TERC (Telomerase RNA Component)

The activation of THP-1 cells induced by MPO protein directly impaired in vitro microvascular structure via increasing the expression of IL-6 and TNFα regulated by NF-κB p65 of THP-1 cells. Together, the noncatalytic functions entail MPO and PON in modulating the involvement of monocytes and endothelial cells in atherosclerosis.

By integrating germline (GWAS-based) and somatic evidence, this study provides a comprehensive view of HCC pathogenesis. This integrated strategy successfully identified a core set of genes and proteins with potential causal links to HCC, elucidating their functional convergence in cancer biology. These findings offer novel molecular insights and candidate targets for precise diagnosis, prognostic assessment, and targeted therapy of HCC, laying a solid foundation for future translational research.

Importantly, LTL was significantly associated with both OS and DFS (p = 0.008 and 0.044 respectively) in combined stage II and stage III patients. Our results show that LTL is predictive of OS and DFS for stage II and III CRC patients, particularly over a longer follow-up, extending beyond five years after a diagnosis of CRC, and certain SNPs in genes involved in telomere maintenance are significantly associated with patient outcomes, independent of telomere length.

Early-stage HCC induces a reversible, systemic immunosuppressive transcriptome captured by a monocyte-derived 23-gene blood signature; tumor removal partially restores this profile within three months. These results highlight the potential of blood-derived monocyte signatures as noninvasive biomarkers of HCC-associated immunosuppression and clinical outcome.

No difference was observed in the number of goblet cells between WT and TRPV6KO mice; however, the expression of intercellular junction proteins, including E-cadherin, claudin-3, and occludin, was significantly suppressed in TRPV6KO mice compared with WT mice. These findings suggest that TRPV6 protects against DSS-induced colitis, potentially by regulating epithelial barrier function through intracellular junction protein expressions.

Compared with the blank serum, JTG-CS showed increased content of 46 amino acids and decreased content of 20 amino acids. JTG-CS inhibited the proliferation, migration, invasion, and inflammation of FLS stimulated by TNF-α by inhibiting the activation of the PI3K/Akt pathway.

These findings reveal PERK-driven EMT as a key mechanism linking ER stress to glioma progression, with hypoxia reinforcing this axis. Targeting the PERK signaling axis or SPP1-CD44 interactions may offer novel therapeutic strategies against aggressive gliomas.

Many near-road and intersection locations harbor a high risk of exposure. The source-resolved, size-aware CFD-ELCR framework reveals strong spatial heterogeneity and age-dependent vulnerability that cannot be captured by sparse fixed-site monitoring alone, and it provides a transferable tool to identify traffic-related UFP risk hotspots and support targeted mitigation in dense urban microenvironments.

Blockade of S100A8/A9 with specific inhibitors effectively suppressed the development of TDI-induced asthma, suggesting that S100A8/A9-targeted therapy holds potential as a clinical intervention for patients with MGA.

Hirudin inhibits hematogenous metastasis of breast cancer through suppression of HIF-1α-controlled DSG2-mediated desmosome junctions, ultimately leading to the disintegration of CTC clusters. Our findings highlight the therapeutic potential of targeting HIF-1α-controlled DSG2-mediated desmosome junction conversion and position hirudin as a promising CTC clusters dissociator optimized for the clinical prevention of breast cancer metastasis.

RNH1 acts as a biomarker for CRC, influencing tumor growth via disulfidptosis, tumor microenvironment alterations, and metabolic pathways. Its high expression correlates with immune escape. This study suggests RNH1 as a potential therapeutic target for CRC, warranting further exploration of its mechanistic roles and treatment potential.

Overexpressed ESM1 may mediate a reduced level of immune cell infiltration in TME through immune signalling pathways. ESM1 can be used as a predictive biomarker for immune-related and clinical progression in BC.