3,591 research outputs found

    p21(WAF1/CIP1) expression in gestational trophoblastic disease: correlation with clinicopathological parameters, and Ki67 and p53 gene expression

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    Background--The p21(WAF1/CIP1) gene mediates growth arrest by inhibiting G 1 cyclin dependent kinases and has been considered as a downstream effector of the tumour suppressor gene p53. Aim--To analyse the role of p21(WAF1/CIP1) in gestational trophoblastic disease. Methods--The immunohistochemical expression of p21(WAF1/CIP1) gene was measured in 33 placentas, 28 partial hydatidiform moles, 54 complete hydatidiform moles, and 13 choriocarcinomas in paraffin wax embedded tissue. The results were correlated with p53 (DO7) and Ki67 (MIB1) immunoreactivity as well as clinical progress. Results--p21(WAF1/CIP1) immunoreactivity was found predominantly in the nuclei of the syncytiotrophoblasts. p21(WAF1/CIP1) protein expression correlated with gestational age in normal placentas (p = 0.0001) but not in hydatidiform moles (p = 0.89). Complete hydatidiform moles and choriocarcinomas had a significantly higher p21(WAF1/CIP1) expression compared with normal placentas and partial hydatiform moles (p 0.05) in p21(WAF1/CIP1) expression between the 17 patients who developed persistent gestational trophoblastic disease and those who did not. Conclusions--This study suggests that p21(WAF1/CIP1) expression in trophoblastic disease may be induced by a p53 independent pathway. The proliferative activity of gestational trophoblastic diseases might not be determined solely by the control of the cell cycle operated by p21(WAF1/CIP1). p21(WAF1/CIP1) expression is not an accurate prognostic indicator of gestational trophoblastic disease.published_or_final_versio

    Telomerase activity in gestational trophoblastic disease

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    Aims - To investigate the pattern of telomerase activity in hydatidiform mole as compared with normal placenta and choriocarcinoma, and to determine the prognostic significance of telomerase activity in hydatidiform mole. Methods - Telomerase activity in 35 cases of hydatidiform mole, 35 normal placentas, one choriocarcinoma sample, and two choriocarcinoma cell lines (JAR, JEG3) was determined using the sensitive polymerase chain reaction based telomeric repeat amplification protocol (TRAP) assay. Two cases of breast carcinoma and two cases of ovarian carcinoma were also included as positive controls in the telomerase assay. Results - Telomerase activity was detected in 11 of 30 early placentas (36.7%), one of five term placentas (20%), five of 27 hydatidiform moles which regressed spontaneously (18.5%), and six of eight hydatidiform moles which developed persistent trophoblastic disease (75%) (including three which developed metastases). Hydatidiform moles which subsequently developed persistent disease, especially those which metastasised, were more likely to express telomerase activity (p < 0.01). However, there was no significant difference in the frequency of telomerase activity between early placentas and hydatidiform mole. Strong telomerase activity was observed in choriocarcinoma tissue, choriocarcinoma cell lines, and ovarian and breast carcinomas. Conclusions - Telomerase activation occurs in hydatidiform mole with a similar incidence to early normal placentas. This supports the concept that hydatidiform mole is essentially an abnormal conceptus. There is an association between telomerase activation and the development of persistent trophoblastic disease. Further study is warrant to confirm the prognostic significance of telomerase activity in hydatidiform mole.published_or_final_versio

    Nested Fermi surface and electronic instability in Ca3Ru2O7

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    High-resolution angular resolved photoemission data reveal well-defined quasiparticle bands of unusually low weight, emerging in line with the metallic phase of Ca 3 Ru 2 O 7 below ∼ 30     K . At the bulk structural phase transition temperature of 48 K, we find clear evidence for an electronic instability, gapping large parts of the underlying Fermi surface that appears to be nested. Metallic pockets are found to survive in the small, non-nested sections, constituting a low-temperature Fermi surface with 2 orders of magnitude smaller volume than in all other metallic ruthenates. The Fermi velocities and volumes of these pockets are in agreement with the results of complementary quantum oscillation measurements on the same crystal batches

    3D time series analysis of cell shape using Laplacian approaches

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    Background: Fundamental cellular processes such as cell movement, division or food uptake critically depend on cells being able to change shape. Fast acquisition of three-dimensional image time series has now become possible, but we lack efficient tools for analysing shape deformations in order to understand the real three-dimensional nature of shape changes. Results: We present a framework for 3D+time cell shape analysis. The main contribution is three-fold: First, we develop a fast, automatic random walker method for cell segmentation. Second, a novel topology fixing method is proposed to fix segmented binary volumes without spherical topology. Third, we show that algorithms used for each individual step of the analysis pipeline (cell segmentation, topology fixing, spherical parameterization, and shape representation) are closely related to the Laplacian operator. The framework is applied to the shape analysis of neutrophil cells. Conclusions: The method we propose for cell segmentation is faster than the traditional random walker method or the level set method, and performs better on 3D time-series of neutrophil cells, which are comparatively noisy as stacks have to be acquired fast enough to account for cell motion. Our method for topology fixing outperforms the tools provided by SPHARM-MAT and SPHARM-PDM in terms of their successful fixing rates. The different tasks in the presented pipeline for 3D+time shape analysis of cells can be solved using Laplacian approaches, opening the possibility of eventually combining individual steps in order to speed up computations

    Detection of putative new mutacins by bioinformatic analysis using available web tools

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    In order to characterise new bacteriocins produced by Streptococcus mutans we perform a complete bioinformatic analyses by scanning the genome sequence of strains UA159 and NN2025. By searching in the adjacent genomic context of the two-component signal transduction system we predicted the existence of many putative new bacteriocins' maturation pathways and some of them were only exclusive to a group of Streptococcus. Computational genomic and proteomic analysis combined to predictive functionnal analysis represent an alternative way for rapid identification of new putative bacteriocins as well as new potential antimicrobial drugs compared to the more traditional methods of drugs discovery using antagonism tests

    Functional diversity of marine ecosystems after the Late Permian mass extinction event

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    Article can be accessed from http://www.nature.com/ngeo/journal/v7/n3/full/ngeo2079.htmlThe Late Permian mass extinction event was the most severe such crisis of the past 500 million years and occurred during an episode of global warming. It is assumed to have had significant ecological impact, but its effects on marine ecosystem functioning are unknown and the patterns of marine recovery are debated. We analysed the fossil occurrences of all known Permian-Triassic benthic marine genera and assigned each to a functional group based on their inferred life habit. We show that despite the selective extinction of 62-74% of marine genera there was no significant loss of functional diversity at the global scale, and only one novel mode of life originated in the extinction aftermath. Early Triassic marine ecosystems were not as ecologically depauperate as widely assumed, which explains the absence of a Cambrian-style Triassic radiation in higher taxa. Functional diversity was, however, significantly reduced in particular regions and habitats, such as tropical reefs, and at these scales recovery varied spatially and temporally, probably driven by migration of surviving groups. Marine ecosystems did not return to their pre-extinction state, however, and radiation of previously subordinate groups such as motile, epifaunal grazers led to greater functional evenness by the Middle Triassic

    Morphology-Controllable Synthesis of CeO2on a Pt Electrode

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    Nanoscale cerium dioxides with shape of nanoparticles, nanorods, and nanotubes were electrochemically synthesized. The morphology of CeO2was modulated by changing electrode potential and potential direction. CeO2nanorods and CeO2nanotubes were synthesized via the potentiostatic and cyclic voltammeteric methods, respectively. The morphology and structure of the obtained CeO2were characterized by field emission scanning electron microscope (FESEM) and X-ray diffraction (XRD). A possible formation mechanism has been suggested to illuminate the relationship between the preparation condition and the morphology of CeO2

    Vascular endothelial growth factor (VEGF) upregulates BCL-2 and inhibits apoptosis in human and murine mammary adenocarcinoma cells

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    Tumour progression is regulated by the balance of proliferation and apoptosis in the tumour cell population. To date, the role of vascular endothelial growth factor (VEGF) in tumour growth has been attributed to the induction of angiogenesis. VEGF has been shown to be a survival factor for endothelial cells, preventing apoptosis by inducing Bcl-2 expression. In both murine (4T1) and human (MDA-MB-231) metastatic mammary carcinoma cell lines, we found that VEGF upregulated Bcl-2 expression and anti-VEGF antibodies reduced Bcl-2 expression. These alterations in Bcl-2 expression were reflected by the levels of tumour cell apoptosis. VEGF resulted in reduced tumour cell apoptosis, whereas its inhibition with anti-VEGF neutralizing antibodies induced apoptosis directly in tumour cells. Therefore, in addition to its role in angiogenesis and vessel permeability, VEGF acts as a survival factor for tumour cells, inducing Bcl-2 expression and inhibiting tumour cell apoptosis. © 2001 Cancer Research Campaign http://www.bjcancer.co
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