Functional Cooperation Research Articles

Safe Human Dual-Robot Interaction Based on Control Barrier Functions and Cooperation Functions

Safe Human Dual-Robot Interaction Based on Control Barrier Functions and Cooperation Functions

Calixarene incorporated molecular imprinting on covalent organic framework for supramolecular recognition and specific extraction of citrinin

Specific recognition and selective extraction of mycotoxin in environmental and food matrixes is significant to guarantee public health. Covalent organic frameworks (COFs) are promising adsorbents with tailorable functionality, but their low binding affinity and poor selectivity hamper their wide application for selective extraction of trace mycotoxin from complex matrix. Herein, we report calixarene incorporated molecular imprinting on COF to prepare molecularly imprinted calix[4]arene-containing COF (MICOF-CX4) for supramolecular recognition and specific adsorption of citrinin. Calixarene with host-guest chemistry was used as a functional monomer, while amine units with different topologies and function groups were selected to regulate MICOF-CX4 to match with citrinin. The complementary shape and supramolecular interactions of MICOF-CX4 gave highly selective recognition for citrinin. Moreover, MICOF-CX4 with vast accessible surface and plentiful imprinting sites exhibited faster adsorption kinetics and 4-fold higher adsorption capacity for citrinin adsorption than no-imprinted COF-CX4. Combination of MICOF-CX4 based solid-phase extraction with high-performance liquid chromatography-mass spectrometry allowed interference free determination of trace citrinin in real samples with a low detection limit of 0.03 ng mL−1, good precision of 4.5 % and quantitative recovery of 88.2 %−101.4 %. The cooperative functions of calixarene and molecular imprinting make COF promising adsorbent for specific adsorption of trace targets in complex matrixes.

Molecular mechanism for regulating APOBEC3G DNA editing function by the non-catalytic domain

APOBEC3G, part of the AID/APOBEC cytidine deaminase family, is crucial for antiviral immunity. It has two zinc-coordinated cytidine-deaminase domains. The non-catalytic N-terminal domain strongly binds to nucleic acids, whereas the C-terminal domain catalyzes C-to-U editing in single-stranded DNA. The interplay between the two domains is not fully understood. Here, we show that DNA editing function of rhesus macaque APOBEC3G on linear and hairpin loop DNA is enhanced by AA or GA dinucleotide motifs present downstream in the 3’-direction of the target-C editing sites. The effective distance between AA/GA and the target-C sites is contingent on the local DNA secondary structure. We present two co-crystal structures of rhesus macaque APOBEC3G bound to ssDNA containing AA and GA, revealing the contribution of the non-catalytic domain in capturing AA/GA DNA. Our findings elucidate the molecular mechanism of APOBEC3G’s cooperative function, which is critical for its antiviral role and its contribution to mutations in cancer genomes.

Integrated multi-omics analysis of PBX1 in mouse adult neural stem- and progenitor cells identifies a transcriptional module that functionally links PBX1 to TCF3/4.

Developmental transcription factors act in networks, but how these networks achieve cell- and tissue specificity is still poorly understood. Here, we explored pre-B cell leukemia homeobox 1 (PBX1) in adult neurogenesis combining genomic, transcriptomic, and proteomic approaches. ChIP-seq analysis uncovered PBX1 binding to numerous genomic sites. Integration of PBX1 ChIP-seq with ATAC-seq data predicted interaction partners, which were subsequently validated by mass spectrometry. Whole transcriptome spatial RNA analysis revealed shared expression dynamics of Pbx1 and interacting factors. Among these were class I bHLH proteins TCF3 and TCF4. RNA-seq following Pbx1, Tcf3 or Tcf4 knockdown identified proliferation- and differentiation associated genes as shared targets, while sphere formation assays following knockdown argued for functional cooperativity of PBX1 and TCF3 in progenitor cell proliferation. Notably, while physiological PBX1-TCF interaction has not yet been described, chromosomal translocation resulting in genomic TCF3::PBX1 fusion characterizes a subtype of acute lymphoblastic leukemia. Introducing Pbx1 into Nalm6 cells, a pre-B cell line expressing TCF3 but lacking PBX1, upregulated the leukemogenic genes BLK and NOTCH3, arguing that functional PBX1-TCF cooperativity likely extends to hematopoiesis. Our study hence uncovers a transcriptional module orchestrating the balance between progenitor cell proliferation and differentiation in adult neurogenesis with potential implications for leukemia etiology.

Abnormal functional lateralization and cooperation in bipolar disorder are associated with neurotransmitter and cellular profiles

BackgroundHemispheric lateralization and cooperation are essential for efficient brain function, and aberrations in both have been found in psychiatric disorders such as schizophrenia. This study investigated alterations in hemispheric lateralization and cooperation among patients with bipolar disorder (BD) and associations with neurotransmitter and cell-type density distributions to identify potential molecular and cellular pathomechanisms. MethodsSixty-seven BD patients and 127 healthy controls (HCs) were examined by resting-state functional MRI (rs-fMRI). Whole-brain maps of the autonomy index (AI) and connectivity between functionally homotopic voxels (CFH) were constructed to reveal BD-specific changes in brain functional lateralization and interhemispheric cooperation, respectively. Spatial associations of regional AI and CFH abnormalities with neurotransmitter and cell-type density distributions were examined by correlation analyses. ResultsBipolar disorder patients exhibited higher AI values in left superior parietal gyrus, cerebellar right Crus I, and cerebellar right Crus II, and these regional abnormalities were associated with the relative densities (proportions) of oligodendrocyte precursor cells and microglia. Patients also exhibited lower CFH values in right inferior parietal gyrus, bilateral middle occipital gyrus, left postcentral gyrus, and bilateral cerebellar crus II, and these regional abnormalities were associated with the densities of serotonin 1A and dopamine D2 receptors, oligodendrocyte precursor cells, astrocytes, and neurons. ConclusionsThese findings indicate that abnormal functional lateralization and cooperation in BD with potential molecular and cellular basis.

Increases in 4-Acetaminobutyric Acid Generated by Phosphomevalonate Kinase Suppress CD8+ T Cell Activation and Allow Tumor Immune Escape.

Certain metabolites in the tumor microenvironment (TME) can alter innate immunity. Here, it is shown how phosphomevalonate kinase (PMVK) allows hepatocellular carcinoma (HCC) cells to overcome the anti-tumor immunity mediated by CD8+ T cells. In HCCs, depletion of PMVK is required to facilitate CD8+ T cell activation and their subsequent suppression of tumor growth. Mechanistically, PMVK phosphorylates and stabilizes glutamate decarboxylase 1 (GAD1), thus increasing the synthesis of γ-aminobutyric acid (GABA), which normally functions as a neurotransmitter. However, PMVK also recruits acetyl-CoA acetyltransferase 1 (ACAT1) and allows it to convert GABA, to 4-acetaminobutyric acid (4-Ac-GABA), which is released into the TME. There, 4-Ac-GABA activates the GABAA receptor (GABAAR) on CD8+ T cells, which inhibits AKT1 signaling. This in turn suppresses CD8+ T cell activation, intratumoral infiltration, and the anti-tumor response. Inhibiting PMVK or GABAAR in HCC mouse models overcomes resistance to anti-PD-1 immune checkpoint therapy. These findings reveal non-canonical and cooperative functions among the key metabolic enzymes PMVK, GAD1, and ACAT1 that reprogram glutamine metabolism to synthesize a potent CD8+ T cell inhibitor 4-Ac-GABA. Blocking 4-Ac-GABA signaling in CD8+ T cells, particularly when combined with immune checkpoint inhibition, potentially represents a new and potent form of immunotherapy.

Exploring the transcriptional cooperation between RUNX2 and its associated elncRNA RAIN

Recent insights into the mechanisms controlling gene expression identified enhancer-associated long non-coding RNAs (elncRNAs) as master players of transcription in cancers. RUNX2, a mammalian RUNT-related transcription factor, is increasingly recognized in cancer biology for its role in supporting survival and progression also in thyroid cancer (TC). We recently identified, within the RUNX2 locus, a novel elncRNA that we named RAIN (RUNX2 associated intergenic lncRNA). We showed that RAIN and RUNX2 expression correlate in TC, both in vitro and in vivo, and that RAIN promotes RUNX2 expression by interacting with and affecting the activity of the RUNX2 P2 promoter through two distinct mechanisms. Here, we took forward these observations to explore the genome-wide transcriptional function of RAIN and its contribution to the RUNX2-dependent gene expression program in TC. By combining multiple omics data, we demonstrated that RAIN functionally cooperates with RUNX2 to the regulation of a subset of functionally related genes involved in promoting matrix remodeling, migration, and loss of differentiation. We showed that RAIN interacts with RUNX2 and its expression is required for the efficient recruitment of this TF to its target regulatory regions. In addition, our data revealed that besides RUNX2, RAIN governs a hierarchically organized complex transcriptional program by controlling a core of cancer-associated TFs that, in turn, orchestrate the expression of downstream genes. This evidence indicates that the functional cooperation observed between RAIN and RUNX2 can be a diffuse work mechanism for this elncRNA.

Characteristics and transcriptional regulators of spontaneous epithelial–mesenchymal transition in genetically unperturbed patient-derived non-spindled breast carcinoma

BackgroundAlthough tumor cells undergoing epithelial–mesenchymal transition (EMT) typically exhibit spindle morphology in experimental models, such histomorphological evidence of EMT has predominantly been observed in rare primary spindle carcinomas. The characteristics and transcriptional regulators of spontaneous EMT in genetically unperturbed non-spindled carcinomas remain underexplored.MethodsWe used primary culture combined with RNA sequencing (RNA-seq), single-cell RNA-seq (scRNA-seq), and in situ RNA-seq to explore the characteristics and transcription factors (TFs) associated with potential spontaneous EMT in non-spindled breast carcinoma.ResultsOur primary culture revealed carcinoma cells expressing diverse epithelial–mesenchymal traits, consistent with epithelial–mesenchymal plasticity. Importantly, carcinoma cells undergoing spontaneous EMT did not necessarily exhibit spindle morphology, even when undergoing complete EMT. EMT was a favored process, whereas mesenchymal–epithelial transition appeared to be crucial for secondary tumor growth. Through scRNA-seq, we identified TFs that were sequentially and significantly upregulated as carcinoma cells progressed through the EMT process, which correlated with increasing VIM expression. Once upregulated, the TFs remained active throughout the EMT process. ZEB1 was a key initiator and sustainer of EMT, as indicated by its earliest significant upregulation in the EMT process, its exact correlation with VIM expression, and the reversal of EMT and downregulation of EMT-upregulated TFs upon ZEB1 knockdown. The correlation between ZEB1 and vimentin expression in triple-negative breast cancer and metaplastic breast carcinoma tumor cohorts further highlighted its role. The immediate upregulation of ZEB2 following that of ZEB1, along with the observation that the knockdown of ZEB1 or ZEB2 downregulates both ZEB1 and ZEB2 concomitant with the reversal of EMT, suggests their functional cooperation in EMT. This finding, together with that of a lack of correlation of SNAI1, SNAI2, and TWIST1 expression with the mesenchymal phenotype, indicated EMT-TFs have a context-dependent role in EMT. Upregulation of EMT-related gene signatures during EMT correlated with poor patient outcomes, highlighting the biological importance of the model. Elevated EMT gene signatures and increased ZEB1 and ZEB2 expression in vimentin-positive compared to vimentin-negative carcinoma cells within the corresponding primary tumor tissue confirmed ZEB1 and ZEB2 as intrinsic, instead of microenvironmentally-induced, EMT regulators, and vimentin as an in vivo indicator of EMT.ConclusionsOur findings provide insights into the characteristics and transcriptional regulators of spontaneous EMT in primary non-spindled carcinoma.

RBPMS promotes contractile phenotype splicing in human embryonic stem cell derived vascular smooth muscle cells.

Differentiated Vascular Smooth Muscle Cells (VSMCs) express a unique network of mRNA isoforms via smooth muscle specific alternative splicing (SM-AS) in functionally critical genes, including those comprising the contractile machinery. We previously described RNA Binding Protein Multiple Splicing (RBPMS) as a potent driver of differentiated SM-AS in the rat PAC1 VSMC cell line. What is unknown is how RBPMS affects VSMC phenotype and behaviour. Here, we aimed to dissect the role of RBPMS in SM-AS in human cells and determine the impact on VSMC phenotypic properties. We used human embryonic stem cell-derived VSMCs (hESC-VSMCs) as our platform. hESC-VSMCs are inherently immature and we found that they display only partially differentiated SM-AS patterns while RBPMS protein levels are low. We found that RBPMS overexpression induces SM-AS patterns in hESC-VSMCs akin to the contractile tissue VSMC splicing patterns. We present in silico and experimental findings that support RBPMS' splicing activity as mediated through direct binding and via functional cooperativity with splicing factor RBFOX2 on a significant subset of targets. We also demonstrate that RBPMS can alter the motility and the proliferative properties of hESC-VSMCs to mimic a more differentiated state. Overall, this study emphasizes a critical role for RBPMS in establishing the contractile phenotype splicing program of human VSMCs.

The Reinvigoration of the Organization of Turkic States amid Ongoing Geopolitical Unrest and Economic Uncertainty

The recent regional events and the geopolitical consequences of the Russo-Ukrainian war have had a profound impact on the dynamics among Türkiye, Azerbaijan, and the Central Asian Turkic states (Kazakhstan, Uzbekistan, and Kyrgyzstan). This shifting geopolitical landscape has been the catalyst of collaboration and integration for these countries under the Organization of Turkic States (OTS), an intergovernmental organization that aims to foster cooperation among Turkic-speaking nations. Being established in 2009, this emerging bloc has pursued a relatively low-profile policy on geopolitical issues in the past decade. However, after years of relatively little activity, things have started to change drastically due to the global situation that is being shaped by wider geopolitical factors. The OTS steadily began to pursue a more ambitious agenda and eventually helped bolster relations and stimulate regional socio-economic development efforts during the last four years, focusing on building stronger regional cooperation through ethnocultural links. The article examines how the Turkic alliance has stimulated functional cooperation through the facilitation of trade, investment, and economic cooperation among its members and observer states.

Cooperative nuclear action of RNA-binding proteins PSF and G3BP2 to sustain neuronal cell viability is decreased in aging and dementia.

Dysfunctional RNA-binding proteins (RBPs) have been implicated in several geriatric diseases, including Alzheimer's disease (AD). However, little is known about the nuclear molecular actions and cooperative functions mediated by RBPs that affect gene regulation in sporadic AD or aging. In the present study, we investigated aging- and AD-associated changes in the expression of PSF and G3BP2, which are representative RBPs associated with sex hormone activity. We determined that both PSF and G3BP2 levels were decreased in aged brains compared to young brains of mice. RNA sequencing (RNA-seq) analysis of human neuronal cells has shown that PSF is responsible for neuron-specific functions and sustains cell viability. In addition, we showed that PSF interacted with G3BP2 in the nucleus and stress granules (SGs) at the protein level. Moreover, PSF-mediated gene regulation at the RNA level correlated with G3BP2. Interestingly, PSF and G3BP2 target genes are associated with AD development. Mechanistically, quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis demonstrated that the interaction of RBPs with the pre-mRNA of target genes enhanced post-transcriptional mRNA stability, suggesting a possible role for these RBPs in preserving neuronal cell viability. Notably, in the brains of patients with sporadic AD, decreased expression of PSF and G3BP2 in neurons was observed compared to non-AD patients. Overall, our findings suggest that the cooperative action of PSF and G3BP2 in the nucleus is important for preventing aging and AD development.

Reasons for Barries in Family-School Cooperation

The concept of family-school cooperation was proposed very early, and its importance has always been emphasized. However, due to the excessive acceleration of the life cycle and the extension of working hours, families have unilaterally delegated the responsibility for children's education to schools. This negative situation for student growth needs to be reversed. Families must realize that the role of the school is to complement the work initiated by the family, not to replace it. Schools also need to realize that without the cooperation of families, school functions and outcomes will be limited. However, awareness is not enough, it is necessary to know the causes of this phenomenon. Therefore, this paper conducted a systematic review of previously published research on the causes of barriers to family-school cooperation. Based on Bronfenbrenner's ecological systems theory and Epstein's overlapping spheres of influence theory, the reasons for obstacles in family-school cooperation will be analyzed from different perspectives

Genesis of regional innovation ecosystems: review and modern interpretation

The article deals with problems in the application of the innovative ecosystem concept. The research is based on systems theory, innovation system theory, the theory of regional innovation systems, and the concept of open innovation. The purpose of the study is to determine the theoretical basis for applying the ecosystem concept to the development of innovation systems in regions. In the course of the study the preconditions for the formation of innovative ecosystems in the regions (acceleration of innovation; complexity of the innovation process and interdisciplinary approach to innovation; application of the concept of open innovation; acceleration of introducing the innovation to the market; possibility of functional complementarity and cooperation; possibility of joint and more efficient use of resources and infrastructure; regional differentiation; innovation risks sharing) were identified. During the work the approaches to the concept of innovation ecosystem that reflect the multidimensionality of innovation ecosystems were revealed. The article clarifies the features of the innovative ecosystems (complexity, openness, interdependence and complementarity of elements, dynamism, non-linearity) and the innovative ecosystems principles (emergence, synergy, adaptability, self-development, sustainability, self-organization, co-evolution). The study highlights the mechanisms of interactions among subjects of the innovation ecosystem (cooperation, competition, coordination, regulation, joint management) that lead to a synergetic effect for the actors of the innovation ecosystem. The obtained results systematize knowledge about innovative ecosystems and form a theoretical basis for the features of their formation and development in the regions, which can find practical application when identifying instruments of regional innovation policy.

Connecting and integrating cooperation within and between species.

There has long been a fundamental divide in the study of cooperation: researchers focus either on cooperation within species, including but not limited to sociality, or else on cooperation between species, commonly termed mutualism. Here, we explore the ecologically and evolutionarily significant ways in which within- and between-species cooperation interact. We highlight two primary cross-linkages. First, cooperation of one type can change the context in which cooperation of the other type functions, and thus potentially its outcome. We delineate three possibilities: (i) within-species cooperation modulates benefits for a heterospecific partner; (ii) between-species cooperation affects the dynamics of within-species cooperation; and (iii) both processes take place interactively. The second type of cross-linkage emerges when resources or services that cooperation makes available are obtainable either from members of the same species or from different species. This brings cooperation at the two levels into direct interaction, to some extent obscuring the distinction between them. We expand on these intersections between within- and between-species cooperation in a diversity of taxa and interaction types. These interactions have the potential to weave together social networks and trophic dynamics, contributing to the structure and functioning of ecological communities in ways that are just beginning to be explored. This article is part of the theme issue 'Connected interactions: enriching food web research by spatial and social interactions'.

SCA44- and SCAR13-associated GRM1 mutations affect metabotropic glutamate receptor 1 function through distinct mechanisms.

Metabotropic glutamate receptor 1 (mGlu1) is a promising therapeutic target for neurodegenerative CNS disorders including spinocerebellar ataxias (SCAs). Clinical reports have identified naturally-occurring mGlu1 mutations in rare SCA subtypes and linked symptoms to mGlu1 mutations. However, how mutations alter mGlu1 function remains unknown, as does amenability of receptor function to pharmacological rescue. Here, we explored SCA-associated mutation effects on mGlu1 cell surface expression, canonical signal transduction and allosteric ligand pharmacology. Orthosteric agonists, positive allosteric modulators (PAMs) and negative allosteric modulators (NAMs) were assessed at two functional endpoints (iCa2+ mobilisation and inositol 1-phosphate [IP1] accumulation) in FlpIn Trex HEK293A cell lines expressing five mutant mGlu1 subtypes. Key pharmacological parameters including ligand potency, affinity and cooperativity were derived using operational models of agonism and allostery. mGlu1 mutants exhibited differential impacts on mGlu1 expression, with a C-terminus truncation significantly reducing surface expression. Mutations differentially influenced orthosteric ligand affinity, efficacy and functional cooperativity between allosteric and orthosteric ligands. Loss-of-function mutations L454F and N885del reduced orthosteric affinity and efficacy, respectively. A gain-of-function Y792C mutant mGlu1 displayed enhanced constitutive activity in IP1 assays, which manifested as reduced orthosteric agonist activity. The mGlu1 PAMs restored glutamate potency in iCa2+ mobilisation for loss-of-function mutations and mGlu1 NAMs displayed enhanced inverse agonist activity at Y792C relative to wild-type mGlu1. Collectively, these data highlight distinct mechanisms by which mGlu1 mutations affect receptor function and show allosteric modulators may present a therapeutic strategy to restore aberrant mGlu1 function in rare SCA subtypes.

Broadening the scope: Multiple functional connectivity networks underlying threat conditioning and extinction

Abstract Threat learning processes are thought to be foundational to anxiety and fear-related disorders. However, the study of these processes in the human brain has largely focused on specific brain regions, owing partly to the ease of translating between these regions in human and nonhuman animals. Moving beyond analyzing focal regions of interest to whole-brain dynamics and connectivity during threat learning is essential for understanding the neuropathology of fear-related disorders in humans. In this study, 223 participants completed a 2-day Pavlovian threat conditioning paradigm while undergoing fMRI. Participants completed threat acquisition and extinction. Extinction recall was assessed 48 hours later. Using a data-driven group independent component analysis (ICA), we examined large-scale functional connectivity networks during each phase of threat learning. Connectivity networks were tested to see how they responded to conditioned stimuli during early and late phases of threat acquisition and extinction as well as during early trials of extinction recall. A network overlapping with the default mode network involving hippocampus, ventromedial prefrontal cortex (vmPFC), and posterior cingulate was implicated in threat acquisition and extinction. Another network overlapping with the salience network involving dorsal anterior cingulate cortex (dACC), mPFC, and inferior frontal gyrus was implicated both in threat acquisition and in extinction recall. Other networks overlapping with parts of the salience, somatomotor, visual, and frontoparietal networks were involved in the acquisition or in the extinction of learned threat responses. These findings help support the functional cooperation of specific brain regions during threat learning in a model-free fashion while introducing new findings of spatially independent functional connectivity networks during threat and safety learning. Rather than being a single process in a core network of regions, threat learning involves multiple brain networks operating in parallel performing different functions at different timescales. Understanding the nature and interplay of these dynamics will be critical for comprehensive understanding of the multiple processes that may be at play in the neuropathology of anxiety and fear-related disorders.

Analysis of Farmer's Perception and Constraints on Dairy Cooperatives in Amhara Region, Ethiopia

This study was done to examine the farmer’s perception and constraints on dairy cooperatives in Amhara region, Ethiopia. A sample of 266 smallholder dairy farmers was selected using a multi-stage sampling technique. Perception of farmers was analyzed using relative importance index, and constraints of dairy cooperative performance were analyzed using Henry Garrett's ranking technique. The result indicates that farmers have a positive perception of certain attributes of dairy cooperatives; such as increasing social networks, improving income, and serving as a saving source. This suggests that farmers believe these aspects of dairy cooperatives are beneficial. Conversely, farmers have concerns and dissatisfaction with the way the cooperative is running, the loyalty of members to the cooperative, member's treatment by cooperatives, and the decision-making process. The study also identified that lack of milk processing facilities, poor member awareness, and member involvement in the decision-making process are the foremost internal challenges of dairy cooperatives, while high cost of cross-breed cows, occurrence of animal disease, and low productivity of local breed cows are external constraints hindering dairy cooperative performance. Thus, to enhance farmers' perception and participation in cooperative activities, emphasis should be given to addressing concerns and improving the overall functioning of dairy cooperatives.

Altered tumor microenvironment heterogeneity of penile cancer during progression from non-lymphatic to lymphatic metastasis.

Lymphatic metastasis is the major challenge in the treatment of penile cancer. The prognosis of individuals with lymphatic metastasis is extremely poor. Therefore, early identification of disease progression and lymphatic metastasis is an urgent task for researchers in penile cancer worldwide. In this study, using single-cell RNA sequencing, an immune landscape was established for the cancer ecosystem based on 46,861 cells from six patients with penile cancer (four with lymphatic metastasis [stage IV] and two without lymphatic metastasis [stage I]). Using bulk RNA sequencing, the discrepancy between the cancers and their respective metastatic lymph nodes was depicted based on seven patients with penile cancer. The interaction between epithelial cells, fibroblasts, and endothelial cells, and the functional cooperation among invasion, epithelial-mesenchymal transition, and angiogenesis were found to be important landscapes in the penile cancer ecosystem, playing important roles in progression of cancer and lymph node metastasis. This study is the first to investigate the altered tumor microenvironment heterogeneity of penile cancer as it evolves from non-lymphatic to lymphatic metastasis and provides insights into the mechanisms underlying malignant progression, the premetastatic niche, and lymphatic metastasis in penile cancer.

Flexible Hydrazone‐Linked Metal‐Covalent Organic Frameworks with Copper Clusters for Efficient Electrocatalytic Oxygen Evolution Reaction

AbstractDespite the challenges associated with the synthesis of flexible metal‐covalent organic frameworks (MCOFs), these offer the unique advantage of maximizing the atomic utilization efficiency. However, the construction of flexible MCOFs with flexible building units or linkages has rarely been reported. In this study, novel flexible MCOFs are constructed using flexible building blocks and copper clusters with hydrazone linkages. The heterometallic frameworks (Cu, Co) are prepared through the hydrazone linkage coordination method and evaluated as catalysts for the oxygen evolution reaction (OER). Owing to the spatial separation and functional cooperation of the heterometallic MCOF catalysts, the as‐synthesized MCOFs exhibited outstanding catalytic activities with an overpotential of 268.8 mV at 10 mA cm–2 for the OER in 1 M KOH, which is superior to those of the reported covalent organic frameworks (COFs)‐based OER catalysts. Theoretical calculations further elucidated the synergistic effect of heterometallic active sites within the linkages and frameworks, contributing to the enhanced OER activity. This study thus introduces a novel approach to the fundamental design of flexible MCOF catalysts for the OER, emphasizing their enhanced atomic utilization efficiency.

Evolution of cooperation in social dilemmas with assortment in finite populations

We investigate conditions for the evolution of cooperation in social dilemmas in finite populations with assortment of players by group founders and general payoff functions for cooperation and defection within groups. Using a diffusion approximation in the limit of a large population size that does not depend on the precise updating rule, we show that the first-order effect of selection on the fixation probability of cooperation when represented once can be expressed as the difference between time-averaged payoffs with respect to effective time that cooperators and defectors spend in direct competition in the different group states. Comparing this fixation probability to its value under neutrality and to the corresponding fixation probability for defection, we deduce conditions for the evolution of cooperation. We show that these conditions are generally less stringent as the level of assortment increases under a wide range of assumptions on the payoffs such as additive, synergetic or discounted benefits for cooperation, fixed cost for cooperation and threshold benefit functions. This is not necessarily the case, however, when payoffs in pairwise interactions are multiplicatively compounded within groups.