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Multi-label feature selection attracts considerable attention from multi-label learning. Information-theory based multi-label feature selection methods intend to select the most informative features and reduce the uncertain amount of information of labels. Previous methods regard the uncertain amount of information of labels as constant. In fact, as the classification information of the label set is captured by features, the remaining uncertainty of each label is changing dynamically. In this paper, we categorize labels into two groups: one contains the labels with few remaining uncertainty, which means that most of classification information with respect to the labels has been obtained by the already-selected features; another group contains the labels with extensive remaining uncertainty, which means that the classification information of these labels is neglected by already-selected features. Feature selection aims to select the new features with highly relevant to the labels in the second group. Existing methods do not distinguish the difference between two label groups and ignore the dynamic change amount of information of labels. To this end, a Relevancy Ratio is designed to clarify the dynamic change amount of information of each label under the condition of the already-selected features. Afterwards, a Weighted Feature Relevancy is defined to evaluate the candidate features. Finally, a new multi-label Feature Selection method based on Weighted Feature Relevancy (WFRFS) is proposed. The experiments obtain encouraging results of WFRFS in comparison to six multi-label feature selection methods on thirteen real-world data sets.

A spike-like double yolk–shell structured TiO2@ZnIn2S4 (D-Y-TiO2@ZnIn2S4) photocatalyst was designed, which possesses superior photocatalytic CO2 reduction efficiency.

Table S1: Differentially expressed miRNAs related to cisplatin sensitivity in hepatocellular carcinoma based on GSE55806 dataset; Table S2: Differentially expressed genes between high and low miR-27a-3p expression group based on TCGA-LIHC dataset; Table S3: Table S3. Differentially expressed genes between Huh7 cells transfected with miR-27a-3p mimics and Huh7 cells transfected with NC based on GSE206246 dataset; Table S4: 79 DEGs related to MAPK signaling pathway in PPI networks based on GSE206246 dataset ranked by degree method.

The ADAMs (a disintegrin and metalloproteinase) are a family of cell surface proteins with crucial roles in the regulation of cell adhesion, cell proliferation to migration, proteolysis and cell signaling transduction pathways. Among these enzymes, the ADAM17 shows significant effects in the “ectodomain shedding” of its substrates such as cytokines (e.g., tumor necrosis factor α, TNFα), growth factors (e.g., epidermal growth factor, EGF), adhesion proteins (e.g., L-selectin), and their receptors (e.g., IL-6R and TNFα). Several studies focus on the underlying molecular mechanisms of ADAM17 in diseased conditions. Here, we took several different approaches to elucidate the function of ADAM17, the participation of ADAM17 in several human diseases, and the potential as targeted therapy reagents. As more and more studies verify the miRNA-mediated expression variation of ADAM17, the specific regulation network of miRNAs and ADAM17 was exploited in this review as well.

Hepatocellular carcinoma (HCC) is an aggressive disease with a high degree of tumor heterogeneity. Genetic lesions of mTOR-related genes, including

Emerging evidence has suggested that long non-coding RNA (lncRNA) colorectal neoplasia differentially expressed (CRNDE) is upregulated in hepatocellular carcinoma (HCC) and is associated with cell invasion, migration, and growth. However, the potential modulation mechanism remains to be elucidated. MiR-33a-5p and cyclin-dependent kinase 6 (CDK6) also participate in the pathophysiology of HCC. This work aims to investigate the effect of CRNDE on HCC apoptosis, invasion, and migration and elucidate the role of miR-33a-5p and CDK6 therein. CRNDE and CDK6 were upregulated in HCC tissues and cells, while miR-33a-5p was downregulated. Inhibition of CRNDE suppressed the invasion, migration, and proliferation of HCC cells and enhanced apoptosis by modulating proteins associated with mitochondrial apoptosis (caspase 3, Bax, cytochrome-c, Bcl-2), which were the same as the function of miR-33a-5p overexpression. The dual-luciferase reporter assay demonstrated that miR-33a-5p was a target of CRNDE, and in turn, CRNDE inhibition enhanced the level of miR-33a-5p. CDK6 was also revealed as a target of miR-33a-5p, and both CRNDE inhibition and miR-33a-5p overexpression suppressed CDK6 expression and led to G0/G1 phase block in HCC cells. In vivo experiments using a mouse xenograft tumor model further verified the interaction between CRNDE and miR-33a-5p, showing that miR-33a-5p overexpression or CRNDE inhibition suppressed CDK6 expression and HCC tumorigenesis. Overall, the present work indicated that CRNDE plays an oncogenic function in HCC through regulating the miR-33a-5p/CDK6 axis, revealing a potential therapeutic target in HCC.

Photocatalytic hydrogen evolution (PHE) over semiconductor photocatalysts is usually constrained by the limited light-harvesting and separation of photogenerated electron-hole pairs. Most of the reported systems focusing on PHE are facilitated by consuming the photoinduced holes with organic sacrificial electron donors (SEDs). The introduction of the SEDs not only causes the environmental problem, but also increases the cost of the reaction. Herein, a dual-functional photocatalyst is developed with the morphology of sandwiched-like hollowed Pd@TiO

Pyroptosis, which is a mode of programmed cell death, has proven effective for cancer therapy. However, efficient pyroptosis inducers for tumor treatment are limited. This study proposes biodegradable K3ZrF7:Yb/Er upconversion nanoparticles (ZrNPs) as pyroptosis inducers for cancer immunotherapy. ZrNPs, which are similar to ion reservoirs, can be dissolved inside cancer cells and release high amounts of K+ and [ZrF7]3- ions, resulting a surge in intracellular osmolarity and homeostasis imbalance. This further induces an increase in reactive oxygen species (ROS), caspase-1 protein activation, gasdermin D (GSDMD) cleavage, and interleukin-1β (IL-1β) maturity, and results in cytolysis. In vivo tests confirm that ZrNPs-induced pyroptosis exhibits superior antitumor immunity activity confirmed by enhanced dendritic cells (DCs) maturity and frequency of effector-memory T cells, as well as observably inhibiting tumor growth and pulmonary metastasis. This work is believed to extend the biomedical applications of upconversion nanomaterials and deepen the understanding of intrinsic immunomodulatory activity of nanomaterials.

Glioma is a life-threatening malignant tumor. Resistance to traditional treatments and tumor recurrence present major challenges in treating and managing this disease, consequently, new therapeutic strategies must be developed. Crossing the blood-brain barrier (BBB) is another challenge for most drug vectors and therapy medications. Filamentous bacteriophage can enter the brain across the BBB. Compared to traditional drug vectors, phage-based drugs offer thermodynamic stability, biocompatibility, homogeneity, high carrying capacity, self-assembly, scalability, and low toxicity. Tumor-targeting peptides from phage library and phages displaying targeting peptides are ideal drug delivery agents. This review summarized recent studies on phage-based glioma therapy and shed light on the developing therapeutics phage in the personalized treatment of glioma.

Pancreatic cancer is a digestive system malignant tumor with high mortality and poor prognosis, but the mechanisms of progression remain unclear in pancreatic cancer. It’s necessary to identify the hub genes in pancreatic cancer and explore the novel potential predictors in the prognosis of pancreatic cancer. We downloaded two mRNA expression profiles from Gene Expression Omnibus and The Cancer Genome Atlas Pancreatic Cancer (TCGA-PAAD) datasets to screen the commonly differentially expressed genes in pancreatic cancer by limma package in R. Subsequently, measurement of the functional similarity among the 38 DEGs in common was performed to identify the hub genes using GOSemSim package. Then, survival analysis and Cox regression were applied to explore prognosis-related hub genes using the survival package. Statistics analysis by two-tailed Student’s t-test or one-way based on TCGA-PAAD datasets and qPCR detection in clinical samples were performed to explore the correlations between expression of hub genes in pancreatic cancer tissues and clinical parameters. Based on integrated analysis of TCGA and GEO datasets, we screened 38 DEGs in common, which were all up-regulated. The functional similarity results showed that 10 DEGs including TSPAN1, MSLN, C1orf116, PKP3, CEACAM6, BAIAP2L1, PPL, RAB25, ERBB3, and AP1M2 in the DEGs in common, which had the higher average functional similarity, were considered as the hub genes. Survival analysis results and Cox regression analysis showed that TSPAN1, CEACAM6, as well as ERBB3 were all associated with poor overall survival of PC. qPCR results showed that the expression levels of TSPAN1 and ERBB3 were significantly upregulated in the PC tissues. The statistical analysis results revealed that TSPAN1 expression correlated significantly with histologic grade, T stage, clinical stage, and vital status by two-tailed Student’s t-test or one-way ANOVA; ERBB3 expression correlated significantly with T stage, clinical stage, and vital status by two-tailed Student’s t-test or one-way ANOVA. We found that TSPAN1 and ERBB3 could be independent predictors of poor survival in pancreatic cancer.

Background: Patients with low response rates to cancer vaccines, short duration of anti-tumor response after vaccination, and relatively weak curative effects are problems that have not been resolved effectively during the development and application of cancer vaccines. With the continuous improvement of knowledge and awareness regarding the immune system and cancer cells, many researches have helped to explain the reasons for poor vaccine efficacy. Input from researchers accompanied by some newly emerged strategies could bring hope to improve the therapeutic effects of vaccines. Methods: Data were collected from Web of Science, Medline, Pubmed, through searching of these keywords: “cancer vaccine”, “cancer stem cell”, “targeted agent”, “immune checkpoint blockade” and “neoantigen”. Results: It may be more effective in immunotherapy of human cancers, including cancer stem cell vaccines, combination vaccines with targeted agents or immune checkpoint blockade, and neoantigen-based vaccines. Conclusion: Personalized vaccines will become the mainstream solution of cancer treatment program with the continuous improvement of human understanding of the immune system and the progress of related experiments.

Pancreatic cancer is one of the most malignant tumors worldwide, and pancreatic ductal adenocarcinoma is the most common type. In pancreatic cancer, glycolysis is the primary way energy is produced to maintain the proliferation, invasion, migration, and metastasis of cancer cells, even under normoxia. However, the potential molecular mechanism is still unknown. From this perspective, this review mainly aimed to summarize the current reasonable interpretation of aerobic glycolysis in pancreatic cancer and some of the newest methods for the detection and treatment of pancreatic cancer. More specifically, we reported some biochemical parameters, such as newly developed enzymes and transporters, and further explored their potential as diagnostic biomarkers and therapeutic targets.

Cervical cancer (CC) remains a major disease burden on the female population worldwide. Chemotherapy with cisplatin (cis-diamminedichloroplatinum (II); CDDP) and related drugs are the main treatment option for CC; however, their efficacy is limited by the development of drug resistance. Noncoding RNAs (ncRNAs) have been found to play critical roles in numerous physiological and pathological cellular processes, including drug resistance of cancer cells. In this review, we describe some of the ncRNAs, including miRNAs, lncRNAs and circRNAs, that are involved in the sensitivity/resistance of CC to CDDP-based chemotherapy and discuss their mechanisms of action. We also describe some ncRNAs that could be therapeutic targets to improve the sensitivity of CC to CDDP-based chemotherapy.

Numerous studies have shown that berberine and its derivatives demonstrate important anti-tumor effects. However, the specific underlying mechanism remains unclear. Therefore, based on systems pharmacology, this review summarizes the information available on the anti-tumor effects and mechanism of berberine and its derivatives. The action and potential mechanism of action of berberine and its derivatives when used in the treatment of complex cancers are systematically examined at the molecular, cellular, and organismic levels. It is concluded that, with further in-depth investigations on their toxicity and efficacy, berberine and its derivatives have the potential for use as drugs in cancer therapy, offering improved clinical efficacy and safety.

Deep blue luminescent materials play a crucial role in the organic light-emitting diodes (OLEDs). In this work, a novel deep blue molecule based on hybridized local and charge-transfer (HLCT) excited state was reported with the emission wavelength of 423 nm. The OLED based on this material achieved high maximum external quantum efficiency (EQE) of 4% with good color purity. The results revealed that the locally-excited (LE)-dominated HLCT excited state had obvious advantages in short wavelength and narrow spectrum emission. What is more, the experimental and theoretical combination was used to describe the excited state characteristic and to understand photophysical property.

Vascular disrupting agents (VDAs) have great potential for cancer treatment. Poly(l‐glutamic acid)‐combretastatin A4 conjugate (PLG‐CA4) is a novel class of VDAs. Though it has notable antitumor activity, it can induce host immune responses that promote tumor growth. Here, PLG‐CA4 induces the polarization of tumor‐associated macrophages (TAMs) toward the M2‐like phenotype in 4T1 metastatic breast cancer (Control 30% vs PLG‐CA4 53%; p < 0.05). Compared to the monotherapy of PLG‐CA4, inhibition of phosphoinositide 3‐kinase gamma (PI3Kγ) attenuates the immunosuppressive effect of PLG‐CA4 treatment by decreasing the number of M2‐like TAMs (2.0 × 104 to 1.5 × 104 per tumor) and potential enhancement of cytotoxic T lymphocyte (3.0 × 104 to 5.7 × 104 per tumor). Importantly, PI3Kγ inhibitor synergizing with PLG‐CA4 significantly extends the mean survival time from 52 days in monotherapy‐treated mice to 61.8 days. Additionally, the combination of PLG‐CA4 and PI3Kγ inhibitor improves the tumor therapeutic effect of NLG919, an inhibitor of immune checkpoint indoleamine 2,3‐dioxygenase (IDO). As far as it is known, this is the first demonstrated study that VDAs induce the reshaping of macrophages to the M2‐like phenotype. The findings also indicate a potential therapeutic strategy of the combination VDAs with an accurate immune modifier in the tumor to reverse the immune resistance.

Herbal medicines, as an important part of traditional Chinese medicine (TCM), have been used to treat digestive system malignancies (DSM) for many years, and have gradually gained recognition worldwide. The role of herbal medicines in the comprehensive treatment of DSM is being improved from adjuvant treatment of the autologous immune function in cancer patients, to the treatment of both the symptoms and disease, direct inhibition of tumor cell growth and proliferation, and induction of tumor cell autophagy and apoptosis. Their specific mechanisms in these treatments are also being explored. The paper reviews the current anti-tumor mechanisms of TCM, including single herbal medicines, Chinese herbal formulations, Chinese medicine preparations and TCM extract, and their application in the comprehensive treatment of digestive system tumors, providing a reference for clinical application of TCM.

The phosphoinositide 3-kinase (PI3K) pathway shows frequent aberrant alterations and pathological activation in breast cancer cells. While PI3K inhibitors have not achieved expectant therapeutic efficacy in clinical trials, and several studies provide promising combination strategies to substantially maximize therapeutic outcomes. Besides its direct impact on regulating cancer cells survival, PI3K inhibitors are also demonstrated to have an immunomodulatory impact based on the tumor microenvironment. Inhibition of the leukocyte-enriched PI3K isoforms may break immune tolerance and restore cytotoxic T cell activity by reprogramming the tumor microenvironment. In addition, PI3K inhibitors have pleiotropic effects on tumor angiogenesis and even induce tumor vascular normalization. In this review, we discuss the mechanism of PI3K inhibitor suppression of breast cancer cells and modulation of the tumor microenvironment in order to provide further thoughts for breast cancer treatment.

Sarcomatoid carcinoma (SC) is an extremely rare and complicated malignant neoplasm that consists of both malignant epithelial components and atypical spindle cells that express an epithelial phenotype. The presents study reported a case of SC of the pancreas (SCP), along with a brief review of the literature. A 63‑year‑old man was admitted to The Second Hospital of Jilin University hospital with complaints of epigastralgia and jaundice of one month in duration. Based on preoperative laboratory blood tests and radiography, a mass at the distal common bile duct was suspected. Intraoperative examination discovered a 2.5x2x1.8‑cm mass in the pancreatic head, with invasion of the distal bile duct. Pancreaticoduodectomy was performed. Histopathology and immunohistochemistry of the specimen confirmed the diagnosis of SCP. The patient succumbed 18 months after surgery due to multiple hepatic metastases.

Primary liver cancer is a common kind of digestive cancers with high malignancy, causing 745,500 deaths each year. Hepatocellular carcinoma is the major pathological type of primary liver cancer. Traditional treatment methods for patients with hepatocellular carcinoma have shown poor efficacy in killing residual cancer cells for a long time. In recent years, tumor immunotherapy has emerged as a promising method owing to its safety and efficacy with respect to delaying the progression of advanced tumors and protecting postoperative patients against tumor relapse and metastasis. Immune tolerance and suppression in tumor microenvironments are the theoretical basis of immunotherapy. Adoptive cell therapy functions by stimulating and cultivating autologous lymphocytes ex vivo and then reinfusing them into the patient to kill cancer cells. Cancer vaccination is performed using antigenic substances to activate tumor-specific immune responses. Immune checkpoint inhibitors can reactivate tumor-specific T cells and develop an antitumor effect by suppressing checkpoint-mediated signaling. Oncolytic viruses may selectively replicate in tumor cells and cause lysis without harming normal tissues. Here, we briefly introduce the mechanism of immunosuppression in hepatocellular carcinoma and summarize the rationale of the four major immunotherapeutic approaches with their current advances.

The induction of lesions in nuclear and mitochondrial DNA by cisplatin is only a small component of its cytostatic/cytotoxic activity. The signaling pathway network in the nucleus and cytoplasm may contribute to chemotherapeutic resistance. Peroxisome proliferator-activated receptor-coactivator 1α (PGC1α)-mediated mitochondrial biogenesis regulates mitochondrial structural and the functional adaptive response against chemotherapeutic stress, and may be a therapeutic target. However, this regulatory network is complex and depends upon tumor types and environments, which require further investigation. Our previous study found that cisplatin-resistant ovarian epithelial carcinoma was more dependent on mitochondrial aerobic oxidation to support their growth, suggesting the association between mitochondrial function and chemotherapeutic resistance. In the present study, it was demonstrated that the expression of PGC1α and level of mitochondrial biogenesis were higher in cisplatin-resistant SKOV3/DDP cells compared with cisplatin-sensitive SKOV3 cells. Furthermore, SKOV3/DDP cells upregulated the expression of PGC1α and maintained mitochondrial structural and functional integrity through mitochondrial biogenesis under cisplatin stress. Inhibiting the expression of PGC1α using short hairpin RNA led to the downregulation of mitochondrial biogenesis and high levels of apoptosis in the SKOV3/DDP cells, and cisplatin resistance was reversed in the PGC1α-deficient SKOV3/DDP cells. Collectively, the present study provided evidence that cisplatin stimulated the expression of PGC1α and the upregulation of mitochondrial biogenesis through PGC1α, promoting cell viability and inhibiting apoptosis in response to cisplatin treatment, thus triggering cisplatin resistance in ovarian cancer cells.

Hepatocellular carcinoma (HCC) accounts for a significant proportion of liver cancer, which has become the second most common cause of cancer-related mortality worldwide. To investigate the potential mechanisms of invasion and progression of HCC, bioinformatics analysis and validation by qRT-PCR were performed. We found 237 differentially expressed genes (DEGs) including EGR1, FOS, and FOSB, which were three cancer-related transcription factors. Subsequently, we constructed TF-gene network and miRNA-TF-mRNA network based on data obtained from mRNA and miRNA expression profiles for analysis of HCC. We found that 42 key genes from the TF-gene network including EGR1, FOS, and FOSB were most enriched in the p53 signaling pathway. The qRT-PCR data confirmed that mRNA levels of EGR1, FOS, and FOSB all were decreased in HCC tissues. In addition, we confirmed that the mRNA levels of CCNB1, CCNB2, and CHEK1, three key markers of the p53 signaling pathway, were all increased in HCC tissues by bioinformatics analysis and qRT-PCR validation. Therefore, we speculated that miR-181a-5p, which was upregulated in HCC tissues, could regulate FOS and EGR1 to promote the invasion and progression of HCC by p53 signaling pathway. Overall, the study provides support for the possible mechanisms of progression in HCC.

Non-invasive brain stimulation (NBS) is a promising treatment for major depressive disorder (MDD), which is an affective processing disorder involving abnormal emotional processing. Many studies have shown that repetitive transcranial magnetic stimulation (rTMS) and transcranial direct current stimulation (tDCS) over the prefrontal cortex can play a regulatory role in affective processing. Although the clinical efficacy of NBS in MDD has been demonstrated clinically, the precise mechanism of action remains unclear. Therefore, this review article summarizes the current status of NBS methods, including rTMS and tDCS, in the treatment of MDD. The article explores possible correlations between depressive symptoms and affective processing, highlighting the relevant affective processing mechanisms. Our review provides a reference for the safety and efficacy of NBS methods in the clinical treatment of MDD.

Background Epilepsy is a chronic brain disease that is caused by various factors and characterized by recurrent, episodic and temporary central nervous system dysfunction which results due to excessive discharge of brain neurons. In the past decades, despite the continuous development of antiepileptic drugs, there are still many patients with epilepsy progressing to drugresistant epilepsy. Currently, surgical treatment is one of important way to cure drug-resistant epilepsy. Methods Data were collected from Web of Science, Medline, Pubmed, through searching of these keywords: "surgery" and "drug-resistant epilepsy". Results An increasing number of studies have shown that surgery plays an important role in the treatment of drug-resistant epilepsy. Moreover, the comprehensive treatment mainly based on surgery can achieve the remission and even cure of drug-resistant epilepsy. Conclusion In this review, we discuss the pathogenesis of drug-resistant epilepsy and the comprehensive treatment mainly based on surgery; this review may provide a reference for the clinical treatment of drug-resistant epilepsy.

Chronic pain, as a stress state, is one of the critical factors for determining depression, and their coexistence tends to further aggravate the severity of both disorders. Unfortunately, their association remains unclear, which creates a bottleneck problem for managing chronic pain-induced depression. In recent years, studies have found considerable overlaps between pain- and depression-induced neuroplasticity changes and neurobiological mechanism changes. Such overlaps are vital to facilitating the occurrence and development of chronic pain and chronic pain-induced depression. In this review, we summarized the role of neuroplasticity in the occurrence and development of the two disorders in question and explored individualized application strategies of analgesic drugs and antidepressants that have different pharmacological effects in the treatment of chronic pain-induced depression. Therefore, this review may provide new insights into the understanding of association between chronic pain and depression.