CKD facilitates the development of biomarker-assessed mMF and DD in hypertensive HFpEF patients.
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    Predictors of mortality and poor outcome in cancer patients with E. faecium bloodstream infection
    (Gobierno de Navarra, 2015) Landecho, M.F. (Manuel F.); Pérez-García, A. (Alejandra); Mauleón, E. (E.); Pozo, J.C. (Juan C.) del; Beunza, J.J. (Juan José); Gea, A. (Alfredo)
    Background. To analyze predictors of mortality and poor outcome in cancer patients diagnosed with E. faecium bloodstream infection. Methods. Demographic, clinical and microbiological data were collected (January 1998-June 2011). Results. After multivariate analysis, presence of a urinary catheter was associated with a worse 7-day prognosis, and higher mortality at discharge. A high Charlson index was also associated with higher 7-day mortality. Conclusion. Presence of a urinary catheter was associated with poor 7-day prognosis and higher mortality at discharge in the present series.
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    Mortality Prediction in Patients Undergoing Non-Invasive Ventilation in Intermediate Care
    (San Francisco CA: Public Library of Science, 2015) Landecho, M.F. (Manuel F.); Garcia-Mouriz, A. (Alberto); Lucena-Ramírez, J.F. (Juan Felipe); Huerta, A. (Ana); Alegre, F. (Félix); Fernandez-Ros, N. (Nerea); Martinez-Urbistondo, D. (Diego); Carmona-Torre, F. (Francisco de A.); Garcia, N. (Nicolás); Quiroga, J. (Jorge); Nuñez-Cordoba, J.M. (Jorge M.)
    Background Intermediate Care Units (ImCU) have become an alternative scenario to perform Non-Inva- sive Ventilation (NIV). The limited number of prognostic studies in this population support the need of mortality prediction evaluation in this context. Objective The objective of this study is to analyze the performance of Simplified Acute Physiology Score (SAPS) II and 3 in patients undergoing NIV in an ImCU. Additionally, we searched for new variables that could be useful to customize these scores, in order to improve mortality prediction. Design Cohort study with prospectively collected data from all patients admitted to a single center ImCU who received NIV. The SAPS II and 3 scores with their respective predicted mortality rates were calculated. Discrimination and calibration were evaluated by calculating the area under the receiver operating characteristic curve (AUC) and with the Hosmer-Lemeshow goodness of fit test for the models, respectively. Binary logistic regression was used to iden- tify new variables to customize the scores for mortality prediction in this setting. Patients The study included 241 patients consecutively admitted to an ImCU staffed by hospitalists from April 2006 to December 2013. Key Results The observed in-hospital mortality was 32.4% resulting in a Standardized Mortality Ratio (SMR) of 1.35 for SAPS II and 0.68 for SAPS 3. Mortality discrimination based on the AUC was 0.73 for SAPS II and 0.69 for SAPS 3. Customized models including immunosuppres- sion, chronic obstructive pulmonary disease (COPD), acute pulmonary edema (APE), lactic acid, pCO2 and haemoglobin levels showed better discrimination than old scores with simi- lar calibration power. Conclusions These results suggest that SAPS II and 3 should be customized with additional patient-risk factors to improve mortality prediction in patients undergoing NIV in intermediate care.
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    Antagonic effect of ghrelin and LEAP-2 on hepatic stellate cell activation and liver fibrosis in obesity-associated nonalcoholic fatty liver disease
    (Oxford University Press, 2023) Landecho, M.F. (Manuel F.); Valenti, V. (Víctor); Ezquerro-Ezquerro, S. (Silvia); Hanley, K.P. (Karen Piper); Catalan, V. (Victoria); Becerril, S. (Sara); Frühbeck, G. (Gema); Tuero, C. (Carlota); Mocha, F. (Fátima); Silva, C. (Camilo); Gomez-Ambrosi, J. (Javier); Rodriguez, A. (Amaia); Escalada, J. (Javier); Moncada-Durruti, R. (Rafael)
    Background: Growing evidence suggests the key role of ghrelin in the onset and progression of nonalcoholic fatty liver disease (NAFLD). The potential participation of ghrelin and the ghrelin receptor antagonist, LEAP-2, in the onset of liver fibrosis in patients with severe obesity and NAFLD through the regulation of TGF-β1-induced hepatic stellate cell (HSC) activation was investigated.