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1.
Journal of Sun Yat-sen University(Medical Sciences) ; (6): 262-270, 2023.
Article in Chinese | WPRIM | ID: wpr-965841

ABSTRACT

ObjectiveTo assess the prognostic value of 18F-FDG PET/CT parameters for predicting therapeutic response in diffuse large B-cell lymphoma (DLBCL). MethodsWe retrospectively analyzed the clinical data and 18F-FDG PET/CT radiomics features of 81 DLBCL patients enrolled between June 2015 and October 2020. Multivariate logistic regression analysis was used to identify the predictive factors for therapeutic response of DLBCL, based on which a predictive model was developed accordingly. The performance of the model was evaluated by receiver operating characteristic (ROC) curves and calibration plots. ResultsDuring the two years after first chemotherapy, 23 patients (28.3%) developed relapse and 58 patients (71.7%) had progression-free survival (PFS). The analysis for the predictive capability of the binary logistic regression model incorporating the PET/CT features revealed that the imaging features of 18F-FDG PET/CT after chemotherapy were independent prognostic factors for PFS. Among them, SUVTHR-mean2 was the most important factor for predicting therapeutic response in DLBCL patients after chemotherapy, with a cutoff value of 2.00 (AUC=0.81). Conclusions18F-FDG PET/CT showed a valuable prognostic performance for PFS in DLBCL patients after chemotherapy, with the imaging feature after chemotherapy SUVTLR-mean2 being the optimal independent predictor. Our predictive model of imaging features might have an important prognostic value in assessing the risk of disease progression, guiding the treatment and follow-up protocol, improving therapeutic efficiency and cutting down the medical cost.

2.
Chinese Journal of Experimental Ophthalmology ; (12): 218-222, 2012.
Article in Chinese | WPRIM | ID: wpr-635578

ABSTRACT

BackgroundOur previous study determined that tetrandrine (Tet) has an inhibitory effect on the proliferation of human Tenon capsule fibroblasts ( TCFs ) in vitro,but its mechanism is poorly understood.ObjectiveThis study was to investigate the effect mechanism of Tet on human TCFs.MethodsHuman TCFs were isolated and cultured from scleral tissue of donor using explant technique.The cells were identified by vimentin antibody staining and morphology.The third generation of cells were seeded in the culture plate at the density of 1 × 105 cells/ml.Twenty-four hours after inoculation,the Tet of 1 × 10-5 mol/L was added in the well of culture plate,and the cells cultured only in 1640 medium served as the control group.The apoptosis of the cells was assessed by TUNEL,and the expressions of bax,bel-2,transforming growth factor-β2 (TGF-β2 ) in TCFs were detected using immunochemistry.Results The cultured cells showed the features of the fibroblasts in shape with the positive response for vimentin.A number of TUNEL positive cells were seen in Tet group and no TUNEL positive response was found in control group.The expression levels (A value) of bax,bcl-2 and TGF-~ protein in TCFs were 0.577 ± 0.009,0.430±0.012 and 0.341 ±0.017 in Tet group,and those in control group were 0.320±0.015,0.819±0.021 and 0.624±0.014 respectively,showing statistically significant differences between two groups( t =33.277,-35.356,-28.093,P<0.01 ).Conclusions Tet suppresses the proliferation of human TCFs through up-regulating the expression of bax and down-regulating the expressions of bcl-2 and TGF-β2 in vitro.

3.
Chinese Medical Journal ; (24): 1545-1550, 2011.
Article in English | WPRIM | ID: wpr-353947

ABSTRACT

<p><b>BACKGROUND</b>Accumulating evidence indicates that both innate and adaptive mechanisms are responsible for the postnatal development of the mammalian visual cortex. Most of the studies, including gene expression analysis, were performed on the visual cortex during the critical period; few efforts were made to elucidate the molecular changes in the visual cortex during much earlier postnatal stages. The current study aimed to gain a general insight into the molecular mechanisms in the developmental process of the rat visual cortex using microarray to display the gene expression profiles of the visual cortex on postnatal days.</p><p><b>METHODS</b>All age-matched Sprague-Dawley rats in various groups including postnatal day 0 (P0, n = 20), day 10 (P10, n = 15), day 20 (P20, n = 15) and day 45 (P45, n = 10) were sacrificed respectively. Fresh visual cortex from the binocular area (Area 17) was dissected for extraction of total RNA for microarray analyses. Taking advantage of annotation information from the gene ontology and pathway database, the gene expression profiles were systematically and globally analyzed.</p><p><b>RESULTS</b>Of the 31 042 gene sequences represented on the rat expression microarray, more than 4000 of the transcripts significantly altered at days 45, 20 or 10 compared to day 0. The most obvious alteration of gene expression occurred in the first ten days of the postnatal period and the genomic activities of the visual cortex maintained a high level from birth to day 45. Compared to the gene expression at birth, there were 2630 changed transcripts that shared in three postnatal periods. The up-regulated genes in most signaling pathways were more than those of the down-regulated genes.</p><p><b>CONCLUSIONS</b>Analyzing gene expression patterns, we provide a detailed insight into the molecular organization of the developing visual cortex in the earlier postnatal rat. The most obvious alteration of gene expression in visual cortex occurred in the first ten days. Our data were a basis to identify new relevant candidate genes that control visual cortex development.</p>


Subject(s)
Animals , Rats , Gene Expression Profiling , Gene Expression Regulation, Developmental , Genetics , Physiology , Oligonucleotide Array Sequence Analysis , Visual Cortex , Metabolism
4.
Chinese Medical Sciences Journal ; (4): 44-48, 2007.
Article in English | WPRIM | ID: wpr-243560

ABSTRACT

<p><b>OBJECTIVE</b>To investigate the role of Caspase-3 in retinal damage caused by light exposure in rats.</p><p><b>METHODS</b>Light injury to retina was induced by persistent exposure to illumination (intensity: 30 000 +/- 50 lux) of operating microscope for 30 minutes in the right eyes of Sprague-Dawley rats. The pathological changes of retina were observed under optical and electron microscopies at different time points, which were 6 hours, 1, 3, 7, and 15 days after the light exposure. Apoptosis of retinal cells was analyzed by flow cytometry. The activity of Caspase-3 was evaluated by using the Caspase-3 assay kit. At the same time, the expression of Caspase-3 protease was determined with Western blot analysis.</p><p><b>RESULTS</b>The examination results of optical and transmission electron microscopes showed that edema of inner and outer segments of the retina, especially the chondriosome inside the inner segment, became obvious 6 hours after the light exposure. The change was deteriorated along with the increasing time. The structures of the discoidal valve dissociated in the outer segment simultaneously. Disorderly arranged nuclei, karyopycnosis, and thinning in the outer nuclear layer were observed. The retinal pigment epithelium almost disappeared during the later stage. The staining results of Annexin-V combined with PI demonstrated that the proportion of apoptotic cells increased with time. The proportion between 7th day (82.7%) and 15th day (80.4%), however, showed no significant difference. Caspase-3 became remarkably active with the lapse of time, which increased from 0.02 at 6th hour to the peak of 9.8 at 7th day before it started to descend. The Western blot detected a expression of the active form of Caspase-3 at 7th day and 15th day.</p><p><b>CONCLUSION</b>Apoptosis of photoreceptor cells is markedly involved in the light damage and Caspase-3 protease may play an important role in the apoptotic process of the retina after light exposure in rats.</p>


Subject(s)
Animals , Rats , Apoptosis , Radiation Effects , Caspase 3 , Genetics , Metabolism , Radiation Effects , Dose-Response Relationship, Radiation , Enzyme Activation , Gene Expression Regulation, Enzymologic , Radiation Effects , Light , Rats, Sprague-Dawley , Retina , Pathology , Radiation Effects
5.
Journal of Southern Medical University ; (12): 603-605, 2006.
Article in Chinese | WPRIM | ID: wpr-282970

ABSTRACT

<p><b>OBJECTIVE</b>To observe the changes of nuclear factor-kappa B (NF-kappaB) in the course of N-methyl-N-nitrosourea (MNU)-induced apoptosis of rat retinal photoreceptor cells and investigate the mechanism of MNU-induced retinal damage.</p><p><b>METHODS</b>A single intraperitoneal injection of 60 mg/kg MNU was given to 50-day-old female rats, which were sacrificed at different intervals after MNU treatment. The retinal damage was examined with optical microscopy and photoreceptor cell apoptosis detected by TUNEL assay. Western blotting was performed to analyze the changes in NF-kappaB.</p><p><b>RESULTS</b>Pyknosis of the photoreceptor cell nuclei and disorientation of the outer segment of the photoreceptor layer was observed 24 h after MNU treatment, and the outer nuclear layer and photoreceptor layer were almost completely lost on day 7. Photoreceptor cell apoptosis peaked at 24 h, and in the apoptotic cascade, NF-kappaB p65 protein was only detected 12 and 24 h after MNU treatment, whereas the amount of I kappa B alpha, in contrast, markedly increased in the cytoplasm as well as in the nuclei.</p><p><b>CONCLUSION</b>MNU-induced retinal damage might be mediated through the signaling pathway of NF-kappaB/I kappa B alpha.</p>


Subject(s)
Animals , Female , Rats , Apoptosis , Blotting, Western , I-kappa B Proteins , Metabolism , In Situ Nick-End Labeling , Methylnitrosourea , Toxicity , NF-kappa B , Metabolism , Rats, Sprague-Dawley , Retinal Diseases , Metabolism , Pathology
6.
Acta Pharmaceutica Sinica ; (12): 690-694, 2005.
Article in Chinese | WPRIM | ID: wpr-353427

ABSTRACT

<p><b>AIM</b>To study the protective effect of ligustrazine against photoreceptor cell injury induced by N-methyl-N-nitrosourea (MNU) in Sprague-Dawley (SD) rats.</p><p><b>METHODS</b>Ligustrazine injections of different doses were injected intraperitoneally into 47-day female SD rats once a day and a single intraperitoneal injection of MNU 60 mg x kg(-1) was given to 50-day rats. At different intervals after MNU treatment,the animals were sacrificed. The apoptotic index of photoreceptor cells was calculated by TUNEL labeling at 24 h following MNU treatment; peripheral retinal damage was evaluated based on retinal thickness at the d 7 after MNU treatment, and the expression of c-jun and c-fos genes was detected by RT-PCR technique.</p><p><b>RESULTS</b>Ligustrazine injection could remarkably increase total thickness of peripheral retina and decrease apoptotic index of photoreceptor cells induced by MNU in a dose-dependent manner. Compared with MNU-treated rats, the gene expression of c-jun and c-fos was time-dependently down-regulated in ligustrazine-treated group.</p><p><b>CONCLUSION</b>Ligustrazine injection partially protects against MNU-induced retinal damage by down-modulating the expression of c-jun and c-fos genes to inhibit apoptosis of photoreceptor cells.</p>


Subject(s)
Animals , Female , Rats , Apoptosis , Dose-Response Relationship, Drug , Genes, fos , Genes, jun , Injections, Intraperitoneal , Ligusticum , Chemistry , Methylnitrosourea , Photoreceptor Cells , Photoreceptor Cells, Vertebrate , Pathology , Plants, Medicinal , Chemistry , Protective Agents , Pharmacology , Pyrazines , Pharmacology , Rats, Sprague-Dawley , Retina , Metabolism , Pathology
7.
International Eye Science ; (12): 19-22, 2005.
Article in Chinese | WPRIM | ID: wpr-641801

ABSTRACT

· AIM: To explore the dynamic expression and correlation among telomerase catalytic subunit (TERT), proliferating cell nuclear antigen ( PCNA) and antiapoptosis protein Bd-2 which relate to cell proliferation in epiretinal membrane of rat traumatic proliferative vitreoretinopathy(PVR).· METHODS: S-P technique was applied for immunohistochemical staining of epiretinal membrane of traumatic PVR with TERT, PCNA and Bcl-2 antibody. HE staining was also carried out. The staining results were analyzed with image analysis system.· RESULTS: The positive rate and average A of PCNA protein were upregulated at first and then down-regulated, with the peak value in 14d Group, which was significantly different from those in 7d Group and 28d Group.The positive rate and average A of TERT and Bcl-2 were also upregulated at first and then down-regulated, with the peak value in 14d Group and 21d Group, which were significantly different from those in 7d Group. There was significant correlation among PCNA, Bcl-2 and TERT protein expression (P≤0.01).· CONCLUSTON: TERT and Bcl-2 take part in the regulation of proliferative cells in epiretinal membrane of traumatic proliferative PVR, with high correlation with the dynamic changes of cell proliferation.

8.
Chinese Medical Journal ; (24): 1081-1086, 2005.
Article in English | WPRIM | ID: wpr-288276

ABSTRACT

<p><b>BACKGROUND</b>Previous studies have showed that photooxidative stress can lead to down-modulation of nuclear factor-kappa B (NF-kappaB) activity causing apoptosis of cultured photoreceptor cells. This study aimed at investigating whether NF-kappaB was involved in photoreceptor cells apoptosis induced by N-methyl-N-nitrosourea (MNU) in rats.</p><p><b>METHODS</b>A single intraperitoneal injection of 60 mg/kg MNU was given to 50-day-old female rats. At different intervals after MNU treatment, the animals were sacrificed. Retinal damage was examined by a light microscope. The apoptotic index of the photoreceptor cells was detected by terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick-end labeling (TUNEL). NF-kappaB was analysed by Western blot and Transcriptin Factor Assay Kits.</p><p><b>RESULTS</b>The pyknosis of the photoreceptor nuclei and the disorientation of the outer segment of the photoreceptor layer was seen after MNU treatment for 24 hours. The outer nuclear layer and photoreceptor layer were almost completely lost at 7 days. Photoreceptor cells apoptosis reached the peaked value at 24 hours. In apoptotic cascade, the protein levels of NF-kappaB p65 were only detected after MNU treatment for 12 and 24 hours in the nucleus. Conversely, the amounts of IkappaBalpha were markedly increased in the cytoplasm as well as in the nucleus. The activity of NF-kappaB p65 in the nucleus was down-modulated in the end.</p><p><b>CONCLUSIONS</b>MNU-induced photoreceptor cell destruction was attributed to the apoptotic process by down-regulating the activation of NF-kappaB p65.</p>


Subject(s)
Animals , Female , Rats , Apoptosis , Cell Nucleus , Metabolism , I-kappa B Proteins , Physiology , Methylnitrosourea , Toxicity , NF-KappaB Inhibitor alpha , NF-kappa B , Physiology , Photoreceptor Cells , Chemistry , Pathology , Rats, Sprague-Dawley , Retina , Pathology
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