Characterisation of electrical power systems based on electrical curves and their properties

[Abstract]: Due to the proliferation of renewable energy systems, the study of voltage and frequency stability is a crucial aspect. Recently, this problem has been approached from a purely geometrical point of view with interesting results. The present work investigates the properties of the so-called electrical curves described by arbitrary voltage or current vectors in Euclidean spaces. Through the invariants of these curves, certain indices can be constructed to detect abnormal operation or irregular characteristics in electrical power systems. Different scenarios and examples have been solved in this work to support the proposed theory

Matrix Metalloproteinases and Bladder Cancer : What is New?

Urothelial bladder cancer represents a heterogeneous disease with divergent pathways of tumorigenesis. Tumor invasion and progression are a multifactorial process promoted by microenvironmental changes that include overexpression of matrix metalloproteinases (MMPs). Recent data clearly challenge the classic dogma that MMPs promote metastasis only by modulating the remodeling of extracellular matrix. Indeed, MMPs have also been attributed as an impact on tumor cell behavior in vivo as a consequence of their ability to cleave growth factors, cell surface receptors, cell adhesion molecules, and chemokines/cytokines. Levels of the different MMPs can be measured in several sample types, including tissue, blood (serum and plasma), and urine, and using different methodologies, such as immunohistochemistry, real-time PCR, western and northern blot analyses, enzyme-linked immunosorbent assay, and zymography. Several MMPs have been identified as having potential diagnostic or prognostic utility, whether alone or in combination with cytology. Although MMP inhibitors have shown limited efficacy, advances in the understanding of the complex physiologic and pathologic roles of MMPs might permit the development of new MMP-specific and tumor-specific therapies. In this paper we update the understanding of MMPs based on a systematic PubMed search encompassing papers published up to December 2011

Relationship between serum prolactin levels and protein composition of breast secretions in nonlactating women

En esta interesante se describe la relación entre los niveles séricos de prolactina (PRL) basales y tras estimulación con hormona liberadora de tirotropina (TRH), y la composición proteica de la secreción del pezón en 54 mujeres premenopáusicas y no lactantes durante la fase lútea de su ciclo menstrual. Las mujeres incluidas en este estudio se clasificaron en cuatro grupos teniendo en cuenta la presencia o ausencia de patología mamaria y el patrón proteico de sus secreciones mamarias. Los fluidos mamarios tipo I contenían Zn-α2-glicoproteina, apolipoproteina D y la proteína 15 de la enfermedad macroquistica mamaria; mientras que los fluidos tipo II se caracterizaron por la presencia de algunas proteínas de la leche como la lactoferrina, lisozima y α-lactoalbumina. Los niveles basales de PRL, progesterona, LH, FSH, T3 y T4 estuvieron dentro de rangos normales y no se identificó ninguna diferencia entre los grupos de mujeres incluidas en el estudio. Sin embargo, después de una prueba de estimulación con TRH si se objetivaron diferencias entre los grupos. En ausencia de patología mamaria, el aumento de PRL fue significativamente superior en mujeres con secreciones tipo II frente a las que tenían secreción tipo I (64 ± 6.8 µg/L vs. 7 ± 3.9 µg/L, p<0.02). De manera similar, cuando se consideraron las concentraciones de PRL en pacientes con enfermedad mamaria benigna, aquellas con fluidos mamarios tipo II tuvieron un aumento de la PRL significativamente superior en comparación con las que tenían fluidos a las que les faltaban estas proteínas (77.1 ± 6.2 µg/L vs. 58.8 ± 5.1 µg/L; P<0.05). Estos resultados muestran que la presencia de proteínas de la leche en la secreción del pezón de mujeres no lactantes se asocia con un incremento de la PRL en el suero tras la estimulación con TRH. Con ello, se abre la posibilidad de utilizar este análisis como un procedimiento no invasivo para el estudio en el efecto putativo de la PRL en el desarrollo de enfermedades mamarias benignas y malignas.Comisión Interministerial de Ciencia y Tecnología, Plan Nacional de I

The Pit-1/Pou1f1 transcription factor regulates and correlates with prolactin expression in human breast cell lines and tumors

The transcription factor Pit-1/Pou1f1 regulates GH and prolactin (PRL) secretion in the pituitary gland. Pit-1 expression and GH regulation by Pit-1 have also been demonstrated in mammary gland. However, no data are available on the role of Pit-1 on breast PRL. To evaluate this role, several human breast cancer cell lines were transfected with either the Pit-1 expression vector or a Pit-1 small interference RNA construct, followed by PRL mRNA and protein evaluation. In addition, transient transfection of MCF-7 cells by a reporter construct containing the proximal PRL promoter, and ChIP assays were performed. Our data indicate that Pit-1 regulates mammary PRL at transcriptional level by binding to the proximal PRL promoter. We also found that Pit-1 raises cyclin D1 expression before increasing PRL levels, suggesting a PRL-independent effect of Pit-1 on cell proliferation. By using immunohistochemistry, we found a significant correlation between Pit-1 and PRL expression in 94 human breast invasive ductal carcinomas. Considering the possible role of PRL in breast cancer disorders, the function of Pit-1 in breast should be the focus of further research

DNA methylation alterations in grade II- and anaplastic pleomorphic xanthoastrocytoma

Background: Pleomorphic xanthoastrocytoma (PXA) is a rare WHO grade II tumor accounting for less than 1% of all astrocytomas. Malignant transformation into PXA with anaplastic features, is unusual and correlates with poorer outcome of the patients. Methods: Using a DNA methylation custom array, we have quantified the DNA methylation level on the promoter sequence of 807 cancer-related genes of WHO grade II (n = 11) and III PXA (n = 2) and compared to normal brain tissue (n = 10) and glioblastoma (n = 87) samples. DNA methylation levels were further confirmed on independent samples by pyrosequencing of the promoter sequences. Results: Increasing DNA promoter hypermethylation events were observed in anaplastic PXA as compared with grade II samples. We further validated differential hypermethylation of CD81, HCK, HOXA5, ASCL2 and TES on anaplastic PXA and grade II tumors. Moreover, these epigenetic alterations overlap those described in glioblastoma patients, suggesting common mechanisms of tumorigenesis. Conclusions: Even taking into consideration the small size of our patient populations, our data strongly suggest that epigenome-wide profiling of PXA is a valuable tool to identify methylated genes, which may play a role in the malignant progression of PXA. These methylation alterations may provide useful biomarkers for decision-making in those patients with low-grade PXA displaying a high risk of malignant transformation

DNA methylation alterations in grade II- and anaplastic pleomorphic xanthoastrocytoma

BACKGROUND: Pleomorphic xanthoastrocytoma (PXA) is a rare WHO grade II tumor accounting for less than 1% of all astrocytomas. Malignant transformation into PXA with anaplastic features, is unusual and correlates with poorer outcome of the patients. METHODS: Using a DNA methylation custom array, we have quantified the DNA methylation level on the promoter sequence of 807 cancer-related genes of WHO grade II (n = 11) and III PXA (n = 2) and compared to normal brain tissue (n = 10) and glioblastoma (n = 87) samples. DNA methylation levels were further confirmed on independent samples by pyrosequencing of the promoter sequences. RESULTS: Increasing DNA promoter hypermethylation events were observed in anaplastic PXA as compared with grade II samples. We further validated differential hypermethylation of CD81, HCK, HOXA5, ASCL2 and TES on anaplastic PXA and grade II tumors. Moreover, these epigenetic alterations overlap those described in glioblastoma patients, suggesting common mechanisms of tumorigenesis. CONCLUSIONS: Even taking into consideration the small size of our patient populations, our data strongly suggest that epigenome-wide profiling of PXA is a valuable tool to identify methylated genes, which may play a role in the malignant progression of PXA. These methylation alterations may provide useful biomarkers for decision-making in those patients with low-grade PXA displaying a high risk of malignant transformation

Aberrant DNA methylation in non-small cell lung cancer-associated fibroblasts

Epigenetic changes through altered DNA methylation have been implicated in critical aspects of tumor progression, and have been extensively studied in a variety of cancer types. In contrast, our current knowledge of the aberrant genomic DNA methylation in tumor-associated fibroblasts (TAFs) or other stromal cells that act as critical coconspirators of tumor progression is very scarce. To address this gap of knowledge, we conducted genome-wide DNA methylation profiling on lung TAFs and paired control fibroblasts (CFs) from non-small cell lung cancer patients using the HumanMethylation450 microarray. We found widespread DNA hypomethylation concomitant with focal gain of DNA methylation in TAFs compared to CFs. The aberrant DNA methylation landscape of TAFs had a global impact on gene expression and a selective impact on the TGF-β pathway. The latter included promoter hypermethylation-associated SMAD3 silencing, which was associated with hyperresponsiveness to exogenous TGF-β1 in terms of contractility and extracellular matrix deposition. In turn, activation of CFs with exogenous TGF-β1 partially mimicked the epigenetic alterations observed in TAFs, suggesting that TGF-β1 may be necessary but not sufficient to elicit such alterations. Moreover, integrated pathway-enrichment analyses of the DNA methylation alterations revealed that a fraction of TAFs may be bone marrow-derived fibrocytes. Finally, survival analyses using DNA methylation and gene expression datasets identified aberrant DNA methylation on the EDARADD promoter sequence as a prognostic factor in non-small cell lung cancer patients. Our findings shed light on the unique origin and molecular alterations underlying the aberrant phenotype of lung TAFs, and identify a stromal biomarker with potential clinical relevance