104 research outputs found

    Orthodontic and orthopaedic treatment for anterior open bite in children (Review)

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    Background: Anterior open bite occurs when there is a lack of vertical overlap of the upper and lower incisors. The aetiology is multifactorial including: oral habits, unfavourable growth patterns, enlarged lymphatic tissue with mouth breathing. Several treatments have been proposed to correct this malocclusion, but interventions are not supported by strong scientific evidence. Objectives: The aim of this systematic review was to evaluate orthodontic and orthopaedic treatments to correct anterior open bite in children. Search methods: The following databases were searched: the Cochrane Oral Health Group's Trials Register (to 14 February 2014); the Cochrane Central Register of Controlled Trials (CENTRAL)(The Cochrane Library 2014, Issue 1); MEDLINE via OVID (1946 to 14 February 2014); EMBASE via OVID (1980 to 14 February 2014); LILACS via BIREME Virtual Health Library (1982 to 14 February 2014); BBO via BIREME Virtual Health Library (1980 to 14 February 2014); and SciELO (1997 to 14 February 2014). We searched for ongoing trials via ClinicalTrials.gov (to 14 February 2014). Chinese journals were handsearched and the bibliographies of papers were retrieved. Selection criteria: All randomised or quasi-randomised controlled trials of orthodontic or orthopaedic treatments or both to correct anterior open bite in children. Data collection and analysis: Two review authors independently assessed the eligibility of all reports identified. Risk ratios (RRs) and corresponding 95% confidence intervals (CIs) were calculated for dichotomous data. The continuous data were expressed as described by the author. Main results: Three randomised controlled trials were included comparing: effects of Frankel's function regulator-4 (FR-4) with lip-seal training versus no treatment; repelling-magnet splints versus bite-blocks; and palatal crib associated with high-pull chincup versus no treatment.The study comparing repelling-magnet splints versus bite-blocks could not be analysed because the authors interrupted the treatment earlier than planned due to side effects in four of ten patients.FR-4 associated with lip-seal training (RR = 0.02 (95% CI 0.00 to 0.38)) and removable palatal crib associated with high-pull chincup (RR = 0.23 (95% CI 0.11 to 0.48)) were able to correct anterior open bite.No study described: randomisation process, sample size calculation, there was not blinding in the cephalometric analysis and the two studies evaluated two interventions at the same time. These results should be therefore viewed with caution. Authors' conclusions: There is weak evidence that the interventions FR-4 with lip-seal training and palatal crib associated with high-pull chincup are able to correct anterior open bite. Given that the trials included have potential bias, these results must be viewed with caution. Recommendations for clinical practice cannot be made based only on the results of these trials. More randomised controlled trials are needed to elucidate the interventions for treating anterior open bite

    Efeitos da nutrição parenteral total associada à infecção bacteriana na função hepatobiliar de ratos da cepa Wistar

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    OBJECTIVE: To evaluate the hepatic alterations associated to parenteral nutrition inrats.MATERIAL AND METHODS: Four groups with 10 rats each: Group I (control group) -rats were orally fed with a regular diet; Group II - rats received a regular diet, and wereinfected with Escherichia coli through intraperitoneal inoculation; Group III - rats receivedparenteral nutrition; and group IV, rats received parenteral nutrition, and were infectedwith Escherichia coli. Serum concentrations of AST, ALT, GGT, and 5’ N were measuredon the first day of the experiment, and on the eighth day of parenteral nutrition (the dayanimals were sacrificed). Histological study of the liver of the rats included: evaluationof hydropic degeneration, dilation of the central lobular vein, cholestasis, sinusoidaldilation, proliferation of Kupffer cells, cellular necrosis, and steatosis. All alterationswere graded from 0 to 4+.RESULTS: The lab exams did not present consistent alterations at the end of theexperiment. Group IV presented a reduction in GGT concentration; in addition, thisgroup presented the largest variations in AST and ALT concentration, possibly as aresult of being submitted to more intense aggression to the hepatic parenchyma. Froma histological point-of-view, all animals (with the exception of one) presented dilation ofthe central lobular vein and of the sinusoids. Such findings were more frequent amonginfected animals. The animals did not present steatosis or cholestasis.CONCLUSIONS: 1) The proposed model of intraperitoneal inoculation of Escherichiacoli was appropriate for the study of bacterial infection in young rats of the Wistarstrain; 2) our results indicate that the association of parenteral nutrition and infectiondetermined histologic alterations which were unspecific, but more intense than thealterations determined by each of these situations in isolation.OBJETIVO: Avaliar as alterações hepáticas associadas à nutrição parenteral em ratos.MATERIAIS E MÉTODOS: Foram avaliados quatro grupos com 10 ratos cada: grupoI - controles alimentados, via oral, com dieta habitual; grupo II - em dieta habitual einfectados com Escherichia Coli inoculada por via intra peritoneal; grupo III - emnutrição parenteral; e grupo IV - em nutrição parenteral e infectados. Foram analisadasas concentrações séricas de AST, ALT, GGT e 5’N no primeiro dia do experimento eno oitavo dia da nutrição parenteral, por ocasião do sacrifício dos animais. O estudohistológico do fígado dos 40 ratos consistiu na avaliação de degeneração hidrópica,dilatação da veia centro-lobular, colestase, dilatação sinusoidal, proliferação de célulasde Kupffer, necrose celular e esteatose. As alterações foram graduadas de 0 a 4+.RESULTADOS: Os exames laboratoriais não foram consistentemente alterados aofinal do experimento. No grupo IV houve redução na concentração de GGT; alémdisso, este foi o grupo que apresentou as maiores variações de AST e ALT,possivelmente devido à maior agressão do parênquima hepático. Do ponto de vistahistológico, todos os animais submetidos à nutrição parenteral (com apenas umaexceção) apresentaram dilatação da veia centro-lobular e dos sinusóides. Estesachados foram mais comuns nos animais infectados. Não foram observadas esteatosee/ou colestase.CONCLUSÕES: 1) O modelo proposto de inoculação intra-peritoneal com EscherichiaColi foi adequado para estudar infecção em ratos jovens da cepa Wistar; 2) osresultados obtidos indicaram que a associação entre nutrição parenteral e infecçãodeterminou alterações histológicas inespecíficas, porém mais intensas do que asalterações determinadas em cada uma dessas situações isoladamente

    Brazilian Morus nigra

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    Morus nigra has been used popularly for several proposes, including diabetic. In an attempt to support medicinal value, the acute hypoglycemic, hypolipidemic, and antioxidant effects of the ethanolic extract of Morus nigra (EEMn 200 or 400 mg/kg b.w.) were evaluated in normal and alloxan-induced diabetic treated for 14 days. Serum biochemical and antioxidant analysis were performed at the end of experiment. Oral glucose tolerance test was performed at 10th and 15th days. Chromatographic analysis by HPLC-DAD of EEMn was performed. Insulin was used as positive control to glycemic metabolism as well as fenofibrate to lipid metabolism. EEMn (400 mg/kg/day) reduced fasting and postprandial glycaemia, improved oral glucose tolerance, and reduced lipolysis and proteolysis in diabetic rats. EEMn decreased the blood levels of total cholesterol and increased HDL level when compared to the diabetic control rats. At higher levels, EEMn reduced triglycerides and VLDL levels in diabetic rats. Also, EEMn reduced malondialdehyde and increased the reduced glutathione levels in liver of diabetic rats. Chromatographic analysis identified the presence of the flavonoids rutin, isoquercetin, and kaempferitrin. Acute EEMn treatment reduced hyperglycemia, improved oral glucose tolerance, and minimized dyslipidemia and oxidative stress leading to a reduction in atherogenic index in alloxan-induced diabetic rats

    A cyclopalladated complex interacts with mitochondrial membrane thiol-groups and induces the apoptotic intrinsic pathway in murine and cisplatin-resistant human tumor cells

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    <p>Abstract</p> <p>Background</p> <p>Systemic therapy for cancer metastatic lesions is difficult and generally renders a poor clinical response. Structural analogs of cisplatin, the most widely used synthetic metal complexes, show toxic side-effects and tumor cell resistance. Recently, palladium complexes with increased stability are being investigated to circumvent these limitations, and a biphosphinic cyclopalladated complex {Pd<sub>2 </sub>[<it>S<sub>(-)</sub></it>C<sup>2</sup>, N-dmpa]<sub>2 </sub>(μ-dppe)Cl<sub>2</sub>} named C7a efficiently controls the subcutaneous development of B16F10-Nex2 murine melanoma in syngeneic mice. Presently, we investigated the melanoma cell killing mechanism induced by C7a, and extended preclinical studies.</p> <p>Methods</p> <p>B16F10-Nex2 cells were treated <it>in vitro </it>with C7a in the presence/absence of DTT, and several parameters related to apoptosis induction were evaluated. Preclinical studies were performed, and mice were endovenously inoculated with B16F10-Nex2 cells, intraperitoneally treated with C7a, and lung metastatic nodules were counted. The cytotoxic effects and the respiratory metabolism were also determined in human tumor cell lines treated <it>in vitro </it>with C7a.</p> <p>Results</p> <p>Cyclopalladated complex interacts with thiol groups on the mitochondrial membrane proteins, causes dissipation of the mitochondrial membrane potential, and induces Bax translocation from the cytosol to mitochondria, colocalizing with a mitochondrial tracker. C7a also induced an increase in cytosolic calcium concentration, mainly from intracellular compartments, and a significant decrease in the ATP levels. Activation of effector caspases, chromatin condensation and DNA degradation, suggested that C7a activates the apoptotic intrinsic pathway in murine melanoma cells. In the preclinical studies, the C7a complex protected against murine metastatic melanoma and induced death in several human tumor cell lineages <it>in vitro</it>, including cisplatin-resistant ones. The mitochondria-dependent cell death was also induced by C7a in human tumor cells.</p> <p>Conclusions</p> <p>The cyclopalladated C7a complex is an effective chemotherapeutic anticancer compound against primary and metastatic murine and human tumors, including cisplatin-resistant cells, inducing apoptotic cell death via the intrinsic pathway.</p

    Timp1 interacts with beta-1 integrin and CD63 along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway independently of Akt phosphorylation

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    Background: Anoikis resistance is one of the abilities acquired along tumor progression. This characteristic is associated with metastasis development, since tumorigenic cells must survive independently of cell-matrix interactions in this process. in our laboratory, it was developed a murine melanocyte malignant transformation model associated with a sustained stressful condition. After subjecting melan-a melanocytes to 1, 2, 3 and 4 cycles of anchorage impediment, anoikis resistant cells were established and named 1C, 2C, 3C and 4C, respectively. These cells showed altered morphology and PMA independent cell growth, but were not tumorigenic, corresponding to pre-malignant cells. After limiting dilution of 4C pre-malignant cells, melanoma cell lines with different characteristics were obtained. Previous data from our group showed that increased Timp1 expression correlated with anoikis-resistant phenotype. Timp1 was shown to confer anchorage-independent growth capability to melan-a melanocytes and render melanoma cells more aggressive when injected into mice. However, the mechanisms involved in anoikis regulation by Timp1 in tumorigenic cells are not clear yet.Methods: the beta 1-integrin and Timp1 expression were evaluated by Western blotting and CD63 protein expression by flow cytometry using specific antibodies. To analyze the interaction among Timp1, CD63 and beta 1-integrin, immunoprecipitation assays were performed, anoikis resistance capability was evaluated in the presence or not of the PI3-K inhibitors, Wortmannin and LY294002. Relative expression of TIMP1 and CD63 in human metastatic melanoma cells was analyzed by real time PCR.Results: Differential association among Timp1, CD63 and beta 1-integrins was observed in melan-a melanocytes, 4C pre-malignant melanocytes and 4C11- and 4C11+ melanoma cells. Timp1 present in conditioned medium of melanoma cells rendered melan-a melanocytes anoikis-resistant through PI3-K signaling pathway independently of Akt activation. in human melanoma cell lines, in which TIMP1 and beta-1 integrin were also found to be interacting, TIMP1 and CD63 levels together was shown to correlate significantly with colony formation capacity.Conclusions: Our results show that Timp1 is assembled in a supramolecular complex containing CD63 and beta 1-integrins along melanoma genesis and confers anoikis resistance by activating PI3-K signaling pathway, independently of Akt phosphorylation. in addition, our data point TIMP1, mainly together with CD63, as a potential biomarker of melanoma.Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)Universidade Federal de São Paulo, Dept Pharmacol, São Paulo, BrazilUniversidade Federal de São Paulo, Microbiol Immunol & Parasitol Dept, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biochem, São Paulo, BrazilLudwig Inst Canc Res, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Pharmacol, São Paulo, BrazilUniversidade Federal de São Paulo, Microbiol Immunol & Parasitol Dept, São Paulo, BrazilUniversidade Federal de São Paulo, Dept Biochem, São Paulo, BrazilFAPESP: 2011/12306-1FAPESP: 2010/18715-8CAPES: 2867/10Web of Scienc
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