Multifunctional Electrocatalysts: Ru–M (M = Co, Ni, Fe) for Alkaline Fuel Cells and Electrolyzers
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Solid additives are crucial in layer-by-layer (LBL) polymer solar cells (PSCs). Despite its importance, the simultaneous application of solid additives into both donor and acceptor layers has been largely overlooked. In this work, two multifunctional solid additives are actively designed, and investigated the synergistic effect on both donor and acceptor layers. Incorporating the multifunctional solid additives into the donor layer could effectively enhance the aggregation and molecular stacking of the donor polymer, leading to reduced energy disorder and minimizing ΔE 2 . When the multifunctional solid additives are introduced into the acceptor layer, they just play a role in optimizing the morphology, thereby reducing the ΔE 3 . Excitedly, the simultaneous addition of the multifunctional solid additives into both donor and acceptor layers produced a synergistic effect for decreasing ΔE 2 and ΔE 3 simultaneously, especially adding SA2, thus enabling an excellent power conversion efficiency (PCE) of 19.95% (certified as 19.68%) with an open-circuit voltage (V oc ) of 0.921 V, a short circuit current density (J sc ) of 27.08 mA cm -2 and a fill factor (FF) of 79.98%. The work highlights the potential of multifunctional solid additives in independently regulating the properties of donor and acceptor layers, which is expected as a promising approach for further developing higher performance PSCs.
Type III polyketide synthases (PKSs) play an important role in biosynthesis of various plant secondary metabolites and plant adaptation to environmental stresses. Aquilaria sinensis (A. sinensis) is the main plant species for production of agarwood, little is known about its PKS family. In this study, AsCHS1 and two new type III PKSs, AsPKS1 and AsPKS2, were isolated and characterized in A. sinensis calli. The comparative sequence and phylogenetic analysis indicated that AsPKS1 and AsPKS2 belonged to non-CHS group different from AsCHS1. The recombinant AsPKS1 and AsPKS2 produced the lactone-type products, suggesting their different enzyme activities from AsCHS1. Three PKS genes had a tissues-specific pattern in A. sinensis. Moreover, we examined the expression profiles of three PKS genes in calli under different abiotic stresses and hormone treatments. AsCHS1 transcript was most significantly induced by salt stress, AsPKS1 abundance was most remarkably enhanced by CdCl{sub 2} treatment, while AsPKS2 expression was most significantly induced by mannitol treatment. Furthermore, AsCHS1, AsPKS1 and AsPKS2 expression was enhanced upon gibberellins (GA3), methyl jasmonate (MeJA), or salicylic acid (SA) treatment, while three PKS genes displayed low transcript levels at the early stage under abscisic acid (ABA) treatment. In addition, three GFP:PKSs fusion proteins were localized in the cytoplasm and cell wall in Nicotiana benthamiana cells. These results indicated the multifunctional role of three type III PKSs in polyketide biosynthesis, plant resistance to abiotic stresses and signal transduction. - Highlights: • Two new PKS genes (AsPKS1 and AsPKS2) were isolated and characterized from A. sinensis. • The recombinant AsPKS1 and AsPKS2 catalyzed lactone-type products in vitro. • AsCHS1, AsPKS1 and AsPKS2 were involved in plant responses to abiotic stresses and hormone stimuli. • Our results also indicated that AsCHS1, AsPKS1 and AsPKS2 were predominantly localized in the cytoplasm and cell wall.
Flexible perovskite solar cells (F-PSCs), prized for their nature of soft and high power-weight compatibility, have attracted intensive attention. However, inferior buried perovskite-substrate interfaces due to low interfacial adhesion between perovskites and substrates and large deformation of flexible substrates have greatly limited the performance of F-PSCs. Here, we add organic molecule Entinostat (ET) into hole extraction material Poly[bis(4-phenyl)(2,4,6-trimethylphenyl)amine] (PTAA) to enhance the adhesion at the perovskite/substrate interface using the interactions of ET with perovskites, PTAA and indium tin oxide (ITO) through its multiple function groups. Meanwhile, ET added into perovskites reduces the voids at the bottom perovskite film, due to its capability to tune the crystallization of perovskites by forming adduct with lead. Consequently, the inverted small area F-PSCs achieved an efficiency of 23.4%. The flexible perovskite minimodule with an area of 9 cm 2 achieved an aperture efficiency of ~19.0% certified by National Renewable Energy Laboratory. Furthermore, the optimized unencapsulated flexible minimodule retained 84% of the initial efficiency after 5000 bending cycles and retained 90% of the initial PCE (T90) after light soaking for >750 hours.
This project focused on the development of metal halide perovskite-polymeric nanofiber nanocomposites for robust and efficient solar cells. Metal halide perovskite solar cells are a potentially disruptive technology with high efficiencies and low-cost solution processability amenable with roll-to-roll fabrication of flexible devices. However, perovskites exhibit extreme brittleness, high internal film stresses, and chemical instabilities that significantly limit service lifetimes under normal operating conditions. To date, most work addressing these shortcomings has been focused on encapsulating devices between thick layers of rigid materials such as glass, which increases the total weight and cost of devices. Furthermore, these rigid and heavy encapsulants do not translate well to emerging solar markets vital for national security, including integrated mobile power, emergency deployments for disaster relief and military engagement, and lightweight power for space. It is therefore critical to improve the thermomechanical and chemical stability of perovskite devices in a way that is compatible with flexible and lightweight substrates. In this project, we integrated nylon-6,6 nanofibers into MAPbI3 to mechanically reinforce the perovskite, demonstrating films that exhibited fracture energies 5-fold greater than pristine MAPbI3 while also maintaining similar power conversion efficiencies due to beneficial light scattering effects from the polymeric nanofibers. These results required successful development of approaches to control the deposition thickness of nanofiber mats down to 100s of nanometers, and to ensure the polymer nanofibers did not inhibit charge transport to the at the perovskite-transport layer interface.
Thin/tunable liquid/gas diffusion layers (TT-LGDLs) or porous transport layers (TT-PTLs), have exhibited superior multifunctional performance in proton exchange membrane electrolyzer cells (PEMECs), which can be attributed to their unique structures, such as planar surface, straight-through pores, thin thickness, etc. For achieving better PEMEC performance, TT-LGDLs with smaller pore size are desired. However, in this case, mass diffusion issues are brought in when some of the pores are covered by the flow field lands or shoulders. The coverage of the pores can lead to very high transport resistance, which may reduce the number of active oxygen evolution reaction sites, and therefore lower down the PEMEC performance. The in-plane transport enhancement layer for TT-LGDLs/PTLs are proposed to develop a dual-layer LGDL/PTL structure for improving the mass diffusion and the PEMEC performance. The results of this research reveal that the dual-layer LGDL/PTL structure exhibits smaller ohmic resistance and mass transport resistance, and therefore improve the PEMEC performance, without obvious changes in kinetic losses. The total ohmic resistance and mass transport resistance can be reduced by about 23% and 41%, respectively, with an ~830 um pore TT-LGDL/PTL stacking on a ~100 um pore TT-LGDL/PTL. The results indicate the feasibility of stacking the in-plane transport enhancement layer with large pore sizes onto a small pore TT-LGDLs/PTLs for high efficiency and low cost PEMEC practical applications.
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DEAD-box helicase 1 (DDX1) is a multifunction protein involved in diverse cellular processes including transcription, viral replication, mRNA/miRNA processing, and tRNA splicing. Here, we report a novel function of DDX1 in mRNA alternative splicing in pancreatic β cells. By performing integrated data analysis of high-throughput RNA sequencing (RNA-Seq), and cross-linking and immunoprecipitation coupled with deep sequencing (CLIP-Seq), we identify hundreds of alternative splicing genes that are targeted by DDX1. These DDX1-targeted alternative splicing genes are mainly associated with calcium ion binding, high voltage-gated calcium channel, and transmembrane transporter. Functionally, silencing DDX1 impairs calcium influx and insulin secretion in the pancreatic β cells. These results reveal an important role for DDX1 in the regulation of gene alternative splicing and insulin secretion in pancreatic β cells.
The 37/67 kDa laminin receptor (LAMR) is a multifunctional protein, acting as an extracellular receptor, localizing to the nucleus, and playing roles in rRNA processing and ribosome assembly. LAMR is important for cell viability; however, it is unclear which of its functions are essential. We developed a silent mutant LAMR construct, resistant to siRNA, to rescue the phenotypic effects of knocking down endogenous LAMR, which include inhibition of protein synthesis, cell cycle arrest, and apoptosis. In addition, we generated a C-terminal-truncated silent mutant LAMR construct structurally homologous to the Archaeoglobus fulgidus S2 ribosomal protein and missing the C-terminal 75 residues of LAMR, which displays more sequence divergence. We found that HT1080 cells stably expressing either silent mutant LAMR construct still undergo arrest in the G{sub 1} phase of the cell cycle when treated with siRNA. However, the expression of full-length silent mutant LAMR rescues cell viability, whereas the expression of the C-terminal-truncated LAMR does not. Interestingly, we also found that both silent mutant constructs restore protein translation and localize to the nucleus. Our findings indicate that the ability of LAMR to regulate viability is associated with its C-terminal 75 residues. Furthermore, this function is distinct from its role in cell proliferation, independent of its ribosomal functions, and may be regulated by a nonnuclear localization.
Highlights: {yields} A yeast two-hybrid screen revealed testin bound to the calcium-sensing receptor. {yields} The second zinc finger of LIM domain 1 of testin is critical for interaction. {yields} Testin bound to a region of the receptor tail important for cell signalling. {yields} Testin and receptor interaction was confirmed in mammalian (HEK293) cells. {yields} Overexpression of testin enhanced receptor-mediated Rho signalling in HEK293 cells. -- Abstract: The calcium-sensing receptor (CaR) plays an integral role in calcium homeostasis and the regulation of other cellular functions including cell proliferation and cytoskeletal organisation. The multifunctional nature of the CaR is manifested through ligand-dependent stimulation of different signalling pathways that are also regulated by partner binding proteins. Following a yeast two-hybrid library screen using the intracellular tail of the CaR as bait, we identified several novel binding partners including the focal adhesion protein, testin. Testin has not previously been shown to interact with cell surface receptors. The sites of interaction between the CaR and testin were mapped to the membrane proximal region of the receptor tail and the second zinc-finger of LIM domain 1 of testin, the integrity of which was found to be critical for the CaR-testin interaction. The CaR-testin association was confirmed in HEK293 cells by coimmunoprecipitation and confocal microscopy studies. Ectopic expression of testin in HEK293 cells stably expressing the CaR enhanced CaR-stimulated Rho activity but had no effect on CaR-stimulated ERK signalling. These results suggest an interplay between the CaR and testin in the regulation of CaR-mediated Rho signalling with possible effects on the cytoskeleton.
CD147 is a multifunctional trans-membrane glycoprotein, which is highly expressed in many cancers. However, the mechanism by which CD147 modulates cell proliferation is not fully understood. The aim of this study is to investigate the role of CD147 in cell proliferation associated with the TGF-β/Smad4 signaling pathway. Here, we used cell viability and clone formation assays in LNCaP prostate cancer cells to demonstrate that CD147 promotes cell proliferation. The luciferase assay and western blotting show that silencing CD147 using shRNA enhances transcription and expression of p21{sup WAF1}. Using immunofluorescence and nuclear-cytoplasmic separation, we show that this is primarily attributed to transport of Smad4 from the cytoplasm to nucleus. Other assays (GST pull-down, co-immunoprecipitation and immunofluorescence) demonstrate that Smad4 is a new interaction partner of CD147, with the Smad4 MH2 domain and CD147 intracellular domain (CD147-ICD) being involved in the interaction. Furthermore, we report that a phosphoserine (pSer) in CD147 (pSer252) is responsible for this interaction and inhibition of the Smad4/p21{sup WAF1} signal that promotes cell proliferation. Our results provide a novel molecular mechanism for CD147-induced cell proliferation associated with Smad4 signal inhibition. - Highlights: • Smad4 interacts with CD147 via the MH2 domain. • CD147 prevents Smad4 translocation into the nuclear to regulate p21 transcription. • CD147 inhibits p21 transcription and expression independent on p53. • pCD147-S252 is responsible for interaction with Smad4 and p21 down-regulation.
Integrin-linked kinase (ILK) is a multifunctional serine/threonine kinase. Accumulating evidences suggest that ILK are involved in cell–matrix interactions, cell proliferation, invasion, migration, angiogenesis and Epithelial–mesenchymal transition (EMT). However, the underlying mechanisms remain largely unknown. EMT has been postulated as a prerequisite for metastasis. The reports have demonstrated that EMT was implicated in metastasis of oral squamous cell carcinomas. Therefore, here we further postulate that ILK might participate in EMT of tongue cancer. We showed that ILK siRNA inhibited EMT with low N-cadherin, Vimentin, Snail, Slug and Twist as well as high E-cadherin expression in vivo and in vitro. We found that knockdown of ILK inhibited cell proliferation, migration and invasion as well as changed cell morphology. We also demonstrated that ILK siRNA inhibited phosphorylation of downstream signaling targets Akt and GSK3β as well as reduced expression of MMP2 and MMP9. Furthermore, we found that the tongue tumor with high metastasis capability showed higher ILK, Vimentin, Snail, Slug and Twist as well as lower E-cadherin expression in clinical specimens. Finally, ILK siRNA led to the suppression for tumorigenesis and metastasis in vivo. Our findings suggest that ILK could be a novel diagnostic and therapeutic target for tongue cancer. Highlights: • ILK siRNA influences cell morphology, cell cycle, migration and invasion. • ILK siRNA affects the expression of proteins associated with EMT. • ILK expression is related to EMT in clinical human tongue tumors. • ILK siRNA inhibits metastasis of the tongue cancer cells through suppressing EMT.
Highlights: • LIF treatment was found to stimulate the synthesis of ECM in-vitro cultured NPCs. • LIF could activate the ERK1/2 signaling pathway to regulate ECM synthesis. • The therapeutic effect of LIF on deferring the degenerative process of disc was proved in vivo. Extracellular matrix (ECM) anabolism and catabolism imbalance is key feature of chondrocyte and intervertebral disc nucleus pulposus (NP) cell degeneration. The role of LIF as a multifunctional cytokine in the ECM metabolism of chondrocytes is controversial, but no relevant research in the ECM metabolism of NP cells. This study aimed to explore the biofunction and related mechanisms of LIF in the degenerative NP cells. We obtained an increase in the expression of LIF in the human degenerated NP specimens. The addition of recombinant human leukemia inhibitory factor (rhLIF) to the degenerated NP cells cultured in vitro was found to stimulate the synthesis of ECM, and rhLIF could activate the ERK1/2 signaling pathway. However, coculture with PD98059, a signal inhibitor of ERK1/2, blocked the effect of rhLIF on the synthesis of ECM. To furtherly clarify the role of LIF, we carried out animal experiments and found that rhLIF treatment could successfully delay the degree of degeneration of the intervertebral disc in a rabbit model; but with the addition of PD98059, the function of rhLIF for degeneration protection disappeared. In summary, this study demonstrates that LIF plays a role in promoting ECM synthesis in the degenerated NP cells as a protective role in intervertebral disc degeneration (IDD), which is related to the activation of ERK1/2 signaling pathway.
Designed and engineered protein and DNA nanopores can be used to sense and characterize single molecules and control transmembrane transport of molecular species. However, designed biomolecular pores are less than 100 nm in length and are used primarily for transport across lipid membranes. Nanochannels that span longer distances could be used as conduits for molecules between nonadjacent compartments or cells. We design micrometer-long, 7-nm-diameter DNA nanochannels that small molecules can traverse according to the laws of continuum diffusion. Binding DNA origami caps to channel ends eliminates transport and demonstrates that molecules diffuse from one channel end to the other rather than permeating through channel walls. These micrometer-length nanochannels can also grow, form interconnects, and interface with living cells. This work thus shows how to construct multifunctional, dynamic agents that control molecular transport, opening ways of studying intercellular signaling and modulating molecular transport between synthetic and living cells.
The activities presented are a broad based approach to advancing key hydrogen related technologies in areas such as fuel cells, hydrogen production, and distributed sensors for hydrogen-leak detection, laser instrumentation for hydrogen-leak detection, and cryogenic transport and storage. Presented are the results from research projects, education and outreach activities, system and trade studies. The work will aid in advancing the state-of-the-art for several critical technologies related to the implementation of a hydrogen infrastructure. Activities conducted are relevant to a number of propulsion and power systems for terrestrial, aeronautics and aerospace applications. Sensor systems research was focused on hydrogen leak detection and smart sensors with adaptive feedback control for fuel cells. The goal was to integrate multifunction smart sensors, low-power high-efficiency wireless circuits, energy harvesting devices, and power management circuits in one module. Activities were focused on testing and demonstrating sensors in a realistic environment while also bringing them closer to production and commercial viability for eventual use in the actual operating environment.
Using additive manufacturing (AM) technology, a fundamental material and structure innovation was proposed to significantly increase the energy efficiency, and to reduce the weight, volume and component quantity of proton exchange membrane electrolyzer cells (PEMECs). Four conventional parts (liquid/gas diffusion layer, bipolar plate, gasket, and current distributor) in a PEMEC were integrated into one multifunctional AM plate without committing to tools or molds for the first time. In addition, since the interfacial contact resistances between those parts were eliminated, the comprehensive in-situ characterizations of AM cells showed that an excellent energy efficiency of up to 86.48% was achieved at 2 A/cm2 and 80 degrees C, and the hydrogen generation rate was increased by 61.81% compared to the conventional cell. More importantly, the highly complex inner structures of the AM integrated multifunctional plates also exhibit the potential to break limitations of conventional manufacture methods for hydrogen generation and to open a door for the development of other energy conversion devices, including fuel cells, solar cells and batteries.
The high density of the extracellular matrix in solid tumors is an important obstacle to nanocarriers for reaching deep tumor regions and has severely limited the efficacy of administrated nanotherapeutics. The use of proteolytic enzymes prior to nanoparticle administration or directly attached to the nanocarrier surface has been proposed to enhance their penetration, but the low in vivo stability of these macromolecules compromises their efficacy and strongly limits their application. Herein, we have designed a multifunctional nanocarrier able to transport cytotoxic drugs to deep areas of solid tumors and once there, to be engulfed by tumoral cells causing their destruction. This system is based on mesoporous silica nanocarriers encapsulated within supported lipid bilayers (SLBs). The SLB avoids premature release of the housed drug while providing high colloidal stability and an easy to functionalize surface. The tumor penetration property is provided by attachment of engineered polymeric nanocapsules that transport and controllably unveil and release the proteolytic enzymes that in turn digest the extracellular matrix, facilitating the nanocarrier diffusion through the matrix. Additionally, targeting properties were endowed by conjugating an antibody specific to the investigated tumoral cells to enhance binding, internalization, and drug delivery. This multifunctional design improves the therapeutic efficacy of the transported drug as a consequence of its more homogeneous distribution throughout the tumoral tissue.
The long-term operational stability of perovskite solar cells (PSCs) remains a key challenge impeding their commercialization, particularly due to ambient environments (e.g., moisture, oxygen, heat)-induced degradation. Carbon electrode-based PSCs have emerged as cost-effective and relatively stable alternatives to metal electrode-based devices due to carbon materials' hydrophobic behavior, yet they still lag in both long-term durability and power conversion efficiency (PCE). In this work, an ultrathin hydrophobic ligand-modified core–shell Cd(S,Se)/ZnS quantum dots (QDs) capping layer is introduced as a multifunctional interfacial modifier for carbon-electrode-based PSCs. This oleic acid ligand-modified QDs capping layer exhibits inherent hydrophobicity, effectively serving as a moisture barrier to retard perovskite degradation under ambient conditions. Furthermore, the strong interfacial bonding between the QDs and perovskite halide surfaces leads to efficient trap state passivation, reducing trap density and creating a more uniform electrical contact. The modified QDs/perovskite interface also features an elevated conduction band edge, promoting improved charge extraction. As a result, devices incorporating this quantum dot capping layer retain 98% of their initial PCE after 450 h of ambient aging and achieve a champion efficiency of 20.74%. As a result, this strategy highlights the potential of hydrophobic ligand-modified chalcogenide QDs as surface modifiers to enhance both the stability and performance of carbon-based PSCs, offering a promising route toward scalable fabrication of durable perovskite solar modules.