Construction of multifunctional hydrogel containing pH-responsive gold nanozyme for bacteria-infected wound healing.

Nanozymes have become promising alternative antibacterial agents for bacteria-infected wounds. In this study, fucoidan-confined gold nanoparticles (Fuc@AuNPs) are developed by in situ reduction, and stabilized by sulfate groups of fucoidan. Fuc@AuNPs exhibit pH-responsive catalytic activity that can mimic oxidase (OXD) under acidic bacterial infection conditions and mimic superoxide dismutase (SOD) under normal physiological conditions.

Sensitize Tumor Immunotherapy: Immunogenic Cell Death Inducing Nanosystems.

Low immunogenicity of tumors poses a challenge in the development of effective tumor immunotherapy. However, emerging evidence suggests that certain therapeutic approaches, such as chemotherapy, radiotherapy, and phototherapy, can induce varying degrees of immunogenic cell death (ICD). This ICD phenomenon leads to the release of tumor antigens and the maturation of dendritic cells (DCs), thereby enhancing tumor immunogenicity and promoting immune responses.

Bioinformatics-based analysis of potential candidates chromatin regulators for immune infiltration in osteoarthritis.

Background: Through the bioinformatics analysis to screen out the potential chromatin regulators (CRs) under the immune infiltration of osteoarthritis (OA), thus providing some theoretical support for future studies of epigenetic mechanisms under OA immune infiltration.

Methods: By integrating CRs and the OA gene expression matrix, we performed weighted gene co-expression network analysis (WGCNA), differential analysis, and further screened Hub genes by protein-protein interaction (PPI) analysis. Using the OA gene expression matrix, immune infiltration extraction and quantification were performed to analyze the correlations and differences between immune infiltrating cells and their functions.

A transcriptome-wide association study provides new insights into the etiology of osteoarthritis.

Background: Osteoarthritis (OA) is a common clinical disease caused by a variety of factors, including genetic variants. Although genome-wide association studies (GWAS) have been performed to elucidate the genetic basis of OA, some loci of risk located in noncoding regions of the genome have been neglected. Therefore, we integrated multiple data types to detect the genetic component of gene expression in OA patients through transcriptome-wide association studies (TWAS) and summary-data-based Mendelian randomization (SMR) analysis.

Potential involvement of more than one locus in trait manifestation for individuals with Leber congenital amaurosis.

Leber congenital amaurosis (LCA) is a clinically and genetically heterogeneous retinal dystrophy. The causes of LCA have been unraveled partially at the molecular level. At least 14 genes have been reported that, when mutated, result in LCA.

Mutation survey of known LCA genes and loci in the Saudi Arabian population.

Purpose: The purpose of this study was to perform a comprehensive survey of all known Leber congenital amaurosis (LCA) genes and loci in a collection of 37 consanguineous LCA families from Saudi Arabia.

Methods: Direct PCR and sequencing were used to screen 13 known LCA genes (GUCY2D, CRX, RPE65, TULP1, AIPL1, CRB1, RPGRIP1, LRAT, RDH12, IMPDH1, CEP290, RD3, LCA5). In addition, families without mutations identified were further screened with STR markers around these 13 known LCA genes and two loci.

High-precision, whole-genome sequencing of laboratory strains facilitates genetic studies.

Whole-genome sequencing is a powerful technique for obtaining the reference sequence information of multiple organisms. Its use can be dramatically expanded to rapidly identify genomic variations, which can be linked with phenotypes to obtain biological insights. We explored these potential applications using the emerging next-generation sequencing platform Solexa Genome Analyzer, and the well-characterized model bacterium Bacillus subtilis.

Identification and functional analysis of ZIC3 mutations in heterotaxy and related congenital heart defects.

Mutations in the zinc finger transcription factor ZIC3 cause X-linked heterotaxy and have also been identified in patients with isolated congenital heart disease (CHD). To determine the relative contribution of ZIC3 mutations to both heterotaxy and isolated CHD, we screened the coding region of ZIC3 in 194 unrelated patients, including 61 patients with classic heterotaxy, 93 patients with heart defects characteristic of heterotaxy, and 11 patients with situs inversus totalis. Five novel ZIC3 mutations in three classic heterotaxy kindreds and two sporadic CHD cases were identified.