Vitamin D (1,25(OH)2D3) induces α-1-antitrypsin synthesis by CD4+ T cells, which is required for 1,25(OH)2D3-driven IL-10.

Studies to identify novel immune-regulatory functions of active vitamin D (1,25(OH)2D3) in human CD4+ T cells revealed that 1,25(OH)2D3 potently induced expression of the gene SERPINA1, encoding the anti-protease α-1-antitrypsin. We confirmed α-1-antitrypsin protein expression by 1,25(OH)2D3-treated CD4+ T cells, but not in CD8+ T cells or monocytes. α-1-Antitrypsin promotes anti-inflammatory IL-10 synthesis in other immune cell populations. We therefore investigated its immune-regulatory effects in CD4+ T cells. Plasma-derived α-1-antitrypsin drove IL-10 synthesis by CD4+ T cells, which was not dependent on anti-protease activity, but appeared to require a serum-binding factor, since this could not be achieved with recombinant protein. α-1-Antitrypsin is reported to bind complement components, which regulate T cell function. A role for this interaction was therefore probed. Plasma-derived, but not recombinant α-1-antitrypsin contained C3a. Surface Plasmon Resonance and Microscale Thermophoresis demonstrated α-1-antitrypsin binding to C3a. Addition of C3a to CD4+ T cells cultured with recombinant α-1-antitrypsin restored induction of IL-10, whereas neutralisation of C3a abrogated IL-10 induced by plasma-derived α-1-antitrypsin. To interrogate an endogenous role for the α-1-antitrypsin-C3a axis in 1,25(OH)2D3-driven CD4+ T cell IL-10 synthesis, we treated cells from healthy or α-1-antitrypsin-deficient individuals (which transcribe SERPINA1 but do not secrete protein) with 1,25(OH)2D3. A significant correlation was identified between SERPINA1 and IL10 gene expression in healthy donor CD4+ T cells, which was absent in cells from α-1-antitrypsin-deficient individuals. Therefore, α-1-antitrypsin is required for 1,25(OH)2D3-induced IL-10 expression in CD4+ T cells, interacting with C3a to drive IL-10 expression.

Efficient Computational Modeling of Human Ventricular Activation and Its Electrocardiographic Representation: A Sensitivity Study.

Patient-specific models of the ventricular myocardium, combined with the computational power to run rapid simulations, are approaching the level where they could be used for personalized cardiovascular medicine. A major remaining challenge is determining model parameters from available patient data, especially for models of the Purkinje-myocardial junctions (PMJs): the sites of initial ventricular electrical activation. There are no non-invasive methods for localizing PMJs in patients, and the relationship between the standard clinical ECG and PMJ model parameters is underexplored. Thus, this study aimed to determine the sensitivity of the QRS complex of the ECG to the anatomical location and regional number of PMJs. The QRS complex was simulated using an image-based human torso and biventricular model, and cardiac electrophysiology was simulated using Cardioid. The PMJs were modeled as discrete current injection stimuli, and the location and number of stimuli were varied within initial activation regions based on published experiments. Results indicate that the QRS complex features were most sensitive to the presence or absence of four "seed" stimuli, and adjusting locations of nearby "regional" stimuli provided finer tuning. Decreasing number of regional stimuli by an order of magnitude resulted in virtually no change in the QRS complex. Thus, a minimal 12-stimuli configuration was identified that resulted in physiological excitation, defined by QRS complex feature metrics and ventricular excitation pattern. Overall, the sensitivity results suggest that parameterizing PMJ location, rather than number, be given significantly higher priority in future studies creating personalized ventricular models from patient-derived ECGs.

1α,25-dihydroxyvitamin D3 acts via transforming growth factor-ß to up-regulate expression of immunosuppressive CD73 on human CD4+ Foxp3- T cells.

Vitamin D deficiency is associated with increased incidence and severity of various immune-mediated diseases. Active vitamin D (1α,25-dihydroxyvitamin D3; 1,25(OH)2 D3) up-regulates CD4(+) T-cell expression of the purine ectonucleotidase CD39, a molecule that is associated with the generation of anti-inflammatory adenosine. Here we aimed to investigate the direct impact of 1,25(OH)2 D3 on expression of the downstream ecto-5'-nucleotidase CD73 by human CD4 T cells, and components of the transforming growth factor-ß (TGF-ß) pathway, which have been implicated in the modulation of CD73 by murine T cells. At 10(-8) to 10(-7) m, 1,25(OH)2 D3 significantly increased expression of CD73 on peripheral human CD4(+) T cells. Although 1,25(OH)2 D3 did not affect the mRNA expression of latent TGF-ß1 , 1,25(OH)2 D3 did up-regulate expression of TGF-ß-associated molecules [latency-associated peptide (LAP), glycophorin A repetitions predominant (GARP), GP96, neuropilin-1, thrombospondin-1 and αv integrin] which is likely to have contributed to the observed enhancement in TGF-ß bioactivity. CD73 was highly co-expressed with LAP and GARP following 1,25(OH)2 D3 treatment, but unexpectedly, each of these cell surface molecules was expressed primarily on CD4(+) Foxp3(-) T cells, rather than CD4(+) Foxp3(+) T cells. Notably, neutralization of TGF-ß significantly impaired 1,25(OH)2 D3-mediated induction of CD73. Collectively, we show that 1,25(OH)2 D3 enhances expression of CD73 on CD4(+) Foxp3(-) T cells in a process that is at least partially TGF-ß-dependent. These data reveal an additional contributing mechanism by which vitamin D may be protective in immune-mediated disease.

Distinct endotypes of steroid-resistant asthma characterized by IL-17A(high) and IFN-γ(high) immunophenotypes: Potential benefits of calcitriol.

BACKGROUND: A small population of patients with severe asthma does not respond to glucocorticoids (steroid resistant [SR]). They have high morbidity, highlighting an urgent need for strategies to enhance glucocorticoid responsiveness. OBJECTIVE: We investigated the immunologic differences between steroid-sensitive (SS) and SR asthmatic patients and the effect on immunophenotype of oral calcitriol treatment because it has been previously shown to beneficially modulate the clinical response to glucocorticoids in patients with SR asthma. METHODS: CD8-depleted PBMCs were isolated from 12 patients with SS and 23 patients with SR asthma and cultured for 7 days with anti-CD3 and IL-2 with or without dexamethasone. Cytokine production was assessed in supernatants by using the Cytometric Bead Array. Patients with SR asthma were subsequently randomized to oral calcitriol or placebo therapy, and identical studies were repeated. RESULTS: Patients with SR asthma produced significantly increased IL-17A and IFN-γ levels compared with those in patients with SS asthma, although it was evident that cells from individual patients might overproduce one or the other of these cytokines. Production of IL-17A was inversely and production of IL-13 was positively associated with the clinical response to prednisolone. Oral calcitriol, compared with placebo, therapy of the patients with SR asthma significantly improved dexamethasone-induced IL-10 production in vitro while suppressing dexamethasone-induced IL-17A production. This effect mirrored the previously demonstrated improvement in clinical response to oral glucocorticoids in calcitriol-treated patients with SR asthma. CONCLUSIONS: IL-17A(high) and IFN-γ(high) immunophenotypes exist in patients with SR asthma. These data identify immunologic pathways that likely underpin the beneficial clinical effects of calcitriol in patients with SR asthma by directing the SR cytokine profile toward a more SS immune phenotype, suggesting strategies for identifying vitamin D responder immunophenotypes.

A high-resolution computational model of the deforming human heart.

Modeling of the heart ventricles is one of the most challenging tasks in soft tissue mechanics because cardiac tissue is a strongly anisotropic incompressible material with an active component of stress. In most current approaches with active force, the number of degrees of freedom (DOF) is limited by the direct method of solution of linear systems of equations. We develop a new approach for high-resolution heart models with large numbers of DOF by: (1) developing a hex-dominant finite element mixed formulation and (2) developing a Krylov subspace iterative method that is able to solve the system of linearized equations for saddle-point problems with active stress. In our approach, passive cardiac tissue is modeled as a hyperelastic, incompressible material with orthotropic properties, and mixed pressure-displacement finite elements are used to enforce incompressibility. Active stress is generated by a model with force dependence on length and velocity of muscle shortening. The ventricles are coupled to a lumped circulatory model. For efficient solution of linear systems, we use Flexible GMRES with a nonlinear preconditioner based on block matrix decomposition involving the Schur complement. Three methods for approximating the inverse of the Schur complement are evaluated: inverse of the pressure mass matrix; least squares commutators; and sparse approximate inverse. The sub-matrix corresponding to the displacement variables is preconditioned by a V-cycle of hybrid geometric-algebraic multigrid followed by correction with several iterations of GMRES preconditioned by sparse approximate inverse. The overall solver is demonstrated on a high-resolution two ventricle mesh based on a human anatomy with roughly 130 K elements and 1.7 M displacement DOF. Effectiveness of the numerical method for active contraction is shown. To the best of our knowledge, this solver is the first to efficiently model ventricular contraction using an iterative linear solver for the mesh size demonstrated and therefore opens the possibility for future very high-resolution models. In addition, several relatively simple benchmark problems are designed for a verification exercise to show that the solver is functioning properly and correctly solves the underlying mathematical model. Here, the output of the newly designed solver is compared to that of the mechanics component of Chaste ('Cancer, Heart and Soft Tissue Environment'). These benchmark tests may be used by other researchers to verify their newly developed methods and codes.

Depigmented-polymerised allergoids favour regulatory over effector T cells: enhancement by 1α, 25-dihydroxyvitamin D3.

BACKGROUND: Allergen immunotherapy (SIT) is the only treatment for allergic disease capable of modifying disease long term. To reduce the risk of anaphylaxis from SIT, allergen-extracts have been modified by polymerisation with glutaraldehyde to reduce IgE binding. It is suggested that these allergoid extracts also have reduced T cell activity, which could compromise clinical efficacy. Effective SIT is thought to act through regulatory T cells (Tregs) rather than activation of effector T cells. There is no published data on the activity of modified extracts on Tregs. RESULTS: We compared the capacity of modified (depigmented-polymerised) versus unmodified (native) allergen extracts of grass pollen and house dust mite to stimulate proliferation/cytokine production and to modulate Treg/effector T cell frequency in cultures of peripheral blood mononuclear cells (PBMC), from volunteers sensitised to both allergens in vitro. Depigmented-polymerised allergen extracts stimulated less proliferation of PBMC, and reduced effector cell numbers after 7 days in culture than did native extracts. However, the frequency of Foxp3+ Tregs in cultures were similar to those seen with native extract so that ratios of regulatory to effector T cells were significantly increased in cultures stimulated with depigmented-polymerised extracts. Addition of 1α, 25-dihydroxyvitamin D3 further favoured Treg, and reduced effector cytokine production, but not interleukin-10. CONCLUSIONS: Depigmented-polymerised allergen extracts appear to favour Treg expansion over activation of effector T cells and this may relate to their demonstrated efficacy and safety in SIT. 1α, 25-dihydroxyvitamin D3 further reduces effector T cell activation by allergen extracts and may be a useful adjuvant for SIT.

1α,25-dihydroxyvitamin D3 in combination with transforming growth factor-ß increases the frequency of Foxp3⁺ regulatory T cells through preferential expansion and usage of interleukin-2.

A high prevalence of vitamin D insufficiency and deficiency exists worldwide, which is associated with an increased incidence and severity of a range of immune-mediated diseases. This has resulted in considerable interest in the immunodulatory functions of vitamin D. The active form of vitamin D, 1α,25-dihydroxyvitamin D3 [1,25(OH)2D3], has been shown to increase the frequency of Foxp3(+) CD4(+) T regulatory (Treg) cells when present at high concentrations or under strong T-cell stimulation in culture. Supporting evidence exists in vivo for a positive association between serum 25(OH)D and Foxp3(+) Treg cell numbers in humans. The aim of this work was to identify the cytokine milieu required in vitro to promote Foxp3(+) Treg cells in cultures containing 1,25(OH)2D3 at more moderate concentrations (10(-7) M). Stimulation of human CD4(+) T cells with a combination of 1,25(OH)2D3 and transforming growth factor-ß (TGF-ß) greatly increased the frequency of Foxp3(+) Treg cells, which is proposed to result from the preferential expansion of Foxp3(+) Treg cells, as compared with the Foxp3(-) effector T cells, in culture. The differential effect on proliferation may result from enhanced availability and usage of interleukin-2 by the Foxp3(+) Treg cells compared with Foxp3(-) effector T cells. In summary, modulation of the cytokine environment to one high in TGF-ß in the presence of 1,25(OH)2D3(10(-7) M) significantly increased Foxp3(+) Treg cell frequency. These data provide additional evidence for the important immunomodulatory properties of 1,25(OH)2D3 that exist and may help to control inflammatory diseases.

Defective IL-10 expression and in vitro steroid-induced IL-17A in paediatric severe therapy-resistant asthma.

BACKGROUND: Understanding of immune mechanisms underpinning asthma has emerged from studies in adults. It is increasingly recognised, both immunologically and in the development of novel therapies, that adult responses cannot be used accurately to predict those of children. METHODS: Using a well-defined paediatric cohort of severe therapy-resistant asthma (STRA) patients, we investigated cytokine profiles in the airway by analysis of bronchoalveolar lavage fluid. The in vitro capacity of peripheral blood mononuclear cells (PBMCs) for cytokine production was also assessed following polyclonal T cell activation in culture, in the absence or presence of dexamethasone and 1α,25-dihydroxyvitamin D3. RESULTS: Children with both moderate and STRA had significantly diminished levels of anti-inflammatory interleukin (IL)-10 in airway lavage samples when compared with non-asthmatic controls (p<0.001). Their PBMCs also demonstrated significantly impaired capacity to secrete IL-10 in culture (p<0.001). Dexamethasone regulated the balance between PBMC IL-10 and IL-13 production, increasing IL-10 secretion (p<0.001) and decreasing IL-13 (p<0.001) but unexpectedly enhanced IL-17A production in all groups-most strikingly in the STRA cohort (p<0.001). The inclusion of the active form of vitamin D, 1α,25-dihydroxyvitamin D3, in culture enhanced dexamethasone-induced IL-10 (p<0.05) without marked effects on IL-13 or IL-17A production. Furthermore, systemic vitamin D status directly correlated with airway IL-10 (r=0.6, p<0.01). CONCLUSIONS: These findings demonstrate reduced peripheral and local IL-10 synthesis in paediatric asthma, and support therapeutic augmentation of low circulating vitamin D in severe, difficult-to-treat asthma, in order to correct impaired IL-10 levels. Conversely, steroids enhanced IL-17A levels, and therefore any steroid-sparing properties of vitamin D may have additional benefit in STRA.

Molecular dynamics simulations of classical stopping power.

Molecular dynamics can provide very accurate tests of classical kinetic theory; for example, unambiguous comparisons can be made for classical particles interacting via a repulsive 1/r potential. The plasma stopping power problem, of great interest in its own right, provides an especially stringent test of a velocity-dependent transport property. We have performed large-scale (~10(4)-10(6) particles) molecular dynamics simulations of charged-particle stopping in a classical electron gas that span the weak to moderately strong intratarget coupling regimes. Projectile-target coupling is varied with projectile charge and velocity. Comparisons are made with disparate kinetic theories (both Boltzmann and Lenard-Balescu classes) and fully convergent theories to establish regimes of validity. We extend these various stopping models to improve agreement with the MD data and provide a useful fit to our results.

Wave packet spreading and localization in electron-nuclear scattering.

The wave packet molecular dynamics (WPMD) method provides a variational approximation to the solution of the time-dependent Schrödinger equation. Its application in the field of high-temperature dense plasmas has yielded diverging electron width (spreading), which results in diminishing electron-nuclear interactions. Electron spreading has previously been ascribed to a shortcoming of the WPMD method and has been counteracted by various heuristic additions to the models used. We employ more accurate methods to determine if spreading continues to be predicted by them and how WPMD can be improved. A scattering process involving a single dynamic electron interacting with a periodic array of statically screened protons is used as a model problem for comparison. We compare the numerically exact split operator Fourier transform method, the Wigner trajectory method, and the time-dependent variational principle (TDVP). Within the framework of the TDVP, we use the standard variational form of WPMD, the single Gaussian wave packet (WP), as well as a sum of Gaussian WPs, as in the split WP method. Wave packet spreading is predicted by all methods, so it is not the source of the unphysical diminishing of electron-nuclear interactions in WPMD at high temperatures. Instead, the Gaussian WP's inability to correctly reproduce breakup of the electron's probability density into localized density near the protons is responsible for the deviation from more accurate predictions. Extensions of WPMD must include a mechanism for breakup to occur in order to yield dynamics that lead to accurate electron densities.

Towards real-time simulation of cardiac electrophysiology in a human heart at high resolution.

We have developed the capability to rapidly simulate cardiac electrophysiological phenomena in a human heart discretised at a resolution comparable with the length of a cardiac myocyte. Previous scientific investigation has generally invoked simplified geometries or coarse-resolution hearts, with simulation duration limited to 10s of heartbeats. Using state-of-the-art high-performance computing techniques coupled with one of the most powerful computers available (the 20 PFlop/s IBM BlueGene/Q at Lawrence Livermore National Laboratory), high-resolution simulation of the human heart can now be carried out over 1200 times faster compared with published results in the field. We demonstrate the utility of this capability by simulating, for the first time, the formation of transmural re-entrant waves in a 3D human heart. Such wave patterns are thought to underlie Torsades de Pointes, an arrhythmia that indicates a high risk of sudden cardiac death. Our new simulation capability has the potential to impact a multitude of applications in medicine, pharmaceuticals and implantable devices.

Enhanced production of IL-17A in patients with severe asthma is inhibited by 1α,25-dihydroxyvitamin D3 in a glucocorticoid-independent fashion.

BACKGROUND: TH17 cells are proposed to play a role in the pathology of asthma, including steroid-resistant (SR) disease. We previously identified a steroid-enhancing function of vitamin D in patients with SR asthma in restoring the impaired response to steroids for production of the anti-inflammatory cytokine IL-10. OBJECTIVE: We sought to investigate the production of the TH17-associated cytokines IL-17A and IL-22 in culture in patients with moderate-to-severe asthma defined on the basis of their clinical response to steroids and the susceptibility of this response to inhibition by steroids and the active form of vitamin D, 1α,25-dihydroxyvitamin D3 (1,25[OH]2D3). METHODS: PBMCs were stimulated in culture with or without dexamethasone and 1,25(OH)2D3. A cytometric bead array, ELISA, and intracellular cytokine staining were used to assess cytokine production. The role of CD39 in inhibition of the TH17 response was studied by using quantitative real-time PCR, flow cytometry, and addition of the antagonist POM-1 to culture. RESULTS: Asthmatic patients synthesized much higher levels of IL-17A and IL-22 than nonasthmatic control subjects, with patients with SR asthma expressing the highest levels of IL-17A. Glucocorticoids did not inhibit IL-17A cytokine expression in patients and enhanced production in cultures from control subjects. Treatment with 1,25(OH)2D3 with or without dexamethasone significantly reduced both IL-17A and IL-22 levels. An antagonist of the ectonucleotidase CD39 reversed 1,25(OH)2D3-mediated inhibition of the IL-17A response. CONCLUSION: Patients with severe asthma exhibit increased levels of TH17 cytokines, which are not inhibited by steroids. 1,25(OH)2D3 inhibits TH17 cytokine production in all patients studied, irrespective of their clinical responsiveness to steroids, identifying novel steroid-enhancing properties of vitamin D in asthmatic patients.

Molecular dynamics simulations and generalized Lenard-Balescu calculations of electron-ion temperature equilibration in plasmas.

We study the problem of electron-ion temperature equilibration in plasmas. We consider pure H at various densities and temperatures and Ar-doped H at temperatures high enough so that the Ar is fully ionized. Two theoretical approaches are used: classical molecular dynamics (MD) with statistical two-body potentials and a generalized Lenard-Balescu (GLB) theory capable of treating multicomponent weakly coupled plasmas. The GLB is used in two modes: (1) with the quantum dielectric response in the random-phase approximation (RPA) together with the pure Coulomb interaction and (2) with the classical (ℏ→0) dielectric response (both with and without local-field corrections) together with the statistical potentials. We find that the MD results are described very well by classical GLB including the statistical potentials and without local-field corrections (RPA only); worse agreement is found when static local-field effects are included, in contradiction to the classical pure-Coulomb case with like charges. The results of the various approaches are all in excellent agreement with pure-Coulomb quantum GLB when the temperature is high enough. In addition, we show that classical calculations with statistical potentials derived from the exact quantum two-body density matrix produce results in far better agreement with pure-Coulomb quantum GLB than classical calculations performed with older existing statistical potentials.

The role of 1α,25-dihydroxyvitamin D3 and cytokines in the promotion of distinct Foxp3+ and IL-10+ CD4+ T cells.

1α,25-Dihydroxyvitamin D3 (1α25VitD3) has potent immunomodulatory properties. We have previously demonstrated that 1α25VitD3 promotes human and murine IL-10-secreting CD4(+) T cells. Because of the clinical relevance of this observation, we characterized these cells further and investigated their relationship with Foxp3(+) regulatory T (Treg) cells. 1α25VitD3 increased the frequency of both Foxp3(+) and IL-10(+) CD4(+) T cells in vitro. However, Foxp3 was increased at high concentrations of 1α25VitD3 and IL-10 at more moderate levels, with little coexpression of these molecules. The Foxp3(+) and IL-10(+) T-cell populations showed comparable suppressive activity. We demonstrate that the enhancement of Foxp3 expression by 1α25VitD3 is impaired by IL-10. 1α25VitD3 enables the selective expansion of Foxp3(+) Treg cells over their Foxp3(-) T-cell counterparts. Equally, 1α25VitD3 maintains Foxp3(+) expression by sorted populations of human and murine Treg cells upon in vitro culture. A positive in vivo correlation between vitamin D status and CD4(+) Foxp3(+) T cells in the airways was observed in a severe pediatric asthma cohort, supporting the in vitro observations. In summary, we provide evidence that 1α25VitD3 enhances the frequency of both IL-10(+) and Foxp3(+) Treg cells. In a translational setting, these data suggest that 1α25VitD3, over a broad concentration range, will be effective in enhancing the frequency of Treg cells.

Self-diffusivity and interdiffusivity of molten aluminum-copper alloys under pressure, derived from molecular dynamics.

We use molecular dynamics (MD) to simulate diffusion in molten aluminum-copper (AlCu) alloys. The self-diffusivities and Maxwell-Stefan diffusivities are calculated for AlCu mixtures using the Green-Kubo formulas at temperatures from 1000 to 4000 K and pressures from 0 to 25 GPa, along with additional points at higher temperatures and pressures. The diffusivities are corrected for finite-size effects. The Maxwell-Stefan diffusivity is compared to the diffusivity calculated from the self-diffusivities using a generalization of the Darken equation. We find that the effects of cross-correlation are small. Using the calculated self-diffusivities, we have assessed whether dilute hard-sphere and dilute Lennard-Jones models apply to the molten mixture. Neither of the two dilute gas diffusivities describes the diffusivity in molten Al and Cu. We report generalized analytic models for the self-diffusivities and interdiffusivity (mutual diffusivity) that fit the MD results well. The MD-derived transport coefficients are in good agreement with the available experimental data. We also report MD calculations of the viscosity and an analytic fit to those results. The ionic thermal conductivity is discussed briefly.

1α,25-dihydroxyvitamin D3 promotes CD200 expression by human peripheral and airway-resident T cells.

BACKGROUND: CD200, a cell-surface immunoglobulin-like molecule expressed by immune and stromal cells, dampens the pro-inflammatory activity of tissue-resident innate cells via its receptor, CD200R. This interaction appears critical for peripheral immune tolerance, particularly in the airways where excessive inflammation is undesirable. Vitamin D contributes to pulmonary health and promotes regulatory immune pathways, therefore its influence on CD200 and CD200R was investigated. METHODS: CD200 and CD200R expression were assessed by qPCR and immunoreactivity of human lymphoid, myeloid and epithelial cells following 1α,25-dihydroxyvitamin D3 (1α,25VitD3) exposure in vitro and in peripheral T cells following 1α,25VitD3 oral ingestion in vivo. The effect of 1α25VitD3 was also assessed in human airway-resident cells. RESULTS: 1α25VitD3 potently upregulated CD200 on peripheral human CD4+ T cells in vitro, and in vivo there was a trend towards upregulation in healthy, but not asthmatic individuals. CD200R expression was not modulated in any cells studied. CD200 induction was observed to a lesser extent in CD8+ T cells and not in B cells or airway epithelium. T cells isolated from the human airway also responded strongly to 1α25VitD3 to upregulate CD200. CONCLUSIONS: The capacity of 1α,25-dihydroxyvitamin D3 to induce CD200 expression by peripheral and respiratory tract T cells identifies an additional pathway via which vitamin D can restrain inflammation in the airways to maintain respiratory health.

Molecular dynamics simulations of electron-ion temperature equilibration in an SF6 plasma.

We use classical molecular dynamics to investigate electron-ion temperature equilibration in a two-temperature SF6 plasma. We choose a density of 1.0 x 10;{19}SF_{6} molecules per cm;{3} and initial temperatures of T_{e} = 100 eV and T_{S} = T_{F} = 15 eV, in accordance with experiments currently underway at Los Alamos National Laboratory. Our computed relaxation time lies between two oft-used variants of the Landau-Spitzer relaxation formula which invoke static screening. Discrepancies are also found when comparing to the predictions made by more recent theoretical approaches. These differences should be large enough to be measured in the upcoming experiments.