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Biomedical subjects

F Montalenti

Publications and source records attributed to F Montalenti.

9 recordsLinked to original sources
PubMed2006

Self-ordering of a Ge island single layer induced by Si overgrowth.

We provide a direct experimental proof and the related modeling of the role played by Si overgrowth in promoting the lateral ordering of Ge islands grown by chemical vapor deposition on Si(001). The deposition of silicon induces a shape transformation, from domes to truncated pyramids with a larger base, generating an array of closely spaced interacting islands. By modeling, we show that the resulting gradient in the chemical potential across the island should be the driving force for a selective flow of both Ge and Si atoms at the surface and, in turn, to a real motion of the dots, favoring the lateral order.

Journal Article↗
PubMed2004

Atomic-scale pathway of the pyramid-to-dome transition during ge growth on Si(001).

By high resolution scanning tunneling microscopy, we investigate the morphological transition from pyramid to dome islands during the growth of Ge on Si(001). We show that pyramids grow from top to bottom and that, from a critical size on, incomplete facets are formed. We demonstrate that the bunching of the steps delimiting these facets evolves into the steeper dome facets. Based on first principles and Tersoff-potential calculations, we develop a microscopic model for the onset of the morphological transition, able to reproduce closely the experimentally observed behavior.

Journal Article↗
PubMed2004

Structure and mobility of defects formed from collision cascades in MgO.

We study radiation-damage events in MgO on experimental time scales by augmenting molecular dynamics cascade simulations with temperature accelerated dynamics, molecular statics, and density functional theory. At 400 eV, vacancies and mono- and di-interstitials form, but often annihilate within milliseconds. At 2 and 5 keV, larger clusters can form and persist. While vacancies are immobile, interstitials aggregate into clusters (In) with surprising properties; e.g., an I4 is immobile, but an impinging I2 can create a metastable I6 that diffuses on the nanosecond time scale but is stable for years.

Journal Article↗
PubMed2001

Closing the gap between experiment and theory: crystal growth by temperature accelerated dynamics.

We present atomistic simulations of crystal growth where realistic experimental deposition rates are reproduced, without needing any a priori information on the relevant diffusion processes. Using the temperature accelerated dynamics method, we simulate the deposition of 4 monolayers (ML) of Ag/Ag(100) at the rate of 0.075 ML/s, thus obtaining a boost of several orders of magnitude with respect to ordinary molecular dynamics. In the temperature range analyzed (0-70 K), steering and activated mechanisms compete in determining the surface roughness.

Journal Article↗
PubMed2001

Cell cycle effects of gemcitabine.

Gemcitabine (2',2'-difluoro-2'-deoxycytidine, or dFdC) is a promising anticancer agent with demonstrated clinical activity in solid tumours currently undergoing clinical trials. Despite extensive studies on the biochemical mechanism of action, cell cycle perturbations induced by dFdC have not yet been thoroughly investigated, apart from the expected inhibition of DNA synthesis. The aim of our study was to clarify whether cell population kinetics is a vital factor in the cytotoxicity of dFdC in single or repeated treatments and in the dFdC-cisplatin combination. Ovarian cancer cells growing in vitro were treated with dFdC for 1 hr in a range of concentrations from 10 nM to 10 microM. Cell kinetics was investigated by DNA-bromodeoxyuridine flow cytometry, using different experimental protocols to measure either the time course of DNA-synthesis inhibition or the fate of cells in G(1), S or G(2)M at the time of dFdC treatment or 24 hr later. A modified sulforhodamine B test was used to assess the growth inhibition caused by dFdC given alone or with cisplatin. Although dFdC promptly inhibited DNA synthesis, cytotoxicity on proliferating cells was not specific for cells initially in the S phase. DNA synthesis was restored after a G(1) block of variable, dose-dependent length, but recycling cells were intercepted at the subsequent checkpoints, resulting in delays in the G(2)M and G(1) phases. The activity of repeated treatment with dFdC + dFdC or dFdC + cisplatin was highly dependent on the interval length between them. These results suggest that the kinetics of cell recycling from a first dFdC treatment strongly affects the outcome of a second treatment with either dFdC itself or cisplatin.

Antimetabolites, Antineoplastic↗
PubMed2000

Probability of dimer reassociation in two dimensions

We study the problem of dimer dissociation and reassociation in two dimensions through a random-walk-like calculation. In order to find the probability of dimer reassociation after a given number of hops, we give the exact analytical solution for the probability of a first return into a given region (rhombus) for a two-dimensional random walker on a squared lattice.

Journal Article↗
PubMed2000

Long jumps in the strong-collision model

The jump-length probability distribution for a classical particle diffusing in a periodic potential is calculated in the framework of a strong-collision model, where each collision of the particle with the thermal bath reequilibrates the velocity. Exact numerical results are obtained by the matrix-continued-fraction method, and two different analytical approximations are developed. In the first approximations it is assumed that an activated particle is always retrapped in the cell where it suffers the first collision; in the second approximation it is assumed that only the collisions giving a final total energy which is lower than the activation barrier are effective for retrapping. This second analytical approximation is in excellent agreement with the numerical data.

Journal Article↗
PubMed1999

Measuring the complexity of cell cycle arrest and killing of drugs: kinetics of phase-specific effects induced by taxol.

BACKGROUND: Paclitaxel (Taxol) is known to act mainly in mitosis, interfering with microtubule dynamics, but effects on the other cells cycle phases have been reported also. However, a comparative picture of perturbation and killing in the G(1), S and G(2)M phases after drug treatment is lacking. The approach developed by our group tackles the problem of the complexity of cell cycle effects with the aid of a computer program simulating cell cycle progression and new quantities measuring cell-cycle arrest and death. METHODS: The program generates data that were compared with those given by absolute cell counts and by different flow cytometry techniques, enabling us to follow the fate of G(1) and G(2)M blocked cells either re-entering the cycle or dying, distinguishing cytostatic and cytotoxic effects. Apoptosis was analyzed in order to refine the description of cytotoxic effects. RESULTS: We estimated the number of blocked and dead cells after short-term Taxol treatments in a range of concentrations and post-drug incubation times. G(2)M block was immediately active at low concentrations but was reversible, becoming irreversible only at the highest concentrations. G(1)block became active later, allowing cell cycle progression of cells initially in G(1), but was still active 48 h post-treatment, at intermediate concentrations. S-phase delay was detected after 24 h. The death rate was much higher within G(1)than G(2)M blocked cells. CONCLUSIONS: Our analysis unraveled the complexity of cell cycle effects of the drug, and revealed the activity of G(1) checkpoint, hidden by a prompter but less cytotoxic G(2)M block.

Antineoplastic Agents, Phytogenic↗