Smoothed particle hydrodynamics for modelling cold-water coral habitats in changing oceans

The importance of the growth, proliferation and longevity of reef-forming cold-water corals is paramount as they support various complex bio-diverse habitats and provide many essential ecosystem services. These cold-water coral reefs consist of layers of living coral tissue that grow on top of large masses of coral skeleton. Here, the Goldilocks Principle is used to simulate growth in optimal conditions and model how cold-water corals engineer their habitat to survive and prosper. A computational fluid dynamics model is created based on the Smoothed Particle Hydrodynamics method, a mesh-free Lagrangian numerical method. The SPH solver is written in the C++ programming language and parallelised with OpenMP to improve its efficiency and reduce the execution times. The solver is validated against analytical and numerical solutions and the growth model is then validated against in situ data of real cold-water coral colonies. The numerical results suggest that the longevity of cold-water corals depends on how well they can manage their energetic reserves when exposed to sub-optimal prey-catching conditions

Smoothed particle hydrodynamics for modelling cold-water coral habitats in changing oceans

The importance of the growth, proliferation and longevity of reef-forming cold-water corals is paramount as they support various complex bio-diverse habitats and provide many essential ecosystem services. These cold-water coral reefs consist of layers of living coral tissue that grow on top of large masses of coral skeleton. Here, the Goldilocks Principle is used to simulate growth in optimal conditions and model how cold-water corals engineer their habitat to survive and prosper. A computational fluid dynamics model is created based on the Smoothed Particle Hydrodynamics method, a mesh-free Lagrangian numerical method. The SPH solver is written in the C++ programming language and parallelised with OpenMP to improve its efficiency and reduce the execution times. The solver is validated against analytical and numerical solutions and the growth model is then validated against in situ data of real cold-water coral colonies. The numerical results suggest that the longevity of cold-water corals depends on how well they can manage their energetic reserves when exposed to sub-optimal prey-catching conditions

A comparative investigation of the efficacy of CO2 and high power diode lasers for the forming of EN3 mild steel sheets

A comparative investigation of the effectiveness of a high power diode laser (HPDL) and a CO2 laser for the forming of thin section EN3 mild steel sheet has been conducted. The buckling mechanism was identified as the laser forming mechanism responsible for the induced bending. For both lasers it was found that the induced bending angles increased with an increasing number of irradiations and high laser powers, whilst decreasing as the traverse speed was increased. Also, it was apparent from the experimental results that the laser bending angle was only linearly proportional to the number of irradiations when the latter was small due to local material thickening along the bend edge with a high number of irradiations. Owing to the mild steel’s greater beam absorption at the HPDL wavelength, larger bending angles were induced when using the HPDL. However, under certain conditions the performance of the CO2 laser in terms of induced bending angle was seen to approach that of the HPDL. Nevertheless, similar results between the two lasers were only achieved with increasing irradiations, thus it was concluded that the efficacy of the HPDL was higher than that of the CO2 laser insofar as it was more efficient. From graphical results and the employment of an analytical procedure, the laser line energy range in which accurate control of the HPDL bending of the mild steel sheets could be exercised efficiently was found to be 53 J mm-1 < P/v < 78 J mm-1, whilst for the CO2 laser the range was 61 J mm-1 < P/v < 85 J mm-1

Differences in bioactivity between human insulin and insulin analogues approved for therapeutic use- compilation of reports from the past 20 years

In order to provide comprehensive information on the differences in bioactivity between human insulin and insulin analogues, published in vitro comparisons of human insulin and the rapid acting analogues insulin lispro (Humalog®), insulin aspart ( NovoRapid®), insulin glulisine (Apidra®), and the slow acting analogues insulin glargine (Lantus®), and insulin detemir (Levemir®) were gathered from the past 20 years (except for receptor binding studies). A total of 50 reports were retrieved, with great heterogeneity among study methodology. However, various differences in bioactivity compared to human insulin were obvious (e.g. differences in effects on metabolism, mitogenesis, apoptosis, intracellular signalling, thrombocyte function, protein degradation). Whether or not these differences have clinical bearings (and among which patient populations) remains to be determined

Using the Goldilocks Principle to model coral ecosystem engineering

The occurrence and proliferation of reef-forming corals is of vast importance in terms of the biodiversity they support and the ecosystem services they provide. The complex three-dimensional structures engineered by corals are comprised of both live and dead coral, and the function, growth and stability of these systems will depend on the ratio of both. To model how the ratio of live : dead coral may change, the ‘Goldilocks Principle’ can be used, where organisms will only flourish if conditions are ‘just right’. With data from particle imaging velocimetry and numerical smooth particle hydrodynamic modelling with two simple rules, we demonstrate how this principle can be applied to a model reef system, and how corals are effectively optimizing their own local flow requirements through habitat engineering. Building on advances here, these approaches can be used in conjunction with numerical modelling to investigate the growth and mortality of biodiversity supporting framework in present-day and future coral reef structures

Insulin Detemir Reduces Weight Gain as a Result of Reduced Food Intake in Patients With Type 1 Diabetes

Insulin detemir lacks the usual propensity for insulin to cause weight gain. We investigated whether this effect was a result of reduced energy intake and/or increased energy expenditure

Gene Silencing of Phogrin Unveils Its Essential Role in Glucose-Responsive Pancreatic β-Cell Growth

OBJECTIVE—Phogrin and IA-2, autoantigens in insulin-dependent diabetes, have been shown to be involved in insulin secretion in pancreatic β-cells; however, implications at a molecular level are confusing from experiment to experiment. We analyzed biological functions of phogrin in β-cells by an RNA interference technique

Insulin Promotes Glycogen Storage and Cell Proliferation in Primary Human Astrocytes

In the human brain, there are at least as many astrocytes as neurons. Astrocytes are known to modulate neuronal function in several ways. Thus, they may also contribute to cerebral insulin actions. Therefore, we examined whether primary human astrocytes are insulin-responsive and whether their metabolic functions are affected by the hormone.Commercially available Normal Human Astrocytes were grown in the recommended medium. Major players in the insulin signaling pathway were detected by real-time RT-PCR and Western blotting. Phosphorylation events were detected by phospho-specific antibodies. Glucose uptake and glycogen synthesis were assessed using radio-labeled glucose. Glycogen content was assessed by histochemistry. Lactate levels were measured enzymatically. Cell proliferation was assessed by WST-1 assay.We detected expression of key proteins for insulin signaling, such as insulin receptor β-subunit, insulin receptor substrat-1, Akt/protein kinase B and glycogen synthase kinase 3, in human astrocytes. Akt was phosphorylated and PI-3 kinase activity increased following insulin stimulation in a dose-dependent manner. Neither increased glucose uptake nor lactate secretion after insulin stimulation could be evidenced in this cell type. However, we found increased insulin-dependent glucose incorporation into glycogen. Furthermore, cell numbers increased dose-dependently upon insulin treatment.This study demonstrated that human astrocytes are insulin-responsive at the molecular level. We identified glycogen synthesis and cell proliferation as biological responses of insulin signaling in these brain cells. Hence, this cell type may contribute to the effects of insulin in the human brain

The Insulin-Mediated Modulation of Visually Evoked Magnetic Fields Is Reduced in Obese Subjects

BACKGROUND: Insulin is an anorexigenic hormone that contributes to the termination of food intake in the postprandial state. An alteration in insulin action in the brain, named "cerebral insulin resistance", is responsible for overeating and the development of obesity. METHODOLOGY/PRINCIPAL FINDINGS: To analyze the direct effect of insulin on food-related neuronal activity we tested 10 lean and 10 obese subjects. We conducted a magnetencephalography study during a visual working memory task in both the basal state and after applying insulin or placebo spray intranasally to bypass the blood brain barrier. Food and non-food pictures were presented and subjects had to determine whether or not two consecutive pictures belonged to the same category. Intranasal insulin displayed no effect on blood glucose, insulin or C-peptide concentrations in the periphery; however, it led to an increase in the components of evoked fields related to identification and categorization of pictures (at around 170 ms post stimuli in the visual ventral stream) in lean subjects when food pictures were presented. In contrast, insulin did not modulate food-related brain activity in obese subjects. CONCLUSIONS/SIGNIFICANCE: We demonstrated that intranasal insulin increases the cerebral processing of food pictures in lean whereas this was absent in obese subjects. This study further substantiates the presence of a "cerebral insulin resistance" in obese subjects and might be relevant in the pathogenesis of obesity