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Adoptive transfer of T cell receptor-engineered T cells (TCR-T) is a promising strategy for immunotherapy against solid tumors. However, the potential of [CD4.sup.+] T cells in mediating tumor regression has been neglected. Nasopharyngeal cancer is consistently associated with EBV. Here, to evaluate the therapeutic potential of CD4 TCR-T in nasopharyngeal cancer, we screened for CD4 TCRs recognizing EBV nuclear antigen 1 (EBNA1) presented by HLA-DP5. Using mass spectrometry, we identified [EBNA1.sub.567-581], a peptide naturally processed and presented by HLA-DP5. We isolated TCR135, a CD4 TCR with high functional avidity, that can function in both [CD4.sup.+] and [CD8.sup.+] T cells and recognizes HLA-DP5-restricted [EBNA1.sub.567-581]. TCR135-transduced T cells functioned in two ways: directly killing [HLA-DP5.sup.+][EBNA1.sup.+] tumor cells after recognizing EBNA1 presented by tumor cells and indirectly killing HLA-DP5-negative tumor cells after recognizing EBNA1 presented by antigen- presenting cells. TCR135-transduced T cells preferentially infiltrated into the tumor microenvironment and significantly inhibited tumor growth in xenograft nasopharyngeal tumor models. Additionally, we found that 62% of nasopharyngeal cancer patients showed 50%-100% expression of HLA-DP on tumor cells, indicating that nasopharyngeal cancer is well suited for CD4 TCR-T therapy. These findings suggest that TCR135 may provide a new strategy for EBV-related nasopharyngeal cancer immunotherapy in [HLA-DP5.sup.+] patients., Introduction Recent advances in immunotherapy have shown promising results in the treatment of solid tumors. Adoptive transfer of T cell receptor- engineered (TCR-engineered) T cells (TCR-T) is a promising approach [...]

Individuals with spinal cord injury (SCI) suffer from permanent disabilities such as severe motor, sensory and autonomic dysfunction. Neural stem cell transplantation has proven to be a potential strategy to promote regeneration of the spinal cord, since NSCs can produce neurotrophic growth factors and differentiate into mature neurons to reconstruct the injured site. However, it is necessary to optimize the differentiation of NSCs before transplantation to achieve a better regenerative outcome. Inhibition of Notch signaling leads to a transition from NSCs to neurons, while the underlying mechanism remains inadequately understood. Our results demonstrate that overexpression of fucosyltransferase 9 (Fut9), which is upregulated by Wnt4, promotes neuronal differentiation by suppressing the activation of Notch signaling through disruption of furin-like enzyme activity during S1 cleavage. In an in vivo study, Fut9-modified NSCs efficiently differentiates into neurons to promote functional and histological recovery after SCI. Our research provides insight into the mechanisms of Notch signaling and a potential treatment strategy for SCI.

Osteosarcoma (OS) is a prevalent bone solid malignancy that primarily affects adolescents, particularly boys aged 14–19. This aggressive form of cancer often leads to deadly lung cancer due to its high migration ability. Experimental evidence suggests that programmed cell death (PCD) plays a crucial role in the development of osteosarcoma. Various forms of PCD, including apoptosis, ferroptosis, autophagy, necroptosis, and pyroptosis, contribute significantly to the progression of osteosarcoma. Additionally, different signaling pathways such as STAT3/c‐Myc signal pathway, JNK signl pathway, PI3k/AKT/mTOR signal pathway, WNT/β‐catenin signal pathway, and RhoA signal pathway can influence the development of osteosarcoma by regulating PCD in osteosarcoma cell. Therefore, targeting PCD and the associated signaling pathways could offer a promising therapeutic approach for treating osteosarcoma. [ABSTRACT FROM AUTHOR]

Background Method Results Conclusion The potential link between environmental pollutants, including metals, and schizophrenia development remains debated. This study aimed to explore the association between plasma levels of three non‐essential metals—barium (Ba), tungsten (W), and uranium (U)—and schizophrenia risk among Chinese individuals.We recruited a total of 221 patients and 219 healthy controls. Plasma levels of three non‐essential metals were measured using inductively coupled plasma mass spectrometry. We employed unconditional logistic regression and Bayesian kernel machine regression (BKMR) to explore the relationship between exposure to multiple metals and the risk of schizophrenia.Logistic regression analysis revealed that the highest quartile (Q4) of W had an odds ratio (OR) of 1.87 (95% CI: 1.08–3.21) compared to the lowest quartile (Q1), with a significant P‐trend of 0.017. For U, the ORs (95% CI) for Q2, Q3, and Q4 were 2.06 (1.19–3.56), 1.99 (1.15–3.44), and 1.74 (1.00–3.00), respectively. BKMR analyses revealed a progressive increase in the risk of schizophrenia with increasing cumulative levels of the three metals at concentrations below 35%, with U playing a major role in this association. U showed a non‐linear positive correlation with schizophrenia, particularly at the 75th percentile level. Moreover, potential interactions were observed between W and Ba, as well as between W and U.Higher plasma W and U concentrations were positively associated with the risk of schizophrenia, which was potentially related to the severity of symptoms in schizophrenic patients. [ABSTRACT FROM AUTHOR]

Background: Triple‐negative breast cancer (TNBC) is a pathological subtype with a high mortality, and the development of inhibitors in the ubiquitin–proteasome system (UPS) component could be a novel therapeutic tool. Methods: Triple‐negative breast cancer data were obtained from The Cancer Genome Atlas (TCGA), and subtype analysis was performed by consistent clustering analysis to identify molecular subtypes of TNBC according to UPS characteristics. Differential analysis, COX and least absolute shrinkage and selection operator (LASSO) COX regression analyses were performed to select genes associated with overall survival in TNBC. The final prognostic model (UPS score) was determined using the LASSO COX model. The model performance was assessed using receiver operating characteristic (ROC) curves and survival curves. In addition, the results of the UPS score on analyzing the abundance of immune cell infiltration and immunotherapy were explored. Finally, we developed a nomogram for TNBC survival prediction. Results: Two UPS subtypes (UPSMS1 and UPSMS2) showing significant survival differences were classified. COX regression analysis on differentially expressed genes in UPSMS1 and UPSMS2 filtered five genes that affected overall survival. Based on the regression coefficients and expression data of the five genes, we built a prognostic assessment system (UPS score). The UPS score showed consistent prognostic and therapeutic guidance values. Finally, the ROC curve of the nomogram and UPS score showed the highest predictive efficacy compared with traditional clinical prognostic indicators. Conclusion: The UPS score represented a promising prognostic tool to predict overall survival and immune status and guide personalized treatment selection in TNBC patients, and this study may provide a more practical alternative for clinical monitoring and management of TNBC. [ABSTRACT FROM AUTHOR]

Metal oxide-based memristors usually exhibit robust resistive switching characteristics but poor mechanical tolerance, limiting their applications in wearable intelligent electronics. Here, we report a highly flexible and robust hafnium oxide-based memristor by using the ultrathin substrate for wearable in-memory computing. The fabricated memristor can display reliable resistive switching behaviors, including low switching voltage, good endurance, and excellent uniformity, under an extremely bending state with the radius of 0.8 mm. The mechanical behavior of the flexible memristor with varying substrate thickness is systematically analyzed using the finite element method. Moreover, typical synaptic plasticity including long-term potentiation and long-term depression was verified under the extremely bending state. Based on the highly flexible and robust memristor device, a three-layer neural network was constructed using a software simulator, achieving a recognition accuracy of 90.49% for handwritten digit recognition under the bending state. These results demonstrate our robust memristor synapse shows high mechanical flexibility, paving a promising way to realizing wearable in-memory computing. [ABSTRACT FROM AUTHOR]

This study investigates how Chinese female wanghongs on Douyin self-frame their image and identity, and how interactions between wanghongs and their followers co-frame the image of contemporary female Internet celebrities. We discovered that the four dominant self-frames of wanghongs are beauty, talent, personality traits, and gender expression through a qualitative coding analysis of the selected 30 female wanghongs’ posts and media interview narratives, along with viewer comments. Besides, we found that the co-framing of influencers and fans as a collective strategy assists women in breaking the aesthetic framework of traditional patriarchal culture. Furthermore, when conflicts arise between framing actors like wanghongs, fans, media, and political parties, female wanghongs tend to respond with resistance or compromise. We argue that examining the identity framing process of female wanghongs on social media can reflect the dilemma that Chinese feminists face when attempting to highlight women’s accomplishments in multiple roles. [ABSTRACT FROM AUTHOR]

Neural stem cells (NSCs) transplantation has been considered as a potential strategy to reconnect the neural circuit after spinal cord injury (SCI) but the therapeutic effect was still unsatisfied because of the poor inflammatory micro‐environment of SCI. Previous study reported that neuroprotection and inflammatory immunomodulation were considered to be most important mechanism of NSCs transplantation. In addition, Wnt4 has been considered to be neurogenesis and anti‐inflammatory so that it would be an essential assistant agent for NSCs transplantation. Our single cells sequence indicates that macrophages are the most important contributor of inflammatory response after SCI and the interaction between macrophages and astrocytes may be the most crucial to inflammatory microenvironment of SCI. We further report the first piece of evidence to confirm the interaction between Wnt4‐modified NSCs and macrophages using NSCs‐macrophages co‐cultured system. Wnt4‐modified NSCs induce M2 polarization and inhibit M1 polarization of macrophages through suppression of TLR4/NF‐κB signal pathway; furthermore, M2 cells promote neuronal differentiation of NSCs through MAPK/JNK signal pathway. In vivo, transplantation of Wnt4‐modified NSCs improves inflammatory micro‐environment through induce M2 polarization and inhibits M1 polarization of macrophages to promote axonal regeneration and tissue repair. The current study indicated that transplantation of Wnt4‐modified NSCs mediates M2 polarization of macrophages to promote spinal cord injury repair. Our novel findings would provide more insight of SCI and help with identification of novel treatment strategy. [ABSTRACT FROM AUTHOR]

Spinal cord injury (SCI) is a common traumatic disease of the nervous system. The pathophysiological process of SCI includes primary injury and secondary injuries. An excessive inflammatory response leads to secondary tissue damage, which in turn exacerbates cellular and organ dysfunction. Due to the irreversibility of primary injury, current research on SCI mainly focuses on secondary injury, and the inflammatory response is considered the primary target. Thus, modulating the inflammatory response has been suggested as a new strategy for the treatment of SCI. In this study, microglial cell lines, primary microglia, and a rat SCI model were used, and we found that WKYMVm/FPR2 plays an anti-inflammatory role and reduces tissue damage after SCI by suppressing the extracellular signal-regulated kinases 1 and 2 (ERK1/2) and nuclear factor-κB (NF-κB) signaling pathways. FPR2 was activated by WKYMVm, suppressing the secretion of tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6), and interleukin-1β (IL-1β) by inhibiting M1 microglial polarization. Moreover, FPR2 activation by WKYMVm could reduce structural disorders and neuronal loss in SCI rats. Overall, this study illustrated that the activation of FPR2 by WKYMVm repressed M1 microglial polarization by suppressing the ERK1/2 and NF-κB signaling pathways to alleviate tissue damage and locomotor decline after SCI. These findings provide further insight into SCI and help identify novel treatment strategies. [ABSTRACT FROM AUTHOR]

We reported here a cobalt‐catalyzed [5+1] annulation with 1,5‐diarylpenta‐1,4‐dien‐3‐ones and 2‐methylquinolines. 3,4,5‐Triarylcyclohexanones were furnished in moderate to good yields and excellent diastereoselectivity under simple reaction conditions. Moreover, we preliminarily studied anticancer activities of the obtained products in vitro by MTT {3‐(4,5‐dimethylthiazol‐2‐yl)‐2, 5‐diphenyltetrazolium bromide} assay. [ABSTRACT FROM AUTHOR]

We are using Drosophila as a model system for analysis of immunity and tumor formation and have conducted two types of screens using enhancer detector strains to find genes related to these processes: genes expressed in the immune system (type A; hemocytes, lymph glands and fat body) and genes increased in expression by bacterial infection (type B). For type A, tissue-specific reporter gene activity was determined. For type B, a variation of enhancer detection was devised in which [Beta]-galactosidase is assayed spectrophotometrically with and without bacterial infection. Because of immune system involvement in melanotic tumor formation, a third type was hypothesized to be found among types A and B: genes that, when mutated, have a melanotic tumor phenotype. Enhancer detector strains (2800) were screened for type A, 900 for B, and 11 retained for further analysis. Complementation tests, cytological mapping, P-element mobilization, and determination of lethal phase and mutant phenotype have identified six novel genes, Dorothy, wizard, toto, viking, Thor and dappled, and one previously identified gene, Collagen IV. All are associated with reporter gene expression in at least one immune system tissue. Thor has increased expression upon infection. Mutations of wizard and dappled have a melanotic tumor phenotype.

Chimeric antigen receptor (CAR) T cell is a novel approach, which utilizes anti-tumor immunity for cancer treatment. As compared to the traditional cell-mediated immunity, CAR-T possesses the improved specificity of tumor antigens and independent cytotoxicity from major histocompatibility complex molecules through a monoclonal antibody in addition to the T-cell receptor. CAR-T cell has proven its effectiveness, primarily in hematological malignancies, specifically where the CD 19 CAR-T cells were used to treat B-cell acute lymphoblastic leukemia and B-cell lymphomas. Nevertheless, there is little progress in the treatment of solid tumors despite the fact that many CAR agents have been created to target tumor antigens such as CEA, EGFR/EGFRvIII, GD2, HER2, MSLN, MUC1, and other antigens. The main obstruction against the progress of research in solid tumors is the tumor microenvironment, in which several elements, such as poor locating ability, immunosuppressive cells, cytokines, chemokines, immunosuppressive checkpoints, inhibitory metabolic factors, tumor antigen loss, and antigen heterogeneity, could affect the potency of CAR-T cells. To overcome these hurdles, researchers have reconstructed the CAR-T cells in various ways. The purpose of this review is to summarize the current research in this field, analyze the mechanisms of the major barriers mentioned above, outline the main solutions, and discuss the outlook of this novel immunotherapeutic modality. [ABSTRACT FROM AUTHOR]

Colorectal cancer (CRC) is the third most common cancer worldwide and its pathogenesis has been extensively explored over the past decades. Recently, microorganisms in the gastrointestinal tract have emerged as potential etiological agents. In particular, a direct proportional association between Fusobacterium and CRC has been described. Since then, the functional impact of Fusobacterium in CRC development has been studied using various mouse models. Although some epidemiologic studies did not establish an obvious relationship between Fusobacterium and CRC, numerous pathogenic mechanisms leading to the disease have been described. For instance, Fusobacterium can activate the E-cadherin/β-catenin signaling pathway and is associated with particular epigenetic phenotype, such as microsatellite instability (MSI) and hypermethylation, via its strong adhesive and invasive abilities resulting in malignant transformation of epithelial cells. Also, Fusobacterium could alter the tumor microenvironment (TME) significantly by myeloid-derived suppressor cells (MDSCs), tumor associated macrophages (TAMs), and tumor associated neutrophils (TANs) recruitment and local immune suppression. Herein, we provide an in-depth review of the relationship between Fusobacterium and colorectal cancer. In light of the emergence of microbiome-based therapeutics, potential therapies and preventive strategies for colorectal cancer related to Fusobacterium are also discussed. [ABSTRACT FROM AUTHOR]

Low fall efficacy can lead to activity restriction and loss of independence, which may cause severe adverse consequences. The purpose of this study was to explore fall efficacy among elders with knee osteoarthritis and influential factors in three communities in Beijing, China. A correlational descriptive study design was used with a sample of 117 participants from July 2014 to November 2014. Results showed that participants had low fall efficacy and that fall efficacy correlated with age, gender, body mass index, marital status, education, disease duration, frequency of falls, number of co-morbidities, pain, stiffness, physical function, depression, lower-extremity muscle strength and balance ( r = −0.594 to 0.234, P < 0.05 to 0.001). Multiple regression analysis revealed that 52% of variance in fall efficacy was explained by fall frequency, age, body mass index, gender, pain and balance function. Findings suggest that strategies to prevent falls, reduce body weight, improve effective pain management and enhance balance function may improve fall efficacy in this population. [ABSTRACT FROM AUTHOR]

• High salt diet accelerates progression of breast cancer and lung metastasis. • High salt diet increases proportion of Th17 lymphocytes in vivo. • Th17 lymphocytes facilitate progression of breast cancer through IL-17F. • Th17 lymphocytes activate MAPK/ERK signaling pathway through IL-17F. • Application of ERK inhibitor and 1, 25 -vitamin D 3 ameliorates Th17-promoted breast cancer. Dietary patterns are believed to regulate tumor progression by altering the tumor microenvironment. Of note, a high salt diet is a risk factor for various diseases. However, the role of high salt intake in the progression of cancers remains unknown. We constructed an in vivo high salt diet model in MMTV-PyVT mice with spontaneous tumor-forming properties to explore the role of a high salt diet in the progression of breast cancer as well as the modulation of the tumor microenvironment. Also, in vitro experiments were performed to understand the mechanism. High salt diet accelerated the development (P < 0.05) and lung metastasis (P < 0.05) of breast cancer in MMTV-PyVT mice, compared to the normal diet model. Moreover, higher frequency of Th17 cells in circulation, tumor tissue and draining lymph node tissue were observed in the high salt diet model (P < 0.05 for all). In vitro, co-culture with Th17 cells facilitated the proliferation, migration and invasion of MCF-7 human breast cancer cells, while these enhanced aggressive behaviors could be reversed by application of 1,25-vitamin D 3 which could inhibit the differentiation of Th17 cells (P < 0.001 for all). In vitro, co-culture with Th17 cells activated MAPK signaling in MCF-7 cells (P < 0.001 for all). Consistently, activated MAPK/ERK signaling was observed by immunohistochemistry in breast cancer cell nodes in the high salt diet model (P < 0.05 for all). Mechanistically, higher level of IL-17F could be detected in breast tumors and serum from the high salt diet model through qRT-PCR and ELISA (P < 0.05 for all). IL-17F treatment facilitated the proliferation, migration and invasion of MCF-7 human breast cancer cells and activated MAPK/ERK signaling in MCF-7 cells (P < 0.001 for all). Moreover, the tumor-promoting function induced by Th17 cells and IL-17F could be inhibited by the administration of ERK inhibitor (sch772894) (P < 0.001 for all). Lastly, high concentration NaCl-induced Th17 cells promoted the proliferation, migration and invasion of MCF-7 human breast cancer cells and activated MAPK/ERK signaling in MCF-7 cells which could be inhibited by neutralizing anti-IL-17F (P < 0.001 for all). High salt intake accelerates the growth of breast cancer and facilitates lung metastasis, as well as increases the level of Th17 cells. Increased Th17 cells might promote the growth of breast cancer via the secretion of IL-17F to activate the MAPK signaling pathway in breast cancer cells. [ABSTRACT FROM AUTHOR]

SET domain-containing 2 (SETD2), the primary methyltransferase for histone 3 lysine-36 trimethylation (H3K36me3) in mammals, is associated with many hematopoietic diseases when mutated. Previous works have emphasized its role in maintaining adult hematopoietic stem cells or tumorigenesis, however, whether and how SETD2 regulates erythropoiesis during embryonic development is relatively unexplored. In this study, using a conditional SETD2 knockout (KO) mouse model, we reveal that SETD2 plays an essential role in fetal erythropoiesis. Loss of Setd2 in hematopoietic cells ablates H3K36me3, and leads to anemia with a significant decrease in erythroid cells in the peripheral blood at E18.5. This is due to impaired erythroblast differentiation in both spleen and liver. We also find increased proportions of nucleated erythrocytes in the blood of Setd2 KO embryos. Lastly, we ascribe embryonic erythropoiesis-related genes Vegfc , Vegfr3 , and Prox1 , as likely downstream targets of SETD2 regulation. Our study reveals a critical role of SETD2 in fetal erythropoiesis that precedes adult hematopoiesis, and provide unique insights into the defects in erythroid lineages, such as anemia. • Loss of Setd2 leads to anemia and postnatal death in mice. • SETD2 regulates fetal erythropoiesis, particularly in terminal differentiation of erythroblasts. • SETD2 affects the expression of erythropoiesis-related genes Vegfc , Vegfr3 , and Prox1. • Setd2 's impact on fetal erythropoiesis suggests early intervention for Setd2 mutation-associated hematopoietic diseases. [ABSTRACT FROM AUTHOR]

• A novel MET SEMA domain duplication was identified in a non-small cell lung cancer patient. • Off-label use of the kinase inhibitor crizotinib led to a marked response of the patient. • Cellular analyses provide a functional basis for the oncogenic role of the structural MET alteration. • The novel MET mutation may represent actionable targets in lung cancer patients. Aberrant MET activation, which promotes cell proliferation and tumor metastasis, occurs in many types of cancer and results from multiple mechanisms. A novel MET duplication mutation was found in a non-small cell lung cancer (NSCLC) patient. The clinical response to crizotinib was investigated and the functional relevance was characterized in cellular models. Next-generation sequencing (NGS) was performed on the tumor tissue and circulating tumor DNA (ctDNA) of a patient with advanced NSCLC. In vitro studies including western blot, proliferation assays and colony formation assays were used to confirm the clinical observations. The patient was identified to harbor a duplication of the MET SEMA domain. After a month of treatment, the patient showed a marked response to crizotinib, a multikinase inhibitor with potent activity against MET. Functional in vitro studies demonstrated that expression of MET SEMA duplication in NIH-3T3 cells stimulated the activation of MET signaling. Crizotinib treatment obviously repressed cell proliferation, colony formation, and MET signaling pathway. Crizotinib treatment resulted in a clinical response in a patient with MET SEMA duplication. Results of cellular analyses together with the clinical data suggest that this novel alteration may represent an actionable target in NSCLC patients. [ABSTRACT FROM AUTHOR]

Neuropathic pain (NP) is a frequent finding in patients diagnosed with spinal cord injuries (SCIs). To improve our understanding of the maladaptive changes taking place in the lumbar spinal cord that can lead to the development of NP and to find alternative options to treat this condition, we aimed to investigate the effects of voluntary exercise on NP after SCI and to elucidate its potential mechanisms. A rat model of post-SCI NP induced by compression of the posterior or lateral cervical spinal cord was used to evaluate the effects of voluntary exercise by measuring the bilateral withdrawal of the hind paws using the Von Frey filament and Hargreaves tests. The place escape/avoid paradigm was used to evaluate supraspinal pain processing and somatosensory evoked potentials (SEPs) were used to examine disturbances in proprioception. Locomotor function was evaluated using Basso, Beattie, and Bresnahan (BBB) scoring. Pathologic findings in hematoxylin and eosin-stained tissue and magnetic resonance imaging were used to evaluate the morphological changes after SCI. The lesion size within the cervical spinal cord was evaluated by staining with Eriochrome cyanine R. Quantitative polymerase chain reaction and immunohistochemistry were used to assess the expression of calcitonin gene-related peptide (CGRP) and ionized calcium-binding adapter molecule 1 (Iba-1) in the lumbar dorsal horns. All injured rats developed mechanical hypersensitivity, hyposensitivity, and thermal hyperalgesia in the contralateral hind paws at 1 week post-injury. Rats that underwent lateral compression injury developed NP in the ipsilateral hind paws 1 week later than rats with a posterior compression injury. Our findings revealed that voluntary exercise ameliorated mechanical allodynia and thermal hyperalgesia, and significantly improved proprioception as measured by SEP, but had no impact on mechanical hypoalgesia or motor recovery and provided no significant neuroprotection after recovery from an acute SCI. SCI-induced NP was accompanied by increased expression of CGRP and Iba-1 in the lumbar dorsal horn. These responses were reduced in rats that underwent voluntary exercise. Voluntary exercise ameliorates NP that develops in rats after compression injury. Increased expression of CGRP and Iba-1 in the lumbar dorsal horns of rats exhibiting symptoms of NP suggests that microglial activation might play a crucial role in its development. Collectively, voluntary exercise may be a promising therapeutic modality to treat NP that develops clinically in response to SCI. • Voluntary exercise ameliorates NP that develops in rats after compression cervical SCI; • SCI-induced NP was accompanied by increased expression of CGRP and Iba-1 in the lumbar dorsal horn; • Increased expression of CGRP and Iba-1 were reduced in rats that underwent voluntary exercise; • Voluntary exercise may be a promising therapeutic modality to treat NP that develops clinically in response to SCI. [ABSTRACT FROM AUTHOR]

• Various modified CL-20 crystalline composites with graphene/polydopamine as the dopants have been prepared; • These CL-20 based composites have improved thermal stability, and lower mechanical sensitivity; • Some of the abovementioned CL-20 based composites have even higher density with exclusion of polymorphic transition; Hexanitrohexaazaisowurtzitane (CL-20) is a well-known high energy density nitramine, but it is of high sensitivity and has the problem of polymorphic transition. In order to reduce the sensitivity of ε-CL-20 and improve the stability of its crystal structure, the polydopamine (PDA)-coated graphene oxide (GO) was used to dope ε-CL-20 crystals by strategy of in-situ coating followed with a solvent-non-solvent crystallization process. It has been shown that modified CL-20 crystals with the best performances are of polygon shape with a smooth surface and with the average diameter of 16 μm, much smaller than that of raw ε-CL-20 (140 μm). In addition, the doping can either improve the polymorphic transition temperature up to 19.0 °C or exclude such a transition due to formation of completely new crystal phase with better stability, depending on the type and content of the dopants. The density of a certain GO@PDA modified CL-20 is even slightly higher than that of pristine ε-CL-20 due to better assembling of the molecules under the nucleation of the dopants. CL-20/PDAG-2 does not show any polymorphic transition peak. Moreover, the XRD spectrum of CL-20/PDAG-2 also demonstrates that it is a completely new crystal phase better than the other four reported ones in terms of thermal stability. [ABSTRACT FROM AUTHOR]