The Orowan Stress Measurement of Twinning Dislocations in Magnesium

The interaction between a lattice dislocation and non-shearable precipitates has been well explained by the Orowan bypass mechanism. The calculated additional shear stress facilitates the evaluation of precipitation hardening in metallic alloys. The lack of information about how a twinning dislocation behaves in the same scenario hinders our understanding of the strengthening against twin-mediated plasticity in magnesium alloys. In the current study, the bowing and bypassing of a twining dislocation impeded by impenetrable obstacles are captured by atomistic simulations. The Orowan stress measurement is realized by revealing the stick-slip dynamics of a twinning dislocation. The measured Orowan stress significantly deviate from what classic theory predicts. This deviation implies that the line tension approximation may generally overestimate the Orowan stress for twinning dislocations.

Analytic study on chiral phase transition in holographic QCD

The chiral symmetry breaking (χsb) is one of the most fundamental problems in QCD. In this paper, we calculate quark condensation analytically in a holographic QCD model dual to the Einstein-Maxwell-Dilaton (EMD) system coupled to a probe scalar field. We find that the black hole phase transition in the EMD system seriously affects χsb. At small chemical potential, χsb behaves as a crossover. For large chemical potential μ > μc, χsb becomes first order with exactly the same transition temperature as the black hole phase transition by a bypass mechanism. The phase diagram we obtained is qualitatively consistent with the recent results from lattice QCD simulations and NJL models.

The HLTF–PARP1 interaction in the progression and stability of damaged replication forks caused by methyl methanesulfonate

Human HLTF participates in the lesion-bypass mechanism through the fork reversal structure, known as template switching of post-replication repair. However, the mechanism by which HLTF promotes the replication progression and fork stability of damaged forks remains unclear. Here, we identify a novel protein–protein interaction between HLTF and PARP1. The depletion of HLTF and PARP1 increases chromosome breaks, further reduces the length of replication tracks, and concomitantly increases the number of stalled forks after methyl methanesulfonate treatment according to a DNA fiber analysis. The progression of replication also depends on BARD1 in the presence of MMS treatment. By combining 5-ethynyl-2′-deoxyuridine with a proximity ligation assay, we revealed that the HLTF, PARP1, and BRCA1/BARD1/RAD51 proteins were initially recruited to damaged forks. However, prolonged stalling of damaged forks results in fork collapse. HLTF and PCNA dissociate from the collapsed forks, with increased accumulation of PARP1 and BRCA1/BARD1/RAD51 at the collapsed forks. Our results reveal that HLTF together with PARP1 and BARD1 participates in the stabilization of damaged forks, and the PARP1–BARD1 interaction is further involved in the repair of collapse forks.

A Novel Precipitate-Type Architected Metamaterial Strengthened via Orowan Bypass-Like Mechanism

The objective of the study is to investigate the strengthening mechanism of embedded meta-precipitates in the design of architected metamaterials. Four precipitate-type architected metamaterials are designed and prepared by fused deposition modelling (FDM). The difference of mechanical properties and deformation mode of these structures is analyzed. The strengthening effect of the introduced meta-precipitates is then compared with Orowan bypass strengthening mechanism. The similarities and discrepancies of metallurgical hardening principles and that found in architected metamaterials are established. It is found that due to the introduction of embedded meta-precipitates, the deformation of the structure changes significantly from diagonal crushing to a meander route, thus improves the mechanical properties and energy absorption abilities. The hindering effect and the influence of volume fraction of meta-precipitates is similar to Orowan bypass mechanism.

DNA polymerases in the risk and prognosis of colorectal and pancreatic cancers

Human cancers arise from the alteration of genes involved in important pathways that mainly affect cell growth and proliferation. DNA replication and DNA damages recognition and repair are among these pathways and DNA polymerases that take part in these processes are frequently involved in cancer onset and progression. For example, damaging alterations within the proofreading domain of replicative polymerases, often reported in patients affected by colorectal cancer (CRC), are considered risk factors and drivers of carcinogenesis as they can lead to the accumulation of several mutations throughout the genome. Thus, replicative polymerases can be involved in cancer when losses of their physiological functions occur. On the contrary, reparative polymerases are often involved in cancer precisely because of their physiological role. In fact, their ability to repair and bypass DNA damages, which confers genome stability, can also counteract the effect of most anticancer drugs. In addition, the altered expression can characterise some type of cancers, which exacerbates this aspect. For example, all of the DNA polymerases involved a damage bypass mechanism, known as translesion synthesis, with the only exception of polymerase theta, are downregulated in CRC. Conversely, in pancreatic ductal adenocarcinoma (PDAC), most of these polymerase result upregulated. This suggests that different types of cancer can rely on different reparative polymerases to acquire drug resistance. Here we will examine all of the aspects that link DNA polymerases with CRC and PDAC.