Mathematical model of interaction and Coliphages.

We propose a mathematical model based in ordinary differential equations between bacterial pathogen and Bacteriophages to describe the infection dynamics of these populations, for which we use a nonlinear function with an inhibitory effect. We study the stability of the model using the Lyapunov theory and the second additive compound matrix and perform a global sensitivity analysis to elucidate the most influential parameters in the model, besides we make a parameter estimation using growth data of bacteria in presence of Coliphages (bacteriophages that infect ) with different multiplicity of infection. We found a threshold that indicates whether the bacteriophage concentration will coexist with the bacterium (the coexistence equilibrium) or become extinct (phages extinction equilibrium), the first equilibrium is locally asymptotically stable while the other is globally asymptotically stable depending on the magnitude of this threshold.

Design of Optimal Coils for Deep Transcranial Magnetic Stimulation.

In this work, a stream function inverse boundary element method (IBEM) has been used for designing different deep transcranial magnetic stimulation (dTMS)coils to activate the prefrontal cortex and the temporal lobe have been set as the target regions. In addition, the performances of these coils have been described and the electric field induced by them has been obtained by using a computational forward technique. These results show that the stream function IBEM is an ideal approach to design optimal dTMS coils capable of producing deep stimulation in the target brain regions.

Design of TMS coils with reduced Lorentz forces: application to concurrent TMS-fMRI.

Objective: Interleaving TMS (transcranial magnetic stimulation) with fMRI (functional Magnetic Resonance Imaging) is a promising technique to study functional connectivity in the human brain, but its development is being restricted by technical limitations, such as that due to the interaction of the TMS current pulses with the magnetic fields of an MRI scanner. In this work, a TMS coil design method capable of controlling Lorentz forces experienced by the coil in the presence of static magnetic fields is presented.

Approach: The suggested approach is based on an existing inverse boundary element method (IBEM) for TMS coil design, in which new electromagnetic computational models of the Lorentz forces have been included to be controlled in the design process.

Molecular mechanism of sphingosine-1-phosphate action in Duchenne muscular dystrophy.

Duchenne muscular dystrophy (DMD) is a lethal muscle-wasting disease. Studies in Drosophila showed that genetic increase of the levels of the bioactive sphingolipid sphingosine-1-phosphate (S1P) or delivery of 2-acetyl-5-tetrahydroxybutyl imidazole (THI), an S1P lyase inhibitor, suppresses dystrophic muscle degeneration. In the dystrophic mouse (mdx), upregulation of S1P by THI increases regeneration and muscle force.

Increased sphingosine-1-phosphate improves muscle regeneration in acutely injured mdx mice.

Background: Presently, there is no effective treatment for the lethal muscle wasting disease Duchenne muscular dystrophy (DMD). Here we show that increased sphingosine-1-phoshate (S1P) through direct injection or via the administration of the small molecule 2-acetyl-4(5)-tetrahydroxybutyl imidazole (THI), an S1P lyase inhibitor, has beneficial effects in acutely injured dystrophic muscles of mdx mice.

Methods: We treated mdx mice with and without acute injury and characterized the histopathological and functional effects of increasing S1P levels.

Drosophila as a starting point for developing therapeutics for the rare disease Duchenne Muscular Dystrophy.

Progress into developing therapeutics for rare diseases can be accelerated for those diseases that can be modeled in genetically tractable organisms. Here we comment on one disease, Duchenne Muscular Dystrophy (DMD), modeled in Drosophila that brought together disparate lines of research toward the goal of developing a therapeutic. Though the bioactive lipid sphingosine 1-phosphate (S1P) has been implicated in many anabolic processes in many cell types and tissues, including muscle, this work confirmed the therapeutic potential of assessing this pathway for DMD.

Genetic elevation of sphingosine 1-phosphate suppresses dystrophic muscle phenotypes in Drosophila.

Duchenne muscular dystrophy is a lethal genetic disease characterized by the loss of muscle integrity and function over time. Using Drosophila, we show that dystrophic muscle phenotypes can be significantly suppressed by a reduction of wunen, a homolog of lipid phosphate phosphatase 3, which in higher animals can dephosphorylate a range of phospholipids. Our suppression analyses include assessing the localization of Projectin protein, a titin homolog, in sarcomeres as well as muscle morphology and functional movement assays.

Dystroglycan and mitochondrial ribosomal protein L34 regulate differentiation in the Drosophila eye.

Mutations that diminish the function of the extracellular matrix receptor Dystroglycan (DG) result in muscular dystrophies, with associated neuronal migration defects in the brain and mental retardation e.g. Muscle Eye Brain Disease.

Genetic modifier screens reveal new components that interact with the Drosophila dystroglycan-dystrophin complex.

The Dystroglycan-Dystrophin (Dg-Dys) complex has a capacity to transmit information from the extracellular matrix to the cytoskeleton inside the cell. It is proposed that this interaction is under tight regulation; however the signaling/regulatory components of Dg-Dys complex remain elusive. Understanding the regulation of the complex is critical since defects in this complex cause muscular dystrophy in humans.

Agrobacterium type IV secretion is a two-step process in which export substrates associate with the virulence protein VirJ in the periplasm.

Type IV secretion systems are virulence determinants in many bacteria and share extensive homology with many conjugal transfer systems. Although type IV systems and their homologues have been studied widely, the mechanism by which substrates are secreted remains unclear. In Agrobacterium, we show that type IV secretion substrates that lack signal peptides form a soluble complex in the periplasm with the virulence protein VirJ.