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Interleukin (IL)-36 is a family of cytokines that belongs to the larger IL-1 superfamily. IL-36 agonist/antagonist binds to the interleukin-36 receptor involving in physiological inflammation regulation and pathogenesis of many inflammatory diseases. In inflammatory joint diseases, the expression of IL-36 changes, and some studies have initially explored the role of IL-36 in these diseases. In psoriatic arthritis, IL-36 signal mediates plasma cell and fibroblast-like synoviocyte crosstalk presenting IL-36 agonist/antagonist imbalance. In rheumatoid arthritis, IL-36 agonists induce fibroblast-like synoviocyte to produce pro-inflammatory factors, while IL-36 antagonist deficiency leads to lesion progression. In osteoarthritis, IL-36 agonists induce chondrocytes to produce catabolic enzymes and pro-inflammatory factors. This article reviews the expression and function of IL-36 in different inflammatory joint diseases to provide a reference for revealing their pathogenic mechanisms and discovering therapeutic targets.
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Humanos , Interleucinas , Artritis Reumatoide , Osteoartritis/patología , Artritis Psoriásica/metabolismo , CitocinasRESUMEN
To give full play to the important role of courses for ideological and political education in moral cultivation, teaching group in the course of oral histology and pathology in Zhejiang University systematically studied the teaching model of which ideological and political education integrated into the course of oral histology and pathology, and put forward a quality evaluation index system of the course. This paper emphatically introduces the general framework of the course, as well as the experience and practices in the aspects of resource mining, teaching design, curriculum evaluation, etc. The quality of the course was evaluated by using the system, which showed that the grade of the course was AAA (excellent) and 95.5% (275/288) students agreed to integrate ideological and political content into the course. The teaching group believes that the integration of the ideological and political content in the course reflects the complementary effect of "teaching" and "educating", and the ideological and political quality as well as the professional level of the teachers are the primary factor to determine the quality of the course. This paper aims at providing a reliable reference for promoting the construction of courses for ideological and political education in the area of oral medical education.
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Metabolomics methods were applied in the study of the toxicity of environmental pollutants. It has been shown that exposure to heavy metals such as mercury, arsenic, cadmium, chromium and lead could cause significant changes in energy, lipids, nucleic acids and amino acids in mammalian cells. After exposure to benzo(a)pyrene [B(a)P], the glands of Pinctada pumila could produce various changes, such as energy metabolic disorder, cell damage, signal transduction disorder, oxidative stress and osmotic disorder. Persistent organic compounds polychlorinated biphenyls (PCBs) could exert toxic effects on Zebrafish embryos through affecting amino acid metabolism, DNA and protein methylation and biosynthesis. After exposure to endocrine disruptors, such as nonylphenol, octylenediester phthalate and bisphenol propane, goldfish showed energy, lipid and nucleic acid metabolic disorders.
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Animales , Benzo(a)pireno , Contaminantes Ambientales , Metabolómica , Estrés OxidativoRESUMEN
Cytochrome P450(CYP450),one of the most important enzymes in the human body,medi?ates the activation and toxicity of indirect poisons as well as indirect carcinogens. CYP450 is a super?family mainly composed of CYP1A, CYP1B, CYP2A, CYP2B, CYP2C, CYP2E, CYP2W, CYP3A and their activities are widely modulated by epigenetic manners, such as DNA methylation, histone modifi?cation and microRNA interference.Indirect carcinogens including benzo(a)pyrene,2,3,7,8-tetrachlorod?ibenzo-p-dioxin,diethylstilbestrol,aflatoxin B1 and cyclophosphamide,can change epigenetic modifica?tions, such as specific changes in DNA methylation, histone acetylation, methylation or ubiquitination, and up-or down-regulation of microRNA expression,which affect the function of the major subtypes of CYP450 and their role in indirect carcinogen activation.
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The gene polymorphisms of human being will cause abnormality in the expression of corresponding gene,which is closely related to the physiological function and disease.Cytochrome P450,cyclooxygenase and lipoxygenase are vital enzymes that mediated the oxidative metabolism process for exogenous chemicals,and play important roles in activating the indirect carcinogens and metabolizing clinical drug;the gene polymorphisms of these enzymes can change the expression and activity of enzymes,affect the metabolic transformation of carcinogens,and then give rise to difference in the susceptibility to neoplasms.Studying the relationship between the gene polymorphisms of oxidative metabolism enzyme for endogenous and exogenous chemicals and the susceptibility to neoplasms can provide scientific basis for probing into the genetic markers and the pathogenesis of neoplasms.
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5-Lipoxygenase, one of lipoxygenase isozymes, is a well-studied oxidative metabolism enzyme. It widely exists in various human tissues and cells, participates in the oxidative metabolism of endogenous and exogenous chemicals, and produces a variety of metabolites, all of which contribute to the occurrence of human diseases, such as inflammation, asthma, atherosclerosis, and tumor and so on. The expression of 5-lipoxygenase is at low level in normal human tissues while at high level in abnormal tissues. 5-Lipoxygenase is closely related to many kinds of diseases in human ovary, brain, cardiovascular system, lung, liver, pancreas and other tissues. The abnormal expression of 5-lipoxygenase tends to promote the development of the disease.
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Humanos , Araquidonato 5-Lipooxigenasa , Fisiología , Aterosclerosis , Inflamación , NeoplasiasRESUMEN
<p><b>BACKGROUND</b>Oral squamous cell carcinoma (OSCC) is one of the most common malignancies in the oral and maxillofacial region. Yes-associated protein 1 (YAP1) has been implicated as a bona fide oncogene in solid tumors. We seek to elucidate the role of YAP1 in OSCC tissue.</p><p><b>METHODS</b>We identified YAP1 gene and protein overexpression in 30 OSCC patients and 10 normal oral mucosa tissues by immunohistochemistry, Western blotting and reverse transcription polymerase chain reaction (RT-PCR).</p><p><b>RESULTS</b>In the normal oral mucosa by immunohistochemical staining, YAP1 mainly located in both the cytoplasm and nucleus mainly the nuclei of the basal cells. In OSCC, the expression of YAP1 translocated from the nucleus to cytoplasm; YAP1 being mainly located in both the cytoplasm and nucleus of the adjacent mucosa. The expression of YAP1 gradual increased in normal oral mucosa, tumor adjacent mucosa and low grade, middle grade, high grade OSCC tissue by Western blotting. Significant difference was found between the expressions of the normal oral mucosa and OSCC tissue (P < 0.05). The coincidence was detected between the normal oral mucosa and OSCC tissue by RT-PCR (P < 0.05).</p><p><b>CONCLUSIONS</b>YAP1 is involved in the carcinogenesis and development of OSCC. There is a transformation between nucleus and cytoplasm.</p>
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Humanos , Proteínas Adaptadoras Transductoras de Señales , Genética , Metabolismo , Western Blotting , Carcinoma de Células Escamosas , Genética , Metabolismo , Técnicas In Vitro , Neoplasias de la Boca , Genética , Metabolismo , Fosfoproteínas , Genética , Metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa InversaRESUMEN
<p><b>OBJECTIVE</b>The oxidation of benzo (a) pyrene mediated by 5-lipoxygenase (5-LOX) were investigated in HBE cells in order to provide further proof that lipoxygenase is the alternative pathway for the oxidation of xenobiotics.</p><p><b>METHODS</b>Enzymic experiment: Soybean lipoxygenase (SLO), substrate (benzo[a] pyrene) and other component react in the enzymic system and the reaction product are detected by spectrophotometry. At the same time, in vitro detect of benzo (a) pyrene-DNA adducts with a UV spectrophotometer and HPLC. Cellular experiment: After HBE cells exposure to different poison (B[a]P 4, 8, 16, 32, 64, 128µmol/L, AA-861, naproxen or α- naphthoflavone 0.1, 1, 10 µmol/L) for 24 hours, the effect of benzo (a) -pyrene on cell survival rate were assessed by reductions of tetrazolium dye (MTT) and flow cytometry in cultured HBE cells, and the protein expressions of 5-lipoxygenase in the cells are tested by western-blot, and the DNA damages by the single cell gel electrophoresis. And then, the effect of the specific inhibitor of 5-lipoxygenase (AA-861) on 5-lipoxygenase protein expression and DNA damage in the cells are detected.</p><p><b>RESULTS</b>SLO can catalyze the co-oxidation of benzo (a) pyrene to generate benzo (a) pyrene-7,8-epoxide in the presence of hydrogen peroxide. GTP can inhibit the reaction , the IC50 value is 0.46 mg/L, the model equation is Probit (P) = 0.8985+2.6824 Log (dose). SLO can catalyze the co-oxidation of benzo (a) pyrene to generate a new product, but fail to form DNA adducts in vitro. HBE cell viability decreased with the benzo (a) pyrene concentration increased , but AA-861 and naproxen can inhibit it. Flow cytometry and single cell gel electrophoresis experiments show, Benzo (a) pyrene can induce 5-lipoxygenase protein expression, but AA-861 cannot in HBE. Benzo (a) pyrene causes toxic action and DNA damage in HBE, which can significantly inhibit by AA-861, the difference is statistically significant (P < 0.05).</p><p><b>CONCLUSIONS</b>The co-oxidate of benzo (a) pyrene by 5-LOX turns into electrophiles that covalently bind to DNA and induce DNA damage, which can be significantly inhibited by AA-861.</p>
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Humanos , Benzo(a)pireno , Metabolismo , Células Cultivadas , Aductos de ADN , Metabolismo , Daño del ADN , Células Epiteliales , Metabolismo , Lipooxigenasa , FarmacologíaRESUMEN
<p><b>OBJECTIVE</b>To systemically investigate receptor activator of nuclear factor-kappaB ligand (RANKL) and macrophage colony-stimulating factor (M-CSF) induced differentiation of osteoclasts.</p><p><b>METHODS</b>Mouse protein-protein interaction(PPI) database NIA and published microarray dataset GES16749 were used to construct and analyze PPI network of RANKL and M-CSF induced mouse monocyte RAW264.7.</p><p><b>RESULTS</b>In the PPI network, transforming growth factor beta receptor 1 (TGFBR1), Rous sarcoma oncogene (SRC), myelocytomatosis oncogene(MYC) and integrin beta 3 (ITGB3) were able to interact with more proteins and they were the key nodes in the signaling transduction.</p><p><b>CONCLUSION</b>TGFBR1, SRC, MYC and ITGB3 might be the key points of RANKL and M-CSF induced differentiation of osteoclasts.</p>
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Animales , Ratones , Proteínas Portadoras , Diferenciación Celular , Factor Estimulante de Colonias de Macrófagos , Glicoproteínas de Membrana , Osteoclastos , Mapas de Interacción de Proteínas , Ligando RANK , Receptor Activador del Factor Nuclear kappa-BRESUMEN
<p><b>OBJECTIVE</b>To investigate the effects of overexpression of exogenous Notch1 in human tongue squamous cell carcinoma (TSCC) cells on cell growth and expression of epidermal growth factor receptor (EGFR) in vitro.</p><p><b>METHODS</b>Human TSCC cell line Tca8113 cells were transiently transfected with the eukaryotic expression plasmid pRAMIC-IRES2-EGFP encoding exogenous intracellular fragment of Notch1 and control plasmid pIRES2-EGFP by Lipofectamine 2000, respectively. Untransfected parental Tca8113 cells served as control. The cell proliferation was evaluated by methyl thiazolyl tetrazolium(MTT) assay. The apoptosis was assessed by flow cytometry. The mRNA and protein levels of Notch1 and EGFR in Tca8113 cells were detected by reverse transcriptase-polymerase chain reaction (RT-PCR) and Western blot. The expression of EGFR protein in Tca8113 cells was detected by immunocytochemistry.</p><p><b>RESULTS</b>MTT assay showed that the cell proliferation of Tca8113 cells transfected with pRAMIC-IRES2-EGFP was significantly inhibited as compared with controls (P < 0.05). After transfected with pRAMIC-IRES2-EGFP for 48 h, the apoptosis rate of Tca8113 cells was significantly higher than those of Tca8113 cells transfected with pIRES2-EGFP and untransfected Tca8113 cells (P < 0.05), and Notch1 expression was significantly increased at mRNA (P < 0.05) and protein (P < 0.05) levels, while EGFR expression was significantly decreased at mRNA (P < 0.05) and protein (P < 0.05) levels.</p><p><b>CONCLUSION</b>Overexpression of exogenous Notch1 may inhibit cell growth and down-regulate EGFR expression in TSCC cells.</p>
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Humanos , Apoptosis , Carcinoma de Células Escamosas , Línea Celular Tumoral , Proliferación Celular , Regulación hacia Abajo , Técnicas In Vitro , ARN Mensajero , Receptores ErbB , Neoplasias de la Lengua , TransfecciónRESUMEN
<p><b>OBJECTIVE</b>To investigate the effects of epidermal growth factor receptor (EGFR) gene silencing mediated by short hairpin RNA (shRNA) on proliferation and apoptosis of human tongue carcinoma cells.</p><p><b>METHODS</b>shRNA eukaryotic expression vector targeting the specific sequence of human EGFR gene was constructed and termed shEGFR. The control vector targeting the unrelated sequence was also constructed and termed shNC. The vectors were transiently transfected into Tca8113 cells of human tongue squamous cell carcinoma by Lipofectamine 2000, respectively. The mRNA and protein levels of EGFR in Tca8113 cells were detected by reverse transcriptase polymerase chain reaction (RT-PCR) and Western blotting. The cell proliferation of Tca8113 cells was evaluated by methyl thiazolyl tetrazolium (MTT) assay. The apoptosis of Tca8113 cells was assessed by flow cytometry.</p><p><b>RESULTS</b>EGFR expression in Tca8113 cells transfected with shEGFR were obviously decreased at mRNA level (81.6%) and protein level (72.0%) (P < 0.05) 48 h after transfection of shEGFR compared with untransfected Tca8113 cells. The proliferation activity of Tca8113 cells transfected with shEGFR was significantly lower than that of Tca8113 cells transfected with shNC and untransfected Tca8113 cells (P < 0.05). The early apoptotic rate of Tca8113 cells transfected with shEGFR was significantly higher than that of Tca8113 cells transfected with shNC and untransfected Tca8113 cells [(39.4 +/- 7.7)%, (4.3 +/- 1.2)%, (2.5 +/- 0.9)%, P < 0.05] 48 h after transfection of shEGFR.</p><p><b>CONCLUSIONS</b>EGFR gene silencing mediated by shRNA may inhibit cell proliferation and induce apoptosis in human tongue carcinoma cells.</p>
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Humanos , Apoptosis , Carcinoma de Células Escamosas , Genética , Metabolismo , Patología , Línea Celular Tumoral , Proliferación Celular , Silenciador del Gen , ARN Mensajero , Genética , ARN Interferente Pequeño , Genética , Receptores ErbB , Genética , Neoplasias de la Lengua , Genética , Metabolismo , Patología , TransfecciónRESUMEN
<p><b>OBJECTIVE</b>To investigate the expression of Notch1 in human tongue squamous carcinoma (TSCC) and precancerous lesion, and to explore the potential relation between Notch1 and epidermal growth factor receptor (EGFR).</p><p><b>METHODS</b>The expression of Notch1 and EGFR was detected in human TSCC (n = 41), tongue leukoplakia (LP) (n = 39) and normal tongue mucosa (n = 7) by immunohistochemistry.</p><p><b>RESULTS</b>In normal tongue mucosa and LP, the positive staining of Notch1 was mainly distributed in stratum corneum, partially in stratum granulosum and stratum spinosum, but not in stratum basale, while the positive staining of EGFR was mainly distributed in stratum basale, rarely in stratum spinosum, but not in stratum granulosum and stratum corneum. In TSCC, Notch1 expression was mainly distributed in locations of squamous metaplasia, but not in peripheral cells of carcinomas, while EGFR expression was detected mainly in peripheral cells of carcinomas, but not in locations of squamous metaplasia.</p><p><b>CONCLUSION</b>Notch1 promotes the differentiation of epithelial cells in tongue mucosa and acts as a tumor suppressor in TSCC. EGFR may act as a negative regulator of Notch1 expression in epithelium of tongue mucosa and TSCC, for maintaining cell proliferation and promoting the tumorigenesis and progression of TSCC.</p>
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Humanos , Carcinoma de Células Escamosas , Diferenciación Celular , Proliferación Celular , Células Epiteliales , Epitelio , Inmunohistoquímica , Leucoplasia Bucal , Mucosa Bucal , Receptores ErbB , Lengua , Neoplasias de la LenguaRESUMEN
<p><b>OBJECTIVE</b>To investigate the effect of intracellular 5-lipoxygenase on oxidation of benzidine in HBE cells and to provide further evidence that lipoxygenase is an alternative pathway for the oxidation of xenobiotics mediated by cytochrome P450.</p><p><b>METHODS</b>Enzyme system test: Soybean lipoxygenase (SLO), substrate (benzidine) and other components reacted in the enzyme system, followed by detection of the reaction products by spectrophotometry. In vitro test: After HBE cells were exposed to benzidine, the protein levels of 5-lipoxygenase in HBE cells were assessed by Western-blot, and the DNA damage by the single cell gel electrophoresis. At last, the effect of the specific inhibitor of 5-lipoxygenase (AA861) on 5-lipoxygenase protein expression and DNA damage in HBE cells were detected.</p><p><b>RESULTS</b>SLO could catalyze the co-oxidation of benzidine to generate benzidine diimine in the presence of hydrogen peroxide. Under optimal condition, numax value of the oxidation of benzidine catalyzed by SLO was 1.42 nmol*min(-1) SLO, and the Km value of benzidine was 1.48 mmol/L. EGCG could inhibit the oxidation of benzidine by SLO. Benzidine could induce 5-lipoxygenase protein expression in HBE cells, but AA861 was invalid. Benzidine caused DNA damage in HBE cells, which could be significantly inhibited by AA861.</p><p><b>CONCLUSION</b>5-LOX protein expression in HBE cells can be regulated by benzidine, which suggests that the co-oxidation of benzidine by 5-LOX could produce into electrophile that could covalently bind to DNA and induce DNA damage, which could be one of the mechanisms for carcinogenesis of BZD. 5-LOX inhibitor AA861 can inhibit this effect.</p>
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Humanos , Araquidonato 5-Lipooxigenasa , Metabolismo , Bencidinas , Farmacocinética , Toxicidad , Células Cultivadas , Daño del ADN , Células Epiteliales , MetabolismoRESUMEN
Lipoxygenase is a protein with non-heme iron atom, which has been discovered in many animals and plants. Lipoxygenase which has a close relationship with human tumors, inflammatory diseases, asthma, arteriosclerosis, and toxic action of chemicals could not only di-oxygenate endogenous polyunsaturated fatty acid to yield bioactive factors such as leukotrienes(LTs), but also has co-oxidation activity to activate xenobiotics. Lipoxygenase inhibitors include hydroxamic acid derivatives, nordihydroguaiaretic acid, flavonoids, FLAP inhibitors and so on. All of them can effectively restrain the catalytic action of lipoxygenase. Literatures demonstrate that the inhibitors can block the formation of relevant bioactive factors and toxic products of xenobiotics clinically which are used to prevent and cure the relevant diseases to keep people healthy.
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Animales , Humanos , Flavonoides , Farmacología , Leucotrienos , Metabolismo , Inhibidores de la Lipooxigenasa , Farmacología , Masoprocol , Farmacología , Oxidación-Reducción , Xenobióticos , MetabolismoRESUMEN
<p><b>OBJECTIVE</b>To investigate the expression of JAK, ERK and Cyclin D proteins in squamous-cell carcinoma of tongue.</p><p><b>METHODS</b>The expression of JAK, ERK and Cyclin D1 proteins was determined with SP immunohistochemical method in 30 cases of lingual Squamous cell carcinoma, 20 of normal lingual mucosa, 10 of mild epithelial dysplasia and 20 of severe epithelial dysplasia.</p><p><b>RESULTS</b>The expression of pJAK in lingual squamous-cell carcinoma and epithelial dysplasia was stronger than that of normal lingual mucosa (chi2=37.54, P<0.01), and the expression of pJAK in lingual squamous-cell carcinoma was significantly higher than that of the epithelial dysplasia (chi2=6.83, P<0.05). pJAK expression in squamous-cell carcinoma of low-middle differentiation was stronger than that of high differentiation. There was no significant difference in pERK expression among lingual squamous-cell carcinoma, normal lingual mucosa and epithelial dysplasia. There was a significantly positive correlation between pJAK and Cyclin D1 expression in SCC (r=0.619, P<0.05). There was no significant correlation between the expression of pERK and Cyclin D1 (r=0.231, P>0.05).</p><p><b>CONCLUSION</b>Over-expression of pJAK and Cyclin D1 may be associated with the occurrence and development of squamous-cell carcinoma of the tongue.</p>
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Humanos , Carcinoma de Células Escamosas , Metabolismo , Patología , Ciclina D1 , Metabolismo , Quinasas MAP Reguladas por Señal Extracelular , Metabolismo , Inmunohistoquímica , Quinasas Janus , Metabolismo , Fosforilación , Neoplasias de la Lengua , Metabolismo , PatologíaRESUMEN
<p><b>OBJECTIVE</b>To investigate the effect of anterior disc displacement on the expression of urokinase plasminogen activator and its inhibitor-1 (uPA/PAI-1) in synovial tissues.</p><p><b>METHODS</b>Forty Japanese white rabbits were used in this study. The animals were killed at 4 days, 1, 2, 4, 8 and 12 weeks postoperatively, respectively. In situ hybridization technology was applied to detect the expression of uPA/PAI-1 mRNA in synovial membrane.</p><p><b>RESULTS</b>In normal synovial tissues, synovial lining cells and a few fibrosblasts with mild positive staining were occasionally seen. More synovial lining cells and fibrosblasts with moderate postive signals were found 1 week after operation. Since then, the degree of staining for uPA/PAI-1 increased gradually. By the end of 12 weeks postoperatively, strong signals of uPA/PAI-1 mRNA were detected.</p><p><b>CONCLUSION</b>There is a harmonized uPA/PAI-1 system existing in synovial tissues. The high expression of uPA and PAI-1 mRNA in synovial tissues indicates that the uPA/PAI-1 system may play an important role in the process of synovitis resulted from anterior disc displacement.</p>
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Animales , Conejos , Hibridación in Situ , Plasminógeno , Inhibidor 1 de Activador Plasminogénico , ARN Mensajero , Membrana Sinovial , Activador de Plasminógeno de Tipo UroquinasaRESUMEN
<p><b>OBJECTIVE</b>To investigate the relative quantification of cytokeratin 19 transcription in oral squamous cell carcinoma tissues by fluorescent quantitive real-time reverse transcription-polymerase chain reaction ((RT-PCR).</p><p><b>METHODS</b>CK19mRNA level was detected by fluorescent quantitive real-time RT-PCR in cancerous and para-cancerous tissues from 31 oral squamous cell carcinoma patients. According to the 2(-DeltaDeltaCt) equation, the relative quantification fold of CK19mRNA level was calculated in cancerous tissues compared with para-cancerous tissues.</p><p><b>RESULTS</b>CK19mRNA levels in cancerous tissues were 2.21 folds higher than those in para-cancerous tissues, and the amplicon was specific. CK19mRNA level in cancerous tissue correlated significantly with pathological differentiation degree, the poorer the differentiation was, the higher the CK19mRNA level became.</p><p><b>CONCLUSIONS</b>Fluorescent quantitive real-time RT-PCR is accurate and reliable in the detection of relative quantification of CK19 transcription in oral squamous cell carcinoma tissues.</p>
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Adulto , Anciano , Femenino , Humanos , Masculino , Persona de Mediana Edad , Carcinoma de Células Escamosas , Metabolismo , Queratina-19 , Genética , Metabolismo , Neoplasias de la Boca , Metabolismo , ARN Mensajero , Genética , Metabolismo , Reacción en Cadena de la Polimerasa de Transcriptasa Inversa , MétodosRESUMEN
<p><b>OBJECTIVE</b>To investigate the influence of surface potentials of tooth hard tissue on bone remodeling.</p><p><b>METHODS</b>After insured the surface potentials of human extracted teeth with electrochemical methods, teeth sections and artificial hydroxyapatite were implanted into 25 rabbits' tibiae. The rabbits were sacrificed at 1, 2, 4, 6 and 8 weeks after implantation, respectively. The bone regeneration was compared between opposite two sides (cathode side and anode side) of tooth sections using hematoxylin-eosin (HE) staining, tartrate-resistant acid phosphatase (TRAP) activity detecting and tetracycline tracing method.</p><p><b>RESULTS</b>Resorption lacunae was seen in the tibiae facing to the enamel anode and new bone density in the implant bed near the cathode of tooth samples was much higher than that near the anode, while the number of TRAP positive cells near the cathode was smaller than that near the anode (P < 0.01). The fluorescent area of tetracycline tracing near the cathode was larger than that near the anode (P < 0.05).</p><p><b>CONCLUSIONS</b>The cathode of tooth hard tissue (cementum) could improve or trigger new bone formation, while the other side, anode (enamel), could improve the bone resorption. This study suggests that tooth hard tissue's electrochemical characteristic might affect the remodeling of alveolar bone, and tooth supraeruption and the alveolar bone loss after tooth extraction might result from the redundant or lack of root electrochemical stimulation to bone.</p>
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Animales , Femenino , Humanos , Masculino , Conejos , Pérdida de Hueso Alveolar , Remodelación Ósea , Cemento Dental , Fisiología , Esmalte Dental , Fisiología , Dentina , Fisiología , Electroquímica , Tibia , FisiologíaRESUMEN
<p><b>OBJECTIVE</b>To study the expressions of matrix metalloproteinase 2 (MMP2) and E-cadherin (E-CD) in salivary mucoepidermoid carcinoma, and their relationship with clinical stages, pathological grading, lymph node metastasis and prognosis.</p><p><b>METHODS</b>Surgical specimens of salivary mucoepidermiod carcinoma and normal salivary gland tissue were collected. MMP-2 and E-CD were stained immunohistochemically with streptavidin peroxidase method.</p><p><b>RESULTS</b>The expression of MMP-2 was increased and the expression of E-CD was reduced or negative in salivary mucoepidemoid carcinoma compared with those of the normal salivary gland. Expression of MMP-2 and E-CD was closely correlated with lymph node metastasis of the mucoepidermoid carcinoma. MMP-2 was positively correlated with the prognosis of mucoepidermoid carcinoma, and E-CD was negatively correlated to the prognosis of mucoepidermoid carcinoma.</p><p><b>CONCLUSION</b>The expression of MMP-2 and E-CD is closely correlated with the metastasis and prognosis of salivary mucoepidermoid carcinoma.</p>
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Humanos , Cadherinas , Genética , Carcinoma Mucoepidermoide , Metabolismo , Patología , Metaloproteinasa 2 de la Matriz , Genética , Invasividad Neoplásica , Metástasis de la Neoplasia , Pronóstico , Neoplasias de las Glándulas Salivales , Metabolismo , PatologíaRESUMEN
<p><b>BACKGROUND</b>The urokinase plasminogen activator system is believed to play an important role in degradation of the extracellular matrix associated with cartilage and bone destruction; however its precise roles in temporomandibular disorders have not yet been clarified. The aims of this study were to investigate the gene expression of fibrinolytic factors urokinase plasminogen activator (uPA) and plasminogen activator inhibitor-1 (PAI-1) in the articular cartilage of rabbit temporomandibular joint (TMJ) with disc displacement (DD) and to probe the relationship between fibrinolytic activity and cartilage remodeling.</p><p><b>METHODS</b>Disc displacement of right joints was performed in 36 of 78 rabbits under investigation. The animals were sacrificed at 4 days and 1, 2, 4, 8 and 12 weeks after surgery, respectively. The right joints of these animals were harvested and processed for the examination of mRNA expression of uPA and PAI-1 in articular cartilage using in situ hybridization techniques.</p><p><b>RESULTS</b>The expression of uPA and PAI-1 was co-expressed weakly in the chondrocytes from transitive zone to hypertrophic zone and mineralized zone, while no hybridizing signals were shown in proliferative zone and superficial zone in control rabbits. The most striking was the up-regulation of uPA and PAI-1 mRNA in 4-day rabbits postoperatively at the onset of cartilage degeneration. The strongest hybridizing signals for uPA and PAI-1 were seen in 2-week rabbits postoperatively. After 2 weeks, the expression of uPA and PAI-1 began to decrease and reached nearly normal level at 12 weeks.</p><p><b>CONCLUSIONS</b>The expression of the uPA/PAI-1 system coincides with the pathological changes in condylar cartilage after DD. The uPA/PAI-1 system may be one of the essential mediators in articular cartilage remodeling.</p>