Forces between elongated particles in a nematic colloid

Using molecular dynamics simulations we study the interactions between elongated colloidal particles (length to breath ratio ≫1) in a nematic host. The simulation results are compared to the results of a Landau–de Gennes elastic free energy. We find that depletion forces dominate for the sizes of the colloidal particles studied. The tangential component of the force, however, allows us to resolve the elastic contribution to the total interaction. We find that this contribution differs from the quadrupolar interaction predicted at large separations. The difference is due to the presence of nonlinear effects, namely, the change in the positions and structure of the defects and their annihilation at small separations

Defect structures and torque on an elongated colloidal particle immersed in a liquid crystal host

Combining molecular dynamics and Monte Carlo simulation we study defect structures around an elongated colloidal particle embedded in a nematic liquid crystal host. By studying nematic ordering near the particle and the disclination core region we are able to examine the defect core structure and the difference between two simulation techniques. In addition, we also study the torque on a particle tilted with respect to the director, and modification of this torque when the particle is close to the cell wall

Defect structures in nematic liquid crystals around charged particles

We numerically study the orientation deformations in nematic liquid crystals around charged particles. We set up a Ginzburg-Landau theory with inhomogeneous electric field. If the dielectric anisotropy varepsilon_1 is positive, Saturn ring defects are formed around the particles. For varepsilon_1<0, novel "ansa" defects appear, which are disclination lines with their ends on the particle surface. We find unique defect structures around two charged particles. To lower the free energy, oppositely charged particle pairs tend to be aligned in the parallel direction for varepsilon_1>0 and in the perpendicular plane for varepsilon_1<0 with respect to the background director . For identically charged pairs the preferred directions for varepsilon_1>0 and varepsilon_1<0 are exchanged. We also examie competition between the charge-induced anchoring and the short-range anchoring. If the short-range anchoring is sufficiently strong, it can be effective in the vicinity of the surface, while the director orientation is governed by the long-range electrostatic interaction far from the surface.Comment: 10 papes, 12 figures, to appear in European Physical Journal

History of clinical transplantation

How transplantation came to be a clinical discipline can be pieced together by perusing two volumes of reminiscences collected by Paul I. Terasaki in 1991-1992 from many of the persons who were directly involved. One volume was devoted to the discovery of the major histocompatibility complex (MHC), with particular reference to the human leukocyte antigens (HLAs) that are widely used today for tissue matching.1 The other focused on milestones in the development of clinical transplantation.2 All the contributions described in both volumes can be traced back in one way or other to the demonstration in the mid-1940s by Peter Brian Medawar that the rejection of allografts is an immunological phenomenon.3,4 © 2008 Springer New York

Infection and Killing of Multiple Myeloma by Adenoviruses

Oncolytic virotherapy makes use of the natural ability of viruses to infect and kill cancer cells. Adenovirus serotype 5 (Ad5) has been approved for use in humans as a therapy for solid cancers. In this study, we have tested whether Ad5 and low-seroprevalence adenoviruses can be used as oncolytics for multiple myeloma (MM). We show that Ad5 productively infects most myeloma cell lines, replicates to various degrees, and mediates oncolytic cell killing in vitro and in vivo. Comparison of Ad5 with low-seroprevalence Ads on primary marrow samples from MM patients revealed striking differences in the abilities of different adenoviral serotypes to kill normal CD138– cells and CD138+ MM cells. Ad5 and Ad6 from species C and Ad26 and Ad48 from species D all mediated killing of CD138+ cells with low-level killing of CD138– cells. In contrast, Ad11, Ad35, Ad40, and Ad41 mediated weak oncolytic effects in all of the cells. Comparison of cell binding, cell entry, and replication revealed that Ad11 and Ad35 bound MM cells 10 to 100 times better than other serotypes. However, after this efficient interaction, Ad11 and Ad35 viral DNA was not replicated and cell killing did not occur. In contrast, Ad5, Ad6, Ad26, and Ad48 all replicated 10- to 100-fold in MM cells and this correlated with cell killing. These data suggest that Ad5 and other low-seroprevalence adenoviruses may have utility as oncolytic agents against MM and other hematologic malignancies