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1.
Acta Anatomica Sinica ; (6): 73-81, 2024.
Article in Chinese | WPRIM | ID: wpr-1015147

ABSTRACT

Objective Hippocampal atrophy is a clinically important marker for the diagnosis of many psychiatric disorders such as Alzheimer’s disease‚ so accurate segmentation of the hippocampus is an important scientific issue. With the development of deep learning‚ a large number of advanced automatic segmentation method have been proposed. However‚ 3D hippocampal segmentation is still challenging due to the effects of various noises in MRI and unclear boundaries between various classes of the hippocampus. Therefore‚ the aim of this paper is to propose new method to segment the hippocampal head‚ body‚ and tail more accurately. Methods To overcome these challenges‚ this paper proposed two strategies. One was the spatial and frequency domain features adaptive fusion strategy‚ which reduced the influence of noise on feature extraction by automatically selecting the appropriate frequency combination through fast Fourier transform and convolution. The other was an inter-class boundary region enhancement strategy‚ which allowed the network to focus on learning the boundary regions by weighting the loss function of the boundary regions between each class to achieve the goal of pinpointing the boundaries and regulating the size of the hippocampal head‚ body and tail. Results Experiments performed on a 50-case teenager brain MRI dataset show that our method achieves state-of-the-art hippocampal segmentation. Hippocampal head‚ body and tail had been improved compared to the existing method. Ablation experiments demonstrated the effectiveness of our two proposed strategies‚ and we also validated that the network had a strong generalization ability on a 260-case Task04_Hippocampus dataset. It was shown that the method proposed in this paper could be used in more hippocampal segmentation scenarios. Conclusion The method proposed in this paper can help clinicians to observe hippocampal atrophy more clearly and accomplish more accurate diagnosis and follow-up of the condition.

2.
Chinese Journal of Oncology ; (12): 326-329, 2005.
Article in Chinese | WPRIM | ID: wpr-358640

ABSTRACT

<p><b>OBJECTIVE</b>Quercetin, a widely distributed natural flavonoid with a variety of biological functions, can reverse multidrug resistance (MDR) in leukemia according to recent researches. The aim of this study was to investigate the mechanisms of reversal of multi-drug resistance by quercetin mainly in respect of membrane transporters.</p><p><b>METHODS</b>MTT cell viability assay was used to verify the chemo-sensitization to daunorubicin (DNR) by quercetin in HL-60/ADM cell line and determine the effective reversal concentration, the expression of MRP(1) gene and its protein product, multidrug resistant associated protein 1 by RT-PCR and flow cytometry By confocal laser scanning microscopy, the subcellular distribution of DNR in HL-60/S and HL-60/ADM cells was examined before and after quercetin exposure.</p><p><b>RESULTS</b>Compared with HL-60/S, 20-40 micromol/L quercetin in vitro remarkably enhanced the sensitivity of HL-60/ADM cells to daunorubicin, down-regulated the expression of MRP(1) gene and its protein product MRP(1), restored the abnormal subcellular distribution of daunorubicin, so as to reverse MDR. Moreover, such an effective concentration of quercetin was non-toxic to the cells.</p><p><b>CONCLUSION</b>Quercetin could be a candidate of effective multidrug resistance-reversing agent with low toxicity in leukemia chemotherapy.</p>


Subject(s)
Humans , ATP Binding Cassette Transporter, Subfamily B , ATP Binding Cassette Transporter, Subfamily B, Member 1 , Antibiotics, Antineoplastic , Pharmacology , Daunorubicin , Pharmacology , Drug Resistance, Multiple , Drug Resistance, Neoplasm , HL-60 Cells , Quercetin , Pharmacology
3.
Chinese Journal of Oncology ; (12): 461-464, 2005.
Article in Chinese | WPRIM | ID: wpr-358603

ABSTRACT

<p><b>OBJECTIVE</b>To investigate if CYP3A5 gene is involved in the molecular mechanisms for multiple drug resistance in leukemia cells.</p><p><b>METHODS</b>A full length cDNA of CYP3A5 gene was cloned, and a recombinant eukaryotic expression plasmid was constructed, then stably transfected cell lines were established. Furthermore, the sensitivity of those cell lines to several anticancer drugs were assessed by MTT and FCM assay.</p><p><b>RESULTS</b>The recombinant plasmid was designated as pcDNA3-CYP3A5. Transfecting HL-60 cells (which didn't show transcript of CYP3A5 gene) with recombinant plasmid pcDNA3-CYP3A5 generated HL-60/CYP3A5 cell line, and transfecting of HL-60 cells with the parental pcDNA3 vector served as control HL-60/pc cell line. Daunorubicin induced remarkable apoptosis peaks in HL-60 and HL-60/pc cells, while such effect did not occur in HL-60/CYP3A5 cells (apoptosis cell percentage were 7.3%, 6.3% and 1.2%, respectively). Compared with HL-60 and HL-60/pc cells, HL-60/CYP3A5 cells were statistically significantly resistant to daunorubicin, aclacinomycin A, vincristine and harringtonine (resistance multiples were 2.89, 2.01, 4.05 and 2.79 times, respectively, P < 0.05), however the sensitivity to teniposide didn't change (resistance multiple was 1.04 times).</p><p><b>CONCLUSION</b>Transcription of CYP3A5 gene in leukemia cells directly induces resistance to anthracyclines and alkaloids, however the cells are still sensitive to epipodophyllotoxins. Therefore, our findings confirmed a new mechanism of multidrug resistance.</p>


Subject(s)
Humans , Aclarubicin , Pharmacology , Antibiotics, Antineoplastic , Pharmacology , Cytochrome P-450 CYP3A , Cytochrome P-450 Enzyme System , Genetics , Daunorubicin , Pharmacology , Drug Resistance, Multiple , Genetics , Drug Resistance, Neoplasm , Genetics , HL-60 Cells , Phenotype , Plasmids , Genetics , Recombination, Genetic , Transfection , Vincristine , Pharmacology
4.
Chinese Journal of Hematology ; (12): 171-174, 2004.
Article in Chinese | WPRIM | ID: wpr-291423

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the expression of VEGF mRNA and secretion of VEGF protein in NB4 and HL-60 cells affected by all-trans retinoic acid (ATRA) and daunorubincin (DNR) respectively.</p><p><b>METHODS</b>Semi-quantitative RT-PCR and ELISA were used to study the expression of VEGF mRNA and secretion of VEGF protein in NB4 and HL-60 cell lines treated by ATRA and DNR respectively.</p><p><b>RESULTS</b>VEGF was expressed in both NB4 and HL-60 cells. The expression of VEGF mRNA and secretion of VEGF protein could be down-regulated by ATRA and DNR respectively in a time and dose dependent manner.</p><p><b>CONCLUSION</b>Besides inducing apoptosis and restraining proliferation of leukemic cells, ATRA and DNR exerted their anti-leukemia effects by reducing angiogenesis via reduction of angiogenic reaction stimulating signals.</p>


Subject(s)
Humans , Apoptosis , Cell Line, Tumor , Cell Proliferation , Daunorubicin , Pharmacology , Gene Expression Regulation, Leukemic , HL-60 Cells , Leukemia , Drug Therapy , Genetics , Metabolism , Tretinoin , Pharmacology , Vascular Endothelial Growth Factors , Genetics , Metabolism
5.
Chinese Journal of Hematology ; (12): 16-18, 2002.
Article in Chinese | WPRIM | ID: wpr-261449

ABSTRACT

<p><b>OBJECTIVE</b>To compare the gene expression status of NB4 cells before and after arsenic sulfide treatment by cDNA microarray.</p><p><b>METHODS</b>Two cDNA probes were made from mRNA of untreated or arsenic sulfide treated NB4 cells. The cells were labelled with Cy3 or Cy5 fluorescence dyes individually, hybridized with cDNA microarray, and scanned for fluorescent intensity. The altered gene expression was screened through the analysis of difference in gene expression profile.</p><p><b>RESULTS</b>Thirty four genes related to apoptosis, cell cycle and others expressed different after the treatment of arsenic sulfide, 28/34 were up-regulated, 6/34 down-regulated.</p><p><b>CONCLUSION</b>ABC50, PNAS-2 and cyclin G(2) might take part in the process of NB4 cell apoptosis induced by arsenic sulfide.</p>


Subject(s)
Humans , Arsenicals , Pharmacology , Gene Expression Regulation, Neoplastic , Oligonucleotide Array Sequence Analysis , Sulfides , Pharmacology , Tumor Cells, Cultured , Metabolism
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