Biomedical subjects

A Talukder

Publications and source records attributed to A Talukder.

3 recordsLinked to original sources

PubMed2002

Mapping the mesoscale interface structure in polycrystalline materials.

A new experimental approach to the quantitative characterization of polycrystalline microstructure by scanning electron microscopy is described. Combining automated electron backscattering diffraction with conventional scanning contrast imaging and with calibrated serial sectioning, the new method (mesoscale interface mapping system) recovers precision estimates of the 3D idealized aggregate function G(x). This function embodies a description of lattice phase and orientation (limiting resolution approximately 1 degree) at each point x (limiting spatial resolution approximately 100 nm), and, therefore, contains a complete mesoscale description of the interfacial network. The principal challenges of the method, achieving precise spatial registry between adjacent images and adequate distortion correction, are described. A description algorithm for control of the various components of the system is also provided.

Journal Article↗

PubMed2001

A closed-form neural network for discriminatory feature extraction from high-dimensional data.

We consider a new neural network for data discrimination in pattern recognition applications. We refer to this as a maximum discriminating feature (MDF) neural network. Its weights are obtained in closed-form, thereby overcoming problems associated with other nonlinear neural networks. It uses neuron activation functions that are dynamically chosen based on the application. It is theoretically shown to provide nonlinear transforms of the input data that are more general than those provided by other nonlinear multilayer perceptron neural network and support-vector machine techniques for cases involving high-dimensional (image) inputs where training data are limited and the classes are not linearly separable. We experimentally verify this on synthetic examples.

Algorithms↗

PubMed1999

Serine phosphorylation of paxillin by heregulin-beta1: role of p38 mitogen activated protein kinase.

The mechanisms through which heregulin (HRG) regulates the progression of breast cancer cells to a more invasive phenotype are currently unknown. Recently we have shown that HRG treatment of breast cancer cells leads to the formation of lamellipodia/filopodia, and increased cell migration and invasiveness through the phosphatidylinositol 3-kinase (PI-3 kinase). Since the process of cell migration must involve changes in adhesion, we explored the potential HRG regulation of paxillin, a major cytoskeletal phosphoprotein of focal adhesion. We report that HRG stimulation of non-invasive breast cancer cells resulted in stimulation of p38 mitogen-activated protein kinase (p38MAPK), extracellular signal-regulated kinases (ERK) and PI-3K, and a concurrent unexpected increase in the level of paxillin phosphorylation on serine residue which was sensitive to protein-phosphatase 2b but not to protein tyrosine phosphatase 1. In addition, HRG triggered a rapid redistribution of paxillin to the perinuclear regions from the tyrosine-phosphorylated focal adhesions, and increased cell scattering. There was no effect of HRG on the state of phosphorylation and localization of focal adhesion kinase. The HRG-induced increase in serine phosphorylation of paxillin and cell scattering were selectively inhibited by a specific inhibitor of p38MAPK or a dominant-negative p38MAPK mutant, but not by inhibitors of p42/44MAPK or PI-3 kinase pathways. For the first time our results have shown that HRG, a potent migratory growth factor stimulates serine phosphorylation of paxillin. These findings suggest a role of p38MAPK-dependent signal transduction pathway(s) in serine phosphorylation and disassembly of the paxillin from the focal complexes during HRG-induced cell shape alterations and motility.

Breast Neoplasms↗