3D printable elastomers with exceptional strength and toughness.

Three-dimensional (3D) printing has emerged as an attractive manufacturing technique because of its exceptional freedom in accessing geometrically complex customizable products. Its potential for mass manufacturing, however, is hampered by its low manufacturing efficiency (print speed) and insufficient product quality (mechanical properties). Recent progresses in ultra-fast 3D printing of photo-polymers1-5 have alleviated the issue of manufacturing efficiency, but the mechanical performance of typical printed polymers still falls far behind what is achievable with conventional processing techniques. This is because of the printing requirements that restrict the molecular design towards achieving high mechanical performance. Here we report a 3D photo-printable resin chemistry that yields an elastomer with tensile strength of 94.6 MPa and toughness of 310.4 MJ m-3, both of which far exceed that of any 3D printed elastomer6-10. Mechanistically, this is achieved by the dynamic covalent bonds in the printed polymer that allow network topological reconfiguration. This facilitates the formation of hierarchical hydrogen bonds (in particular, amide hydrogen bonds), micro-phase separation and interpenetration architecture, which contribute synergistically to superior mechanical performance. Our work suggests a brighter future for mass manufacturing using 3D printing.

Biomimetic Phthalocyanine-Based Covalent Organic Frameworks with Tunable Pendant Groups for Electrocatalytic CO2 Reduction.

Electrocatalytic carbon dioxide reduction reaction (CO2RR) is an effective way of converting CO2 into value-added products using renewable energy, whose activity and selectivity can be in principle maneuvered by tuning the microenvironment near catalytic sites. Here, we demonstrate a strategy for tuning the microenvironment of CO2RR by learning from the natural chlorophyll and heme. Specifically, the conductive covalent organic frameworks (COFs) linked by piperazine serve as versatile supports for single-atom catalysts (SACs), and the pendant groups modified on the COFs can be readily tailored to offer different push-pull electronic effects for tunable microenvironment. As a result, while all the COFs exhibit high chemical structure stability under harsh conditions and good conductivity, the addition of -CH2NH2 can greatly enhance the activity and selectivity of CO2RR. As proven by experimental characterization and theoretical simulation, the electron-donating group (-CH2NH2) not only reduces the surface work function of COF, but also improves the adsorption energy of the key intermediate *COOH, compared with the COFs with electron-withdrawing groups (-CN, -COOH) near the active sites. This work provides insights into the microenvironment modulation of CO2RR electrocatalysts at the molecular level.

TRIM65 deficiency alleviates renal fibrosis through NUDT21-mediated alternative polyadenylation.

Chronic kidney disease (CKD) is a major global health concern and the third leading cause of premature death. Renal fibrosis is the primary process driving the progression of CKD, but the mechanisms behind it are not fully understood, making treatment options limited. Here, we find that the E3 ligase TRIM65 is a positive regulator of renal fibrosis. Deletion of TRIM65 results in a reduction of pathological lesions and renal fibrosis in mouse models of kidney fibrosis induced by unilateral ureteral obstruction (UUO)- and folic acid. Through screening with a yeast-hybrid system, we identify a new interactor of TRIM65, the mammalian cleavage factor I subunit CFIm25 (NUDT21), which plays a crucial role in fibrosis through alternative polyadenylation (APA). TRIM65 interacts with NUDT21 to induce K48-linked polyubiquitination of lysine 56 and proteasomal degradation, leading to the inhibition of TGF-ß1-mediated SMAD and ERK1/2 signaling pathways. The degradation of NUDT21 subsequently altered the length and sequence content of the 3'UTR (3'UTR-APA) of several pro-fibrotic genes including Col1a1, Fn-1, Tgfbr1, Wnt5a, and Fzd2. Furthermore, reducing NUDT21 expression via hydrodynamic renal pelvis injection of adeno-associated virus 9 (AAV9) exacerbated UUO-induced renal fibrosis in the normal mouse kidneys and blocked the protective effect of TRIM65 deletion. These findings suggest that TRIM65 promotes renal fibrosis by regulating NUDT21-mediated APA and highlight TRIM65 as a potential target for reducing renal fibrosis in CKD patients.

[Mid-term effectiveness of modified arthroscopic suture button fixation Latarjet procedure for treatment of recurrent anterior shoulder dislocations].

Objective: To summarize mid-term effectiveness of modified arthroscopic suture button fixation Latarjet procedure for treatment of recurrent anterior shoulder dislocations. Methods: Between January 2018 and October 2020, 30 patients with recurrent anterior shoulder dislocations were treated with modified arthroscopic suture button fixation Latarjet procedure. There were 19 males and 11 females with an average age of 27.3 years (range, 18-41 years). The shoulder dislocation occurred 3-7 times, with an average of 4.9 times. The time from the last dislocation to operation was 3-10 days, with an average of 4.1 days. Glenoid defects exceeded 20% in all cases. There were 27 cases of Hill-Sachs lesions. The joint pain and function were estimated by visual analogue scale (VAS) score, University of California, Los Angeles (UCLA) score, Rowe score, American Association for Shoulder and Elbow Surgery (ASES) score, Walch-Duplay score, and the range of external rotation at 0° and external rotation at 90° abduction of shoulder before operation and at 1 month, 6 months, and last follow-up. The X-ray film, CT scan and three-dimensional reconstruction were reviewed to observe the position, healing, and absorption of the coracoid graft, correction of glenoid defect, and joint degeneration. Results: The operation time ranged from 51 to 79 minutes, with an average of 68.4 minutes. All incisions healed without complications such as nerve or blood vessel injury. All patients were followed up 36-60 months with an average of 44.6 months. The VAS score, UCLA score, Rowe score, ASES score, Walch-Duplay score, and the range of external rotation at 0° and external rotation at 90° abduction after operation significantly improved when compared with preoperative values ( P<0.05). All indicators further improved with time, and the differences between different time points after operation were significant ( P<0.05). Imaging review showed that the coracoid graft was located in the anteroinferior glenoid at 1 day after operation, and no occurrence of shoulder osteoarthritis was found during follow-up. The anatomical structure of the glenoid was normal, and no delayed healing or non-union of the coracoid graft occurred. At 20 months after operation, arthroscopic re-exploration was performed in 1 case due to fracutre caused by falling injury revealed the good shaping of the coracoid graft, smooth glenoid, and no bone resorption or osteoarthritis. Conclusion: For recurrent anterior shoulder dislocations, the modified arthroscopic suture button fixation Latarjet procedure can obtain good recovery of shoulder function and low incidence of complications and has a good mid-term effectiveness.

AcMYB266, a key regulator of the red coloration in pineapple peel: a case of subfunctionalization in tandem duplicated genes.

Red fruit peel is an attractive target for pineapple breeding. Various pineapple accessions with distinct red coloration patterns exist; however, the precise molecular mechanism accounting for these differences remains unknown, which hinders the pineapple breeding process from combining high fruit quality with red peel. In this study, we characterized a transcription factor, AcMYB266, which is preferentially expressed in pineapple peel and positively regulates anthocyanin accumulation. Transgenic pineapple, Arabidopsis, and tobacco plants overexpressing AcMYB266 exhibited significant anthocyanin accumulation. Conversely, transient silencing of this gene led to decreased anthocyanin accumulation in pineapple red bracts. In-depth analysis indicated that variations of AcMYB266 sequences in the promoter instead of the protein-coding region seem to contribute to different red coloration patterns in peels of three representative pineapple varieties. In addition, we found that AcMYB266 was located in a cluster of four MYB genes exclusive to and conserved in Ananas species. Of this cluster, each was proved to regulate anthocyanin synthesis in different pineapple tissues, illustrating an interesting case of gene subfunctionalization after tandem duplication. In summary, we have characterized AcMYB266 as a key regulator of pineapple red fruit peel and identified an MYB cluster whose members were subfunctionalized to specifically regulate the red coloration of different pineapple tissues. The present study will assist in establishing a theoretical mechanism for pineapple breeding for red fruit peel and provide an interesting case for the investigation of gene subfunctionalization in plants.

HSPE1 enhances aerobic glycolysis to promote progression of lung adenocarcinoma.

OBJECTIVE: This study aimed to explore the role of heat shock protein family E member 1 (HSPE1) in the metabolism of lung adenocarcinoma (LUAD) cells. METHODS: Bioinformatics analysis was applied to examine the expression of HSPE1 in LUAD and its correlation with patient survival. Single-gene Gene Set Enrichment Analysis was conducted for HSPE1. LUAD cell lines or mouse models with up-regulated/down-regulated HSPE1 were constructed. The expression level of HSPE1 was detected by qRT-PCR or immunohistochemical staining. We used CCK-8 assay to measure cell viability and flow cytometry to detect apoptosis levels. Transwell assay was performed to evaluate migration and invasion characteristics. Extracellular Flux Analyzer was employed to detect oxygen consumption rate and extracellular acidification rate. Glucose consumption, adenosine triphosphate production, and lactate levels were measured by Reagent kits. Western blot analysis was conducted to examine the expression levels of GLUT1, HK2, and LDHA. RESULTS: HSPE1 promoted proliferative, migratory, and invasive abilities, and inhibited apoptosis of LUAD cells through the aerobic glycolysis pathway. Specifically, LUAD cells with HSPE1 knockdown exhibited significantly decreased proliferation, migration, and invasion abilities, along with an increased apoptosis rate. Additionally, the expression levels of aerobic glycolysis-related proteins HK2, LADH, and GLUT1 were downregulated, while their levels were increased in LUAD cells with high HSPE1 expression. Suppression of aerobic glycolysis by 2-DG attenuated the promoting effects of HSPE1 overexpression on the proliferation, migration, and invasion of LUAD cells. HSPE1 knockdown inhibited tumor growth and decreased expression levels of HK2, LADH, and GLUT1 in vivo. CONCLUSION: HSPE1 regulated the proliferation, migration, and invasion of LUAD cells through the aerobic glycolysis pathway, thus facilitating malignant development of LUAD. The study suggested that HSPE1 could be useful as a therapeutic target for LUAD.

NAT10 Promotes Prostate Cancer Growth and Metastasis by Acetylating mRNAs of HMGA1 and KRT8.

N4-acetylcytidine (ac4C) is essential for the development and migration of tumor cells. According to earlier research, N-acetyltransferase 10 (NAT10) can increase messenger RNAs (mRNAs) stability by catalyzing the synthesis of ac4C. However, little is known about NAT10 expression and its role in the acetylation modifications in prostate cancer (PCa). Thus, the biological function of NAT10 in PCa is investigated in this study. Compared to paraneoplastic tissues, the expression of NAT10 is significantly higher in PCa. The NAT10 expression is strongly correlated with the pathological grade, clinical stage, Gleason score, T-stage, and N-stage of PCa. NAT10 has the ability to advance the cell cycle and the epithelial-mesenchymal transition (EMT), both of which raise the malignancy of tumor cells. Mechanistically, NAT10 enhance the stability of high mobility group AT-hook 1 (HMGA1) by acetylating its mRNA, thereby promoting cell cycle progression to improve cell proliferation. In addition, NAT10 improve the stability of Keratin 8 (KRT8) by acetylating its mRNA, which promotes the progression of EMT to improve cell migration. This findings provide a potential prognostic or therapeutic target for PCa.

Role of gut microbiota in regulating immune checkpoint inhibitor therapy for glioblastoma.

Glioblastoma (GBM) is a highly malignant, invasive, and poorly prognosed brain tumor. Unfortunately, active comprehensive treatment does not significantly prolong patient survival. With the deepening of research, it has been found that gut microbiota plays a certain role in GBM, and can directly or indirectly affect the efficacy of immune checkpoint inhibitors (ICIs) in various ways. (1) The metabolites produced by gut microbiota directly affect the host's immune homeostasis, and these metabolites can affect the function and distribution of immune cells, promote or inhibit inflammatory responses, affect the phenotype, angiogenesis, inflammatory response, and immune cell infiltration of GBM cells, thereby affecting the effectiveness of ICIs. (2) Some members of the gut microbiota may reverse T cell function inhibition, increase T cell anti-tumor activity, and ultimately improve the efficacy of ICIs by targeting specific immunosuppressive metabolites and cytokines. (3) Some members of the gut microbiota directly participate in the metabolic process of drugs, which can degrade, transform, or produce metabolites, affecting the effective concentration and bioavailability of drugs. Optimizing the structure of the gut microbiota may help improve the efficacy of ICIs. (4) The gut microbiota can also regulate immune cell function and inflammatory status in the brain through gut brain axis communication, indirectly affecting the progression of GBM and the therapeutic response to ICIs. (5) Given the importance of gut microbiota for ICI therapy, researchers have begun exploring the use of fecal microbiota transplantation (FMT) to transplant healthy or optimized gut microbiota to GBM patients, in order to improve their immune status and enhance their response to ICI therapy. Preliminary studies suggest that FMT may enhance the efficacy of ICI therapy in some patients. In summary, gut microbiota plays a crucial role in regulating ICIs in GBM, and with a deeper understanding of the relationship between gut microbiota and tumor immunity, it is expected to develop more precise and effective personalized ICI therapy strategies for GBM, in order to improve patient prognosis.

TRIM65 promotes renal cell carcinoma through ubiquitination and degradation of BTG3.

As a typical E3 ligase, TRIM65 (tripartite motif containing 65) is involved in the regulation of antiviral innate immunity and the pathogenesis of certain tumors. However, the role of TRIM65 in renal cell carcinoma (RCC) and the underlying mechanism has not been determined yet. In this study, we identified TRIM65 as a novel oncogene in RCC, which enhanced the tumor cell proliferation and anchorage-independent growth abilities both in vitro and in vivo. Moreover, we found that TRIM65-regulated RCC proliferation mainly via direct interaction with BTG3 (BTG anti-proliferation factor 3), which in turn induced the K48-linked ubiquitination and subsequent degradation through K41 amino acid. Furthermore, TRIM65 relieved G2/M phase cell cycle arrest via degradation of BTG3 and regulated downstream factors. Further studies revealed that TRIM65 acts through TRIM65-BTG3-CyclinD1 axis and clinical sample IHC chip data indicated a negative correction between TRIM65 and BTG3. Taken together, our findings demonstrated that TRIM65 promotes RCC cell proliferation via regulation of the cell cycle through degradation of BTG3, suggesting that TRIM65 may be a promising target for RCC therapy.

Research Progress on the Correlation Between Hypertension and Gut Microbiota.

Among cardiovascular diseases, hypertension is the most important risk factor for morbidity and mortality worldwide, and its pathogenesis is complex, involving genetic, dietary and environmental factors. The characteristics of the gut microbiota can vary in response to increased blood pressure (BP) and influence the development and progression of hypertension. This paper describes five aspects of the relationship between hypertension and the gut microbiota, namely, the different types of gut microbiota, metabolites of the gut microbiota, sympathetic activation, gut-brain interactions, the effects of exercise and dietary patterns and the treatment of the gut microbiota through probiotics, faecal microbiota transplantation (FMT) and herbal remedies, providing new clues for the future prevention of hypertension. Diet, exercise and traditional Chinese medicine may contribute to long-term improvements in hypertension, although the effects of probiotics and FMT still need to be validated in large populations.

Graded decisions in the human brain.

Decision-makers objectively commit to a definitive choice, yet at the subjective level, human decisions appear to be associated with a degree of uncertainty. Whether decisions are definitive (i.e., concluding in all-or-none choices), or whether the underlying representations are graded, remains unclear. To answer this question, we recorded intracranial neural signals directly from the brain while human subjects made perceptual decisions. The recordings revealed that broadband gamma activity reflecting each individual's decision-making process, ramped up gradually while being graded by the accumulated decision evidence. Crucially, this grading effect persisted throughout the decision process without ever reaching a definite bound at the time of choice. This effect was most prominent in the parietal cortex, a brain region traditionally implicated in decision-making. These results provide neural evidence for a graded decision process in humans and an analog framework for flexible choice behavior.

FLRT2 mediates chondrogenesis of nasal septal cartilage and mandibular condyle cartilage.

Nasal septal cartilages (NSCs) and mandibular condyle cartilages (MCCs) are two important cartilages for craniomaxillofacial development. However, the role of FLRT2 in the formation of NSCs and MCCs remains undiscovered. NSCs and MCCs were used for immunocytochemistry staining of collagen II, toluidine blue staining, and alcian blue staining. Quantitative reverse transcription­PCR and western blot were used to detect mRNA and protein expressions of FLRT2, N-cadherin, collagen II, aggrecan, and SOX9. Cell proliferation of MCCs and NSCs was tested by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and cell counting kit­8 assay. Cell migration of MCCs and NSCs was examined by wound healing assay and Transwell. Chondrogenesis of MCCs and NSCs were similar in morphological characteristics, while different in cell proliferation, migration, and extracellular matrix. FLRT2 promotes the proliferation and migration of NSCs. There were up-regulation of N-cadherin and down-regulation of collagen II, aggrecan, and SOX9 in NSC with knock down FLRT2. The current study, as demonstrated by Xie et al., reveals that FLRT2 overexpression in Sprague-Dawley neonatal rats promotes the proliferation and migration of NSCs and MCCs, decreases N-cadherin while increases collagen II, aggrecan, and SOX9 in NSC and MCCs. Altogether, FLRT2 mediates chondrogenesis of NSCs and MCCs.

GPR65 sensing tumor-derived lactate induces HMGB1 release from TAM via the cAMP/PKA/CREB pathway to promote glioma progression.

BACKGROUND: Lactate has emerged as a critical regulator within the tumor microenvironment, including glioma. However, the precise mechanisms underlying how lactate influences the communication between tumor cells and tumor-associated macrophages (TAMs), the most abundant immune cells in glioma, remain poorly understood. This study aims to elucidate the impact of tumor-derived lactate on TAMs and investigate the regulatory pathways governing TAM-mediated tumor-promotion in glioma. METHODS: Bioinformatic analysis was conducted using datasets from TCGA and CGGA. Single-cell RNA-seq datasets were analyzed by using UCSC Cell Browser and Single Cell Portal. Cell proliferation and mobility were evaluated through CCK8, colony formation, wound healing, and transwell assays. Western blot and immunofluorescence staining were applied to assess protein expression and cell distribution. RT-PCR and ELISA were employed to identify the potential secretory factors. Mechanistic pathways were explored by western blotting, ELISA, shRNA knockdown, and specific inhibitors and activators. The effects of pathway blockades were further assessed using subcutaneous and intracranial xenograft tumor models in vivo. RESULTS: Elevated expressions of LDHA and MCT1 were observed in glioma and exhibited a positive correlation with M2-type TAM infiltration. Lactate derived from glioma cells induced TAMs towards M2-subtype polarization, subsequently promoting glioma cells proliferation, migration, invasion, and mesenchymal transition. GPR65, highly expressed on TAMs, sensed lactate-stimulation in the TME, fueling glioma cells malignant progression through the secretion of HMGB1. GPR65 on TAMs triggered HMGB1 release in response to lactate stimulation via the cAMP/PKA/CREB signaling pathway. Disrupting this feedback loop by GPR65-knockdown or HMGB1 inhibition mitigated glioma progression in vivo. CONCLUSION: These findings unveil the intricate interplay between TAMs and tumor cells mediated by lactate and HMGB1, driving tumor progression in glioma. GPR65, selectively highly expressed on TAMs in glioma, sensed lactate stimulation and fostered HMGB1 secretion via the cAMP/PKA/CREB signaling pathway. Blocking this feedback loop presents a promising therapeutic strategy for GBM.

Comparative transcriptome analysis identifies candidate genes related to sucrose accumulation in longan (Dimocarpus longan Lour.) pulp.

Sucrose content is one of the important factors to determine longan fruit flavor quality. To gain deep insight of molecular mechanism on sucrose accumulation in longan, we conducted comparative transcriptomic analysis between low sucrose content longan cultivar 'Qingkebaoyuan' and high sucrose content cultivar 'Songfengben'. A total of 12,350 unique differentially expressed genes (DEGs) were detected across various development stages and different varieties, including hexokinase (HK) and sucrose-phosphate synthase (SPS), which are intricately linked to soluble sugar accumulation and metabolism. Weighted gene co-expression network analysis (WGCNA) identified magenta module, including DlSPS gene, was significantly positively correlated with sucrose content. Furthermore, transient expression unveiled DlSPS gene play crucial role in sucrose accumulation. Moreover, 5 transcription factors (MYB, ERF, bHLH, C2H2, and NAC) were potentially involved in DlSPS regulation. Our findings provide clues for sucrose metabolism, and lay the foundation for longan breeding in the future.

Elevated serum irisin levels in boys with central precocious puberty independent of BMI.

INTRODUCTION: Central precocious puberty (CPP) is a prevalent endocrine disorder. Research has indicated that pubertal development is linked to nutritional metabolism. Irisin, a novel myokine/adipokine, has been identified as a potential predictor of CPP in girls. This study aims to examine the relationship between serum irisin levels and CPP in boys. MATERIAL AND METHODS: An enzyme-linked immunosorbent assay (ELISA) was used to measure serum irisin levels in 32 boys diagnosed with CPP and 33 prepubertal age-matched boys as normal controls (NC). To assess the impact of body mass index (BMI) on irisin levels, both the CPP and NC groups were divided into overweight/obese and normal-weight subgroups. Spearman correlation analysis was employed to assess the connection between irisin and clinical and biochemical parameters. Additionally, a receiver operating characteristic curve was utilised to determine the optimal threshold value for irisin. RESULTS: In the normal-weight subgroups, boys with CPP exhibited elevated irisin levels compared to controls, but not in the overweight/obese subgroups. The optimal cut-off value for irisin levels to predict CPP in the normal-weight groups was 93.09 ng/mL, yielding a sensitivity of 47.6% and a specificity of 100%. Furthermore, a positive correlation was noted between irisin levels and bone age (BA), bone age advancement (BA-CA), and BMI. CONCLUSIONS: Serum irisin levels correlate with BMI and pubertal development. Given its limited sensitivity, irisin level can only be utilised as a supplementary rather than a standalone diagnostic indicator for CPP.

PSE-Net: Channel pruning for Convolutional Neural Networks with parallel-subnets estimator.

Channel Pruning is one of the most widespread techniques used to compress deep neural networks while maintaining their performances. Currently, a typical pruning algorithm leverages neural architecture search to directly find networks with a configurable width, the key step of which is to identify representative subnet for various pruning ratios by training a supernet. However, current methods mainly follow a serial training strategy to optimize supernet, which is very time-consuming. In this work, we introduce PSE-Net, a novel parallel-subnets estimator for efficient channel pruning. Specifically, we propose a parallel-subnets training algorithm that simulate the forward-backward pass of multiple subnets by droping extraneous features on batch dimension, thus various subnets could be trained in one round. Our proposed algorithm facilitates the efficiency of supernet training and equips the network with the ability to interpolate the accuracy of unsampled subnets, enabling PSE-Net to effectively evaluate and rank the subnets. Over the trained supernet, we develop a prior-distributed-based sampling algorithm to boost the performance of classical evolutionary search. Such algorithm utilizes the prior information of supernet training phase to assist in the search of optimal subnets while tackling the challenge of discovering samples that satisfy resource constraints due to the long-tail distribution of network configuration. Extensive experiments demonstrate PSE-Net outperforms previous state-of-the-art channel pruning methods on the ImageNet dataset while retaining superior supernet training efficiency. For example, under 300M FLOPs constraint, our pruned MobileNetV2 achieves 75.2% Top-1 accuracy on ImageNet dataset, exceeding the original MobileNetV2 by 2.6 units while only cost 30%/16% times than BCNet/AutoAlim.

Inducing spin polarization via Co doping in the BiVO4 cell to enhance the built-in electric field for promotion of photocatalytic CO2 reduction.

The efficiency of CO2 photocatalytic reduction is severely limited by inefficient separation and sluggish transfer. In this study, spin polarization was induced and built-in electric field was strengthened via Co doping in the BiVO4 cell to boost photocatalytic CO2 reduction. Results showed that owing to the generation of spin-polarized electrons upon Co doping, carrier separation and photocurrent production of the Co-doped BiVO4 were enhanced. CO production during CO2 photocatalytic reduction from the Co-BiVO4 was 61.6 times of the BiVO4. Notably, application of an external magnetic field (100 mT) further boosted photocatalytic CO2 reduction from the Co-BiVO4, with 68.25 folds improvement of CO production compared to pristine BiVO4. The existence of a built-in electric field (IEF) was demonstrated through density functional theory (DFT) simulations and kelvin probe force microscopy (KPFM). Mechanism insights could be elucidated as follows: doping of magnetic Co into the BiVO4 resulted in increased the number of spin-polarized photo-excited carriers, and application of a magnetic field led to an augmentation of intrinsic electric field due to a dipole shift, thereby extending carrier lifetime and suppressing charges recombination. Additionally, HCOO- was a crucial intermediate in the process of CO2RR, and possible pathways for CO2 reduction were proposed. This study highlights the significance of built-in electric fields and the important role of spin polarization for promotion of photocatalytic CO2 reduction.

Reprogramming Photoresponsive Liquid Crystalline Elastomer via Force-Directed Evaporation.

Incorporating photothermal agents into thermoresponsive liquid crystalline elastomers (LCEs) offers remote and spatio-temporal control in actuation. Typically, both the light responsiveness and actuation behaviors are fixed since the agent doping and mesogen alignment are conducted before network formation. Here, we report an approach that enables programming photoresponsive LCEs after synthesis via force-directed evaporation. Different photothermal agents can be doped or removed by swelling the fully cross-linked LCEs in a specific solution, achieving the introduction and erasing of the photoresponsiveness. Moreover, the network swelling deletes the registered alignment, which allows for redefining the molecular order via re-evaporating the solvent with force imposed. This "one stone, two birds" strategy paves the way to simultaneously program/reprogram the actuation mode and responsiveness of LCEs, even in a spatio-selective manner to achieve complex actuations. Our approach is expandable to three-dimensional (3D) printed LCEs to access geometrically sophisticated shape-changing.