Solving the time-dependent Schr\"odinger equation with absorbing boundary conditions and source terms in Mathematica 6.0

In recent decades a lot of research has been done on the numerical solution of the time-dependent Schr\"odinger equation. On the one hand, some of the proposed numerical methods do not need any kind of matrix inversion, but source terms cannot be easily implemented into this schemes; on the other, some methods involving matrix inversion can implement source terms in a natural way, but are not easy to implement into some computational software programs widely used by non-experts in programming (e.g. Mathematica). We present a simple method to solve the time-dependent Schr\"odinger equation by using a standard Crank-Nicholson method together with a Cayley's form for the finite-difference representation of evolution operator. Here, such standard numerical scheme has been simplified by inverting analytically the matrix of the evolution operator in position representation. The analytical inversion of the N x N matrix let us easily and fully implement the numerical method, with or without source terms, into Mathematica or even into any numerical computing language or computational software used for scientific computing.Comment: 15 pages, 7 figure

Increased Lysis of Stem Cells but Not Their Differentiated Cells by Natural Killer Cells; De-Differentiation or Reprogramming Activates NK Cells

The aims of this study are to demonstrate the increased lysis of stem cells but not their differentiated counterparts by the NK cells and to determine whether disturbance in cell differentiation is a cause for increased sensitivity to NK cell mediated cytotoxicity. Increased cytotoxicity and augmented secretion of IFN-γ were both observed when PBMCs or NK cells were co-incubated with primary UCLA oral squamous carcinoma stem cells (UCLA-OSCSCs) when compared to differentiated UCLA oral squamous carcinoma cells (UCLA-OSCCs). In addition, human embryonic stem cells (hESCs) were also lysed greatly by the NK cells. Moreover, NK cells were found to lyse human Mesenchymal Stem Cells (hMSCs), human dental pulp stem cells (hDPSCs) and human induced pluripotent stem cells (hiPSCs) significantly more than their differentiated counterparts or parental lines from which they were derived. It was also found that inhibition of differentiation or reversion of cells to a less-differentiated phenotype by blocking NFκB or targeted knock down of COX2 in monocytes significantly augmented NK cell cytotoxicity and secretion of IFN-γ. Taken together, these results suggest that stem cells are significant targets of the NK cell cytotoxicity. However, to support differentiation of a subset of tumor or healthy untransformed primary stem cells, NK cells may be required to lyse a number of stem cells and/or those which are either defective or incapable of full differentiation in order to lose their cytotoxic function and gain the ability to secrete cytokines (split anergy). Therefore, patients with cancer may benefit from repeated allogeneic NK cell transplantation for specific elimination of cancer stem cells

Theology, News and Notes - Vol. 14, No. 03

Theology News & Notes was a theological journal published by Fuller Theological Seminary from 1954 through 2014.https://digitalcommons.fuller.edu/tnn/1030/thumbnail.jp

Tritium labeling of potential lipophilic myelin probes

Two potential lipophilic myelin imaging agents (1,1,2,2‐tetrafluoro‐1,2‐diphenylethane and 1‐fluoroadamantane) were tritium labeled. The most effective method employed the microwave discharge activation of tritium gas technique and resulted in specific activities of 177 mCi/mmol for 1,1,2,2‐tetrafluoro‐1,2‐diphenylethane and 593 mCi/mmol for 1‐fluoroadamantane. Using this tritiation method significant amounts of tritium‐for‐fluorine substitution was also observed in the labeling of 1‐fluoroadamatane, resulting in nearly equivalent amounts of tritiated adamantane and fluoroadamantane.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/90398/1/2580210110_ftp.pd

Three-body Interactions Improve the Prediction of Rate and Mechanism in Protein Folding Models

Here we study the effects of many-body interactions on rate and mechanism in protein folding, using the results of molecular dynamics simulations on numerous coarse-grained C-alpha-model single-domain proteins. After adding three-body interactions explicitly as a perturbation to a Go-like Hamiltonian with native pair-wise interactions only, we have found 1) a significantly increased correlation with experimental phi-values and folding rates, 2) a stronger correlation of folding rate with contact order, matching the experimental range in rates when the fraction of three-body energy in the native state is ~ 20%, and 3) a considerably larger amount of 3-body energy present in Chymotripsin inhibitor than other proteins studied.Comment: 9 pages, 2 tables and 5 figure

Extended surfaces modulate and can catalyze hydrophobic effects

Interfaces are a most common motif in complex systems. To understand how the presence of interfaces affect hydrophobic phenomena, we use molecular simulations and theory to study hydration of solutes at interfaces. The solutes range in size from sub-nanometer to a few nanometers. The interfaces are self-assembled monolayers with a range of chemistries, from hydrophilic to hydrophobic. We show that the driving force for assembly in the vicinity of a hydrophobic surface is weaker than that in bulk water, and decreases with increasing temperature, in contrast to that in the bulk. We explain these distinct features in terms of an interplay between interfacial fluctuations and excluded volume effects---the physics encoded in Lum-Chandler-Weeks theory [J. Phys. Chem. B 103, 4570--4577 (1999)]. Our results suggest a catalytic role for hydrophobic interfaces in the unfolding of proteins, for example, in the interior of chaperonins and in amyloid formation.Comment: 22 pages, 5 figure

The Canadian Neuromuscular Disease Registry 2010-2019: A Decade of Facilitating Clinical Research Througha Nationwide, Pan-NeuromuscularDisease Registry

We report the recruitment activities and outcomes of a multi-disease neuromuscular patient registry in Canada. The Canadian Neuromuscular Disease Registry (CNDR) registers individuals across Canada with a confirmed diagnosis of a neuromuscular disease. Diagnosis and contact information are collected across all diseases and detailed prospective data is collected for 5 specific diseases: Amyotrophic Lateral Sclerosis (ALS), Duchenne Muscular Dystrophy (DMD), Myotonic Dystrophy (DM), Limb Girdle Muscular Dystrophy (LGMD), and Spinal Muscular Atrophy (SMA). Since 2010, the CNDR has registered 4306 patients (1154 pediatric and 3148 adult) with 91 different neuromuscular diagnoses and has facilitated 125 projects (73 academic, 3 not-for-profit, 3 government, and 46 commercial) using registry data. In conclusion, the CNDR is an effective and productive pan-neuromuscular registry that has successfully facilitated a substantial number of studies over the past 10 years

Potential for modulation of the hydrophobic effect inside chaperonins

Despite the spontaneity of some in vitro protein folding reactions, native folding in vivo often requires the participation of barrel-shaped multimeric complexes known as chaperonins. Although it has long been known that chaperonin substrates fold upon sequestration inside the chaperonin barrel, the precise mechanism by which confinement within this space facilitates folding remains unknown. In this study, we examine the possibility that the chaperonin mediates a favorable reorganization of the solvent for the folding reaction. We begin by discussing the effect of electrostatic charge on solvent-mediated hydrophobic forces in an aqueous environment. Based on these initial physical arguments, we construct a simple, phenomenological theory for the thermodynamics of density and hydrogen bond order fluctuations in liquid water. Within the framework of this model, we investigate the effect of confinement within a chaperonin-like cavity on the configurational free energy of water by calculating solvent free energies for cavities corresponding to the different conformational states in the ATP- driven catalytic cycle of the prokaryotic chaperonin GroEL. Our findings suggest that one function of chaperonins may be to trap unfolded proteins and subsequently expose them to a micro-environment in which the hydrophobic effect, a crucial thermodynamic driving force for folding, is enhanced

Microsecond folding dynamics of the F13W G29A mutant of the B domain of staphylococcal protein A by laser-induced temperature jump

The small size (58 residues) and simple structure of the B domain of staphylococcal protein A (BdpA) have led to this domain being a paradigm for theoretical studies of folding. Experimental studies of the folding of BdpA have been limited by the rapidity of its folding kinetics. We report the folding kinetics of a fluorescent mutant of BdpA (G29A F13W), named F13W*, using nanosecond laser-induced temperature jump experiments. Automation of the apparatus has permitted large data sets to be acquired that provide excellent signal-to-noise ratio over a wide range of experimental conditions. By measuring the temperature and denaturant dependence of equilibrium and kinetic data for F13W*, we show that thermodynamic modeling of multidimensional equilibrium and kinetic surfaces is a robust method that allows reliable extrapolation of rate constants to regions of the folding landscape not directly accessible experimentally. The results reveal that F13W* is the fastest-folding protein of its size studied to date, with a maximum folding rate constant at 0 M guanidinium chloride and 45°C of 249,000 (s-1). Assuming the single-exponential kinetics represent barrier-limited folding, these data limit the value for the preexponential factor for folding of this protein to at least ≈2 x 10(6) s(-1)

Control of pathogenic effector T-cell activities in situ by PD-L1 expression on respiratory inflammatory dendritic cells during respiratory syncytial virus infection

Respiratory syncytial virus (RSV) infection is a leading cause of severe lower respiratory tract illness in young infants, the elderly and immunocompromised individuals. We demonstrate here that the co-inhibitory molecule programmed cell death 1 (PD-1) is selectively upregulated on T cells within the respiratory tract during both murine and human RSV infection. Importantly, the interaction of PD-1 with its ligand PD-L1 is vital to restrict the pro-inflammatory activities of lung effector T cells in situ, thereby inhibiting the development of excessive pulmonary inflammation and injury during RSV infection. We further identify that PD-L1 expression on lung inflammatory dendritic cells is critical to suppress inflammatory T-cell activities, and an interferon-STAT1-IRF1 axis is responsible for increased PD-L1 expression on lung inflammatory dendritic cells. Our findings suggest a potentially critical role of PD-L1 and PD-1 interactions in the lung for controlling host inflammatory responses and disease progression in clinical RSV infection