ABSTRACT
Objective ToexplorethevalueofMRIiterativedecompositionofwaterandfatwithechoasymmetryandleastsquares estimationquantificationsequence(IDEALIQ)techniquetoevaluatemyelosuppressionduringradiotherapyandchemotherapyincervicalcancer. Methods 25femalesubjectswereenrolledinthisstudy,whowereclinicallydiagnosedascervicalcancerandacceptedtheradiotherapyand chemotherapy.AllthesubjectswereperformedwithsagittalMRIIDEALIQscansineachweek’streatmentandattheendofwhole fiveweeks’therapy,soeachpatienthad6timesMRIscans.ROIweremanuallyplacedonL4,L5andS1vertebralbodyandsubcutaneousfatto measurethefatfraction.ThefatfractioncolorimageswerereconstructedonaAW (AdvantageWorkstation)4.6workstation.Results Asthe radiationandchemotherapyprocess,thevaluesoffatfractionincreasedprogressivelyonL4,L5andS1vertebralbody(P<0.001), whilethefatfractionvaluesinsubcutaneousfatappearedstableallthetime(P=0.987).Conclusion MRIIDEALIQtechniquecan evaluatethereal-timefatfraction,andradiotherapyandchemotherapyplansmaybeoptimizedaccordingtothefatfractionresult.
ABSTRACT
Objective:To investigate the effects of Mor-platin, a novel mitochondrial platinum complex, on proliferation and migration of human hepatoma carcinoma HepG2 cells. Methods:Cell counting kit-8 (CCK-8) assay was used to analyze cell proliferation of Mor-platin and classic anticancer drugs, particularly cisplatin, in HepG2 cells. A laser confocal microscope was used to observe whether Mor-platin can target mitochondria. The morphological changes in cellular mitochondria after treatment with Mor-platin were ob-served on a transmission electron microscope. Cell apoptosis was measured by flow cytometry, and cell invasion was evaluated by three-dimensional tumor spheroid model. Results:Mor-platin can inhibit cell proliferation and is dose dependent. The half inhibitory concentration (IC50) of Mor-platin is lower than that of cisplatin. Laser confocal images showed that Mor-platin can target cell mito-chondria and enrich cell mitochondria. Transmission electron microscopy images showed that cell mitochondrial morphology changed after Mor-platin treatment. Furthermore, cell mitochondrial membrane is incomplete and mitochondrial cristae are reduced. Cell apoptosis caused by Mor-platin is dose dependent. The three-dimensional tumor spheroid model showed that the cell areas of the group subjected to Mor-platin treatment are smaller than those of the control group. Conclusion:Mor-platin can target cell mitochon-dria, change the cell mitochondrial morphology, inhibit cell proliferation, and thus promote cell apoptosis. It also showed better anti-cancer effects than cisplatin. Furthermore, Mor-platin can inhibit three-dimensional tumor spheroid invasion. These results suggest that Mor-platin is a potential antitumor drug.
ABSTRACT
BACKGROUND:RADA16 is a mature amphiphilic self-assembling peptide, which can be assembled into nanofibers, and promote MC3T3 E1 cellattachment, spreading and proliferation. OBJECTIVE:To observe the effects of the new-type self-assembling peptide hydrogel NBD/RADA16 on osteogenic differentiation of mouse preosteoblasts MC3T3 E1. METHODS:The MC3T3 E1 cells were inoculated in NBD/RADA16 self-assembling peptide hydrogel and RADA16 hydrogel for osteogenic induction. cells undergoing simple osteogenic induction served as controls. After culture for 1, 3, 6 days, the activity of alkaline phosphatase was detected. After 7 days, western blot assay was used to determine the expression of bone morphogenetic protein-2. After 21 days, alizarin red staining was used to observe calcified nodules. RESULTS AND CONCLUSION:MC3T3 E1 cells grew wel on the NBD/RADA16 peptide hydrogel, which were superior to those on the RADA16 hydrogel. The activity of alkaline phoshpatase was higher in the NBD/RADA16 group than the RADA16 and control groups (P<0.01). Compared with the RADA16 hydrogel, mineralized matrix deposition and expression of bone morphogenetic protein-2 were higher on the NBD/RADA16 peptide hydrogel (P<0.01). These findings indicate that the NBD/RADA16 peptide hydrogel is superior to the RADA16 hydrogel for promoting the osteogenic differentiation of MC3T3 E1 cells.