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The preparation and characterization of carbon nanotubes (CNTs)/epoxy composites are analyzed for microwave absorption, which frequency is from 2 to 6 GHz. Two-layer coating with CNTs/epoxy resin and graphite/epoxy resin composites are examined in order to widen the frequencies range of CNTs microwave sorbent in the low microwave frequency application.

Abstract Background Targeted delivery of chemotherapeutic drugs to tumour cells is a major challenge for cancer chemotherapy. Recent studies show that tumour cell-derived microparticles can be used as vectors to package chemotherapeutic drugs, and selectively deliver drugs to tumour cells. Nevertheless, since the particle size range of microparticles is relatively wide, the sizes may exhibit different pharmacokinetic characteristics in the body, which will have a great impact on the application of drug-loaded microparticles. Here in this report, we compare the characteristics, distribution in vivo and antitumour efficacy of small microparticles (SMPs, ≤ 200 nm) and large microparticles (LMPs, > 200 nm) which loaded with methotrexate, in order to screen out more suitable carrier sizes. Results In vivo and in vitro studies have proved that the drug-loaded vesicles of SMPs (mainly 100–200 nm) are more reasonable, and the drug content and maintenance in tumour tissues. The time is significantly higher than that of LMPs (mainly 400–500 nm). At the same time, we found that SMPs can be better taken up and processed by DC cells to promote the proliferation of specific T cells. SMPs show obvious advantages in both drug delivery and immune activation, which is verified by the comparison of the efficacy of SMPs and LMPs in the treatment of solid tumours in mice. Conclusions The present data demonstrate that the SMPs had a higher cumulative concentration in tumour tissue, and the tumour suppressive effect was also significantly better than that of LMPs. It provides important process parameters for the drug-loaded vesicle delivery system. Future works will aim to expand production scale and improve the separation and purification process of the microparticles. Although the research and application of drug-loaded vesicles derived from tumour cells is still in its infancy, it has broad prospects for tumour therapy.

Abstract Patient‐derived cancer cells (PDCs) and patient‐derived xenografts (PDXs) are often used as tumor models, but have many shortcomings. PDCs not only lack diversity in terms of cell type, spatial organization, and microenvironment but also have adverse effects in stem cell cultures, whereas PDX are expensive with a low transplantation success rate and require a long culture time. In recent years, advances in three‐dimensional (3D) organoid culture technology have led to the development of novel physiological systems that model the tissues of origin more precisely than traditional culture methods. Patient‐derived cancer organoids bridge the conventional gaps in PDC and PDX models and closely reflect the pathophysiological features of natural tumorigenesis and metastasis, and have led to new patient‐specific drug screening techniques, development of individualized treatment regimens, and discovery of prognostic biomarkers and mechanisms of resistance. Synergistic combinations of cancer organoids with other technologies, for example, organ‐on‐a‐chip, 3D bio‐printing, and CRISPR‐Cas9‐mediated homology‐independent organoid transgenesis, and with treatments, such as immunotherapy, have been useful in overcoming their limitations and led to the development of more suitable model systems that recapitulate the complex stroma of cancer, inter‐organ and intra‐organ communications, and potentially multiorgan metastasis. In this review, we discuss various methods for the creation of organ‐specific cancer organoids and summarize organ‐specific advances and applications, synergistic technologies, and treatments as well as current limitations and future prospects for cancer organoids. Further advances will bring this novel 3D organoid culture technique closer to clinical practice in the future.

Abstract Background Lung cancer is one of the most common malignant tumors threatening human health. The aim of this study was to investigate the function of miR‐21‐5p in lung cancer progression. Methods We analyzed the expression levels of miR‐21‐5p in lung cancer tissues and cell lines. The qRT‐PCR and MTT assays were performed after transfection with miR‐21‐5p mimic, inhibitor and negative control into lung cancer cells. Results Luciferase reporter assays showed miR‐21‐5p directly target SMAD7. The miR‐21‐5p inhibitor significantly suppressed lung cancer cell proliferation, invasion and migration. We found that SMAD7 was upregulated in lung cancer tissue. In addition, we found that SMAD7 inhibited lung cancer cell proliferation and miR‐21‐5p mimic damaged the inhibitory effect of SMAD7. Conclusions miRNA‐21‐5p may promote cell proliferation, migration and invasion by spoiling SMAD7 expression in lung cancer cells.

Purpose: The aim of the study was to investigate the functional role of L1.2, the zebrafish paralog of L1.1 and ortholog of mammalian L1CAM in adult zebrafish spinal cord regeneration after injury. L1CAM and L1.1 have shown beneficial features in ameliorating nervous system dysfunctions in different experimental paradigms. It thus deemed important to characterize the L1.2 member of the L1CAM family, the functions of which are unknown. Methods: Spinal cord transection of adult zebrafish, application of anti-sense morpholino to reduce L1.2 expression, qPCR, immunohistology, immunoblotting, in situ hybridization, retrograde tracing, anterograde tracing. Results: Similar to L1.1, L1.2 expression in adult zebrafish is upregulated after spinal cord transection. By co-localization of in situ hybridization and immunohistology, L1.2 is expressed in neurons and, in contrast to L1.1, it is also expressed in GFAP-immunoreactive glia. Reducing L1.2 protein levels leads to impaired locomotor recovery and reduction of regrowth of severed descending axons from a brain stem nucleus which is composed of neurons innately capable of axonal regrowth. Conclusions: Our findings support the speculation that paralogs of duplicated genes can exert similar functions and may thus represent an advantage over other species that do not carry duplicated genes. [ABSTRACT FROM AUTHOR]

Immune checkpoint inhibitors (ICIs) significantly improve the survival of patients with non-small-cell lung cancer (NSCLC), but only some patients obtain clinical benefits. Predictive biomarkers for ICIs can accurately identify people who will benefit from immunotherapy. Lipid metabolism signaling plays a key role in the tumor microenvironment (TME) and immunotherapy. Hence, we aimed to explore the association between the mutation status of the lipid metabolism pathway and the prognosis of patients with NSCLC treated with ICIs. We downloaded the mutation data and clinical data of a cohort of patients with NSCLC who received ICIs. Univariate and multivariate Cox regression models were used to analyze the association between the mutation status of the lipid metabolism signaling and the prognosis of NSCLC receiving ICIs. Additionally, The Cancer Genome Atlas (TCGA)–NSCLC cohort was used to explore the relationships between the different mutation statuses of lipid metabolism pathways and the TME. Additionally, we found that patients with high numbers of mutations in the lipid metabolism pathway had significantly enriched macrophages (M0- and M1-type), CD4 + T cells (activated memory), CD8 + T cells, Tfh cells and gamma delta T cells, significantly increased expression of inflammatory genes [interferon-γ (IFNG), CD8A, GZMA, GZMB, CXCL9, and CXCL10] and enhanced immunogenic factors [neoantigen loads (NALs), tumor mutation burden (TMB), and DNA damage repair pathways]. In the local-NSCLC cohort, we found that the group with a high number of mutations had a significantly higher tumor mutation burden (TMB) and PD-L1 expression. High mutation status in the lipid metabolism pathway is associated with significantly prolonged progression-free survival (PFS) in NSCLC, indicating that this marker can be used as a predictive indicator for patients with NSCLC receiving ICIs.

Abstract Menstrual blood-derived stem cells (MenSCs) have great potential in the treatment of various diseases. As a novel type of mesenchymal stem cells (MSCs), MenSCs have attracted more interest due to their therapeutic effects in both animal models and clinical trials. Here, we described the differentiation, immunomodulation, paracrine, homing, and engraftment mechanisms of MenSCs. These include differentiation into targeting cells, immunomodulation with various immune cells, the paracrine effect on secreting cytokines, and homing and engraftment into injured sites. To better conduct MenSC-based therapy, some novel hotspots were proposed such as CRISPR (clustered regularly interspaced short palindromic repeats)/cas9-mediated gene modification, exosomes for cell-free therapy, single-cell RNA sequence for precision medicine, engineered MenSC-based therapy for the delivery platform, and stem cell niches for improving microenvironment. Subsequently, current challenges were elaborated on, with regard to age of donor, dose of MenSCs, transplantation route, and monitoring time. The management of clinical research with respect to MenSC-based therapy in diseases will become more normative and strict. Thus, a more comprehensive horizon should be considered that includes a combination of traditional solutions and novel strategies. In summary, MenSC-based treatment has a great potential in treating diseases through diverse strategies, and more therapeutic mechanisms and novel strategies need to be elucidated for future regenerative medicine and clinical applications.

The use of programmed cell-death protein 1 (PD-1)/programmed cell-death ligand 1 (PD-L1) inhibitors is the standard therapy for the first-line or second-line treatment of patients with non-small-cell lung cancer (NSCLC). In contrast to current traditional treatments such as chemotherapy or radiotherapy, anti-PD-1 and anti-PD-L1 treatments can directly attenuate tumour-mediated exhaustion and effectively modulate the host anti-tumour immune response in vivo . In addition, compared with traditional therapy, PD-1/PD-L1 inhibitor monotherapy can significantly prolong survival without obvious side effects in the treatment of advanced NSCLC. Ideally, several biomarkers could be used to monitor the safety and effectiveness of anti-PD-1 and anti-PD-L1 treatments; however, the current lack of optimal prognostic markers remains a widespread limitation and challenge for further clinical applications, as does the possibility of immune-related adverse events and drug resistance. In this review, we aimed to summarise the latest progress in anti-PD-1/anti-PD-L1 treatment of advanced NSCLC, worldwide, including in China. An exploration of underlying biomarker identification and future challenges will be discussed in this article to facilitate translational studies in cancer immunotherapy.