Application status and optimization suggestions of tumor organoids and CAR-T cell co-culture models.

Tumor organoids, especially patient-derived organoids (PDOs) exhibit marked similarities in histopathological morphology, genomic alterations, and specific marker expression profiles to those of primary tumour tissues. They are applied in various fields including drug screening, gene editing, and identification of oncogenes. However, CAR-T therapy in the treatment of solid tumours is still at an exploratory stage. Tumour organoids offer unique advantages over other preclinical models commonly used for CAR-T therapy research, which the preservation of the biological characteristics of primary tumour tissue is critical for the study of early-stage solid tumour CAR-T therapies. Although some investigators have used this co-culture model to validate newly targeted CAR-T cells, optimise existing CAR-T cells and explore combination therapy strategies, there is still untapped potential in the co-culture models used today. This review introduces the current status of the application of tumour organoid and CAR-T cell co-culture models in recent years and commented on the limitations of the current co-cultivation model. Meanwhile, we compared the tumour organoid model with two pre-clinical models commonly used in CAR-T therapy research. Eventually, combined with the new progress of organoid technologies, optimization suggestions were proposed for the co-culture model from five perspectives: preserving or reconstructing the tumor microenvironment, systematization, vascularization, standardized culture procedures, and expanding the tumor organoids resource library, aimed at assisting related researchers to better utilize co-culture models.

Glutathione-Responsive Organosilica Hybrid Nanosystems for Targeted Dual-Starvation Therapy in Luminal Breast Cancer.

Starvation therapy is an innovative approach in cancer treatment aimed at depriving cancer cells of necessary resources by impeding tumor angiogenesis or blocking the energy supply. In addition to the commonly observed anaerobic glycolysis energy supply mode, adipocyte-rich tumor tissue triggers the fatty acid energy supply pathway, which fuels the proliferation and metastasis of cancer cells. To completely disrupt these dual-energy-supply pathways, we developed an exceptional nanoreactor. This nanoreactor consisted of yolk-shell mesoporous organosilica nanoparticles (YSMONs) loaded with a fatty acid transport inhibitor (Dox), conjugated with a luminal breast-cancer-specific targeting aptamer, and integrated with a glucose oxidation catalyst (GOx). Upon reaching cancer cells with the assistance of the aptamer, the nanoreactor underwent a structural collapse of the shell triggered by the high concentration of glutathione within cancer cells. This collapse led to the release of GOx and Dox, achieving targeted delivery and exhibiting significant efficacy in starving therapy. Additionally, the byproducts of glucose metabolism, gluconic acid and H2O2, enhanced the acidity and reactive oxygen species levels of the intracellular microenvironment, inducing oxidative damage to cancer cells. Simultaneously, released Dox acted as a potent broad-spectrum anticancer drug, inhibiting the activity of carnitine palmitoyltransferase 1A and exerting marked effects. Combining these effects ensures high anticancer efficiency, and the "dual-starvation" nanoreactor has the potential to establish a novel synergistic therapy paradigm with considerable clinical significance. Furthermore, this approach minimizes damage to normal organs, making it highly valuable in the field of cancer treatment.

Facile Preparation of Photothermal Superhydrophobic Melamine Sponge Decorated with MXene and Lignin Particles for Efficient Oil/Water Separation, Fast Crude Oil Recovery, and Active Deicing.

Frequent oil spills and the discharge of oily wastewaters have caused a serious threat to the environment, ecosystems, and human beings. Herein, a photothermal and superhydrophobic melamine sponge (MS) decorated with MXene and lignin particles has been prepared for the separation of oil/water mixtures, the recovery of crude oils, and active deicing. The obtained superhydrophobic melamine sponge shows a water contact angle (WCA) of 152.3° and an oil contact angle of ∼0° and possesses good chemical stability, thermal stability, and mechanical durability in terms of being immersed in various liquids (i.e., corrosive solutions, organic solvents, and boiling water) and being abrased by sandpapers. This superhydrophobic MS displays a high oil adsorption capacity of CCl4, up to 91.6 times its own weight and a high separation efficiency of 99.4%. Furthermore, the maximum surface temperature of the superhydrophobic MS reaches 57.5 °C under sunlight irradiation (1.0 kW/m2) due to the excellent photothermal heating conversion performance of MXene and lignin particles. When exposed to sunlight, the superhydrophobic MS can quickly absorb viscous crude oils up to 72 times its own weight. Also, the WCA of the superhydrophobic MS remains above 146° after 50 icing/deicing cycles, showing excellent photothermal anti-icing properties. Thus, this study presents an easy and low-cost method for designing photothermal superhydrophobic melamine sponges and opens a new avenue to the applications of efficient oil/water separation, fast crude oil recovery, and active deicing.

Efficacy and safety of low-dose cyclophosphamide combined with lenvatinib, pembrolizumab and TACE for unresectable hepatocellular carcinoma: A single-center, prospective, single-arm clinical trial.

Objective: Unresectable hepatocellular carcinoma (uHCC) continues to pose effective treatment options. The objective of this study was to assess the efficacy and safety of combining low-dose cyclophosphamide with lenvatinib, pembrolizumab and transarterial chemoembolization (TACE) for the treatment of uHCC. Methods: From February 2022 to November 2023, a total of 40 patients diagnosed with uHCC were enrolled in this small-dose, single-center, single-arm, prospective study. They received a combined treatment of low-dose cyclophosphamide with lenvatinib, pembrolizumab, and TACE. Study endpoints included progression-free survival (PFS), objective response rate (ORR), and safety assessment. Tumor response was assessed using the modified Response Evaluation Criteria in Solid Tumors (mRECIST), while survival analysis was conducted through Kaplan-Meier curve analysis for overall survival (OS) and PFS. Adverse events (AEs) were evaluated according to the National Cancer Institute Common Terminology Criteria for Adverse Events (version 5.0). Results: A total of 34 patients were included in the study. The median follow-up duration was 11.2 [95% confidence interval (95% CI), 5.3-14.6] months, and the median PFS (mPFS) was 15.5 (95% CI, 5.4-NA) months. Median OS (mOS) was not attained during the study period. The ORR was 55.9%, and the disease control rate (DCR) was 70.6%. AEs were reported in 27 (79.4%) patients. The most frequently reported AEs (with an incidence rate >10%) included abnormal liver function (52.9%), abdominal pain (44.1%), abdominal distension and constipation (29.4%), hypertension (20.6%), leukopenia (17.6%), constipation (17.6%), ascites (14.7%), and insomnia (14.7%). Abnormal liver function (14.7%) had the most common grade 3 or higher AEs. Conclusions: A combination of low-dose cyclophosphamide with lenvatinib, pembrolizumab, and TACE is safe and effective for uHCC, showcasing a promising therapeutic strategy for managing uHCC.

Enterovirus 71 enters human brain microvascular endothelial cells through an ARF6-mediated endocytic pathway.

Infection of the central nervous system caused by enterovirus 71 (EV71) remains the main cause of death in hand-foot-and-mouth disease. However, the mechanism responsible for how EV71 breaks through the blood-brain barrier to infect brain cells has yet to be elucidated. By performing a high-throughput small interfering RNA (siRNA) screening and validation, we found that the infection of human brain microvascular endothelial cells (HBMECs) by EV71 was independent of the endocytosis pathways mediated by caveolin, clathrin, and macropinocytosis but dependent on ADP-ribosylation factor 6 (ARF6), a small guanosinetriphosphate (GTP)-binding protein of the Ras superfamily. The specific siRNA targeting ARF6 markedly inhibited HBMECs susceptibility to EV71. EV71 infectivity was inhibited by NAV-2729, a specific inhibitor of ARF6, in a dose-dependent manner. The subcellular analysis demonstrated the co-localization of the endocytosed EV71 and ARF6, while knockdown of ARF6 with siRNA remarkably influenced EV71 endocytosis. By immunoprecipitation assays, we found a direct interaction of ARF6 with EV71 viral protein. Furthermore, ARF1, another small GTP-binding protein, was also found to participate in ARF6-mediated EV71 endocytosis. Murine experiments demonstrated that NAV-2729 significantly alleviated mortality caused by EV71 infection. Our study revealed a new pathway by which EV71 enters the HBMECs and provides new targets for drug development.

Photothermal, Magnetic, and Superhydrophobic PU Sponge Decorated with a Fe3O4/MXene/Lignin Composite for Efficient Oil/Water Separation.

Frequent oil spills and the discharge of industrial oily wastewaters have become a serious threat to the environment, ecosystem, and human beings. Herein, a photothermal, magnetic, and superhydrophobic PU sponge decorated with a Fe3O4/MXene/lignin composite (labeled as S-Fe3O4/MXene/lignin@PU sponge) has been designed and prepared. The obtained superhydrophobic/superoleophilic PU sponge possesses excellent chemical stability, thermal stability, and mechanical durability in terms of being immersed in corrosive solutions and organic solvents and boiling water and being abrased by sandpapers, respectively. The oil adsorption capacities of the S-Fe3O4/MXene/lignin@PU sponge for various organic liquids range from 29.1 to 70.3 g/g, and the oil adsorption capacity for CCl4 can remain 69.6 g/g even after 15 cyclic adsorption tests. The separation efficiencies of the S-Fe3O4/MXene/lignin@PU sponge for n-hexane and CCl4 are higher than 98% in different environments (i.e., water, hot water, 1 mol/L NaOH, 1 mol/L NaCl, and 1 mol/L HCl). More importantly, the introduction of three light absorbers (i.e., Fe3O4, MXene, and lignin) into the S-Fe3O4/MXene/lignin@PU sponge shows a synergistic effect in the photothermal heat conversion performance, and the maximum surface temperature reaches 64.4 °C under sunlight irradiation (1.0 kW/m2). The separation flux of the S-Fe3O4/MXene/lignin@PU sponge for viscous LT147 vacuum pump oil reaches 35,469 L m-2 h-1 under sunlight irradiation, showing an increase of 27.3% compared to that of oil adsorption processes without the photothermal effect. Thus, the rational design of superhydrophobic sponges by introducing proper photothermal heat absorbers provides new insights into facile and cost-effective preparation of sponges for efficient oil/water separation.

Binding mechanism of oseltamivir and influenza neuraminidase suggests perspectives for the design of new anti-influenza drugs.

Oseltamivir is a widely used influenza virus neuraminidase (NA) inhibitor that prevents the release of new virus particles from host cells. However, oseltamivir-resistant strains have emerged, but effective drugs against them have not yet been developed. Elucidating the binding mechanisms between NA and oseltamivir may provide valuable information for the design of new drugs against NA mutants resistant to oseltamivir. Here, we conducted large-scale (353.4 µs) free-binding molecular dynamics simulations, together with a Markov State Model and an importance-sampling algorithm, to reveal the binding process of oseltamivir and NA. Ten metastable states and five major binding pathways were identified that validated and complemented previously discovered binding pathways, including the hypothesis that oseltamivir can be transferred from the secondary sialic acid binding site to the catalytic site. The discovery of multiple new metastable states, especially the stable bound state containing a water-mediated hydrogen bond between Arg118 and oseltamivir, may provide new insights into the improvement of NA inhibitors. We anticipated the findings presented here will facilitate the development of drugs capable of combating NA mutations.

Remission effect of Canagliflozin in patients with newly diagnosed type 2 diabetes mellitus: a protocol for a multicenter, parallel-group, randomized, controlled, open-label trial.

BACKGROUND: Studies reporting the effects of metabolic surgery, lifestyle intervention, and intensive insulin therapy for the remission of type 2 diabetes (T2DM) has been increasing, with fruitful results better conducted and yielded. However, there are only a few studies on the remission of T2DM using oral hypoglycemic drugs. Therefore, this study aims to investigate the remission effect of canagliflozin and metformin on participants with newly diagnosed T2DM and its possible underlying mechanism(s) through which these two medications elicit diabetes remission. METHOD: To this end, we performed a multicenter, parallel-group, randomized, controlled, and open-label trial. A total of 184 participants with a ≤ 3-year course of T2DM will be enrolled and randomly assigned to the canagliflozin or metformin treatment group in a ratio of 1:1. Participants in each group will maintain their medication for 3 months after achieving the target blood glucose level and then stop it. These participants will be followed up for one year to determine remission rates in both groups. DISCUSSION: In this study, we will establish that whether canagliflozin is superior to metformin in terms of remission rate in participants with newly diagnosed T2DM. The results of this trial may provide robust evidence regarding the efficacy and mechanisms of the action of sodium-glucose cotransporter-2 inhibitors (SGLT2is) in T2DM remission. TRIAL REGISTRATION: ChiCTR2100043770(February 28, 2021).

Dexmedetomidine alleviates acute lung injury by promoting Tregs differentiation via activation of AMPK/SIRT1 pathway.

OBJECTIVES: To explore the anti-inflammatory effect and the potential mechanism of dexmedetomidine in ARDS/ALI. MATERIALS AND METHODS: C57BL/6 mice and EL-4 cells were used in this research. The ALI model was established by CLP. The level of inflammatory cytokines in the lung and blood, the severity of lung injury, the expression of Foxp3, and the proportion of Tregs were detected before and after dexmedetomidine treatment. The expression of the AMPK/SIRT1 after dexmedetomidine treatment was detected in vivo and in vitro. After blocking the AMPK/SIRT1 pathway or depleting Tregs in vivo, the level of the inflammatory response, tissue injury, and Tregs differentiation were detected again to clarify the effect of dexmedetomidine. RESULTS: Dexmedetomidine significantly reduced systemic inflammation and lung injury in CLP mice. Dexmedetomidine enhanced the Foxp3 expression in the lungs and the frequency of Tregs in the spleen. Dexmedetomidine up-regulated the protein expression of p-AMPK and SIRT1 in lungs and EL-4 cells and facilitated the differentiation of naïve CD4+ T cells into Tregs in vitro. Meanwhile, DEX also increased the expression of Helios in Treg cells. CONCLUSIONS: DEX could improve ARDS/ALI by facilitating the differentiation of Tregs from naïve CD4+ T cells via activating the AMPK/SIRT1 pathway.

Advancements in understanding mechanisms of hepatocellular carcinoma radiosensitivity: A comprehensive review.

Primary liver cancer is a significant health problem worldwide. Hepatocellular carcinoma (HCC) is the main pathological type of primary liver cancer, accounting for 75%-85% of cases. In recent years, radiotherapy has become an emerging treatment for HCC and is effective for various stages of HCC. However, radiosensitivity of liver cancer cells has a significant effect on the efficacy of radiotherapy and is regulated by various factors. How to increase radiosensitivity and improve the therapeutic effects of radiotherapy require further exploration. This review summarizes the recent research progress on the mechanisms affecting sensitivity to radiotherapy, including epigenetics, transportation and metabolism, regulated cell death pathways, the microenvironment, and redox status, as well as the effect of nanoparticles on the radiosensitivity of liver cancer. It is expected to provide more effective strategies and methods for clinical treatment of liver cancer by radiotherapy.

MICAL1 facilitates pancreatic cancer proliferation, migration, and invasion by activating WNT/ß-catenin pathway.

BACKGROUND: MICAL1 is involved in the malignant processes of several types of cancer; however, the role of MICAL1 in pancreatic cancer (PC) has not been well-characterized. This study aimed to investigate the expression and function of MICAL1 in PC. METHODS: RT-qPCR and immunohistochemistry were used to detect MICAL1 expression in PC and adjacent nontumor tissues. Cell Counting Kit-8, EdU, clone formation, wound healing, and Transwell assays as well as animal models were used to investigate the effects of overexpression or inhibition of MICAL1 expression on the proliferation, invasion, and metastasis of PC cells. RNA-seq was used to explore the main pathway underlying the functions of MICAL1. Proteomics, mass spectrometry, and co-immunoprecipitation assays were used to investigate the interaction of proteins with MICAL1. Rescue experiments were conducted to validate these findings. RESULTS: Both MICAL1 mRNA and protein levels were upregulated in PC tissues compared with matched adjacent nontumor tissues. The expression level of MICAL1 was associated with the proliferative and metastatic status of PC. Repression of MICAL1 significantly inhibited PC cell growth, migration, and invasion in vitro and in vivo. RNA sequencing analysis indicated that MICAL1 was closely correlated with the WNT pathway. Overexpression of MICAL1 (1) promoted the phosphorylation of TBC1D1 at the Ser660 site, (2) facilitated the distribution of FZD7 on the cytomembrane, (3) inhibited the degradation of FZD7 in the lysosome, and (4) activated the WNT pathway. CONCLUSIONS: MICAL1 was upregulated in PC and involved in stimulating the progression of PC cells by activating the WNT/ß-catenin signaling pathway. Therefore, MICAL1 is a potential therapeutic target for PC.

Phosphorylated ATF1 at Thr184 promotes metastasis and regulates MMP2 expression in gastric cancer.

BACKGROUND: Studies have revealed an important role of activating transcription factor 1 (ATF1) and phosphorylated ATF1 at Ser63 in tumors. Our previous study identified Thr184 as a novel phosphorylation site of ATF1. However, the role of phosphorylated ATF1 at Thr184 (p-ATF1-T184) in tumor is unclear. This study figured out the role of p-ATF1-T184 in the metastasis of gastric cancer (GC) and in the regulation of Matrix metallopeptidase 2 (MMP2). METHODS: Immunohistochemical analysis (IHC) was performed to analyze the level of p-ATF1-T184 and its relationship with clinicopathological characteristics. Wound scratch test, Transwell assay were used to observe the role of p-ATF1-T184 in the invasion and metastasis of GC. The regulation of MMP2 by p-ATF1-T184 was investigated by a series of experiments including quantitative RT-PCR, western blot, gelatin zymography assay, Chromatin immunoprecipitation (ChIP), luciferase reporter assay and cycloheximide experiment. The Cancer Genome Atlas (TCGA) data were used to analyze the expression and prognostic role of ATF1 and MMP2 in GC. Mass spectrometry (MS) following co-immunoprecipitation (co-IP) assay was performed to identify potential upstream kinases that would phosphorylate ATF1 at Thr184. RESULTS: High expression level of p-ATF1-T184 was found and significantly associated with lymph node metastasis and poor survival in a GC cohort of 126 patients. P-ATF1-T184 promoted migration and invasion of gastric cancer cells. Phosphorylation of ATF1-T184 could regulate the mRNA, protein expression and extracellular activity of MMP2. P-ATF1-T184 further increased the DNA binding ability, transcription activity, and stabilized the protein expression of ATF1. Moreover, TCGA data and IHC results suggested that the mRNA level of ATF1 and MMP2, and protein level of p-ATF1-T184 and MMP2 could be prognosis markers of GC. Two protein kinase related genes, LRBA and S100A8, were identified to be correlated with the expression ATF1 in GC. CONCLUSION: Our results indicated that p-ATF1-T184 promoted metastasis of GC by regulating MMP2.

Sodium formononetin-3'-sulphonate alleviates cerebral ischemia-reperfusion injury in rats via suppressing endoplasmic reticulum stress-mediated apoptosis.

BACKGROUND: Sodium formononetin-3'-sulphonate (Sul-F) may alleviate I/R injury in vivo with uncertain mechanism. Endoplasmic reticulum (ER) stress-mediated apoptosis participates in the process of cerebral ischemia-reperfusion (I/R) injury. Our aim is to figure out the effect of Sul-F on cerebral I/R injury and to verify whether it works through suppressing ER stress-mediated apoptosis. RESULTS: The cerebral lesions of middle cerebral artery occlusion (MCAO) model in SD rats were aggravated after 24 h of reperfusion, including impaired neurological function, increased infarct volume, intensified inflammatory response and poor cell morphology. After intervention, the edaravone (EDA, 3 mg/kg) group and Sul-F high-dose (Sul-F-H, 80 mg/kg) group significantly alleviated I/R injury via decreasing neurological score, infarct volume and the serum levels of inflammatory factors (TNF-α, IL-1ß and IL-6), as well as alleviating pathological injury. Furthermore, the ER stress level and apoptosis rate were elevated in the ischemic penumbra of MCAO group, and were significantly blocked by EDA and Sul-F-H. In addition, EDA and Sul-F-H significantly down-regulated the ER stress related PERK/eIF2α/ATF4 and IRE1 signal pathways, which led to reduced cell apoptosis rate compared with the MCAO group. Furthermore, there was no difference between the EDA and Sul-F-H group in terms of therapeutic effect on cerebral I/R injury, indicating a therapeutic potential of Sul-F for ischemic stroke. CONCLUSIONS: Sul-F-H can significantly protects against cerebral I/R injury through inhibiting ER stress-mediated apoptosis in the ischemic penumbra, which might be a novel therapeutic target for ischemic stroke.

Evidence of Kinetically Relevant Consistency in Thermal and Photo-Thermal HCOOH Decomposition over Pd/LaCrO3 /C3 N4 Composite.

Photo-thermal catalysis has been an attractive alternative strategy to promote chemical reactions for years, however, how light cooperates with thermal energy is still unclear. We meet this demand by exploring reaction mechanism via pressure dependency studies as well as H/D exchange experiments with HCOOH decomposition as a probe over a palladium nanoparticle (Pdn ) and isolated Pd (Pd1 ) decorated LaCrO3 /C3 N4 composite catalyst, in which the H2 formation rate shows a first-order dependence on HCOOH and inverse first-order dependence on CO partial pressures no matter the reaction was driven by thermal or photo-thermal energy. Additionally, negligible kinetic isotopic effects (KIEs: kH /kD ) were determined under both dark and light conditions at 1.04 and 1.18 when the HCOOH was replaced by HCOOD. Besides, when the reactant HCOOH was further replaced by DCOOD, the KIE values of 1.55 (dark) and 1.92 (light) were obtained, which indicates that the HCOOH decomposition follows kinetically relevant (KR) of C-H bond rupture within HCOOH molecule under both thermal and photo-thermal reaction conditions and the catalytic surface was found to be densely covered by CO based on the pressure dependency studies as well as the in situ Fourier transform infrared spectroscopy (FTIR) analysis. Clearly, the HCOOH decomposition driven by thermal and photo-thermal energy follows the same reaction mechanism. Nevertheless, light induced hot electrons and the derived thermal effect do cause the enhancement of the reaction activity in some circumstances compared with bare thermal catalysis, which clarifies the confusion on cooperation mechanism of photo and thermal energies from the kinetic perspective. Hot electrons induced by photo-illumination was confirmed by in situ FTIR CO chemisorption with ∼10 cm-1 redshift identified of the CO feature once light was introduced. Meanwhile, the photo thermal reaction system suffers from severe electron-hole re-combination at high reaction temperatures and make the thermal effect of photo irradiation dominant with respect to the effect at low reaction temperatures. This research provides insight to the mechanism on how photo-thermal reaction works and draws attention to the photo-thermal reaction process in boosting catalytic activity.

Anthocyanins Inhibit Airway Inflammation by Downregulating the NF-κB Pathway via the miR-138-5p/SIRT1 Axis in Asthmatic Mice.

OBJECTIVE: Asthma, caused by chronic inflammation, is a common disease. Anthocyanins are involved in asthma treatment. This study explored the mechanism of anthocyanins on airway inflammation in asthmatic mice by regulating nuclear factor-κB (NF-κB) via the miR-138-5p/sirtuin-1 (SIRT1) axis. METHODS: The asthmatic mouse model was established by ovalbumin (OVA) induction and treated with anthocyanins or simultaneously injected with the lentivirus miR-138-5p mimic, followed by the measurement of lung inflammatory injury and IL-4, IL-5, IL-13, and IFN-γ levels in bronchoalveolar lavage fluid. Human bronchial epithelial (HBE) cells 16HBE14o-160 were induced by OVA to establish an asthmatic cell model, treated with anthocyanins and manipulated with miR-138-5p mimic and pcDNA3.1-SIRT1. The releases of inflammatory cytokines, the nuclear translocation of p-p65/p65 in the NF-κB pathway, and the levels of miR-138-5p and SIRT1 mRNA were detected. RESULTS: In vivo experiments showed that anthocyanins could reduce the OVA-induced airway hyperresponsiveness and airway inflammation, improve the inflammatory infiltration and mucus in lung tissues, and diminish the miR-138-5p level in asthmatic mice. Infection with the miR-138-5p mimic averted the remission effect of anthocyanins in asthmatic mice. In vitro experiments showed that in HBE cells exposed to OVA, anthocyanins reduced the miR-138-5p level, increased the SIRT1 level, inhibited the release of inflammatory factors, and reduced the nuclear translocation of NF-κB p65. miR-138-5p targeted SIRT1. miR-138-5p overexpression partially reversed the therapeutic effect of anthocyanins, while SIRT1 overexpression antagonized the effect of miR-138-5p overexpression. CONCLUSION: Anthocyanins inhibited the NF-κB pathway by regulating the miR-138-5p/SIRT1 axis, thus inhibiting airway inflammation in asthmatic mice.

Mussel-Inspired Durable TiO2/PDA-Based Superhydrophobic Paper with Excellent Self-Cleaning, High Chemical Stability, and Efficient Oil/Water Separation Properties.

Oceanic oil spill and the discharge of industrial oily wastewaters can cause significant threats to the ecological environment and human health. Herein, we design a durable TiO2/PDA-based superhydrophobic paper for efficient oil/water separation. Bioinspired from mussel adhesive proteins, the mechanical durability of the as-prepared superhydrophobic paper is enhanced by the deposition of polydopamine (PDA) onto cellulosic fibers via self-polymerization of dopamine. The TiO2/PDA-based superhydrophobic paper shows a high water contact angle of 168.2° and an oil contact angle of ∼0°, exhibiting excellent superhydrophobicity and superoleophilicity. Furthermore, the as-prepared superhydrophobic paper possesses excellent chemical stability, thermal stability, and mechanical durability in terms of being immersed in corrosive solutions and solvents and boiling water and being subjected to the sandpaper abrasion test, respectively. More importantly, the separation efficiency of the TiO2/PDA-based superhydrophobic paper for an oil/water mixture is 97.2%, and it maintains a separation efficiency above 94.3% even after 15 cyclic separation processes. Furthermore, the separation efficiency for water-in-oil emulsions is higher than 93.7% after 15 cyclic separation tests, showing its excellent recyclable stability for water-in-oil emulsions. Therefore, the rationally designed TiO2/PDA-based superhydrophobic paper shows great potential in the practical applications of self-cleaning, antifouling, and oil/water separation.

Enhanced Surface Icephobicity on an Elastic Substrate.

Ice accumulation on exposed surfaces is unavoidable as time elapses and the temperature decreases sufficiently. To mitigate icing problems, various types of icephobic substrates have been rationally designed, including superhydrophobic substrates (SHSs), aqueous lubricating layers, organic lubricating layers, organogels, polyelectrolyte brush layers, electrolyte-based hydrogels, elastic substrates, and multicrack initiator-promoted surfaces. Among these surfaces, elastic substrates show excellent enhanced surface icephobicity during dynamic processes (i.e., water-impacting and de-icing tests). Herein, we summarize recent progress in elastic icephobic substrates and discuss the reasons that surface icephobicity can be enhanced on elastic substrates in terms of enhanced water repellency and further lowering the ice adhesion strength. For enhanced water repellency, we focus on reducing the contact time of water impacting such that water droplets can be easily shed from an elastic substrate before ice occurs. Reducing the contact time of water impacting various substrates (i.e., micro/nanostructured rigid SHSs, macrotextured rigid SHSs, and elastic SHSs) is discussed, followed by exploring their mechanisms. We argue that the ice adhesion strength can be further lowered on an elastic substrate by rationally tuning the elastic modulus and surface textures (i.e., surface textured and hollow subsurface textured) and combining elastic substrate with other passive anti-icing strategies (or functioning passive icephobic substrates with an electrothermal or photothermal stimulus). In short, the introduction of an elastic substrate into a passive or active icephobicity surface opens an avenue toward designing a versatile icephobic surface, providing great potential for outdoor anti-icing applications.

Vinyl azide as a synthon for DNA-compatible divergent transformations into N-heterocycles.

Inspired by diversity-oriented synthesis, we have developed a series of DNA-compatible transformations utilizing on-DNA vinyl azide as a synthon to forge divergent N-heterocyclic scaffolds. Polysubstituted imidazoles and isoquinolines were efficiently obtained with moderate-to-excellent conversions. Besides, the "one-pot" strategy to prepare in-house on-DNA vinyl azides afforded synthons readily. Results from substrate scope exploration and enzymatic ligation further demonstrate the feasibility of these N-heterocycle syntheses in DNA-encoded chemical library construction.

Gas-particle partitioning of polycyclic aromatic hydrocarbons from oil combustion involving condensate, diesel and heavy oil.

This study focuses on the gas-particle (G-P) partitioning of 16 polycyclic aromatic hydrocarbons (PAHs) from oil combustion, which is one of the important contributors of anthropogenic PAHs but has been rarely studied. The combustions of different types of oils involving ultra-light to heavy oils were investigated, and the PAH partitioning mechanism was determined by the widely used Junge-Pankow adsorption model, Koa absorption model, and dual sorption model, respectively. The results show that the source-specific diagnostic ratios of Ant/(Ant+Phe) are between 0.09 and 0.24, the estimated regression slopes of G-P partition coefficients (KP) of the total PAHs on their sub-cooled liquid vapor pressures (PLO) are in the range of - 0.34 to - 0.25, and the predicted fractions of PAHs in the particle phase (φ) by Koa absorption model are close to the measured values, while the log KPvalues of the LMW PAHs from the combustions of diesel and heavy oil are better represented by the dual sorption model. Our findings indicate that PAHs are derived from mixed sources that include the unburned original oil and combustion products, and the PAH partitioning mechanism is governed by the process of absorption into organic matter because of the unburned oil, but both adsorption and absorption exist simultaneously in the lighter PAHs from the combustions of heavier oils (i.e., diesel and heavy oil). Based on these findings, the understanding of the fate and transport of PAH emissions and the optimization of the emergency responses to accidents such as marine oil spills would be potentially improved.

MSA-MOT: Multi-Stage Association for 3D Multimodality Multi-Object Tracking.

Three-dimensional multimodality multi-object tracking has attracted great attention due to the use of complementary information. However, such a framework generally adopts a one-stage association approach, which fails to perform precise matching between detections and tracklets, and, thus, cannot robustly track objects in complex scenes. To address this matching problem caused by one-stage association, we propose a novel multi-stage association method, which consists of a hierarchical matching module and a customized track management module. Specifically, the hierarchical matching module defines the reliability of the objects by associating multimodal detections, and matches detections with trajectories based on the reliability in turn, which increases the utilization of true detections, and, thus, guides accurate association. Then, based on the reliability of the trajectories provided by the matching module, the customized track management module sets maximum missing frames with differences for tracks, which decreases the number of identity switches of the same object and, thus, further improves the association accuracy. By using the proposed multi-stage association method, we develop a tracker called MSA-MOT for the 3D multi-object tracking task, alleviating the inherent matching problem in one-stage association. Extensive experiments are conducted on the challenging KITTI benchmark, and the results show that our tracker outperforms the previous state-of-the-art methods in terms of both accuracy and speed. Moreover, the ablation and exploration analysis results demonstrate the effectiveness of the proposed multi-stage association method.