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Introduction: Dermatofibrosarcoma protuberans (DFSP) is a slow-growing cutaneous neoplasm with high cure rates following complete surgical resection. However, 5-15% of classic DFSP cases undergo fibrosarcomatous transformation, resulting in fibrosarcomatous DFSP (FS-DFSP), a more aggressive variant with significantly higher rates of local recurrence, metastasis, and mortality. This case presents a rare myxoid variant of FS-DFSP with complex anatomical involvement requiring multidisciplinary management. Case Presentation: A 56-year-old female presented with a giant recurrent chest mass measuring 15 × 12 × 6 cm, initially misdiagnosed as fibroma 19 years prior. Advanced imaging revealed an 8 × 13 × 12 cm poorly defined soft tissue mass involving the pectoralis major and extending to the sternocleidomastoid muscles, with compression of the proximal right jugular vein. Histopathological examination confirmed FS-DFSP with myxoid differentiation, characterized by diffuse spindle cell infiltration in a herringbone pattern. Immunohistochemistry revealed CD34+, EMA+, and Actin+ staining with negative desmin, S100, and STAT-6. COL1A1-FISH analysis demonstrated COL1A1/PDGFB fusion in 8% of cells. Management included tumor vascular embolization, surgical resection with 3 cm margins, skin grafting, local flap repair, and adjuvant radiation therapy due to anatomical constraints and residual tumor involvement of the anterior sternum. Conclusion: This case highlights the myxoid variant of FS-DFSP, emphasizing the importance of comprehensive histopathological evaluation, multidisciplinary treatment planning, and long-term surveillance. The successful management with combined surgical and radiation therapy demonstrates the need for individualized treatment approaches in complex anatomical locations. Four-year follow-up shows no evidence of recurrence, supporting the efficacy of aggressive multimodal therapy in preventing local recurrence in FS-DFSP.

Background Accumulating evidence shows that long noncoding RNAs (lncRNAs) are important regulator molecules involved in diverse biological processes. Acquired drug resistance is a major challenge in the clinical treatment of glioblastoma (GBM), and lncRNAs have been shown to play a role in chemotherapy resistance. However, the underlying mechanisms by which lncRNA mediates TMZ resistance in GBM remain poorly characterized. Methods Quantitative reverse transcription PCR (qRT-PCR) and fluorescence in situ hybridization assays were used to detect small nucleolar RNA host gene 12 (SNHG12) levels in TMZ-sensitive and TMZ-resistant GBM cells and tissues. The effects of SNHG12 on TMZ resistance were investigated through in vitro assays (western blots, colony formation assays, flow cytometry assays, and TUNEL assays). The mechanism mediating the high expression of SNHG12 in TMZ-resistant cells and its relationships with miR-129-5p, mitogen-activated protein kinase 1 (MAPK1), and E2F transcription factor 7 (E2F7) were determined by bioinformatic analysis, bisulfite amplicon sequencing, methylation-specific PCR, dual luciferase reporter assays, chromatin immunoprecipitation assays, RNA immunoprecipitation assays, immunofluorescence, qRT-PCR, and western blot. For in vivo experiments, an intracranial xenograft tumor mouse model was used to investigate SNHG12 function. Results SNHG12 was upregulated in TMZ-resistant cells and tissues. Overexpression of SNHG12 led to the development of acquired TMZ resistance, while knockdown of SNHG12 restored TMZ sensitivity. An abnormally low level of DNA methylation was detected within the promoter region of SNHG12, and loss of DNA methylation made this region more accessible to the Sp1 transcription factor (SP1); this indicated that methylation and SP1 work together to regulate SNHG12 expression. In the cytoplasm, SNHG12 served as a sponge for miR-129-5p, leading to upregulation of MAPK1 and E2F7 and endowing the GBM cells with TMZ resistance. Disinhibition of MAPK1 regulated TMZ-induced cell apoptosis and the G1/S cell cycle transition by activating the MAPK/ERK pathway, while E2F7 dysregulation was primarily associated with G1/S cell cycle transition. Clinically, SNHG12 overexpression was associated with poor survival of GBM patients undergoing TMZ treatment. Conclusion Our results suggest that SNHG12 could serve as a promising therapeutic target to surmount TMZ resistance, thereby improving the clinical efficacy of TMZ chemotherapy.

Several commercial seismometers now support CSTP, the real-time communication protocol used in the China Earthquake Early Warning System, but there is still no simple, flexible, and low-cost solution to archive CSTP streams or integrate them into existing data processing systems. In this study, we design and implement SharpCEEWPServer, a lightweight, out-of-the-box graphical server that integrates client management, real-time data reception, visualization, and archiving, and can, via RingServer, convert CSTP real-time streams into widely supported SeedLink streams. Hardware compatibility is evaluated using four commercial CSTP-capable instruments, a forwarding chain is built to assess forwarding functionality and reliability, and concurrency performance is tested using simulated networks with different station counts. The stability under network impairment scenarios and the performance of the forwarding system were also analyzed. The results show that the server can reliably receive and forward real-time data streams, and that laptop-class hardware is sufficient to withstand the load imposed by an M7.0 earthquake scenario when receiving real-time streams from 1000 three-component seismometers. However, the current version’s latency performance can only meet the needs of non-early warning networks. Overall, the proposed server significantly lowers the deployment and usage threshold for new CSTP-capable instruments and provides an efficient, low-cost integration solution for temporary networks in earthquake emergency response and seismic arrays.

The development of lymphoma is a complex multistep process that integrates numerous experimental findings and clinical data that have not yet yielded a definitive explanation. Studies of oncogenic viruses can help to deepen insight into the pathogenesis of lymphoma, and identifying associations between lymphoma and viruses that are established and unidentified should lead to cellular and pharmacologically targeted antiviral strategies for treating malignant lymphoma. This review focuses on the pathogenesis of lymphomas associated with hepatitis B and C, Epstein-Barr, and human immunodeficiency viruses as well as Kaposi sarcoma-associated herpesvirus to clarify the current status of basic information and recent advances in the development of virus-associated lymphomas.

Long noncoding RNAs (lncRNAs) are involved in glioma initiation and progression. Glioma stem cells (GSCs) are essential for tumor initiation, maintenance, and therapeutic resistance. However, the biological functions and underlying mechanisms of lncRNAs in GSCs remain poorly understood. Here, we identified that LINC00839 was overexpressed in GSCs. A high level of LINC00839 was associated with GBM progression and radiation resistance. METTL3-mediated m6A modification on LINC00839 enhanced its expression in a YTHDF2-dependent manner. Mechanistically, LINC00839 functioned as a scaffold promoting c-Src-mediated phosphorylation of β-catenin, thereby inducing Wnt/β-catenin activation. Combinational use of celecoxib, an inhibitor of Wnt/β-catenin signaling, greatly sensitized GSCs to radiation. Taken together, our results showed that LINC00839, modified by METTL3-mediated m6A, exerts tumor progression and radiation resistance by activating Wnt/β-catenin signaling.

Capacitive deionization (CDI) is considered a promising technology for desalination of sea or brackish water. In this study, a ZnS/g-C3N4 composite was synthesized through a one-step high-temperature method and used as the main material to fabricate CDI electrodes. The results of SEM and TEM showed that spherical-like nanoparticles of ZnS were uniformly distributed on the g-C3N4 sheet. The g-C3N4 phase facilitates the ZnS particles precipitate and restrain their agglomeration, which contributes to a high specific surface area of ZnS. Furthermore, the electrochemical test results indicated that ZnS/g-C3N4 composite had a good capacitance characteristic, low resistance, and high electrochemical stability. Finally, the desalinization performance of the ZnS/g-C3N4 composite electrodes was tested in traditional mode and membrane capacitive deionization (MCDI) mode. The results showed that ZnS/g-C3N4//ZnS/g-C3N4 (MCDI) exhibited an optimal desalination capacity. The adsorption amount was 27.65, 50.26, and 65.34 mg/g for NaCl initial concentration of 200, 400, and 600 mg/L, respectively, with the voltage of 1.2 V and flow rate of 5 mL/min. Increasing initial concentration enhanced the conductivity and ion migration rate so as to increase the NaCl adsorption amount. ZnS/g-C3N4 composite can be used as potential electrode material for high performance of MCDI.

Glioblastoma (GBM) is the most lethal primary brain tumor with intra-tumoral hierarchy of glioblastoma stem cells (GSCs). The heterogeneity of GSCs within GBM inevitably leads to treatment resistance and tumor recurrence. Molecular mechanisms of different cellular state GSCs remain unclear. Here, we find that classical (CL) and mesenchymal (MES) GSCs are enriched in reactive immune region and high CL-MES signature informs poor prognosis in GBM. Through integrated analyses of GSCs RNA sequencing and single-cell RNA sequencing datasets, we identify specific GSCs targets, including MEOX2 for the CL GSCs and SRGN for the MES GSCs. MEOX2-NOTCH and SRGN-NFκB axes play important roles in promoting proliferation and maintaining stemness and subtype signatures of CL and MES GSCs, respectively. In the tumor microenvironment, MEOX2 and SRGN mediate the resistance of CL and MES GSCs to macrophage phagocytosis. Using genetic and pharmacologic approaches, we identify FDA-approved drugs targeting MEOX2 and SRGN. Combined CL and MES GSCs targeting demonstrates enhanced efficacy, both in vitro and in vivo. Our results highlighted a therapeutic strategy for the elimination of heterogeneous GSCs populations through combinatorial targeting of MEOX2 and SRGN in GSCs. The molecular mechanisms underlying the function of different cellular states in glioblastoma stem cells (GSCs) remain poorly understood. Here, the authors perform integrated single cell and bulk analysis of GSCs and identify potential therapeutic targets.

To date, the effects of ocean acidification on toxic metals accumulation and the underlying molecular mechanism remains unknown in marine bivalve species. In the present study, the effects of the realistic future ocean p CO 2 levels on the cadmium (Cd) accumulation in the gills, mantle and adductor muscles of three bivalve species, Mytilus edulis , Tegillarca granosa and Meretrix meretrix, were investigated. The results obtained suggested that all species tested accumulated significantly higher Cd ( p  < 0.05) in the CO 2 acidified seawater during the 30 days experiment and the health risk of Cd (based on the estimated target hazard quotients, THQ) via consumption of M. meretrix at pH 7.8 and 7.4 significantly increased 1.21 and 1.32 times respectively, suggesting a potential threat to seafood safety. The ocean acidification-induced increase in Cd accumulation may have occurred due to (i) the ocean acidification increased the concentration of Cd and the Cd 2+ /Ca 2+ in the seawater, which in turn increased the Cd influx through Ca channel; (ii) the acidified seawater may have brought about epithelia damage, resulting in easier Cd penetration; and (iii) ocean acidification hampered Cd exclusion.

The aim of the study was to assess the association between the geriatric nutritional risk index (GNRI) and incidence of CKD progression, all-cause mortality, and cardiovascular events in the elderly patients with chronic kidney disease (CKD) before dialysis initiation. We performed a post hoc analysis of the CKD-ROUTE database, which included 538 pre-dialysis CKD patients aged ≥65 years in this prospective cohort study. Associations between GNRI and clinical outcomes were estimated using Cox proportional hazards model analysis. Multivariable linear mixed regression models with random intercepts were used to assess the association between GNRI and estimated glomerular filtration rate (eGFR) decline per year. During the median follow-up period of 2.92 years, there were 123 (22.86%) CKD progression events, 44 (8.18%) deaths, and 76 (14.13%) cardiovascular events. After adjusting for multiple confounding factors, the hazard ratios (HRs) for CKD progression in patients with GNRI <92 were 1.99 (95% CI, 1.34-2.97;  < 0.001), when compared with a GNRI of ≥92. Patients with a lower GNRI also had a significantly greater rate of eGFR decline over time than well-nourished patients (mean annual difference, -1.69; 95% CI, -2.62 to -0.77;  < 0.001). In the secondary outcomes, this association was consistent for all-cause mortality. Moreover, the associations were generally consistent across several subgroup and sensitivity analyses. The lower GNRI is significantly associated with higher risks of renal prognosis and all-cause mortality in elderly patients with CKD.

Background Glucose metabolic reprogramming is a significant hallmark of malignant tumors including GBM. Previous studies suggest that microRNAs play key roles in modulating this process in GBM cells. miR-181b acts as a tumor suppressor miRNA in influencing glioma tumorigenesis. Our previous results showed that miR-181b was down-regulated in glioma cells and tissues. Methods The extracellular acidification rate (ECAR), colony formation assay and levels of Glut1 and PKM2 were measured to assess the glucose metabolic and proliferation changes in GBM cells overexpressing miR-181b. Immunoblotting and luciferase reporter assay were performed to confirm the expression and role of SP1 as a direct target of miR-181b. ChIP assay was used to figure out the transcriptional regulation of SP1 on Glut1 and PKM2. In vivo study was examined for the role of miR-181b in GBM cells. Results MiR-181b overexpression significantly reduced the glucose metabolic and colony formation ability of GBM cells. And, SP1 was confirmed as a direct target of miR-181b while upregulation of SP1 could reverse the influence of overexpression of miR-181b. Furthermore, Glut1 and PKM2 could be regulated by SP1. Finally, miR-181b could inhibit the tumor growth in vivo. Conclusions Our article demonstrated the inhibitory effect of miR-181b on glucose metabolism and proliferation in GBM by suppressing SP1 expression.