16 research outputs found
Building Energy Flexibility: A Sensitivity Analysis and Key Performance Indicator Comparison
No full textThis thesis has two objectives, the first is to analyze the impact of insulation level, thermalmass, type of heating system, control strategy, outdoor temperature, solar radiation and type ofbuilding (office or single family house), on the flexibility function and the two key performanceindicators developed by IEA EBC Annex 67. This sensitivity analysis is based on raw data from6 case studies, and to assess the influence on the different parameters, ANOVA tests are used.The results are then ranked according to their influence on the different flexibility characteristicsand key performance indicators. Furthermore, another sensitivity analysis is performed to morespecifically analyze the impact of insulation level, thermal mass, heating system and controlstrategy on the flexibility characteristics.The results showed that insulation level has the largest influence on all the flexibilitycharacteristics and key performance indicators, except the total time of increased energy demand.Thermal mass is also found to have a significant influence on the flexibility characteristics,especially on low insulated building.The validity of the sensitivity analysis results on the total time of increase/decrease energydemand are questionable. Based on analysis and result from other studies, the ranking ordershould be different. Insulation level and thermal mass should be the parameters that have thelargest influence.The results also showed that only insulation level has an influence on the cost/savings by applyingflexibility. This can be more related to the decrease of energy consumption from a low insulatedto a high insulated building.The second objective of this thesis is so analyze and compare different key performance indicatorsto the ones developed by IEA EBC Annex 67. For comparison, a graph with results from boththe respective and key performance indicators developed by IEA EBC Annex 67 is used. In total,11 key performance indicators were analyzed, and it was found that they can be categorized intofour categories.The comparison showed that 8 of the 11 analyzed key performance indicators were eithercomparable to shifted flexible load or efficiency of flexible operation, or, if only consideringthe KPIs that can assess the flexibility potential on a yearly basis, 8 of the 9 analyzed keyperformance indicators were comparable to the IEA EBC Annex 67 key performance indicators.<br/
Detecting fingerprint alterations by orientation field and minutiae orientation analysis
No full text
Building Energy Flexibility:A Sensitivity Analysis and Key Performance Indicator Comparison
No full textBuildings are a key active element of the future Smart Grids with large shares of renewable energy, as they can provide flexible energy usage to help balancing power production intermittence. There is currently no consensus yet on how to quantify building energy flexibility. The various KPIs found in literature can be classified into 4 main categories: load shifting ability, power adjustment, energy efficiency and cost efficiency. Most of them use a reference scenario. Moreover, the envelope performance appears to be the most important parameter with regards to all aspects of building energy flexibility when using indoor temperature set point modulation.Buildings are a key active element of the future Smart Grids with large shares of renewable energy, as they can provide flexible energy usage to help balancing power production intermittence. There is currently no consensus yet on how to quantify building energy flexibility. The various KPIs found in literature can be classified into 4 main categories: load shifting ability, power adjustment, energy efficiency and cost efficiency. Most of them use a reference scenario. Moreover, the envelope performance appears to be the most important parameter with regards to all aspects of building energy flexibility when using indoor temperature set point modulation
Increased number of islet-associated macrophages in type 2 diabetes
No full textActivation of the innate immune system in obesity is a risk factor for the development of type 2 diabetes. The aim of the current study was to investigate the notion that increased numbers of macrophages exist in the islets of type 2 diabetes patients and that this may be explained by a dysregulation of islet-derived inflammatory factors. Increased islet-associated immune cells were observed in human type 2 diabetic patients, high-fat-fed C57BL/6J mice, the GK rat, and the db/db mouse. When cultured islets were exposed to a type 2 diabetic milieu or when islets were isolated from high-fat-fed mice, increased islet-derived inflammatory factors were produced and released, including interleukin (IL)-6, IL-8, chemokine KC, granulocyte colony-stimulating factor, and macrophage inflammatory protein 1alpha. The specificity of this response was investigated by direct comparison to nonislet pancreatic tissue and beta-cell lines and was not mimicked by the induction of islet cell death. Further, this inflammatory response was found to be biologically functional, as conditioned medium from human islets exposed to a type 2 diabetic milieu could induce increased migration of monocytes and neutrophils. This migration was blocked by IL-8 neutralization, and IL-8 was localized to the human pancreatic alpha-cell. Therefore, islet-derived inflammatory factors are regulated by a type 2 diabetic milieu and may contribute to the macrophage infiltration of pancreatic islets that we observe in type 2 diabetes
The role of systemically perturbed PTEN and PKBß/AKT2 signaling in accumulation of hepatic lipids
No full textNon-alcoholic fatty liver disease (NAFLD) is a major health problem and occurs frequently in the context of obesity and type 2 diabetes mellitus (T2D). Insulin resistance of the liver and/or peripheral tissues is considered to drive ectopic lipid accumulation in hepatocytes, but individual contributions are not fully understood. Hepatocyte-specific Pten-deficiency in mice was shown previously to result in hepatic steatosis due to hyperactivated PKBb in the liver. However, the role of peripheral insulin sensitive tissues on PTEN/PKBb-dependent development of NAFLD has not been addressed.
The aim of this thesis is to characterize the effects of systemically perturbed PTEN/PKBb signaling on hepatic lipid content using Pten-haplodeficient (Pten+/-/Pkbb+/+) mice and Pten-haplodeficient mice lacking Pkbb (Pten+/-/Pkbb-/-). We found that Pten+/-/Pkbb+/+ mice have a more than 2-fold reduction in hepatic lipid content compared to control mice, similar to the low level observed in Pten+/-/Pkbb-/- mice. Pten+/-/Pkbb+/+ mice showed enhanced insulin signaling in the liver indicating that extra-hepatic factors prevent hepatic lipid accumulation. Further results suggested that augmented PKBb activity in the skeletal muscle of Pten+/-/Pkbb+/+ mice might reduce hepatic lipid content. Indeed, skeletal muscle-specific expression of constitutively active PKBb reduced hepatic lipids in Pten+/+Pkbb+/+ mice and dominant negative PKBb increased hepatic lipid content in both Pten+/+Pkbb+/+ and Pten+/-/Pkbb+/+ mice.
The results obtained during this study show that PKBb activity in skeletal muscle regulates lipid accumulation in the livers of Pten+/+Pkbb+/+ and Pten+/-/Pkbb+/+ mice, and emphasizes the role of skeletal muscle in the pathophysiology of NAFLD
Glycoprotein 130 receptor signaling mediates α-cell dysfunction in a rodent model of type 2 diabetes
No full textDysregulated glucagon secretion accompanies islet inflammation in type 2 diabetes. We recently discovered that interleukin (IL)-6 stimulates glucagon secretion from human and rodent islets. IL-6 family cytokines require the glycoprotein 130 (gp130) receptor to signal. In this study, we elucidated the effects of α-cell gp130 receptor signaling on glycemic control in type 2 diabetes. IL-6 family cytokines were elevated in islets in rodent models of this disease. gp130 receptor activation increased STAT3 phosphorylation in primary α-cells and stimulated glucagon secretion. Pancreatic α-cell gp130 knockout (agp130KO) mice showed no differences in glycemic control, α-cell function, or α-cell mass. However, when subjected to streptozotocin plus high-fat diet to induce islet inflammation and pathophysiology modeling type 2 diabetes, agp130KO mice had reduced fasting glycemia, improved glucose tolerance, reduced fasting insulin, and improved α-cell function. Hyperinsulinemic-euglycemic clamps revealed no differences in insulin sensitivity. We conclude that in a setting of islet inflammation and pathophysiology modeling type 2 diabetes, activation of α-cell gp130 receptor signaling has deleterious effects on α-cell function, promoting hyperglycemia. Antagonism of α-cell gp130 receptor signaling may be useful for the treatment of type 2 diabetes. © 2014 by the American Diabetes Association
The development of a novel rugby league match simulation protocol
No full textThe effectiveness of recovery interventions following prolonged multiple sprint team sports matches has rarely been studied despite the potential for exercise-induced muscle damage to adversely affect training in the days following games. The lack of research related to this topic is probably owing to the wide variability that exists in the movement demands of players between matches and the impact that this has on the subsequent rate and magnitude of recovery which makes it difficult to detect meaningful differences when conducting research with small sample sizes. Therefore, the purpose of this thesis was to develop a rugby league-specific match simulation protocol that replicates the movement demands, physiological responses and subsequent recovery from matches in order to study the effectiveness of recovery interventions. Hence, two time-motion analysis studies were conducted using a semi-automated image recognition system to inform the development of the rugby league match simulation protocol (RLMSP). Whilst mean total distance covered over the duration of the match was 8,503 m, ball in play and stoppage work-to-rest ratios were 1:6.9 and 1:87.4, respectively, for all players. Furthermore, a significant decline in high and very high intensity running locomotive rates were observed between the initial and final 20 min periods of the match. Thus a RLMSP was devised to replicate the overall movement demands, intra-match fatigue and recovery from a senior elite rugby league match. Not only was there a low level of variability in the movement demands during the RLMSP over consecutive trials, but with the exception of creatine kinase, the rate and magnitude of recovery following the RLMSP was similar to that that has been published following competitive matches. Therefore, the RLMSP devised in this thesis may be a more appropriate research tool for assessing the effectiveness of recovery interventions following match related exercise than following actual match play.Sponsored by Warrington Wolves Rugby League Football Clu
Interplay between inflammation, autoimmunity and regeneration in the NOD mouse model of type 1 diabetes and Sjogren’s Syndrome.
No full textPhDA continuous process of tissue remodelling and regeneration is a fundamental feature of the
homeostatic response of the target organ of several autoimmune diseases. In type 1 diabetes (T1D)
the β cell mass is in a constant process of death and renewal in order to regenerate the islets
damaged by the autoimmune process. The relationship linking inflammation and regeneration
during autoimmunity remains elusive. Reg genes, a multigene family discovered using cDNA
libraries derived from rat regenerating islets, have been suggested to play an important role in
epithelial regeneration not only in the pancreas but also in the salivary glands (SG) of Sjogren’s
Syndrome (SS) during autoimmune sialoadenitis.
Both in patients and animal models of T1D and SS, the chronic inflammatory/autoimmune process
is heterogeneous and display high immunological variability. In particular, in a sizeable subset of
cases, inflammatory lesions display ectopic lymphoid structures (ELS) characterised by T/B cell
segregation, follicular dendritic cells networks and differentiation of germinal center B cells.
However, there is limited evidence on the cellular and molecular mechanisms underlying ELS
formation and their contribution to autoimmunity in the pancreas during autoimmune insulitis and
in SG during autoimmune sialoadenitis. In this PhD project, I used the NOD mouse model of T1D
and SS in order to investigate i) the cellular and molecular mechanisms regulating ELS formation,
ii) the functionality of ELS in supporting in situ autoreactive B cell differentiation and iii) the
relationship between formation of ELS and the expression of REG genes.
In this work I showed that ELS formation was preceded by local up-regulation of lymphotoxins
(LTαβ) and lymphoid chemokines CXCL13 and CCL19 and that, once formed, ELS were fully
functional in promoting autoreactive B cell activation. Importantly, inhibition of the LT-β pathway
prevented the formation of ELS and B cell autoimmunity. Finally, I showed that the expression
pattern of Reg genes was strictly related to the development of inflammatory infiltrates in NOD
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mice and that Reg proteins were target of the autoimmune process itself, as shown by the
development of anti-Reg1 antibodies in patients with T1D. Overall, these results suggest that the
processes of destruction and regeneration occurring in chronic autoimmune/inflammatory diseases
are strongly interdependent whereby autoimmunity may be further enhanced by the attempt to
regenerate
