Renormalization of Higher Derivative Operators in the Matrix Model

$M$-theory is believed to be described in various dimensions by large $N$ field theories. It has been further conjectured that at finite $N$, these theories describe the discrete light cone quantization (DLCQ) of $M$ theory. Even at low energies, this is not necessarily the same thing as the DLCQ of supergravity. It is believed that this is only the case for quantities which are protected by non-renormalization theorems. In 0+1 and 1+1 dimensions, we provide further evidence of a non-renormalization theorem for the $v^4$ terms, but also give evidence that there are not such theorems at order $v^8$ and higher.Comment: 14 pages latex. Note added in light of recent development

NMDAR-Activated PP1 Dephosphorylates GluN2B to Modulate NMDAR Synaptic Content.

In mature neurons, postsynaptic N-methyl-D-aspartate receptors (NMDARs) are segregated into two populations, synaptic and extrasynaptic, which differ in localization, function, and associated intracellular cascades. These two pools are connected via lateral diffusion, and receptor exchange between them modulates synaptic NMDAR content. Here, we identify the phosphorylation of the PDZ-ligand of the GluN2B subunit of NMDARs (at S1480) as a critical determinant in dynamically controlling NMDAR synaptic content. We find that phosphorylation of GluN2B at S1480 maintains NMDARs at extrasynaptic membranes as part of a protein complex containing protein phosphatase 1 (PP1). Global activation of NMDARs leads to the activation of PP1, which mediates dephosphorylation of GluN2B at S1480 to promote an increase in synaptic NMDAR content. Thus, PP1-mediated dephosphorylation of the GluN2B PDZ-ligand modulates the synaptic expression of NMDARs in mature neurons in an activity-dependent manner, a process with profound consequences for synaptic and structural plasticity, metaplasticity, and synaptic neurotransmission

Resistance mechanisms to targeted therapy in BRAF-mutant melanoma - A mini review

Background The introduction of targeted therapies for the treatment of BRAF-mutant melanomas have improved survival rates in a significant proportion of patients. Nonetheless, the emergence of resistance to treatment remains inevitable in most patients. Scope of review Here, we review known and emerging molecular mechanisms that underlay the development of resistance to MAPK inhibition in melanoma cells and the potential strategies to overcome these mechanisms. Major conclusions Multiple genetic and non-genetic mechanisms contribute to treatment failure, commonly leading to the reactivation of the MAPK pathway. A variety of resistance mechanisms are enabled by the underlying heterogeneity and plasticity of melanoma cells. Moreover, it has become apparent that resistance to targeted therapy is underpinned by early functional adaptations involving the rewiring of cell states and metabolic pathways. General significance The evidence presented suggest that the use of a combinatorial treatment approach would delay the emergence of resistance and improve patient outcomes

Structure of a liquid crystalline fluid around a macroparticle: Density functional theory study

The structure of a molecular liquid, in both the nematic liquid crystalline and isotropic phases, around a cylindrical macroparticle, is studied using density functional theory. In the nematic phase the structure of the fluid is highly anisotropic with respect to the director, in agreement with results from simulation and phenomenological theories. On going into the isotropic phase the structure becomes rotationally invariant around the macroparticle with an oriented layer at the surface.Comment: 10 pages, 6 figues. Submitted to Phys. Rev.