Search

• A high- efficiency, stable, and printable CeO 2 /FaSnI 3 /Spiro-OMeTAD perovskite solar cell is proposed. • Effect of different parameters such as thickness, defect density, and donor density on photovoltaic characteristic parameters is investigated. • Effect of conventional TiO 2 substitution with CeO 2 on efficiency improvement of devices is discussed. • Role of capture cross section of electrons, and holes is explained. After an abrupt rise in the efficiency of perovskite solar cells (PSCs), hole transport layer (HTL) as an essential factor for fabricating efficient PSC devices attract attentions. The pristine spiro-OMeTADspiro-OMeTAD, as most widely used HTL, still suffers from poor electrical conductivity, low hole mobility, and low oxidation rate. In this research, the spiro-OMeTAD is replaced by nitrogen doped TiO 2 (N-TiO 2) HTL. Then, the variation in the device design key parameters such as the thickness and bulk defect density of perovskite layer, simultaneous modifications of defect density and defect energy level, and acceptor doping concentration in absorber layer, and operating temperature are examined with their impact on the photovoltaic characteristic parameters. The standard lead-free CsSnI 3 –based PSCs with spiro-OMeTAD HTL is simulated using SCAPS-1D software. The CsSnI 3 -based solar cell with N-TiO 2 as HTL showed higher efficiency of 27.03 % than the standard device with PCE of 23.63 % for conventional spiro-OMeTAD HTL. [Display omitted] [ABSTRACT FROM AUTHOR]

Research has been conducted on peroxisome-proliferator-activated receptor delta. The authors demonstrate that targeted activation of this receptor in adipose tissue induces gene expressions which are important for fatty acid oxidation and energy dissipation.

Objective Alternative activation (M2) of adipose tissue resident macrophage (ATM) inhibits obesity-induced metabolic inflammation. The underlying mechanisms remain unclear. Recent studies have shown that dysregulated lipid homeostasis caused by increased lipolysis in white adipose tissue (WAT) in the obese state is a trigger of inflammatory responses. We investigated the role of M2 macrophages in lipotoxicity-induced inflammation. Methods We used microarray experiments to profile macrophage gene expression regulated by two M2 inducers, interleukin-4 (Il-4), and peroxisome proliferator-activated receptor delta/gamma (Pparδ/Pparγ) agonists. Functional validation studies were performed in bone marrow-derived macrophages and mice deprived of the signal transducer and activator of transcription 6 gene ( Stat6 ; downstream effector of Il-4) or Pparδ/Pparγ genes (downstream effectors of Stat6). Palmitic acid (PA) and β-adrenergic agonist were employed to induce macrophage lipid loading in vitro and in vivo , respectively. Results Profiling of genes regulated by Il-4 or Pparδ/Pparγ agonists reveals that alternative activation promotes the cell survival program, while inhibiting that of inflammation-related cell death. Deletion of Stat6 or Pparδ/Pparγ increases the susceptibility of macrophages to PA-induced cell death. NLR family pyrin domain containing 3 (Nlrp3) inflammasome activation by PA in the presence of lipopolysaccharide is also increased in Stat6 −/− macrophages and to a lesser extent, in Pparδ/γ −/− macrophages. In concert, β-adrenergic agonist-induced lipolysis results in higher levels of cell death and inflammatory markers in ATMs derived from myeloid-specific Pparδ/γ −/− or Stat6 −/− mice. Conclusions Our data suggest that ATM cell death is closely linked to metabolic inflammation. Within WAT where concentrations of free fatty acids fluctuate, M2 polarization regulated by the Stat6-Ppar axis enhances ATM's tolerance to lipid-mediated stress, thereby maintaining the homeostatic state. [ABSTRACT FROM AUTHOR]

In this paper, Cu 2 ZnSn(S,Se) 4 (CZTSSe) thin-films were prepared by sulfo-selenization of metal precursors in H 2 S environment instead of using metal selenides/sulfides as precursors. High quality CZTSSe thin films were obtained using multi-stacking metallic nanolayer precursors undergoing a fast ramping process. For the preparation of metallic stacked nanolayer precursors, we have developed a 9-layer sequential deposition of Sn/Zn/Cu metal stack onto Mo-coated soda lime glass substrate by RF-sputtering. Due to inevitable metal inter-diffusion during the sulfo-selenization, we further studied the effect of the Sn/Zn/Cu metal stacking number (therefore, the layer thickness) on the quality of thin film with respect to its device performance. In the device prepared with conventional 3-layer stack, due to insufficient inter-diffusion of precursors, excessive Cu-rich secondary phase was formed at the back contact region and resulted in poor performance of devices. By using the modified 9-layer stacked precursor and fast ramping heating process the device efficiency can be improved from 4.9% to 7.7% and open circuit voltage from 0.44 to 0.5 V. This improvement can be ascribed to a compact, smooth microstructure, presence of bronze formation and the suppression of Cu-rich bi-layer formation in the 9-layer approach. [ABSTRACT FROM AUTHOR]

Several studies provide evidence supporting a beneficial effect from the traditional Mediterranean diet (MedDiet) on the risk of type 2 diabetes mellitus (T2DM) and metabolic syndrome (MetS). This review summarizes the current scientific evidence from epidemiologic studies and clinical trials on the relation between the MedDiet and T2DM and MetS and the possible mechanisms underlying the reported associations. A recent meta-analysis of prospective cohort studies showed that greater adherence to the MedDiet was associated with a significant reduction in the risk of diabetes. The MedDiet has also been found to be beneficial in the prevention of gestational diabetes. Four large prospective studies have observed inverse associations between the MedDiet and MetS or its components. Few randomized controlled trials (RCTs) have evaluated the effect of the MedDiet on T2DM and MetS. Results from the landmark PREvención con DIeta MEDiterránea (PREDIMED) nutrition intervention trial showed that participants assigned to the MedDiet had a significant 30% reduction in the risk of T2DM and that it also promoted the reversion of MetS and its components, hyperglycemia and central obesity. In addition, 5 RCTs showed the beneficial effects of the MedDiet compared with other dietary patterns on glycemic control in patients with T2DM. A recent meta-analysis of RCTs revealed that, compared with a variety of control diets, the MedDiet was associated with beneficial effects on all MetS components. Bioactive components of the MedDiet synergize to affect various metabolic pathways, leading to a reduced cardiometabolic disease risk. The abundance of healthy, nutrient-dense foods that make up the plant-based MedDiet predicts its bioactivity and potential to beneficially influence metabolic pathways that lead to MetS and T2DM, as well as other chronic conditions. Abundant epidemiologic and clinical trial evidence supports the role of the MedDiet on the prevention and management of T2DM and MetS. [ABSTRACT FROM AUTHOR]

Summary Mast cells (MCs) contribute to the pathogenesis of obesity and diabetes. This study demonstrates that leptin deficiency slants MCs toward anti-inflammatory functions. MCs in the white adipose tissue (WAT) of lean humans and mice express negligible leptin. Adoptive transfer of leptin-deficient MCs expanded ex vivo mitigates diet-induced and pre-established obesity and diabetes in mice. Mechanistic studies show that leptin-deficient MCs polarize macrophages from M1 to M2 functions because of impaired cell signaling and an altered balance between pro- and anti-inflammatory cytokines, but do not affect T cell differentiation. Rampant body weight gain in ob/ob mice, a strain that lacks leptin, associates with reduced MC content in WAT. In ob/ob mice, genetic depletion of MCs exacerbates obesity and diabetes, and repopulation of ex vivo expanded ob/ob MCs ameliorates these diseases. [ABSTRACT FROM AUTHOR]

Summary Mitochondria undergo architectural/functional changes in response to metabolic inputs. How this process is regulated in physiological feeding/fasting states remains unclear. Here we show that mitochondrial dynamics (notably fission and mitophagy) and biogenesis are transcriptional targets of the circadian regulator Bmal1 in mouse liver and exhibit a metabolic rhythm in sync with diurnal bioenergetic demands. Bmal1 loss-of-function causes swollen mitochondria incapable of adapting to different nutrient conditions accompanied by diminished respiration and elevated oxidative stress. Consequently, liver-specific Bmal1 knockout (LBmal1KO) mice accumulate oxidative damage and develop hepatic insulin resistance. Restoration of hepatic Bmal1 activities in high-fat-fed mice improves metabolic outcomes, whereas expression of Fis1, a fission protein that promotes quality control, rescues morphological/metabolic defects of LBmal1KO mitochondria. Interestingly, Bmal1 homolog AHA-1 in C. elegans retains the ability to modulate oxidative metabolism and lifespan despite lacking circadian regulation. These results suggest clock genes are evolutionarily conserved energetics regulators. [ABSTRACT FROM AUTHOR]

Summary: Through unknown mechanisms, insulin activates the sterol regulatory element-binding protein (SREBP1c) transcription factor to promote hepatic lipogenesis. We find that this induction is dependent on the mammalian target of rapamycin (mTOR) complex 1 (mTORC1). To further define the role of mTORC1 in the regulation of SREBP1c in the liver, we generated mice with liver-specific deletion of TSC1 (LTsc1KO), which results in insulin-independent activation of mTORC1. Surprisingly, the LTsc1KO mice are protected from age- and diet-induced hepatic steatosis and display hepatocyte-intrinsic defects in SREBP1c activation and de novo lipogenesis. These phenotypes result from attenuation of Akt signaling driven by mTORC1-dependent insulin resistance. Therefore, mTORC1 activation is not sufficient to stimulate hepatic SREBP1c in the absence of Akt signaling, revealing the existence of an additional downstream pathway also required for this induction. We provide evidence that this mTORC1-independent pathway involves Akt-mediated suppression of Insig2a, a liver-specific transcript encoding the SREBP1c inhibitor INSIG2. [ABSTRACT FROM AUTHOR]

Summary: The transcriptional corepressor SMRT utilizes two major receptor-interacting domains (RID1 and RID2) to mediate nuclear receptor (NR) signaling through epigenetic modification. The physiological significance of such interaction remains unclear. We find SMRT expression and its occupancy on peroxisome proliferator-activated receptor (PPAR) target gene promoters are increased with age in major metabolic tissues. Genetic manipulations to selectively disable RID1 (SMRTmRID1) demonstrate that shifting SMRT repression to RID2-associated NRs, notably PPARs, causes premature aging and related metabolic diseases accompanied by reduced mitochondrial function and antioxidant gene expression. SMRTmRID1 cells exhibit increased susceptibility to oxidative damage, which could be rescued by PPAR activation or antioxidant treatment. In concert, several human Smrt gene polymorphisms are found to nominally associate with type 2 diabetes and adiponectin levels. These data uncover a role for SMRT in mitochondrial oxidative metabolism and the aging process, which may serve as a drug target to improve health span. [ABSTRACT FROM AUTHOR]

Tricarboxylic acid (TCA) cycle deregulation may predispose to cardiovascular diseases, but the role of TCA cycle-related metabolites in the development of atrial fibrillation (AF) and heart failure (HF) remains unexplored. This study sought to investigate the association of TCA cycle-related metabolites with risk of AF and HF. We used two nested case-control studies within the PREDIMED study. During a mean follow-up for about 10 years, 512 AF and 334 HF incident cases matched by age (±5 years), sex and recruitment center to 616 controls and 433 controls, respectively, were included in this study. Baseline plasma levels of citrate, aconitate, isocitrate, succinate, malate and d / l -2-hydroxyglutarate were measured with liquid chromatography-tandem mass spectrometry. Multivariable conditional logistic regression models were fitted to estimate odds ratios (OR) and 95% confidence intervals (95% CI) for metabolites and the risk of AF or HF. Potential confounders included smoking, family history of premature coronary heart disease, physical activity, alcohol intake, body mass index, intervention groups, dyslipidemia, hypertension, type 2 diabetes and medication use. Comparing extreme quartiles of metabolites, elevated levels of succinate, malate, citrate and d / l -2-hydroxyglutarate were associated with a higher risk of AF [OR Q4 vs. Q1 (95% CI): 1.80 (1.21–2.67), 2.13 (1.45–3.13), 1.87 (1.25–2.81) and 1.95 (1.31–2.90), respectively]. One SD increase in aconitate was directly associated with AF risk [OR (95% CI): 1.16 (1.01–1.34)]. The corresponding ORs (95% CI) for HF comparing extreme quartiles of malate, aconitate, isocitrate and d / l -2-hydroxyglutarate were 2.15 (1.29–3.56), 2.16 (1.25–3.72), 2.63 (1.56–4.44) and 1.82 (1.10–3.04), respectively. These associations were confirmed in an internal validation, except for aconitate and AF. These findings underscore the potential role of the TCA cycle in the pathogenesis of cardiac outcomes. • Tricarboxylic acid (TCA) cycle deregulation may predispose to cardiovascular disease. • The role of TCA cycle metabolites in the development of atrial fibrillation (AF) and heart failure (HF) remains unexplored. • Baseline plasma TCA cycle metabolites were associated with a higher risk of AF, HF in high cardiovascular risk individuals. • Our results suggest that a dysregulation of aerobic energy metabolism may precede the development of both cardiac outcomes. [ABSTRACT FROM AUTHOR]

Summary: The polarization of adipose tissue-resident macrophages toward the alternatively activated, anti-inflammatory M2 phenotype is believed to improve insulin sensitivity. However, the mechanisms controlling tissue macrophage activation remain unclear. Here we show that adipocytes are a source of Th2 cytokines, including IL-13 and to a lesser extent IL-4, which induce macrophage PPARδ/β (Ppard/b) expression through a STAT6 binding site on its promoter to activate alternative activation. Coculture studies indicate that Ppard ablation renders macrophages incapable of transition to the M2 phenotype, which in turns causes inflammation and metabolic derangement in adipocytes. Remarkably, a similar regulatory mechanism by hepatocyte-derived Th2 cytokines and macrophage PPARδ is found to control hepatic lipid metabolism. The physiological relevance of this paracrine pathway is demonstrated in myeloid-specific PPARδ−/− mice, which develop insulin resistance and show increased adipocyte lipolysis and severe hepatosteatosis. These findings provide a molecular basis to modulate tissue-resident macrophage activation and insulin sensitivity. [Copyright &y& Elsevier]

Peroxisome proliferator-activated receptor-γ (PPARγ), a fatty acid receptor, has received particular attention as the molecular target of insulin-sensitizing drugs, and as a regulator of lipid accumulation by the coronary artery macrophages known as foam cells. Controversial results have been reported regarding the consequences of PPARγ activation in the inflammatory response, the progression or improvement of the atherosclerotic lesion, and the identity of target tissues (muscle or fat) for PPARγ-specific antidiabetic drugs. A clear understanding of how PPARγ functions in each of these processes is therefore necessary to advance its utility as a therapeutic target. Receptor-dependent and -independent actions of PPARγ agonists have been carefully examined with a combination of Pparg-knockout mice, PPARγ-null embryonic stem cells, PPARγ-specific drugs, and mouse models of atherosclerosis. Through those combined studies, a physiological and therapeutic role for PPARγ in lipid management by the macrophage has emerged. [Copyright &y& Elsevier]

Thin films of the ternary compound Tb x Dy 1-x Fe 2-y were prepared by DC magnetron sputtering from a TbDyFe alloy target with the composition same as Terfenol-D alloy (Tb 0.32 Dy 0.68 Fe 1.92) onto 400 °C Si (001) substrates. The influence of post annealing temperature at 550 °C, 700 °C or 850 °C for 6 h are studied systematically on a series of Tb x Dy 1-x Fe 2-y samples. However, the annealing process leads to the incorporation of oxygen impurity into the thin film. To understand the effects of annealing temperature on the microstructural and crystalline degree of oxidation of RFe 2 thin film, different characterisation techniques such as anomalous X-ray scattering and electron probe micro-analyzer were performed. These measurements show that Fe clusters phase gets segregated from the bulk matrix during annealing at 550 °C and 850 °C but do not segregate while annealing at 700 °C. In this work, we present an anomalous X-ray diffraction measurement on Tb x Dy 1-x Fe 2-y to determine the composition ratio of rare earth oxides in thin film and compositional analysis. • Determination of the composition ratio of RE oxides in thin film using AXS. • Post annealing effects at 550 °C, 700 °C or 850 °C for 6 h are discussed. • Importance of substrates role to produce stoichiometrically correct film with Laves phase. [ABSTRACT FROM AUTHOR]

Gas-phase photocatalytic reactions to convert carbon dioxide and water into oxygen and hydrocarbons are the foundation of life on earth. However, the efficiency of photosynthesis is relatively low (~1%), which leaves much room for artificial photosynthesis to reach the benchmark of the solar cells (>15%). In this work, carbon implanted SnS 2 thin films (C–SnS 2) were prepared to study photocatalytic activity and adsorbate-catalyst surface interactions during CO 2 photoreduction. The electron density distribution in C–SnS 2 and its contribution toward the photogenerated charge transfer process has been analyzed by the angle-dependent X-ray absorption near-edge structure (XANES) study. The C–SnS 2 surface affinity toward the CO 2 molecule was monitored by in-situ dark current and Raman spectroscopy measurements. By optimizing the dose during ion implantation, SnS 2 thin film with 1 wt% carbon incorporation shows 108 times enhancement in the CO 2 conversion efficiency and more than 89% product selectivity toward CH 4 formation compared with the as-grown SnS 2 without carbon incorporation. The improved photocatalytic activity can be ascribed to enhanced light harvesting, pronounced charge-transfer between SnS 2 and carbon with improved carrier separation and the availability of highly active carbon sites that serve as favorable CO 2 adsorption sites. Image 1 • Carbon implanted SnS 2 thin-film and its contribution toward the photogenerated charge transfer process for CO 2 reduction. • The C-SnS 2 shows 108 times enhancement in the CO 2 conversion efficiency and higher product selectivity compared with SnS 2. • The CO 2 interactions with the catalyst surface and their implications on heterogeneous photocatalytic CO 2 reduction. [ABSTRACT FROM AUTHOR]

Herein, we demonstrate a facile method for transferring thin films to achieve polymer solar cells having stacked structures. By controlling the swelling/de-swelling properties of Polydimethylsiloxane (PDMS) via solvent treatment, we formed uniform organic films upon the PDMS surface and then transferred them to target substrates. We prepared bilayer and graded bilayer structures after transferring indene-C60 bis-adduct (ICBA) and ratio-controlled poly(3-hexylthiophene) (P3HT:ICBA) blends, respectively, onto the P3HT layer. The optimal graded bilayer solar cell exhibited a power conversion efficiency (PCE) of 5.13% an impressive value compared with that obtained for the corresponding bilayer cell (3.67%). We attribute this enhancement in PCE to the greater number of junction interfaces and the balanced carrier transfer properties. This residue-free and place-lift-off transferring method appears to have great promise in the solution processing of multilayer stacked thin film optoelectronics. A facile transfer printing method controlled from swelling de-swelling of PDMS for realizing bilayer and graded organic solar cells. Image 1 • Controlling surface energy of PDMS stamp by exploiting its natural properties of swelling for transfer printing. • Residue-free transfer from PDMS to target substrates without the need for heat or pressure unlike conventional techniques. • Demonstration of transfer printing approach by printing large area and fabricating bilayer and graded bilayer OSC's. • This technique provides new route for fabrication of multi-stack optoelectronic devices for potential commercialization. [ABSTRACT FROM AUTHOR]

Abstract: Using polarized neutron reflectivity (PNR) measurements together with associated simulation, magnetic structures of two Ni80Fe20 (111)/Ru (0001) multilayer samples with Ru thickness of 9 and 21Å were investigated under various external magnetic fields at room temperature. The results reveal the existence of layer thickness, interface roughness, magnetic moment, interlayer coupling angle and non-collinear coupling. The former three are independent of Ru thickness; while the latter two are strongly dependent of Ru thickness. [Copyright &y& Elsevier]