930 resultados para Non proliferation regime
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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In this work we investigate a possible magnetic moment generation for massive neutral particles with spins-1 and -2 coupled non-minimally, in a specific way, to an external electromagnetic field. It is found that, in the nonrelativistic limit, these particles present g = 1. This result, worked out in the framework of Relativistic Quantum Mechanics, seems to suggest that g = 1 for all massive and neutral particles of any spin ≤ 2. We also compare with the results obtained for massive charged particles of spins-1 and -2, in the same regime (nonrelativistic), in order to investigate the role played by the spin separetely from the charge. Copyright © owned by the author(s) under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike Licence.
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Includes bibliography
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Background: Uterine Leiomyomas (ULs) are the most common benign tumours affecting women of reproductive age. ULs represent a major problem in public health, as they are the main indication for hysterectomy. Approximately 40-50% of ULs have non-random cytogenetic abnormalities, and half of ULs may have copy number alterations (CNAs). Gene expression microarrays studies have demonstrated that cell proliferation genes act in response to growth factors and steroids. However, only a few genes mapping to CNAs regions were found to be associated with ULs. Methodology: We applied an integrative analysis using genomic and transcriptomic data to identify the pathways and molecular markers associated with ULs. Fifty-one fresh frozen specimens were evaluated by array CGH (JISTIC) and gene expression microarrays (SAM). The CONEXIC algorithm was applied to integrate the data. Principal Findings: The integrated analysis identified the top 30 significant genes (P<0.01), which comprised genes associated with cancer, whereas the protein-protein interaction analysis indicated a strong association between FANCA and BRCA1. Functional in silico analysis revealed target molecules for drugs involved in cell proliferation, including FGFR1 and IGFBP5. Transcriptional and protein analyses showed that FGFR1 (P = 0.006 and P<0.01, respectively) and IGFBP5 (P = 0.0002 and P = 0.006, respectively) were up-regulated in the tumours when compared with the adjacent normal myometrium. Conclusions: The integrative genomic and transcriptomic approach indicated that FGFR1 and IGFBP5 amplification, as well as the consequent up-regulation of the protein products, plays an important role in the aetiology of ULs and thus provides data for potential drug therapies development to target genes associated with cellular proliferation in ULs. © 2013 Cirilo et al.
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The exploitation of non-timber forest products is often considered a low-impact activity in tropical forests. However, assessments of the impacts of such activity are mostly focused on the harvested species and not on the plant community, thus limiting our understanding for establishing forest management recommendations. We investigated the consequences of Euterpe edulis palm heart harvesting on the seed rain in the Brazilian Atlantic rainforest. We compared the density of E. edulis individuals, as well as the density of E. edulis seeds, and the density, richness and functional composition of seed rain of the whole plant community, before and after palm heart harvesting in a 10 ha permanent plot. This assessment was carried out in preserved (typical old-growth Atlantic rainforest) and in disturbed (more open habitat dominated by the native bamboo Guadua tagoara) forest patches. Palm harvesting reduced the E. edulis population from 202.16 to 25.67 ind/ha and its seed rain density from 0.362 to 0.3 seeds/m2 and from 2.395 to 0.15 seeds/m2 in preserved and disturbed forest patches, respectively. Seed density of light-dependent climbers, pioneer trees, bamboo and animal-dispersed seeds increased after palm harvesting, especially in the disturbed forest patches, where palm harvesting was more intense and may have changed the light regime of the understory. On the other hand, species richness of the plant community declined by half. We observed a remarkable decline in the number of animal-dispersed species, especially for those with large seeds, suggesting that the activity of seed dispersers, including many species attracted by E. edulis fruits, was reduced. Therefore, harvesting of E. edulis palm heart may change the regeneration dynamics of the Atlantic rainforest, both due to shifts in forest structure, mediated by the removal of individuals from the forest canopy, and in community functioning, mediated by the interference on the activity of seed dispersers. © 2013 Elsevier B.V. All rights reserved.
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Os regimes térmicos e hídricos do solo se comportam de maneiras diferentes em anos de ocorrência dos fenômenos El Niño, La niña e ano de não ocorrência de nenhum dos dois fenômenos. Para estudar estes comportamentos utilizou-se dados de totais horários e mensais da precipitação pluviométrica, dados médios horários e mensais da temperatura do solo nas profundidades de 2cm e 10cm e umidade do solo nas profundidades de 5cm e 20cm, para os anos representativos dos eventos pesquisados. Os resultados mostram que o ano sob a influência do fenômeno El Niño, apresentou maiores valores de temperatura e menores valores de umidade do solo, quando comparado com o ano que esteve sob a influência do fenômeno La Niña. Por outro lado, o ano em que não houve ocorrência dos fenômenos La Niña e El Niño, apresentou valores de temperatura (umidade) do solo maiores (menores) do que o ano de La Niña, porém menores (maiores) do que no ano de El Niño.
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Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
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Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP)
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Pós-graduação em Engenharia Mecânica - FEIS
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The plasma density evolution in sawtooth regime on the Tore Supra tokamak is analyzed. The density is measured using fast-sweeping X-mode reflectometry which allows tomographic reconstructions. There is evidence that density is governed by the perpendicular electric flows, while temperature evolution is dominated by parallel diffusion. Postcursor oscillations sometimes lead to the formation of a density plateau, which is explained in terms of convection cells associated with the kink mode. A crescent-shaped density structure located inside q = 1 is often visible just after the crash and indicates that some part of the density withstands the crash. 3D full MHD nonlinear simulations with the code XTOR-2F recover this structure and show that it arises from the perpendicular flows emerging from the reconnection layer. The proportion of density reinjected inside the q = 1 surface is determined, and the implications in terms of helium ash transport are discussed. (C) 2012 American Institute of Physics. [http://dx.doi.org/10.1063/1.4766893]
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Background. Transforming growth factor alpha (TGF alpha) is an important mitogen that binds to epidermal growth factor receptor and is associated with the development of several tumors. Aims. Assessment of the immunoexpression of TGF alpha in hepatocellular carcinoma (HCC) and in non-neoplastic liver tissue and its relationship to morphological patterns of HCC. Material and methods. The immunohistochemical expression of TGF alpha was studied in 47 cases of HCC (27 multinodular, 20 nodular lesions). Five lesions measured up to 5 cm and 15 lesions above 5 cm. Thirty-two cases were graded as I or II and 15 as III or IV. The non-neoplastic tissue was examined in 40 cases, of which 22 had cirrhosis. HBsAg and anti-HCV were positive in 5/38 and 15/37 patients, respectively. The statistical analysis for possible association of immunostaining of TGF alpha and pathological features was performed through chi-square test. Results. TGF alpha was detected in 31.9% of the HCC and in 42.5% of the non-neoplastic. There was a statistically significant association between the expression of TGF alpha and cirrhosis (OR = 8.75, 95% CI = [1.93, 39.75]). The TGF alpha was detected more frequently in patients anti-HCV(+) than in those HBsAg(+). The immunoexpression of TGF alpha was not found related to tumor size or differentiation. In conclusion the TGF alpha is present in hepatocarcinogenesis in HBV negative patients. Further analysis is needed to examine the involvement of TGF alpha in the carcinogenesis associated with HCV and other possible agents. In addition, TGF alpha has an higher expression in hepatocyte regeneration and proliferation in cirrhotic livers than in HCC.
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Background: Canova activates macrophages and indirectly induces lymphocyte proliferation. Here we evaluated the effects of Canova in cyclophosphamide-treated non-human primates. Methods: Twelve Cebus apella were evaluated. Four animals were treated with Canova only. Eight animals were treated with two doses of cyclophosphamide (50 mg/kg) and four of these animals received Canova. Body weight, biochemistry and hematologic analyses were performed for 40 days. Micronucleus and comet assays were performed for the evaluation of DNA damage. Results: We observed that cyclophosphamide induced abnormal WBC count in all animals. However, the group treated with cyclophosphamide plus Canova presented a higher leukocyte count than that which received only cyclophosphamide. Cyclophosphamide induced micronucleus and DNA damage in all animals. The frequency of these alterations was significantly lower in the Canova group than in the group without this medicine. Conclusions: Our results demonstrated that Canova treatment minimizes cyclophosphamide myelotoxicity in C. apella. (C) 2012 Elsevier Ltd. All rights reserved.
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The study of RNA and DNA oncogenic viruses has proved invaluable in the discovery of key cellular pathways that are rendered dysfunctional during cancer progression. An example is high risk human papillomavirus (HPV), the etiological agent of cervical cancer. The role of HPV oncogenes in cellular immortalization and transformation has been extensively investigated. We reported the differential expression of a family of human mitochondrial non-coding RNAs (ncRNAs) between normal and cancer cells. Normal cells express a sense mitochondrial ncRNA (SncmtRNA) that seems to be required for cell proliferation and two antisense transcripts (ASncmtRNAs). In contrast, the ASncmtRNAs are down-regulated in cancer cells. To shed some light on the mechanisms that trigger down-regulation of the ASncmtRNAs, we studied human keratinocytes (HFK) immortalized with HPV. Here we show that immortalization of HFK with HPV-16 or 18 causes down-regulation of the ASncmtRNAs and induces the expression of a new sense transcript named SncmtRNA-2. Transduction of HFK with both E6 and E7 is sufficient to induce expression of SncmtRNA-2. Moreover, E2 oncogene is involved in down-regulation of the ASncmtRNAs. Knockdown of E2 in immortalized cells reestablishes in a reversible manner the expression of the ASncmtRNAs, suggesting that endogenous cellular factors(s) could play functions analogous to E2 during non-HPV-induced oncogenesis.
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Periodontitis comprises a group of multifactorial diseases in which periodontopathogens accumulate in dental plaque and trigger host chronic inflammatory and immune responses against periodontal structures, which are determinant to the disease outcome. Although unusual cases of non-inflammatory destructive periodontal disease (NIDPD) are described, their pathogenesis remains unknown. A unique NIDPD case was investigated by clinical, microbiological, immunological and genetic tools. The patient, a non-smoking dental surgeon with excessive oral hygiene practice, presented a generalized bone resorption and tooth mobility, but not gingival inflammation or occlusion problems. No hematological, immunological or endocrine alterations were found. No periodontopathogens (A. actinomycetemcomitans, P. gingivalis, F. nucleatum and T. denticola) or viruses (HCMV, EBV-1 and HSV-1) were detected, along with levels of IL-1 beta and TNF-alpha in GCF compatible with healthy tissues. Conversely ALP, ACP and RANKL GCF levels were similar to diseased periodontal sites. Genetic investigation demonstrated that the patient carried some SNPs, as well HLA-DR4 (*0404) and HLA-B27 alleles, considered risk factors for bone loss. Then, a less vigorous and diminished frequency of toothbrushing was recommended to the patient, resulting in the arrest of alveolar bone loss, associated with the return of ALP, ACP and RANKL in GCF to normality levels. In conclusion, the unusual case presented here is compatible with the previous description of NIDPD, and the results that a possible combination of excessive force and frequency of mechanical stimulation with a potentially bone loss prone genotype could result in the alveolar bone loss seen in NIDPD.
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The down-regulation of the tumor-suppressor gene RASSF1A has been shown to increase cell proliferation in several tumors. RASSF1A expression is regulated through epigenetic events involving the polycomb repressive complex 2 (PRC2); however, the molecular mechanisms modulating the recruitment of this epigenetic modifier to the RASSF1 locus remain largely unknown. Here, we identify and characterize ANRASSF1, an endogenous unspliced long noncoding RNA (lncRNA) that is transcribed from the opposite strand on the RASSF1 gene locus in several cell lines and tissues and binds PRC2. ANRASSF1 is transcribed through RNA polymerase II and is 5'-capped and polyadenylated; it exhibits nuclear localization and has a shorter half-life compared with other lncRNAs that bind PRC2. ANRASSF1 endogenous expression is higher in breast and prostate tumor cell lines compared with non-tumor, and an opposite pattern is observed for RASSF1A. ANRASSF1 ectopic overexpression reduces RASSF1A abundance and increases the proliferation of HeLa cells, whereas ANRASSF1 silencing causes the opposite effects. These changes in ANRASSF1 levels do not affect the RASSF1C isoform abundance. ANRASSF1 overexpression causes a marked increase in both PRC2 occupancy and histone H3K27me3 repressive marks, specifically at the RASSF1A promoter region. No effect of ANRASSF1 overexpression was detected on PRC2 occupancy and histone H3K27me3 at the promoter regions of RASSF1C and the four other neighboring genes, including two well-characterized tumor suppressor genes. Additionally, we demonstrated that ANRASSF1 forms an RNA/DNA hybrid and recruits PRC2 to the RASSF1A promoter. Together, these results demonstrate a novel mechanism of epigenetic repression of the RASSF1A tumor suppressor gene involving antisense unspliced lncRNA, in which ANRASSF1 selectively represses the expression of the RASSF1 isoform overlapping the antisense transcript in a location-specific manner. In a broader perspective, our findings suggest that other non-characterized unspliced intronic lncRNAs transcribed in the human genome might contribute to a location-specific epigenetic modulation of genes.