Objective To investigate the expression of prolyl hydroxylase 2(EGLN1) and solute carrier family 27 member 6(SLC27A6) in nasopharyngeal carcinoma(NPC) tissues, their correlation with stemness genes, and their prognostic significance. Methods A total of 132 NPC patients diagnosed and treated in the Department of Otolaryngology at Affiliated Hospital of Guizhou Medical University from March 2018 to March 2020 were selected as the research subjects. Quantitative real-time PCR(qPCR) was used to detect the m RNA expression levels of EGLN1, SLC27A6, and stemness-related genes [octamer-binding transcription factor 4(OCT4), sex-determining region Y box protein 2(SOX2), and NANOG]in NPC tissues,and Pearson correlation analysis was performed to assess their relationships. Immunohistochemistry was used to detect the protein expression of EGLN1 and SLC27A6 in NPC tissues. Kaplan-Meier survival analysis and Cox regression were used to identify risk factors affecting the prognosis of NPC patients. Results The m RNA expression levels of EGLN1, SLC27A6,OCT4, SOX2, and NANOG in NPC tissues were significantly higher than those in adjacent normal tissues(t/P = 46.841/<0.001, 44.102/<0.001, 46.396/<0.001, 52.522/<0.001, 45.576/<0.001). The m RNA expression of EGLN1 and SLC27A6 in NPC tissues was positively correlated with OCT4, SOX2, and NANOG(r = 0.708, 0.692, 0.669; 0.641, 0.721, 0.784, all P <0.001). The positive rates of EGLN1 and SLC27A6 protein expression in NPC tissues were 62.12%(82/132) and 60.61%(80/132), respectively, which were significantly higher than those in adjacent tissues [9.09%(12/132) and 6.06%(8/132)](χ2=80.951, 88.364, both P <0.001). The positive rates of EGLN1 and SLC27A6 in cancer tissues were significantly higher in NPC patients with TNM stage Ⅲ–Ⅳ than in those with stageⅠ–Ⅱ, and also higher in patients with lymph node metastasis than in those without lymph node metastasis(χ2/P = 31.034/<0.001, 14.314/<0.001, 5.811/0.016, 10.725/0.001). The 5-year survival rates of patients in the EGLN1-positive and EGLN1-negative groups were 56.10%(46/82) and 88.00%(44/50), respectively,with a statistically significant difference(Log-rank χ2= 14. 530, P = 0. 004). The 5-year survival rates of patients in the SLC27A6-positive and SLC27A6-negative groups were 55.00%(44/80) and 88.46%(46/52), respectively, with a statistically significant difference(Log-rank χ2= 15.860, P <0.001). TNM stage Ⅲ–Ⅳ, lymph node metastasis, EGLN1 positivity, and SLC27A6 positivity were independent risk factors affecting the prognosis of NPC patients [OR(95%CI) = 1.602(1.166-2.200), 1.540(1.242-1.911), 1.379(1.124-1.690), 1.302(1.075-1.578)]. Conclusion The expression of EGLN1 and SLC27A6 is upregulated in NPC and positively correlated with the expression of stemness-related genes, suggesting their potential as novel tumor markers for prognostic evaluation of NPC.

Objective To elucidate the molecular mechanism by which tyrosine phosphatase SHP2 regulates macrophage M2 polarization in the tumor microenvironment and its inhibitory effect on the invasion and metastasis of nasopharyngeal carcinoma(NPC). Methods The experiment was conducted in the laboratory of the Medical Research Center of Kailuan General Hospital in June 2024. A lentiviral vector overexpressing SHP2 was constructed and used to infect THP-1 monocytes to establish a stable macrophage model overexpressing SHP2(SHP2-THP-1). Cells were divided into blank control group,THP-1 group, and SHP2-THP-1 group, and co-cultured with conditioned medium from NPC CNE-1 cells. Quantitative realtime PCR(qRT-PCR) and Western blot were used to detect the expression of M2 polarization markers(IL-10, Arg1, CD163,CD206) and key proteins in the IL-6/STAT3 and PI3K/AKT signaling pathways. The effects of supernatants from each group on the migration and invasion abilities of CNE-1 cells were evaluated using wound healing and Transwell assays. Results Compared with the blank control group, the m RNA expression levels of M2 markers(IL-10, Arg1, CD163, CD206) in THP-1 cells treated with CNE-1 conditioned medium were significantly increased(P <0.05). Compared with the THP-1 group, the SHP2 overexpression group(SHP2-THP-1) showed a significant decrease in the expression of these M2 markers(P <0.05).Western blot analysis revealed that overexpression of SHP2 significantly inhibited the protein expression of IL-6, p-STAT3(Tyr705), p-PI3K, and p-AKT(Ser473)(P <0.05). Functional assays demonstrated that the migration rate and invasion number of CNE-1 cells were significantly higher in the THP-1 supernatant group than in the blank control group(P <0.05), whereas these parameters were significantly lower in the SHP2-THP-1 supernatant group compared with the THP-1 supernatant group(P <0.05). Conclusion SHP2 inhibits tumor microenvironment-induced M2 polarization of macrophages by suppressing IL-6/STAT3 and PI3K/AKT signaling, thereby attenuating NPC cell invasion and metastasis. These findings highlight the therapeutic potential of targeting the SHP2-immunometabolic axis in NPC.

We present three cases of autoimmune glial fibrillary acidic protein astrocytopathy(GFAP-A) with detailed clinical information and review the relevant literature.

This article reports the clinical data of 3 patients with Ig G4 hyper-secretory Castleman disease and reviews the relevant literature.

Alzheimer' s disease(AD) is a neurodegenerative disorder characterised primarily by progressive cognitive impairment and memory loss, with existing single-target drug treatments showing limited efficacy. Fufang Congrong Yizhi capsule exerts its pharmacological mechanisms through multi-component, multi-target interventions in AD pathological processes,including inhibition of β-amyloid deposition and tau protein phosphorylation, anti-neuroinflammation, antioxidative stress, and neuroprotection. This article aims to provide a reference for in-depth research and rational clinical application of Fufang Congrong Yizhi capsule, and to clarify the need for future large-scale, long-term randomised controlled trials to verify its long-term efficacy and safety, offering new approaches for AD treatment.