Augmented Extraction Efficiency of a Hot D Exciton in MoS2 via Intervalley Scattering.

Prolonging hot carrier cooling, a crucial factor in optoelectronic applications, including hot carrier photovoltaics, presents a significant challenge. High-energy band-nesting excitons within parallel bands offer a promising and underexplored avenue for addressing this issue. Here, we exploit an exceptional D exciton cooling prolongation of 2 to 3 orders of magnitude compared to sub-picosecond in typical transition metal dichalcogenides (TMDs) owing to the complex Coulomb environment and the sequential and mismatch-valley relaxation. Simultaneously, the intervalley scattering upconversion of band-edge excitons with the slow D exciton formation in the metastable Γ valley/hill also reduces the cooling rate. We successfully extract D and C excitons as hot carriers through integrating with various thicknesses of TiOx, achieving the highest efficiency of 98% and 85% at a Ti thickness of 2 nm. Our findings highlight the potential of band-nesting excitons for extending hot carrier cooling time, paving the way for advancements in hot carrier-based optoelectronic devices.

Systematic mapping of TF-mediated cell fate changes by a pooled induction coupled with scRNA-seq and multi-omics approaches.

Transcriptional regulation controls cellular functions through interactions between transcription factors (TFs) and their chromosomal targets. However, understanding the fate conversion potential of multiple TFs in an inducible manner remains limited. Here, we introduce iTF-seq as a method for identifying individual TFs that can alter cell fate toward specific lineages at a single-cell level. iTF-seq enables time course monitoring of transcriptome changes, and with biotinylated individual TFs, it provides a multi-omics approach to understanding the mechanisms behind TF-mediated cell fate changes. Our iTF-seq study in mouse embryonic stem cells identified multiple TFs that trigger rapid transcriptome changes indicative of differentiation within a day of induction. Moreover, cells expressing these potent TFs often show a slower cell cycle and increased cell death. Further analysis using bioChIP-seq revealed that GCM1 and OTX2 act as pioneer factors and activators by increasing gene accessibility and activating the expression of lineage specification genes during cell fate conversion. iTF-seq has utility in both mapping cell fate conversion and understanding cell fate conversion mechanisms.

The transcriptional regulatory network modulating human trophoblast stem cells to extravillous trophoblast differentiation.

During human pregnancy, extravillous trophoblasts play crucial roles in placental invasion into the maternal decidua and spiral artery remodeling. However, regulatory factors and their action mechanisms modulating human extravillous trophoblast specification have been unknown. By analyzing dynamic changes in transcriptome and enhancer profile during human trophoblast stem cell to extravillous trophoblast differentiation, we define stage-specific regulators, including an early-stage transcription factor, TFAP2C, and multiple late-stage transcription factors. Loss-of-function studies confirm the requirement of all transcription factors identified for adequate differentiation, and we reveal that the dynamic changes in the levels of TFAP2C are essential. Notably, TFAP2C pre-occupies the regulatory elements of the inactive extravillous trophoblast-active genes during the early stage of differentiation, and the late-stage transcription factors directly activate extravillous trophoblast-active genes, including themselves as differentiation further progresses, suggesting sequential actions of transcription factors assuring differentiation. Our results reveal stage-specific transcription factors and their inter-connected regulatory mechanisms modulating extravillous trophoblast differentiation, providing a framework for understanding early human placentation and placenta-related complications.

Boosting internal quantum efficiency via ultrafast triplet transfer to 2H-MoTe2 film.

Organic systems often allow to create two triplet spin states (triplet excitons) by converting an initially excited singlet spin state (a singlet exciton). An ideally designed organic/inorganic heterostructure could reach the photovoltaic energy harvest over the Shockley-Queisser (S-Q) limit because of the efficient conversion of triplet excitons into charge carriers. Here, we demonstrate the molybdenum ditelluride (MoTe2)/pentacene heterostructure to boost the carrier density via efficient triplet transfer from pentacene to MoTe2 using ultrafast transient absorption spectroscopy. We observe carrier multiplication by nearly four times by doubling carriers in MoTe2 via the inverse Auger process and subsequently doubling carriers via triplet extraction from pentacene. We also verify efficient energy conversion by doubling the photocurrent in the MoTe2/pentacene film. This puts a step forward to enhancing photovoltaic conversion efficiency beyond the S-Q limit in the organic/inorganic heterostructures.

Obstacles to Health Big Data Utilization Based on the Perceptions and Demands of Health Care Workers in South Korea: Web-Based Survey Study.

BACKGROUND: This study focuses on the potential of health big data in the South Korean context. Despite huge data reserves and pan-government efforts to increase data use, the utilization is limited to public interest research centered in public institutions that have data. To increase the use of health big data, it is necessary to identify and develop measures to meet the various demands for such data from individuals, private companies, and research institutes. OBJECTIVE: The aim of this study was to identify the perceptions of and demands for health big data analysis and use among workers in health care-related occupations and to clarify the obstacles to the use of health big data. METHODS: From May 8 to May 18, 2022, we conducted a web-based survey among 390 health care-related workers in South Korea. We used Fisher exact test and analysis of variance to estimate the differences among occupations. We expressed the analysis results by item in frequency and percentage and expressed the difficulties in analyzing health big data by mean and standard deviation. RESULTS: The respondents who revealed the need to use health big data in health care work-related fields accounted for 86.4% (337/390); 65.6% (256/390) of the respondents had never used health big data. The lack of awareness about the source of the desired data was the most cited reason for nonuse by 39.6% (153/386) of the respondents. The most cited obstacle to using health big data by the respondents was the difficulty in data integration and expression unit matching, followed by missing value processing and noise removal. Thus, the respondents experienced the greatest difficulty in the data preprocessing stage during the health big data analysis process, regardless of occupation. Approximately 91.8% (358/390) of the participants responded that they were willing to use the system if a system supporting big data analysis was developed. As suggestions for the specific necessary support system, the reporting and provision of appropriate data and expert advice on questions arising during the overall process of big data analysis were mentioned. CONCLUSIONS: Our findings indicate respondents' high awareness of and demand for health big data. Our findings also reveal the low utilization of health big data and the need to support health care workers in their analysis and use of such data. Hence, we recommend the development of a customized support system that meets the specific requirements of big data analysis by users such as individuals, nongovernmental agencies, and academia. Our study is significant because it identified important but overlooked failure factors. Thus, it is necessary to prepare practical measures to increase the utilization of health big data in the future.

Isolation and identification of extracellular matrix proteins from oil-based CASPERized mouse brains for matrisomal analysis.

The extracellular matrix (ECM) components present within all tissues and organs help to maintain the cytoskeletal architecture and tissue morphology. Although the ECM plays a role in cellular events and signaling pathways, it has not been well studied due its insolubility and complexity. Brain tissue has a higher cell density and weaker mechanical strength than other tissues in the body. When removing cells using a general decellularization method to produce scaffolds and obtain ECM proteins, various problems must be considered because tissues are easily damaged. To retain the brain shape and ECM components, we performed decellularization in combination with polymerization. We immersed mouse brains in oil for polymerization and decellularization via O-CASPER (Oil-based Clinically and Experimentally Applicable Acellular Tissue Scaffold Production for Tissue Engineering and Regenerative Medicine) and then isolated ECM components using sequential matrisome preparation reagents (SMPRs), namely, RIPA, PNGase F, and concanavalin A. Adult mouse brains were preserved with our decellularization method. Western blot and LC-MS/MS analyses revealed that ECM components, including collagen and laminin, were isolated efficiently from decellularized mouse brains using SMPRs. Our method will be useful to obtain matrisomal data and perform functional studies using adult mouse brains and other tissues.

Generation of multilineage liver organoids with luminal vasculature and bile ducts from human pluripotent stem cells via modulation of Notch signaling.

BACKGROUND: The generation of liver organoids recapitulating parenchymal and non-parenchymal cell interplay is essential for the precise in vitro modeling of liver diseases. Although different types of multilineage liver organoids (mLOs) have been generated from human pluripotent stem cells (hPSCs), the assembly and concurrent differentiation of multiple cell types in individual mLOs remain a major challenge. Particularly, most studies focused on the vascularization of mLOs in host tissue after transplantation in vivo. However, relatively little information is available on the in vitro formation of luminal vasculature in mLOs themselves. METHODS: The mLOs with luminal blood vessels and bile ducts were generated by assembling hepatic endoderm, hepatic stellate cell-like cells (HscLCs), and endothelial cells derived entirely from hPSCs using 96-well ultra-low attachment plates. We analyzed the effect of HscLC incorporation and Notch signaling modulation on the formation of both bile ducts and vasculature in mLOs using immunofluorescence staining, qRT-PCR, ELISA, and live-perfusion imaging. The potential use of the mLOs in fibrosis modeling was evaluated by histological and gene expression analyses after treatment with pro-fibrotic cytokines. RESULTS: We found that hPSC-derived HscLCs are crucial for generating functional microvasculature in mLOs. HscLC incorporation and subsequent vascularization substantially reduced apoptotic cell death and promoted the survival and growth of mLOs with microvessels. In particular, precise modulation of Notch signaling during a specific time window in organoid differentiation was critical for generating both bile ducts and vasculature. Live-cell imaging, a series of confocal scans, and electron microscopy demonstrated that blood vessels were well distributed inside mLOs and had perfusable lumens in vitro. In addition, exposure of mLOs to pro-fibrotic cytokines induced early fibrosis-associated events, including upregulation of genes associated with fibrotic induction and endothelial cell activation (i.e., collagen I, α-SMA, and ICAM) together with destruction of tissue architecture and organoid shrinkage. CONCLUSION: Our results demonstrate that mLOs can reproduce parenchymal and non-parenchymal cell interactions and suggest that their application can advance the precise modeling of liver diseases in vitro.

Electrodeposition of Stable Noble-Metal-Free Co-P Electrocatalysts for Hydrogen Evolution Reaction.

Hydrogen production via water splitting has been extensively explored over the past few decades, and considerable effort has been directed toward finding more reactive and cost-effective electrocatalysts by engineering their compositions, shapes, and crystal structures. In this study, we developed hierarchical cobalt phosphide (Co-P) nanosphere assemblies as non-noble metal electrocatalysts via one-step electrodeposition. The morphologies of the Co-P nanostructures and their electrocatalytic activities towards the hydrogen evolution reactions (HER) were controlled by the applied potentials during electrodeposition. The physicochemical properties of the as-prepared Co-P nanostructures in this study were characterized by field-emission scanning electron microscopy, X-ray photoemission spectroscopy and X-ray diffraction. Linear sweep voltammetry revealed that the Co-P grown at -0.9 V showed the best HER performance exhibiting the highest electrochemical active surface area and lowest interfacial charge transfer resistance. The Co-P electrocatalysts showed superior long-term stability to electrodeposited Pt, indicating their potential benefits.

The Relation between Korean Children's Autonomy and Motor Development Mediated by Teacher-Child Relationships: A Focus on Gender Difference.

This study was conducted to identify the relation between children's autonomy and motor development mediated by teacher-child relationships. Are there differences between teacher-child relationships and motor development according to the gender of the child? To answer this question, the fundamental movement skills of 292 children were measured, and teacher-child relationship and children's autonomy data were collected from the teachers. There was a gender difference in locomotion skills; however, there was no difference in object control skills. In the case of girls, a conflict teacher-child relationship mediates the association between autonomy and object control skills. This study highlights the importance of teacher-child relationships, which are mainly discussed in relation to conventional social-emotional development, and provides examples of whole-child development.

Shinjulactone A Blocks Vascular Inflammation and the Endothelial-Mesenchymal Transition.

Objective: The endothelial inflammatory response plays an important role in atherogenesis by inducing nuclear factor (NF)κB-dependent cell adhesion molecule expression and monocyte recruitment. Here, we screened for natural ligands and investigated the ability of shinjulactone A to inhibit interleukin-1ß (IL-1ß)-induced endothelial inflammatory signaling. Methods: The natural compound library included 880 single compounds isolated from medicinal plants by the Korean Medicinal Material Bank. Primary endothelial cells were pretreated with single compounds before stimulation with IL-1ß to induce endothelial inflammation. Endothelial inflammation was measured by assaying NFκB activation and monocyte adhesion. The endothelial-mesenchymal transition (EndMT) was evaluated using cell type-specific marker protein expression and morphology. Results: Shinjulactone A was identified as an efficient blocker of IL-1ß -induced NFκB activation, with a half-maximal inhibitory concentration of approximately 1 µM, and monocyte recruitment in endothelial cells. However, it did not affect lipopolysaccharide-induced NFκB activation in macrophages. Compared to Bay 11-782, a well-known NFκB inhibitor that shows considerable cytotoxicity during long-term treatment, shinjulactone A did not affect endothelial cell viability. Furthermore, it also significantly inhibited the EndMT, which is known to promote atherosclerosis and plaque instability. Conclusion: We suggest that shinjulactone A may be an effective and safe drug candidate for atherosclerosis because it targets and inhibits both endothelial inflammation and the EndMT, without impairing NFκB-dependent innate immunity in macrophages.

Two-dimensional Transition metal Dichalcogenides as an Emerging Platform for Singlet Fission Solar Cells.

Singlet fission, a rapid exciton doubling process via inverse Auger recombination, is recognized as one of the most practical and feasible means for overcoming the Shockley-Queisser limit. Singlet fission solar cells are generally developed by integrating photon downconversion organic semiconductors into conventional photovoltaic devices to break the maximum photovoltaic response of the host semiconductors by virtue of extra triplet excitons. In this regard, proper matching of two different semiconductors and heterointerface engineering are both crucial for highly efficient singlet fission solar cells. Therefore, the aim of this study is to review the prerequisite conditions for efficient triplet transfer at the heterointerfaces and thus highlight the robust spin and valley degrees of freedom of transition metal dichalcogenides with the ultimate goal of stimulating research into next-generation singlet fission solar cells.

Induction of human trophoblast stem-like cells from primed pluripotent stem cells.

The placenta is a transient but important multifunctional organ crucial for healthy pregnancy for both mother and fetus. Nevertheless, limited access to human placenta samples and the paucity of a proper in vitro model system have hampered our understanding of the mechanisms underlying early human placental development and placenta-associated pregnancy complications. To overcome these constraints, we established a simple procedure with a short-term treatment of bone morphogenetic protein 4 (BMP4) in trophoblast stem cell culture medium (TSCM) to convert human primed pluripotent stem cells (PSCs) to trophoblast stem-like cells (TSLCs). These TSLCs show not only morphology and global gene expression profiles comparable to bona fide human trophoblast stem cells (TSCs) but also long-term self-renewal capacity with bipotency that allows the cells to differentiate into functional extravillous trophoblasts (EVT) and syncytiotrophoblasts (ST). These indicate that TSLCs are equivalent to genuine human TSCs. Our data suggest a straightforward approach to make human TSCs directly from preexisting primed PSCs and provide a valuable opportunity to study human placenta development and pathology from patients with placenta-related diseases.

Network-based integrated analysis for toxic effects of high-concentration formaldehyde inhalation exposure through the toxicogenomic approach.

Formaldehyde is a colorless, pungent, highly reactive, and toxic environmental pollutant used in various industries and products. Inhaled formaldehyde is a human and animal carcinogen that causes genotoxicity, such as reactive oxygen species formation and DNA damage. This study aimed to identify the toxic effects of inhaled formaldehyde through an integrated toxicogenomic approach utilizing database information. Microarray datasets (GSE7002 and GSE23179) were collected from the Gene Expression Omnibus database, and differentially expressed genes were identified. The network analyses led to the construction of the respiratory system-related biological network associated with formaldehyde exposure, and six upregulated hub genes (AREG, CXCL2, HMOX1, PLAUR, PTGS2, and TIMP1) were identified. The expression levels of these genes were verified via qRT-PCR in 3D reconstructed human airway tissues exposed to aerosolized formaldehyde. Furthermore, NRARP was newly found as a potential gene associated with the respiratory and carcinogenic effects of formaldehyde by comparison with human in vivo and in vitro formaldehyde-exposure data. This study improves the understanding of the toxic mechanism of formaldehyde and suggests a more applicable analytic pipeline for predicting the toxic effects of inhaled toxicants.

Release of Notch activity coordinated by IL-1ß signalling confers differentiation plasticity of airway progenitors via Fosl2 during alveolar regeneration.

While the acquisition of cellular plasticity in adult stem cells is essential for rapid regeneration after tissue injury, little is known about the underlying mechanisms governing this process. Our data reveal the coordination of airway progenitor differentiation plasticity by inflammatory signals during alveolar regeneration. Following damage, interleukin-1ß (IL-1ß) signalling-dependent modulation of Jag1 and Jag2 expression in ciliated cells results in the inhibition of Notch signalling in secretory cells, which drives the reprogramming and acquisition of differentiation plasticity. We identify the transcription factor Fosl2 (also known as Fra2) for secretory cell fate conversion to alveolar type 2 cells that retain the distinct genetic and epigenetic signatures of secretory lineages. We also reveal that human secretory cells positive for KDR (also known as FLK-1) display a conserved capacity to generate alveolar type 2 cells via Notch inhibition. Our results demonstrate the functional role of an IL-1ß-Notch-Fosl2 axis in the fate decision of secretory cells during injury repair, proposing a potential therapeutic target for human lung alveolar regeneration.

Nanoparticles: Weighing the Pros and Cons from an Eco-genotoxicological Perspective.

The exponential growth of nanotechnology and the industrial production have raised concerns over its impact on human and environmental health and safety (EHS). Although there has been substantial progress in the assessment of pristine nanoparticle toxicities, their EHS impacts require greater clarification. In this review, we discuss studies that have assessed nanoparticle eco-genotoxicity in different test systems and their fate in the environment as well as the considerable confounding factors that may complicate the results. We highlight key mechanisms of nanoparticle-mediated genotoxicity. Then we discuss the reliability of endpoint assays, such as the comet assay, the most favored assessment technique because of its versatility to measure low levels of DNA strand breakage, and the micronucleus assay, which is complementary to the former because of its greater ability to detect chromosomal DNA fragmentation. We also address the current recommendations on experimental design, including environmentally relevant concentrations and suitable exposure duration to avoid false-positive or -negative results. The genotoxicity of nanoparticles depends on their physicochemical features and the presence of co-pollutants. Thus, the effect of environmental processes (e.g., aggregation and agglomeration, adsorption, and transformation of nanoparticles) would account for when determining the actual genotoxicity relevant to environmental systems, and assay procedures must be standardized. Indeed, the engineered nanoparticles offer potential applications in different fields including biomedicine, environment, agriculture, and industry. Toxicological pathways and the potential risk factors related to genotoxic responses in biological organisms and environments need to be clarified before appropriate and sustainable applications of nanoparticles can be established.

Depletion of Mitochondrial Components from Extracellular Vesicles Secreted from Astrocytes in a Mouse Model of Fragile X Syndrome.

Mitochondrial dysfunction contributes to neurodegenerative diseases and developmental disorders such as Fragile X syndrome (FXS). The cross-talk between mitochondria and extracellular vesicles (EVs) suggests that EVs may transfer mitochondrial components as intermediators for intracellular communication under physiological and pathological conditions. In the present study, the ability of EVs to transfer mitochondrial components and their role in mitochondrial dysfunction in astrocytes were examined in the brains of Fmr1 knockout (KO) mice, a model of FXS. The amounts of mitochondrial transcription factor NRF-1, ATP synthases ATP5A and ATPB, and the mitochondrial membrane protein VDAC1 in EVs were reduced in cerebral cortex samples and astrocytes from Fmr1 KO mice. These reductions correspond to decreased mitochondrial biogenesis and transcriptional activities in Fmr1 KO brain, along with decreased mitochondrial membrane potential (MMP) with abnormal localization of vimentin intermediate filament (VIF) in Fmr1 KO astrocytes. Our results suggest that mitochondrial dysfunction in astrocytes is associated with the pathogenesis of FXS and can be monitored by depletion of components in EVs. These findings may improve the ability to diagnose developmental diseases associated with mitochondrial dysfunction, such as FXS and autism spectrum disorders (ASD).

Therapeutic potential of CKD-506, a novel selective histone deacetylase 6 inhibitor, in a murine model of rheumatoid arthritis.

OBJECTIVES: Histone deacetylase (HDAC) 6 promotes inflammation. We investigated the anti-arthritic effects of CKD-506, a novel HDAC6 inhibitor, in vitro and in a murine model of arthritis as a novel treatment option for rheumatoid arthritis (RA). METHODS: HDAC6 was overexpressed in mouse peritoneal macrophages and RAW 264.7 cells, and the effects of a HDAC6 inhibitor CKD-506 on cytokine production and activity of NF-κB and AP-1 signaling were examined. Peripheral blood mononuclear cells (PBMCs) from RA patients and fibroblast-like synoviocytes (FLS) were activated in the presence of CKD-506. Next, regulatory T cells (Tregs) were induced from RA patients and co-cultured with healthy effector T cells (Teffs) and cell proliferation was analyzed by flow cytometry. Finally, the effects of the inhibitor on the severity of arthritis were assessed in a murine model of adjuvant-induced arthritis (AIA). RESULTS: Overexpression of HDAC6 induced macrophages to produce TNF-α and IL-6. The inhibitory effect of CKD-506 was mediated via blockade of NF-κB and AP-1 activation. HDAC6 inhibition reduced TNF-α and IL-6 production by activated RA PBMCs. CKD-506 inhibited production of MMP-1, MMP-3, IL-6, and IL-8 by activated FLS. In addition, CKD-506 inhibited proliferation of Teffs directly and indirectly by improving iTreg function. In AIA rats, oral CKD-506 improved clinical arthritis in a dose-dependent manner. A combination of sub-therapeutic CKD-506 and methotrexate exerted a synergistic effect. CONCLUSION: The novel HDAC6 inhibitor CKD-506 suppresses inflammatory responses by monocytes/macrophages, improves Treg function, and ameliorates arthritis severity in a murine model of RA. Thus, CKD-506 might be a novel and effective treatment option for RA.

Electrocatalytic glycerol oxidation enabled by surface plasmon polariton-induced hot carriers in Kretschmann configuration.

Plasmonic hot carrier generation has attracted increasing attention due to its ability to convert light to electrical energy. The generation of plasmon-induced hot carriers can be achieved via Landau damping in the non-radiative decay process of the plasmonic excitation energy. Localized surface plasmons (LSPs) undergo both radiative and non-radiative decays, while surface plasmon polaritons (SPPs) dissipate only via the non-radiative decay. Thus, it is a challenging task to exploit the surface plasmon polaritons for the efficient generation of hot carriers and their applications. In this study, a model hot-carrier-mediated electrocatalytic conversion system was demonstrated using an Au thin film in Kretschmann configuration, which is the representative platform to excite SPPs. AgPt-decorated Au nanobipyramids (AuNBPs) were designed and introduced onto the Au film, creating hot-spots to revolutionize the thin film-based photon-to-carrier conversion efficiency. The glycerol electro-oxidation reaction enabled by such SPP-induced hot carriers was evaluated and exhibited a photon-to-hot carrier conversion efficiency of 2.4 × 10-3%, which is ∼2.5 times enhanced as compared to the efficiency based on the neat Au film.

Super-enhancer-guided mapping of regulatory networks controlling mouse trophoblast stem cells.

Trophectoderm (TE) lineage development is pivotal for proper implantation, placentation, and healthy pregnancy. However, only a few TE-specific transcription factors (TFs) have been systematically characterized, hindering our understanding of the process. To elucidate regulatory mechanisms underlying TE development, here we map super-enhancers (SEs) in trophoblast stem cells (TSCs) as a model. We find both prominent TE-specific master TFs (Cdx2, Gata3, and Tead4), and >150 TFs that had not been previously implicated in TE lineage, that are SE-associated. Mapping targets of 27 SE-predicted TFs reveals a highly intertwined transcriptional regulatory circuitry. Intriguingly, SE-predicted TFs show 4 distinct expression patterns with dynamic alterations of their targets during TSC differentiation. Furthermore, depletion of a subset of TFs results in dysregulation of the markers for specialized cell types in placenta, suggesting a role during TE differentiation. Collectively, we characterize an expanded TE-specific regulatory network, providing a framework for understanding TE lineage development and placentation.

Systematic Discovery of Endogenous Human Ribonucleoprotein Complexes.

RNA-binding proteins (RBPs) play essential roles in biology and are frequently associated with human disease. Although recent studies have systematically identified individual RNA-binding proteins, their higher-order assembly into ribonucleoprotein (RNP) complexes has not been systematically investigated. Here, we describe a proteomics method for systematic identification of RNP complexes in human cells. We identify 1,428 protein complexes that associate with RNA, indicating that more than 20% of known human protein complexes contain RNA. To explore the role of RNA in the assembly of each complex, we identify complexes that dissociate, change composition, or form stable protein-only complexes in the absence of RNA. We use our method to systematically identify cell-type-specific RNA-associated proteins in mouse embryonic stem cells and finally, distribute our resource, rna.MAP, in an easy-to-use online interface (rna.proteincomplexes.org). Our system thus provides a methodology for explorations across human tissues, disease states, and throughout all domains of life.