Nanoengineering Natural Leather for Dynamic Thermal Management and Electromagnetic Interference Shielding.

Unpredictable and extreme weather conditions, along with increasing electromagnetic pollution, have resulted in a significant threat to human health and productivity, causing irreversible damage to society's well-being and economy. However, existing personal temperature management and electromagnetic protection materials lack adaptability to dynamic environmental changes. To address this, a unique asymmetric bilayer leather/a-MWCNTs/CA fabric is developed by vacuum-infiltrating interconnected a-MWCNTs networks into natural leather's microfiber backbone and spraying porous acetic acid (CA) on the reverse side. Such fabric achieves simultaneous passive radiation cooling, heating, and anti-electromagnetic interference functions without external energy input. The fabric's cooling layer has high solar reflectance (92.0%) and high infrared emissivity (90.2%), providing an average subambient radiation cooling effect of 10 °C, while the heating layer has high solar absorption (98.0%), enabling excellent passive radiative heating and effective compensation for warming via Joule heating. Additionally, the fabric's 3D conductive a-MWCNTs network provides electromagnetic interference shielding effectiveness of 35.0 dB mainly through electromagnetic wave absorption. This multimode electromagnetic shielding fabric can switch between cooling and heating modes to adapt to dynamic cooling and heating scenarios, providing a new avenue for sustainable temperature management and electromagnetic protection applications.

A Zero-Energy, Zero-Emission Air Conditioning Fabric.

High indoor humidity/temperature pose serious public health threat and hinder industrial productivity, thus adversely impairing the wellness and economy of the entire society. Traditional air conditioning systems for dehumidification and cooling involve significant energy consumption and have accelerated the greenhouse effect. Here, this work demonstrates an asymmetric bilayer cellulose-based fabric that enables solar-driven continuous indoor dehumidification, transpiration-driven power generation, and passive radiative cooling using the same textile without any energy input. The multimode fabric (ABMTF) consists of a cellulose moisture absorption-evaporation layer (ADF) and a cellulose acetate (CA) radiation layer. The ABMTF exhibits a high moisture absorption capacity and water evaporation rate, which quickly reduces the indoor relative humidity (RH) to a comfortable level (40-60% RH) under 1 sun illumination. The evaporation-driven continuous capillary flow generates a maximum open-circuit voltage (Voc ) of 0.82 V, and a power density (P) up to 1.13 µW cm-3 . When a CA layer with high solar reflection and mid-infrared (mid-IR) emissivity faces outward, it realizes subambient cooling of ≈12 °C with average cooling power of ≈106 W m-2 at midday under radiation of 900 W m-2 . This work brings a new perspective to develop the next-generation, high performance environmentally friendly materials for sustainable moisture/thermal management and self-powered applications.

Stat4 isoforms differentially regulate inflammation and demyelination in experimental allergic encephalomyelitis.

Experimental allergic encephalomyelitis (EAE) is a T cell-mediated autoimmune disease model of multiple sclerosis. Signal transducer and activator of transcription 4 (Stat4) is a transcription factor activated by IL-12 and IL-23, two cytokines known to play important roles in the pathogenesis of EAE by inducing T cells to secrete IFN-gamma and IL-17, respectively. We and others have previously shown that therapeutic intervention or targeted disruption of Stat4 was effective in ameliorating EAE. Recently, a splice variant of Stat4 termed Stat4beta has been characterized that lacks 44 amino acids at the C terminus of the full-length Stat4alpha. In this study we examined whether T cells expressing either isoform could affect the pathogenesis of EAE. We found that transgenic mice expressing Stat4beta on a Stat4-deficient background develop an exacerbated EAE compared with wild-type mice following immunization with myelin oligodendrocyte glycoprotein peptide 35-55, while Stat4alpha transgenic mice have greatly attenuated disease. The differential development of EAE in transgenic mice correlates with increased IFN-gamma and IL-17 in Stat4beta-expressing cells in situ, contrasting increased IL-10 production by Stat4alpha-expressing cells. This study demonstrates that Stat4 isoforms differentially regulate inflammatory cytokines in association with distinct effects on the onset and severity of EAE.

Dap1p, a heme-binding protein that regulates the cytochrome P450 protein Erg11p/Cyp51p in Saccharomyces cerevisiae.

Alkylating agents chemically modify DNA and cause mutations that lead to cancer. In the budding yeast Saccharomyces cerevisiae, resistance to the alkylating agent methyl methanesulfonate (MMS) is mediated in part by Dap1p (damage resistance protein 1). Dap1p is related to cytochrome b5, which activates cytochrome P450 proteins, elevating the metabolism of lipids and xenobiotic compounds. We have found that Dap1p, like cytochrome b5, binds to heme and that Dap1p targets the cytochrome P450 protein Erg11p/Cyp51p. Genetic analysis indicates that Erg11p acts downstream of Dap1p. Furthermore, Dap1p regulates the stability of Erg11p, and Erg11p is stabilized in dap1Delta cells by the addition of heme. Thus, Dap1p utilizes heme to stabilize Erg11p, which in turn regulates ergosterol synthesis and MMS resistance. Dap1p homologues have been identified in numerous eukaryotes, including mammals, suggesting that the Dap1p-cytochrome P450 protein pathway is broadly conserved in eukaryotic species.

A systematic study of yeast sterol biosynthetic protein-protein interactions using the split-ubiquitin system.

Sterol biosynthesis occurs in the ER and most sterol biosynthetic enzymes have transmembrane domains. However, due to difficulties in characterizing membrane protein-protein interactions, the nature of the sterol biosynthetic complex as well as in vivo interactions between various enzymes have not been described. We employed a split-ubiquitin membrane protein yeast two-hybrid system to characterize interactions between sterol biosynthetic proteins. Fourteen bait constructs were co-transformed into a reporter yeast strain with 14 prey constructs representing all sterol enzymatic reactions beginning with the synthesis of squalene. Our results not only confirmed several previous interactions, but also allowed us to identify novel interactions. Based on these results, ergosterol biosynthetic enzymes display specific protein-protein interactions forming a functional complex we designate, the ergosome. In this complex, Erg11p, Erg25p, Erg27p, and Erg28p appear to form a core center that can interact with other enzymes in the pathway. Also Erg24p and Erg2p, two enzymes that are sensitive to morpholine antifungals, appear to interact with one another; however, the profile of protein interaction partners appears to be unique. Erg2p and Erg3p, two enzymes catalyzing sequential reactions also appear to have different interaction partners. Our results provide a working model as to how sterol biosynthetic enzymes are topologically organized not only in yeast but in plant and animal systems that share many of these biosynthetic reactions.

The ERG28-encoded protein, Erg28p, interacts with both the sterol C-4 demethylation enzyme complex as well as the late biosynthetic protein, the C-24 sterol methyltransferase (Erg6p).

In Saccharomyces cerevisiae, the C-24 sterol methyltransferase (Erg6p) converts zymosterol to fecosterol, an enzymatic step following C-4 demethylation of 4,4-dimethylzymosterol. Our previous study showed that an endoplasmic reticulum (ER) transmembrane protein, Erg28p, functions as a scaffold to tether the C-4 demethylation enzymatic complex (Erg25p-Erg26p-Erg27p) to the ER. To determine whether Erg28p also interacts with other ergosterol biosynthetic proteins, we compared protein levels of Erg3p, Erg6p, Erg7p, Erg11p and Erg25p in three pairs of erg28 and ERG28 strains. In erg28 strains, the Erg6p level in the ER fraction was decreased by about 50% relative to the wild-type strain, while ER protein levels of the four other ergosterol proteins showed no significant differences. Co-immunoprecipitation experiments, using an erg28 strain transformed with the epitope-tagged plasmid pERG28-HA and proteins detected with anti-HA and anti-Erg6p antibodies, indicated that Erg6p and Erg28p reciprocally co-immunoprecipitate. Further, the split ubiquitin yeast membrane two-hybrid system designed to detect protein interactions between membrane bound proteins also indicated an Erg28p-Erg6p interaction when pERG6-Cub was used as the bait and pERG28-NubG was used as the prey. We conclude that Erg28p may not only anchor the C-4 demethylation enzyme complex to the ER but also acts as a protein bridge to the Erg6p enzyme required for the next ergosterol biosynthetic step.

Differential regulation of CD4(+) T helper cell responses by curcumin in experimental autoimmune encephalomyelitis.

Nutraceuticals and phytochemicals are important regulators of human health and diseases. Curcumin is a polyphenolic phytochemical isolated from the rhizome of the plant Curcuma longa (turmeric) that has been traditionally used for the treatment of inflammation and wound healing for centuries. Systematic analyses have shown that curcumin exerts its beneficial effects through antioxidant, antiproliferative and anti-inflammatory properties. We and others have shown earlier that curcumin ameliorates experimental autoimmune encephalomyelitis (EAE) model for multiple sclerosis. In this study, we show that C57BL/6 mice induced to develop EAE express elevated levels of interferon (IFN) γ and interleukin (IL)-17 in the central nervous system (CNS) and lymphoid organs that decreased significantly following in vivo treatment with curcumin. The EAE mice also showed elevated expression of IL-12 and IL-23 that decreased after treatment with curcumin. Ex vivo and in vitro treatment with curcumin resulted in a dose-dependent decrease in the secretion of IFNγ, IL-17, IL-12 and IL-23 in culture. The inhibition of EAE by curcumin was also associated with an up-regulation of IL-10, peroxisome proliferator activated receptor γ and CD4(+)CD25(+-)Foxp3(+) Treg cells in the CNS and lymphoid organs. These findings highlight that curcumin differentially regulates CD4(+) T helper cell responses in EAE.

PPARgamma regulates LIF-induced growth and self-renewal of mouse ES cells through Tyk2-Stat3 pathway.

Embryonic stem (ES) cells are genetically normal, pluripotent cells, capable of self-renewal and multi-lineage differentiation. Leukemia inhibitory factor (LIF) is a growth factor that can maintain the pluripotency of mouse ES cells in culture. Peroxisome proliferator-activated receptors (PPARs) are nuclear receptor transcription factors that regulate growth and differentiation of many cell types. We have shown earlier that 15-Deoxy-(12,14)-Prostaglandin J2 (15d-PGJ2), a natural ligand for PPARgamma, inhibits LIF-induced proliferation of mouse ES cells in culture. In this study we demonstrate that the PPARgamma antagonist Bisphenol A diglycidyl ether (BADGE) and 2-Chloro-5-nitro-N-(4-pyridyl)benzamide (T0070907) reverse the inhibition of ES cell proliferation by PPARgamma agonists. Stable transfection of ES cells with a dominant negative PPARgamma1 mutant also reduced the inhibition of proliferation by PPARgamma agonists. While 15d-PGJ2 and ciglitazone-induced growth-arrest in ES cells by blocking LIF signaling, PPARgamma antagonists and dominant negative PPARgamma1 mutant reversed proliferation by restoring LIF-induced Tyk2-Stat3 signaling. These results suggest that PPARgamma regulates LIF-induced growth and self-renewal of mouse ES cells through Tyk2-Stat3 pathway.

Erg28p is a key protein in the yeast sterol biosynthetic enzyme complex.

Previously, a microarray expression study in the yeast Saccharomyces cerevisiae indicated that the ERG28 gene was strongly coregulated with ergosterol biosynthesis. Subsequently, Erg28p was shown to function as an endoplasmic reticulum transmembrane protein, acting as a scaffold to tether the C-4 demethylation enzymatic complex and also to interact with a downstream enzyme, Erg6p. To understand all possible protein interactions involving Erg28p in sterol biosynthesis, a yeast two-hybrid system designed to assess interactions between membrane proteins was used. The Erg28p fusion protein was used as bait to assess interactions with all 14 sterol biosynthetic proteins in a pairwise study based on two reporter systems as well as Western blots demonstrating the release of a transcription factor. Our results indicated that Erg28p not only interacted with the C-4 demethylation enzymes and Erg6p but also with Erg11p and Erg1p. Interactions between Erg28p and seven ergosterol biosynthetic enzymes were confirmed by coimmunoprecipitation experiments. Furthermore, by comparing the reporter gene expression levels, we demonstrate that Erg28p is most closely associated with Erg27p, Erg25p, Erg11p, and Erg6p and less with Erg26p and Erg1p. Based on these results, we suggest that many if not all sterol biosynthetic proteins may be tethered as a large complex.