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

https://www.seas.upenn.edu/%7Edischer/pdfs/Cell_on_Gel-CELLpaper.pdf

Matrix elasticity directs stem cell lineage specification.

/pdf/self-assembled-monolayers-of-thiolates-on-metals-as-a-form-1neb0hj3k4.pdf

Self-assembled monolayers of thiolates on metals as a form of nanotechnology.

Normal tissue cells are generally not viable when suspended in a fluid and are therefore said to be anchorage dependent. Such cells must adhere to a solid, but a solid can be as rigid as glass or softer than a baby's skin. The behavior of some cells on soft materials is characteristic of important phenotypes; for example, cell growth on soft agar gels is used to identify cancer cells. However, an understanding of how tissue cells-including fibroblasts, myocytes, neurons, and other cell types-sense matrix stiffness is just emerging with quantitative studies of cells adhering to gels (or to other cells) with which elasticity can be tuned to approximate that of tissues. Key roles in molecular pathways are played by adhesion complexes and the actinmyosin cytoskeleton, whose contractile forces are transmitted through transcellular structures. The feedback of local matrix stiffness on cell state likely has important implications for development, differentiation, disease, and regeneration.

/pdf/tissue-cells-feel-and-respond-to-the-stiffness-of-their-6dx0rumap6.pdf

Tissue Cells Feel and Respond to the Stiffness of Their Substrate

Memory disturbances generated from the neocortex in dementia impair the control of emotions generated from the limbic system. These are one class of the origin and characteristics of the behavioral and psychological symptoms of dementia (BPSD). Differentially, we commonly think of memory disturbance as a core symptom and BPSD as a peripheral symptom. But is it true? We have previously suggested that dementia with declined cognitive function shows relatively intact emotional functions using the Mini-Emotional State Examination. Dementia is defined as a state of abnormality of brain function resulting in impairment of social function and interaction. If older people gently yielded to their caregiver’s advice on activities, such as taking a bath and eating, but without showing BPSD, then this is not a case of dementia, even if cognition is somewhat blurred, perhaps when sitting quietly on the veranda. In contrast to dementia, what would happen if memory function is preserved, but emotional function is extremely impaired? Hannah Arendt argued that Adolf Eichmann, a historical criminal of World War II and a member of the Nazi party, was a person who lacked emotional function. Eichmann was captured after the war and tried as a war criminal. He insisted that he was innocent, because he was just obeying orders from his superiors when killing Jews. Arendt had anticipated that Eichmann would be close to insane after killing tens of thousands of Jews, but he was an ordinary man, except that he expressed no opinion on anything criminal in the court. Arendt argues that “absence of thinking” lies at the root of Eichmann’s crimes. Here, the sense of “thinking” is not at the level of knowledge, but rather, the ability to judge good and evil, beautiful things and ugly things. He could carry out these hideous acts almost clerically, without consciousness of any feelings of guilt. Eichmann is a historical figure, but Arendt warns that ordinary people in modern society can also become like Eichmann when they lack emotional function. Consider another example. When juice is poured into a cup in front of chimpanzees, they only look at the juice. When the same is done in front of human infants of approximately 3 years-of-age, they watch the person who is pouring the juice as well as the juice itself. These infants are thought to be wondering what motivated the person to pour the juice for them. It has been suggested that the difference between chimpanzees and humans is that humans have the ability to comprehend the emotions of the person who is kindly pouring the juice for them. It is concluded that the ability to consider the other’s kindness distinguishes humans from chimpanzees. Humans act on the basis of emotions generated from the limbic system, so the limbic system controls purpose. The neocortex is merely a tool that is used to accomplish this purpose. In this sense, the purpose would be a core symptom and the tool for the purpose would be a peripheral symptom. BPSD could potentially be relieved by taking all possible steps, and dementia would be a more treatable disease irrespective of the reduction of peripheral symptoms of cognitive dysfunction. Average Japanese older adults aged approximately 100 years show impairment of cognitive function. As cognitive decline is an unavoidable consequence of aging, like many of the systemic organs of the body, it would be difficult to treat dementia as long as medical treatment focuses solely on the cognitive decline manifested in peripheral symptoms. When the person becomes older with degraded tools, the person would have modest purposes that are suitable for the degraded tools, a balanced aging between purpose and tools. The first step, therefore, in treating dementia is to distinguish between core symptoms and peripheral symptoms, and to appreciate the importance of the limbic system in contrast to simply cognition.

Core symptoms and peripheral symptoms of dementia.

Figure 2, "Accuracy of in-plane tractions as a function of Poisson's ratio when out-of-plane components of displacements are neglected" is incorrect. The correct file can be found here: 





The color bar in Figure 4, "Balance of forces considered in MSM" is incorrectly displayed to range from 0 to 15Pa. Correct range is 0 to 150Pa. The correct version of Figure 4 can be found here:

Correction: Monolayer Stress Microscopy: Limitations, Artifacts, and Accuracy of Recovered Intercellular Stresses

Forces, Flows, Fluorescence, and μFluidics

For migration of the single cell studied in isolation, loss of function of the tumor suppressor p53 is thought to increase cell motility. Here by contrast we used the 2-D confluent cell layer and the 3-D multicellular spheroid to investigate how p53 impacts dissemination and invasion of cellular collectives. We used two human carcinoma cell lines, the bladder carcinoma EJ and the colorectal carcinoma HCT116. We began by replicating single cell invasion in the traditional Boyden chamber assay, and found that the number of invading cells increased with loss of p53, as expected. In the confluent 2-D cell layer, however, for both EJ and HCT, speeds and effective diffusion coefficients for the p53 null types compared to their p53 expressing counterparts were significantly smaller. Compared to p53 expressers, p53 null cells exhibited more organized cortical actin rings together with reduced front-rear cell polarity. Furthermore, loss of p53 caused cells to exert smaller traction forces upon their substrates, and reduced formation of cryptic lamellipodia. In a 3-D collagen matrix, p53 consistently promoted invasion of the multicellular spheroids into surrounding matrix. Together, these results show that p53 expression in these carcinoma model systems increases collective cellular migration and invasion. As such, these studies point to paradoxical contributions of p53 in single cell versus collective cellular migration.

https://www.biorxiv.org/content/biorxiv/early/2018/07/30/380600.full.pdf

The tumor suppressor p53 promotes carcinoma invasion and collective cellular migration

/pdf/on-the-relationship-between-velocities-tractions-and-27bn7hr49a.pdf

James P. Butler

Papers

Core symptoms and peripheral symptoms of dementia.

Correction: Monolayer Stress Microscopy: Limitations, Artifacts, and Accuracy of Recovered Intercellular Stresses

Forces, Flows, Fluorescence, and μFluidics

The tumor suppressor p53 promotes carcinoma invasion and collective cellular migration

On the relationship between velocities, tractions, and intercellular stresses in the migrating epithelial monolayer