Influence of Social and Behavioural Characteristics of Users on Their Evaluation of Subjective Loudness and Acoustic Comfort in Shopping Malls

A large-scale subjective survey was conducted in six shopping malls in Harbin City, China, to determine the influence of social and behavioural characteristics of users on their evaluation of subjective loudness and acoustic comfort. The analysis of social characteristics shows that evaluation of subjective loudness is influenced by income and occupation, with correlation coefficients or contingency coefficients of 0.10 to 0.40 (p<0.05 or p<0.01). Meanwhile, evaluation of acoustic comfort evaluation is influenced by income, education level, and occupation, with correlation coefficients or contingency coefficients of 0.10 to 0.60 (p<0.05 or p<0.01). The effect of gender and age on evaluation of subjective loudness and acoustic comfort is statistically insignificant. The effects of occupation are mainly caused by the differences in income and education level, in which the effects of income are greater than that of education level. In terms of behavioural characteristics, evaluation of subjective loudness is influenced by the reason for visit, frequency of visit, and length of stay, with correlation coefficients or contingency coefficients of 0.10 to 0.40 (p<0.05 or p<0.01). Evaluation of acoustic comfort is influenced by the reason for visit to the site, the frequency of visit, length of stay, and also season of visit, with correlation coefficients of 0.10 to 0.30 (p<0.05 or p<0.01). In particular, users who are waiting for someone show lower evaluation of acoustic comfort, whereas users who go to shopping malls more than once a month show higher evaluation of acoustic comfort. On the contrary, the influence of the period of visit and the accompanying persons are found insignificant

Application of functionalized nanofluid in thermosyphon

A water-based functionalized nanofluid was made by surface functionalizing the ordinary silica nanoparticles. The functionalized nanofluid can keep long-term stability. and no sedimentation was observed. The functionalized nanofluid as the working fluid is applied in a thermosyphon to understand the effect of this special nanofluid on the thermal performance of the thermosyphon. The experiment was carried out under steady operating pressures. The same work was also explored for traditional nanofluid (consisting of water and the same silica nanoparticles without functionalization) for comparison. Results indicate that a porous deposition layer exists on the heated surface of the evaporator during the operating process using traditional nanofluid; however, no coating layer exists for functionalized nanofluid. Functionalized nanofluid can enhance the evaporating heat transfer coefficient, while it has generally no effect on the maximum heat flux. Traditional nanofluid deteriorates the evaporating heat transfer coefficient but enhances the maximum heat flux. The existence of the deposition layer affects mainly the thermal performance, and no meaningful nanofluid effect is found in the present study

5-HTR3 and 5-HTR4 located on the mitochondrial membrane and functionally regulated mitochondrial functions

5-HT has been reported to possess significant effects on cardiac activities, but activation of 5-HTR on the cell membrane failed to illustrate the controversial cardiac reaction. Because 5-HT constantly comes across the cell membrane via 5-HT transporter (5-HTT) into the cytoplasm, whether 5-HTR is functional present on the cellular organelles is unknown. Here we show 5-HTR3 and 5-HTR4 were located in cardiac mitochondria, and regulated mitochondrial activities and cellular functions. Knock down 5-HTR3 and 5-HTR4 in neonatal cardiomyocytes resulted in significant increase of cell damage in response to hypoxia, and also led to alternation in heart beating. Activation of 5-HTR4 attenuated mitochondrial Ca2+ uptake under the both normoxic and hypoxic conditions, whereas 5-HTR3 augmented Ca2+ uptake only under hypoxia. 5-HTR3 and 5-HTR4 exerted the opposite effects on the mitochondrial respiration: 5-HTR3 increased RCR (respiration control ratio), but 5-HTR4 reduced RCR. Moreover, activation of 5-HTR3 and 5-HTR4 both significantly inhibited the opening of mPTP. Our results provided the first evidence that 5-HTR as a GPCR and an ion channel, functionally expressed in mitochondria and participated in the mitochondria function and regulation to maintain homeostasis of mitochondrial [Ca2+], ROS, and ATP generation efficiency in cardiomyocytes in response to stress and O2 tension

A compare between myocardial topical negative pressure levels of -25 mmHg and -50 mmHg in a porcine model

<p>Abstract</p> <p>Background</p> <p>Topical negative pressure (TNP), widely used in wound therapy, is known to stimulate wound edge blood flow, granulation tissue formation, angiogenesis, and revascularization. We have previously shown that application of a TNP of -50 mmHg to the myocardium significantly increases microvascular blood flow in the underlying tissue. We have also shown that a myocardial TNP levels between -75 mmHg and -150 mmHg do not induce microvascular blood flow changes in the underlying myocardium. The present study was designed to elucidate the difference between -25 mmHg and -50 mmHg TNP on microvascular flow in normal and ischemic myocardium.</p> <p>Methods</p> <p>Six pigs underwent median sternotomy. The microvascular blood flow in the myocardium was recorded before and after the application of TNP using laser Doppler flowmetry. Analyses were performed before left anterior descending artery (LAD) occlusion (normal myocardium), and after 20 minutes of LAD occlusion (ischemic myocardium).</p> <p>Results</p> <p>A TNP of -25 mmHg significantly increased microvascular blood flow in both normal (from 263.3 ± 62.8 PU before, to 380.0 ± 80.6 PU after TNP application, * <it>p </it>= 0.03) and ischemic myocardium (from 58.8 ± 17.7 PU before, to 85.8 ± 20.9 PU after TNP application, * <it>p </it>= 0.04). A TNP of -50 mmHg also significantly increased microvascular blood flow in both normal (from 174.2 ± 20.8 PU before, to 240.0 ± 34.4 PU after TNP application, * <it>p </it>= 0.02) and ischemic myocardium (from 44.5 ± 14.0 PU before, to 106.2 ± 26.6 PU after TNP application, ** <it>p </it>= 0.01).</p> <p>Conclusion</p> <p>Topical negative pressure of -25 mmHg and -50 mmHg both induced a significant increase in microvascular blood flow in normal and in ischemic myocardium. The increase in microvascular blood flow was larger when using -25 mmHg on normal myocardium, and was larger when using -50 mmHg on ischemic myocardium; however these differences were not statistically significant.</p

Sp1 Is Essential for p16(INK4a) Expression in Human Diploid Fibroblasts during Senescence

BACKGROUND: p16 (INK4a) tumor suppressor protein has been widely proposed to mediate entrance of the cells into the senescent stage. Promoter of p16 (INK4a) gene contains at least five putative GC boxes, named GC-I to V, respectively. Our previous data showed that a potential Sp1 binding site, within the promoter region from −466 to −451, acts as a positive transcription regulatory element. These results led us to examine how Sp1 and/or Sp3 act on these GC boxes during aging in cultured human diploid fibroblasts. METHODOLOGY/PRINCIPAL FINDINGS: Mutagenesis studies revealed that GC-I, II and IV, especially GC-II, are essential for p16 (INK4a) gene expression in senescent cells. Electrophoretic mobility shift assays (EMSA) and ChIP assays demonstrated that both Sp1 and Sp3 bind to these elements and the binding activity is enhanced in senescent cells. Ectopic overexpression of Sp1, but not Sp3, induced the transcription of p16 (INK4a). Both Sp1 RNAi and Mithramycin, a DNA intercalating agent that interferes with Sp1 and Sp3 binding activities, reduced p16 (INK4a) gene expression. In addition, the enhanced binding of Sp1 to p16 (INK4a) promoter during cellular senescence appeared to be the result of increased Sp1 binding affinity, not an alteration in Sp1 protein level. CONCLUSIONS/SIGNIFICANCE: All these results suggest that GC- II is the key site for Sp1 binding and increase of Sp1 binding activity rather than protein levels contributes to the induction of p16 (INK4a) expression during cell aging

GW501516, a PPARδ Agonist, Ameliorates Tubulointerstitial Inflammation in Proteinuric Kidney Disease via Inhibition of TAK1-NFκB Pathway in Mice

Peroxisome proliferator-activated receptors (PPARs) are a nuclear receptor family of ligand-inducible transcription factors, which have three different isoforms: PPARα, δ and γ. It has been demonstrated that PPARα and γ agonists have renoprotective effects in proteinuric kidney diseases; however, the role of PPARδ agonists in kidney diseases remains unclear. Thus, we examined the renoprotective effect of GW501516, a PPARδ agonist, in a protein-overload mouse nephropathy model and identified its molecular mechanism. Mice fed with a control diet or GW501516-containing diet were intraperitoneally injected with free fatty acid (FFA)-bound albumin or PBS(−). In the control group, protein overload caused tubular damages, macrophage infiltration and increased mRNA expression of MCP-1 and TNFα. These effects were prevented by GW501516 treatment. In proteinuric kidney diseases, excess exposure of proximal tubular cells to albumin, FFA bound to albumin or cytokines such as TNFα is detrimental. In vitro studies using cultured proximal tubular cells showed that GW501516 attenuated both TNFα- and FFA (palmitate)-induced, but not albumin-induced, MCP-1 expression via direct inhibition of the TGF-β activated kinase 1 (TAK1)-NFκB pathway, a common downstream signaling pathway to TNFα receptor and toll-like receptor-4. In conclusion, we demonstrate that GW501516 has an anti-inflammatory effect in renal tubular cells and may serve as a therapeutic candidate to attenuate tubulointerstitial lesions in proteinuric kidney diseases

<em>Enterococcus faecalis</em> Infection Causes Inflammation, Intracellular Oxphos-Independent ROS Production, and DNA Damage in Human Gastric Cancer Cells

Background: Achlorhydria caused by e.g. atrophic gastritis allows for bacterial overgrowth, which induces chronic inflammation and damage to the mucosal cells of infected individuals driving gastric malignancies and cancer. Enterococcus faecalis (E. faecalis) can colonize achlohydric stomachs and we therefore wanted to study the impact of E. faecalis infection on inflammatory response, reactive oxygen species (ROS) formation, mitochondrial respiration, and mitochondrial genetic stability in gastric mucosal cells. Methods: To separate the changes induced by bacteria from those of the inflammatory cells we established an in vitro E. faecalis infection model system using the gastric carcinoma cell line MKN74. Total ROS and superoxide was measured by fluorescence microscopy. Cellular oxygen consumption was characterized non-invasively using XF24 microplate based respirometry. Gene expression was examined by microarray, and response pathways were identified by Gene Set Analysis (GSA). Selected gene transcripts were verified by quantitative real-time polymerase chain reaction (qRT-PCR). Mitochondrial mutations were determined by sequencing. Results: Infection of MKN74 cells with E. faecalis induced intracellular ROS production through a pathway independent of oxidative phosphorylation (oxphos). Furthermore, E. faecalis infection induced mitochondrial DNA instability. Following infection, genes coding for inflammatory response proteins were transcriptionally up-regulated while DNA damage repair and cell cycle control genes were down-regulated. Cell growth slowed down when infected with viable E. faecalis and responded in a dose dependent manner to E. faecalis lysate. Conclusions: Infection by E. faecalis induced an oxphos-independent intracellular ROS response and damaged the mitochondrial genome in gastric cell culture. Finally the bacteria induced an NF-kappa B inflammatory response as well as impaired DNA damage response and cell cycle control gene expression