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"Huang, Zhao"
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Fabrication of triboelectric polymer films via repeated rheological forging for ultrahigh surface charge density
Triboelectric polymer with high charge density is the foundation to promote the wide range of applications of triboelectric nanogenerators. This work develops a method to produce triboelectric polymer based on repeated rheological forging. The fluorinated ethylene propylene film fabricated by repeated forging method not only has excellent mechanical properties and good transmittance, but also can maintain an ultrahigh tribo-charge density. Based on the film with a thickness of 30 μm, the output charge density from contact-separation nanogenerator reaches 352 μC·m
−2
. Then, the same film is applied for the nanogenerator with air-breakdown mode and a charge density of 510 μC·m
−2
is further achieved. The repeated forging method can effectively regulate the composition of surface functional groups, the crystallinity, and the dielectric constants of the fluorinated ethylene propylene, leading to the superior capability of triboelectrification. Finally, we summarize the key parameters for elevating the electrification performance on the basis of molecular structure and related fabrication crafts, which can guide the further development of triboelectric polymers.
High charge density is the foundation to promote a wide range of applications of triboelectric nanogenerators. Here, authors propose a processing method based on the repeated rheological forging of triboelectric polymers achieving an enhanced triboelectricity and further study its mechanism.
Journal Article
The role of long noncoding RNAs in hepatocellular carcinoma
Hepatocellular carcinoma (HCC) is the most frequent subtype of primary liver cancer and one of the leading causes of cancer-related death worldwide. However, the molecular mechanisms underlying HCC pathogenesis have not been fully understood. Emerging evidences have recently suggested the crucial role of long noncoding RNAs (lncRNAs) in the tumorigenesis and progression of HCC. Various HCC-related lncRNAs have been shown to possess aberrant expression and participate in cancerous phenotypes (e.g. persistent proliferation, evading apoptosis, accelerated vessel formation and gain of invasive capability) through their binding with DNA, RNA or proteins, or encoding small peptides. Thus, a deeper understanding of lncRNA dysregulation would provide new insights into HCC pathogenesis and novel tools for the early diagnosis and treatment of HCC. In this review, we summarize the dysregulation of lncRNAs expression in HCC and their tumor suppressive or oncogenic roles during HCC tumorigenesis. Moreover, we discuss the diagnostic and therapeutic potentials of lncRNAs in HCC.
Journal Article
Neoantigens: promising targets for cancer therapy
Recent advances in neoantigen research have accelerated the development and regulatory approval of tumor immunotherapies, including cancer vaccines, adoptive cell therapy and antibody-based therapies, especially for solid tumors. Neoantigens are newly formed antigens generated by tumor cells as a result of various tumor-specific alterations, such as genomic mutation, dysregulated RNA splicing, disordered post-translational modification, and integrated viral open reading frames. Neoantigens are recognized as non-self and trigger an immune response that is not subject to central and peripheral tolerance. The quick identification and prediction of tumor-specific neoantigens have been made possible by the advanced development of next-generation sequencing and bioinformatic technologies. Compared to tumor-associated antigens, the highly immunogenic and tumor-specific neoantigens provide emerging targets for personalized cancer immunotherapies, and serve as prospective predictors for tumor survival prognosis and immune checkpoint blockade responses. The development of cancer therapies will be aided by understanding the mechanism underlying neoantigen-induced anti-tumor immune response and by streamlining the process of neoantigen-based immunotherapies. This review provides an overview on the identification and characterization of neoantigens and outlines the clinical applications of prospective immunotherapeutic strategies based on neoantigens. We also explore their current status, inherent challenges, and clinical translation potential.
Journal Article
Self-poled piezoelectric polymer composites via melt-state energy implantation
Lightweight flexible piezoelectric polymers are demanded for various applications. However, the low instinctively piezoelectric coefficient (
i.e
. d33) and complex poling process greatly resist their applications. Herein, we show that introducing dynamic pressure during fabrication is capable for poling polyvinylidene difluoride/barium titanate (PVDF/BTO) composites with d33 of ~51.20 pC/N at low density of ~0.64 g/cm
3
. The melt-state dynamic pressure driven energy implantation induces structure evolutions of both PVDF and BTO are demonstrated as reasons for self-poling. Then, the porous material is employed as pressure sensor with a high output of ~20.0 V and sensitivity of ~132.87 mV/kPa. Besides, the energy harvesting experiment suggests power density of ~58.7 mW/m
2
can be achieved for 10 N pressure with a long-term durability. In summary, we not only provide a high performance lightweight, flexible piezoelectric polymer composite towards sustainable self-powered sensing and energy harvesting, but also pave an avenue for electrical-free fabrication of piezoelectric polymers.
Lightweight flexible piezoelectric polymers are demanded for various applications, but restricted by the low instinctively piezoelectric coefficient and complex poling process. Here, the authors develop a high performance lightweight, flexible self-poled piezoelectric polymer composite towards sustainable self-powered sensing and energy harvesting.
Journal Article
Correlation analysis between disease severity and inflammation-related parameters in patients with COVID-19: a retrospective study
Background
COVID-19 is highly contagious, and the crude mortality rate could reach 49% in critical patients. Inflammation concerns on disease progression. This study analyzed blood inflammation indicators among mild, severe and critical patients, helping to identify severe or critical patients early.
Methods
In this cross-sectional study, 100 patients were included and divided into mild, severe or critical groups according to disease condition. Correlation of peripheral blood inflammation-related indicators with disease criticality was analyzed. Cut-off values for critically ill patients were speculated through the ROC curve.
Results
Significantly, disease severity was associated with age (
R
= -0.564,
P
< 0.001), interleukin-2 receptor (IL2R) (
R
= -0.534,
P
< 0.001), interleukin-6 (IL-6) (
R
= -0.535,
P
< 0.001), interleukin-8 (IL-8) (
R
= -0.308,
P
< 0.001), interleukin-10 (IL-10) (
R
= -0.422,
P
< 0.001), tumor necrosis factor α (TNFα) (
R
= -0.322,
P
< 0.001), C-reactive protein (CRP) (
R
= -0.604,
P
< 0.001), ferroprotein (
R
= -0.508,
P
< 0.001), procalcitonin (
R
= -0.650,
P
< 0.001), white cell counts (WBC) (
R
= -0.54,
P
< 0.001), lymphocyte counts (LC) (
R
= 0.56,
P
< 0.001), neutrophil count (NC) (
R
= -0.585,
P
< 0.001) and eosinophil counts (EC) (
R
= 0.299,
P
< 0.001). With IL2R > 793.5 U/mL or CRP > 30.7 ng/mL, the progress of COVID-19 to critical stage should be closely observed and possibly prevented.
Conclusions
Inflammation is closely related to severity of COVID-19, and IL-6 and TNFα might be promising therapeutic targets.
Journal Article
Elesclomol induces copper‐dependent ferroptosis in colorectal cancer cells via degradation of ATP7A
Cancer cells reprogram their copper metabolism to adapt to adverse microenvironments, such as oxidative stress. The copper chelator elesclomol has been reported to have considerable anticancer efficacy, but the underlying mechanisms remain largely unknown. In this study, we found that elesclomol‐mediated copper overload inhibits colorectal cancer (CRC) both in vitro and in vivo. Elesclomol alone promotes the degradation of the copper transporter copper‐transporting ATPase 1 (ATP7A), which retards the proliferation of CRC cells. This property distinguishes it from several other copper chelators. Combinational treatment of elesclomol and copper leads to copper retention within mitochondria due to ATP7A loss, leading to reactive oxygen species accumulation, which in turn promotes the degradation of SLC7A11, thus further enhancing oxidative stress and consequent ferroptosis in CRC cells. This effect accounts for the robust antitumour activity of elesclomol against CRC, which can be reversed by the administration of antioxidants and ferroptosis inhibitors, as well as the overexpression of ATP7A. In summary, our findings indicate that elesclomol‐induced copper chelation inhibits CRC by targeting ATP7A and regulating ferroptosis. In this study, we describe the molecular mechanisms by which elesclomol‐mediated copper (Cu2+) overload inhibits colorectal cancer (CRC) both in vitro and in vivo. Elesclomol elevated Cu2+ levels in mitochondria and decreased the expression of the Cu2+ transporter ATP7A, leading to Cu2+ retention and the subsequent accumulation of reactive oxygen species. The process promoted the degradation of SLC7A11, which further enhanced oxidative stress and induced ferroptosis in CRC cells.
Journal Article
Oral squamous cell carcinomas: state of the field and emerging directions
Oral squamous cell carcinoma (OSCC) develops on the mucosal epithelium of the oral cavity. It accounts for approximately 90% of oral malignancies and impairs appearance, pronunciation, swallowing, and flavor perception. In 2020, 377,713 OSCC cases were reported globally. According to the Global Cancer Observatory (GCO), the incidence of OSCC will rise by approximately 40% by 2040, accompanied by a growth in mortality. Persistent exposure to various risk factors, including tobacco, alcohol, betel quid (BQ), and human papillomavirus (HPV), will lead to the development of oral potentially malignant disorders (OPMDs), which are oral mucosal lesions with an increased risk of developing into OSCC. Complex and multifactorial, the oncogenesis process involves genetic alteration, epigenetic modification, and a dysregulated tumor microenvironment. Although various therapeutic interventions, such as chemotherapy, radiation, immunotherapy, and nanomedicine, have been proposed to prevent or treat OSCC and OPMDs, understanding the mechanism of malignancies will facilitate the identification of therapeutic and prognostic factors, thereby improving the efficacy of treatment for OSCC patients. This review summarizes the mechanisms involved in OSCC. Moreover, the current therapeutic interventions and prognostic methods for OSCC and OPMDs are discussed to facilitate comprehension and provide several prospective outlooks for the fields.
Journal Article
Mitochondrial adaptation in cancer drug resistance: prevalence, mechanisms, and management
Drug resistance represents a major obstacle in cancer management, and the mechanisms underlying stress adaptation of cancer cells in response to therapy-induced hostile environment are largely unknown. As the central organelle for cellular energy supply, mitochondria can rapidly undergo dynamic changes and integrate cellular signaling pathways to provide bioenergetic and biosynthetic flexibility for cancer cells, which contributes to multiple aspects of tumor characteristics, including drug resistance. Therefore, targeting mitochondria for cancer therapy and overcoming drug resistance has attracted increasing attention for various types of cancer. Multiple mitochondrial adaptation processes, including mitochondrial dynamics, mitochondrial metabolism, and mitochondrial apoptotic regulatory machinery, have been demonstrated to be potential targets. However, recent increasing insights into mitochondria have revealed the complexity of mitochondrial structure and functions, the elusive functions of mitochondria in tumor biology, and the targeting inaccessibility of mitochondria, which have posed challenges for the clinical application of mitochondrial-based cancer therapeutic strategies. Therefore, discovery of both novel mitochondria-targeting agents and innovative mitochondria-targeting approaches is urgently required. Here, we review the most recent literature to summarize the molecular mechanisms underlying mitochondrial stress adaptation and their intricate connection with cancer drug resistance. In addition, an overview of the emerging strategies to target mitochondria for effectively overcoming chemoresistance is highlighted, with an emphasis on drug repositioning and mitochondrial drug delivery approaches, which may accelerate the application of mitochondria-targeting compounds for cancer therapy.
Journal Article
Epithelial–mesenchymal transition: The history, regulatory mechanism, and cancer therapeutic opportunities
Epithelial–mesenchymal transition (EMT) is a program wherein epithelial cells lose their junctions and polarity while acquiring mesenchymal properties and invasive ability. Originally defined as an embryogenesis event, EMT has been recognized as a crucial process in tumor progression. During EMT, cell–cell junctions and cell–matrix attachments are disrupted, and the cytoskeleton is remodeled to enhance mobility of cells. This transition of phenotype is largely driven by a group of key transcription factors, typically Snail, Twist, and ZEB, through epigenetic repression of epithelial markers, transcriptional activation of matrix metalloproteinases, and reorganization of cytoskeleton. Mechanistically, EMT is orchestrated by multiple pathways, especially those involved in embryogenesis such as TGFβ, Wnt, Hedgehog, and Hippo, suggesting EMT as an intrinsic link between embryonic development and cancer progression. In addition, redox signaling has also emerged as critical EMT modulator. EMT confers cancer cells with increased metastatic potential and drug resistant capacity, which accounts for tumor recurrence in most clinic cases. Thus, targeting EMT can be a therapeutic option providing a chance of cure for cancer patients. Here, we introduce a brief history of EMT and summarize recent advances in understanding EMT mechanisms, as well as highlighting the therapeutic opportunities by targeting EMT in cancer treatment. Epithelial–mesenchymal transition contributes to multiple hallmarks of cancer, including metastasis activation, metabolic reprogramming, stemness acquisition, and chronic inflammation, which is regulated by complex signaling network and is highly context dependent. It provides both difficulties and opportunities for cancer treatment via targeting EMT.
Journal Article