Search Results (148)

The methanol oxidation reaction (MOR) of direct methanol fuel cells (DMFCs) is limited by the slow kinetic process and high reaction energy barrier, significantly restricting the commercial application of DMFCs. Therefore, developing MOR catalysts with high activity and stability is very important. In this paper, oxygen-functionalised activated carbon (FAC) with controllable oxygen-containing functional groups was prepared by adjusting the volume ratio of H₂SO₃/HNO₃ mixed acid, and Pd/AC and Pd/FAC catalysts were synthesised via the hydrazine hydrate reduction method. A series of characterisation techniques and electrochemical performance tests were used to study the catalyst. The results showed that when V(H₂SO₃):V(HNO₃) = 2:3, more defects were generated on the surface of the AC, and more oxygen-containing functional groups represented by C=O and C–OH were attached to the surface of the support, which increased the anchor sites of Pd and improved the dispersion of Pd nanoparticles (Pd NPs) on the support. At the same time, the mass–specific activity of Pd/FAC for MOR was 2320 mA·mg_Pd, which is 1.5 times that of Pd/AC, and the stability was also improved to a certain extent. In situ infrared spectroscopy further confirmed that oxygen functionalisation treatment promoted the formation and transformation of *COOH intermediates, accelerated the transformation of CO_L into CO_B, reduced the poisoning of CO_ads species adsorbed to the catalyst, optimised the reaction path and improved the catalytic kinetic performance. Full article

Post-traumatic stress disorder (PTSD) has traditionally been viewed as a psychiatric disorder of fear, memory, and emotional regulation. However, growing evidence implicates systemic and neuroinflammation as key contributors. Individuals with PTSD often exhibit elevated blood levels of pro-inflammatory cytokines such as IL-1β, IL-6, TNF-α, and C-reactive protein, indicating immune dysregulation. Dysfunctions in the hypothalamic–pituitary–adrenal (HPA) axis marked by reduced cortisol levels impair the body’s ability to regulate inflammation, allowing persistent immune activation. Circulating cytokines cross a weakened blood–brain barrier and activate microglia, which release additional inflammatory mediators. This neuroinflammatory loop can damage brain circuits critical to emotion processing including the hippocampus, amygdala, and prefrontal cortex, and disrupt neurotransmitter systems like serotonin and glutamate, potentially explaining PTSD symptoms such as hyperarousal and persistent fear memories. Rodent models of PTSD show similar inflammatory profiles, reinforcing the role of neuroinflammation in disease pathology. Bromo-epi-androsterone (BEA), a synthetic analog of dehydroepiandrosterone (DHEA), has shown potent anti-inflammatory effects in clinical trials, significantly reducing IL-1β, IL-6, and TNF-α. By modulating immune activity, BEA represents a promising candidate for mitigating neuroinflammation and its downstream effects in PTSD. These findings support the rationale for initiating clinical trials of BEA as a novel therapeutic intervention for PTSD. Full article

Background/Objectives: CD318 (also known as CDCP1) is a transmembrane protein that is overexpressed in many cancers and contributes to tumor progression, invasion, and metastasis by activating SRC family kinases through phosphorylation. Emerging evidence also suggests that CD318 plays a role in modulating the tumor immune microenvironment, although its precise mechanism in tumor progression is still not well understood. Methods: To investigate this, we analyzed the expression and immune-related functions of CD318 using the publicly available data from The Cancer Genome Atlas (TCGA) across colorectal adenocarcinoma (COAD), cervical squamous cell carcinoma (CESC), lung adenocarcinoma (LUAD), and pancreatic adenocarcinoma (PAAD). Results: All four cancers exhibited a high level of CD318 expression. Notably, in CESC, LUAD, and PAAD, plasmin-mediated cleavage of CD318 leads to phosphorylation of SRC and protein kinase C delta (PKCδ), which activates HIF1α and/or p38 MAPK. These downstream effectors translocate to the nucleus and promote the transcriptional upregulation of TGFβ1, fostering an immunosuppressive tumor microenvironment through Treg cell recruitment. In contrast, this signaling cascade appears to be absent in COAD. Instead, our analysis indicate that intact CD318 in COAD interacts with the surface receptors CD96 and CD160, which are found on CD8⁺ T cells and NK cells. Conclusions: This interaction enhances cytotoxic immune responses in COAD by promoting CD8⁺ T cell and NK cell activity, offering a possible explanation for the favorable prognosis associated with high CD318 expression in COAD, compared to the poorer outcomes observed in CESC, LUAD, and PAAD. Full article

Ulcerative colitis (UC) is a chronic inflammatory bowel disease characterized by mucosal inflammation and debilitating symptoms that considerably impair life quality. UC is particularly prevalent in younger populations, where early diagnosis remains challenging owing to nonspecific symptoms and the potential progression to colitis-associated cancer (CAC). The GSE177044 dataset, consisting of whole blood samples, was analyzed to identify differentially expressed genes, perform gene annotation, analyze key signaling pathways, and detect key hub genes in UC using protein–protein interaction networks. Multiple UC datasets composed of colonic samples were used for validation and examination of methylation and age-related gene expression patterns. Further analyses were performed to explore the association between these key hub genes and colon adenocarcinoma (COAD). We identified four key hub genes—lipocalin-2 (LCN2), matrix metalloproteinase-9 (MMP9), S100 calcium-binding protein A9 (S100A9), and olfactomedin-4 (OLFM4)—significantly up-regulated in UC, with S100A9 showing epigenetic regulation and age-dependent expression patterns. Additionally, S100A9 was strongly associated with poor prognosis in COAD, displaying hypo-methylation and elevated expression, especially in myeloid cell types, and links to altered immune and molecular subtypes. Our findings confirmed the hypo-methylation-driven up-regulation of LCN2, S100A9, and OLFM4 in UC, suggesting their potential as blood-based diagnostic biomarkers. Notably, S100A9 has emerged as a promising biomarker for the early diagnosis of ulcerative colitis, particularly in pediatric and adolescent patients with UC. Moreover, S100A9 holds potential as a precision target to prevent progression from UC to CAC. Full article

Background: Colorectal cancer (CRC) heterogeneity is strongly influenced by molecular subtypes and tumor stroma interactions. The meprin/A5/PTPmu (MAM) domain, a conserved structural motif in transmembrane proteins, remains undercharacterized in CRC pathogenesis. Methods: We analyzed RNA-seq data from TCGA-COAD to evaluate MAM domain gene expression. Immunohistochemistry and Western blotting were conducted to validate the results of the database analysis. Results: Bioinformatics analysis revealed that MAM domain-containing protein 2 (MAMDC2) was enriched in mesenchymal subtype 4 (CMS4) colorectal cancer (p < 0.001). IHC confirmed MAMDC2 overexpression in MSS colorectal cancer with a high tumor stroma ratio (TSR) and peritoneal metastatic lesions (p < 0.01). WB and real-time PCR analyses confirmed that MAMDC2 has a role in regulating epithelial–mesenchymal transition (EMT) development in CRC. Importantly, we identified that cancer cell-derived MAMDC2 promotes MYLK expression in cancer-associated fibroblasts (CAFs) through paracrine signaling. Conclusions: Our findings suggest MAMDC2 may function as a stromal-associated regulator in MSS colorectal cancer with a high tumor stromal ratio (TSR). Full article

Background: Colorectal cancer (CRC) ranks as the third most prevalent cancer globally, with its incidence and recurrence rates steadily rising. To explore the relationship between CRC and longevity-associated genes (LAGs), and to offer new therapeutic avenues for CRC treatment, we developed a prognostic model based on these genes to predict the outcomes for CRC patients. Additionally, we conducted an immune correlation analysis. Methods: We conducted a comprehensive analysis of the effects of 81 LAGs in CRC by integrating multiple omics datasets. This analysis led to the identification of two distinct molecular subtypes and revealed that alterations in LAGs across various layers were linked to clinicopathological features, prognosis, and cell infiltration characteristics within the tumor microenvironment (TME). The training and validation cohorts for the models were derived from the TCGA-COAD, TCGA-READ, and GSE35279 datasets. Subsequently, we developed a risk score model, and the Kaplan–Meier method was employed to estimate overall survival (OS). Ultimately, we established a prognostic model based on five LAGs: BEDN3, EXOC3L2, CDKN2A, IL-13, and CAPN9. Furthermore, we assessed the correlations between the risk score and factors such as immune cell infiltration, microsatellite instability, and the stem cell index. Results: Our comprehensive bioinformatics analysis revealed a strong association between longevity genes and CRC. The risk score derived from the five newly identified LAGs was determined to be an independent prognostic factor for CRC. Patients categorized by this risk score demonstrated significant differences in immune status and microsatellite instability. Conclusions: Our comprehensive multi-omic analysis of LAGs highlighted their potential roles in the tumor immune microenvironment, clinicopathological features, and prognosis, offering new insights for the treatment of CRC. Full article

Background/Objectives: Colon adenocarcinoma (COAD), the most prevalent form of colorectal cancer, remains a leading cause of cancer-related mortality. Advances in various treatments for COAD have significantly improved treatment outcomes. However, therapeutic limitations persist, highlighting the need for personalized strategies driven by novel biomarkers. The aim was to identify key hub genes that could be potential biomarkers of COAD using comprehensive bioinformatic analyses. Methods: Differentially expressed genes (DEGs) and co-DEGs were identified from COAD gene expression datasets. Functional enrichment analyses, including Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis, were performed. Hub genes were extracted from protein–protein interaction (PPI) networks and validated epigenetically using microRNA (miRNA) and DNA methylation datasets. Their expression patterns were further examined via single-cell RNA sequencing (scRNA-seq) and immune cell infiltration analysis. Prognostic relevance was assessed based on tumor metastasis and survival outcomes. Results: Gene expression profiling identified 118 co-DEGs, with GO and KEGG pathway analyses revealing significant pathway enrichment. PPI network analysis pinpointed 27 key co-DEGs. Epigenetic profiling indicated that both miRNA interference and DNA methylation regulate CLDN1, INHBA, and CXCL12 expression levels. scRNA-seq analysis showed elevated CLDN1 expression in epithelial cells and INHBA in myeloid cells, and reduced CXCL12 expression in stromal cells. Prognostic analysis further demonstrated that CLDN1 and INHBA are significantly associated with poor COAD outcomes. Conclusions: We identified some potential prognostic biomarkers for patients with COAD. Further experimental validation is required to translate these findings into precision medicine for COAD. Full article

Aquaponics integrates aquaculture and hydroponics, promoting circularity through the recirculation of water and nutrients. However, waste management remains a challenge. This study aimed to evaluate the anaerobic digestion (AD) of aquaponic effluent (AE) combined with cattle manure (CM) for biogas production. An Indian model biodigester was fed with AE, CM and 1:1, 1:3, and 3:1 W (Water):CM, under anaerobic mono-digestion (MoAD) and 1:1, 1:3, and 3:1 AE:CM under anaerobic co-digestion (CoAD) conditions. The chemical characteristics of the substrates and digestates were assessed, as well as the potential for biogas production over 19 weeks. Overall, CoAD provided better results regarding the chemical characterization of the substrates aimed at biogas production. Notably, the 1:3 AE:CM ratio resulted in the most promising outcomes among the tested conditions. This ratio demonstrated higher efficiency, initiating biogas production by the third week and reaching the highest accumulated volume. It is probable that AE increased the dissolved organic load, optimizing the conversion of organic matter and eliminating the need for additional water in the process. Thus, the CoAD of AE and CM emerged as a promising alternative for waste valorization in aquaponics, contributing to renewable energy generation, agricultural sustainability, and the promotion of the circular economy. Full article

SPS is characterized by progressive spasmodic muscular rigidity. SPS is thought to be an autoimmune disease with a prominent feature of antibodies against glutamic acid decarboxylase (GAD). GAD is responsible for the enzymatic conversion of glutamic acid (glutamate) into the inhibitory neurotransmitter gamma-aminobutyric acid (GABA). Reduced GABA activity leads to increased excitability in the central nervous system, resulting in muscle rigidity and spasms characteristic of SPS. While SPS is rare, anti-GAD antibodies seen in SPS are also seen in the much more common autoimmune disease, type 1 diabetes (T1D). There is evolving research showing that the anti-GAD antibodies of T1D are produced in response to the presence of mycobacterial heat shock protein 65 (mHSP65), and the mHSP65 is produced in response to an occult infection by a bacterium, Mycobacterium avium subspecies Paratuberculosis (MAP). Humans are broadly exposed to MAP in food, water, and air. There are linear and conformational similarities between the epitopes of GAD and mHSP65. This article proposes that MAP is also an infectious trigger for SPS. Dehydroepiandrosterone (DHEA) is a principal component of the steroid metabolome; it plateaus in young adults and then steadily declines. Bromo-epi-androsterone (BEA) is a potent synthetic analog of DHEA; unlike DHEA, it is non-androgenic, non-anabolic, and an effective modulator of immune dysregulation. BEA is also an anti-infective agent and has been shown to benefit mycobacterial infections, including tuberculosis and leprosy. With the immune stabilizing capacity of BEA as well as its anti-mycobacterial properties, there is reason to believe that a randomized clinical trial with BEA may be beneficial for SPS. Full article

Pt catalysts are investigated for methanol oxidation in direct methanol fuel cells, utilizing the electrochemical quartz microbalance method (EQCM) with exceptional resolution and sensitivity. Pt catalysts were deposited onto the gas-diffusion layer of carbon using stationary potential electrodeposition. Physical characterization and electrochemical tests were performed. SEM results showed that Pt presented dendrite crystals with nanoscale facets. Cyclic voltammetry (CV) demonstrated that the current density for the methanol oxidation reaction highly reached 1020 mA·cm⁻² for the deposited Pt catalyst by EQCM. The dendrite crystal structures of deposited Pt provide much area for high catalytic activity. It found that the peak density of the Pt catalysts for the methanol oxidation reaction decreased after five cycles. Furthermore, the response frequency for the adsorption of the deposited Pt catalysts was investigated using EQCM and compared with commercial PtRu catalysts. The results showed that the response frequency of the Pt catalysts decreased more rapidly than that of the PtRu catalysts. It is possible for the adsorption of small organic molecules on Pt catalysts to occur during the methanol electro-oxidation with CO_ad intermediates. The reaction mechanism is preliminarily discussed by the electrochemical measurement combined with EQCM. Full article

Colon adenocarcinoma (COAD) demonstrates significant clinical heterogeneity across disease stages, gender, and age groups, posing challenges for unified therapeutic strategies. This study establishes a multi-dimensional stratification framework through integrative analysis of miRNA–gene co-expression networks, employing the MRNETB algorithm coupled with Markov flow entropy (MFE) centrality quantification. Analysis of TCGA-COAD cohorts revealed stage-dependent regulatory patterns centered on CDX2-hsa-miR-22-3p-MUC13 interactions, with progressive dysregulation mirroring tumor progression. Gender-specific molecular landscapes have emerged, characterized by predominant SLC26A3 expression in males and GPA33 enrichment in females, suggesting divergent pathogenic mechanisms between genders. Striking age-related disparities were observed, where early-onset cases exhibited molecular signatures distinct from conventional COAD, highlighted by marked XIST expression variations. Drug-target network analysis identified actionable candidates including CEACAM5-directed therapies and differentiation-modulating agents. Our findings underscore the critical need for heterogeneity-aware clinical decision-making, providing a roadmap for stratified intervention paradigms in precision oncology. Full article

Despite being the leading cause of death worldwide, cancer still lacks precise biomarkers for effective targeting, limiting efforts to reduce mortality rates. This review explores the role and clinical significance of a newly identified long non-coding RNA, MYOSLID, in cancer progression. MYOSLID has emerged as a critical modulator in cancer progression by influencing key hallmarks such as proliferation, immune evasion, metastasis, and metabolic reprogramming. It promotes tumor cell growth by stabilizing hypoxia-inducible factor 1 and acting as a competing endogenous RNA (ceRNA) to sequester tumor-suppressive microRNAs like miR-29c-3p, thereby enhancing oncogene expression. It facilitates immune evasion by upregulating PD-L1, suppressing T cell activation, and modulating necroptosis pathways involving RIPK1 and RIPK3. Additionally, MYOSLID drives metastasis by regulating epithelial–mesenchymal transition markers such as LAMB3 and Slug while promoting RAB13-mediated cytoskeletal remodeling and enhancing cancer cell invasion. We have obtained the expression of MYOSLID from TCGA and the ENCORI database. The expression of colorectal adenocarcinoma (COAD) and head and neck squamous cell carcinoma (HNSCC) is associated with poor prognosis and lower survival rate. Given its significant potential as a diagnostic biomarker and therapeutic target, further research is required to elucidate its precise molecular mechanisms and therapeutic applications in cancer treatment. Full article

The shedding of leaves by Posidonia oceanica (P. oceanica) in autumn results in the accumulation of shoreline debris, contributing to significant economic, social, and environmental problems. Due to the lack of alternative solutions, this waste biomass is disposed of in landfills, incurring an economic cost for the disposal process. In the context of the circular economy, anaerobic digestion (AD) can serve as a highly efficient biological alternative for treating and valorizing wastes with a high organic load. The aim of this research was to comparatively evaluate the performance and kinetics of the AD of ashore P. oceanica biomass and its anaerobic co-digestion (co-AD) with different nitrogen-rich co-substrates. To evaluate the effect of the nitrogen source in the co-AD system, peptone, casein, synthetic casein, urea, and the microalgae Raphidocelis subcapitata were used as co-substrates in biomethanization tests at a mesophilic temperature (35 ± 2 °C). The lowest methane yield was achieved for the sole AD of P. oceanica (79 ± 3 NL CH₄ kg⁻¹ VS), while the highest yields were found for the three co-ADs of P. oceanica with proteins (i.e., peptone, casein, and synthetic casein), showing no significant differences among them (380 ± 30 − 420 ± 30 NL CH₄ kg⁻¹ VS). Additionally, the first-order kinetics and the transference function model were proven and allowed for adequately fitting the experimental results of methane production with time. Full article

Lecithin cholesterol acyltransferase (LCAT) is a crucial enzyme in high-density lipoprotein (HDL) metabolism that is often dysregulated in cancers, affecting tumor growth and therapy response. We extensively studied LCAT expression in various malignancies, linking it to clinical outcomes and genetic/epigenetic alterations. We analyzed LCAT expression in multiple cancers and used the Cox regression model to correlate it with patient survival metrics, including overall survival (OS), disease-specific survival (DSS), and progression-free interval (PFI). We also examined the copy number variations (CNVs), single-nucleotide variations (SNVs), DNA methylation, and N6-methyladenosine (m6A) modifications of LCAT and their connections to tumor immune responses and drug sensitivity. LCAT expression varies among cancers and correlates with patient outcomes. Low expression is linked to poor prognosis in low-grade glioma (LGG) and liver hepatocellular carcinoma (LIHC), while high expression is associated with better outcomes in adrenocortical carcinoma (ACC) and colon adenocarcinoma (COAD). In kidney renal papillary cell carcinoma (KIRP) and uterine corpus endometrial carcinoma (UCEC), LCAT CNV and methylation levels are prognostic markers. LCAT interacts with m6A modifiers and immune molecules, suggesting a role in immune evasion and as a biomarker for immunotherapy response. LCAT expression correlates with chemotherapeutic drug IC50 values, indicating potential for predicting treatment response. In ACC and COAD, LCAT may promote tumor growth, while in LGG and LIHC, it may inhibit progression. LCAT expression and activity regulation could be a new cancer therapy target. As a key molecule linking lipid metabolism, immune modulation, and tumor progression, the potential of LCAT in cancer therapy is significant. Our findings provide new insights into the role of LCAT in cancer biology and support the development of personalized treatment strategies. Full article