Estrategias de aprendizaje del profesorado europeo: género y etapa educativa [Learning strategies of European teachers: gender and period of teaching]

INTRODUCTION. The lack of teaching professionals with continuous training affects quality in educational systems and quality of teaching. That is why we believe that teachers must increase or improve their professional competences once they have finished their initial training. To do so, learning strategies are needed, but they vary according to training aspirations and gender. OCDE (2007) and Quesada-Pallarès, Fernández-de-Álava and Rebollar-Sánchez (2015) show differences between men and women. METHOD. This article uses the last data collected with the PIAAC survey, administered in 2012. 23 countries participated in the PIAAC survey, obtaining a total of 157,000 responses. We opt for a quantitative methodology for determining if the use of learning strategies of European teachers varies according to gender, and period of teaching. RESULTS. The main results of this article show that men, compared to women, and university and higher education teachers, compared to those who teach in other teaching periods, make greater use of learning strategies. DISCUSSION. These outcomes help towards the building of a unified framework for continuous training and learning strategies; pointing out that learning strategies are determined by work demands, and activities carried out by teachers according to their period of teaching. Likewise, the results pose some challenges related to the teacher profile, and the non-use of learning strategies by women for self-promotion

Transcription factors Sp1 and p73 control the expression of the proapoptotic protein NOXA in the response of testicular embryonal carcinoma cells to cisplatin

Testicular germ cell tumors (TGCTs) are highly responsive to and curable by cisplatin-based chemotherapy even in advanced stages. We have studied the molecular mechanisms involved in the induction of apoptosis in response to cisplatin, and found that proapoptotic Noxa is transcriptionally up-regulated following cisplatin exposure, even in the absence of p53, in NTERA2 cisplatin-sensitive cells but not in 1411HP-resistant cells. Blockade of Noxa reduced the apoptotic response of embryonal carcinoma (EC) NTERA2 cells to cisplatin. A detailed analysis of the Noxa promoter revealed that p73 and Sp1-like factors, Sp1 and KLF6, played key roles in the transcriptional control of this gene. Overexpression of TAp73 induced Noxa whereas the dominant negative isoform ΔNp73, reduced the levels of Noxa after cisplatin exposure in NTERA2 and 2102EP. Interestingly, down-regulation of Sp1 increased Noxa expression in response to cisplatin. However, blockade of KLF6 decreased cisplatin-induced up-regulation of Noxa in EC cell lines. In addition, tissue microarray analyses of TGCTs revealed that expression of Noxa correlates with good clinical prognosis in patients with embryonal carcinoma. Thus, our data show the transcriptional network that regulates Noxa in EC cells, which is key for their apoptotic response to cisplatin-based chemotherapy, and propose Noxa as a predictive factor of therapeutic response

Imatinib inhibits proliferation of Ewing tumor cells mediated by the stem cell factor/KIT receptor pathway, and sensitizes cells to vincristine and doxorubicin-induced apoptosis

Purpose and Experimental Design: The stem cell factor/ KIT receptor loop may represent a novel target for molecular- based therapies of Ewing tumor. We analyzed the in vitro impact of KIT blockade by imatinib in Ewing tumor cell lines. Results: KIT expression was detected in 4 of 4 Ewing tumor cell lines and in 49 of 110 patient samples (44.5%) by immunohistochemistry and/or Western blot analysis. KIT expression was stronger in Ewing tumors showing EWSFLI1 nontype 1 fusions. Despite absence of c-kit mutations, constitutive and ligand-inducible phosphorylation of KIT was found in all tumor cell lines, indicating an active receptor. Treatment with KIT tyrosine kinase inhibitor imatinib (0.5–20 M) induced down-regulation of KIT phosphorylation and dose response inhibition of cell proliferation (IC50, 12–15 M). However, imatinib administered alone at doses close to IC50 for growth inhibition (10 M) did not induce a significant increase in apoptosis. We then analyzed if blockade of KIT loop through imatinib (10 M) was able to increase the antitumor in vitro effect of doxorubicin (DXR)and vincristine (VCR), drugs usually used in Ewing tumor treatment. Addition of imatinib decreased in 15–20 and 15–36% of the proliferative rate of Ewing tumor cells exposed to DXR and VCR, respectively, and increased in 15 and 30% of the apoptotic rate of Ewing tumor cells exposed to the same drugs. Conclusions: Inhibition of Ewing tumor cell proliferation by imatinib is mediated through blockade of KIT receptor signaling. Inhibition of KIT increases sensitivity of these cells to DXR and VCR. This study supports a potential role for imatinib in the treatment of Ewing tumor

Correlation functions in the two-dimensional random-field Ising model

Transfer-matrix methods are used to study the probability distributions of spin-spin correlation functions $G$ in the two-dimensional random-field Ising model, on long strips of width $L = 3 - 15$ sites, for binary field distributions at generic distance $R$, temperature $T$ and field intensity $h_0$. For moderately high $T$, and $h_0$ of the order of magnitude used in most experiments, the distributions are singly-peaked, though rather asymmetric. For low temperatures the single-peaked shape deteriorates, crossing over towards a double-$\delta$ ground-state structure. A connection is obtained between the probability distribution for correlation functions and the underlying distribution of accumulated field fluctuations. Analytical expressions are in good agreement with numerical results for $R/L \gtrsim 1$, low $T$, $h_0$ not too small, and near G=1. From a finite-size {\it ansatz} at $T=T_c (h_0=0)$, $h_0 \to 0$, averaged correlation functions are predicted to scale with $L^y h_0$, $y =7/8$. From numerical data we estimate y=0.875 \pm 0.025$, in excellent agreement with theory. In the same region, the RMS relative width$W$of the probability distributions varies for fixed$R/L=1$as$W \sim h_0^{\kappa} f(L h_0^u)$with$\kappa \simeq 0.45$,$u \simeq 0.8$;$f(x)$appears to saturate when$x \to \infty$, thus implying$W \sim h_0^{\kappa}$in$d=2$.Comment: RevTeX code for 8 pages, 7 eps figures, to appear in Physical Review E (1999

The current situation of gender differences in non-formal and informal learning activities in the Spanish adult population

INTRODUCTION. The need of continuous and lifelong training is an issue that has prevailed since the last century (European Commission, 1995; European Council, 1975; Delors, 1996; Marsick & Watkins, 1990). In this regard, we obverse changes in the ways of learning highlighting those that take place outside formal educational and training institution and that do not depend directly on the trainer or structured processes. METHOD. This paper starts from the results obtained in the Adult Education Survey (EADA, by its Spanish acronym). Specifically, the collection method is a computer-assisted personal interview, through stratified random sampling, of 153 items to 17,829 Spanish persons. In this sense, it has a twofold aim (1) to analyze if there are gender differences in non-formal and informal activities carried out; and, if so, (2) to identify the variables associated with these differences. Therefore, we use descriptive and inferential statistics of the most important variables. RESULTS. The outcomes indicate significant differences between male and female sexes in regards to age, nationality and social class for taking part in non-formal and informal learning activities. DISCUSSION. Finally, we point out the limitations of these variables in women’s professional development, and we make proposals for progressing in the elimination of these differences

Transcription factors Sp1 and p73 control the expression of the proapoptotic protein NOXA in the response of testicular embryonal carcinoma cells to cisplatin

Testicular germ cell tumors (TGCTs) are highly responsive to and curable by cisplatin-based chemotherapy even in advanced stages. We have studied the molecular mechanisms involved in the induction of apoptosis in response to cisplatin, and found that proapoptotic Noxa is transcriptionally up-regulated following cisplatin exposure, even in the absence of p53, in NTERA2 cisplatin-sensitive cells but not in 1411HP-resistant cells. Blockade of Noxa reduced the apoptotic response of embryonal carcinoma (EC) NTERA2 cells to cisplatin.Adetailed analysis of the Noxa promoter revealed that p73 and Sp1-like factors, Sp1 and KLF6, played key roles in the transcriptional control of this gene. Overexpression of TAp73 induced Noxa whereas the dominant negative isoform ΔNp73, reduced the levels of Noxa after cisplatin exposure in NTERA2 and 2102EP. Interestingly, down-regulation of Sp1 increased Noxa expression in response to cisplatin. However, blockade of KLF6 decreased cisplatin-induced up-regulation of Noxa in EC cell lines. In addition, tissue microarray analyses of TGCTs revealed that expression of Noxa correlates with good clinical prognosis in patients with embryonal carcinoma. Thus, our data show the transcriptional network that regulates Noxa in EC cells, which is key for their apoptotic response to cisplatin-based chemotherapy, and propose Noxa as a predictive factor of therapeutic response. © 2012 by The American Society for Biochemistry and Molecular Biology, Inc.This work was supported by Instituto de Salud Carlos III Grants RD06/0020/0074 (to J.L. F.-L.), RD06/0020/0059 (to E.A.), RD06/0020/0017 (to M.D.D.) (Red Tematica de Investigacion Cooperativa en Cancer), PI11/00397 (to M.D.D.), and PI081491 (to X.G.); and a grant from Instituto de Formacion e Investigación Marqués de Valdecilla (IFIMAV), API2011-04 (to J.L. F.-L.).Peer Reviewe

Imatinib inhibits proliferation of Ewing tumor cells mediated by the stem cell factor/KIT receptor pathway, and sensitizes cells to vincristine and doxorubicin-induced apoptosis

Purpose and Experimental Design: The stem cell factor/ KIT receptor loop may represent a novel target for molecular- based therapies of Ewing tumor. We analyzed the in vitro impact of KIT blockade by imatinib in Ewing tumor cell lines. Results: KIT expression was detected in 4 of 4 Ewing tumor cell lines and in 49 of 110 patient samples (44.5%) by immunohistochemistry and/or Western blot analysis. KIT expression was stronger in Ewing tumors showing EWSFLI1 nontype 1 fusions. Despite absence of c-kit mutations, constitutive and ligand-inducible phosphorylation of KIT was found in all tumor cell lines, indicating an active receptor. Treatment with KIT tyrosine kinase inhibitor imatinib (0.5–20 M) induced down-regulation of KIT phosphorylation and dose response inhibition of cell proliferation (IC50, 12–15 M). However, imatinib administered alone at doses close to IC50 for growth inhibition (10 M) did not induce a significant increase in apoptosis. We then analyzed if blockade of KIT loop through imatinib (10 M) was able to increase the antitumor in vitro effect of doxorubicin (DXR)and vincristine (VCR), drugs usually used in Ewing tumor treatment. Addition of imatinib decreased in 15–20 and 15–36% of the proliferative rate of Ewing tumor cells exposed to DXR and VCR, respectively, and increased in 15 and 30% of the apoptotic rate of Ewing tumor cells exposed to the same drugs. Conclusions: Inhibition of Ewing tumor cell proliferation by imatinib is mediated through blockade of KIT receptor signaling. Inhibition of KIT increases sensitivity of these cells to DXR and VCR. This study supports a potential role for imatinib in the treatment of Ewing tumor

Whole-genome sequencing identifies recurrent mutations in chronic lymphocytic leukaemia

Chronic lymphocytic leukaemia (CLL), the most frequent leukaemia in adults in Western countries, is a heterogeneous disease with variable clinical presentation and evolution. Two major molecular subtypes can be distinguished, characterized respectively by a high or low number of somatic hypermutations in the variable region of immunoglobulin genes. The molecular changes leading to the pathogenesis of the disease are still poorly understood. Here we performed whole-genome sequencing of four cases of CLL and identified 46 somatic mutations that potentially affect gene function. Further analysis of these mutations in 363 patients with CLL identified four genes that are recurrently mutated: notch 1 (NOTCH1), exportin 1 (XPO1), myeloid differentiation primary response gene 88 (MYD88) and kelch-like 6 (KLHL6). Mutations in MYD88 and KLHL6 are predominant in cases of CLL with mutated immunoglobulin genes, whereas NOTCH1 and XPO1 mutations are mainly detected in patients with unmutated immunoglobulins. The patterns of somatic mutation, supported by functional and clinical analyses, strongly indicate that the recurrent NOTCH1, MYD88 and XPO1 mutations are oncogenic changes that contribute to the clinical evolution of the disease. To our knowledge, this is the first comprehensive analysis of CLL combining whole-genome sequencing with clinical characteristics and clinical outcomes. It highlights the usefulness of this approach for the identification of clinically relevant mutations in cancer

Sarcoma classification by DNA methylation profiling

Sarcomas are malignant soft tissue and bone tumours affecting adults, adolescents and children. They represent a morphologically heterogeneous class of tumours and some entities lack defining histopathological features. Therefore, the diagnosis of sarcomas is burdened with a high inter-observer variability and misclassification rate. Here, we demonstrate classification of soft tissue and bone tumours using a machine learning classifier algorithm based on array-generated DNA methylation data. This sarcoma classifier is trained using a dataset of 1077 methylation profiles from comprehensively pre-characterized cases comprising 62 tumour methylation classes constituting a broad range of soft tissue and bone sarcoma subtypes across the entire age spectrum. The performance is validated in a cohort of 428 sarcomatous tumours, of which 322 cases were classified by the sarcoma classifier. Our results demonstrate the potential of the DNA methylation-based sarcoma classification for research and future diagnostic applications