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Event-related potentials (ERPs) have previously been used to confirm the existence of the fast optical signal (FOS) but validation methods have mainly been limited to exploring the temporal correspondence of FOS peaks to those of ERPs. The purpose of this study was to systematically quantify the relationship between FOS and ERP responses to a visual oddball task in both time and frequency domains. Near-infrared spectroscopy (NIRS) and electroencephalography (EEG) sensors were co-located over the prefrontal cortex while participants performed a visual oddball task. Fifteen participants completed 2 data collection sessions each, where they were instructed to keep a mental count of oddball images. The oddball condition produced a positive ERP at 200 ms followed by a negativity 300–500 ms after image onset in the frontal electrodes. In contrast to previous FOS studies, a FOS response was identified only in DC intensity signals and not in phase delay signals. A decrease in DC intensity was found 150–250 ms after oddball image onset with a 400-trial average in 10 of 15 participants. The latency of the positive 200 ms ERP and the FOS DC intensity decrease were significantly correlated for only 6 (out of 15) participants due to the low signal-to-noise ratio of the FOS response. Coherence values between the FOS and ERP oddball responses were found to be significant in the 3–5 Hz frequency band for 10 participants. A significant Granger causal influence of the ERP on the FOS oddball response was uncovered in the 2–6 Hz frequency band for 7 participants. Collectively, our findings suggest that, for a majority of participants, the ERP and the DC intensity signal of the FOS are spectrally coherent, specifically in narrow frequency bands previously associated with event-related oscillations in the prefrontal cortex. However, these electro-optical relationships were only found in a subset of participants. Further research on enhancing the quality of the event-related FOS signal is required before it can be practically exploited in applications such as brain-computer interfacing.

Tumor eradication is one of the most important challengeable categories in oncological studies. In this account, besides the molecular genetics methods including cell therapy, gene therapy, immunotherapy, and general cancer therapy procedures like surgery, radiotherapy, and chemotherapy, photodynamic adjuvant therapy is of great importance. Photodynamic therapy (PDT) as a relatively noninvasive therapeutic method utilizes the irradiation of an appropriate wavelength which is absorbed by a photosensitizing agent in the presence of oxygen.

DNA methylation is a significant regulator of gene expression, and its role in carcinogenesis recently has been a subject of remarkable interest. The aim of this review is to analyze the mechanism and cell regulatory effects of both hypo- and hyper-DNA methylation on cancer. In this review, we report new developments and their implications regarding the effects of DNA methylation on cancer development. Indeed, alteration of the pattern of DNA methylation has been a constant finding in cancer cells of the same type and differences in the pattern of DNA methylation not only occur in a variety of tumor types, but also in developmental processes Furthermore, the pattern of histone modification appears to be a predicator of the risk of recurrence of human cancers. It is well known that hypermethylation represses transcription of the promoter sections of tumor-suppressor genes leading to gene silencing. However, hypomethylation also has been identified as a cause of oncogenesis. Furthermore, experiments concerning the mechanism of methylation and its control have led to the discovery of many regulatory enzymes and proteins. This review reports on methods developed for the detection of 5-hydroxymethylcytosine methylation at the 5-methylcytosine of protein domains in the CpG context compared to non-methylated DNA, histone modification, and microRNA change.

Perception and generation of affective movements are essential for achieving the expressivity required for a fully engaging human-machine interaction. This paper develops a computational model for recognizing and generating affective hand movements for display on anthropomorphic and non-anthropomorphic structures. First, time-series features of these movements are aligned and converted to fixed-length vectors using piece-wise linear re-sampling. Next, a feature transformation best capable of discriminating between the affective movements is obtained using functional principal component analysis (FPCA). The resulting low-dimensional feature transformation is used for classification and regeneration. A dataset consisting of one movement type, closing and opening the hand, is considered for this study. Three different expressions, sadness, happiness and anger, were conveyed by a demonstrator through the same general movement. The performance of the developed model is evaluated objectively using leave-one-out cross validation and subjectively through a user study, where participants evaluated the regenerated affective movements as well as the original affective movements reproduced both on a human-like model and a non-anthropomorphic structure. The proposed approach achieves zero leave-one-out cross validation errors, on both the training and testing sets. No significant difference is observed between participants’ evaluation of the regenerated movements as compared to the original movement, which confirms successful regeneration of the affective movement. Furthermore, a significant effect of structure on the perception of affective movements is observed.

Exosomes which are membrane vesicles released by cells have gained significant interest in the field of cancer therapy as a novel means of intercellular communication. Their role in immune activation and their pathophysiological functions in cancer therapy have been recognized. Exosomes carry diverse bioactive components including proteins, mRNA, microRNAs, and bioactive lipids. These molecules have therapeutic potential in promoting tissue regeneration, supporting stem cell activity, preventing cell death, modulating immune responses, and promoting the growth of new blood vessels. However, the precise roles of exosomes derived from mesenchymal stem cells (MSCs) in the treatment of various cancers are still not fully understood. Consequently, cancer stem cells (CSCs) can self-renew and differentiate into various cell types. Understanding the mechanisms that sustain their persistence is crucial for developing effective therapies. Exosomes have recently gained interest as vehicles for intercellular communication between CSCs and non-CSCs, influencing cancer progression and the microenvironment. Research is ongoing on the utilization of exosomes derived from cancer stem cells (CSC-Exosome) for cancer treatment. The composition of extracellular vesicles is influenced by the specific type and condition of the cells from which they are secreted. Circulating exosomes contain stable RNA molecules such as mRNAs, microRNAs, and long non-coding RNAs (lncRNAs). In this review, we will explore the significance of exosomes and their diverse cellular combinations in the context of cancer therapy. Graphical Abstract

Glioblastoma multiforme (GBM) is the most common harmful high-grade brain tumor with high mortality and low survival rate. Importantly, besides routine diagnostic and therapeutic methods, modern and useful practical techniques are urgently needed for this serious malignancy. Correspondingly, the translational medicine focusing on genetic and epigenetic profiles of glioblastoma, as well as the immune framework and brain microenvironment, based on these challenging findings, indicates that key clinical interventions include immunotherapy, such as immunoassay, oncolytic viral therapy, and chimeric antigen receptor T (CAR T) cell therapy, which are of great importance in both diagnosis and therapy. Relatively, vaccine therapy reflects the untapped confidence to enhance GBM outcomes. Ongoing advances in immunotherapy, which utilizes different methods to regenerate or modify the resistant body for cancer therapy, have revealed serious results with many different problems and difficulties for patients. Safe checkpoint inhibitors, adoptive cellular treatment, cellular and peptide antibodies, and other innovations give researchers an endless cluster of instruments to plan profoundly in personalized medicine and the potential for combination techniques. In this way, antibodies that block immune checkpoints, particularly those that target the program death 1 (PD-1)/PD-1 (PD-L1) ligand pathway, have improved prognosis in a wide range of diseases. However, its use in combination with chemotherapy, radiation therapy, or monotherapy is ineffective in treating GBM. The purpose of this review is to provide an up-to-date overview of the translational elements concentrating on the immunotherapeutic field of GBM alongside describing the molecular mechanism involved in GBM and related signaling pathways, presenting both historical perspectives and future directions underlying basic and clinical practice.

Introduction Suppression within the tumor microenvironment (TME) hampered natural killer (NK) cells and their role in cancer immunotherapy. This study explores how interleukin (IL) signaling (IL‐12A, IL‐12B, IL‐15, IL‐18) and interferon gamma (IFNG or IFN‐γ) interact with microRNAs to regulate NK cell function in cancer. Methods We identify the targeted microRNAs (miRNAs) for these genes and the key pathways influencing various cancers through comprehensive analyses, including protein–protein interaction networks, protein co‐expression, miRNA targeting prediction, homology, mRNA‐miRNA regulatory networks, gene set enrichment, and signaling pathway analysis. Results Our analysis revealed a significant association between genes encoding interleukins and IFNG with NK cell infiltration across various cancers. Additionally, we identified several miRNAs (hsa‐miR‐590‐3p, hsa‐miR‐340‐5p, hsa‐miR‐495‐3p, hsa‐miR‐5692a, hsa‐miR‐130a‐3p) that potentially regulate NK cell function by targeting these genes. These miRNAs participate in critical pathways essential for NK cell function. Notably, our findings suggest a key role for mRNA‐miRNA co‐regulation in suppressing NK cells within the tumor microenvironment. Conclusion This study highlights the potential of targeting these identified miRNAs as a strategy to enhance NK cell function and improve the efficacy of cancer immunotherapy.

Gastric cancer is among the commonplace causes of cancer death worldwide. Sonic hedgehog (Shh) signaling is an important pathway which may be dysregulated in many cancers.CDX1/2, and KLF5are key transcription factors involved in Shh pathway and cancer stem cells. The aim of this study was to investigate the expression and epigenetic alterations of these genes in gastric cancer patients. DNA methylation’s modifications of CDX1, KLF5 and CDX2 genes alongside with the expressions of these genes in gastric cancer tissues and their non-tumoral counterparts (margin tissues) were analyzed using methylation specific sequencing, and Real time PCR Taq man assays, respectively. The expression of CDX1 (P = 0.002) and KLF5 (P = 0.010) were decreased significantly, but it was considerably increased for CDX2 (P = 0.001). Relatively, the results for the regulatory region methylation status of each CpG site had shown a notable fluctuation in these genes with no significant difference in most places. The creation of metastatic lymph nodes in patients was significantly associated with increased expression of CDX2 gene. The modifications of these genes expression can be considered as a cancer biomarker in future studies. Methylation of the investigated genes is not the main mechanism of gastric cancer development.

Objective Glioblastoma, one of the most aggressive brain tumors, is distinguished by its resistance to standard treatments. So, studying practical therapeutic methods is of great importance. In this project, the effects of combined chemotherapy drugs, including bevacizumab, carmustine, and metformin, on the expression of IL-6, TLR2, and TLR6 in the glioblastoma cell line of U87MG were investigated. Methods U87MG cells were treated with bevacizumab, carmustine, and metformin alone or in combined groups. Cell viability was measured using the MTT assay. Apoptotic rates and cell cycle were analyzed by flow cytometry. Gene and protein expression levels of TLR2 , TLR6 , and IL-6 were evaluated by Real-Time PCR and Western blotting, respectively. In addition, bioinformatic analyses, including protein-protein interaction (PPI) network construction and pathway enrichment, were performed using Cytoscape (GeneMANIA) and R (ClusterProfiler). Results The triple-drug combination(bevacizumab, carmustine, and metformin )significantly reduced cell viability and induced a substantial increase in apoptosis and G0/G1 cell cycle arrest. Treatment also led to a marked downregulation of TLR2 , TLR6 , and IL-6 gene expression. Bioinformatic analysis revealed these genes to be central in pathways associated with immune regulation, inflammation, and tumor progression. Conclusion The combination of bevacizumab, carmustine, and metformin exerts a potent synergistic antitumor effect in U87MG glioblastoma cells through modulation of inflammation-associated genes, induction of apoptosis, and disruption of cell cycle progression. These findings provide a mechanistic rationale for multi-targeted combination therapy in glioblastoma and support further preclinical evaluation.

Therapeutic methods are very important in the prevalence of opportunistic fungal infections, which are an important cause of human diseases. In this study, air pollution agents that are in direct contact with microorganisms, and the effects of carbon sources using CO2 and MTBE on growth of fungi, and particularly the evaluation of changes in the expression of interfering genes in susceptibility and drug resistance in these fungi, were investigated.Collecting samples and isolating Candida glabrata and Candida albicans with phenotypic methods were accomplished. We then evaluated the minimum inhibitory concentration (MIC) with the M27A4 protocol of CLSI. We adjusted 20 strains of C. albicans and 10 strains of C. glabrata whose sensitivity was evaluated in the MIC test with 5% CO2 and 5mg/ml methyl tert-butyl ether (MTBE) considered as air pollutants, and followed by re-evaluating MIC testing to separate azole-resistant strains. Interfering agents were also considered.Upregulation of some genes on the two mentioned yeasts had led to drug resistance in them; they were previously sensitive to both drugs. Correspondingly, 41% of C. glabrata samples in sputum showed sensitivity to these drugs. Upregulation of ERG11 (71%) and EPA1 (90%) were observed in resistant strains. Upregulation of genes associated with aspartate proteins and downregulation of SAP3 genes were recognized in C. glabrata in sputum and a 15% downregulation of bronchoalveolar lavage (BAL) isolate and 50% upregulation of SAP1 gene in C. albicans sensitive samples were observed and compared to fluconazole and itraconazole with the oral and joint sources. Remarkably, decreased SAP2 expression in oral sources and a 60% increase in resistant strains in C. albicans were observed. The downregulation of SAP3 expression showed in the joint samples. An increase in HWP1 expression (30%) was noted in isolated and drug-sensitive samples at the sputum and BAL source. CDR1 expression was increased in MTBE-affected species; however, it decreased in the vicinity of CT.Air pollutants such as CO2 and MTBE eventually caused drug resistance in Candida, which can be one of the causes of drug resistance in candidiasis infections.