Tumor cell-released LC3-positive EVs promote lung metastasis of breast cancer through enhancing premetastatic niche formation.

Most breast cancer-related deaths are caused by metastasis in vital organs including the lungs. Development of supportive metastatic microenvironments, referred to as premetastatic niches (PMNs), in certain distant organs before arrival of metastatic cells, is critical in metastasis. However, the mechanisms of PMN formation are not fully clear. Here, we demonstrated that chemoattractant C-C motif chemokine ligand 2 (CCL2) could be stimulated by heat shock protein 60 (HSP60) on the surface of murine 4 T1 breast cancer cell-released LC3+ extracellular vesicles (LC3+ EVs) via the TLR2-MyD88-NF-κB signal cascade in lung fibroblasts, which subsequently promoted lung PMN formation through recruiting monocytes and suppressing T cell function. Consistently, reduction of LC3+ EV release or HSP60 level or neutralization of CCL2 markedly attenuated PMN formation and lung metastasis. Furthermore, the number of circulating LC3+ EVs and HSP60 level on LC3+ EVs in the plasma of breast cancer patients were positively correlated with disease progression and lung metastasis, which might have potential value as biomarkers of lung metastasis in breast cancer patients (AUC = 0.898, 0.694, respectively). These findings illuminate a novel mechanism of PMN formation and might provide therapeutic targets for anti-metastasis therapy for patients with breast cancer.

Low-cost polymer-film spiral inertial microfluidic device for label-free separation of malignant tumor cells.

We developed a low-cost polymer-film spiral inertial microfluidic device for the effective size-dependent separation of malignant tumor cells. The device was fabricated in polymer films by rapid laser cutting and chemical bonding. After fabricating the prototype device, the separation performance of our device was evaluated using particles and cells. The effects of operational flow rate, cell diameter, and cell concentration on the separation performance were explored. Our device successfully separated tumor cells from polydisperse white blood cells according to their different migration modes and lateral positions. Then, the separation of rare cells was carried out using the high-concentration lysed blood spiked with 200 tumor cells. Experimental results showed that 83.90% of the tumor cells could be recovered, while 99.87% of white blood cells could be removed. We successfully employed our device for processing clinical pleural effusion samples from patients with advanced metastatic breast cancer. Malignant tumor cells with an average purity of 2.37% could be effectively enriched, improving downstream diagnostic accuracy. Our device offers the advantages of label-free operation, low cost, and fast fabrication, thus being a potential tool for effective cell separation.

Identification of Potential Prognostic and Predictive Biomarkers for Immune-Checkpoint Inhibitor Response in Small Cell Lung Cancer.

BACKGROUND Immune-checkpoint inhibitors have propelled the field of therapeutics for small cell lung cancer (SCLC) treatment, but are only beneficial to some patients. The objective of this study was to identify valid biomarkers for good potential response to immunotherapy. MATERIAL AND METHODS We performed an integrated analysis of the available datasets from the Gene Expression Omnibus (GEO) projects, Cancer Cell Line Encyclopedia (CCLE), TISIDB database, and Lung Cancer Explorer (LCE) database. Six prognosis-related genes (MCM2, EZH2, CENPK, CHEK1, CDKN2A, and EXOSC2) were identified utilizing the meta workflow of data analysis methods. We performed subclass mapping to compare their expression profiles to other datasets of patients who responded to immunotherapy. A drug sensitivity predictive model was used to predict the chemotherapeutic response to cisplatin and etoposide. RESULTS Our results showed that the expression of the 6 key genes was significantly associated with the overall survival of patients with SCLC. Lower expression of these 6 genes was correlated to the response to anti-PD-1 treatment. Additionally, low expression of MCM2, EZH2, CENPK, and CHEK1 was correlated with increased sensitivity to cisplatin, but not etoposide. CONCLUSIONS Overall, our data showed that MCM2, EZH2, CENPK, CHEK1, CDKN2A, and EXOSC2 are potential prognostic and predictive biomarkers for response to immune-checkpoint inhibitor treatment in patients with SCLC. Further studies with large sample sizes are required to validate our findings and to explore the detailed mechanisms underlying the role of these genes in SCLC.

Hyperspectral imaging analysis of a photonic crystal bead array for multiplex bioassays.

For multiplex bioassays, one effective strategy is to employ microfluidic chips based on an array of photonic crystal beads (PCBs) that are encoded by their characteristic reflection spectrum (CRS). In this paper, we report a hyperspectral imaging system and algorithms for the high throughput decoding of a PCB array and subsequent detection. The results showed that the decoding accuracy of up to ∼500 PCBs is 98.56% with an excellent ability to extract low-intensity fluorescence intensities. The results also demonstrated hyperspectral imaging techniques which can simultaneously obtain both spatial and spectral information as powerful tools in the analysis of multiplex bioassays or microfluidic chips.

Clinical value of serum polyunsaturated fatty acids in patients with gastric polyps.

Polyunsaturated fatty acids (PUFAs) are vital nutrients in human physiology and are implicated in various chronic diseases. However, the relationship between PUFAs and gastric polyps remains unclear. This study employed liquid chromatography-tandem mass spectrometry (LC-MS/MS) to assess PUFA levels in the serum of 350 patients, along with analyzing the ω-6 to ω-3 ratio. The results revealed significant differences in the levels of C16:1, C18:1, C18:2, α-C18:3, γ-C18:3, C20:1, C20:4, C20:5, ω-3-C22:5, ω-6-C22:5, and C22:6, as well as ω-6 to ω-3 ratio between the control and gasteic polyp groups. Moreover, setting the threshold for ω-6: ω-3 at 10 revealed a close correlation between polyp occurrence and this ratio. These findings suggest that PUFAs and the ω-6 to ω-3 ratio hold promise as potential early screening markers for gastric polyps. However, further research is imperative to elucidate the underlying mechanisms and therapeutic potential of PUFAs in managing gastric polyps.

Multicolor Photochemical Printing Inside Polymer Matrices for Advanced Photonic Anticounterfeiting.

Conventional security inks, generally directly printed on the data page surface, are vulnerable to counterfeiters, thereby raising the risk of chemical structural deciphering. In fact, polymer film-based data pages with customized patterns embedded within polymer matrix, rather than printed on the surface, emerge as a promising solution. Therefore, the key lies in developing fluorophores offering light dose-controlled fluorescent color inside polymer matrices. Though conventional fluorophores often suffer from photobleaching and uncontrolled photoreactions, disqualifying them for this purpose. Herein a diphenanthridinylfumaronitrile-based phototransformers (trans-D5) that undergoes photoisomerization and subsequent photocyclization during photopolymerization of the precursor, successively producing cis- and cyclo-D5 with stepwise redshifted solid-state emissions is developed. The resulting cyclo-D5 exhibits up to 172 nm emission redshift in rigidifying polymer matrices, while trans-D5 experiences a slightly blueshifted emission (≈28 nm), cis-D5 undergoes a modest redshift (≈14 nm). The markedly different rigidochromic behaviors of three D5 molecules within polymer matrices enable multicolor photochemical printing with a broad hue ranging from 38 to 10 via an anticlockwise direction in Munsell color space, yielding indecipherable fluorescent patterns in polymer films. This work provides a new method for document protection and implements advanced security features that are unattainable with conventional inks.

PDL1/HER2-Targeted Lipid-Encapsulated Oxygen Nanobubbles Combined with Photodynamic Therapy for HER2+ Breast Cancer Immunotherapy.

Programmed death (PD) 1/PD ligand 1 (PDL1) inhibitors are immune checkpoint inhibitors (ICIs) that may facilitate HER2-positive breast cancer treatment; however, their clinical efficacy remains elusive. Oxygen-enhanced photodynamic therapy (PDT) increases immunogenic cell death (ICD), providing a promising strategy to render the tumor microenvironment more sensitive to the ICIs. Lipid-encapsulated oxygen nanobubbles (Lipo-NBs-O2) obtained using nanobubbles (NBs) water for oxygen delivery in vivo can facilitate enhanced PDT. Here, dual-receptor targeted Lipo-NBs-O2 (DRT@Lipo-NBs-O2) is prepared by modifying Lipo-NBs-O2 with anti-PDL1 scFv and the fusion protein anti-HER2 scFv-tandem-repeat cytochrome c (anti-HER2-nCytc). Copper phthalocyanine is the photosensitizer (PS). DRT@Lipo-PS-NBs-O2 plus near-infrared irradiation leads to robust ICD induction, increasing DC activation and CD8+ T-cell numbers. Modification with anti-PDL1 scFv improves tumor distribution of DRT@Lipo-PS-NBs-O2 and plays the ICI role, invigorating CD8+ T cells and boosting the effects of immunotherapy. Oxygen supplied through DRT@Lipo-PS-NBs-O2 reduces P-glycoprotein expression. Enhanced PDT and Cytc can cause tumor cell death, thereby reducing the immune burden. Under dual receptor targeting and laser local irradiation, tumor cells become subject to the combination effects of PDT, ICD, ICIs, and apoptosis; this effectively suppresses tumor growth and metastasis. Lipo-NBs-O2 affords a combination of oxygen delivery and multidrug therapy to alleviate HER2-positive breast cancer.

Tumour cell-released autophagosomes promote lung metastasis by upregulating PD-L1 expression in pulmonary vascular endothelial cells in breast cancer.

PURPOSE: Establishing an immunosuppressive premetastatic niche (PMN) in distant organs is crucial for breast cancer metastasis. Vascular endothelial cells (VECs) act as barriers to transendothelial cell migration. However, the immune functions of PMNs remain unclear. Tumour cell-released autophagosomes (TRAPs) are critical modulators of antitumour immune responses. Herein, we investigated the mechanism through which TRAPs modulate the immune function of pulmonary VECs in lung PMN in breast cancer. METHODS: Immortalised mouse pulmonary microvascular endothelial cells were incubated with TRAPs in vitro. RNA sequencing, flow cytometry, and western blotting were employed to assess immunosuppressive function and mechanism. In vivo, TRAP-trained and autophagy-deficient tumour mice were used to detect immunosuppression, and high-mobility group box 1 (HMGB1)-deficient TRAP-trained and TLR4 knockout mice were utilised to investigate the underlying mechanisms of pulmonary VECs. Additionally, the efficacy of anti-programmed cell death ligand-1 (PD-L1) immunotherapy was evaluated in early tumour-bearing mice. RESULTS: HMGB1 on TRAPs surfaces stimulated VECs to upregulate PD-L1 via a TLR4-MyD88-p38/STAT3 signalling cascade that depended on the cytoskeletal movement of VECs. Importantly, PD-L1 on TRAP-induced VECs can inhibit T cell function, promote lung PMN immunosuppression, and result in more pronounced lung metastasis. Treatment with anti-PD-L1 reduces lung metastasis in early stage tumour-bearing mice. CONCLUSIONS: These findings revealed a novel role and mechanism of TRAP-induced immunosuppression of pulmonary VECs in lung PMN. TRAPs and their surface HMGB1 are important therapeutic targets for reversing immunosuppression, providing a new theoretical basis for the treatment of early stage breast cancer using an anti-PD-L1 antibody.

Tumor cell-released autophagosomes (TRAPs) induce PD-L1-decorated NETs that suppress T-cell function to promote breast cancer pulmonary metastasis.

BACKGROUND: Lung metastasis is the primary cause of breast cancer-related mortality. Neutrophil extracellular traps (NETs) are involved in the progression of breast cancer. However, the mechanism of NET formation is not fully understood. This study posits that tumor cell-released autophagosomes (TRAPs) play a crucial role in this process. METHODS: TRAPs were isolated from breast cancer cell lines to analyze their impact on NET formation in both human and mouse neutrophils. The study used both in vitro and in vivo models, including Toll-like receptor 4 (TLR4-/-) mice and engineered breast cancer cell lines. Immunofluorescence, ELISA, Western blotting, RNA sequencing, and flow cytometry were employed to dissect the signaling pathways leading to NET production and to explore their immunosuppressive effects, particularly focusing on the impact of NETs on T-cell function. The therapeutic potential of targeting TRAP-induced NETs and their immunosuppressive functions was evaluated using DNase I and αPD-L1 antibodies. Clinical relevance was assessed by correlating circulating levels of TRAPs and NETs with lung metastasis in patients with breast cancer. RESULTS: This study showed that TRAPs induced the formation of NETs in both human and mouse neutrophils by using the high mobility group box 1 and activating the TLR4-Myd88-ERK/p38 signaling axis. More importantly, PD-L1 carried by TRAP-induced NETs inhibited T-cell function in vitro and in vivo, thereby contributing to the formation of lung premetastatic niche (PMN) immunosuppression. In contrast, Becn1 KD-4T1 breast tumors with decreased circulating TRAPs in vivo reduced the formation of NETs, which in turn attenuated the immunosuppressive effects in PMN and resulted in a reduction of breast cancer pulmonary metastasis in murine models. Moreover, treatment with αPD-L1 in combination with DNase I that degraded NETs restored T-cell function and significantly reduced tumor metastasis. TRAP levels in the peripheral blood positively correlated with NET levels and lung metastasis in patients with breast cancer. CONCLUSIONS: Our results demonstrate a novel role of TRAPs in the formation of PD-L1-decorated NETs, which may provide a new strategy for early detection and treatment of pulmonary metastasis in patients with breast cancer.

Intestine-inspired wrinkled MXene microneedle dressings for smart wound management.

Composite MXene-based materials are prone to crack propagation, thus limiting their tensile properties. Numerous efforts have been devoted to removing material constraints and fabricating unitary MXene elastic films. Here, for the first time, inspired by the intestinal wrinkles and villi structure, we presented a ductile, biologically friendly, and highly conductive MXene-based microneedle (MMN) dressing composed of stacked MXene film and superfine microneedle arrays through a simple stretching and laser engraving strategy for wound healing. By utilizing photothermal responsive MXene, periodic porous structures, and a temperature-responsive polymer to construct the MMN dressing, the system can act as an effective route for facilitating controllable drug delivery controlled by near-infrared (NIR) irradiation. In addition, superior conductivity imparts them with the capacity to realize continuous and steady monitoring of motion sensing. The practical performance further demonstrated that the versatile MMN dressing showed obvious therapeutic efficacy in vivo animal wound models. Thus, it is believed that MMN dressings with biomimetic structures, controllable drug release, and conductive pathways will open a new chapter for wound management and widen other practical applications in biomedical fields, such as artificial tendons and soft robotics. STATEMENT OF SIGNIFICANCE: MXene-based materials have been demonstrated as critical tools in advancing our understanding of wound healing. However, the rapid crack propagation is a constraint on their tensile properties. Here, inspired by the intestinal wrinkles and villi structure, a single-step method has also been discussed to present a MXene-based microneedle dressing composed of unitary MXene elastic film and superfine microneedle arrays. At the same time, the dressing with biomimetic structures, controllable drug release, and conductive pathways has prospects in intelligent wound management and varieties of related biomedical fields.

Comprehensive Explorations of CCL28 in Lung Adenocarcinoma Immunotherapy and Experimental Validation.

Background: Chemokines have been reported to play an important role in cancer immunotherapy. This study aimed to explore the chemokines involved in lung cancer immunotherapy. Methods: All the public data were downloaded from The Cancer Genome Atlas Program database. Quantitative real time-PCR was used to detect the mRNA level of specific molecules and Western blot was used for the protein level. Other experiments used include luciferase reporter experiments, flow cytometric analysis, Chromatin immunoprecipitation assay, ELISA and co-cultured system. Results: We found that the CCL7, CCL11, CCL14, CCL24, CCL25, CCL26, CCL28 had a higher level, while the CCL17, CCL23 had a lower level in immunotherapy non-responders. Also, we found that immunotherapy non-responders had a higher level of CD56dim NK cells, NK cells, Th1 cells, Th2 cells and Treg, yet a lower level of iDC and Th17 cells. Biological enrichment analysis indicated that in the patients with high Treg infiltration, the pathways of pancreas beta cells, KRAS signaling, coagulation, WNT BETA catenin signaling, bile acid metabolism, interferon alpha response, hedgehog signaling, PI3K/AKT/mTOR signaling, apical surface, myogenesis were significantly enriched in. CCL7, CCL11, CCL26 and CCL28 were selected for further analysis. Compared with the patients with high CCL7, CCL11, CCL26 and CCL28 expression, the patients with low CCL7, CCL11, CCL26 and CCL28 expression had a better performance of immunotherapy response and this effect might partly be due to Treg cells. Furthermore, biological exploration and clinical correlation of CCL7, CCL11, CCL26 and CCL28 were conducted, Finally, CCL28 was selected for validation. Experiments showed that under the hypoxia condition, HIF-1α was upregulated, which can directly bind to the promoter region of CCL28 and lead to its higher level. Also, CCL28 secreted by lung cancer cells could induce Tregs infiltration. Conclusion: Our study provides a novel insight focused on the chemokines in lung cancer immunotherapy. Also, CCL28 was identified as an underlying biomarker for lung cancer immunotherapy.

Core-shell SERS nanotags-based western blot.

Western blot (WB) is the most commonly used scheme for protein identification in life science, but it still faces great challenges in the accurate quantitative detection of low-abundance proteins. Here, we proposed a novel surface-enhanced Raman scattering-based Western blot (SERS-WB) to solve this challenge. SERS nanotags were used as quantitative labels of proteins, which were composed of gold-silver core-shell nanoparticles, and Nile blue A (NBA) molecules were anchored on the interface of the core and shell. The results show that the SERS-WB possessed excellent sensitivity with detection limit of glyceraldehyde-3-phosphate dehydrogenase (GAPDH) protein of 0.15 pg, as well as wide linear dynamic range (LDR) of 382 fg to 382 ng. In addition, the target protein on nitrocellulose (NC) membrane could be directly identified by colorimetric signal due to the aggregation effect of nanoparticles, which greatly simplifies the procedure. This as-proposed strategy will bring new thoughts to technological innovation of WB.

Correction: A graphene hybrid supramolecular hydrogel with high stretchability, self-healable and photothermally responsive properties for wound healing.

[This corrects the article DOI: 10.1039/D0RA09106E.].

The cross-talk of cancer-associated fibroblasts assist in prognosis and immunotherapy in patients with breast carcinoma.

The association between cancer-associated fibroblasts (CAFs) and tumor microenvironment (TME) is a key factor in promoting tumor progression. However, the correlation between CAFs and TME in breast carcinoma has not been elucidated. Thus, further study about the cross-effect between CAFs and TME can provide novel strategies for breast carcinoma treatment, particularly targeted immunotherapy. First, we systematically analyzed cell communication in a single-cell dataset and identified the interacted genes between CAFs and TME components. Then, a robust fibroblast-related score (FRS) model was developed using the LASSO algorithm. The FRS can be a reliable adverse prognostic factor in three cohorts with breast carcinoma. Functional enrichment analysis and single-sample Gene Set Enrichment Analysis showed that patients with a high FRS had cold tumors with active proliferation and immunosuppression. Patients with a low FRS presented with hot tumors with active immune and cell-killing functions. Genomic variation analysis revealed that patients with a low FRS had a higher somatic mutation load and copy number variation burden. Finally, patients with a low FRS were more sensitive to chemotherapy and immunotherapy, particularly anti-PD-1 therapy. In conclusion, a reliable FRS model was constructed not only reliable for predicting prognosis but also competent to estimate clinical immunotherapy and chemotherapy response for patients with BRCA, which might provide significant clinical implications for guiding clinical decision-making for patients with BRCA.

Development and validation of a combined ferroptosis- and pyroptosis-related gene signatures for the prediction of clinical outcomes in lung adenocarcinoma.

Lung adenocarcinoma (LUAD) is a very heterogeneous cancer with a bad prognosis. Pyroptosis and ferroptosis are two newly discovered forms of regulated cell death, which can trigger inflammation-related immunosuppression in tumor microenvironments, thereby promoting tumor growth. So far, there has been no thorough systematic investigation of the predictive values of ferroptosis and pyroptosis-related genes in LUAD. Therefore, in this study, we conducted a combined analyses in the gene expression of ferroptosis and pyroptosis and identified four distinct subgroups: immobility, ferroptosis, pyroptosis, and mixed. The gene sets most closely associated to both ferroptosis and pyroptosis were utilized to build a risk prediction model based on their variations in survival and biological activities. More importantly, our conclusions from bioinformatics analyses were validated by external experiments in patients with LUAD. In conclusion, the establishment of LUAD subgroups based on the ferroptosis- and pyroptosis-related gene expression profile provided new insights into understanding the roles of programmed cell death in oncogenesis and might contribute to the development of individualized therapy.

Machine Learning Revealed Ferroptosis Features and a Novel Ferroptosis-Based Classification for Diagnosis in Acute Myocardial Infarction.

Acute myocardial infarction (AMI) is a leading cause of death and disability worldwide. Early diagnosis of AMI and interventional treatment can significantly reduce myocardial damage. However, owing to limitations in sensitivity and specificity, existing myocardial markers are not efficient for early identification of AMI. Transcriptome-wide association studies (TWASs) have shown excellent performance in identifying significant gene-trait associations and several cardiovascular diseases (CVDs). Furthermore, ferroptosis is a major driver of ischaemic injury in the heart. However, its specific regulatory mechanisms remain unclear. In this study, we screened three Gene Expression Omnibus (GEO) datasets of peripheral blood samples to assess the efficiency of ferroptosis-related genes (FRGs) for early diagnosis of AMI. To the best of our knowledge, for the first time, TWAS and mRNA expression data were integrated in this study to identify 11 FRGs specifically expressed in the peripheral blood of patients with AMI. Subsequently, using multiple machine learning algorithms, an optimal prediction model for AMI was constructed, which demonstrated satisfactory diagnostic efficiency in the training cohort (area under the curve (AUC) = 0.794) and two external validation cohorts (AUC = 0.745 and 0.711). Our study suggests that FRGs are involved in the progression of AMI, thus providing a new direction for early diagnosis, and offers potential molecular targets for optimal treatment of AMI.

Highly sensitive detection of free testosterone assisted by magnetic nanobeads and gap-enhanced SERS nanotags.

The quantitative determination of trace free testosterone (FT) is of great significance for the diagnosis of androgen-related endocrine diseases. Herein, a fascinating detection protocol was developed for highly sensitive FT analysis through a competitive immunoassay mechanism, which was composed of magnetic nanobeads (MNBs) and gap-enhanced surface enhanced Raman scattering (SERS) nanotags. With the MNBs as detection carriers, trace FT could be enriched by simple magnetic separation. The SERS nanotag constructed with silver-gold core-shell nanoparticle was acted as quantitative label, and Raman indicators were located at the interface between silver core and gold shell. It is demonstrated that the as-proposed protocol achieves high detection sensitivity for FT of 12.11 fg mL-1, and wider linear dynamic detection range (LDR) in the concentration of 100 fg mL-1 to 100 ng mL-1 with R2 value of 0.979, which is due to the enhanced Raman signal of the gap-enhanced SERS nanotag and the high surface-to-volume ratio of the MNB, respectively. Taking advantages of such sensitivity and accuracy approach, the as-developed powerful strategy presents potential applications for rapid disease diagnosis through analyzing trace levels of FT, and can also provide guidance for the exploitation of analysis project of other analytes.

Harnessing molecular isomerization in polymer gels for sequential logic encryption and anticounterfeiting.

Using smart photochromic and luminescent tissues in camouflage/cloaking of natural creatures has inspired efforts to develop synthetic stimuli-responsive materials for data encryption and anticounterfeiting. Although many optical data-encryption materials have been reported, they generally require only one or a simple combination of few stimuli for decryptions and rarely offer output corruptibility that prevents trial-and-error attacks. Here, we report a series of multiresponsive donor-acceptor Stenhouse adducts (DASAs) with unprecedented switching behavior and controlled reversibility via diamine conformational locking and substrate free-volume engineering and their capability of sequential logic encryption (SLE). Being analogous to the digital circuits, the output of DASA gel-based data-encryption system depends not only on the present input stimulus but also on the sequence of past inputs. Incorrect inputs/sequences generate substantial fake information and lead attackers to the point of no return. This work offers new design concepts for advanced data-encryption materials that operate via SLE, paving the path toward advanced encryptions beyond digital circuit approaches.

Ultrasensitive and facile detection of multiple trace antibiotics with magnetic nanoparticles and core-shell nanostar SERS nanotags.

Ultrasensitive, multiplex, rapid, and accurate quantitative determination of trace antibiotics remains a challenging issue, which is of importance to public health and safety. Herein, we presented a multiplex strategy based on magnetic nanoparticles and surface-enhanced Raman scattering (SERS) nanotags for simultaneous detection of chloramphenicol (CAP) and tetracycline (TTC). In practice, SERS nanotags based on Raman reporter probes (RRPs) encoded gold-silver core-shell nanostars were used as detection labels for identifying different types of antibiotics, and the magnetic nanoparticles could be separated simply by magnetic force, which significantly improves the detection efficiency, reduces the analysis cost, and simplifies the operation. Our results demonstrate that the as-proposed assay possesses the capacities of high sensitivity and multiplexing with the limits of detection (LODs) for CAP and TTC of 159.49 and 294.12 fg mL-1, respectively, as well as good stability and reproducibility, and high selectivity and reliability. We believe that this strategy holds a great promising perspective for the detection of trace amounts of antibiotics in microsystems, which is crucial to our life. Additionally, the assay can also be used to detect other illegal additives by altering the appropriate antibodies or aptamers.

A graphene hybrid supramolecular hydrogel with high stretchability, self-healable and photothermally responsive properties for wound healing.

Wound healing is a ubiquitous healthcare problem in clinical wound management. In this paper, the fabrication of a graphene hybrid supramolecular hydrogel (GS hydrogel) for wound dressing applications is demonstrated. The hydrogel is composed of two components, including N-acryloyl glycinamide (NAGA) as the scaffold and graphene as the photothermally responsive active site for photothermal therapy. Based on the multiple hydrogen bonds between the dual amide motifs in the side chain of N-acryloyl glycinamide, the hydrogel exhibits high tensile strength (≈1.7 MPa), good stretchability (≈400%) and self-recoverability. In addition, the GS hydrogel shows excellent antibacterial activity towards methicillin-resistant Staphylococcus aureus (MRSA), benefiting from the addition of graphene that possesses great photothermal transition activity (≈85%). Significantly, in vivo animal experiments also demonstrated that the GS hydrogel effectively accelerates the wound healing processes by eradicating microbes, promoting collagen deposition and angiogenesis. In summary, this GS hydrogel demonstrates excellent mechanical performance, photothermal antimicrobial activity, and promotes skin tissue regeneration, and so has great application potential as a promising wound dressing material in clinical use.