Amina i Musa, els nostres amics. 'Amina y Musa, nuestros amigos'.

Resumen del documento en catalán

Amina i Musa van a l'escola. 'Amina y Musa van a la escuela'.

Resumen del documento en catalán

Amina i Musa aprenen : la importància de l'educació. 'Amina i Musa aprenden : la importancia de la educación'.

Musa tiene 8 años y quiere ser veterinario. Amina, que tiene 12, sueña que será profesora o alcaldesa. Los dos van a la escuela, colaboran con sus padres en las faenas de casa, juegan con los amigos. Un árbol del pueblo donde viven, en Tanzania, muestra la vida cotidiana de sus habitantes y como a lo largo de los años ha podido constatar que la educación mejora la calidad de vida de las personas. Resumen del documento en catalán.

Espectro de gotas e potencial de deriva de caldas contendo o herbicida 2,4-d amina em misturas em tanque

Pós-graduação em Agronomia (Energia na Agricultura) - FCA

Amina Goodwin, Kniestück

Signatur des Originals: S 36/F10735

La Sonnambula. Act I. Scene XI. : Elvino: Al nuovo amante, sconoseente t'abbandono. Amina: Oh crudo istante! Deh mudite io rea von sono. ; Elvino: I abandon thee ungrateful, to thy new lover. Amina: Oh, cruel moment! I am not guilty.

Signatur des Originals: S 36/G03300

Jenny Lind als Amina, Rollenbild, in: Vincenzo Bellini: La sonnambula

Signatur des Originals: S 36/G14178

Clusterin facilitates COMMD1 and I-kB degradation to enhance NF-kB activity in prostate cancer cells

Secretory clusterin (sCLU) is a stress-activated, cytoprotective chaperone that confers broad-spectrum cancer treatment resistance, and its targeted inhibitor (OGX-011) is currently in phase II trials for prostate, lung, and breast cancer. However, the molecular mechanisms by which sCLU inhibits treatment-induced apoptosis in prostate cancer remain incompletely defined. We report that sCLU increases NF-κB nuclear translocation and transcriptional activity by serving as a ubiquitin-binding protein that enhances COMMD1 and I-κB proteasomal degradation by interacting with members of the SCF-βTrCP E3 ligase family. Knockdown of sCLU in prostate cancer cells stabilizes COMMD1 and I-κB, thereby sequestrating NF-κB in the cytoplasm and decreasing NF-κB transcriptional activity. Comparative microarray profiling of sCLU-overexpressing and sCLU-knockdown prostate cancer cells confirmed that the expression of many NF-κB–regulated genes positively correlates with sCLU levels. We propose that elevated levels of sCLU promote prostate cancer cell survival by facilitating degradation of COMMD1 and I-κB, thereby activating the canonical NF-κB pathway.

Clusterin is a critical downstream mediator of stress-induced YB-1 transactivation in prostate cancer

Clusterin is a stress-activated, cytoprotective chaperone that confers broad-spectrum treatment resistance in cancer. However, the molecular mechanisms mediating CLU transcription following anticancer treatment stress remain incompletely defined. We report that Y-box binding protein-1 (YB-1) directly binds to CLU promoter regions to transcriptionally regulate clusterin expression. In response to endoplasmic reticulum stress inducers, including paclitaxel, YB-1 is translocated to the nucleus to transactivate clusterin. Furthermore, higher levels of activated YB-1 and clusterin are seen in taxane-resistant, compared with parental, prostate cancer cells. Knockdown of either YB-1 or clusterin sensitized prostate cancer cells to paclitaxel, whereas their overexpression increased resistance to taxane. Clusterin overexpression rescued cells from increased paclitaxel-induced apoptosis following YB-1 knockdown; in contrast, however, YB-1 overexpression did not rescue cells from increased paclitaxel-induced apoptosis following clusterin knockdown. Collectively, these data indicate that YB-1 transactivation of clusterin in response to stress is a critical mediator of paclitaxel resistance in prostate cancer. Mol Cancer Res; 9(12); 1755–66.

Mathematical Models of Tumor-Immune System Dynamics

"This collection of papers offers a broad synopsis of state-of-the-art mathematical methods used in modeling the interaction between tumors and the immune system. These papers were presented at the four-day workshop on Mathematical Models of Tumor-Immune System Dynamics held in Sydney, Australia from January 7th to January 10th, 2013. The workshop brought together applied mathematicians, biologists, and clinicians actively working in the field of cancer immunology to share their current research and to increase awareness of the innovative mathematical tools that are applicable to the growing field of cancer immunology. Recent progress in cancer immunology and advances in immunotherapy suggest that the immune system plays a fundamental role in host defense against tumors and could be utilized to prevent or cure cancer. Although theoretical and experimental studies of tumor-immune system dynamics have a long history, there are still many unanswered questions about the mechanisms that govern the interaction between the immune system and a growing tumor. The multidimensional nature of these complex interactions requires a cross-disciplinary approach to capture more realistic dynamics of the essential biology. The papers presented in this volume explore these issues and the results will be of interest to graduate students and researchers in a variety of fields within mathematical and biological sciences."--Publisher website