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Porous carbon nanosheets have shown great potential in electrochemical energy storage devices, yet their intrinsic limited volumetric capacity and energy density remain a great concern. Herein, lamellar porous carbon framework hybrids (LPCFHs) have been facilely developed by thermal-induced bulk self-assembly of block copolymers with precisely controllable molecular structure, followed by stepwise chemical crosslinking and morphology-persistent carbonization processes. The as-obtained LPCFHs consist of densely covalent connected alternate layers (porous carbon nanosheets and porous carbon spacers) and homogenously dispersed metal sulfide nanoparticles. The ordered compact stacking structure of carbon nanosheets endows LPCFHs with a high tap density and fast electron transfer both in lateral and vertical dimension, while the porous carbon spacers enable fast channels for ion transfer. Moreover, the metal sulfide nanoparticles strongly interacted with carbon nanosheets are homogenously distributed in LPCFHs, resulting in sufficient active sites. As a result, when used as anode materials in lithium-ion batteries (LIBs), tin sulfide-decorated LPCFHs (LPCFHs-SnS) deliver a volumetric capacity of up to 1285 mAh cm−3; meanwhile, high-rate capability (488 mAh g−1 at 5 A g−1) and excellent cycling stability (capacity retention of 88.3 % after 500 cycles at 1 A g−1) are also achieved, demonstrating great potential for practical application in LIBs. [Display omitted] [ABSTRACT FROM AUTHOR]

Selective modulation of the types of reactive oxygen species (ROS) for the treatment of acute lung injury (ALI) has not been tackled, whereas the usually applied hydrophobic nanoparticles (NPs) are easily excreted and metabolized. Herein, a zwitterionic-segment containing polyurethane was synthesized to formulate into Pazopanib (Pazo)-loaded NPs (PUSB@Pazo NPs), which had the ability to selectively enhance the expression of H 2 O 2 but suppress other types of ROS, and achieved long retention in lung and thereby improved treatment efficacy. The zwitterionic group of PUSB effectively decreased the clearance rate of PUSB@Pazo NPs in vivo , and prolonged their resident time in lung post inhalation up to 48 h. The increase of local H 2 O 2 concentration decreased the permeability of lung epithelial cells, accompanied by the significantly reduced tissue edema and inflammatory cell recruitment. The system also reduced the expression of various inflammatory factors, revealing its effective and promising treatment for ALI. [Display omitted] • Zwitterionic ROS-responsive polyurethane (PUSB) was synthesized. • PUSB@Pazo NPs had longer residence in alveoli and selectively enhanced H 2 O 2 secretion. • Cytokine storm in ALI was suppressed with downregulated inflammatory factors. • New insights for delivery of therapeutic aerosols with significance in ALI therapy. [ABSTRACT FROM AUTHOR]

Chemotherapy is a crucial adjuvant method of treating breast cancer, but it fails to achieve preferable prognosis as the malignant cells eventually develop drug-resistance. Reduced chemotherapeutic sensitivity is primarily caused by endogenous and exogenous resistance during the treatment. Cuproptosis is a newly discovered immunogenic cell death (ICD), characterized by accumulation of copper (Cu) ions inside tumor cells. However, intracellular Cu ion concentrations can hardly reach desired levels to induce cuproptosis due to limited import via existing Cu ionophores and synchronous export via ATP-Cu pump. Herein, our research developed an elesclomol (ES) loaded cuprous oxide (Cu 2 O) nanocomposite, called PEG@Cu 2 O-ES, to solve this dilemma. Our designed PEG@Cu 2 O-ES could efficiently enter the breast cancer cells, release encapsulated ES and Cu 2 O, while the photothermal (PTT) effect of Cu 2 O induced by near-infrared II region (NIR-II) radiation could in turn accelerate the releasing process. Cu 2 O discharged substantial amounts of Cu in cytoplasm, which directly engaged in the tricarboxylic acid (TCA) cycle in mitochondria, resulting in cuproptosis to some extent. As a result of PTT-enhanced Fenton-like reactions, Cu 2 O generated a substantial quantity of reactive oxygen species (ROS) that attacked the ATP-Cu pump on cancer cells' membranes, thereby reducing the outflow of Cu ions and aggravating cuproptosis. Additionally, free ES further promoted Cu from the tumor microenvironment (TME) to enter breast cancer cells, and exacerbated cuproptosis with higher efficiency. In vivo , PEG@Cu 2 O-ES nanocomposites showed strong anti-tumor effect by inducing cuproptosis, as well as the ability to reprogram the TME and increase the response-sensitivity to programmed cell death protein-1 antibody (αPD-1). In conclusion, this study provides a promising strategy by combining a nano-drug with αPD-1 for sensitizing immunotherapy of chemotherapy-resistant breast cancer. [Display omitted] • PEG@Cu 2 O-ES discharged substantial amounts of Cu in cytoplasm, which directly engaged in TCA cycle in mitochondria to induce cuproptosis. • PEG@Cu 2 O-ES with PTT and CDT effects could generate ROS to attack ATP-Cu pump, thereby reducing the outflow of Cu ions and aggravating cuproptosis. • Released ES from PEG@Cu 2 O-ES further promoted Cu from TME to enter breast cancer cells, and exacerbated cuproptosis with higher efficiency. • PEG@Cu 2 O-ES showed strong anti-tumor effect by inducing cuproptosis, reprogramming TME and thus increasing the response-sensitivity to αPD-1. [ABSTRACT FROM AUTHOR]

To investigate the association between habitual tea consumption and transitions between frailty states among older adults in China. A prospective cohort study based on the Chinese Longitudinal Healthy Longevity Study. A total of 23,720 older adults aged ≥65 years with complete data regarding frailty status and tea consumption were recruited. The frequency and consistency of tea consumption were introduced to evaluate levels of tea consumption. The frailty index was used to define frailty status (frail and nonfrail). Frailty transition was classified into remaining nonfrail, improvement, worsening, and remaining frail groups. Logistic regression models were applied. The overall frailty prevalence at baseline was 19.1%, being lower among consistent daily tea drinkers (12.5%) and higher among non-tea drinkers (21.9%). Logistic regression analyses showed that the risk of frailty was significantly reduced among consistent daily tea drinkers after adjusting for all confounders [odds ratio (OR), 0.81; 95% CI, 0.67–0.98]. During the 3-year follow-up, improvement in frailty status was more common among consistent daily tea drinkers (50.9%) than non-tea drinkers (40.9%), and this trend was opposite in participants with worsened frailty status (consistent daily tea drinkers: 12.2%) vs non-tea drinkers: 19.2%). Further analysis showed that consistent daily tea drinkers were significantly associated with improvement in frailty status (OR, 3.24; 95% CI, 1.02–10.31) and remaining in a nonfrail state (OR, 1.35; 95% CI, 1.00–1.83). In addition, daily tea consumption was observed to be positively associated with remaining in a nonfrail state and inversely associated with worsened frailty status in men, but not in women. Older people consuming tea daily tend to have an improved frailty status in the future. Men with daily tea consumption were less likely to have a worsened frailty status. Advocating for the traditional lifestyle of drinking tea could be a promising way to advance healthy aging for older adults. [ABSTRACT FROM AUTHOR]

Acute kidney injury (AKI) was reported to be one of the initiators of chronic kidney disease (CKD) development. Necroinflammation may contribute to the progression from AKI to CKD. Dexmedetomidine (Dex), a highly selective α 2 -adrenoreceptor (AR) agonist, has cytoprotective and "anti-" inflammation effects. This study was designed to investigate the anti-fibrotic properties of Dex in sepsis models. C57BL/6 mice were randomly treated with an i.p. injection of lipopolysaccharides (LPS) (10 mg/kg) alone, LPS with Dex (25 μg/kg), or LPS, Dex and Atipamezole (Atip, an α 2 -adrenoreceptor antagonist) (500 μg/kg) (n=5/group). Human proximal tubular epithelial cells (HK2) were also cultured and then exposed to LPS (1 μg/ml) alone, LPS and Dex (1 μM), transforming growth factor-beta 1 (TGF-β1) (5 ng/ml) alone, TGF-β1 and Dex, with or without Atip (100 μM) in culture media. Epithelial-mesenchymal transition (EMT), cell necrosis, necroptosis and pyroptosis, and c-Jun N-terminal kinase (JNK) phosphorylation were then determined. Dex treatment significantly alleviated LPS-induced AKI, myofibroblast activation, NLRP3 inflammasome activation, and necroptosis in mice. Atip counteracted its protective effects. Dex attenuated LPS or TGF-β1 induced EMT and also prevented necrosis, necroptosis, and pyroptosis in response to LPS stimulation in the HK2 cells. The anti-EMT effects of Dex were associated with JNK phosphorylation. Dex reduced EMT following LPS stimulation whilst simultaneously inhibiting pyroptosis and necroptosis via α 2 -AR activation in the renal tubular cells. The "anti-fibrotic" and cytoprotective properties and its clinical use of Dex need to be further studied. [ABSTRACT FROM AUTHOR]