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Highly effective and highly efficient decontamination of mercury from aqueous media remains a serious task for public health and ecosystem protection. Here we report that this task can be addressed by creating a mercury ‘nano-trap’ as illustrated by functionalizing a high surface area and robust porous organic polymer with a high density of strong mercury chelating groups. The resultant porous organic polymer-based mercury ‘nano-trap’ exhibits a record-high saturation mercury uptake capacity of over 1,000 mg g −1 , and can effectively reduce the mercury(II) concentration from 10 p.p.m. to the extremely low level of smaller than 0.4 p.p.b. well below the acceptable limits in drinking water standards (2 p.p.b.), and can also efficiently remove >99.9% mercury(II) within a few minutes. Our work therefore presents a new benchmark for mercury adsorbent materials and provides a new perspective for removing mercury(II) and also other heavy metal ions from contaminated water for environmental remediation. Decontamination of mercury pollution from fresh water is a serious environmental issue. Here, the authors report a porous organic polymer-based nano-trap, functionalized with mercury chelating groups, capable of efficient and rapid mercury removal from aqueous media.

Herein, we report a strategy to construct highly efficient perfluorooctanoic acid (PFOA) adsorbents by installing synergistic electrostatic/hydrophobic sites onto porous organic polymers (POPs). The constructed model material of PAF-1-NDMB (NDMB = N,N-dimethyl-butylamine) demonstrates an exceptionally high PFOA uptake capacity over 2000 mg g −1 , which is 14.8 times enhancement compared with its parent material of PAF-1. And it is 32.0 and 24.1 times higher than benchmark materials of DFB-CDP (β-cyclodextrin (β-CD)-based polymer network) and activated carbon under the same conditions. Furthermore, PAF-1-NDMB exhibits the highest k 2 value of 24,000 g mg −1 h −1 among all reported PFOA sorbents. And it can remove 99.99% PFOA from 1000 ppb to <70 ppt within 2 min, which is lower than the advisory level of Environmental Protection Agency of United States. This work thus not only provides a generic approach for constructing PFOA adsorbents, but also develops POPs as a platform for PFOA capture. The performance of adsorbents for perfluorooctanoic acid (PFOA) removal often suffers from long equilibrium times, weak binding affinities and poor stability. Here the authors report a highly efficient PFOA adsorbents by functionalizing porous organic polymers with electrostatic and hydrophobic binding sites.

Effective capture of radioactive organic iodides from nuclear waste remains a significant challenge due to the drawbacks of current adsorbents such as low uptake capacity, high cost, and non-recyclability. We report here a general approach to overcome this challenge by creating radioactive organic iodide molecular traps through functionalization of metal-organic framework materials with tertiary amine-binding sites. The molecular trap exhibits a high CH 3 I saturation uptake capacity of 71 wt% at 150 °C, which is more than 340% higher than the industrial adsorbent Ag 0 @MOR under identical conditions. These functionalized metal-organic frameworks also serve as good adsorbents at low temperatures. Furthermore, the resulting adsorbent can be recycled multiple times without loss of capacity, making recyclability a reality. In combination with its chemical and thermal stability, high capture efficiency and low cost, the adsorbent demonstrates promise for industrial radioactive organic iodides capture from nuclear waste. The capture mechanism was investigated by experimental and theoretical methods. Capturing radioactive organic iodides from nuclear waste is important for safe nuclear energy usage, but remains a significant challenge. Here, Li and co-workers fabricate a stable metal–organic framework functionalized with tertiary amine groups that exhibits high capacities for radioactive organic iodides uptake.

Crystalline porous materials such as covalent organic frameworks (COFs), metal-organic frameworks (MOFs) and porous organic cages (POCs) have been widely applied in various fields with outstanding performances. However, the lack of general and effective methodology for large-scale production limits their further industrial applications. In this work, we developed a general approach comprising high pressure homogenization (HPH), which can realize large-scale synthesis of crystalline porous materials including COFs, MOFs, and POCs under benign conditions. This universal strategy, as illustrated in the proof of principle studies, has prepared 4 COFs, 4 MOFs, and 2 POCs. It can circumvent some drawbacks of existing approaches including low yield, high energy consumption, low efficiency, weak mass/thermal transfer, tedious procedures, poor reproducibility, and high cost. On the basis of this approach, an industrial homogenizer can produce 0.96 ~ 580.48 ton of high-performance COFs, MOFs, and POCs per day, which is unachievable via other methods. The large-scale production of crystalline porous materials remains a challenge. Here the authors report a general approach of high-pressure homogenization that can realize large-scale synthesis of crystalline porous materials under benign conditions.

Background Few recognized, valid and reliable tools are used to assess the current quality of care at the very end-of-life from the bereaved relative’s perspective in Mainland China. The purpose of this study was to validate the Chinese version of the international Care Of the Dying Evaluation (i-CODE) questionnaire by assessing its reliability and validity. Methods From June 2023 to January 2024, participants were 216 bereaved relatives who were the primary caregivers of the deceased patients. Confirmatory Factor Analyses (CFA) were conducted, concurrent and discriminant validity was examined by correlating scores from the Chinese version of the i-CODE with Good Death Inventory (GDI), Care Evaluation Scale (CES), and Patient Health Questionnaire (PHQ-9). Internal reliability was assessed with Cronbach alpha (α) and test-retest reliability was assessed using Intraclass Correlation Coefficients (ICC). Results The Chinese version of the i-CODE had four dimensions and 27 items were confirmed based on confirmatory factor analysis of the factor structure proposed by the authors of the original version. The fit indices were acceptable: Root Mean Square Error of Approximation (RMSEA) was 0.069, Standardised Root Mean Square Residual (SRMR) was 0.063, Comparative Fit Index (CFI) was 0.879, and Tucker-Lewis Index (TLI) was 0.864. The i-CODE was moderately correlated with the GDI ( r  = 0.50, p  < 0.001) and CES ( r  = 0.31, p  < 0.001) and not correlated with PHQ-9 ( r  = 0.02, p  = 0.765). The internal consistency was excellent (Cronbach’s α = 0.91) and the test-retest reliability was good (ICC = 0.73). Conclusions The Chinese version of the i-CODE demonstrated acceptable preliminary psychometric properties and broadly supported the original four-factor structure, indicating suitability for assessing the quality of care in the last days of life from the perspective of bereaved relatives in Mainland China. Further validation in larger and more diverse samples is needed, and the scale may be useful for clinical evaluation, quality improvement and cross-cultural research in end-of-life care.

Cardiac hypertrophy is a compensatory response to mechanical stimuli and neurohormonal factors, ultimately progresses to heart failure. The proteins of some transient receptor potential (TRP) channels, Ca2+‐permeable nonselective cation channel, are highly expressed in cardiomyocytes, and associated with the occurrence of cardiac hypertrophy. Transient receptor potential vanilloid 3 (TRPV3) is a member of TRP, however, the functional role of TRPV3 in cardiac hypertrophy remains unclear. TRPV3 was elevated in pathological cardiac hypertrophy, but not in swimming exercise‐induced physiological cardiac hypertrophy in rats. TRPV3 expression was also increased in Ang II–induced cardiomyocyte hypertrophy in vitro, which was remarkably increased by carvacrol (a nonselective TRPV channel agonist), and reduced by ruthenium red (a nonselective TRPV channel antagonist). Interestingly, we found that activated TRPV3 in Ang II–induced cardiomyocyte hypertrophy was accompanied with increasing intracellular calcium concentration, promoting calcineurin, and phosphorylated CaMKII protein expression, and enhancing NFATc3 nuclear translocation. However, blocking or knockdown of TRPV3 could inhibit the expressions of calcineurin, phosphorylated CaMKII and NFATc3 protein by Western blot. In conclusion, the activation of TRPV3 aggravated pathological cardiac hypertrophy through calcineurin/NFATc3 signalling pathway and correlated with the protein expression levels of calcineurin, phosphorylated CaMKII and NFATc3, revealing that TRPV3 might be a potential therapeutic target for cardiac hypertrophy.

Background: The skeletal system is a common site for metastasis from breast cancer. In our prior work, we developed induced tumor-suppressing cells (iTSCs) capable of secreting a set of tumor-suppressing proteins. In this study, we examined the possibility of identifying anticancer peptides (ACPs) from trypsin-digested protein fragments derived from iTSC proteomes. Methods: The efficacy of ACPs was examined using an MTT-based cell viability assay, a Scratch-based motility assay, an EdU-based proliferation assay, and a transwell invasion assay. To evaluate the mechanism of inhibitory action, a fluorescence resonance energy transfer (FRET)-based GTPase activity assay and a molecular docking analysis were conducted. The efficacy of ACPs was also tested using an ex vivo cancer tissue assay and a bone microenvironment assay. Results: Among the 12 ACP candidates, P18 (TDYMVGSYGPR) demonstrated the most effective anticancer activity. P18 was derived from Arhgdia, a Rho GDP dissociation inhibitor alpha, and exhibited inhibitory effects on the viability, migration, and invasion of breast cancer cells. It also hindered the GTPase activity of RhoA and Cdc42 and downregulated the expression of oncoproteins such as Snail and Src. The inhibitory impact of P18 was additive when it was combined with chemotherapeutic drugs such as Cisplatin and Taxol in both breast cancer cells and patient-derived tissues. P18 had no inhibitory effect on mesenchymal stem cells but suppressed the maturation of RANKL-stimulated osteoclasts and mitigated the bone loss associated with breast cancer. Furthermore, the P18 analog modified by N-terminal acetylation and C-terminal amidation (Ac-P18-NH2) exhibited stronger tumor-suppressor effects. Conclusions: This study introduced a unique methodology for selecting an effective ACP from the iTSC secretome. P18 holds promise for the treatment of breast cancer and the prevention of bone destruction by regulating GTPase signaling.

Cardiac fibrosis is pathological damage associated with nearly all forms of heart disease. AMP-activated protein kinase (AMPK) is an evolutionary conserved energy-sensing enzyme. Emerging evidences indicate that AMPK plays an important role in cardiac fibrosis and cell proliferation. However, less is known about the detailed mechanism of AMPK activation on cardiac fibrosis. In this study, we found the AMPK activation improved the impaired cardiac function of cardiac fibrosis rats and decreased interstitial fibrosis. Further results indicated AMPK activation promoted p21 and p27 and inhibited CDK2 and cyclin E protein expressions both in vivo and in vitro. Moreover, AMPK activation repressed downstream transcription factor hepatocyte nuclear factor 4 alpha (HNF-4α) expression and decreased the binding of HNF-4α to TGF-β1 promoters, which eventually resulted in TGF-β1 downregulation and miR-29 family upregulation. Furthermore, miR-29, in turn, inhibited the progression of cardiac fibrosis through suppressing its target CDK2. Taken together, activation of AMPK, on the one hand, upregulated p21 and p27 expression, further inhibited CDK2 and cyclin E complex, and finally suppressed the progression of cardiac fibrosis, and, on the other hand, repressed HNF-4α expression, further downregulated the activity of TGF-β1 promoter, promoted miR-29 expression, and finally prevented the development of cardiac fibrosis.

PDAC (pancreatic ductal adenocarcinoma) is a highly aggressive malignant tumor. We have previously developed induced tumor-suppressing cells (iTSCs) that secrete a group of tumor-suppressing proteins. Here, we examined a unique procedure to identify anticancer peptides (ACPs), using trypsin-digested iTSCs-derived protein fragments. Among the 10 ACP candidates, P04 (IGEHTPSALAIMENANVLAR) presented the most efficient anti-PDAC activities. P04 was derived from aldolase A (ALDOA), a glycolytic enzyme. Extracellular ALDOA, as well as P04, was predicted to interact with epidermal growth factor receptor (EGFR), and P04 downregulated oncoproteins such as Snail and Src. Importantly, P04 has no inhibitory effect on mesenchymal stem cells (MSCs). We also generated iTSCs by overexpressing ALDOA in MSCs and peripheral blood mononuclear cells (PBMCs). iTSC-derived conditioned medium (CM) inhibited the progression of PDAC cells as well as PDAC tissue fragments. The inhibitory effect of P04 was additive to that of CM and chemotherapeutic drugs such as 5-Flu and gemcitabine. Notably, applying mechanical vibration to PBMCs elevated ALDOA and converted PBMCs into iTSCs. Collectively, this study presented a unique procedure for selecting anticancer P04 from ALDOA in an iTSCs-derived proteome for the treatment of PDAC.

Chromatin architecture is highly dynamic, undergoing nanoscale rearrangements throughout the cell cycle and in response to environmental cues. In this study, we employed high-resolution stochastic optical reconstruction microscopy (STORM) to visualize chromatin organization and cellular plasticity at the nanoscale in two osteosarcoma cell lines, U2OS and MG63. To promote a tumor-suppressive bone microenvironment, we applied three biophysical modalities, namely mechanical vibration, electrical stimulation, and optical pulses, each previously linked to altered tumor behavior by reprogramming cells and generating induced tumor-suppressing (iTS) cells. These stimuli enlarged nuclear size and disrupted nuclear envelope integrity, as revealed by increased surface roughness. Critically, all three modalities transiently scattered nucleosome clusters, indicating chromatin decondensation as a hallmark of iTS cell generation. iTS cells exhibited elevated expression of histone demethylases lysine demethylase 3A (KDM3A) and lysine demethylase 4 (KDM4), accompanied by reduced levels of trimethylated histone H3 lysine 9 (H3K9me3). Consistently, pharmacological agents—Trichostatin A as a histone deacetylase inhibitor and chaetocin as a histone methyltransferase inhibitor—induced nucleosome scattering and converted U2OS cells into iTS cells, whose conditioned media exerted tumor-suppressive effects. Our findings highlight nucleosome clustering as a key epigenetic feature responsive to both biophysical and chemical cues, underscoring its role in microscale chromatin remodeling and reprogramming of the tumor microenvironment.