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Biomedical subjects

D Domínguez

Publications and source records attributed to D Domínguez.

At least 19 recordsLinked to original sources
PubMed2002

Nonlinear ac resistivity in s-wave and d-wave disordered granular superconductors.

We model s-wave and d-wave disordered granular superconductors with a three-dimensional lattice of randomly distributed Josephson junctions. The nonlinear ac resistivity rho(2) of these systems was calculated using Langevin dynamical equations. The current amplitude dependence of rho(2) at the peak position is found to be a power law characterized by exponent alpha, which is not universal but depends on the self-inductance and current regimes. In the weak current regime alpha is independent of the self-inductance and alpha = 0.5+/-0.1 for both s- and d-wave materials. In accord with experiments, we find alpha approximately 1 for some interval of inductance in the strong current regime.

Journal Article↗
PubMed2001

Renal cell carcinoma with syncytial giant cell component.

We report a case of clear cell renal cell carcinoma in which a prominent multinucleated giant cell component was intermingled with clear, granular, and spindle cells. Histological, ultrastructural, cytometric, and cytogenetic features of giant cells were similar to those of mononucleated cells in the tumor, and therefore they were not from stromal or osteoclast derivation. These giant cells had homogeneous, finely granular, abundant cytoplasm, often with scalloped cell borders, and contained from 5 to more than 50 nuclei, all of them very similar in size and shape, with prominent central nucleoli. Occasionally, surrounding inflammatory cells were also engulfed in the cytoplasm. This syncytial appearance was more similar to that of some giant cell carcinomas from the lung than to the pleomorphic giant cells often encountered in high grade renal cell tumors. Although the patient is alive and free of disease 6 years after diagnosis, a longer follow-up will be required to assess the potential prognostic influence of this peculiar histological appearance.

Carcinoma, Giant Cell↗
PubMed2001

Nonequilibrium transitions in fully frustrated Josephson junction arrays.

We study the effect of thermal fluctuations in a fully frustrated Josephson junction array driven by a current I larger than the apparent critical current I(c)(T). We calculate numerically the behavior of the chiral order parameter of Z2 symmetry and the transverse helicity modulus [related to the U(1) symmetry] as a function of temperature. We find that the Z2 transition occurs at a temperature T(Z2)(I) which is lower than the temperature T(U(1))(I) for the U(1) transition. Both transitions could be observed experimentally from measurements of the longitudinal and transverse voltages.

Journal Article↗
PubMed2001

Mode locking in ac-driven vortex lattices with random pinning.

We find mode-locking steps in simulated current-voltage characteristics of ac-driven vortex lattices with random pinning. For low frequencies there is mode locking above a finite ac force amplitude, while for large frequencies there is mode locking for any small ac force. This is correlated with the nature of temporal order in the different regimes in the absence of ac drive. The mode-locked state is a frozen solid pinned in the moving reference of frame, and the depinning from the step shows plastic flow and hysteresis.

Journal Article↗
PubMed2001

Loss of E-cadherin expression in melanoma cells involves up-regulation of the transcriptional repressor Snail.

Malignant transformation of melanocytes frequently coincides with loss of E-cadherin expression. Here we show that loss of E-cadherin in melanoma cell lines does not involve mutations in the E-cadherin gene, promoter methylation, or alterations in expression of AP-2 transcription factors as suggested previously. In a panel of different melanoma cell lines, E-cadherin expression was negatively regulated by up-regulation of the transcription factor Snail. In comparison with primary human melanocytes, where Snail expression was not detected by reverse transcription-polymerase chain reaction, significant expression was found in all eight melanoma cell lines. In parallel, Western blot and reverse transcription-polymerase chain reaction analysis revealed strong reduction of E-cadherin expression in the melanoma cells. Consistently, transient transfection of a Snail expression plasmid into human primary melanocytes led to significant down-regulation of E-cadherin, whereas transient and stable transfection of an antisense Snail construct induced reexpression of E-cadherin in Mel Ju and Mel Im melanomas. In summary, we conclude that activation of Snail expression plays an important role in down-regulation of E-cadherin and tumorigenesis of malignant melanomas.

Blotting, Western↗
PubMed2000

The transcription factor snail is a repressor of E-cadherin gene expression in epithelial tumour cells.

The adhesion protein E-cadherin plays a central part in the process of epithelial morphogenesis. Expression of this protein is downregulated during the acquisition of metastatic potential at late stages of epithelial tumour progression. There is evidence for a transcriptional blockage of E-cadherin gene expression in this process. Here we show that the transcription factor Snail, which is expressed by fibroblasts and some E-cadherin-negative epithelial tumour cell lines, binds to three E-boxes present in the human E-cadherin promoter and represses transcription of E-cadherin. Inhibition of Snail function in epithelial cancer cell lines lacking E-cadherin protein restores the expression of the E-cadherin gene.

Binding Sites↗
PubMed1998

Protein kinase C-alpha activity inversely modulates invasion and growth of intestinal cells.

The phorbol ester phorbol 12-myristate 13-acetate induces remarkable phenotypic changes in intestinal HT-29 M6 cells; these changes consist of loss of homotypic adhesion and inactivation of E-cadherin. In parallel, cell growth is retarded. We have transfected HT-29 M6 cells with an activated form of the conventional protein kinase Calpha (cPK-Calpha). Expression of this isoform induced the acquisition of a scattered phenotype, similar to that adopted by cells after addition of phorbol 12-myristate 13-acetate, with very low cell-to-cell aggregation and undetectable levels of functional E-cadherin. These cell clones were highly motile and rapidly invaded embryonic chick heart fragments. Furthermore, cells expressing activated-cPK-Calpha showed decreased proliferation in comparison to control clones. We have also studied how these two apparently antagonistic changes affect the tumorigenic ability of HT-29 M6 cells. When the different cell clones were xenografted into athymic mice, the effect on cell growth seemed to predominate. Expression of activated-cPK-Calpha significantly reduced the size of the tumors; the cells with the highest level of expression did not even form subcutaneous tumors. Besides their smaller size, the morphology of these tumors was clearly different from those originated by HT-29 M6 cells, and they could be defined as infiltrative on anatomo-pathological basis. These results indicate that cPK-Calpha controls both cell-to-cell adhesion and proliferation of intestinal cells.

Animals↗