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Objective @#To explore the etiology, clinical manifestations, diagnosis and treatment of multiple idiopathic root resorption to provide a reference for clinical diagnosis and treatment. @*Methods@# The clinical data of a case of multiple idiopathic root resorption were analyzed retrospectively, and the related literature was reviewed.@*Results@#The patient had no history of orthodontic correction, occlusal trauma, trauma history or other causes of root resorption. Clinical examination revealed full-mouth gingival congestion, redness, a loose texture, and variable degrees of destruction of the alveolar bone. Imaging examination showed that teeth 13, 16, 26, 36, 46 had idiopathic root resorption. The diagnoses were multiple idiopathic root resorption and periodontitis. The pathology tests showed that a large number of osteoclasts were present in the soft tissue surrounding the teeth. Whole-exome sequencing showed that there was a strong correlation between gene mutations (WNT7a and HSPG2) and the present phenotype. Root resorption of teeth without periodontitis was stopped after periodontal treatment during the 19-month follow-up. Tooth 13 was removed, and extraction socket preservation was performed. The etiology of idiopathic root resorption may be related to gene mutations, but it is not clear. At present, there is no effective treatment. @* Conclusion @#Multiple idiopathic root resorption has an unknown etiology, but it may be related to WNT7A and HSPG2 gene mutations. The rate of root resorption can be slowed by controlling periodontal inflammation.
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Objective:To observe the expression of microRNA (miRNA, miR)-5787 in breast cancer tissues and various cell lines, analyze the effect of overexpression of miR-5787 on breast cancer cell invasion and proliferation, and explore its possible molecular mechanism.Methods:Real-time fluorescence quantitative polymerase chain reaction (qRT-PCR) method was used to detect the expression of miR-5787 in 47 breast cancer tissues and adjacent tissues, 4 breast cancer cell lines and normal breast epithelial cells. Breast cancer cell lines with the lowest miR-5787 expression were selected and transfected with miR-5787 mimics (experimental group) and control NC mimics (control group), respectively. qRT-PCR was used to detect the expression of miR-5787 in cells of the two groups. Transwell invasion experiment and cell counting kit-8 (CCK-8) were used to detect the effect of miR-5787 overexpression on breast cancer cell invasion and proliferation. Bioinformatics software and dual luciferase reporter gene experiments were used to predict and verify the target genes that miR-5787 could complementally bind. qRT-PCR and Western blot were used to detect the expression of target gene mRNA and protein.Results:Compared with adjacent tissues (5.05±0.82), the expression of miR-5787 in breast cancer tissues (1.32±0.33) was significantly reduced ( P<0.01). Compared with normal breast epithelial cells, the expression of miR-5787 in the four breast cancer cell lines was reduced ( P<0.05), and the expression in HCC1937 cells was the lowest ( P<0.01). After transfection of miR-5787 mimics, the expression of miR-5787 in HCC1937 cells in the experimental group was significantly higher than that in the control group ( P<0.01). Overexpression of miR-5787 could inhibit the invasion ( P<0.05) and proliferation ( P<0.05) of breast cancer HCC1937 cells. Bioinformatics software showed that the target gene of miR-5787 might be heparan sulfate proteoglycan 2 (HSPG2), and miR-5787 could complement HSPG2 mRNA ( P<0.01). qRT-PCR and Western blot indicated that overexpression of miR-5787 could significantly inhibit the expression of HSPG2 gene ( P<0.01), with the decreased expression of Vimentin, N-cadherin, Ki67 and PCNA. Conclusions:miR-5787 expression was low in breast cancer tissues and cell lines. Overexpression of miR-5787 could inhibit the invasion and proliferation of breast cancer HCC1937 cells by interfering with the expression of HSPG2 gene.
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Aims: The main objective of this paper is to review the technologies used for the detection of Hepatocellular Carcinoma. Study Design: Convective cooling protects the cancer cells from thermal destruction and decreases the necrosed volume. A major objective of the method development is to achieve a virtually complete necrosis of tumors close to major blood vessels and to avoid blood vessel damage and, hence, the needed treatment planning. Place and Duration of Study: We found from this three-dimensional three-field coupling study that in large blood vessels, both convective cooling and acoustic streaming may change the temperature considerably near the blood vessel. Acoustic streaming velocity magnitude can be several times larger than the blood vessel velocity. Methodology: Different methods and techniques were proposed so far in the automatic detection of Hepatocellular Carcinoma. However the performance of the technologies till now not completely matched to the performance of human expert. Results: This review paper have analyzed the recent technologies in Liver Cancer Identification (24%), Liver Tumor Risks (16%), MR Imaging (22%), Liver Tumor Prevention (16%) and Liver Tumor Therapy (18%). The results presented in the current work can be further used to construct a surgical planning platform. Conclusions: Also we give some directions about the technologies and this can be useful for the researches to develop a new technology for the detection of Hepatocellular Carcinoma.
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For decades, various systemic therapies have been explored for the treatment of advanced hepatocellular carcinoma (HCC), the fifth most common cancer and the third leading cause of cancer-related deaths worldwide. Nevertheless, no satisfactory results have been obtained so far. Glypican-3 (GPC-3) is a cell-surface heparan sulfate proteoglycans (HSPGs) that emerged as a promising diagnostic marker as well as target for therapy. Therefore; we investigated antitumor activity of antiglypican-3 (antiGPC3), a specific antibody aginst GPC-3, against HepG2, human HCC, cell line. HepG2 cells were treated with AntiGPC3 at (5, 10 and 20 μg/ml). HepG2 cell proliferation was measured by MTT and lactate dehydrogenase (LDH) assays. GPC-3, HSPG and sulfatase-2 (SULF2) levels were measured by ELISA. Moreover, apoptosis was assessed by measuring Caspase-3 activity. We found that, antiGPC3 reduced HepG2 cells survival and showed cell cytotoxicity in a dose-dependent manner. In addition, antiGPC3 was able to increase the apoptosis measured by capase-3 activity in hepG2 cells. Finally, antiGPC3 restored HSPG level without affecting SULF2 in HepG2 cells. We can conclude that, antiGPC3 possesses cytotoxic effects, which can be partially explained by restoration of HSPGs and increase of caspase-3 apoptotic pathway. GPC-3 represents a promising target of HCC therapy.
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PURPOSE: We describe the changes of rat glomerular epithelial cells when exposed to high levels of glucose and advanced glycosylation endproducts(AGE) in the in vitro diabetic condition. We expect morphological alteration of glomerular epithelial cells and permeability changes experimentally and we may correlate the results with a mechanism of proteinuria in DM. METHODS: We made 0.2 M glucose-6-phsphate solution mixed with PBS(pH 7.4) containing 50 mg/mL BSA and protease inhibitor for preparation of AGE. As control, we used BSA. We manufactured and symbolized five culture dishes as follows; B5 - normal glucose(5 mM) + BSA, B30 - high glucose(30 mM) + BSA, A5 - normal glucose(5 mM) + AGE, A30 - high glucose(30 mM) + AGE, A/B 25 - normal glucose(5 mM) + 25 mM of mannitol(osmotic control). After the incubation period of both two days and seven days, we measured the amount of heparan sulfate proteoglycan(HSPG) in each dish by ELISA and compared them with the B5 dish at 2nd and 7th incubation days. We observed the morphological changes of epithelial cells in each culture dish using scanning electron microscopy(SEM). We tried the permeability assay of glomerular epithelial cells using cellulose semi-permeable membrane measuring the amount of filtered BSA through the apical chamber for 2 hours by sandwich ELISA. RESULTS: On the 2nd incubation day, there was no significant difference in the amount of HSPG between the 5 culture dishes. But on the 7th incubation day, the amount of HSPG increased by 10% compared with the B5 dish on the 2nd day except the A30 dish(P0.05). In the osmotic control group (A/B 25) no significant correlation was observed. On the SEM, we could see the separated intercellular junction and fused microvilli of glomerular epithelial cells in the culture dishes where AGE was added. The permeability of BSA increased by 19% only in the A30 dish on the 7th day compared with B5 dish on the 7th day in the permeability assay(P<0.05). CONCLUSION: We observed not only the role of a high level of glucose and AGE in decreasing the production of HSPG of glomerular epithelial cells in vitro, but also their additive effect. However, the role of AGE is greater than that of glucose. These results seems to correlate with the defects in charge selective barrier. Morphological changes of the disruption of intercellular junction and fused microvilli of glomerular epithelial cells seem to correlate with the defects in size-selective barrier. Therefore, we can explain the increased permeability of glomerular epithelial units in the in vitro diabetic condition.
Subject(s)
Animals , Rats , Cellulose , Enzyme-Linked Immunosorbent Assay , Epithelial Cells , Glucose , Glycosylation , Heparan Sulfate Proteoglycans , Heparitin Sulfate , Intercellular Junctions , Membranes , Microvilli , Permeability , Protease Inhibitors , ProteinuriaABSTRACT
BACKGROUND: Minimal Change Nephrotic Syndrome (MCNS) is one of the most common primary nephrotic syndromes in children and its pathogenesis has not been exactly known. Interleukin-8 (IL-8) and tumor necrosis factor-alpha (TNF-alpha ) may be involved in the pathogenesis of this disese, because they are increased in blood and/or urine during relapse. This study was conducted to see changes of IL-8 and TNF-alpha in children with MCNS and to see the effects of IL-8 and TNF-alpha on the abundance of HSPG mRNA in rats glomerular epithelial cells (GECs). METHODS: Study patients consisted of 19 biopsy-proven MCNS children aged 2-15 years old. Ten age-matched healthy children were used as controls. Both blood and urinary IL-8 and TNF-alpha were measured using ELISA kit. GECs were cultured until confluent. IL-8 or TNF-alpha were added at various concentrations. Total RNA was extracted at 12 or 24 hours after adding IL-8 or TNF-alpha . RT-PCR using HSPG-specific primers and beta-actin as internal controls was done. Densities and areas of GBM HSPG corresponding bands to beta-actin bands were measured. RESULTS: Values of urinary IL-8 (ng/mg'cr) were 13,996+/-2,811, 2,811+/-3,734, and 5,331+/-6,403, during relapse, remission, and in control, respectively. Urinary IL-8 'during relapse' was significantly measured increased compared to 'during remission' and in controls (p<0.05). Values of urinary TNF-alpha (ng/mg'cr) were 364.4+/-512.1, 155.3+/-208.0, and 36.0+/-45.0, during relapse, remission, and in control, respectively. Urinary TNF-alpha during relapse was also significantly increased compared to 'during remission' and 'control' (p<0.05). Values of Blood IL-8 (ng/mL) were 1.19+/-1.23, 0.51+/-0.84, and 0.77+/-0.62, during relapse, remission, and in control, respectively. Blood IL-8 during relapse was significantly increased compared to 'during remission' and 'in control' (p<0.05). No significant change was seen in blood TNF-alpha. And no significant difference was seen in abdundance of HSPG mRNA after adding various concentraons IL-8 or TNF-alpha into rats GEC. CONCLUSION: The values of plasma and urinary IL-8 and TNF-alpha during relapse were increased compared to those of remission period and in control. but neither IL-8 nor TNF-alpha affect the abundance of HSPG-mRNA in rats GECs at various concentraions. So, it seems that both IL-8 and TNF-alpha do not play a direct role in GBM permeability and the elevated values of these cytokines in plasma and/or urine are secondary effects.
Subject(s)
Animals , Child , Humans , Rats , Actins , Cytokines , Enzyme-Linked Immunosorbent Assay , Epithelial Cells , Heparan Sulfate Proteoglycans , Heparitin Sulfate , Interleukin-8 , Nephrosis, Lipoid , Nephrotic Syndrome , Permeability , Plasma , Recurrence , RNA , RNA, Messenger , Tumor Necrosis Factor-alphaABSTRACT
Aim To observe the anti-tumor activity and the mechanism of heparan sulfate proteoglycan(HSPG) on C3H mice transplanted tumors.Methods Tumor model was established and randomly divided into five groups.HSPG groups(5,10,50 mg?kg-1),positive group and control group,intraperitoneal injection was performed once a day for 22 days and the volume of tumors was measured.Mice were treated on 24th day,then tumor weight was examined,thymus index,and spleen index were calculated,the apoptosis was determined by TdT-mediated Dutp nick end labeling(TUNEL) assay in situ,the expression of vascular endothelial growth factor(VEGF) was detected by immunohistochemistry.Results The tumor volume in HSPG groups was reduced without the decrease of thymus index,spleen index.TUNEL assay in situ showed numerous heavy blue apoptosis cells in the HSPG groups significantly higher than in control groups.The tumors in HSPG groups showed significantly lower VEGF expression than those in control group.Conclusion HSPG had significant anti-tumor effects on C3H mice transplantable breast cancer.The mechanisms may be associated with the effects of inducing tumor cell apoptosis and inhibiting the VEGF expression.