Objective To investigate the relationship between chromosome 6p copy number alterations (CNAs) and postoperative intrahepatic recurrence of hepatocellular carcinoma (HCC);and to screen for the target genes in CNA(s).Methods Array comparative genomic hybridization (CGH) and expression arrays were used to detect CNAs and differences in gene expression, respectively.The associations between CNAs in 6p and HCC recurrence were analyzed using the log-rank test, the Kaplan-Meier curves and the Cox proportional hazards models on 66 patients who had been follow-up for 2.6 ～ 73.3 months.The differentially expression of genes in the potentially recurrence-related CNAs were further evaluated by the MannWhitney U test on 117 HCCs, which included 109 cases with paired array CGH and expression data.Results 6p CNAs were detected in 46 (69.7％) of the 66 HCCs.Of the 8 CNAs with the most frequent recurrence of over 20％ , a gain at 6p21.1 was independently associated with a 2.3-fold (95％ CI =1.1 ～ 5.1, P ＜ 0.05) increased risk for intrahepatic recurrence and with a more pronounced 3.3-fold (95％ CI =1.4 ～ 8.2, P ＜0.05) risk for early recurrence (≤ 1 year).A panel of 9 genes, including BYSL and RPL7L1 within the documented 6p21.1, were observed to be upregulated in HCCs with 6p21.1 gain when compared with HCCs without (all P ＜ 0.05).A high BYSL expression significantly correlated with a larger tumor size (＞ 6 cm), vascular invasion and advanced tumor stage (all P ＜ 0.05), and high RPL7L1 expression significantly correlated with vascular invasion and advanced tumor stage (all P ＜ 0.05).Conclusion A gain at 6p21.1 was an independently prognostic marker for intrahepatic recurrence of postoperative HCC, particular for early recurrence, and BYSL and RPL7L1 might be the target genes in the recurrence-related 6p21.1 gain.

Tissue engineering bone technology, grounded in seed cells, cytokines, and scaffold supports, provides an effective solution for addressing extensive bone defects, demonstrating significant potentials in the field of bone repair. However, this technology still faces numerous challenges. Focusing on vascularization in engineered bones, this article reviews various methods to enhance vascularization within tissue-engineered bones, including multicellular co-culture, application of angiogenic factors, advanced 3D printing, and aid of surgical interventions. This article also analyses the latest research developments and the limitations of the methods, and speculates future research directions for tissue engineered bone.

Themedical's () infantgenre in western Hunan Province is one of the most famous infantgenres in China. Based on physiological and pathological characteristics of infants, generation-inhibition theory of five-elements andmedical's promotion-inhibition theory of five-meridians, theprotocol of "" was flexibly adjusted; according to different constitution types, including lung-deficiency type, spleen-deficiency type, kidney-deficiency type,-deficiency type,-deficiency type,-deficiency type, phlegm-wet type, phlegm-heat type, different protocols were adopted to prevent or reduce the asthma recurrence and reach the aim of regulating constitution and disease prevention.

OBJECTIVE: To analyze transforming growth factor-β1( TGF-β1)-induced differentially expressed genes( DEGs) in human embryonic lung fibroblast( IMR-90) using microarray,and to screen the key genes and signaling pathways related to trans-differentiation of fibroblast.METHODS: The gene chip GSE17518,attained from TGF-β1 stimulated IMR-90 cells,was downloaded from the Gene Expression Omnibus database.The DEGs were screened by GENE-E software.Then,the DEGs were imported into the DAVID online database for Gene Ontology( GO) functional enrichment analysis and Kyoto Encyclopedia of Genes and Genomes( KEGG) pathway enrichment analysis.The proteinprotein interaction( PPI) network was constructed and the hub genes were screened using STRING database and Cytoscape software.RESULTS: A total of 394 DEGs related to TGF-β1 stimulation were identified,including 171 down-regulated genes and 223 up-regulated genes.The results of GO analysis showed that the DEGs were widely distributed in cytoplasm,cell membrane,extracellular matrix( ECM) and exosomes,regulating biological functions such as ECM organization,cell migration and adhesion,cell proliferation and apoptosis.The results of the KEGG pathway analysis indicated that most of DEGs were enriched in cell focal adhesion,ECM-receptor interaction and phosphoinositide 3 kinase-Protein kinase B( PI3K-Akt) signaling pathways.The PPI network screened 10 core genes,included nucleolar protein 2( NOP2),succinate dehydrogenase B,glutamyl-prolyl-tRNA synthetase( EPRS),FtsJ homolog 3( FTSJ3),prefoldin subunit 4,Ras-related C3 botulinum toxin substrate 2,signal recognition particle receptor subunit beta,succinate-Co A ligase GDPforming beta subunit,pumilio RNA binding family member 3( KIAA0020),and general vesicular transport factor p115.NOP2,EPRS,FTSJ3,KIAA0020 were mainly distributed in M1 module.The NOP2 is the core gene with the highest number of nodes in M1 module.CONCLUSION: A total of 10 core differential genes and 7 signaling pathways related to TGF-β1 stimulation were screened.Among them,focal adhesion,ECM-receptor interaction,PI3K-Akt and NOP2,EPRS,FTSJ3,KIAA0020 may provide new direction for research of mechanisms of abnormal activation of fibrotic diseases including silicosis in incidence and development of multiple lung fibrotic diseases.

Radiotherapy (RT) can potentially induce systemic immune responses by initiating immunogenic cell death (ICD) of tumor cells. However, RT-induced antitumor immunologic responses are sporadic and insufficient against cancer metastases. Herein, we construct multifunctional self-sufficient nanoparticles (MARS) with dual-enzyme activity (GOx and peroxidase-like) to trigger radical storms and activate the cascade-amplified systemic immune responses to suppress both local tumors and metastatic relapse. In addition to limiting the Warburg effect to actualize starvation therapy, MARS catalyzes glucose to produce hydrogen peroxide (H₂O₂), which is then used in the Cu⁺-mediated Fenton-like reaction and RT sensitization. RT and chemodynamic therapy produce reactive oxygen species in the form of radical storms, which have a robust ICD impact on mobilizing the immune system. Thus, when MARS is combined with RT, potent systemic antitumor immunity can be generated by activating antigen-presenting cells, promoting dendritic cells maturation, increasing the infiltration of cytotoxic T lymphocytes, and reprogramming the immunosuppressive tumor microenvironment. Furthermore, the synergistic therapy of RT and MARS effectively suppresses local tumor growth, increases mouse longevity, and results in a 90% reduction in lung metastasis and postoperative recurrence. Overall, we provide a viable approach to treating cancer by inducing radical storms and activating cascade-amplified systemic immunity.