Fabrication of polycarbonate ultrafiltration mixed matrix membranes including modified halloysite nanotubes and graphene oxide nanosheets for olive oil/water emulsion separation
SEPARATION AND PURIFICATION TECHNOLOGY
Authors: Amid, Maryam; Nabian, Nima; Delavar, Maedeh
Abstract
In this study, ultrafiltration polycarbonate mixed matrix membranes (MMMs) were synthesized to remove the olive oil from the aqueous solution. To characterize the synthesized membranes in terms of surface morphology, functional groups, hydrophilicity, and mechanical strength, various analyses such as FESEM, FTIR, contact angle, and tensile strength were carried out, respectively. Modified halloysite nanotubes and graphene oxide nanosheets with the loading of 0.25, 0.5, and 0.75 wt% were added to the blank membrane. Membranes including modified halloysite nanotubes exhibited better hydrophilicity and higher pure water flux due to the presence of amphiphilic sodium dodecyl sulfate surfactant at higher nanoparticle loadings, while the agglomeration of graphene oxide nanosheets in the membrane polymeric matrix resulted in the lower pure water flux compared to the blank PC membrane. Moreover, the pure water flux data were modeled by Design-Expert software, and the highest pure water flux of 1340 L/m(2) h was reported for PC-MHNT0.75 MMM. Then, the optimized membranes based on the output of the design expert software were used in the ultrafiltration tests for olive oil removal. All the selected membranes reached 100% rejection efficiency of olive oil; however, they were different based on the time to reach this efficiency and the permeate flux. Performance evaluation of membranes in ultrafiltration tests at different feed concentrations showed that the PC-MHNT0.75 mixed matrix membrane possessed the lowest time (165 min at 100 ppm feed concentration) to reach 100% rejection efficiency and subsequently selected as the optimal membrane. The regeneration process using 20% (v/v) acetone solution was implemented for the optimal membrane and the obtained membrane water flux after three cycles of regeneration was more than 96%, introducing the fabricated MMMs as suitable candidates for olive oil separation.
MicroRNA-23a acts as an oncogene in pancreatic carcinoma by targeting TFPI-2
EXPERIMENTAL AND THERAPEUTIC MEDICINE
Authors: Wang, Wei; Ning, Jin-Zhuo; Tang, Zhi-Gang; He, Ying; Yao, Li-Chao; Ye, Lin; Wu, Lun
Abstract
Pancreatic carcinoma (PC) is a rapidly progressive, fatal malignant tumor with the poorest prognosis among all major carcinoma types. MicroRNAs (miRNAs/miRs) have been indicated to be key post-transcriptional regulatory factors, which are involved in cancer development. The present study was designed to investigate the effect of miR-23a on PC cell proliferation, metastasis and apoptosis. The expression of miR-23a was detected in a normal pancreatic ductal epithelial cell line and three PC cell lines, and miR-23a inhibitor or mimics were transfected into the Panc-1 and MiaPaCa2 PC cells. The association between miR-23a and tissue factor pathway inhibitor (TFPI)-2 was examined using a luciferase reporter assay. MTT and flow cytometry assays were used to assess cell viability and apoptosis, respectively. Furthermore, wound-healing, Transwell and Matrigel assays were used to evaluate cell migration and invasion abilities, and the protein expression level of TFPI-2 was determined using western blot analysis. The results of the present study revealed that miR-23a was upregulated in PC cells. Furthermore, TFPI-2 was identified as a downstream target of miR-23a, and TFPI-2 expression was found to be increased following miR-23a knockdown. In addition, functional assays revealed that downregulation of miR-23a decreased PC cell proliferation, migration and invasiveness and promoted cell apoptosis, while miR-23a overexpression exerted the opposite effects. Furthermore, TFPI-2 knockdown rescued the biological effects on PC cells, which were induced by miR-23a knockdown. The results of the present study indicated that miR-23a negatively modulated TFPI-2 expression in vitro and enhanced the malignant phenotypes of PC cells. Therefore, miR-23a may be a potential marker and/or target for the diagnosis and treatment of PC.