Biomedical subjects

Alessandro Flammini

Publications and source records attributed to Alessandro Flammini.

8 recordsLinked to original sources

PubMed2006

Scale-free network growth by ranking.

Network growth is currently explained through mechanisms that rely on node prestige measures, such as degree or fitness. In many real networks, those who create and connect nodes do not know the prestige values of existing nodes but only their ranking by prestige. We propose a criterion of network growth that explicitly relies on the ranking of the nodes according to any prestige measure, be it topological or not. The resulting network has a scale-free degree distribution when the probability to link a target node is any power-law function of its rank, even when one has only partial information of node ranks. Our criterion may explain the frequency and robustness of scale-free degree distributions in real networks, as illustrated by the special case of the Web graph.

Journal Article↗

PubMed2006

Geometry of proteins: hydrogen bonding, sterics, and marginally compact tubes.

The functionality of proteins is governed by their structure in the native state. Protein structures are made up of emergent building blocks of helices and almost planar sheets. A simple coarse-grained geometrical model of a flexible tube barely subject to compaction provides a unified framework for understanding the common character of globular proteins. We argue that a recent critique of the tube idea is not well founded.

Computer Simulation↗

PubMed2005

Species lifetime distribution for simple models of ecologies.

Interpretation of empirical results based on a taxa's lifetime distribution shows apparently conflicting results. Species' lifetime is reported to be exponentially distributed, whereas higher-order taxa, such as families or genera, follow a broader distribution, compatible with power-law decay. We show that both forms of evidence are consistent with a simple evolutionary model that does not require specific assumptions on species interaction. The model provides a zero-order description of the dynamics of ecological communities, and its species lifetime distribution can be computed exactly. Different behaviors are found as follows: an initial t(-3/2) power law, emerging from a random walk type of dynamics, which crosses over to a steeper t(-2) branching process-like regime and finally is cut off by an exponential decay that becomes weaker and weaker as the total population increases. Sampling effects also can be taken into account and shown to be relevant. If species in the fossil record were sampled according to the Fisher log-series distribution, lifetime should be distributed according to a t(-1) power law. Such variability of behaviors in a simple model, combined with the scarcity of data available, casts serious doubt on the possibility of validating theories of evolution on the basis of species lifetime data.

Animals↗

PubMed2004

Simulations of action of DNA topoisomerases to investigate boundaries and shapes of spaces of knots.

The configuration space available to randomly cyclized polymers is divided into subspaces accessible to individual knot types. A phantom chain utilized in numerical simulations of polymers can explore all subspaces, whereas a real closed chain forming a figure-of-eight knot, for example, is confined to a subspace corresponding to this knot type only. One can conceptually compare the assembly of configuration spaces of various knot types to a complex foam where individual cells delimit the configuration space available to a given knot type. Neighboring cells in the foam harbor knots that can be converted into each other by just one intersegmental passage. Such a segment-segment passage occurring at the level of knotted configurations corresponds to a passage through the interface between neighboring cells in the foamy knot space. Using a DNA topoisomerase-inspired simulation approach we characterize here the effective interface area between neighboring knot spaces as well as the surface-to-volume ratio of individual knot spaces. These results provide a reference system required for better understanding mechanisms of action of various DNA topoisomerases.

Bacteriophage T4↗

PubMed2004

Stochastic model for the species abundance problem in an ecological community.

We propose a model based on coupled multiplicative stochastic processes to understand the dynamics of competing species in an ecosystem. This process can be conveniently described by a Fokker-Planck equation. We provide an analytical expression for the marginalized stationary distribution. Our solution is found in excellent agreement with numerical simulations and compares rather well with observational data from tropical forests.

Animals↗

PubMed2004

Scale-free behavior and universality in random fragmentation and aggregation.

Two distinct mechanisms underlying the existence of power-law distributions are presented: the distribution is stationary under the process of merging and splitting of classes and the distribution of the entities under study is invariant under changes of the classification scheme. We provide an explanation for the ubiquitous inverse n relationship in the species abundance relationship in ecology and the 1/n(2) distribution of company sizes based on the minimum impact principle.

Journal Article↗

PubMed2003

Global protein function prediction from protein-protein interaction networks.

Determining protein function is one of the most challenging problems of the post-genomic era. The availability of entire genome sequences and of high-throughput capabilities to determine gene coexpression patterns has shifted the research focus from the study of single proteins or small complexes to that of the entire proteome. In this context, the search for reliable methods for assigning protein function is of primary importance. There are various approaches available for deducing the function of proteins of unknown function using information derived from sequence similarity or clustering patterns of co-regulated genes, phylogenetic profiles, protein-protein interactions (refs. 5-8 and Samanta, M.P. and Liang, S., unpublished data), and protein complexes. Here we propose the assignment of proteins to functional classes on the basis of their network of physical interactions as determined by minimizing the number of protein interactions among different functional categories. Function assignment is proteome-wide and is determined by the global connectivity pattern of the protein network. The approach results in multiple functional assignments, a consequence of the existence of multiple equivalent solutions. We apply the method to analyze the yeast Saccharomyces cerevisiae protein-protein interaction network. The robustness of the approach is tested in a system containing a high percentage of unclassified proteins and also in cases of deletion and insertion of specific protein interactions.

Algorithms↗

PubMed2002

Crucial stages of protein folding through a solvable model: predicting target sites for enzyme-inhibiting drugs.

An exactly solvable model based on the topology of a protein native state is applied to identify bottlenecks and key sites for the folding of human immunodeficiency virus type 1 (HIV-1) protease. The predicted sites are found to correlate well with clinical data on resistance to Food and Drug Administration-approved drugs. It has been observed that the effects of drug therapy are to induce multiple mutations on the protease. The sites where such mutations occur correlate well with those involved in folding bottlenecks identified through the deterministic procedure proposed in this study. The high statistical significance of the observed correlations suggests that the approach may be promisingly used in conjunction with traditional techniques to identify candidate locations for drug attacks.

Amino Acids↗