In vitro and in vivo investigation of the inhibitory effects of Sinoporphyrin sodium-mediated Sonodynamic therapy on human oral squamous cell carcinoma.

Objective: Sonodynamic therapy (SDT) is an innovative, non-invasive approach to cancer treatment, by using low-intensity ultrasound to trigger the activation of sonosensitizers localized within cancerous cells. This current study aimed to explore the therapeutic efficacy of a new sonosensitizer, Sinoporphyrin Sodium (DVDMS), under ultrasound irradiation, against oral squamous cell carcinoma (OSCC)-derived SCC-154 cells, both in vitro and in vivo.

Methods: Fluorescence spectra, cytotoxicity assessments, uptake mechanisms, and subcellular distributions of DVDMS within the SCC-154 cell line were detected.

Proximity ligation-triggered DNAzyme for selective fluorescent aptasensing of methicillin-resistant Staphylococcus aureus.

There is an urgent need for novel strategies to accurately and reliably detect pathogenic bacteria to address the global epidemic of antibiotic resistance. This study proposes an innovative approach combining dual aptamer-based target recognition and proximity ligation assay (PLA) triggered DNAzyme recycling cleavage. This method allows for the precise identification and reliable detection of methicillin-resistant Staphylococcus aureus (MRSA).

LogicGep: Boolean networks inference using symbolic regression from time-series transcriptomic profiling data.

Reconstructing the topology of gene regulatory network from gene expression data has been extensively studied. With the abundance functional transcriptomic data available, it is now feasible to systematically decipher regulatory interaction dynamics in a logic form such as a Boolean network (BN) framework, which qualitatively indicates how multiple regulators aggregated to affect a common target gene. However, inferring both the network topology and gene interaction dynamics simultaneously is still a challenging problem since gene expression data are typically noisy and data discretization is prone to information loss.

CircPKM2 aggravates the progression of non-small cell lung cancer by regulating MTDH via miR-1298-5p.

Background: Non-small cell lung cancer (NSCLC) is the most common type of lung cancer with high morbidity and mortality. The role of dysregulated circular RNAs (circRNAs) in human diseases are receiving more and more attention. In this study, we focused on the role and mechanism of circPKM2 in the progression of NSCLC.

CXCL8 induces M2 macrophage polarization and inhibits CD8 T cell infiltration to generate an immunosuppressive microenvironment in colorectal cancer.

The poor prognosis of immunotherapy in patients with colorectal cancer (CRC) necessitates a comprehensive understanding of the immunosuppressive mechanisms within tumor microenvironment (TME). Undoubtedly, the anti-tumor immune cells play an indispensable role in immune tolerance. Therefore, it is imperative to investigate novel immune-related factors that have the capacity to enhance anti-tumor immunity.

[Calnexin (CNX) enhances the killing effect of CD8 T cells on colorectal cancer cells by promoting MHC I expression].

Objective To investigate the killing effect and molecular mechanism of aberrant expression of calnexin (CNX) in the colorectal cancer (CRC) on the CD8 T immune cells. Methods Immunohistochemistry was used to detect CNX protein level in 102 pairs of CRC cancer and adjacent non-cancerous tissues. Western blotting was employed to examine the protein expression of MHC I in the HCT-15 cells overexpressed with CNX or in the SW480 cells whose CNX expressions were knockdown by siRNA.

miR-148a-3p silences the CANX/MHC-I pathway and impairs CD8 T cell-mediated immune attack in colorectal cancer.

Nonresponse, or acquired resistance to immune checkpoint inhibitors in colorectal cancer (CRC) highlight the importance of finding potential tolerance mechanisms. Low expression of major histocompatibility complex, class I (MHC-I) on the cell surface of the tumor is one of the main mechanisms of tumor escape from T-cell recognition and destruction. In this study, we demonstrated that a high level of calnexin (CANX) in the tumors is positively correlated with the overall survival in colorectal cancer patients.

Finite-Horizon Optimal Control of Boolean Control Networks: A Unified Graph-Theoretical Approach.

This article investigates the finite-horizon optimal control (FHOC) problem of Boolean control networks (BCNs) from a graph theory perspective. We first formulate two general problems to unify various special cases studied in the literature: 1) the horizon length is a priori fixed and 2) the horizon length is unspecified but finite for given destination states. Notably, both problems can incorporate time-variant costs, which are rarely considered in existing work, and a variety of constraints.

Learning Asynchronous Boolean Networks From Single-Cell Data Using Multiobjective Cooperative Genetic Programming.

Recent advances in high-throughput single-cell technologies provide new opportunities for computational modeling of gene regulatory networks (GRNs) with an unprecedented amount of gene expression data. Current studies on the Boolean network (BN) modeling of GRNs mostly depend on bulk time-series data and focus on the synchronous update scheme due to its computational simplicity and tractability. However, such synchrony is a strong and rarely biologically realistic assumption.

Infinite-Horizon Optimal Control of Switched Boolean Control Networks With Average Cost: An Efficient Graph-Theoretical Approach.

This study investigates the infinite-horizon optimal control (IHOC) problem for switched Boolean control networks with an average cost criterion. A primary challenge of this problem is the prohibitively high computational cost when dealing with large-scale networks. We attempt to develop a more efficient approach from a novel graph-theoretical perspective.

Mathematical Modeling Reveals the Role of Hypoxia in the Promotion of Human Mesenchymal Stem Cell Long-Term Expansion.

Many experimental studies have found that human mesenchymal stem cells (MSCs) in long-term culture exhibited enhanced cell proliferation and prolonged lifespan under hypoxia (around 1%-7% oxygen) against the normoxic condition (about 21% oxygen). Inspired by the experimental findings, we aimed to investigate the hypoxic effects on MSC expansion quantitatively through mathematical modeling to elucidate the corresponding biological mechanism. A two-compartment model based on ordinary differential equations (ODEs), which incorporate cellular division and senescence via state transition, was developed to describe the MSC expansion process.