53 resultados para migration

em Repositório Institucional UNESP - Universidade Estadual Paulista "Julio de Mesquita Filho"


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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Tinuvin P migration from Polyethyleneterephthalate (PET) bottles was investigated using several fatty-food simulants such as olive oil, soybean oil, n-heptane and iso-octane, at exposure conditions of 2-10 days at 40 degrees C (total immersion). The stability of several UV stabilizers (BHT, Cyasorb UV 5411, Tinuvin P, Tinuvin 326 and Tinuvin 327) in n-heptane and iso-octane was also studied. After 10 days at 40 degrees C, losses of 6% and 20% in iso-octane and n-heptane respectively, were verified for Tinuvin P. Other UV stabilizers at the same experimental conditions showed higher losses (up to 30% for Tinuvin 327). These results confirm that, when carrying out specific migration studies, the stability of the substance of interest should be established in the food simulant to avoid underestimating the real migration behaviour. In order to quantify UV stabilizer migration, n-heptane and iso-octane solutions were concentrated and directly analysed by SIM mode GC-MS. For olive and soybean oils, Tinuvin P was isolated using size-exclusion chromatography and quantified by SIM mode GC-MS. Iso-octane proved to be a move suitable fatty-food simulant than n-heptane for the migration study of Tinuvin P from PET. Higher levels of Tinuvin P migrated to olive and soybean oils rather than to n-heptane. These results suggest that the MERCOSUL recommended official methods for specific migration studies should be revised since the migration levels using n-heptane as a fatty-food simulant could be underestimated when compared to edible oils. Copyright (C) 1999 John Wiley & Sons, Ltd.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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The aim of this work was to identify the degradation compounds produced during irradiation of multilayer polyamide 6 (PA-6) films and to study their migration into water and 95% ethanol food simulant. After irradiation of multilayer PA-6 films at 3, 7 and 12 kGy, degradation compounds were extracted using solid-phase microextraction, for which the time and temperature of extraction and stirring were optimized, and identified by gas chromatography-mass spectrometry. Caprolactam, 2-cyclopentylcyclopentanone and aldehydes, among other compounds, were identified in the headspace of the films. Polydimethylsiloxane was considered the best fiber for extraction. The optimum conditions of time, temperature and stirring to extract the compounds were 20 min, 80 degrees C and 225 rpm. For validation purposes, the compounds were quantified in water and 95% ethanol and the results showed high sensitivity, good precision and accuracy. Migration of compounds from irradiated and non-irradiated multilayer PA-6 films into water and 95% ethanol food simulants was carried out at 40 degrees C for 10 days. The method was efficient for the quantification of decaldehyde, 2-cyclopentylcyclopentanone and caprolactam that migrated from multilayer PA-6 films into food simulants.

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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)

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The migration of diethylhexyl phthalate (DEHP) from PVC bags into LVPS (0.9% NaCl) and LVPS with cyclosporine at concentrations of 2.5 and 0.5 mg/ml was studied. PVC bags were placed in contact with these solutions and stored at 25 1 degrees C. They were taken for analysis each 30 min during 6 h and after this period at each 1 h until 12 h of contact. Water was used as reference, and exposed and analyzed under the same conditions. After contact, the solutions were submitted to extraction with hexane and analyzed by GC-FID. The results showed that DEHP did not migrate into water and LVPS during all the time. Also, no measurable amount of DEHP was detected during the first 3 h of contact between the PVC bag and the diluted cyclosporine solution. However, the amount of released DEHP reached a detectable level after 4 It of contact, increased until 6 h, stabilized, and increased again after 9-10 h. The 12 h of contact showed the highest DEHP levels for both cyclosporine concentrations. The DEHP migrated was 0.02-0.08% of that present in the bag. (c) 2005 Elsevier B.V. All rights reserved.

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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)

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The aim of this study was to investigate cellular migration induced by calcium hydroxide to air-pouch cavities in mice. The migration was more specific to neutrophil and was dose and time dependent (peaking 96 h after stimulation). This migration was inhibited by pretreatment with thalidomide, indomethacin, MK886, meloxicam, dexamethasone, MK886 associated with indomethacin, and MK886 associated with indomethacin and dexamethasone. The air-pouch exudate from animals stimulated with calcium hydroxide showed an increase of leukotriene-B4 (LTB4), interleukin-1 beta, tumor necrosis factor alpha (TNF-alpha), cytokine-induced neutrophil chemoattractant (KC), and macrophage inflammatory protein 2 (MIP-2) release. Pretreatment with 3% thioglycollate increased the macrophage population in the air pouch but did not change neutrophil migration. Depleting the resident mast cells through chronic pretreatment with compound 48/80 did not alter neutrophil migration in response to calcium hydroxide. It was possible to conclude that calcium hydroxide-induced neutrophil migration to the air-pouch cavity in mice is mediated by LTB4, TNF-alpha, KC, MIP-2, and prostaglandins, but it was not dependent on macrophages or mast cells.

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Pathologic tooth migration related to periodontal disease is a common chief complaint of periodontal patients. This paper describes the treatment of a case of severe periodontal disease and disfiguring pathologic migration of maxillary central incisors, which required a multidisciplinary approach. After conventional pert. odontal treatment was performed, the anterior diastema was closed using a combination of orthodontic therapy and restorative treatment. A 6-month follow-up examination of this case revealed resolution of the anterior pathologic migration, with gains in clinical attachment levels and a successful esthetic and functional final result.

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The 5-year survival rate for oral cavity cancer is poorer than for breast, colon or prostate cancer, and has improved only slightly in the last three decades. Hence, new therapeutic strategies are urgently needed. Here we demonstrate by tissue micro array analysis for the first time that RNA-binding protein La is significantly overexpressed in oral squamous cell carcinoma (SCC). Within this study we therefore addressed the question whether siRNA-mediated depletion of the La protein may interfere with known tumor-promoting characteristics of head and neck SCC cells. Our studies demonstrate that the La protein promotes cell proliferation, migration and invasion of lymph node-metastasized hypopharyngeal SCC cells. We also reveal that La is required for the expression of beta-catenin as well as matrix metalloproteinase type 2 (MMP-2) within these cells. Taken together these data suggest a so far unknown function of the RNA-binding protein La in promoting tumor progression of head and neck SCC.

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Background: Suppressor of cytokine signaling 3 (SOCS3) is an inducible endogenous negative regulator of signal transduction and activator of transcription 3 (STAT3). Epigenetic silencing of SOCS3 has been shown in head and neck squamous cell carcinoma (HNSCC), which is associated with increased activation of STAT3. There is scarce information on the functional role of the reduction of SOCS3 expression and no information on altered subcellular localization of SOCS3 in HNSCC.Methodology/Principal Findings: We assessed endogenous SOCS3 expression in different HNSCC cell lines by RT-qPCR and western blot. Immunofluorescence and western blot were used to study the subcellular localization of endogenous SOCS3 induced by IL-6. Overexpression of SOCS3 by CMV-driven plasmids and siRNA-mediated inhibition of endogenous SOCS3 were used to verify the role of SOCS3 on tumor cell proliferation, viability, invasion and migration in vitro. In vivo relevance of SOCS3 expression in HNSCC was studied by quantitative immunohistochemistry of commercially-available tissue microarrays. Endogenous expression of SOCS3 was heterogeneous in four HNSCC cell lines and surprisingly preserved in most of these cell lines. Subcellular localization of endogenous SOCS3 in the HNSCC cell lines was predominantly nuclear as opposed to cytoplasmic in non-neoplasic epithelial cells. Overexpression of SOCS3 produced a relative increase of the protein in the cytoplasmic compartment and significantly inhibited proliferation, migration and invasion, whereas inhibition of endogenous nuclear SOCS3 did not affect these events. Analysis of tissue microarrays indicated that loss of SOCS3 is an early event in HNSCC and was correlated with tumor size and histological grade of dysplasia, but a considerable proportion of cases presented detectable expression of SOCS3.Conclusion: Our data support a role for SOCS3 as a tumor suppressor gene in HNSCC with relevance on proliferation and invasion processes and suggests that abnormal subcellular localization impairs SOCS3 function in HNSCC cells.

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Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)