Intercomparison of Antarctic ice-shelf, ocean, and sea-ice interactions simulated by MetROMS-iceshelf and FESOM 1.4

An increasing number of Southern Ocean models now include Antarctic ice-shelf cavities, and simulate thermodynamics at the ice-shelf/ocean interface. This adds another level of complexity to Southern Ocean simulations, as ice shelves interact directly with the ocean and indirectly with sea ice. Here, we present the first model intercomparison and evaluation of present-day ocean/sea-ice/ice-shelf interactions, as simulated by two models: a circumpolar Antarctic configuration of MetROMS (ROMS: Regional Ocean Modelling System coupled to CICE: Community Ice CodE) and the global model FESOM (Finite Element Sea-ice Ocean Model), where the latter is run at two different levels of horizontal resolution. From a circumpolar Antarctic perspective, we compare and evaluate simulated ice-shelf basal melting and sub-ice-shelf circulation, as well as sea-ice properties and Southern Ocean water mass characteristics as they influence the sub-ice-shelf processes. Despite their differing numerical methods, the two models produce broadly similar results and share similar biases in many cases. Both models reproduce many key features of observations but struggle to reproduce others, such as the high melt rates observed in the small warm-cavity ice shelves of the Amundsen and Bellingshausen seas. Several differences in model design show a particular influence on the simulations. For example, FESOM's greater topographic smoothing can alter the geometry of some ice-shelf cavities enough to affect their melt rates; this improves at higher resolution, since less smoothing is required. In the interior Southern Ocean, the vertical coordinate system affects the degree of water mass erosion due to spurious diapycnal mixing, with MetROMS' terrain-following coordinate leading to more erosion than FESOM's z coordinate. Finally, increased horizontal resolution in FESOM leads to higher basal melt rates for small ice shelves, through a combination of stronger circulation and small-scale intrusions of warm water from offshore

Length of carotid stenosis predicts peri-procedural stroke or death and restenosis in patients randomized to endovascular treatment or endarterectomy.

BACKGROUND: The anatomy of carotid stenosis may influence the outcome of endovascular treatment or carotid endarterectomy. Whether anatomy favors one treatment over the other in terms of safety or efficacy has not been investigated in randomized trials. METHODS: In 414 patients with mostly symptomatic carotid stenosis randomized to endovascular treatment (angioplasty or stenting; n = 213) or carotid endarterectomy (n = 211) in the Carotid and Vertebral Artery Transluminal Angioplasty Study (CAVATAS), the degree and length of stenosis and plaque surface irregularity were assessed on baseline intraarterial angiography. Outcome measures were stroke or death occurring between randomization and 30 days after treatment, and ipsilateral stroke and restenosis ≥50% during follow-up. RESULTS: Carotid stenosis longer than 0.65 times the common carotid artery diameter was associated with increased risk of peri-procedural stroke or death after both endovascular treatment [odds ratio 2.79 (1.17-6.65), P = 0.02] and carotid endarterectomy [2.43 (1.03-5.73), P = 0.04], and with increased long-term risk of restenosis in endovascular treatment [hazard ratio 1.68 (1.12-2.53), P = 0.01]. The excess in restenosis after endovascular treatment compared with carotid endarterectomy was significantly greater in patients with long stenosis than with short stenosis at baseline (interaction P = 0.003). Results remained significant after multivariate adjustment. No associations were found for degree of stenosis and plaque surface. CONCLUSIONS: Increasing stenosis length is an independent risk factor for peri-procedural stroke or death in endovascular treatment and carotid endarterectomy, without favoring one treatment over the other. However, the excess restenosis rate after endovascular treatment compared with carotid endarterectomy increases with longer stenosis at baseline. Stenosis length merits further investigation in carotid revascularisation trials

Status Update and Interim Results from the Asymptomatic Carotid Surgery Trial-2 (ACST-2)

Objectives: ACST-2 is currently the largest trial ever conducted to compare carotid artery stenting (CAS) with carotid endarterectomy (CEA) in patients with severe asymptomatic carotid stenosis requiring revascularization. Methods: Patients are entered into ACST-2 when revascularization is felt to be clearly indicated, when CEA and CAS are both possible, but where there is substantial uncertainty as to which is most appropriate. Trial surgeons and interventionalists are expected to use their usual techniques and CE-approved devices. We report baseline characteristics and blinded combined interim results for 30-day mortality and major morbidity for 986 patients in the ongoing trial up to September 2012. Results: A total of 986 patients (687 men, 299 women), mean age 68.7 years (SD ± 8.1) were randomized equally to CEA or CAS. Most (96%) had ipsilateral stenosis of 70-99% (median 80%) with contralateral stenoses of 50-99% in 30% and contralateral occlusion in 8%. Patients were on appropriate medical treatment. For 691 patients undergoing intervention with at least 1-month follow-up and Rankin scoring at 6 months for any stroke, the overall serious cardiovascular event rate of periprocedural (within 30 days) disabling stroke, fatal myocardial infarction, and death at 30 days was 1.0%. Conclusions: Early ACST-2 results suggest contemporary carotid intervention for asymptomatic stenosis has a low risk of serious morbidity and mortality, on par with other recent trials. The trial continues to recruit, to monitor periprocedural events and all types of stroke, aiming to randomize up to 5,000 patients to determine any differential outcomes between interventions. Clinical trial: ISRCTN21144362. © 2013 European Society for Vascular Surgery. Published by Elsevier Ltd. All rights reserved

Diagnosis and management of glutaric aciduria type I – revised recommendations

Glutaric aciduria type I (synonym, glutaric acidemia type I) is a rare organic aciduria. Untreated patients characteristically develop dystonia during infancy resulting in a high morbidity and mortality. The neuropathological correlate is striatal injury which results from encephalopathic crises precipitated by infectious diseases, immunizations and surgery during a finite period of brain development, or develops insidiously without clinically apparent crises. Glutaric aciduria type I is caused by inherited deficiency of glutaryl-CoA dehydrogenase which is involved in the catabolic pathways of L-lysine, L-hydroxylysine and L-tryptophan. This defect gives rise to elevated glutaric acid, 3-hydroxyglutaric acid, glutaconic acid, and glutarylcarnitine which can be detected by gas chromatography/mass spectrometry (organic acids) or tandem mass spectrometry (acylcarnitines). Glutaric aciduria type I is included in the panel of diseases that are identified by expanded newborn screening in some countries. It has been shown that in the majority of neonatally diagnosed patients striatal injury can be prevented by combined metabolic treatment. Metabolic treatment that includes a low lysine diet, carnitine supplementation and intensified emergency treatment during acute episodes of intercurrent illness should be introduced and monitored by an experienced interdisciplinary team. However, initiation of treatment after the onset of symptoms is generally not effective in preventing permanent damage. Secondary dystonia is often difficult to treat, and the efficacy of available drugs cannot be predicted precisely in individual patients. The major aim of this revision is to re-evaluate the previous diagnostic and therapeutic recommendations for patients with this disease and incorporate new research findings into the guideline

Vascular complications of severe hyperhomocysteinemia in patients with homocysteinuria due to cystathionine beta-synthase deficiency: effects of homocysteine-lowering therapy

Item does not contain fulltex

Intercomparison of Antarctic ice-shelf, ocean, and sea-ice interactions simulated by MetROMS-iceshelf and FESOM 1.4

An increasing number of Southern Ocean models now include Antarctic ice-shelf cavities, and simulate thermodynamics at the ice-shelf/ocean interface. This adds another level of complexity to Southern Ocean simulations, as ice shelves interact directly with the ocean and indirectly with sea ice. Here, we present the first model intercomparison and evaluation of present-day ocean/sea-ice/ice-shelf interactions, as simulated by two models: a circumpolar Antarctic configuration of MetROMS (ROMS: Regional Ocean Modelling System coupled to CICE: Community Ice CodE) and the global model FESOM (Finite Element Sea-ice Ocean Model), where the latter is run at two different levels of horizontal resolution. From a circumpolar Antarctic perspective, we compare and evaluate simulated ice-shelf basal melting and sub-ice-shelf circulation, as well as sea-ice properties and Southern Ocean water mass characteristics as they influence the sub-ice-shelf processes. Despite their differing numerical methods, the two models produce broadly similar results and share similar biases in many cases. Both models reproduce many key features of observations but struggle to reproduce others, such as the high melt rates observed in the small warm-cavity ice shelves of the Amundsen and Bellingshausen seas. Several differences in model design show a particular influence on the simulations. For example, FESOM's greater topographic smoothing can alter the geometry of some ice-shelf cavities enough to affect their melt rates; this improves at higher resolution, since less smoothing is required. In the interior Southern Ocean, the vertical coordinate system affects the degree of water mass erosion due to spurious diapycnal mixing, with MetROMS' terrain-following coordinate leading to more erosion than FESOM's z coordinate. Finally, increased horizontal resolution in FESOM leads to higher basal melt rates for small ice shelves, through a combination of stronger circulation and small-scale intrusions of warm water from offshore

Hyperhomocysteinemia: an independent risk factor for vascular disease.

BACKGROUND: Hyperhomocysteinemia arising from impaired methionine metabolism, probably usually due to a deficiency of cystathionine beta-synthase, is associated with premature cerebral, peripheral, and possibly coronary vascular disease. Both the strength of this association and its independence of other risk factors for cardiovascular disease are uncertain. We studied the extent to which the association could be explained by heterozygous cystathionine beta-synthase deficiency. METHODS: We first established a diagnostic criterion for hyperhomocysteinemia by comparing peak serum levels of homocysteine after a standard methionine-loading test in 25 obligate heterozygotes with respect to cystathionine beta-synthase deficiency (whose children were known to be homozygous for homocystinuria due to this enzyme defect) with the levels in 27 unrelated age- and sex-matched normal subjects. A level of 24.0 mumol per liter or more was 92 percent sensitive and 100 percent specific in distinguishing the two groups. The peak serum homocysteine levels in these normal subjects were then compared with those in 123 patients whose vascular disease had been diagnosed before they were 55 years of age. RESULTS: Hyperhomocysteinemia was detected in 16 of 38 patients with cerebrovascular disease (42 percent), 7 of 25 with peripheral vascular disease (28 percent), and 18 of 60 with coronary vascular disease (30 percent), but in none of the 27 normal subjects. After adjustment for the effects of conventional risk factors, the lower 95 percent confidence limit for the odds ratio for vascular disease among the patients with hyperhomocysteinemia, as compared with the normal subjects, was 3.2. The geometric-mean peak serum homocysteine level was 1.33 times higher in the patients with vascular disease than in the normal subjects (P = 0.002). The presence of cystathionine beta-synthase deficiency was confirmed in 18 of 23 patients with vascular disease who had hyperhomocysteinemia. CONCLUSIONS: Hyperhomocysteinemia is an independent risk factor for vascular disease, including coronary disease, and in most instances is probably due to cystathionine beta-synthase deficiency

Vascular outcome in patients homocystinuria due to cystathionine beta-synthase deficiency treated chronically

Item does not contain fulltex