Connexin37 reduces smooth muscle cell proliferation and intimal hyperplasia in a mouse model of carotid artery ligation
ConclusionThe presence of Cx37 in the media layer of injured arteries restrains VSMC proliferation and limits the development of IH, presumably by interfering with the pro-proliferative effect of Cx43 and the Akt pathway. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 25, 2017 Category: Cardiology Source Type: research

Restitution slope is determined by the steady state action potential duration: law and disorder
This editorial refers to ‘Restitution slope is principally determined by steady-state action potential duration’ by M.J. Shattocket al., pp. 817 –828. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 24, 2017 Category: Cardiology Source Type: research

Tyrosine phosphorylation of eNOS regulates myocardial survival after an ischaemic insult: role of PYK2
ConclusionThe current studies demonstrate that PYK2 is a pivotal regulator of eNOS function in myocardial infarction and identify PYK2 as a novel therapeutic target for cardioprotection. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 20, 2017 Category: Cardiology Source Type: research

Increased collagen within the transverse tubules in human heart failure
ConclusionIncreased expression and labelling of collagen in IDCM samples indicates fibrosis may contribute to t-tubule remodelling in human heart failure. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 20, 2017 Category: Cardiology Source Type: research

Low-dose ionizing radiation induces therapeutic neovascularization in a pre-clinical model of hindlimb ischemia
ConclusionsThese findings disclose an innovative, non-invasive strategy to induce therapeutic neovascularization in a mouse model of HLI, emerging as a novel approach in the treatment of critical limb ischemia patients. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 19, 2017 Category: Cardiology Source Type: research

Inhibition of the cardiac myocyte mineralocorticoid receptor ameliorates doxorubicin-induced cardiotoxicity
ConclusionsWe show here that (i) eplerenone prevents doxorubicin-induced left ventricular dysfunction in mice, and (ii) this beneficial effect is related to inhibition of MR in cardiac myocytes. Together with present clinical trial data our findings suggest that MR antagonism may be appropriate for the prevention of doxorubicin-induced cardiotoxicity. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 18, 2017 Category: Cardiology Source Type: research

Role of phosphatase and tensin homolog in hypoxic pulmonary vasoconstriction
ConclusionOur data indicate a novel interplay between ROCK and [Ca2+]i signalling in HPV via PTEN, in that ROCK mediates interaction of PTEN and TRPC6 which then conjointly translocate to caveolae allowing for Ca2+ influx into and subsequent contraction of PASMC. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 18, 2017 Category: Cardiology Source Type: research

Dr Fauconnier talks to Professor Barbara Casadei, President-Elect of the European Society of Cardiology
Check the interview here:https://youtu.be/MVu9QC7eek8 (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 18, 2017 Category: Cardiology Source Type: research

Anti-arrhythmic potential of the late sodium current inhibitor GS-458967 in murine Scn5a -1798insD +/ − and human SCN5A -1795insD +/− iPSC-derived cardiomyocytes
ConclusionThe INaL inhibitor GS967 decreases repolarization abnormalities and has anti-arrhythmic effects in the absence of deleterious effects on cardiac conduction. Thus, selective inhibition of INaL constitutes a promising pharmacological treatment of cardiac channelopathies associated with enhanced INaL. Our findings furthermore implement hiPSC-CMs as a valuable tool for assessment of novel pharmacological approaches in inherited sodium channelopathies. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 18, 2017 Category: Cardiology Source Type: research

ULK1 prevents cardiac dysfunction in obesity through autophagy-meditated regulation of lipid metabolism
ConclusionThese results provide clear evidence of the critical role of modulating cardiac LPL activity through autophagy-mediated proteolytic clearance as a potential novel strategy to overcome obesity-related cardiomyopathy. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 17, 2017 Category: Cardiology Source Type: research

Inhibition of sarcolemmal FAT/CD36 by sulfo- N -succinimidyl oleate rapidly corrects metabolism and restores function in the diabetic heart following hypoxia/reoxygenation
ConclusionsDiabetic hearts have limited metabolic flexibility and cardiac dysfunction when stressed, which can be rapidly rectified by reducing fatty acid uptake with the FAT/CD36 inhibitor, SSO. This novel therapeutic approach not only reduces fat oxidation but also lipotoxicity, by targeting the primary step in the fatty acid metabolism pathway. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 17, 2017 Category: Cardiology Source Type: research

CKII-SIRT1-SM22 α loop evokes a self-limited inflammatory response in vascular smooth muscle cells
ConclusionOur findings demonstrate that, in response to TNF- α stimulation, CKII-SIRT1-SM22α acts in a loop to reinforce the expression of SM22α, which limits the inflammatory response in VSMCsin vivo andin vitro. The anti-inflammatory effect of SIRT1 may be dependent on SM22 α to some extent. Our data point to targeted activation of SIRT1 in VSMCs as a promising therapeutic avenue in preventing cardiovascular diseases. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 16, 2017 Category: Cardiology Source Type: research

Decreased thromboembolic stroke but not atherosclerosis or vascular remodelling in mice with ROCK2-deficient platelets
ConclusionThese findings indicate that platelet ROCK2 plays important role in platelet function and thrombosis, but does not contribute to the pathogenesis of atherosclerosis and vascular remodeling. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 14, 2017 Category: Cardiology Source Type: research

LAV-BPIFB4 isoform modulates eNOS signalling through Ca 2+ /PKC-alpha-dependent mechanism
ConclusionsWe have identified novel molecular determinants of the beneficial effects of LAV-BPIFB4 on endothelial function, showing the roles of Ca2+ mobilization and PKC α in eNOS activation and of EDHF when eNOS is inhibited. These results highlight the role LAV-BPIFB4 can have in restoring signals that are lost during ageing. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 13, 2017 Category: Cardiology Source Type: research

Impact of acute hypertension transients on diastolic function in patients with heart failure with preserved ejection fraction
AbstractAimTo address the mechanisms responsible for the increase in LV filling pressures induced by acute hypertension transients in patients with heart failure with preserved ejection fraction (HFpEF).Methods and resultsMultiple-beat pressure –volume loops were recorded during inferior vena cava occlusion in 39 HFpEF patients and 20 controls during handgrip and atrial pacing. We measured the contribution of relaxation, elastic recoil, and stiffness to instantaneous diastolic pressure using a novel processing method. Fibrosis was quanti fied from endomyocardial biopsies. HFpEF patients showed higher diastolic pressu...
Source: Cardiovascular Research - April 11, 2017 Category: Cardiology Source Type: research

Caveolae-localized L-type Ca 2+ channels do not contribute to function or hypertrophic signalling in the mouse heart
ConclusionOur results indicate that LTCCs in the caveolae microdomain do not affect cardiac function and are not necessary for the regulation of hypertrophic signaling in the adult mouse heart. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 11, 2017 Category: Cardiology Source Type: research

RAGE-mediated extracellular matrix proteins accumulation exacerbates HySu-induced pulmonary hypertension
ConclusionsActivation of RAGE facilitates the development of hypoxia-induced pulmonary hypertension by increase of ECM deposition in pulmonary arteries. Our results indicate that sRAGE may be a potential biomarker for PAH diagnosis and disease severity, and that RAGE may be a promising target for PAH treatment. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 11, 2017 Category: Cardiology Source Type: research

Prof Stellos talks to Prof Steffens, awardee of the ESC/CBCS outstanding award, for 2016
Check the interview here:https://youtu.be/4Y0cDyl_Kns (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 4, 2017 Category: Cardiology Source Type: research

Dr Vilahur talks to Prof Antoniades, awardee of the ESC/CBCS outstanding achievement award, for 2016
Check the interview here:https://youtu.be/0mSRBMN6dSs (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 4, 2017 Category: Cardiology Source Type: research

Ablation outperforming antiarrhythmic drugs need for more research
Commentary to “Ventricular tachycardia ablation versus escalation of antiarrhythmic drugs” by Sapp JL et al., N Engl J. 2016.1 (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 4, 2017 Category: Cardiology Source Type: research

The rise of epitranscriptomic era: implications for cardiovascular disease
Commentary to ‘m6A RNA methylation promotes XIST mediated transcriptional repression’ by Patil DP et al., Nature, 2016.1 (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 4, 2017 Category: Cardiology Source Type: research

Bringing Cardiovascular Research On life
The editorial team and the Scientists of Tomorrow (http://www.escardio.org/The-ESC/ESC-Young-Community/Scientists-of-Tomorrow) are proud to launch Cardiovascular Research Onlife, the online platform that will link Cardiovascular Research with the wider scientific community. This new initiative aims to stimulate exchange of knowledge between the basic cardiovascular science community, the clinical cardiologists and scientists in other, non-cardiovascular but relevant fields of science. Onlife will highlight new ideas and provide views on what’s going on in the cardiovascular field and outside, brought by the Scientist...
Source: Cardiovascular Research - April 4, 2017 Category: Cardiology Source Type: research

Modelling human calmodulinopathies with induced pluripotent stem cells: progress and challenges
This editorial refers to ‘Elucidating arrhythmogenic mechanisms of long-QT syndrome CALM1-F142L mutation in patient-specific induced pluripotent stem cell-derived cardiomyocytes’ by M. Rocchetti et al., pp. 531–541. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 4, 2017 Category: Cardiology Source Type: research

New thrombolytic strategy providing neuroprotection in experimental ischemic stroke: MMP10 alone or in combination with tissue-type plasminogen activator
AbstractAimsEarly reperfusion with tissue-type plasminogen activator (tPA) is an effective therapeutic strategy to treat acute ischemic stroke, but only 1/3 of tPA-treated patients recover and are free from disability. tPA has also shown neurotoxicity in experimental models of cerebral ischemia. Considering that MMP-10 improves stroke injury, we have examined the therapeutic and protective effect of MMP10 and tPA/MMP10 as clot-dissolving and neuroprotective agent in an experimental model of ischemic stroke and studiedin vitro the molecular pathways involved in MMP10-mediated effects.Methods and resultsCerebral ischemia was...
Source: Cardiovascular Research - April 3, 2017 Category: Cardiology Source Type: research

Early sensitization of myofilaments to Ca 2+ prevents genetically linked dilated cardiomyopathy in mice
ConclusionOur data indicate that decreased myofilament Ca2+ sensitivity is an essential element in the pathophysiology of thin filament linked DCM. Sensitization of myofilaments to Ca2+ in the early stage of DCM may be a useful therapeutic strategy in thin filament linked DCM. (Source: Cardiovascular Research)
Source: Cardiovascular Research - April 3, 2017 Category: Cardiology Source Type: research

Therapeutic inhibition of miR-375 attenuates post-myocardial infarction inflammatory response and left ventricular dysfunction via PDK-1-AKT signalling axis
ConclusionTaken together, our studies demonstrate that anti-miR-375 therapy reduced inflammatory response, decreased cardiomyocyte death, improved LV function, and enhanced angiogenesis by targeting multiple cell types mediated at least in part through PDK-1/AKT signalling mechanisms. (Source: Cardiovascular Research)
Source: Cardiovascular Research - March 28, 2017 Category: Cardiology Source Type: research

Tissue transglutaminase induction in the pressure-overloaded myocardium regulates matrix remodelling
ConclusionsFollowing pressure overload, endogenous tTG mediates matrix cross-linking, while protecting the remodelling myocardium from dilation by exerting matrix-preserving actions. (Source: Cardiovascular Research)
Source: Cardiovascular Research - March 28, 2017 Category: Cardiology Source Type: research

Hypercontractile mutant of ventricular myosin essential light chain leads to disruption of sarcomeric structure and function and results in restrictive cardiomyopathy in mice
ConclusionsAs a result of the E143K-induced myosin hypercontractility, the hearts of RCM mice model exhibited cardiac dysfunction, stiff ventricles and physiological, morphologic, and metabolic remodelling consistent with the development of RCM. Future efforts should be directed toward normalization of myosin motor function and the use of myosin-specific therapeutics to avert the hypercontractile state of E143K-myosin and prevent pathological cardiac remodelling. (Source: Cardiovascular Research)
Source: Cardiovascular Research - March 23, 2017 Category: Cardiology Source Type: research

Sensory innervation of perivascular adipose tissue: a crucial role in artery vasodilatation and leptin release
ConclusionThese data show, for the first time, expression of sensory nerves within PVAT and that PVAT is crucial for sensory neurogenic vasorelaxation and crosstalk with adipocytes leading to leptin release, which may augment CGRP-mediated relaxation; leptin release is abolished after exposure to conditions of reduced oxygenation. (Source: Cardiovascular Research)
Source: Cardiovascular Research - March 23, 2017 Category: Cardiology Source Type: research

Restitution slope is principally determined by steady-state action potential duration
Conclusion(s)Steady-state APD is the principal determinant of the slope of the ventricular electrical restitution curve. In the absence of post-repolarization refractoriness, factors that prolong the action potential would be expected to steepen the restitution curve. However, concomitant changes in tissue refractoriness act to reduce susceptibility to sustained VF. Dependence on steady-state APD may contribute to the failure of restitution slope to predict sudden cardiac death. (Source: Cardiovascular Research)
Source: Cardiovascular Research - March 23, 2017 Category: Cardiology Source Type: research

ELABELA-APJ axis protects from pressure overload heart failure and angiotensin II-induced cardiac damage
ConclusionThe ELA-APJ axis protects from pressure overload-induced heart failure possibly via suppression of ACE expression and pathogenic angiotensin II signalling. The different effects of ELA and Apelin on the expression of ACE and ACE2 implicate fine-tuned mechanisms for a ligand-induced APJ activation and downstream signalling. (Source: Cardiovascular Research)
Source: Cardiovascular Research - March 23, 2017 Category: Cardiology Source Type: research

Novel targets and future strategies for acute cardioprotection: Position Paper of the European Society of Cardiology Working Group on Cellular Biology of the Heart
Ischaemic heart disease and the heart failure that often results, remain the leading causes of death and disability in Europe and worldwide. As such, in order to prevent heart failure and improve clinical outcomes in patients presenting with an acute ST-segment elevation myocardial infarction and patients undergoing coronary artery bypass graft surgery, novel therapies are required to protect the heart against the detrimental effects of acute ischaemia/reperfusion injury (IRI). During the last three decades, a wide variety of ischaemic conditioning strategies and pharmacological treatments have been tested in the clinic &m...
Source: Cardiovascular Research - March 17, 2017 Category: Cardiology Source Type: research

Corrigendum to: A landscape of circular RNA expression in the human heart
[Cardiovasc Res 2016; DOI:10.1093/cvr/cvw250] (Source: Cardiovascular Research)
Source: Cardiovascular Research - March 10, 2017 Category: Cardiology Source Type: research

Corrigendum to: Multilevel analyses of SCN5A mutations in arrhythmogenic right ventricular dysplasia/cardiomyopathy suggest non-canonical mechanisms for disease pathogenesis
[Cardiovasc Res 2016; 113 (1):102-111] (Source: Cardiovascular Research)
Source: Cardiovascular Research - March 10, 2017 Category: Cardiology Source Type: research

An overview of the inflammatory signalling mechanisms in the myocardium underlying the development of diabetic cardiomyopathy
AbstractHeart failure is a highly morbid and mortal clinical condition that represents the last stage of most cardiovascular disorders. Diabetes is strongly associated with an increased incidence of heart failure and directly promotes cardiac hypertrophy, fibrosis, and apoptosis. These changes, in turn, contribute to the development of ventricular dysfunction. The clinical condition associated with the spectrum of cardiac abnormalities induced by diabetes is termed diabetic cardiomyopathy. Myocardial inflammation has recently emerged as a pathophysiological process contributing to cardiac hypertrophy, fibrosis, and dysfunc...
Source: Cardiovascular Research - March 3, 2017 Category: Cardiology Source Type: research

Metabolism in cardiomyopathy: every substrate matters
AbstractCardiac metabolism is highly adaptive to changes in fuel availability and the energy demand of the heart. This metabolic flexibility is key for the heart to maintain its output during the development and in response to stress. Alterations in substrate preference have been observed in multiple disease states; a clear understanding of their impact on cardiac function in the long term is critical for the development of metabolic therapies. In addition, the contribution of cellular metabolism to growth, survival, and other signalling pathways through the generation of metabolic intermediates has been increasingly noted...
Source: Cardiovascular Research - March 3, 2017 Category: Cardiology Source Type: research

Inflammation and metabolic cardiomyopathy
AbstractExcessive feeding is associated with an increase in the incidence of chronic metabolic diseases, such as obesity, insulin resistance, and type 2 diabetes. Metabolic disturbance induces chronic low-grade inflammation in metabolically-important organs, such as the liver and adipose tissue. Many of the inflammatory signalling pathways are directly triggered by nutrients. The pro-inflammatory mediators in adipocytes and macrophages infiltrating adipose tissue promote both local and systemic pro-inflammatory status. Metabolic cardiomyopathy is a chronic metabolic disease characterized by structural and functional altera...
Source: Cardiovascular Research - March 3, 2017 Category: Cardiology Source Type: research

Periostin paves the way for neonatal heart regeneration
This editorial refers to ‘Ablation of periostin inhibits post-infarction myocardial regeneration in neonatal mice mediated by the phosphatidylinositol 3 kinase/glycogen synthase kinase 3β/cyclin D1 signalling pathway’, by Z. Chenet al., pp.620 –632. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 28, 2017 Category: Cardiology Source Type: research

MiR-142-3p is a paracrine mediator between T cells and endothelium during allograft rejection
This editorial refers to ‘Exosomal miR-142-3p is increased during cardiac allograft rejection and augments vascular permeability through down-regulation of endothelial RAB11FIP2 expression’ by I.S. Dewi et al., pp. 440–452. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 28, 2017 Category: Cardiology Source Type: research

Farnesylation of RhoB: the cancer hypothesis of pulmonary hypertension revisited
This editorial refers to ‘Tipifarnib prevents development of hypoxia-induced pulmonary hypertension’ by L. Duluc et al., pp. 276–287. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 28, 2017 Category: Cardiology Source Type: research

Mechanisms regulating Ca 2+ release in cardiomyocytes
This editorial refers to ‘Sensitized signalling between L-type Ca2+ channels and ryanodine receptors in the absence or inhibition of FKBP12.6 in cardiomyocytes’ by Y.-T. Zhao et al., pp. 332–342. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 28, 2017 Category: Cardiology Source Type: research

Cardiac mGluR1 metabotropic receptors in cardioprotection
ConclusionThis study provides the first demonstration that mGluR1 activation at the onset of reperfusion induces cardioprotection and might represent a putative strategy to prevent ischaemia-reperfusion injury. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 27, 2017 Category: Cardiology Source Type: research

Macrophage migration inhibitory factor triggers vascular smooth muscle cell dedifferentiation by a p68-serum response factor axis
ConclusionsOur results demonstrate a novel mechanism for the regulation of VSMC differentiation by MIF involving p68 and SRF. Strategy for targeting of MIF could inhibit aberrant transition of VSMC in cardiovascular pathogenesis, and may be of therapeutic benefit in phenotype-related arterial remodelling. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 27, 2017 Category: Cardiology Source Type: research

New insights into shear stress-induced endothelial signalling and barrier function: cell-free fluid versus blood flow
ConclusionsSS-induced EC NO production occurs in both cell free fluid and blood perfused vessels, whereas SS-induced increases in EC [Ca2+]i and EC gap formation require the presence of RBCs, attributing to SS-induced pannexin-1 channel dependent release of ATP from RBCs. Thus, changes in blood flow alter vascular EC function through both wall SS and SS exerted on RBCs, and RBC released ATP contributes to SS-induced changes in EC barrier function. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 27, 2017 Category: Cardiology Source Type: research

Functional local crosstalk of inositol 1,4,5-trisphosphate receptor- and ryanodine receptor-dependent Ca 2+ release in atrial cardiomyocytes
ConclusionsOur results support the concept of bidirectional interaction between RyRs and InsP3Rs (i.e. Ca2+ sparks and Ca2+ puffs) in atrial myocytes. We conclude that highly efficient InsP3 dependent SR-Ca2+ flux constitute the main mechanism of functional crosstalk between InsP3Rs and RyRs resulting in more Ca2+ sensitized RyRs to trigger subsequent Ca2+-induced Ca2+ release activation. In this way, bidirectional local interaction of both SR-Ca2+ release channels may contribute to the shaping of global Ca2+ transients and thereby to contractility in cardiac myocytes. (Sour...
Source: Cardiovascular Research - February 24, 2017 Category: Cardiology Source Type: research

Shear stress-regulated miR-27b controls pericyte recruitment by repressing SEMA6A and SEMA6D
ConclusionThe present study demonstrates for the first time that shear stress-regulated miR-27b promotes the interaction of endothelial cells with pericytes, partly by repressing SEMA6A and SEMA6D. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2017 Category: Cardiology Source Type: research

Increased BACE1-AS long noncoding RNA and β-amyloid levels in heart failure
ConclusionGiven the neurotoxic role of β-amyloid in AD, dysregulation of the BACE1/BACE1-AS/β-amyloid axis might be relevant in HF pathogenesis, further implicating ncRNAs in the complex scenario of proteotoxicity in cardiac dysfunction. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 23, 2017 Category: Cardiology Source Type: research

Regional acidosis locally inhibits but remotely stimulates Ca 2+ waves in ventricular myocytes
ConclusionAcidosis influences Ca2+ waves via inhibitory Hi+ and stimulatory Nai+ signals (the latter facilitating intracellular Ca2+-loading through modulation of sarcolemmal Na+/Ca2+ exchange activity). During spatial [H+]i-heterogeneity, Hi+-inhibition dominates in acidic regions, while rapid Nai+ diffusion stimulates waves in downstream, non-acidic regions. Local acidosis thus simultaneously inhibits and stimulates arrhythmogenic Ca2+-signalling in the same myocyte. If the principle of remote H+-stimulation of Ca2+ waves also applies in multicellular myocardium, it raises the possibility of electrical disturbances being...
Source: Cardiovascular Research - February 21, 2017 Category: Cardiology Source Type: research

Heterologous desensitization of cardiac β-adrenergic signal via hormone-induced βAR/arrestin/PDE4 complexes
ConclusionsThese data reveal essential roles of β-arrestin 2 and PDE4D in a common mechanism for heterologous desensitization of cardiac βARs under hormonal stimulation, which is associated with impaired cardiac function during the development of pathophysiological conditions. (Source: Cardiovascular Research)
Source: Cardiovascular Research - February 21, 2017 Category: Cardiology Source Type: research

Reply: Glycine as a key element of remote ischaemic conditioning cardioprotective signalling
We appreciate the interest of Prunieret al. in our article on the role of glycine in the humoral-mediated signalling of remote ischaemic conditioning, recently published inCardiovascular Research.1 We agree with these authors on the importance of metabolomic approaches in the study of remote ischaemic conditioning (RIC) mechanisms. The fact that Prunieret al. also found a metabolic fingerprint of RIC by using liquid chromatography coupled to tandem mass spectroscopy2 or their ultra-high-performance liquid chromatography coupled to high-resolution mass spectrometry, and reverse phase and hydrophilic interaction chromatograp...
Source: Cardiovascular Research - February 21, 2017 Category: Cardiology Source Type: research