Experimental Study on Energy-Free Superhydrophobic Radiative Cooling Versatile Film with Enhanced Environmental Tolerance.

Clean, energy-free methods of cooling are an effective way to respond to the global energy crisis. To date, cooling materials using passive daytime radiative cooling (RC) technology have been applied in the fields of energy-efficient buildings, solar photovoltaic cooling, and insulating textiles. However, RC materials frequently suffer from comprehensive damage to their microstructure, resulting in the loss of their initial cooling effect in complex outdoor environments. Here, a superhydrophobic daytime passive RC porous film with environmental tolerance (SRCP film) was fabricated, which integrated strong solar reflectivity (approximately 90%), mid-infrared emissivity (approximately 0.97), and superhydrophobicity (water contact angle (WCA) of 160° and sliding angle of 3°). This study revealed that SRCP film had an average reflectivity of 14.3% higher than SiO2 particles in the 0.3-2.5 µm wavelength region, achieving a cooling effect of 13.2 °C in ambient conditions with a solar irradiance of 946 W·m-2 and a relative humidity of 74% due to the synergistic effect of effective solar reflection and thermal infrared emission. In addition, empirical results showed that the attained films possessed outstanding environmental tolerance, maintaining high WCA (156°), stable cooling effect (8.3 °C), and low SiO2 loss (less than 5.1%) after 30 consecutive days of UV irradiation and 14 days of corrosion with acidic and alkaline solutions. More importantly, this work could be flexibly prepared by various methods without the use of any fluorine-containing reagents, which greatly widens the practical application scope.

A deep-learning pipeline for the diagnosis and discrimination of viral, non-viral and COVID-19 pneumonia from chest X-ray images.

Common lung diseases are first diagnosed using chest X-rays. Here, we show that a fully automated deep-learning pipeline for the standardization of chest X-ray images, for the visualization of lesions and for disease diagnosis can identify viral pneumonia caused by coronavirus disease 2019 (COVID-19) and assess its severity, and can also discriminate between viral pneumonia caused by COVID-19 and other types of pneumonia. The deep-learning system was developed using a heterogeneous multicentre dataset of 145,202 images, and tested retrospectively and prospectively with thousands of additional images across four patient cohorts and multiple countries. The system generalized across settings, discriminating between viral pneumonia, other types of pneumonia and the absence of disease with areas under the receiver operating characteristic curve (AUCs) of 0.94-0.98; between severe and non-severe COVID-19 with an AUC of 0.87; and between COVID-19 pneumonia and other viral or non-viral pneumonia with AUCs of 0.87-0.97. In an independent set of 440 chest X-rays, the system performed comparably to senior radiologists and improved the performance of junior radiologists. Automated deep-learning systems for the assessment of pneumonia could facilitate early intervention and provide support for clinical decision-making.

Dependence of Photothermal Conversion Characteristics on Different Nanoparticle Dispersions.

The efficiency of nanoparticle-based direct absorption solar collector (DASC) is strongly dependent on the materials, where a systematic study is still lacking. This work conducts an experimental study of the photothermal conversion characteristics of a number of nanoparticle dispersions including Au, Si, Fe3O4, Al2O3 and diamond under the same experimental setup. The results show that comparing with the base fluid, the introduction of nanoparticles can increase the photothermal conversion efficiency significantly, and the efficiency increases in the order of Al2O3, diamond, (Fe3O4 and Si) and Au. For a given total mass concentration, the Fe3O4-Au hybrid nanofluid is found to possess a higher efficiency than that of pure Au alone. Three possible mechanisms are proposed for the influence of nanoparticle materials, which can qualitatively explain the experimental results.

EEG biofeedback improves attentional bias in high trait anxiety individuals.

BACKGROUND: Emotion-related attentional bias is implicated in the aetiology and maintenance of anxiety disorders. Electroencephalogram (EEG) biofeedback can obviously improve the anxiety disorders and reduce stress level, and can also enhance attention performance in healthy subjects. The present study examined the effects and mechanisms of EEG biofeedback training on the attentional bias of high trait anxiety (HTA) individuals toward negative stimuli. RESULTS: Event-related potentials were recorded while HTA (n=24) and nonanxious (n=21) individuals performed the color-word emotional Stroop task. During the emotional Stroop task, HTA participants showed longer reaction times and P300 latencies induced by negative words, compared to nonanxious participants.The EEG biofeedback significantly decreased the trait anxiety inventory score and reaction time in naming the color of negative words in the HTA group. P300 latencies evoked by negative stimuli in the EEG biofeedback group were significantly reduced after the alpha training, while no significant changes were observed in the sham biofeedback group after the intervention. CONCLUSION: The prolonged P300 latency is associated with attentional bias to negative stimuli in the HTA group. EEG biofeedback training demonstrated a significant improvement of negative emotional attentional bias in HTA individuals, which may be due to the normalization of P300 latency.

Involvement of MAPK/NF-κB signaling in the activation of the cholinergic anti-inflammatory pathway in experimental colitis by chronic vagus nerve stimulation.

BACKGROUND: Autonomic nervous system dysfunction is implicated in the etiopathogenesis of inflammatory bowel diseases (IBD). Therapies that increase cardiovagal activity, such as Mind-Body interventions, are currently confirmed to be effective in clinical trials in IBD. However, a poor understanding of pathophysiological mechanisms limits the popularization of therapies in clinical practice. The aim of the present study was to explore the mechanisms of these therapies against 2,4,6-trinitrobenzenesulfonic acid (TNBS)-induced colitis in rats using a chronic vagus nerve stimulation model in vivo, as well as the lipopolysaccharide (LPS)-induced inflammatory response in human epithelial colorectal adenocarcinoma cells (Caco-2) by acetylcholine in vitro. METHODS AND RESULTS: Colitis was induced in rats with rectal instillation of TNBS, and the effect of chronic VNS (0.25 mA, 20 Hz, 500 ms) on colonic inflammation was evaluated. Inflammatory responses were assessed by disease activity index (DAI), histological scores, myeloperoxidase (MPO) activity, inducible nitric oxide synthase (iNOS), TNF-α and IL-6 production. The expression of Mitogen-activated protein kinases (MAPK) family members, IκB-α, and nuclear NF-κB p65 were studied by immunoblotting. Heart rate variability (HRV) analysis was also applied to assess the sympathetic-vagal balance. DAI, histological scores, MPO activity, iNOS, TNF-α and IL-6 levels were significantly decreased by chronic VNS. Moreover, both VNS and acetylcholine reduced the phosphorylation of MAPKs and prevented the nuclear translocation of NF-κB p65. Methyllycaconitine (MLA) only reversed the inhibitory effect on p-ERK and intranuclear NF-κB p65 expression by ACh in vitro, no significant change was observed in the expression of p-p38 MAPK or p-JNK by MLA. CONCLUSION: Vagal activity modification contributes to the beneficial effects of the cholinergic anti-inflammatory pathway in IBD-related inflamed colonic mucosa based on the activation of MAPKs and nuclear translocation of NF-κB. Our work may provide key pathophysiological mechanistic evidence for novel therapeutic strategies that increase the cardiovagal activity in IBD patients.

Estrogen improved metabolic syndrome through down-regulation of VEGF and HIF-1α to inhibit hypoxia of periaortic and intra-abdominal fat in ovariectomized female rats.

Metabolic syndrome (MBS), a cluster of metabolic abnormalities and visceral fat accumulation, increases cardiovascular risks in postmenopausal women. In addition to visceral fat, perivascular adipose tissue has been recently found to play an important role in vascular pathophysiology. Hence, the present study investigates the effects of estrogen on both intra-abdominal fat (visceral fat) and periaortic fat (perivascular fat) accumulation as well as hypoxia in ovariectomized female rats. Female rats were divided into sham operation, ovariectomy and ovariectomy with 17ß-estradiol supplementation groups. Twelve weeks later, we found that estrogen improved MBS via reducing body weight gain, the weight of periaortic and intra-abdominal fat, hepatic triglyceride, and total serum cholesterol levels. Estrogen also increased insulin sensitivity through restoring glucose and serum leptin levels. For periaortic fat, western blot showed estrogen inhibited hypoxia by reducing the levels of VEGF and HIF-1α, which is consistent with the results from immunohistochemical staining. The correlation analysis indicated that perivascular fat had a positive correlation with body weight, intra-abdominal fat or serum total cholesterol, but a negative correlation with insulin sensitivity index. For intra-abdominal fat, real-time fluorescent RT-PCR showed estrogen improved fat dysfunction via reducing the levels of relative leptin, MCP-1 but increasing adiponectin mRNA. Estrogen reduced the levels of VEGF and HIF-1α to inhibit hypoxia but restored the levels of PPARγ and Srebp-1c, which are important for lipid capacity function of intra-abdominal fat. These results demonstrated estrogen improved MBS through down-regulating VEGF and HIF-1α to inhibit hypoxia of periaortic and intra-abdominal fat in ovariectomized female rats.

Heart rate variability biofeedback decreases blood pressure in prehypertensive subjects by improving autonomic function and baroreflex.

BACKGROUND: Individuals with prehypertension are at risk of hypertension and cardiovascular diseases, and yet efficient interventions are lagging behind. Studies indicate that heart rate variability-biofeedback (HRV-BF) increases HRV and baroreflex sensitivity (BRS) as well as reduces related pathological symptoms, suggesting potentially beneficial effects of HRV-BF on prehypertension, but little is known about these effects. In this study, these effects were investigated and their mechanisms were explored. OBJECTIVES: The effect of HRV-BF on prehypertension in young adults and its potential mechanism were explored. DESIGN: Forty-three (43) individuals with prehypertension were recruited and classified into three categories: HRV-BF group, slow abdominal breathing group, and control group. All groups were assessed with measurements of noninvasive blood pressure (BP), BRS, respiration, and galvanic skin response (GSR) at pre-intervention, in the entire process of each session, at postintervention, as well as at a 3-month follow-up. INTERVENTIONS: Subjects participated in a 10-session HRV-BF protocol or simple slow abdominal breathing protocol conducted over 5 weeks. A 3-month follow-up was also performed on these individuals. RESULTS: The incidence of prehypertension was as high as 14.5% in young college students. Individuals with prehypertension were lower in BRS (7.5±5.2 ms/mm Hg) and HRV (log10-transformed of the standard deviation of normal-to-normal beats [SDNN]=1.62±0.13 ms, lgTotal power of spectral density in the range of frequencies between 0 and 0.4Hz (TP)=8.02±0.55 ms2) than those with normal blood pressure (BRS=18.4±7.4 ms/mm Hg, lgSDNN=1.79±0.10 ms, lgTP=8.68±0.85 ms2). HRV-BF reduced blood pressure (from 131.7±8.7/79.3±4.7 mm Hg to 118.9±7.3 mm Hg/71.9±4.9 mm Hg, p<0.01), increased BRS (from 7.0±5.9 ms/mm Hg to 15.8±5.3 ms/mm Hg, p<0.01) and increased HRV (lgSDNN from 1.61±0.11 to 1.75±0.05 ms, and lgTP from 8.07±0.54 to 9.08±0.41 ms2, p<0.01). These effects were more obvious than those of the slow-breathing group, and remained for at least 3 months. HRV-BF also significantly increased vagus-associated HRV indices and decreased GSR (indices of sympathetic tone). CONCLUSIONS: These effects suggest that HRV-BF, a novel behavioral neurocardiac intervention, could enhance BRS, improve the cardiac autonomic tone, and facilitate BP adjustment for individuals with prehypertension.

E2-BSA activates caveolin-1 via PI3K/ERK1/2 and lysosomal degradation pathway and contributes to EPC proliferation.

BACKGROUND: The mechanism that estrogen (E(2)) increases the number of endothelial progenitor cells (EPC) is largely unknown. Here we used E(2)-conjugated bovine serum albumin (E(2)-BSA, membrane impermeable) to investigate whether the membrane estrogen receptor (mER) and its related protein caveolin-1 (CAV-1) are involved in these processes. METHODS AND RESULTS: E(2)-BSA promoted [(3)H]-thymidine incorporation of EPC through increasing CAV-1 expression via mER (ERα, but not ERß or GPR30). Both cholesterol depletion and CAV-1 knockdown with use of CAV-1 siRNA significantly attenuated E(2)-BSA-induced [(3)H]-thymidine incorporation. Western blot showed that E(2)-BSA increased membrane CAV-1 protein expression 12h after treatment, whereas mRNA levels of CAV-1 were augmented until 24h after E(2)-BSA treatment. Furthermore, pre-incubated EPC with ICI 182780 (a specific ER antagonist), LY 294002 (a selective PI(3)K inhibitor) or PD 98059 (a specific ERK1/2 inhibitor) before E(2)-BSA inhibited the late-stage effect of E(2)-BSA (≥24 h) on up-regulation of CAV-1 mRNA and protein expression. Pulse chase results demonstrated that E(2)-BSA inhibited lysosome-mediated degradation of CAV-1 protein at the early stage (≤12 h), and then resulted in the increased CAV-1 protein. CONCLUSION: In the present work we demonstrated that E(2)-BSA promotes EPC proliferation through mER (ERα) in CAV-1-dependent manner: prolonging the stability of CAV-1 protein through quick inhibition of the lysosomal degradation pathway at the early stage (≤12 h) and up-regulating CAV-1 at transcription levels through PI(3)K/ERK1/2 signaling pathway at the late stage (≥24 h). These data indicated that a there is a novel mechanism of E(2)-BSA in the regulation of EPC proliferation through CAV-1.

Effect of slow abdominal breathing combined with biofeedback on blood pressure and heart rate variability in prehypertension.

OBJECTIVE: Prehypertension is a new category designated by the Seventh Report of the Joint National Committee on Prevention, Detection, Evaluation, and Treatment of High Blood Pressure (JNC7) in 2003. Managing prehypertension with nonpharmacological intervention is possibly beneficial to the prevention of hypertension. In this study, we observed the effect of slow abdominal breathing combined with electromyographic (EMG) biofeedback training on blood pressure (BP) in prehypertensives and assessed the changes of heart rate variability (HRV) in order to find an optional intervention to prevent hypertension and acquire some experimental data to clarify the underlying neural mechanism. METHODS: Twenty-two (22) postmenopausal women with prehypertension were randomly assigned to either the experiment group or the control group. The experiment group performed 10 sessions of slow abdominal breathing (six cycles/min) combined with frontal electromyographic (EMG) biofeedback training and daily home practice, while the control group only performed slow abdominal breathing and daily home practice. BP and HRV (including R-R interval and standard deviation of the normal-normal intervals [SDNN]) were measured. RESULTS: Participants with prehypertension could lower their systolic blood pressure (SBP) 8.4 mm Hg (p < 0.001) and diastolic blood pressure (DBP) 3.9 mm Hg (p < 0.05) using slow abdominal breathing combined with EMG biofeedback. The slow abdominal breathing also significantly decreased the SBP 4.3 mm Hg (p < 0.05), while it had no effect on the DBP (p > 0.05). Repeated-measures analyses showed that the biofeedback group + abdominal respiratory group (AB+BF) training was more effective in lowering the BP than the slow breathing (p < 0.05). Compared with the control group, the R-R interval increased significantly during the training in the AB+BF group (p < 0.05). The SDNN increased remarkably in both groups during the training (p < 0.05). CONCLUSIONS: Slow abdominal breathing combined with EMG biofeedback is an effective intervention to manage prehypertension. The possible mechanism is that slow abdominal breathing combined with EMG biofeedback could reduce sympathetic activity and meanwhile could enhance vagal activity.

The role of caveolin1 and sprouty1 in genistein's regulation of vascular smooth muscle cell and endothelial cell proliferation.

Genistein prevents atherosclerosis by exerting protective effects on blood vessels. The aim of this study is to investigate the role of caveolin1 and sprouty1 in the regulation of proliferation of vascular smooth muscle cell (VSMC) and endothelial cell by genistein. Using thiazolyl blue tetrazolium bromide(MTT) and [3H]-TdR assay, we found genistein inhibited angiotensin II-induced proliferation in primary cultured VSMC while it stimulated proliferation of quiescent endothelial cells. The effects were attenuated by caveolin1 or sprouty1 siRNA. Western blot analysis indicated that genistein attenuated the phosphorylation of extracellular regulated kinase1/2(ERK1/2) in angiotensin II-induced proliferated VSMC but stimulated the phosphorylation of ERK1/2 in quiescent endothelial cell. Double staining immunofluorescence identified caveolin1 and sprouty1 coexpressed in the cytoplasm of both VSMC and endothelial cell. Genistein increased the expression of caveolin1, p-caveolin1 and sprouty1 in VSMC, while it had opposite effects in quiescent endothelial cell. Co-immunoprecipitation suggested that genistein exerted its effects through interaction of caveolin1 and sprouty1. Our results demonstrate that the inhibition of angiotensin II-induced proliferation of VSMC and stimulation of quiescent endothelial cell by genistein are regulated by caveolin1 and sprouty1, which are implemented through Ras/MAPK pathway.

The role of peroxisome proliferator-activated receptor-gamma and estrogen receptors in genistein-induced regulation of vascular tone in female rat aortas.

BACKGROUND: Genistein (GST) is a phytoestrogen that binds estrogen receptors (ER) to produce a protective cardiovascular effect. It also has been shown binding peroxisome proliferator-activated receptor-gamma (PPAR-gamma). METHODS: In the present study, we assessed the role of PPAR-gamma and ER in GST-mediated regulation of vascular tone in female rat aortas by in vitro tension measurement, immunohistochemistry, immunofluorescence, immunoprecipitation and Western blot analysis. RESULTS: In aortas pretreated with GW9662 (inhibitor of PPAR-gamma), ICI182780 (inhibitor of ER) and a combination of GW9662 and ICI182780, the magnitudes of GST-induced dilatation were attenuated. N(G)-nitro-L-arginine methyl ester had a similar effect. ER-beta and PPAR-gamma colocalized in all 3 layers of the aortas, while ER-alpha and PPAR-gamma colocalized only in the vascular endothelium and adventitia. In GST-treated whole-cell protein samples, we demonstrated coimmunoprecipitation of ER-beta (not ER-alpha) and PPAR-gamma. The expression of ER-beta and PPAR-gamma in nuclear protein from GST-treated samples increased, which was partially reversed by either GW9662 or ICI182780 and more efficiently reversed using a combination of GW9662 and ICI182780. CONCLUSION: Our findings suggest that GST can relax phenylephrine-induced vascular contraction in female rat aortas, which is mediated by PPAR-gamma and ER-beta.

Non-genomic effects of 17beta-estradiol in activation of the ERK1/ERK2 pathway induces cell proliferation through upregulation of cyclin D1 expression in bovine artery endothelial cells.

OBJECTIVE: Growing evidence indicates that estrogen's non-genomic effects play important roles in cellular functions and backs up the hypothesis of the existence of a membrane estrogen receptor (mER) in a number of cell types, but little is known about the complementary effects between traditional genomic and novel non-genomic effects of estrogen. The aim of the present study was to explore the non-genomic activation of ERK1/2 mitogen-activated protein kinase (MAPK) by 17beta-estradiol (E(2)) through mER and its role in cell proliferation. METHODS: On cultured bovine artery endothelial cells (BAECs) we used the [(3)H]thymidine incorporation assay to evaluate the influence of E(2) on cell proliferation and fluorescence microscopy to show the presence of mER on the cell membrane. Scatchard analysis was performed to identify and characterize the mER on a purified membrane fraction of BAECs. RESULTS: E(2) upregulated cyclin D1 protein expression and enhanced cell proliferation. Inhibition of the MAPK cascade with PD98059 or of G protein with pertussis toxin (PTX) completely abolished the above effects, while the estrogen receptor antagonist tamoxifen attenuated E(2)-dependent upregulation of cyclin D1 and cell proliferation. Accordingly, E(2) rapidly led to ERK1/ERK2 activation, which was prevented by tamoxifen or PTX and was entirely reproduced by membrane-impermeable estradiol-bovine serum albumin conjugate (E(2)coBSA). Immunofluorescent staining with E(2)coBSA-fluorescein isothiocyanate resulted in a punctuate staining pattern of the plasma membrane and Scatchard analysis of the E(2)-binding protein in a purified membrane fraction of BAECs showed that E(2) binds to the membrane fraction with a dissociation constant of 0.2394 nmol/l. CONCLUSION: Our findings showed that E(2) induces cell proliferation through upregulation of cyclin D1 via non-genomic activation of the ERK1/ERK2 pathway mediated by mER and G protein.

Estrogen receptor alpha gene polymorphism associated with type 2 diabetes mellitus and the serum lipid concentration in Chinese women in Guangzhou.

BACKGROUND: Estrogen might play an important role in type 2 diabetes mellitus pathogenesis. A number of polymorphisms have been reported in the estrogen receptor alpha (ERalpha) gene (also named ESR1), including the XbaI and PvuII restriction enzyme polymorphisms of ESR1, which may be involved in disease pathogenesis. The aim of this study was to determine whether ERX gene polymorphisms are associated with type 2 diabetes mellitus and serum lipid level. METHODS: Two hundred and ninety-nine patients with type 2 diabetes mellitus were compared with three hundred and forty-one health controls of Guangzhou in China, both were male and postmenopausal female residents at 51 - 70 years. ESR1 genotyping was performed using polymerase chain reaction (PCR) and PvuII and XbaI restriction fragment length polymorphism (PCR-RFLP) analysis. RESULTS: ESR1 allelic frequencies of P, p and X, x alleles were 0.408, 0.592; 0.360, 0.640 in the type 2 diabetes mellitus group and 0.318, 0.682; 0.328, 0.672 in the control group, respectively. In case-control study, there was significant difference in PvuII, but not XbaI, allele frequency between the type 2 diabetes mellitus and control groups (P = 0.001 and P = 0.122). When the group was separated into men and women, the difference was significant in women (P < 0.001) but not in men (P = 0.854) with the PvuII genotype, and the effect of PvuII variant on the development of type 2 diabetes mellitus was improved with aging. In addition, PvuII genotype was associated with blood glucose [fasting blood glucose (FBG), postprandial blood glucose (PBG)] and serum lipid [total cholesterol (TC) and low density lipoprotein (LDL)-c] concentration in healthy women. CONCLUSIONS: PvuII polymorphism of ESR1 increases susceptibility to type 2 diabetes mellitus in Chinese Guangzhou women. ESR1 variants may also impact serum lipid metabolism, which might provide a mechanism connecting ESR1 to type 2 diabetes.

[Possible involvement of caveolin-1 in the inhibition of endothelin-1 induced proliferation of vascular smooth muscle cells by 17beta-estradiol].

The aim of the present study was to investigate the role of caveolin-1 in the inhibition of endothelin-1 induced proliferation of vascular smooth muscle cells (VSMCs) by 17beta-estradiol. In the cultured rat thoracic aortic VSMCs, proliferation of VSMCs was determined by using [(3)H]-thymidine incorporation and the expression of caveolin-1 protein was measured by immunofluorescence assays and Western blotting. The measurement demonstate VSMCs exposed to various concentrations of endothelin-1 (1-100 nmol/L) for 24 h induced an increase in [(3)H]-thymidine incorporation. Pretreament with various concentrations of 17beta-estradiol (0.1-10 nmol/L) for 24 h inhibited the proliferation effect of endothelin-1. Immunofluorescence assays showed that after 24 h treatment of VSMCs with endothelin-1 (100 nmol/L), the expression of caveolin-1 in VSMCs was significantly increased, whereas pretreament with 17beta-estradiol (10 nmol/L) for 24 h inhibited the effect. Western blotting results further proved that endothelin-1 inhibited and 17beta-estradiol increased the expression of caveolin-1 in VSMCs. These results demonstrate that 17beta-estradiol inhibits the VSMCs proliferation induced by endothelin-1, and that the effect of estradiol is probably mediated by caveolin-1.

[Physical simulation of human body metabolism in sealed module on the ground].

OBJECTIVE: To provide a test platform for experimental verification of environmental control and life support system (ECLSS) of manned spacecraft on the ground. METHOD: According to characters of ECLSS ground simulation test, simulation of human body metabolism was divided into different units, and a ground metabolic simulator was designed. RESULT: The ground metabolic simulator accurately simulated human body metabolic oxygen consumption, carbon dioxide production, water and heat productions in the sealed module. CONCLUSION: The physical method for simulating human body metabolism is feasible and has the advantages of high precision and easiness of control. It can be used for verifying and appraising the function of ECLSS.