Prevalence of abnormal glucose metabolism in atrial fibrillation: A case control study in 75-year old subjects

<p>Abstract</p> <p>Background</p> <p>The prevalence of atrial fibrillation (AF) is increasing world wide and amongst factors that aggravate the risk is diabetes mellitus (DM), also in epidemic development.</p> <p>However, although DM is a potentially modifiable risk factor for AF, few, if any, studies have explored the prevalence of undiagnosed dysglycaemia among subjects with AF or if duration of AF are related to parameters of glycaemia or dysglycaemia prevalence.</p> <p>Methods</p> <p>In this case control study, amongst 75-year old subjects with and without AF, the prevalence of dysglycaemia, i.e., impaired fasting glycaemia, impaired glucose tolerance or DM, according to World Health Organisation criteria was assessed by a 75-g oral glucose tolerance test (OGTT).</p> <p>Results</p> <p>Prevalence of undiagnosed DM among the 108 subjects (male/female 73/35, BMI 25.4 ± 3.2) without and the 46 (male/female 34/12, BMI 25.3 ± 3.7) with AF (median AF duration five years) where 3.7% and 13.0%, respectively (p = 0.031, Odds ratio (OR) 3.86 (95% Confidence interval [CI]: 1.01, 16.25)) whereas the overall prevalence of dysglycaemia (prediabetes and DM) where similar (respectively 43.5% and 39.1%, p = 0.46, OR 0.83 [95% CI: 0.41, 1.69]). Patients with AF duration ≥ 5 years had however a higher dysglycaemia prevalence (61.1% [DM 22.2%, prediabetes 38.9%]) as compared to AF duration < 5 years (25% [DM 7.1%, prediabetes 17.9%], p = 0.0014, OR 4.7 [95% CI: 1.30, 16.90]) or no AF (p = 0.17, OR 2.04 [95% CI: 0.73, 5.66]). There was also a significant correlation between the duration of AF and HbA1c (r = 0.408, p = 0.005) and fasting glucose levels (r = 0.353, p = 0.016).</p> <p>Conclusion</p> <p>AF is associated with chronic hyperglycaemia amongst 75-year old subjects. Prediabetes and DM should be pro-actively assessed if AF duration ≥ 5 years.</p

Climate change and new potential spawning sites for Northeast Arctic cod

In this study we investigate both historical and potential future changes in the spatial distribution of spawning habitats for Northeast Arctic cod (NEA cod) based on a literature study on spawning habitats and different physical factors from a downscaled climate model. The approach to use a high resolution regional ocean model to analyze spawning sites is new and provides more details about crucial physical factors than a global low resolution model can. The model is evaluated with respect to temperature and salinity along the Norwegian coast during the last decades and shows acceptable agreement with observations. However, the model does not take into consideration biological or evolutionary factors which also have impact on choice of spawning sites. Our results from the downscaled RCP4.5 scenario suggest that the spawning sites will be shifted further northeastwards, with new locations at the Russian coast close to Murmansk over the next 50 years, where low temperatures for many decades in the last century were a limiting factor on spawning during spring. The regional model gives future temperatures above the chosen lower critical minimum value in larger areas than today and indicates that spawning will be more extensive there. Dependent on the chosen upper temperature boundary, future temperatures may become a limiting factor for spawning habitats at traditional spawning sites south of Lofoten. Finally, the observed long-term latitudinal shifts in spawning habitats along the Norwegian coast the recent decades may be indirectly linked to temperature through the latitudinal shift of the sea ice edge and the corresponding shift in available ice-free predation habitats, which control the average migration distance to the spawning sites. We therefore acknowledge that physical limitations for defining the spawning sites might be proxies for other biophysically related factors.publishedVersio

A gap analysis for automated cargo handling operations with geared vessels frequenting small sized ports

With the Yara Birkeland, the world’s first autonomous cargo ship developed for commercial use, nearing regular unmanned operation, it is crucial to assess the availability and readiness of unmanned cargo handling solutions. While there are already fully automated container terminals at large international ports, the purpose of this study is to consider solutions to support autonomous ships for small sized ports with little infrastructure, typical of coastal harbors in Norway. The analysis centers on geared cargo vessels that can navigate such ports with minimal or no crew onboard, and the primary method used involved workshops and interviews with personnel from relevant industries. An important finding is the lack of skilled crane operators that are willing to follow the ship. The study concludes that it is important to address the following 3 key technological gaps: (1) the autonomous connection and release of break-bulk, (2) automatic securing and lashing of onboard cargo, and (3) shipboard cranes that can operate without an onsite crane operator.publishedVersio

Dipeptidyl Peptidase-4 Inhibitors for the Potential Treatment of Brain Disorders; A Mini-Review With Special Focus on Linagliptin and Stroke

Cerebral stroke is a leading cause of death and persistent disability of elderly in the world. Although stroke prevention by targeting several risk factors such as diabetes and hypertension has decreased the stroke incidence, the total number of strokes is increasing due to the population aging and new preventive therapies are needed. Moreover, post-stroke acute pharmacological strategies aimed to reduce stroke-induced brain injury have failed in clinical trials despite being effective in animal models. Finally, approximately 30% of surviving stroke patients do not recover from stroke and remain permanently dependent on supportive care in activities of daily living. Therefore, strategies to improve stroke recovery in the post-acute phase are highly needed. Linagliptin is a dipeptidyl peptidase-4 inhibitor which is clinically approved to reduce hyperglycemia in type 2 diabetes. The regulation of glycemia by dipeptidyl peptidase-4 inhibition is mainly achieved by preventing endogenous glucagon-like peptide-1 (GLP-1) degradation. Interestingly, linagliptin has also shown glycaemia-independent beneficial effects in animal models of stroke, Parkinson's disease and Alzheimer's disease. In some case the preclinical data have been supported with some clinical data. Although potentially very interesting for the development of new strategies against stroke and neurodegenerative disorders, the mode of action of linagliptin in the brain is still largely unknown and seems to occur in a GLP-1R-independent manner. The purpose of this mini-review is to summarize and discuss the recent experimental and clinical work regarding the effects of linagliptin in the central nervous system, with special emphasis on acute neuroprotection, stroke prevention and post-stroke recovery. We also highlight the main questions in this research field that need to be addressed in clinical perspective

Determinants and prognostic implications of Cardiac Troponin T measured by a sensitive assay in Type 2 Diabetes Mellitus

<p>Abstract</p> <p>Background</p> <p>The cardiac troponins are biomarkers used for diagnosis of myocardial injury. They are also powerful prognostic markers in many diseases and settings. Recently introduced high-sensitivity assays indicate that chronic cardiac troponin elevations are common in response to cardiovascular (CV) morbidity. Type 2 diabetes mellitus (T2DM) confers a high risk of CV disease, but little is known about chronic cardiac troponin elevations in diabetic subjects. Accordingly, we aimed to understand the prevalence, determinants, and prognostic implications of cardiac troponin T (cTnT) elevations measured with a high-sensitivity assay in patients with T2DM.</p> <p>Methods</p> <p>cTnT was measured in stored, frozen serum samples from 124 subjects enrolled in the Asker and Bærum Cardiovascular Diabetes trial at baseline and at 2-year follow-up, if availabe (96 samples available). Results were analyzed in relation to baseline variables, hospitalizations, and group assignment (multifactorial intensive versus conventional diabetes care for lowering CV risk).</p> <p>Results</p> <p>One-hundred thirteen (90 %) had detectable cTnT at baseline and of those, 22 (18 % of the total population) subjects had values above the 99th percentile for healthy controls (13.5 ng/L). Levels at baseline were associated with conventional CV risk factors (age, renal function, gender). There was a strong correlation between cTnT levels at the two time-points (r = 0.92, p > 0.001). Risk for hospitalizations during follow-up increased step-wise by quartiles of hscTnT measured at baseline (p = 0.058).</p> <p>Conclusions</p> <p>Elevations of cTnT above the 99th percentile measured by a highly sensitive assay were encountered frequently in a population of T2DM patients. cTnT levels appeared to be stable over time and associated with conventional CV risk factors. Although a clear trend was present, no statistically robust associations with adverse outcomes could be found.</p

Pooled analysis of Phase III trials indicate contrasting influences of renal function on blood pressure, body weight, and HbA1c reductions with empagliflozin

Sodium glucose cotransporter 2 (SGLT2) inhibitors reduce HbA1c, blood pressure, and weight in patients with type 2 diabetes. To investigate the effect of renal function on reductions in these parameters with the SGLT2 inhibitor empagliflozin, we assessed subgroups by baseline estimated glomerular filtration rate (eGFR; Modification of Diet in Renal Disease) in pooled data from five 24-week trials of 2286 patients with type 2 diabetes randomized to empagliflozin or placebo. Reductions in HbA1c with empagliflozin versus placebo significantly diminished with decreasing baseline eGFR. Reductions in systolic blood pressure (SBP) with empagliflozin were maintained in patients with lower eGFR. The mean placebo-corrected changes from baseline in systolic blood pressure at week 24 with empagliflozin were -3.2 (95% confidence interval -4.9,-1.5) mmHg, -4.0 (-5.4, -2.6) mmHg, -5.5 (-7.6, -3.4) mmHg, and -6.6 (-11.4, -1.8) mmHg in patients with an eGFR of 90 or more, 60 to 89, 30 to 59, and under 30 ml/min/1.73m(2), respectively. Similar trends were observed for diastolic blood pressure. Weight loss with empagliflozin versus placebo tended to be attenuated in patients with a lower eGFR. Results were consistent in a 12-week ambulatory blood pressure monitoring trial in 823 patients with type 2 diabetes and hypertension. Thus, unlike HbA1c reductions, systolic blood pressure and weight reductions with empagliflozin are generally preserved in patients with chronic kidney disease.Peer reviewe