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Recently, magnetoelectric (ME) antennas have become a hot topic in the field of antenna miniaturization in the very-low-frequency (VLF) band because their size can be reduced to one-ten-thousandth of the size of conventional electric antennas. However, they still suffer from narrow transmission/reception bandwidth and weak radiation intensity. To address these issues, VLF thin-film ME antennas with a microbridge structure are designed, and the method of array connection is used. Test results show that the detection limit of the ME antenna unit is 636 pT/√Hz at 23 kHz and the radiant magnetic field intensity at 0.12 m is 0.87 nT (input power of 10 mW). By series-connecting three ME antenna units with the same resonance frequency, the output response has been increased to 1.72 times and the EM wave radiation intensity is increased to 1.9 times compared to a single unit. By parallel-connecting two ME antenna units with different resonance frequencies, the output response bandwidth has been expanded to 1.56 times compared to a single unit, and the signal radiation bandwidth has been expanded to 1.47 times. This work provides a valuable reference for the future larger-scale arraying of ME antennas. [ABSTRACT FROM AUTHOR]

Immune cells can protect against tumor progression by killing cancer cells, while aberrant expression of the immune checkpoint protein PD‐L1 (programmed death ligand 1) in cancer cells facilitates tumor immune escape and inhibits anti‐tumor immunotherapy. As a serine/threonine kinase, CK2 (casein kinase 2) regulates tumor progression by multiple pathways, while it is still unclear the effect of CK2 on tumor immune escape. Here it is found that ING4 induced PD‐L1 autophagic degradation and inhibites non‐small cell lung cancer (NSCLC) immune escape by increasing T cell activity. However, clinical analysis suggests that high expression of CK2 correlates with low ING4 protein level in NSCLC. Further analysis shows that CK2 induce ING4‐S150 phosphorylation leading to ING4 ubiquitination and degradation by JFK ubiquitin ligase. In contrast, CK2 gene knockout increases ING4 protein stability and T cell activity, subsequently, inhibites NSCLC immune escape. Furthermore, the combined CK2 inhibitor with PD‐1 antibody effectively enhances antitumor immunotherapy. These findings provide a novel strategy for cancer immunotherapy. [ABSTRACT FROM AUTHOR]

Esophageal carcinoma is one of the important lethal tumors in the world, but the mechanism of esophageal cancer progression is still unclear. The long non-coding RNAs are known to regulate tumor progression. Here we report that BRAF-activated nonprotein coding RNA (BANCR) is associated with the development of esophageal squamous cell carcinoma (ESCC). The expression levels of BANCR in 132 ESCC tumor tissues detected by quantitative real-time PCR were significantly higher than that in the adjacent normal tissues. The expression level of BANCR was down-regulated by transfecting small interrupting RNA against BANCR (BANCR siRNA) in Eca109 cells. Eca109 and TE-1 cells transfected with BANCR siRNA led to the delayed cell cycles compared to the cells transfected with negative control siRNA. Moreover, MTT assays demonstrated that Eca109 cells transfected with BANCR siRNA resulted in the inhibition of cell proliferation. These results suggested that BANCR advances the development and progression of ESCC cells through regulating their cell cycles.

Simple Summary: Exosomes are nanosized vesicles secreted by living cells and exist in biological fluids. Exosomes contain various bioactive molecules, including proteins, nucleic acids, and lipids, which can reflect the pathophysiological state of donor cells. In recent years, long non-coding RNAs (lncRNAs) in exosomes have attracted wide attention in cancer research. Exosomal lncRNAs play important roles in gastrointestinal cancer progression. Blood samples-derived exosomal lncRNAs also exhibit great potential to serve as important indicators of liquid biopsy, thus providing a novel diagnosis strategy for gastrointestinal cancer. In addition, exosomes-mediated several lncRNAs delivery can exert anti-tumor effects. The aim of this review article is to summarize the recent work conducted in this field and evaluate the opportunities and challenges in utilizing exosomal lncRNAs for the diagnostic and therapeutic purposes of gastrointestinal cancer in the clinical setting. Due to the lack of specific and effective biomarkers and therapeutic targets, the early diagnosis and treatment of gastrointestinal cancer remain unsatisfactory. As a type of nanosized vesicles derived from living cells, exosomes mediate cell-to-cell communication by transporting bioactive molecules, thus participating in the regulation of many pathophysiological processes. Recent evidence has revealed that several long non-coding RNAs (lncRNAs) are enriched in exosomes. Exosomes-mediated lncRNAs delivery is critically involved in various aspects of gastrointestinal cancer progression, such as tumor proliferation, metastasis, angiogenesis, stemness, immune microenvironment, and drug resistance. Exosomal lncRNAs represent promising candidates to act as the diagnosis biomarkers and anti-tumor targets. This review introduces the major characteristics of exosomes and lncRNAs and describes the biological functions of exosomal lncRNAs in gastrointestinal cancer development. The preclinical studies on using exosomal lncRNAs to monitor and treat gastrointestinal cancer are also discussed, and the opportunities and challenges for translating them into clinical practice are evaluated. [ABSTRACT FROM AUTHOR]

Background: Drug resistance is an important factor affecting the efficacy of chemotherapy in patients with colon cancer. However, clinical markers for diagnosing drug resistance of tumor cells are not only a few in number, but also low in specificity, and the mechanism of action of tumor cell drug resistance remains unclear. Methods: Dipeptidase 1 (DPEP1) expression was analyzed using the cancer genome atlas (TCGA) and genotype‐Tissue Expression pan‐cancer data. Survival analysis was performed using the survival package in R software to assess the prognostic value of DPEP1 expression in colon cancer. Correlation and Venn analyses were adopted to identify key genes. Immunohistochemistry, western blot, qRT–PCR, Co‐immunoprecipitation, and dual‐luciferase reporter experiments were carried out to explore the underlying associations between DPEP1 and Achaete scute‐like 2 (ASCL2). MTT assays were used to evaluate the role of DPEP1 and ASCL2 in colon cancer drug resistance. Results: DPEP1 was highly expressed in colon cancer tissues. DPEP1 expression correlated negatively with disease‐specific survival but not with overall survival. Bioinformatics analysis and experiments showed that the expressions of DPEP1 and ASCL2 in colon cancer tissues were markedly positively correlated. Mechanistic research indicated that DPEP1 enhanced the stability of protein ASCL2 by inhibiting its ubiquitination‐mediated degradation. In turn, ASCL2 functioned as a transcription factor to activate the transcriptional activity of the DPEP1 gene and boost its expression. Furthermore, DPEP1 also could enhance the expression of colon cancer stem cell markers (LGR5, CD133, and CD44), which strengthened the tolerance of colon cancer cells to chemotherapy drugs. Conclusions: Our findings reveal that the DPEP1 enhances the stemness of tumor cells by forming a positive feedback loop with ASCL2 to improve resistance to chemotherapy drugs. [ABSTRACT FROM AUTHOR]

Simple Summary: Two fruit fossil species of Ceratophyllum L. are discovered from South China, namely C. cf. muricatum Chamisso from the upper Eocene of the Maoming Basin, Guangdong, and C. demersum L. from the Miocene of the Guiping Basin, Guangxi. Our findings provide evidence for the distribution of Ceratophyllum in South China in the late Eocene, and its wide expansion in subtropical China during the Miocene. Ceratophyllum L. is a cosmopolitan genus of perennial aquatic herbs that occur in quiet freshwaters. Fossils of this genus have been widely reported from the Northern Hemisphere, most of them occurring in the temperate zone. Here, we describe two species of fossil fruits discovered from subtropical areas of China. The fossil fruit discovered from the upper Eocene Huangniuling Formation of the Maoming Basin is designated as C. cf. muricatum Chamisso, and fruits discovered from the Miocene Erzitang Formation of the Guiping Basin are assigned to the extant species C. demersum L. The discovery of these two fossil species indicates that Ceratophyllum had spread to South China by the late Eocene and their distribution expanded in subtropical China during the Miocene. [ABSTRACT FROM AUTHOR]

Background. Several cancers, including lung adenocarcinoma (LUAD), are caused by genes related to necroptosis. However, it is still unknown how necroptosis-related long noncoding RNAs (lncRNAs) may be involved in LUAD. In order to predict the prognosis of LUAD patients and personalize immunotherapy, this study set out to construct a necroptosis-related lncRNA prognostic signature (NLPS). Methods. The Cancer Genome Atlas (TCGA) database was used to download the LUAD transcriptome data and the associated clinical data. lncRNAs associated with necroptosis were screened using coexpression analysis. An NLPS was built using univariate and least absolute shrinkage and selection operator (LASSO) Cox regression analyses. The Gene Expression Omnibus (GEO) database's GSE30219 was used to validate the NLPS. The prognostic value of the risk score was assessed using Kaplan-Meier survival, receiver operating characteristic (ROC) Cox regression, multivariate Cox regression, and nomogram analyses. Then, we looked into the differences between the low- and high-risk groups in the tumor immune microenvironment, immunotherapy response, and half-maximal inhibitory concentration (IC50). Results. The 14 lncRNAs in a novel NLPS were created. With further validation in the GSE30219 dataset, the risk score according to the NLPS was an independent prognostic indicator for LUAD patients. Patients with better overall survival (OS) in the low-risk group, who were characterized by increased immune cell infiltration, tumor mutational burden (TMB), and immunophenoscore (IPS), may have hot tumors and higher immunotherapy response rates. In addition, the risk score was also closely linked to sensitivity to various anticancer medications. Conclusions. We constructed a novel NLPS that could predict OS and sensitivity to immunotherapy in LUAD patients. [ABSTRACT FROM AUTHOR]

The ability of extracellular vesicles (EVs) to regulate a broad range of cellular processes has recently been used to treat diseases. Growing evidence indicates that EVs play a cardioprotective role in heart disease by activating beneficial signaling pathways. Multiple functional components of EVs and intracellular molecular mechanisms are involved in the process. To overcome the shortcomings of native EVs such as their heterogeneity and limited tropism, a series of engineering approaches has been developed to improve the therapeutic efficiency of EVs. In this review, we present an overview of the research and future directions for EVs-based cardiac therapies with an emphasis on EVs-mediated delivery of therapeutic agents. The advantages and limitations of various modification strategies are discussed, and possible opportunities for improvement are proposed. An in-depth understanding of the endogenous properties of EVs and EVs engineering strategies could lead to a promising cell-free therapy for cardiac repair. [ABSTRACT FROM AUTHOR]

Fossil wood of Chinese white pine (Pinus armandii Franch.) from the Late Pleistocene deposits of Maoming Basin of South China provides the first megafossil evidence for glacial expansion of the range of a cold-tolerant species in low latitudes. [ABSTRACT FROM AUTHOR]

Background: Colorectal cancer is an important death‐related disease in the worldwide. However, specific colon cancer tumor markers currently used for diagnosis and treatment are few. The purpose of this study is to screen the potential colon cancer markers by bioinformatics and verify the results with experiments. Methods: Gene expression data were downloaded from two different databases: TCGA database and GEO datasets, which were then analyzed by two different methods (difference analysis and WGCNA method). Venn and PPI analysis obtained the potential core genes, which were then performed the GO enrichment and KEGG pathway analysis. Expressions levels of NKD1 in colon carcinoma tissues were further confirmed by immunohistochemical staining and western blot assays. Moreover, the function was measured by MTT, clone formation, and tumor transplantation experiments. Importantly, co‐immunoprecipitation, immunofluorescence, and protein stability assays were further performed to explore the underlying mechanism of NKD1 promoting cell proliferation. Results: Nine potential core genes highly expressed in colon cancer samples were screened out by bioinformatics analysis. NKD1, one of the hub genes, highly expressed in the colon carcinoma tissues could enhance the proliferation of colon cancer cells. Mechanism research demonstrated that NKD1 was essential for the combination between Wnt signalosome (DVL) and β‐catenin, and that NKD1 knockout remarkably decreased the β‐catenin expression. Immunofluorescence assays further implied that NKD1 knockout significantly inhibited β‐catenin nuclear accumulation. Importantly, the stability of β‐catenin proteins was maintained by NKD1 in the colon cancer cells. Conclusion: We believe that NKD1 well expressed in the colorectal carcinoma tissues can enhance the proliferation of colon cancer cells. Furthermore, the functions that NKD1 may have in colon cancer cells should be different from that NKD1 has played in the zebrafish. Thus, NKD1 could be a specific colorectal cancer marker. [ABSTRACT FROM AUTHOR]

Peripheral nerve injury–induced mechanical allodynia is often accompanied by abnormalities in the higher cortical regions, yet the mechanisms underlying such maladaptive cortical plasticity remain unclear. Here, we show that in male mice, structural and functional changes in the primary somatosensory cortex (S1) caused by peripheral nerve injury require neuron-microglial signaling within the local circuit. Following peripheral nerve injury, microglia in the S1 maintain ramified morphology and normal density but up-regulate the mRNA expression of brain-derived neurotrophic factor (BDNF). Using in vivo two-photon imaging and Cx3cr1CreER;Bdnfflox mice, we show that conditional knockout of BDNF from microglia prevents nerve injury–induced synaptic remodeling and pyramidal neuron hyperactivity in the S1, as well as pain hypersensitivity in mice. Importantly, S1-targeted removal of microglial BDNF largely recapitulates the beneficial effects of systemic BDNF depletion on cortical plasticity and allodynia. Together, these findings reveal a pivotal role of cerebral microglial BDNF in somatosensory cortical plasticity and pain hypersensitivity. This study reveals that brain-derived neurotrophic factor (BDNF) from cerebral microglia contributes to nerve injury-induced synaptic remodeling and neuronal hyperactivity, and ultimately contributes to pain sensitivity in mice; removal of microglial BDNF has beneficial effects on cortical plasticity and pain. [ABSTRACT FROM AUTHOR]

In this paper, we propose generalized hesitant fuzzy soft sets by integrating generalized fuzzy soft sets with hesitant fuzzy sets. Then we investigate several fundamental properties of generalized hesitant fuzzy soft sets. In particular, a system of all the generalized hesitant fuzzy soft sets with narrow strict union and generalized strict intersection operators turns out to be a lattice. Meanwhile, a system of all the generalized hesitant fuzzy soft sets with generalized strict union and narrow strict intersection operators is a lattice. Based on generalized hesitant fuzzy soft sets, we provide an effective approach to decision making. Finally, three examples are presented to illuminate the feasibility of the method. [ABSTRACT FROM AUTHOR]

Various studies have demonstrated that microRNA (miRNA) serves an important role in the development of gastric cancer. However, the expression level, clinical significance and the biological function of miRNA in gastric cancer remain largely unknown. The present study investigated the exact roles of miR-671-5p in gastric cancer, confirmed its target and explored its mechanism. Initially, the low expression levels of miR-671-5p in gastric cancer cells were confirmed by reverse transcription-quantitative polymerase chain reaction. TargetScan and MiRanda databases were utilized to forecast the target genes of miR-671-5p, and the prediction was verified by dual-luciferase reporter assay and western blot analysis. Cell Counting Kit-8 was used for cell proliferation detection. An annexin V-fluorescein isothiocyanate kit was used for cell apoptosis determination. Western blot analysis was adopted to measure the protein expression levels in different groups. The results of the present study revealed that there were lower expression levels of miR-671-5p in gastric cancer cells than in normal gastric cells. Upregulator of cell proliferation (URGCP) is a direct target of miR-671-5p and it may be negatively regulated by miR-671-5p. miR-671-5p mimics induced reduction of MKN28 cell proliferation. miR-671-5p mimics caused upregulation of MKN28 cell apoptosis. In addition, western blotting results indicated that the ratio of B-cell lymphoma 2 (Bcl-2)/Bcl-2-associated X protein was significantly decreased in the miR-671-5p mimic group compared with the negative control group (P<0.01). These results suggested that miR-671-5p had a protective role in gastric cancer through inhibiting gastric cancer cell proliferation and promoting cell apoptosis by targeting URGCP. Therefore, miR-671-5p may be an effective therapeutic target for gastric cancer. [ABSTRACT FROM AUTHOR]