Abstract. Observations and models agree that the Greenland Ice Sheet (GrIS) surface mass balance (SMB) has decreased since the end of the 1990s due to an increase in meltwater runoff and that this trend will accelerate in the future. However, large uncertainties remain, partly due to different approaches for modelling the GrIS SMB, which have to weigh physical complexity or low computing time, different spatial and temporal resolutions, different forcing fields, and different ice sheet topographies and extents, which collectively make an inter-comparison difficult. Our GrIS SMB model intercomparison project (GrSMBMIP) aims to refine these uncertainties by intercomparing 13 models of four types which were forced with the same ERA-Interim reanalysis forcing fields, except for two global models. We interpolate all modelled SMB fields onto a common ice sheet mask at 1 km horizontal resolution for the period 1980–2012 and score the outputs against (1) SMB estimates from a combination of gravimetric remote sensing data from GRACE and measured ice discharge; (2) ice cores, snow pits and in situ SMB observations; and (3) remotely sensed bare ice extent from MODerate-resolution Imaging Spectroradiometer (MODIS). Spatially, the largest spread among models can be found around the margins of the ice sheet, highlighting model deficiencies in an accurate representation of the GrIS ablation zone extent and processes related to surface melt and runoff. Overall, polar regional climate models (RCMs) perform the best compared to observations, in particular for simulating precipitation patterns. However, other simpler and faster models have biases of the same order as RCMs compared with observations and therefore remain useful tools for long-term simulations or coupling with ice sheet models. Finally, it is interesting to note that the ensemble mean of the 13 models produces the best estimate of the present-day SMB relative to observations, suggesting that biases are not systematic among models and that this ensemble estimate can be used as a reference for current climate when carrying out future model developments. However, a higher density of in situ SMB observations is required, especially in the south-east accumulation zone, where the model spread can reach 2 m w.e. yr−1 due to large discrepancies in modelled snowfall accumulation.

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Objective: In women, sex hormones cause increased morbidity and mortality in patients with coronary heart disease (CHD) and adversely affect the coagulation profile. We have studied the effect of physiological testosterone replacement therapy in men on coagulation factor expression, to determine if there is an increased risk of thrombosis. Methods: Double-blind, randomized, placebo-controlled trial of testosterone in 46 men with chronic stable angina. Measurements of free, total and bioavailable testosterone, luteinising hormone (LH) and follicle-stimulating hormone (FSH), estradiol, plasminogen activator inhibitor-1 (PAI-1), fibrinogen, tissue plasminogen activator (tPA) and full blood count were made at 0, 6 and 14 weeks.

Aim:To assess for the first time the vasodilatory effect of testosterone in the human pulmonary circulation utilizing both isolated human pulmonary arteries and isolated perfused human lungs. In addition, a secondary aim was to determine whether there was any difference in the response to testosterone dependant upon gender.Methods:Isolated human pulmonary arteries were studied by wire myography. Vessels were preconstricted with U46619 (1 nM–1 μM) prior to exposing them to either testosterone (1 nM–100 μM) or ethanol vehicle (<0.1%). Isolated lungs were studied in a ventilated and perfused model. They were exposed to KCl (100 mM), prior to the addition of either testosterone (1 nM–100 μM) or ethanol vehicle (<0.1%).Results:Testosterone caused significant vasodilatation in all preparations, but a greater response to testosterone was observed in the isolated perfused lungs, 24.9 ± 2.2% at the 100 μM dose of testosterone in the isolated pulmonary arteries compared to 100 ± 13.6% at the 100 μM dose in the isolated perfused lungs. No significant differences in the response to testosterone were observed between sexes.Conclusion:Testosterone is an efficacious vasodilator in the human pulmonary vasculature and this is not modulated by patient sex. This vasodilator action suggests that testosterone therapy may be beneficial to male patients with pulmonary arterial hypertension.

Vasopressin is a peptide synthesized in the hypothalamus whose primary role is in fluid homeostasis. It has recently gained interest as a potential agent in the treatment of cardiorespiratory arrest. Initial human studies have shown benefits with vasopressin in patients with out of hospital ventricular fibrillation and asystolic cardiac arrest. One subgroup of patients not included in these trials is patients with pulmonary hypertension, who have a five-year mortality rate of 50%. Animal studies have shown vasopressin to be a vasodilator in the pulmonary vascular system of rats, under normoxic and hypoxic conditions, with conflicting results in canines. Human studies have shown conflicting results with increases, decreases and no changes seen in pulmonary artery pressures of patients with a variety of clinical conditions. Research needs to be done in patients with pulmonary hypertension regarding the potential role of vasopressin during cardiac arrest in this subgroup.

AIM:To evaluate the referrals with suspected arrhythmogenic right ventricular cardiomyopathy (ARVC) and compare cardiac MR (cMR) findings against clinical diagnosis. METHODS:A retrospective analysis of 114 (age range 16 to 83, males 55% and females 45%) patients referred for cMR with a suspected diagnosis of ARVC between May 2006 and February 2010 was performed after obtaining institutional approval for service evaluation. Reasons for referral including clinical symptoms and family history of sudden death, electrocardiogram and echo abnormalities, cMR findings, final clinical diagnosis and information about clinical management were obtained. The results of cMR were classified as major, minor, non-specific or negative depending on both functional and tissue characterisation and the cMR results were compared against the final clinical diagnosis. RESULTS:The most common reasons for referral included arrhythmias (30%) and a family history of sudden death (20%). Of the total cohort of 114 patients: 4 patients (4%) had major cMR findings for ARVC, 13 patients (11%) had minor cMR findings, 2 patients had non-specific cMR findings relating to the right ventricle and 95 patients had a negative cMR. Of the 4 patients who had major cMR findings, 3 (75%) had a positive clinical diagnosis. In contrast, of the 13 patients who had minor cMR findings, only 2 (15%) had a positive clinical diagnosis. Out of the 95 negative patients, clinical details were available for 81 patients and none of them had ARVC. Excluding the 14 patients with no clinical data and final diagnosis, the sensitivity of the test was 100%, specificity 87%, positive predictive value 29% and the negative predictive value 100%.CONCLUSION: CMR is a useful tool for ARVC evaluation because of the high negative predictive value as the outcome has a significant impact on the clinical decision-making. Key words: Arrhythmogenic right ventricular cardiomyopathy; Cardiomyopathy; Right ventricular; Arrhythmias; Magnetic resonance imaging; Diagnosis; Implantable cardiac defibrillator Core tip: This study was designed to evaluate the referrals with suspected Arrhythmogenic right ventricular cardiomyopathy (ARVC) and compare the findings of cardiac magnetic resonance imaging (cMR) against clinical diagnosis. Currently the diagnosis depends upon a combination of variety of factors including imaging findings. We evaluated all the referrals in our institution over a 4-year period and found a high sensitivity and specificity of cMR for ARVC diagnosis. We have concluded that cMR is a very useful tool for ARVC evalua- RETROSPECTIVE STUDYSubmit a

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