Contribution of sphingomyelin phosphodiesterase acid-like 3B to the proliferation, migration, and invasion of ovarian cancer cells.

Background: Cancer has the highest mortality rate among gynecological cancers and poses a serious threat to women's lives. However, the treatment options for ovarian cancer are still limited, and exploring effective targeted biomarkers is particularly important for predicting and treating ovarian cancer. Therefore, it is necessary to explore the molecular mechanisms of the occurrence and development of ovarian cancer. Methods: This investigation encompassed the analysis of gene expression profiles, measurement of transcription levels of potential target genes in peripheral blood samples from ovarian cancer patients and characterization of the ovarian cancer-related secretory protein sphingomyelin phosphodiesterase acid-like 3B (SMPDL3B). Through bioinformatics analysis, potential target genes were identified, and their association with overall survival (OS) and progression-free survival (PFS) in ovarian cancer patients was assessed utilizing relevant databases. Subsequently, differences in target gene expression in ovarian cancer tissue samples were validated through protein blotting and quantitative real-time PCR (qRT-qPCR). Cell proliferation assays using the cell count kit-8 (CCK-8) method, as well as transwell chamber assay and pre coated matrix gel chamber assay were employed to elucidate the role of SMPDL3B in ovarian cancer cell migration and invasion. Results: This study revealed a substantial upregulation of SMPDL3B in the serum of ovarian cancer patients, correlating with an unfavorable prognosis. High SMPDL3B expression was linked not only to increased proliferation of ovarian cancer cells, but also enhanced migration and invasion. Remarkably, the knockdown the human alkaline ceramidase 2 (ACER2) gene in cancer cells with heightened SMPDL3B expression significantly inhibited cell proliferation, migration, and invasion induced by SMPDL3B activation (P<0.05), highlighting the functional interplay between ACER2 and SMPDL3B in ovarian cancer. Conclusions: In summary, this study proposes SMPDL3B as a prognostic marker for ovarian cancer, with implications for potential therapeutic intervention targeting the ACER2-SMPDL3B axis.

A novel model for runoff prediction based on the ICEEMDAN-NGO-LSTM coupling.

Prediction of runoff trends is a critical topic in hydrological forecasting. Accurate and reliable prediction models are important for the rational use of water resources. This paper proposes a new coupled model, ICEEMDAN-NGO-LSTM, for runoff prediction in the middle reaches of the Huai River. This model combines the excellent nonlinear processing capability of the Improved Complete Ensemble Empirical Mode Decomposition with Adaptive Noise (ICEEMDAN) algorithm, the perfect optimization strategy of the Northern Goshawk Optimization (NGO) algorithm, and the advantages of the Long Short-Term Memory (LSTM) algorithm in modeling time series data. The results show that the ICEEMDAN-NGO-LSTM model predicts the monthly runoff trend with higher accuracy compared to the actual data variation. The average relative error is 5.95% within 10%, and the Nash Sutcliffe (NS) is 0.9887. These results indicate that the ICEEMDAN-NGO-LSTM coupled model has superior prediction performance and provides a new method for short-term runoff forecasting.

Mindfulness-Based Interventions for Postpartum Depression: A Systematic Review and Meta-Analysis.

Background: We aimed to investigate the intervention effect of mindfulness-based interventions (MBIs) in patients with postpartum depression. Methods: The method of computer and manual keyword retrieval was used to search PubMed, Web of Science, Cochrane Library. Literature included in the study was assessed for quality and meta-analysis was performed using RevMan 5.3 software. Results: Twelve articles were finally included in the study and the meta-analysis showed that 6 articles used the Edinburgh Postnatal Depression Scale (EPDS) to compare MBIs with conventional therapy, and the statistical heterogeneity between the combined results was low (P=0.18, I2=32%). The level of depression in postpartum depression patients was lower in the MBIs group than in the conventional group [MD=3.13, 95%CI (2.57, 3.70), P<0.00001]. Based on the Beck Depression Inventory (BDI), the comparison between MBIs and conventional therapy had low statistical heterogeneity between the combined results (P=0.56, I2=0%). The level of depression in patients with postpartum depression who received MBIs was significantly lower than in the conventional care group [MD=5.89, 95%CI (4.88, 6.91), P<0.00001]. Subgroup analysis showed that the best intervention duration for MBIs for postpartum depression was within 4 weeks (SMD=-1.785), each session ≦60 minutes (SMD=-1.435), and participants had to complete the best three times per week (SMD=-2.185). Conclusion: MBIs can alleviate depression in women, thereby facilitating their adjustment to new life. It is recommended to practice mindfulness meditation for 30 minutes per day.

ML323 suppresses the progression of ovarian cancer via regulating USP1-mediated cell cycle.

Background: Ubiquitin specific protease 1 (USP1) tightly correlates with poor prognosis of multiple cancers. However, whether USP1 underlies ovarian cancer (OV) progression remains unclarified. Methods: First, GSEA strategy and WGCNA analysis were used to screen for anti-ovarian cancer drugs and furthern optimal module, respectively. In addition, functional enrichments of module genes were realized by Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis. Kaplan-Meier was then employed to analyze the prognostic impact of USP1 expression on OV patients. Cell proliferation and cell cycle assays were used to confirm biological functions of USP1 in the final. Results: Through the forementioned methods, we obtained five candidate drugs against OV from 353 anticancer drugs, and proposed ML323 as a novel anti-OV drug. As our hypothesized, ML323 significantly inhibited the proliferation of OV cells. Combined with WGCNA and KEGG analysis, the turquoise module was related to ML323, together with cell cycle. USP1 was subsequently identified as a target of ML323 and according to the TCGA database, USP1 negatively correlated with prognosis in OV, and its reduction and ML323-treatment both inhibited the proliferation of OV cells, blocking the S phase of cell cycle in vitro. Conclusion: Taken together, ML323 exerts its inhibitory effect on the proliferation of OV cells by targeting USP1-regulated cell cycle, providing a therapeutical strategy and potential target against OV.

Knockdown of JARID2 inhibits the viability and migration of placenta trophoblast cells in preeclampsia.

Protein Jumonji (JARID2) is a member of the Jumonji family of proteins and has been demonstrated to regulate cell proliferation and invasion. However, little is known about the role of JARID2 in the metastasis of placenta trophoblast cells. In the present study, the effect and the underlying molecular mechanism of JARID2 on trophoblast cell viability and invasion was investigated. The expression of JARID2 in placental tissues was analyzed by reverse transcription­quantitative polymerase chain reaction and western blotting. HTR8/SVneo cells were transfected with si­JARID2 or scramble for 24 h. Cell viability, migration and invasion in HTR8/SVneo cells were then evaluated. The expression levels of matrix metallopeptidase 2 (MMP2), MMP9, phosphorylated phosphatidylinositol 3­kinase (p­PI3K), PI3K, phosphorylated AKT serine/threonine kinase 1 (p­Akt) and Akt in HTR8/SVneo cells were also detected using western blotting. The results of the present study demonstrated that JARID2 is underexpressed in human preeclamptic placentas. The knockdown of JARID2 significantly inhibited the viability, migration and invasion of HTR8/SVneo cells. In addition, the knockdown of JARID2 significantly decreased the levels of phosphorylated PI3K and Akt in HTR8/SVneo cells. The results of the present study demonstrated that JARID2 may serve a role in the progression of preeclampsia. The knockdown of JARID2 inhibited the viability and invasion of trophoblast cells in preeclampsia by suppressing the PI3K/Akt signaling pathway. Therefore, JARID2 may serve as a novel potential target for treating preeclampsia.