Effect of quilt thermal resistance on bedding system and sleep thermal comfort.

Ambient temperature and the bedding thermal resistance are two key factors affecting sleepers' thermal comfort. Six duvets with thermal resistance of 3.81, 5.12, 6.19, 7.81, 8.75 and 8.93 clo were included to investigate the effects of duvet thermal resistance on the sleep thermal comfort zone. Six males and six females were enrolled in a whole night sleep experiment, and the ambient temperature of the sleep room was adjusted to be thermally comfortable. Skin temperature, bed climate temperature and sleep stages were all acquired. Subjective evaluations including thermal perception and sleep quality were also assessed through questionnaires. The results indicated that increasing the thermal resistance of duvets widened the thermal comfort zone of ambient temperature, with the highest thermal resistance ranging from 8.2 to 17.7 °C and the lowest from 16.4 to 22.2 °C. The upper and lower temperature limits of the comfort zone did not significantly differ in their effect on sleep quality. The recommended bed climate temperature for comfortable sleep would be in the small range of 30-33 °C, and a good quality of sleep can be guaranteed in the scenario.

Effects of quilts on comfortable indoor temperatures and human thermal responses during sleep.

Quilts play a vital role in the thermal comfort of sleeping people. This study aims to investigate the comfortable indoor temperatures and thermal responses when people sleep in different quilts. The experiment tested three kinds of quilts (down, silk, and polyester), and each kind of quilt involved six filling weights. Sixteen participants (eight males and eight females) conducted whole-night sleeping trials to acquire skin temperatures, bedding temperatures, and thermal perceptual responses. The lower and upper limits of air temperatures ( T lower $$ {T}_{lower} $$ and T upper $$ {T}_{upper} $$ ) for comfortable sleeping were obtained. The results indicated that thermal sensation votes were in the range from 0.1 (close to "neutral") to 1.3 (close to "slightly warm") when participants felt comfortable and preferred "no change" in thermal preference. The corresponding comfortable mean skin and bedding temperatures were 34.6 ~ 35.2°C and 31.2 ~ 32.7°C, respectively. T lower $$ {T}_{lower} $$ and T upper $$ {T}_{upper} $$ had good linear correlations with bedding insulations. For the same bedding insulation, the T lower $$ {T}_{lower} $$ and T upper $$ {T}_{upper} $$ were highest for using silk quilts, followed by down and polyester quilts. The comfort ranges of air temperatures and quilt insulations were finally determined. The findings may benefit understanding the thermal requirement of quilts and help people select and design quilts to achieve thermal comfort.

Correction: Mouse Sirt3 promotes autophagy in AngII-induced myocardial hypertrophy through the deacetylation of FoxO1.

[This corrects the article DOI: 10.18632/oncotarget.13429.].

Left atrial morpho-functional remodeling in atrial fibrillation assessed by three dimensional speckle tracking echocardiography and its value in atrial fibrillation screening.

BACKGROUND: Three dimensional speckle tracking echocardiography (3D STE) is a novel technique combining 3D echocardiography and speckle tracking analysis. 3D STE software dedicated to the left atrium (LA) was recently available. Our study aimed to assess (1) atrial fibrillation (AF) related LA morpho-functional remodeling using 3D STE and (2) value of LA function parameters in identifying paroxysmal AF (PAF). METHODS: One hundred thirty-nine PAF, 109 persistent AF (Per-AF) and 59 non-AF subjects underwent 3D STE. LA phasic volumes and total LA emptying fraction (LAEF) were obtained and used to calculate passive (pLAEF) and active LA emptying fraction (aLAEF) based on atrial contraction. LA longitudinal and circumferential strain representing reservoir (LASr/LASrc), conduit (LAScd/LAScdc) and pump (LASct/LASctc) function were also assessed. RESULTS: 3D STE was found to have good reproducibility. Increase of LA volumes and decrease of parameters representing LA reservoir and pump function were independently associated with AF as well as AF burden. The correlations between LA emptying fraction and LA circumferential strain representing the same function were always stronger than those with LA longitudinal strain (p < 0.001). Minimal LA volume, LAEF, aLAEF, LASrc and LASctc can be used to accurately differentiate PAF from non-AF subjects (AUC > 0.8) with great sensitivity and specificity. CONCLUSIONS: Assessing LA remodeling in AF using 3D STE was feasible. AF and AF burden were independently associated with LA enlargement and impairment of reservoir and pump function but not conduit function. LA function parameters can indicate underlying PAF and thus can guide AF screening strategy.

Salidroside Attenuates Doxorubicin-Induced Cardiac Dysfunction Partially Through Activation of QKI/FoxO1 Pathway.

Doxorubicin (DOX) is an effective chemotherapy. However, its usage has been associated with adverse effects. Salidroside (SAL) is an antioxidative drug, which confers protective effects against several diseases. Salidroside can attenuate cardiac dysfunction induced by DOX. Quaking (QKI) is identified as a protective factor that can inhibit cardiotoxicity medicated by DOX through the regulation of cardiac circular RNA expression. The present study investigated the role of QKI on the protective effect of SAL in the DOX-induced cardiotoxicity model. Results indicated that SAL attenuated DOX-induced adverse effects, including cardiac dysfunction, weight loss, and reactive oxygen species (ROS) production, and decreased the expression of BAX, caspase 3, and FoxO1. Also, it increased the Mn-SOD2 and QKI expression in vivo and in vitro. Furthermore, QKI knockdown suppressed anti-cardiotoxicity mediated by SAL. In conclusion, the results of the current study show that salidroside attenuates doxorubicin-induced cardiac dysfunction through activation of QKI/FoxO1 pathway.

SIRT3 Ablation Deteriorates Obesity-Related Cardiac Remodeling by Modulating ROS-NF-κB-MCP-1 Signaling Pathway.

Obesity and the associated complications are a major public health issue as obesity incidence increases yearly, worldwide. Effects of obesity on heart failure have been reported previously. Obesity-related cardiac remodeling includes structural and functional dysfunctions, in which cardiac inflammation and fibrosis play a key role. The main mitochondrial deacetylase, SIRT3 participates in numerous cellular processes; however, its role in obesity-related cardiac remodeling remains unclear. In our study, high-fat diet (HFD) feeding induced downregulation of SIRT3 protein level in mice. SIRT3-KO mice fed on HFD exhibited higher cardiac dysfunction and cardiac remodeling compared with the wild-type controls. Further study revealed increases in collagen accumulation and inflammatory cytokine expression including MCP-1, IL-6, TGF-ß, TNF-α in mice fed on HFD compared with chow diet, with higher levels observed in SIRT3-KO mice. Furthermore, significantly high levels of cardiac MCP-1 expression and macrophage infiltration, and ROS generation and activated NF-κB were observed in HFD-fed SIRT3-KO mice. We presumed that SIRT3 ablation-mediated MCP-1 upregulation is attributed to ROS-NF-κB activation. Thus, we concluded that SIRT3 prevents obesity-related cardiac remodeling by attenuating cardiac inflammation and fibrosis, through modulation of ROS-NF-κB-MCP-1 pathway.

Inhibition of TRPA1 Promotes Cardiac Repair in Mice After Myocardial Infarction.

Recent studies have shown that TRPA1, a nonselective cation channel with high permeability to calcium, is expressed in many tissues of the cardiovascular system and is involved in the pathogenesis of many cardiovascular diseases. However, the role of TRPA1 in cardiac repair after myocardial infarction (MI) has not been clearly defined. The aim of this study was to confirm whether inhibition of TRPA1 could attenuate MI-induced cardiac ischemia injury. The C57BL/6 mice were subjected to ligation of the left anterior descending coronary artery and treated with TRPA1-specific inhibitor HC-030031 (HC) for 4 weeks. Echocardiography was performed to assess cardiac function. The results showed that HC significantly attenuated MI-induced cardiac dysfunction 4 weeks after MI. Similarly, HC reduced cardiac fibrosis and cell apoptosis after MI and significantly increased angiogenesis in the border zone of the infarct. In vitro, we found that HC promoted the proliferation and migration of human umbilical vein endothelial cells (HUVECs). Importantly, HC treatment decreased phosphatase and tensin homolog expression and augmented the expression of phosphorylated Akt in the myocardium post MI and HUVECs. However, treatment of HUVECs with a PI3K inhibitor, LY294002, before HC administration almost completely abolished HC-induced migration in HUVECs. In conclusion, we demonstrate that the inhibition of TRPA1 promotes angiogenesis after MI, thereby alleviating myocardial ischemia injury via mechanisms involving inhibition of phosphatase and tensin homolog expression and subsequent activation of the PI3K/Akt signaling.

Salidroside prevents tumor necrosis factor-α-induced vascular inflammation by blocking mitogen-activated protein kinase and NF-κB signaling activation.

Vascular inflammation is a key factor in the pathogenesis of atherosclerosis. Salidroside is an important active ingredient extracted from the root of the Rhodiola rosea plant, which has been reported to have antioxidative, anti-cancer, neuroprotective and cardioprotective effects. However, the effects of salidroside on vascular inflammation have not been clarified. The purpose of the present study was to investigate the protective effects of salidroside against tumor necrosis factor (TNF)-α-induced vascular inflammation in cardiac microvascular endothelial cells (CMECs), a specific cell type derived from coronary micro-vessels. Over a 24-h period, salidroside did not exert any significant cytotoxicity up to a dose of 100 µM. Additionally, salidroside decreased the expression levels of the cell adhesion molecule vascular cell adhesion molecule-1 (VCAM-1) in TNF-α-stimulated CMECs, thus suppressing monocyte-to-CMEC adhesion. Salidroside also decreased the production of inflammatory cytokines such as interleukin (IL)-1ß, IL-6 and monocyte chemotactic protein 1 (MCP-1) in TNF-α-induced CMECs, as well as suppressing TNF-α-activated mitogen-activated protein kinase (MAPK) and NF-κB activation. Since MAPKs and NF-κB both serve notable roles in regulating the expression of VCAM-1, IL-1ß, IL-6 and MCP-1, the present study provided a preliminary understanding of the mechanism underlying the protective effects of salidroside. Overall, salidroside alleviated vascular inflammation by mediating MAPK and NF-κB activation in TNF-α-induced CMECs. These results indicated that salidroside may have potential applications as a therapeutic agent against vascular inflammation and atherosclerosis.

miR-221-3p inhibits oxidized low-density lipoprotein induced oxidative stress and apoptosis via targeting a disintegrin and metalloprotease-22.

Oxidized low-density lipoprotein (ox-LDL)-induced oxidative stress and apoptosis are considered as a critical contributor to atherosclerosis. MicroRNAs (miRNAs) have been reported versatile functions in all biological processes via directly suppressing target messenger RNA at a posttranscriptional level. Although miRNA-221 has been implied to be involved in the regulation of atherosclerosis, the underlying mechanism remains unclear. Here, we showed that ox-LDL treatment remarkably suppressed the expression of miR-221-3p in a concentration-dependent and time-dependent manner. Transfection of miR-221-3p mimic significantly reduced the foam cell formation and expression of lipid biomarkers, while transfection of the miR-221-3p inhibitor showed completely opposite effects. Moreover, miR-221-3p was also found to inhibit the process of cell apoptosis in macrophages. A disintegrin and metalloprotease-22 (ADAM22) is predicted as a direct target of miR-221-3p, and silencing AMAM22 resulted in a reduced foam cell formation and cell apoptosis. Furthermore, silencing AMAM22 restored the stimulatory effect of the miR-221-3p inhibitor in ox-LDL-induced foam cell formation and apoptosis. These findings suggest that miR-221-3p inhibits ox-LDL and apoptosis via directly targeting ADAM22.

SIRT3 inhibits Ang II-induced transdifferentiation of cardiac fibroblasts through ß-catenin/PPAR-γ signaling.

AIMS: Cardiac fibrosis is an inevitable process of numerous cardiovascular diseases in which the transdifferentiation of cardiac fibroblasts plays a pivotal role. Sirtuin3 (SIRT3) has been believed to protect against cardiac fibrosis. However, the mechanism underlying this beneficial effect has not yet been elucidated. In this study, we investigated the potential mechanism of SIRT3 on the inhibition of fibroblast-to-myoblast transdifferentiation. MAIN METHODS: Cells were stimulated by angiotension II (Ang II) with SIRT3 overexpression or knockdown. Also, PPARγ agonist (Pioglitazone PIO) and inhibitor (GW9662) were used to confirm the antifibrotic effect of PPARγ. Western blot, qRT-PCR, CCK-8 and immunofluorescence staining analysis were used for investigation. KEY FINDINGS: Our data demonstrated that overexpression of SIRT3 prevented the transdifferentiation of CFs while SIRT3 knockdown promoted the process. Simultaneously, SIRT3 overexpression increased total PPARγ expression and suppressed the acetylated PPARγ. Besides, pretreatment with PPARγ agonist, pioglitazone protected CFs from transdifferentiation while PPARγ inhibitor prevented the protective effect of SIRT3. In addition, we have found that SIRT3 upregulated the expression of PPARγ by degeration of ß-catenin. SIGNIFICANCE: Our findings indicate that this newly identified SIRT3/ß-catenin/PPAR-γ axis will provide novel insight into the understanding of the mechanism of transdifferentiation of CFs to myofibroblasts.

SIRT3 attenuates AngII-induced cardiac fibrosis by inhibiting myofibroblasts transdifferentiation via STAT3-NFATc2 pathway.

Cardiac fibrosis is a maladaptive response to various stresses, characterized by increased interstitial collagen deposition and progressive cardiac dysfunction. The transdifferentiation of fibroblasts into myofibroblasts is an essential process in the pathogenesis of cardiac fibrosis. SIRT3, as a mitochondrial NAD+-dependent histone deacetylase, has been demonstrated beneficial in many cardiovascular diseases. However, the specific mechanism of its protective role in cardiac fibrosis needs to be elucidated further. Here, we determined the role of SIRT3 in cardiac fibrosis by subjecting Sirt3-knockout mice to chronic AngII infusion for four weeks in vivo. In this study, the Sirt3-knockout mice developed more serious cardiac fibrosis compared to wild-type controls. In vitro, primary cardiac fibroblasts from Sirt3-knockout mice transdifferentiated into myofibroblasts spontaneously and this phenotype conversion exaggerated after AngII stimulation. The SIRT3-KO myofibroblasts secret more fibrotic mediators including TGF-ß to promote cardiac fibrosis. In addition, the overexpression of SIRT3 by lentivirus transfection attenuated myofibroblasts transdifferentiation. We further demonstrated that SIRT3 directly binds to and deacetylates STAT3 to inhibit its activity. Sequentially the downstream factor, known as NFATc2, showed a reduced expression. Taken together, these results revealed that SIRT3 can protect against cardiac fibrosis by inhibiting myofibroblasts transdifferentiation via the STAT3-NFATc2 signaling pathway.

Mouse Sirt3 promotes autophagy in AngII-induced myocardial hypertrophy through the deacetylation of FoxO1.

Sirt3, a mitochondrial NAD+-dependent histone deacetylase, is the only member proven to promote longevity in mammalian Sirtuin family. The processed short form of Sirt3 has been demonstrated to target many mediators of energy metabolism and mitochondrial stress adaptive program. Autophagy serves as a dynamic recycling mechanism and provides energy or metabolic substrates. Among the mechanisms triggered by cardiac stress, opinions vary as to whether autophagy is a protective or detrimental response. Here, by inducing the Sirt3-knockout mice to myocardial hypertrophy with chronic angiotensin II infusion for four weeks, we determined the role of Sirt3 in myocardial hypertrophy and autophagy. In this study, the Sirt3-knockout mice developed deteriorated cardiac function and impaired autophagy compared to wild-type mice. What's more, the overexpression of Sirt3 by lentivirus transfection attenuated cardiomyocytes hypertrophy by promoting autophagy. We further demonstrated that Sirt3 could bind to FoxO1 and activate its deacetylation. Sequentially, deacetylated FoxO1 translocates to the nucleus where it facilitates downstream E3 ubiquitin ligases such as Muscle RING Finger 1 (MuRF1) and muscle atrophy F-box (MAFbx, Atrogin1). Altogether, these results revealed that Sirt3 activation is essential to improve autophagy flux by reducing the acetylation modification on FoxO1, which in turn alleviates myocardial hypertrophy.