| 1. |
- Risberg, Daniel, et al.
(författare)
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CFD simulations of the indoor climate of a low energy building in a sub-Arctic climate: an evaluationof different heating systems.
- 2013
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Konferensbidrag (refereegranskat)abstract
- Computational Fluid Dynamics (CFD) simulations were used to study the indoor climate in a low energy building in northern Sweden. The building’s low heat requirements raise the prospect of using relatively simple and inexpensive heating systems to maintain an acceptable indoor environment, even in the face of extremely low outdoor temperatures. To explore the viability of this approach, the indoor temperature and air velocity distribution inside the building were studied assuming that it was fitted with one of four different heating systems: radiators, an underfloor heating system, a pellet stove, and an air/air heat pump. The radiators produced a relatively uniform horizontal temperature distribution throughout the house. The underfloor system provided an even more uniform temperature distribution. In contrast, the heat pump created a relatively uneven internal temperature distribution. Several locations for the pump were considered, all of which had significant drawbacks. The pellet stove produced a more even temperature distribution than the pump but not to the same extent as the underfloor system or the radiators. Overall, point source heating systems cost less to fit and operate over a given period of time but produce a less clement indoor environment than distributed heating systems.
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| 2. |
- Vesterlund, Mattias, et al.
(författare)
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Evaluation of losses in district heating system, a case study
- 2013
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Konferensbidrag (refereegranskat)abstract
- To be able to create a model that accurately describes a district heating system, it is important to identify the thermal losses and how they are distributed. However, general methods targeting the determination of losses are scarce in the literature. In the current case the losses for a district heating system in Kiruna, a town in northern Sweden, has been estimated in the year 2010 to be 12%, which is in the range for a typical Swedish network. Unfortunately, detailed information of the thermal losses is lacking.In this paper two methods to determine loss distribution in a district heating system are presented.Two databases of pipe lengths and diameters have been compiled for two piping categories, loops and feeds. Any missing data regarding pipe diameters in the map has then been determined with the two different methods.In the first method average pipe diameters for loops and feeds are calculated. All pipes with unknown diameter are then assumed to have the average one. The second method considers a percentage based distribution of known diameters and assigns the same distribution to the missing pipe diameters. The losses were estimated in the whole system according to the data from a pipe producer catalogue, in which losses are calculated according to current European standard. The results show that the losses in the system are similar to the losses caused by pipes with the lowest insulating capacity.By using the two methods two fictitious pipe series reproducing exactly the losses in the system are created by scaling the calculated losses of the catalogue pipe series which would give the most similar losses (the one with the lowest insulating capacity). This adjustment was +3.1% by using the first method, and +4.9% by using the second method.The major conclusion of this study is that, both methods can be used for calculating the distribution of thermal losses in the district heating system of Kiruna; moreover, this kind of analysis can be an important tool for analyzing investments in the district heating network in Kiruna.
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| 3. |
- Vesterlund, Mattias
(författare)
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The mechanism of action of SOCS2 and its role in metabolism and growth
- 2013
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- A well-known function of Growth Hormone (GH) is the regulation of postnatal longitudinal growth but it also affects other biological processes, for instance metabolism and inflammation. Actions of GH are tightly regulated at several levels and by several different factors and are initiated by GH binding to membrane bound GH receptors (GHR). The intracellular signaling of GH and other related hormones and cytokines is predominately mediated by the JAK-STAT pathway. This pathway is regulated in a negative feedback manner by the Suppressors of Cytokine Signaling (SOCS) family of proteins. One of the family members, SOCS2, is intimately tied to GH by virtue of the phenotype that results from its absence. SOCS2-/- mice are 40% larger than wildtype littermates due to increased GH sensitivity. Here, the molecular mechanism behind SOCS2s negative regulation of GH signaling, and its effects on metabolism and inflammation are described. We demonstrate that SOCS2 assembles a canonical E3 ubiquitin ligase complex with Elongin B, Elongin C, Cullin 5 and Rbx2 and that this complex has intrinsic E3 ligase activity in vitro. Overexpression of SOCS2 and its complex members leads to ubiquitination and proteasomal degradation of the GHR. We also outline the importance of the different domains of SOCS2, and demonstrate the necessity of the SOCS-box for proper SOCS2 activity. In a follow up study the claim that the naturally occurring Ser52Asn polymorphism of SOCS2 affects its activity and may contribute to acromegaly in humans was investigated. The Ser52Asn mutant was however found to be as efficient at regulating GH signaling as the wildtype and we conclude that it is unlikely to contribute to increased GH sensitivity. In Paper III the phenotype of SOCS2-/- mice under conditions of dietary stress is described. We report that SOCS2 deletion protects against high fat diet (HFD) induced hepatic steatosis but simultaneously leads to decreased insulin sensitivity. SOCS2-/- mice were found to have increased triglyceride output from the liver but also increased plasma levels of proinflammatory cytokines without apparent macrophage infiltration. In vitro examination of macrophages revealed increased phagocytic activity and cytokine production in the absence of SOCS2 and suggests a direct role for SOCS2 in the regulation of TLR4 signaling. Finally, the results of a screening effort to identify SOCS2-modulating, drug-like molecules are included. We have identified a prospective hit that binds to and inhibits SOCS2 activity in vitro. In summary, SOCS forms an E3 ligase complex which targets the GHR for degradation. This forms the molecular basis of its physiological actions. SOCS2-/- mice are protected from HFD induced hepatic steatosis but suffer from deteriorated insulin sensitivity related to increased inflammation.
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