Three parallel algorithms for classical molecular dynamics are presented. The first assigns each processor a fixed subset of atoms; the second assigns each a fixed subset of inter-atomic forces to compute; the third assigns each a fixed spatial region. The algorithms are suitable for molecular dynamics models which can be difficult to parallelize efficiently—those with short-range forces where the neighbors of each atom change rapidly. They can be implemented on any distributed-memory parallel machine which allows for message-passing of data between independently executing processors. The algorithms are tested on a standard Lennard-Jones benchmark problem for system sizes ranging from 500 to 100,000,000 atoms on several parallel supercomputers--the nCUBE 2, Intel iPSC/860 and Paragon, and Cray T3D. Comparing the results to the fastest reported vectorized Cray Y-MP and C90 algorithm shows that the current generation of parallel machines is competitive with conventional vector supercomputers even for small problems. For large problems, the spatial algorithm achieves parallel efficiencies of 90% and a 1840-node Intel Paragon performs up to 165 faster than a single Cray C9O processor. Trade-offs between the three algorithms and guidelines for adapting them to more complex molecular dynamics simulations are also discussed.

Fast parallel algorithms for short-range molecular dynamics

抗原变异可使得多种致病微生物易于逃避宿主免疫应答。表达在感染红细胞表面的恶性疟原虫红细胞表面蛋白1（PfPMP1）与感染红细胞、内皮细胞、树突状细胞以及胎盘的单个或多个受体作用，在黏附及免疫逃避中起关键的作用。每个单倍体基因组var基因家族编码约60种成员，通过启动转录不同的var基因变异体为抗原变异提供了分子基础。

疟原虫var基因转换速率变化导致抗原变异[英]／Paul H, Robert P, Christodoulou Z, et al//Proc Natl Acad Sci U S A

Foreign body reaction to biomaterials.

The organization of behavior: A neuropsychological theory

中枢神経系疾患の治療は正常細胞（ニューロン）の機能維持を目的とするが，脳血管障害のように機能障害の原因が細胞の死滅に基づくことは多い．一方，脳腫瘍の治療においては薬物療法や放射線療法といった腫瘍細胞の死滅を目標とするものが大きな位置を占める．いずれの場合にも，細胞死の機序を理解することは各種病態や治療法の理解のうえで重要である．現在のところ最も研究の進んでいる細胞死の型はアポトーシスである．そのなかで重要な位置を占めるミトコンドリアにおける反応および抗アポトーシス因子について概要を紹介する．

Neuroscience 細胞死：最近の知見

Biocompatibility of methylcellulose-based constructs designed for intracerebral gelation following experimental traumatic brain injury.

High rate shear strain of three-dimensional neural cell cultures: a new in vitro traumatic brain injury model.

The mechanism by which mechanical impact to brain tissue is transduced to neuronal impairment remains poorly understood. Using an in vitro model of neuronal stretch, we found that mechanical stretc...

Mechanical stretch to neurons results in a strain rate and magnitude-dependent increase in plasma membrane permeability.

Traumatic injury to the central nervous system (CNS) triggers cell death and deafferentation, which may activate a cascade of cellular and network disturbances. These events often result in the formation of irregularly shaped lesions comprised of necrotic tissue and/or a fluid-filled cavity. Tissue engineering represents a promising treatment strategy for the injured neural tissue. To facilitate minimally invasive delivery of a tissue engineered system, a thermoreversible polymer is an attractive scaffold candidate. We have developed a bioactive scaffold for neural tissue engineering by tethering laminin-1 (LN) to methylcellulose (MC), a thermoresponsive hydrogel. The base MC chain was oxidized via sodium m-periodate to increase MC tethering capacity. Protein immobilization was facilitated by a Schiff base reaction between primary amine groups on LN and the carbonyl groups of the oxidized MC chain. Immunoassays demonstrated tethering of LN at 1.6 +/- 0.5 ng of LN per milligram of MC. Rheological measurements for different MC-LN constructs indicated MC composition- and MC treatment-dependent effects on solution-gelation transition temperature. Cellular assays with primary rat cortical neurons demonstrated enhanced cell adhesion and viability on LN-functionalized MC when compared with base and oxidized MC. This bioadhesive thermoresponsive scaffold may provide a robust delivery vehicle to injured CNS tissue for neural cell transplantation strategies.

Thermoreversible laminin-functionalized hydrogel for neural tissue engineering.

Traumatic brain injury (TBI) and traumatic spinal cord injury (SCI) are acquired when an external physical insult causes damage to the central nervous system (CNS). Functional disabilities resulting from CNS trauma are dependent upon the mode, severity, and anatomical location of the mechanical impact as well as the mechanical properties of the tissue. Although the biomechanical insult is the initiating factor in the pathophysiology of CNS trauma, the anatomical loading distribution and the resulting cellular responses are currently not well understood. For example, the primary response phase includes events such as increased membrane permeability to ions and other molecules, which may initiate complex signaling cascades that account for the prolonged damage and dysfunction. Correlation of insult parameters with cellular changes and subsequent deficits may lead to refined tolerance criteria and facilitate the development of improved protective gear. In addition, advancements in the understanding of injury biomechanics are essential for the development and interpretation of experimental studies at both the in vitro and in vivo levels and may lead to the development of new treatment approaches by determining injury mechanisms across the temporal spectrum of the injury response. Here we discuss basic concepts relevant to the biomechanics of CNS trauma, injury models used to experimentally simulate TBI and SCI, and novel multilevel approaches for improving the current understanding of primary damage mechanisms.

Michelle C. LaPlaca

Papers

Biocompatibility of methylcellulose-based constructs designed for intracerebral gelation following experimental traumatic brain injury.

High rate shear strain of three-dimensional neural cell cultures: a new in vitro traumatic brain injury model.

Mechanical stretch to neurons results in a strain rate and magnitude-dependent increase in plasma membrane permeability.

Thermoreversible laminin-functionalized hydrogel for neural tissue engineering.

CNS injury biomechanics and experimental models.