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1.
Phys Rev E ; 107(4-1): 044116, 2023 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-37198773

RESUMO

Via hydrodynamics-preserving molecular dynamics simulations we study growth phenomena in a phase-separating symmetric binary mixture model. We quench high-temperature homogeneous configurations to state points inside the miscibility gap, for various mixture compositions. For compositions at the symmetric or critical value we capture the rapid linear viscous hydrodynamic growth due to advective transport of material through tubelike interconnected domains. For state points very close to any of the branches of the coexistence curve, the growth in the system, following nucleation of disconnected droplets of the minority species, occurs via a coalescence mechanism. Using state-of-the-art techniques, we have identified that these droplets, between collisions, exhibit diffusive motion. The value of the exponent for the power-law growth, related to this diffusive coalescence mechanism, has been estimated. While the exponent nicely agrees with that for the growth via the well-known Lifshitz-Slyozov particle diffusion mechanism, the amplitude is stronger. For the intermediate compositions we observe initial rapid growth that matches the expectations for viscous or inertial hydrodynamic pictures. However, at later times these types of growth cross over to the exponent that is decided by the diffusive coalescence mechanism.

2.
Cancer Pathog Ther ; 1(3): 195-204, 2023 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-38327834

RESUMO

Prostate cancer (PCa) is the most common malignancy in men. Despite aggressive therapy involving surgery and hormonal treatments, the recurrence and emergence of metastatic castration-resistant prostate cancer (CRPCa) remain a major challenge. Dysregulation of the transforming growth factor-ß (TGF-ß) signaling pathway is crucial to PCa development and progression. This also contributes to androgen receptor activation and the emergence of CRPC. In addition, TGF-ß signaling regulates long non-coding RNA (lncRNA) expression in multiple cancers, including PCa. Here, we discuss the complex regulatory network of lncRNAs and TGF-ß signaling in PCa and their potential applications in diagnosing, prognosis, and treating PCa. Further investigations on the role of lncRNAs in the TGF-ß pathway will help to better understand PCa pathogenesis.

3.
Phys Rev E ; 101(6-1): 062112, 2020 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-32688577

RESUMO

Via Monte Carlo simulations we study nonequilibrium dynamics in the nearest-neighbor Ising model, following quenches to points inside the ordered region of the phase diagram. With the broad objective of quantifying the nonequilibrium universality classes corresponding to spatially correlated and uncorrelated initial configurations, in this paper we present results for the decay of the order-parameter autocorrelation function for quenches from the critical point. This autocorrelation is an important probe for the aging dynamics in far-from-equilibrium systems and typically exhibits power-law scaling. From the state-of-the-art analysis of the simulation results, we quantify the corresponding exponents (λ) for both conserved and nonconserved (order-parameter) dynamics of the model in space dimension d=3. Via structural analysis we demonstrate that the exponents satisfy a bound. We also revisit the d=2 case to obtain more accurate results. It appears that irrespective of the dimension, λ is approximately the same for both conserved and nonconserved dynamics.

4.
J Phys Condens Matter ; 32(18): 184005, 2020 May 01.
Artigo em Inglês | MEDLINE | ID: mdl-31952063

RESUMO

Following quenches of initial configurations having long range spatial correlations, prepared at the demixing critical point, to points inside the miscibility gap, we study aging phenomena in solid binary mixtures. Results on the decay of the two-time order-parameter autocorrelation functions, obtained from Monte Carlo simulations of the two-dimensional Ising model, with Kawasaki exchange kinetics, are analyzed via state-of-the art methods. The outcome is compared with that obtained for the ordering in uniaxial ferromagnets. For the latter, we have performed Monte Carlo simulations of the same model using the Glauber mechanism. For both types of systems we provide comparative discussion of our results with reference to those concerning quenches with configurations having no spatial correlation. We also discuss the role of structure on the decay of these correlations.

5.
J Biol Phys ; 39(1): 1-14, 2013 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-23860831

RESUMO

Chlamydomonas reinhardtii has long been used as a model organism in studies of cell motility and flagellar dynamics. The motility of the well-conserved '9+2' axoneme in its flagella remains a subject of immense curiosity. Using high-speed videography and morphological analyses, we have characterized long-flagella mutants (lf1, lf2-1, lf2-5, lf3-2, and lf4) of C. reinhardtii for biophysical parameters such as swimming velocities, waveforms, beat frequencies, and swimming trajectories. These mutants are aberrant in proteins involved in the regulation of flagellar length and bring about a phenotypic increase in this length. Our results reveal that the flagellar beat frequency and swimming velocity are negatively correlated with the length of the flagella. When compared to the wild-type, any increase in the flagellar length reduces both the swimming velocities (by 26-57%) and beat frequencies (by 8-16%). We demonstrate that with no apparent aberrations/ultrastructural deformities in the mutant axonemes, it is this increased length that has a critical role to play in the motion dynamics of C. reinhardtii cells, and, provided there are no significant changes in their flagellar proteome, any increase in this length compromises the swimming velocity either by reduction of the beat frequency or by an alteration in the waveform of the flagella.


Assuntos
Chlamydomonas reinhardtii/citologia , Chlamydomonas reinhardtii/genética , Flagelos/metabolismo , Movimento , Mutação , Chlamydomonas reinhardtii/metabolismo , Dineínas/metabolismo
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