La formación docente en momentos de cambios: ¿Qué nos dicen los profesores principiantes universiatrios?

Este estudio cualitativo con una metodología de estudios de casos múltiple examina la opinión de los profesores principiantes de la Universidad de Barcelona sobre las consecuencias del proceso de implementación del Espacio Europeo de Educación Superior (EEES). Indaga sobre la valoración que realiza el profesorado sobre la formación recibida en el postgrado de 'Iniciación a la docencia universitaria' y sobre los aprendizajes que les generó la experiencia formativa. La muestra de la investigación ha estado constituida por diez profesores principiantes de diferentes ámbitos de conocimiento de la Universidad de Barcelona y los datos proceden de la realización de entrevistas en profundidad. Entre los hallazgos más importantes, cabe destacar su percepción sobre la implementación del EEES y las propuestas que dan sobre los cambios que debería realizar la Universidad para una verdadera reforma de la formación de los docente

NTN4 partially rescues AKT and ERK phosphorylation in TMZ treated U251MG cells, but not in TMZ treated U87MG cells.

<p>U251MG and U87MG cells were treated with TMZ [100μM] for 3 h, and then cultured in medium containing 10% FCS supplemented with recombinant NTN4 protein [100 ng/ml]. Recombinant NTN4 protein was resupplied every 24 h. The cells were lysed for immunoblotting before (0 h) or after TMZ treatment (3 h), and every 24 h after TMZ treatment (24 h, 48 h, 72 h), total mTOR, total AKT, total ERK, and tubulin were used as loading control. In both U251MG and U87MG cell lines, the levels of p-AKT increased immediately after TMZ treatment and were significantly reduced 72 h later, while p-ERK (marked by arrowhead) was continuously inhibited after TMZ treatment. 72 h after TMZ treatment, NTN4 partially rescued AKT and ERK phosphorylation in U251MG cells (A), but not in U87MG cells (B).</p

U87MG and U251MG glioblastoma cells are sensitive to TMZ induced senescence.

<p>T98G, U118MG, U251MG and U87MG cells were treated with TMZ [100μM] for 3 h, and then cultured in medium containing 10% FCS. The cells were subsequently subjected to a time-course cell senescence assay. The cells were fixed every 24 h and the cell senescence rate was analyzed by beta-gal assay. U87MG cells were observed to be the most sensitive cell line to TMZ, as the percentage of senescence increased already 24 h after TMZ treatment. The U251MG cells responded more slowly, and started to undergo senescence about 48 h after the treatment. In contrast, the T98G and U118MG cells were insensitive to TMZ induced senescence (A). The expression of MGMT in the four glioblastoma cell lines was determined by using both Q-RT-PCR and Western blotting. MGMT was highly expressed in T98G and U118 cells, but undetectable in U251MG and U87MG cells (B, C).  On the basis of 425 primary GBM tumors from TCGA, we calculated the Pearson product-moment correlation coefficient. Bioinformatics analysis revealed that the expression of MGMT does not correlate with the expression of either NTN4 (r value=0.041) or ITGB4 (r value=0.043) (D).  Mean ± SE, <i>n</i> ≥ 3.</p

NTN4 partially prevents TMZ induced cell senescence of U251MG, but not of U87MG cells.

<p>U251MG and U87MG cells were treated with TMZ [100μM] for 3 h, and then cultured in medium containing 10% FCS and recombinant NTN4 protein [100 ng/ml] as indicated. After 4 d (U251MG) or 2 d (U87MG) the cells were subjected to beta-gal staining. NTN4 reduced the senescence rate of TMZ treated U251MG cells (A), but had no significant effects on U87MG cells (B). Both U87MG and U251MG cells were cultured to about 50% confluence, and then lysed for western blotting (WB) analysis. ITGB4 protein was observed in U251MG cells, but was barely detectable in U87MG cells. Tubulin was used as a loading control (C). Mean ± SE, <i>n</i> ≥ 3, ** p-value < 0.01.</p

Overexpression of ITGB4 combined with exogenous NTN4 partially prevents TMZ- induced U87MG cell senescence .

<p>U87MG cells were transfected to overexpress ITGB4. The expression level of ITGB4 in U87MG was confirmed by immunoblotting (A). ITGB4 overexpressing U87MG cells were treated with TMZ [100 μM] for 3 h, and then cultured in medium containing 10% FCS supplemented by recombinant NTN4 protein [100 ng/ml]. After 2 d, the cells were analyzed for senescence by beta-gal staining. Wild type U87MG and empty vector (Mock) transfected U87MG cells were used as controls. In either wild type U87MG or mock transfected cells, NTN4 displayed no significant effects on TMZ induced cell senescence. In the absence of exogenous addition of recombinant NTN4, overexpression of ITGB4 enhanced TMZ induced U87MG cell senescence, whereas in the presence of recombinant NTN4, the cells overexpressing ITGB4 were partially resistant to TMZ induced cell senescence (B, C). U251MG cells were infected by lentivirus harboring ITGB4 shRNAs and nontargeting control shRNA (NT-shRNA). Three days after infection, U251MG cells were treated with TMZ [100μM] for 3 h, and then cultured in medium containing 10% FCS and recombinant NTN4 protein [100 ng/ml]. Four days later, U251MG cells were fixed and analyzed by beta-gal staining. Silencing of ITGB4 increased the number of U251MG cells undergoing senescence. NTN4 reduced the senescence rate of wild type or non-targeting control U251MG cells induced by TMZ treatment, but NTN4 did not affect ITGB4-silenced U251MG cells (D). Mean ± SE, n ≥ 3, **p value < 0.01, * p value < 0.05.</p

In mothers of type 1 diabetic children the presence of C allele in the genotype is associated with an average difference of 3.9 nmol/l in serum 25OHD concentration (<i>p</i> = 0.002) while in mothers of non-diabetic children such an association was not found (<i>p</i> = 0.64) (<i>p</i>_interaction = 0.02).

<p>All analyses were adjusted for the month of sample collection.</p

Association of 25-hydroxyvitamin D concentration with SNPs in the metabolic pathway of vitamin D in all mothers and separately for mothers of type 1 diabetic and non-diabetic children, and according to the presence of the effect allele (EA).

<p>All analyses were adjusted for month of sample collection.</p