ABSTRACT
Domain walls affect significantly ferroelectric and magnetic properties of magnetoelectric multiferroics. The stereotype is that the ferroelectric polarization will reduce at the domain walls due to the incomplete shielding of depolarization field or the effects of gradient energy. By combining transmission electron microscopy and first-principles calculations, we demonstrate that the ferroelectric polarization of tail-to-tail 180° domain walls in ε-Fe2O3 is regulated by the bound charge density. A huge enhancement (43%) of ferroelectric polarization is observed in the type I domain wall with a low bound charge density, while the ferroelectric polarization is reduced to almost zero at the type II domain wall with a high bound charge density. The magnetic coupling across the type I and type II ferroelectric domain walls are antiferromagnetic and ferromagnetic, respectively. Revealing mechanisms for enhancing ferroelectric polarization and magnetic behaviors at ferroelectric domain walls may promote the fundamental research and potential applications of magnetoelectric multiferroics.
ABSTRACT
BACKGROUND: Despite the substantial impact of methylenetetrahydrofolate dehydrogenase 2 (MTHFD2) on cancer progression, its significance in the regulation of hepatocellular carcinoma (HCC) cell proliferation and chemosensitivity remains poorly defined. METHODS: We evaluated MTHFD2 expression in a total of 95 HCC tissues by immunohistochemistry and analyzed the association of MTHFD2 with clinicopathologic features. qRT-PCR and Western blotting were conducted to verify MTHFD2 expression levels. Bioinformatics analysis such as gene set enrichment analysis (GSEA) and kyoto encyclopedia of genes and genomes (KEGG) enrichment analysis were used to predict the signaling pathways involved in MTHFD2. In addition, to investigate the anti-tumor effects of MTHFD2 knockdown, Cell Counting Kit-8 (CCK-8) and EdU assays were used. RESULTS: We found that MTHFD2 was frequently upregulated in HCC, and the combination of increased expression of MTHFD2 and Ki67 was associated with poor HCC prognosis. MTHFD2 knockdown significantly inhibited HCC cell proliferation and effectively sensitized HCC cells to sorafenib and lenvatinib. PI3K/AKT pathway was involved in MTHFD2-mediated modulation of proliferation and chemosensitivity. CONCLUSIONS: These findings indicate that MTHFD2 plays an important role in proliferation and chemosensitivity of HCC, indicating that it may serve as a novel pharmacological target for improving HCC therapy.
Subject(s)
Carcinoma, Hepatocellular , Liver Neoplasms , Methylenetetrahydrofolate Dehydrogenase (NADP) , Humans , Carcinoma, Hepatocellular/drug therapy , Carcinoma, Hepatocellular/genetics , Carcinoma, Hepatocellular/metabolism , Cell Line, Tumor , Cell Proliferation/genetics , Down-Regulation , Liver Neoplasms/drug therapy , Liver Neoplasms/genetics , Liver Neoplasms/metabolism , Phosphatidylinositol 3-Kinases/genetics , Phosphatidylinositol 3-Kinases/metabolism , Proto-Oncogene Proteins c-akt/genetics , Proto-Oncogene Proteins c-akt/metabolism , Methylenetetrahydrofolate Dehydrogenase (NADP)/genetics , Methylenetetrahydrofolate Dehydrogenase (NADP)/metabolismABSTRACT
OBJECTIVES: To summarize the underlying biological correlation of prognostic radiomics and deep learning signatures in patients with lung cancer and evaluate the quality of available studies. METHODS: This study examined databases including the PubMed, Embase, Web of Science Core Collection, and Cochrane Library, for studies that elaborated on the underlying biological correlation with prognostic radiomics and deep learning signatures based on CT or PET/CT for predicting the prognosis in patients with lung cancer. Information about the patient and radiogenomic analyses was extracted for the included studies. The Radiomics Quality Score (RQS) and the Prediction Model Risk of Bias Assessment Tool were used to assess the quality of these studies. RESULTS: Twelve studies were included with 7,338 patients from 2014 to 2022. All studies except for one were retrospective. Supervised machine learning was adopted in six studies, and the remaining used unsupervised machine learning methods. Gene sequencing and histopathological data were analyzed by 83.33% and 16.67% of the included studies, respectively. Gene set enrichment analysis and correlation analysis were most used to explore the biological meaning of prognostic signatures. The median RQS for supervised learning articles was 13.5 (range 12-19) and 7.0 (range 5-14) for unsupervised learning articles. The studies included in this report were assessed to have high risk of bias overall. CONCLUSION: The biological basis for the interpretability of data-driven models mainly focused on genomics and histopathological factors, and it may improve the prognosis of lung cancer with more proper biological interpretation in the future.
Subject(s)
Deep Learning , Lung Neoplasms , Humans , Lung Neoplasms/diagnostic imaging , Lung Neoplasms/genetics , Prognosis , Tomography, X-Ray Computed/methods , Positron Emission Tomography Computed Tomography/methods , RadiomicsABSTRACT
OBJECTIVE: To investigate whether prenatal fibrinogen (FIB) or other related factors could be utilized to evaluate the risk of postpartum hemorrhage (PPH). METHODS: A retrospective study was conducted in a database from January 2015 to December 2019. A total of 128 patients were enrolled and evaluated with FIB, in which 55 patients were assigned to low FIB and 73 in normal FIB. RESULTS: According to the volume of blood loss, the mean of the low FIB group (<4 g/L) was markedly higher than that of the normal FIB group (≥4 g/L). Prenatal FIB was negatively correlated with PPH volume. The receiver operating characteristic (ROC) curve results indicated that the value of prenatal FIB was 0.701 to predict refractory PPH. CONCLUSIONS: Prenatal FIB was significantly related to thrombin time (TT), which may be an independent factor to predict the coagulation state of prenatal pregnancy.
Subject(s)
Hemostatics , Postpartum Hemorrhage , Female , Pregnancy , Humans , Fibrinogen , Retrospective Studies , Postpartum Hemorrhage/diagnosis , Blood Coagulation , VitaminsABSTRACT
Reaction of the 1,2-disilylenes {(DipAr Am)Si}2 (DipAr Am=[(NDip)2 CAr]- , Dip=2,6-diisopropylphenyl, Ar=4-C6 H4 But (Ar') 1 a or Ph 1 b) and two abnormal N-heterocyclic silylenes, (DipAr Am)SiOCSi{(NDip)2 CAr} (Ar=Ar' 3 a or Ph 3 b) with N2 O led to formation of unprecedented examples of uncoordinated silicon analogues of carboxylic acid anhydrides, (DipAr Am)(O=)SiOSi(=O)(DipAr Am) (Ar=Ar' 2 a or Ph 2 b). Both compounds have been fully characterized, and the mechanism of formation of one explored using DFT calculations. Reduction of sila-acid anhydride 2 a with a dimagnesium(I) compound, [{(Mes Nacnac)Mg}2 ] (Mes Nacnac=[(MesNCMe)2 CH]- , Mes=mesityl), led to the one-electron reduction of the anhydride and formation of a magnesium complex of a sila-acid anhydride radical anion [(Mes Nacnac)Mg{(OSi(DipAr' Am)}2 O] 5. A combination of EPR spectroscopic studies and DFT calculations reveal the unpaired electron to largely reside on one of the amidinate ligands of the complex.