Omfördelning av Gränby Sportfälts effektuttag

There is currently a power shortage in the electric grid around Uppsala, which obstructs the local development, since it prevents companies from expanding their businesses. Sportfastigheter is a part of Uppsala municipality and operates the ice halls at Gränby Sportfält, which occasionally require large power outputs. The purpose of this study is, therefore, to examine whether flow batteries could be a possible technique to redistribute the power output from the electric grid. Type, size and steering of a flow battery have been examined through simulations. Flow batteries have also been compared to other energy storage methods and the implementation of a possible capacitor bank has been investigated. The result is, that flow batteries is a possible technique to cut power tops at Gränby sportfält, while other storage methods should be investigated more closely, since flow batteries is a rather new and unproven technique. If the installation would be made today, a more established storage method such as lithium ion batteries would be preferable, even though flow batteries have a promising future potential. The installation of a capacitor bank can be considered since it would compensate the reactive effect and, hence, reduce the power output at Gränby Sportfält.Det råder idag kapacitetsbrist i Uppsalas elnät vilket bromsar den lokala utvecklingen eftersom det hindrar företag från att bygga ut sina verksamheter. Sportfastigheter är en del av Uppsala kommun och förvaltar ishallarna vid Gränby Sportfält, som stundtals kräver mycket stora effektuttag. Syftet med denna studie är att undersöka om flödesbatterier kan vara en möjlig teknik för att omfördela effektuttaget från elnätet. Typ, storlek och styrning av ett flödesbatteri har undersökts genom simuleringar. Flödesbatterier har även jämförts med andra energilagringsmetoder och implementeringen av en eventuell kondensatorbank har undersökts. Resultatet är att flödesbatterier är en möjlig teknik för att kapa effekttopparna för Gränby Sportfält men att andra lagringsmetoder bör undersökas närmare, eftersom flödesbatterier är en relativt ny och obeprövad metod. Om installation skulle göras i dagsläget vore en mer etablerad lagringsmetod såsom litiumjonbatterier att föredra, även om flödesbatterier har en lovande framtidspotential. Installationen av en kondensatorbank kan övervägas då det skulle kompensera för den reaktiva effekten och på sätt minska effektuttaget för Gränby Sportfält

Rapid expansion and long-term persistence of elevated NK cell numbers in humans infected with hantavirus

Acute hantavirus infection in humans triggers a rapid expansion and long-term persistence of NK cells

Load control of electrical space and water heating : A study of the potential in detached houses to contribute to a lower subscripted power of the overhead grid

This study has explored the potential for lowering the subscripted power of 25 MW for one of the connection points between the local power grid and its overhead power grid for a local grid owner. The potential for doing so through hard, direct load control of electrical domestic heating and domestic water heating for detached houses with a fuse size of 16-25 A is evaluated for 12 different scenarios. The scenarios are found by combining a customer participation of 25, 50, 75 and 100 percent with a maximum allowed duration for load control of two, three and four hours respectively. A function describing the need for electrical power for domestic heating as dependent of the outdoor temperature is developed and combined with a model that is used for simulating hot water usage and a model that describes the power demand of a domestic water heater. Furthermore, a control function is incorporated to ensure that households are not subjected to load control for a longer period than allowed and that all households bear the same burden in this respect.  The results show that a power of 1,0-4,1 MWh/h can be redistributed, but that the potential is heavily limited by the returning load that occurs. Due to the long duration of the critical peaks that are being redistributed, up to 5-10 hours, returning load occurs even though load control has not yet been finalized. The returning load leads to a bigger amount of power having to be redistributed and therefore limits the potential for the new subscripted power that can be achieved. Furthermore, the maximum aggregated power for the investigated year amounts to 25,9 MW. Still, a new subscripted power of 21,8–24,9 MW is theoretically deemed to be achievable. The most likely outcome however is thought to be a lowering of the subscripted power to at least 23,4–24,4 MW, having taken the composition of type of heating systems as well as the most likely customer participation into account.

Longitudinal Analysis of the Human T Cell Response during Acute Hantavirus Infection ▿ †

Longitudinal studies of T cell immune responses during viral infections in humans are essential for our understanding of how effector T cell responses develop, clear infection, and provide long-lasting immunity. Here, following an outbreak of a Puumala hantavirus infection in the human population, we longitudinally analyzed the primary CD8 T cell response in infected individuals from the first onset of clinical symptoms until viral clearance. A vigorous CD8 T cell response was observed early following the onset of clinical symptoms, determined by the presence of high numbers of Ki67+CD38+HLA-DR+ effector CD8 T cells. This response encompassed up to 50% of total blood CD8 T cells, and it subsequently contracted in parallel with a decrease in viral load. Expression levels of perforin and granzyme B were high throughout the initial T cell response and likewise normalized following viral clearance. When monitoring regulatory components, no induction of regulatory CD4 or CD8 T cells was observed in the patients during the infection. However, CD8 as well as CD4 T cells exhibited a distinct expression profile of inhibitory PD-1 and CTLA-4 molecules. The present results provide insight into the development of the T cell response in humans, from the very onset of clinical symptoms following a viral infection to resolution of the disease

Lactoferrin-Hexon Interactions Mediate CAR-Independent Adenovirus Infection of Human Respiratory Cells

Virus entry into host cells is a complex process that is largely regulated by access to specific cellular receptors. Human adenoviruses (HAdVs) and many other viruses use cell adhesion molecules such as the coxsackievirus and adenovirus receptor (CAR) for attachment to and entry into target cells. These molecules are rarely expressed on the apical side of polarized epithelial cells, which raises the question of how adenoviruses—and other viruses that engage cell adhesion molecules—enter polarized cells from the apical side to initiate infection. We have previously shown that species C HAdVs utilize lactoferrin—a common innate immune component secreted to respiratory mucosa—for infection via unknown mechanisms. Using a series of biochemical, cellular, and molecular biology approaches, we mapped this effect to the proteolytically cleavable, positively charged, N-terminal 49 residues of human lactoferrin (hLF) known as human lactoferricin (hLfcin). Lactoferricin (Lfcin) binds to the hexon protein on the viral capsid and anchors the virus to an unknown receptor structure of target cells, resulting in infection. These findings suggest that HAdVs use distinct cell entry mechanisms at different stages of infection. To initiate infection, entry is likely to occur at the apical side of polarized epithelial cells, largely by means of hLF and hLfcin bridging HAdV capsids via hexons to as-yet-unknown receptors; when infection is established, progeny virions released from the basolateral side enter neighboring cells by means of hLF/hLfcin and CAR in parallel. IMPORTANCE: Many viruses enter target cells using cell adhesion molecules as receptors. Paradoxically, these molecules are abundant on the lateral and basolateral side of intact, polarized, epithelial target cells, but absent on the apical side that must be penetrated by incoming viruses to initiate infection. Our study provides a model whereby viruses use different mechanisms to infect polarized epithelial cells depending on which side of the cell—apical or lateral/basolateral—is attacked. This study may also be useful to understand the biology of other viruses that use cell adhesion molecules as receptors

NK Cell Activation in Human Hantavirus Infection Explained by Virus-Induced IL-15/IL15R alpha Expression

Clinical infection with hantaviruses cause two severe acute diseases, hemorrhagic fever with renal syndrome (HFRS) and hantavirus pulmonary syndrome (HPS). These diseases are characterized by strong immune activation, increased vascular permeability, and up to 50% case-fatality rates. One prominent feature observed in clinical hantavirus infection is rapid expansion of natural killer (NK) cells in peripheral blood of affected individuals. We here describe an unusually high state of activation of such expanding NK cells in the acute phase of clinical Puumala hantavirus infection. Expanding NK cells expressed markedly increased levels of activating NK cell receptors and cytotoxic effector molecules. In search for possible mechanisms behind this NK cell activation, we observed virus-induced IL-15 and IL-15R alpha on infected endothelial and epithelial cells. Hantavirus-infected cells were shown to strongly activate NK cells in a cell-cell contact-dependent way, and this response was blocked with anti-IL-15 antibodies. Surprisingly, the strength of the IL-15-dependent NK cell response was such that it led to killing of uninfected endothelial cells despite expression of normal levels of HLA class I. In contrast, hantavirus-infected cells were resistant to NK cell lysis, due to a combination of virus-induced increase in HLA class I expression levels and hantavirus-mediated inhibition of apoptosis induction. In summary, we here describe a possible mechanism explaining the massive NK cell activation and proliferation observed in HFRS patients caused by Puumala hantavirus infection. The results add further insights into mechanisms behind the immunopathogenesis of hantavirus infections in humans and identify new possible targets for intervention

Increased HLA class I expression on hantavirus-infected cells inhibits NK cell effector functions.

<p>(A) Degranulation (CD107a) and cytokine production (TNF and IFN-γ) of resting, IL-15 and IFN-α pre-activated CD56^dim NK cells reactive against uninfected (white) or HTNV-infected (black) endothelial cells. Results from 2 independent experiments (n = 6) (*** p≤0.001, ** p≤0.01, * p≤0.05; paired <i>t</i>-test). (B) Representative staining of HLA class I and HLA-E expression on uninfected (white) or HTNV-infected (black) endothelial cells. Isotype control (grey). (C and D) CD56^dim NK cell responses against uninfected and HTNV-infected endothelial cells in the presence of anti-HLA class I or isotype control antibody. (C) Representative FACS analysis of the NK cell responses against uninfected and HTNV-infected endothelial cells in the presence of anti-HLA class I or isotype control antibody is depicted. (D) Frequency of CD56^dim NK cells expressing CD107a (n = 6), TNF (n = 3) and IFN-γ (n = 3) in response to uninfected (white) and HTNV-infected (black) endothelial cells in the presence of anti-HLA class I or isotype control antibody (*** p≤0.001, * p≤0.05; paired <i>t</i>-test).</p

Hantavirus-activated CD56^dim NK cells kill uninfected but not hantavirus-infected endothelial cells.

<p>(A) Experimental set-up: NK cells were incubated with uninfected or HTNV-infected cells for 24 h then transferred and incubated for another 5 h with uninfected or HTNV-infected cells, followed by assessment of NK cell degranulation and cytotoxicity. (B and C) Degranulation (CD107a) of CD56^dim NK cells pre-stimulated with uninfected or HTNV-infected endothelial cells against uninfected and HTNV-infected endothelial cells. (B) FACS analysis of one NK cell donor is shown. (C) CD107a expression on CD56^dim NK cells (n = 9) in response to uninfected and HTNV-infected endothelial cells after pre-stimulation with uninfected (white) or HTNV-infected (black) endothelial cells or medium alone (grey). Results from 3 independent experiments (*** p≤0.001; paired <i>t</i>-test). (D) Degranulation of CD56^dim NK cells (n = 4) against uninfected endothelial cells after pre-stimulation with uninfected (white) and HTNV-infected (black) endothelial cells. When indicated, IL-15 was blocked on endothelial cells during pre-stimulation. Results from 2 independent experiments (* p≤0.05; paired <i>t</i>-test). (E and F) Induction of apoptosis in endothelial cells exposed to NK cells pre-stimulated with uninfected or HTNV-infected endothelial cells. (E) One representative immunofluorescent staining is depicted: DAPI (blue), HTNV-nucleocapsid protein (green), TUNEL-positive cells (red). (F) Percentage of TUNEL-positive uninfected and HTNV-infected endothelial cells after exposure to NK cells (n = 6) pre-stimulated with uninfected (white) and HTNV-infected (black) endothelial cells. Results from 3 independent experiments (** p≤0.01; paired <i>t</i>-test). (G) NK cell-mediated specific lysis of uninfected endothelial cells after pre-stimulation with uninfected (white) or HTNV-infected (black) endothelial cells. Depicted are mean values (+/− SD) from 5 donors and 2 independent experiments (* p≤0.05).</p

CD56^dim NK cells acquire increased functional capacity after contact with hantavirus-infected cells.

<p>(A–C) Degranulation (CD107a) and intracellular cytokine production of CD56^dim NK cells reacting to K562 cells after pre-stimulation with uninfected or HTNV-infected endothelial and epithelial cells. (A) Representative FACS analysis of CD107a, IFN-γ and TNF expression in one NK cell donor is shown. (B and C) Summary of the CD56^dim NK cell responses against K562 cells (n = 9) after pre-stimulation with uninfected (white) or HTNV-infected (black) endothelial (B) and epithelial cells (C). (*** p≤0.001, ** p≤0.01; paired <i>t</i>-test). (D) NK cell-mediated specific lysis of K562 cells after pre-stimulation of NK cells with uninfected (white) and HTNV-infected (black) endothelial cells. Depicted are mean values (+/− SD) from 5 donors and 2 independent experiments (** p≤0.01, *p≤0.05; paired <i>t</i>-test).</p

Induced IL-15 and IL-15Rα expression in hantavirus-infected cells drives CD56^dim NK cell activation.

<p>(A and B) Kinetics of IL-15 and IL-15Rα mRNA-expression in HTNV-infected endothelial (A) and epithelial (B) cells analyzed with RT-qPCR. Fold change compared to the expression level in the respective uninfected cell is depicted. Results of one experiment run in triplicates are shown. (C and D) Expression of IL-15 and IL-15Rα protein in uninfected and HTNV-infected endothelial cells analyzed with flow cytometry after cell permeabilization. (C) One representative FACS analysis is shown. Uninfected cells (white), HTNV-infected cells (black) and isotype control (grey). (D) The expression levels (MFI) of IL-15 and IL-15Rα protein in uninfected (white) or HTNV-infected (black) endothelial cells (n = 3). (E–H) Surface expression of IL-15 and IL-15Rα on uninfected and HTNV-infected endothelial (E and F) and epithelial (G and H). (E and G) Representative FACS analysis of the surface expression of IL-15 and IL-15Rα on uninfected and HTNV-infected endothelial cells and epithelial cells. Uninfected cells (white), HTNV-infected cells (black) and isotype (grey). (F and H) The expression levels (MFI) of IL-15 and IL-15Rα on uninfected (white) or HTNV-infected (black) endothelial (n = 4) and epithelial cells (n = 4) are shown. (I–L) CD69 expression on CD56^dim NK cells after co-incubation with HTNV-infected endothelial cells (I and J) and epithelial cells (K and L) in the presence of anti-IL-15 or isotype control antibody. (I and K) Representative FACS analysis of CD69 expression on CD56^dim NK cells incubated with endothelial cells (I) and epithelial cells (K) in the presence of isotype control (black) or anti-IL-15 antibody (grey). (J and L) Expression levels (MFI) of CD69 on CD56^dim NK cells after co-incubation with endothelial cells (n = 8) (J) and epithelial cells (n = 6) (L). The dashed lines represent upper and lower SEM intervals for means of CD69 expression on CD56^dim NK cells after incubation with the respective uninfected cells.</p