The aim was to optimize the extraction process of Akebia trifoliata seed oil. Using Akebia trifoliata seed as raw material, the oil extraction rate was used as index. The effect of flash extraction on the yield of Akebia trifoliata seed oil was investigated. Taking the liquid-material ratio, extraction voltage, and extraction time as the investigation factors and the oil extraction rate of Akebia trifoliata seed as the response value and on the basis of the single-factor test, the extraction process of Akebia trifoliata seed oil was optimized by the Box-Behnken response surface method. The oil yields of Akebia trifoliata seeds from different origins in China were compared. The experimental results showed that the optimum technological conditions for flash extraction of Akebia trifoliata seed oil were as follows: liquid-material ratio, 12 : 1; extraction voltage, 150 V; extraction time, 90 s; and oil yield of Akebia trifoliata seed, 19.83%. For comparison, it is found that the oil yield of Akebia trifoliata seed produced in Qujing of Yunnan is relatively the highest, followed by Tongren of Guizhou and Zhangjiajie of Hunan; the oil yield of Akebia trifoliata seed produced in Shimian of Sichuan is the lowest. The flash extraction process of Akebia trifoliata seed oil is reasonable, and the oil yield of Akebia trifoliata seed produced in Qujing of Yunnan, China, is relatively the highest. It provides a theoretical and experimental reference for the research and development of Akebia trifoliata seed oil.

Objective: To study the differential lncRNA / mRNA expression profiles of placental tissues in patients with gestational hypertension, analyze their possible mechanisms of action, and explore their target genes and small molecule drug-related lncRNAs. Methods: Three patients with gestational hypertension who were treated in our hospital from May 2018 to May 2019 were selected as the research subjects and three healthy pregnant women who underwent a prenatal examination in the same hospital were selected as the control group. The placental tissues were taken from the patients. RNA-sequencing was performed to construct lncRNA/mRNA differential expression profiles; screening differentially expressed lncRNAs were used to predict target genes, and GO and KEGG enrichment analysis predicted the biological functions of target genes and the enriched signal pathways, respectively. Protein-protein interaction network, lncRNA-miRNA-mRNA network, and differentially expressed gene-small molecule drug association networks were constructed. Results: RNA-seq analysis revealed 19 differentially expressed lncRNA (4 up-regulated; 15 down-regulated) (P<0.05). Moreover, 423 differentially expressed genes (DEGs) (84 up-regulated; 339 down-regulated)(P<0.05). GO and KEGG enrichment analysis found that gestational hypertension is mainly related to endothelial cell damage, inflammatory response, abnormal immune regulation, and abnormal trophoblast invasion. The PPI network and lncRNA-miRNA-mRNA network were constructed. Differentially expressed gene-drug small molecule prediction results found 19 pairs of differentially gene-small drug relationship pairs, mainly including antibody, inhibitor et al. Conclusion: Differently expressed lncRNAs in the placenta of patients with gestational hypertension can participate in the regulation of multiple biological functional level-related signal pathways through targeted regulation of their target genes, and play an important role in the occurrence and development of gestational hypertension. The predicted small molecule drug can be used as a reference for clinical treatment.

Sonodynamic therapy (SDT) triggered by ultrasound (US) has attracted increasing attention owing to its ability to overcome critical limitations, including low tissue-penetration depth and phototoxicity in photodynamic therapy (PDT). Biogenic metal oxide nanoparticles (NPs) have been used as anti-cancer drugs due to their biocompatibility properties with most biological systems. Here, sonosensitizer MWO4-PEG NPs (M = Fe Mn Co Ni) were synthesized as inhibitors to activation-induced cytidine deaminase (AID), thus neutralizing the extensive carcinogenesis of AID in diffuse large B-cell lymphoma (DLBCL). The physiological properties of these nanomaterials were examined using transmission electron microscopy (TEM). The inhibition of NPs to AID was primarily identified by the affinity interaction prediction between reactive oxygen species (ROS) and AID through molecular dynamics and molecular docking technology. The cell apoptosis and ROS generation in US-triggered NPs treated DLBCL cells (with high levels of AID) were also detected to indicate the sonosensitivity and toxicity of MWO4-PEG NPs to DLBCL cells. The anti-lymphoma studies using DLBCL and AID-deficient DLBCL cell lines indicated a concentration-dependent profile. The synthesized MWO4-PEG NPs in this study manifested good sonodynamic inhibitory effects to AID and well treatment for AID-positive hematopoietic cancers.

Adenosine A1 receptor (A1AR) and Adenosine A2A receptor (A2AAR) are AR isoforms that share highly homologous, but play many different roles in terms of regulating arteriolar pressure and urine flow...

Activation-induced cytidine deaminase (AID) plays a crucial role in promoting B cell diversification through somatic hypermutation (SHM) and class switch recombination (CSR). While AID is primarily associated with the physiological function of humoral immune response, it has also been linked to the initiation and progression of lymphomas. Abnormalities in AID have been shown to disrupt gene networks and signaling pathways in both B-cell and T-cell lineage lymphoblastic leukemia, although the full extent of its role in carcinogenesis remains unclear. This review proposes an alternative role for AID and explores its off-target effects in regulating tumorigenesis. In this review, we first provide an overview of the physiological function of AID and its regulation. AID plays a crucial role in promoting B cell diversification through SHM and CSR. We then discuss the off-target effects of AID, which includes inducing mutations of non-Igs, epigenetic modification, and the alternative role as a cofactor. We also explore the networks that keep AID in line. Furthermore, we summarize the off-target effects of AID in autoimmune diseases and hematological neoplasms. Finally, we assess the off-target effects of AID in solid tumors. The primary focus of this review is to understand how and when AID targets specific gene loci and how this affects carcinogenesis. Overall, this review aims to provide a comprehensive understanding of the physiological and off-target effects of AID, which will contribute to the development of novel therapeutic strategies for autoimmune diseases, hematological neoplasms, and solid tumors.