22 research outputs found

    Exergy Analysis for Utilizing Latent Energy of Thermal Energy Storage System in District Heating

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    The thermal energy storage (TES) system stores the district heating (DH) water when the heating load is low. Since a TES system stores heat at atmospheric pressure, the DH water temperature of 115 °C has to be lowered to less than 100 °C. Therefore, the temperature drop of the DH water results in thermal loss during storage. In addition, the DH water must have high pressure to supply heat to DH users a long distance from the CHP plant. If heat is to be stored in the TES system, a pressure drop in the throttling valve occurs. These exergy losses, which occur in the thermal storage process of the general TES system, can be analyzed by exergy analysis to identify the location, cause and the amount of loss. This study evaluated the efficiency improvement of a TES system through exergy calculation in the heat storage process. The method involves power generation technology using the organic Rankine cycle (ORC) and a hydraulic turbine. As a result, the 930 kW capacity ORC and the 270 kW capacity hydraulic turbine were considered suitable for a heat storage system that stores 3000 m3/h. In this case, each power generation facility was 50% of the thermal storage capacity, which was attributed to the variation of actual heat storage from the annual operating pattern analysis. Therefore, it was possible to produce 1200 kW of power by recovering the exergy losses. The payback period of the ORC and the hydraulic turbine will be 3.5 and 7.13 years, respectively

    CD4+CD25+ regulatory T cell depletion modulates anxiety and depression-like behaviors in mice.

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    Stress has been shown to suppress immune function and increase susceptibility to inflammatory disease and psychiatric disease. CD4(+)CD25(+) regulatory T (Treg) cells are prominent in immune regulation. This study was conducted to determine if anti-CD25 antibody (Ab) mediated depletion of Treg cells in mice susceptibility to stress-induced development of depression-like behaviors, as well as immunological and neurochemical activity. To accomplish this, an elevated plus-maze test (EPM), tail suspension test (TST), and forced swim test (FST) were used to examine depression-like behaviors upon chronic immobilization stress. Immune imbalance status was observed based on analysis of serum cytokines using a mouse cytometric bead array in conjunction with flow cytometry and changes in the levels of serotonin (5-HT) and dopamine (DA) in the brain were measured by high performance liquid chromatography (HPLC). The time spent in the open arms of the EPM decreased significantly and the immobility time in the FST increased significantly in the anti-CD25 Ab-treated group when compared with the non stressed wild-type group. In addition, interlukin-6 (IL-6), tumor necrosis factor-á (TNF-á), interlukin-2 (IL-2), interferon-gamma (IFN-γ), interlukin-4 (IL-4) and interlukin-17A (IL-17A) concentrations were significantly upregulated in the stressed anti-CD25 Ab-treated group when compared with the non stressed wild-type group. Furthermore, the non stressed anti-CD25 Ab-treated group displayed decreased 5-HT levels within the hippocampus when compared with the non stressed wild-type group. These results suggest that CD4(+)CD25(+) Treg cell depletion modulated alterations in depressive behavior, cytokine and monoaminergic activity. Therefore, controlling CD4(+)CD25(+) Treg cell function during stress may be a potent therapeutic strategy for the treatment of depression-like symptoms

    Effects of CD4<sup>+</sup>CD25<sup>+</sup> Treg cells deficiency on levels of serotonin (5-HT) (A) and its metabolite, 5-HIAA, (B) within the hippocampus (n = 5–8).

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    <p>After the behavioral tests, the prefrontal cortex and hippocampus were dissected from the mice and homogenized. Each supernatant sample was injected into a reversed phase HPLC column. The amounts of monoamines and metabolites were then determined using an electrochemical detector. Data were analyzed using separate one-way ANOVA followed by a <i>post hoc</i> Newman-Keuls test. * <i>p</i><0.05 <i>vs.</i> the non-stressed control group. Vertical bars indicate the S.E.</p

    Anti-CD25 Ab-induced depletion of CD4<sup>+</sup>CD25<sup>+</sup> Treg cells in mice (n = 8–10).

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    <p>Representative dot plots are shown for CD4<sup>+</sup>CD25<sup>+</sup>FOXP3<sup>+</sup> cells. The efficacy of CD4<sup>+</sup>CD25<sup>+</sup> Treg cell depletion was confirmed by flow cytometry analysis using PE-anti-mouse CD25 and fluorescent isothiocyanate- anti-mouse CD4 (A). Summaries of the percentage of positive cells are shown in (B) for CD4<sup>+</sup>CD25<sup>+</sup>FOXP3<sup>+</sup> cells and are presented as the mean ± SE. *** <i>p</i><0.001 <i>vs.</i> the wild-type mice.</p

    Effects of CD4<sup>+</sup>CD25<sup>+</sup> Treg cells deficiency on serum concentrations of the Th1 cytokines IL-2 (A) and IFN-γ (B) (n = 10–12).

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    <p>After the behavior tests, blood samples were collected from the mice by retro-orbital puncture. The serum prepared from each blood sample was then subjected to duplicate measurements for cytokine analysis using the mouse cytometric bead array (CBA). Data were analyzed using separate one-way ANOVA followed by a <i>post hoc</i> Newman-Keuls test. ** <i>p</i><0.01, * <i>p</i><0.05 <i>vs</i>. the stressed anti-CD25 Ab-treated group. Vertical bars indicate the S.E.</p

    Correlation between the durations of immobility in the forced swim test and levels of cytokines and monoamines (B, C).

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    <p>Correlations in immobility are shown in the scatter-plat with IL-6 and TNF-á (<i>Closed circles = </i>IL-6: <i>closed triangles = </i>TNF-á) (A), 5-HT and 5-HIAA (<i>Closed circles = </i>5-HT : <i>closed triangles = </i>5-HIAA) (B) and DA and DOPAC (<i>Closed circles = </i>DA : <i>closed triangles = </i>DOPAC) (C) plotted separately. Data were analyzed using Pearson’s correlation coefficients (2-tailed).There were significant correlation at the level of 0.05 between the stress condition and changes in cytokines (IL-6, r = 0.48 and TNF-á, r = 0.46) and monoamines (5-HT, r = −0.46; 5-HIAA, r = −0.46; DA, r = −0.47) concentrations.</p

    Schedule of experimental procedures.

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    <p>Mice were divided into non-stressed WT mice, stressed WT mice, non-stressed CD4<sup>+</sup>CD25<sup>+</sup> regulatory T (Treg) cells depleted mice, stressed CD4<sup>+</sup>CD25<sup>+</sup> Treg cells depleted mice; from day 1 to 22, the stressed WT mice and stressed CD4<sup>+</sup>CD25<sup>+</sup> Treg cells depleted mice received daily immobilization stress for 4 h and then were moved back to the home cage (three mice to a cage). An anti-CD25 antibody (Ab) was injected intraperitoneally once 24 h before CIS and then on the 8<sup>th</sup> day after the first CIS. On day 22, EPM, FST and TST were conducted in the afternoon (22 day) to determine depression and anxiety related behaviors after the previous day’s morning CIS.</p

    Effects of CD4<sup>+</sup>CD25<sup>+</sup> Treg cells deficiency on the durations of immobility in the forced swim test (n = 14–16).

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    <p>After 21 days of stress, mice were individually placed in a glass cylinder (20 cm diameter ×25 cm high) containing water. During the 6 min test, the duration of immobility was observed and measured. The immobility time was regarded as the time spent by the mouse floating in the water without struggling. Data were analyzed using separate one-way ANOVA followed by a <i>post hoc</i> Newman-Keuls test. ** <i>p</i><0.01 <i>vs.</i> the non-stressed control group. Vertical bars indicate the S.E.</p
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