Plant’s gypsum affinity shapes responses to specific edaphic constraints without limiting responses to other general constraints

Aims: Harsh edaphic environments harbor species with different soil affinities. Plant’s responses to specific edaphic constraints may be compromised against responses to prevalent stresses shared with other semi-arid environments. We expect that species with high edaphic affinity may show traits to overcome harsh soil properties, while species with low affinity may respond to environmental constraints shared with arid environments. Methods: We quantified the edaphic affinity of 12 plant species co-occurring in gypsum outcrops and measured traits related to plant responses to specific gypsum constraints (rooting and water uptake depth, foliar accumulation of Ca, S and Mg), and traits related to common constraints of arid environments (water use efficiency, macronutrients foliar content). Results: Plants in gypsum outcrops differed in their strategies to face edaphic limitations. A phylogenetic informed PCA segregated species based on their foliar Ca and S accumulation and greater water uptake depths, associated with plant responses to specific gypsum limitations. Species’ gypsum affinity explained this segregation, but traits related to water or nutrient use efficiency did not contribute substantially to this axis. Conclusions: Plant’s specializations to respond to specific edaphic constraints of gypsum soils do not limit their ability to deal with other non-specific environmental constraints

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

Biochemical Diagnosis of Hypertensive Myocardial Fibrosis

A substantial increase in fibrillar collagen has been observed in the left cardiac ventricle of animals and humans with arterial hypertension. Hypertensive myocardial fibrosis is the result of both increased collagen types I and III due to the fact that its synthesis by fibroblasts and myofibroblasts is stimulated and its extracellular collagen degradation unchanged or decreased extracellular collagen degradation. Hemodynamic and non-hemodynamic factors may be involved in the disequilibrium between collagen synthesis and degradation that occurs in hypertension. As shown experimentally and clinically, an exaggerated rise in fibrilar collagen content promotes abnormalities of cardiac function, contributes to the decrease in coronary reserve and facilitates alterations in the electrical activity of the left ventricle. Although microscopic examination of cardiac biopsies is the most reliable method for documenting and measuring myocardial fibrosis, the development of non-invasive methods to indicate the presence of myocardial fibrosis in hypertensive patients would be useful. We have therefore applied a biochemical method based on the measurement of serum peptides derived from the tissue formation when synthesized and degradation of fibrillar collagens to monitor the turnover of these molecules in rats with spontaneous hypertension and patients with essential hypertension

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

Experimental and Simulation Study of Adsorption in Postcombustion Conditions Using a Microporous Biochar. 1. CO2 and N2 Adsorption

The influence of N2 on CO2 adsorption was evaluated using a microporous biochar with a narrow pore size distribution. The adsorption isotherms of pure CO2 and N2 were measured at 0, 30, 50, and 70 °C up to 120 kPa and fitted to the Toth adsorption model. Dynamic breakthrough experiments were carried out in a fixed-bed adsorption unit using binary mixtures with compositions representative of different postcombustion streams (8–30% CO2) from ambient temperature to 70 °C. Dynamic adsorption experiments were simulated to validate the mathematical model of the adsorption process, as a necessary step for its later use for process design. The Ideal Adsorption Solution (IAS) theory, based on the pure component adsorption models, was used to account for competitive adsorption with satisfactory results. The information gathered in the present work will be used to extend the validity of the model to the adsorption of postcombustion streams containing H2O in part 2.Work was carried out with financial support from the HiPerCap Project of the European Union 7th Framework Programme FP7 (2007-2013; Grant Agreement number: 60855). M.G.P. acknowledges funding from the CSIC (JAE-Doc program cofinanced by the European Social Fund). N.Q. acknowledges funding from the Government of the Principado de Asturias (Severo Ochoa Program). The authors also appreciate the support from the technical consultants of AspenTechnology Inc., M.M. and E.L.Peer reviewe

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

Altered cardiac expression of peroxisome proliferator-activated receptor-isoforms in patients with hypertensive heart disease

OBJECTIVE: To investigate whether cardiac expression of the nuclear peroxisome proliferator-activated receptor alpha (PPARalpha) is altered in patients with hypertensive heart disease (HHD). METHODS: We studied endomyocardial septal biopsies from 24 patients with essential hypertension divided into three groups: 6 without left ventricular hypertrophy (LVH) (HT group), 10 with LVH (LVH group), and 8 with LVH and heart failure (HF) (HF group). The expression of two PPARalpha isoforms (the native active and the truncated inhibitory) was analyzed by Western blot and reverse transcription polymerase chain reaction (RT-PCR), and two PPARalpha target genes were evaluated by RT-PCR. Histomorphological features were evaluated in a second myocardial sample from LVH and HF groups. RESULTS: Whereas the expression of native PPARalpha protein was lower (p<0.05) in LVH and HF groups than in the HT group, truncated PPARalpha protein was overexpressed (p<0.001) in the HF group as compared with LVH and HT groups. The mRNA expression of native and truncated PPARalpha was similar in the three groups of hypertensives. In addition, a progressive decrease (p for trend<0.05) in the two PPARalpha target genes mRNA expression was observed among HT, LVH and HF groups. The amount of truncated PPARalpha protein correlates directly with cardiomyocytes apoptosis and inversely with cardiomyocytes density in patients with HHD. In addition, the expression of truncated PPARalpha protein was directly correlated with left ventricular volumes, and inversely with ejection fraction in all hypertensives. CONCLUSIONS: These findings suggest that post-transcriptional regulation of PPARalpha isoforms is altered in patients with HHD, namely in those developing HF. An excess of the truncated inhibitory isoform may be involved in hypertensive left ventricular failure and remodeling

The PdBI Arcsecond Whirlpool Survey (PAWS): The Role of Spiral Arms in Cloud and Star Formation

This is the final version of the article. Available from American Astronomical Society via the DOI in this record.The process that leads to the formation of the bright star-forming sites observed along prominent spiral arms remains elusive. We present results of a multi-wavelength study of a spiral arm segment in the nearby grand-design spiral galaxy M51 that belongs to a spiral density wave and exhibits nine gas spurs. The combined observations of the (ionized, atomic, molecular, dusty) interstellar medium with star formation tracers (H ii regions, young <10 Myr stellar clusters) suggest (1) no variation in giant molecular cloud (GMC) properties between arm and gas spurs, (2) gas spurs and extinction feathers arising from the same structure with a close spatial relation between gas spurs and ongoing/recent star formation (despite higher gas surface densities in the spiral arm), (3) no trend in star formation age either along the arm or along a spur, (4) evidence for strong star formation feedback in gas spurs, (5) tentative evidence for star formation triggered by stellar feedback for one spur, and (6) GMC associations being not special entities but the result of blending of gas arm/spur cross sections in lower resolution observations. We conclude that there is no evidence for a coherent star formation onset mechanism that can be solely associated with the presence of the spiral density wave. This suggests that other (more localized) mechanisms are important to delay star formation such that it occurs in spurs. The evidence of star formation proceeding over several million years within individual spurs implies that the mechanism that leads to star formation acts or is sustained over a longer timescale.S.E.M. and M.Q. acknowledge funding from the Deutsche Forschungsgemeinschaft (DFG) via grant SCHI 536/7-2 as part of the priority program SPP 1573 "ISM-SPP: Physics of the Interstellar Medium." C.L.D. acknowledges funding from the European Research Council for the FP7 ERC starting grant project LOCALSTAR. J.P. acknowledges support from the CNRS programme Physique et Chimie du Milieu Interstellaire (PCMI). M.Q. acknowledges the International Max Planck Research School for Astronomy and Cosmic Physics at the University of Heidelberg (IMPRS-HD). S.G.B. thanks support from Spanish grant AYA2012-32295. We acknowledge financial support to the DAGAL network from the People Programme (Marie Curie Actions) of the European Unions Seventh Framework Programme FP7/2007-2013/ under REA grant agreement number PITN-GA-2011-289313. E.S. thanks NRAO for their support and hospitality during her visits in Socorro. E.S. thanks the Kavli Institute for Theoretical Physics for hospitality during the writing of this paper. IRAM is supported by INSU/CNRS (France), MPG (Germany), and IGN (Spain)