System analysis of the bio-based economy in Colombia: A bottom-up energy system model and scenario analysis

The transition to a sustainable bio‐based economy is perceived as a valid path towards low‐carbon development for emerging economies that have rich biomass resources. In the case of Colombia, the role of biomass has been tackled through qualitative roadmaps and regional climate policy assessments. However, neither of these approaches has addressed the complexity of the bio‐based economy systematically in the wider context of emission mitigation and energy and chemicals supply. In response to this limitation, we extended a bottom‐up energy system optimization model by adding a comprehensive database of novel bio‐based value chains. We included advanced road and aviation biofuels, (bio)chemicals, bioenergy with carbon capture and storage (BECCS), and integrated biorefinery configurations. A scenario analysis was conducted for the period 2015–2050, which reflected uncertainties in the capacity for technological learning, climate policy ambitions, and land availability for energy crops. Our results indicate that biomass can play an important, even if variable, role in supplying 315–760 PJ/y of modern bio‐based products. In pursuit of a deep decarbonization trajectory, the large‐scale mobilization of biomass resources can reduce the cost of the energy system by up to 11 billion $/year, the marginal abatement cost by 62%, and the potential reliance on imports of oil and chemicals in the future. The mitigation potential of BECCS can reach 24–29% of the cumulative avoided emissions between 2015 and 2050. The proposed system analysis framework can provide detailed quantitative information on the role of biomass in low carbon development of emerging economies

Editorial: Human rights and inequity in health access of Central American Migrants

Frontiers in Public Health is very pleased to publish this journal issue focusing on the health access of immigrants. Contributions to this journal issue include five articles that rely on different methodologies while focusing on diverse geographic world regions and target populations. This editorial summarizes these features while also highlighting the unique contributions of each article

Natural hosts of different hantavirus genotypes in south America: who is who?

Gardenal, C.N., Gonzalez-Ittig, R.E., Rivera, P.C., Levis, S., Salazar-Bravo, J., Barquez, R.M

UOLO - automatic object detection and segmentation in biomedical images

We propose UOLO, a novel framework for the simultaneous detection and segmentation of structures of interest in medical images. UOLO consists of an object segmentation module which intermediate abstract representations are processed and used as input for object detection. The resulting system is optimized simultaneously for detecting a class of objects and segmenting an optionally different class of structures. UOLO is trained on a set of bounding boxes enclosing the objects to detect, as well as pixel-wise segmentation information, when available. A new loss function is devised, taking into account whether a reference segmentation is accessible for each training image, in order to suitably backpropagate the error. We validate UOLO on the task of simultaneous optic disc (OD) detection, fovea detection, and OD segmentation from retinal images, achieving state-of-the-art performance on public datasets.Comment: Publised on DLMIA 2018. Licensed under the Creative Commons CC-BY-NC-ND 4.0 license: http://creativecommons.org/licenses/by-nc-nd/4.0

Impact of treatment on myocardial lysyl oxidase expression and collagen cross-linking in patients with heart failure

The aim of this study was to investigate whether torasemide modifies collagen cross-linking in the failing human heart. We analyzed the degree of cross-linking and the expression of the enzyme lysyl oxidase, which regulates cross-linking, in the myocardium of patients with chronic heart failure at baseline and after 8 months of treatment with either torasemide or furosemide in addition to their standard heart failure therapy. Whereas lysyl oxidase protein expression was very scarce in normal hearts, it was highly expressed in failing hearts. Cross-linking was increased (P<0.001) in heart failure patients compared with normal hearts. These 2 parameters decreased (P=0.021 and P=0.034) in torasemide-treated patients and remained unchanged in furosemide-treated patients. In addition, more (P=0.009) patients showed normalization of left ventricular chamber stiffness in the torasemide subgroup than in the furosemide subgroup after treatment. Lysyl oxidase expression correlated with cross-linking (r=0.661; P<0.001), and cross-linking correlated with left ventricular chamber stiffness (r=0.452; P=0.002) in all patients. These findings show for the first time that lysyl oxidase overexpression is associated with enhanced collagen cross-linking in the failing human heart. In addition, we report that the ability of torasemide to correct both lysyl oxidase overexpression and enhanced collagen cross-linking results in normalization of left ventricular chamber stiffness in patients with heart failure. Lysyl oxidase may thus represent a target for reduction of stiff collagen and improvement of left ventricular mechanical properties in heart failure patients

Apoptosis in hypertensive heart disease: a clinical approach

PURPOSE OF REVIEW: It is widely accepted that there are two principal forms of cell death, namely, necrosis and apoptosis. According to the classical view, necrosis is the major mechanism of cardiomyocyte death in cardiac diseases. RECENT DEVELOPMENTS: In the past few years observations have been made showing that cardiomyocyte apoptosis occurs in diverse conditions including hypertensive heart disease, and that apoptosis may be a contributing cause of loss and functional abnormalities of cardiomyocytes in this condition. SUMMARY: This review will summarize recent evidence demonstrating the potential contribution of cardiomyocyte apoptosis to heart failure in hypertensive patients. In addition, some strategies aimed to detect and prevent apoptosis of cardiomyocytes will be considered

Filling pressures and collagen metabolism in hypertensive patients with heart failure and normal ejection fraction

This study was designed to evaluate the association between circulating biomarkers of collagen metabolism and elevated left-sided filling pressures (FPs), as assessed from elevated estimated pulmonary capillary wedge pressure (ePCWP), in hypertensive patients with heart failure with normal ejection fraction. Echocardiography was performed and ePCWP was calculated from the formula ePCWP=1.90+1.24(maximum early transmitral flow velocity in diastole:tissue Doppler early mitral annulus velocity). The biomarkers of collagen synthesis (carboxy-terminal propeptide of procollagen type I) and degradation (matrix metalloproteinase [MMP] 1 and tissue inhibitor of MMP-1 [TIMP-1]) were analyzed by ELISA methods. Seventy-eight patients with normal FPs (ePCWP 15 mm Hg) were included. Compared with controls, the levels of the 3 biomarkers were increased in the 2 groups of patients. The MMP-1:TIMP-1 ratio, an index of MMP-1 activity, was increased in patients with normal FPs and unchanged in patients with elevated FPs. Patients with elevated FPs exhibited higher TIMP-1 levels and a lower MMP-1:TIMP-1 ratio than patients with normal FPs. ePCWP was independently associated with TIMP-1 (r=0.349; P<0.001) and the MMP-1:TIMP-1 ratio (r=-0.240; P<0.01) in all of the patients. Receiver operating characteristic curves showed that a cutoff value of TIMP-1 of 1557 ng/mL provided 64% sensitivity and 67% specificity for predicting elevated FPs with a relative risk of 3.71 (95% CI: 1.91 to 7.22). These findings suggest that, in hypertensive patients with heart failure with normal ejection fraction and elevated FPs, collagen synthesis predominates over degradation because of a relative excess of TIMP-1. This imbalance can facilitate myocardial fibrosis, which, in turn, may contribute to the elevation of FPs in these patients

Association of cardiotrophin-1 with myocardial fibrosis in hypertensive patients with heart failure

Cardiotrophin-1 has been shown to be profibrogenic in experimental models. The aim of this study was to analyze whether cardiotrophin-1 is associated with left ventricular end-diastolic stress and myocardial fibrosis in hypertensive patients with heart failure. Endomyocardial biopsies from patients (n=31) and necropsies from 7 control subjects were studied. Myocardial cardiotrophin-1 protein and mRNA and the fraction of myocardial volume occupied by collagen were increased in patients compared with controls ( P <0.001). Cardiotrophin-1 overexpression in patients was localized in cardiomyocytes. Cardiotrophin-1 protein was correlated with collagen type I and III mRNAs ( r =0.653, P <0.001; r =0.541, P <0.01) and proteins ( r =0.588, P <0.001; r =0.556, P <0.005) in all subjects and with left ventricular end-diastolic wall stress ( r =0.450; P <0.05) in patients. Plasma cardiotrophin-1 and N-terminal pro-brain natriuretic peptide and serum biomarkers of myocardial fibrosis (carboxy-terminal propeptide of procollagen type I and amino-terminal propeptide of procollagen type III) were increased ( P <0.001) in patients compared with controls. Plasma cardiotrophin-1 was correlated with N-terminal pro-brain natriuretic peptide ( r =0.386; P <0.005), carboxy- terminal propeptide of procollagen type I ( r =0.550; P <0.001), and amino-terminal propeptide of procollagen type III ( r =0.267; P <0.05) in all subjects. In vitro, cardiotrophin-1 stimulated the differentiation of human cardiac fibroblast to myofibroblasts ( P <0.05) and the expression of procollagen type I ( P <0.05) and III ( P <0.01) mRNAs. These findings show that an excess of cardiotrophin-1 is associated with increased collagen in the myocardium of hypertensive patients with heart failure. It is proposed that exaggerated cardiomyocyte production of cardiotrophin-1 in response to increased left ventricular end-diastolic stress may contribute to fibrosis through stimulation of fibroblasts in heart failure of hypertensive origi