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The emergence of multi-principal element alloys (MPEAs) holds great promise for the development of high performance metallic materials. However, it remains unclear whether MPEAs can provide previously unknown deformation mechanisms to drastically enhance their mechanical performance. Here we report a new deformation mechanism of mechanically-induced dual phase transformations from the face-centered cubic (FCC) to hexagonal close- packed (HCP) phase and then back to the FCC phase with nanotwins in a CrCoNi medium-entropy alloy (MEA). During the two sequential steps of phase transformation, continued shear occurs in the same < 110 >(FCC) parallel to < 11 (2) over bar0 >(HCP) direction along different {111}(FCC) parallel to (0001)(HCP) planes, producing a total shear transformation strain up to 70%. The dual phase transformations stem from a unique capability of facile slip in between the close-packed {111}(FCC) parallel to (0001)(HCP) atomic layers in both FCC and HCP phases, leading to flexible stacking sequences of those close-packed layers with low stacking fault energies. Our work demonstrates that MPEAs can offer unconventional deformation mechanisms such as dual phase transformations in the CrCoNi MEA, thereby opening opportunities for enhancing the mechanical properties of advanced alloys., QC 20210831

© 2020, Science China Press and Springer-Verlag GmbH Germany, part of Springer Nature. The mechanical size effect of nanostructured, dual-phase CrCoNi medium-entropy alloy (MEA) was investigated by combining in-situ micro-compression testing with post-mortem electron microscopy analysis. The alloy possesses a superior yield strength up to ∼4 GPa, primarily due to its hierarchical microstructure including column nanograins, preferred orientation, a high density of planar defects and the presence of the hexagonal close packed (HCP) phase. While the yield strength of the alloy has shown size-independency, the deformation behaviour was strongly dependent on the sample size. Specifically, with decreasing the pillar diameters, the dominant deformation mode changed from highly localized and catastrophic shear banding to apparently homogeneous deformation with appreciable plasticity. This transition is believed to be governed by the size-dependent critical stress required for a shear band traversing the pillar and mediated by the competition between shear-induced softening and subsequent hardening mechanisms. In addition, an unexpected phase transformation from HCP to face-centered cubic (FCC) was observed in the highly localized deformation zones, leading to strain softening that contributed to accommodating plasticity. These findings provide insights into the criticality of sample dimensions in influencing mechanical behaviors of nanostructured metallic materials used for nanoelectromechanical systems.

FeMnCoCrC high entropy alloy coatings were deposited onto high speed steel substrates using magnetron sputtering under a range of substrate bias voltages. These coatings exhibited a novel α-Mn crystal structure and highly refined columnar grains. Higher bias voltages promoted strong texture development through favouring (332)-oriented grains along the coating growth direction, as well as the formation of well-defined twin boundaries. The -80 V coating possessed a high hardness (~12.5 GPa), more than triple that of its fcc-structured bulk counterpart. This is attributed to the cumulative effects of the α-Mn structure, strong texture, grain refinement and the presence of twin boundaries.

CeO2-x coatings were deposited under variable oxygen flow ratios (%fO2) onto Si substrates by reactive magnetron sputtering. Nanoindentation testing revealed an increase in the hardness, elastic modulus, H/E and H3/E2 ratio with increasing oxygen flow ratio, which in turn increased the adhesion and tribological performance of the coatings. Scratch testing yielded the highest critical load (LC2 = 28.8 N) and CPRS = 103 for the coating deposited with the highest oxygen flow ratio (57 %fO2). Cracking events during scratch testing were initiated by tensile forces behind the scratch stylus, which led to the formation of semi-circular ring cracks. As the normal load increased, transverse cracks emerged extending outwards from the scratch track towards the edge causing the exposure of substrate. Beyond LC2, severe spallation of the CeO2-x coatings led to coating failure. Furthermore, the specific wear rates of the CeO2-x coatings were determined to be within the ~10−15 m3/Nm range influenced by three-body abrasive wear. In-depth analyses from scratch and wear data indicates that these coatings possess good adhesion and durability.

© 2020, Science China Press and Springer-Verlag GmbH Germany, part of Springer Nature. The mechanical size effect of nanostructured, dual-phase CrCoNi medium-entropy alloy (MEA) was investigated by combining in-situ micro-compression testing with post-mortem electron microscopy analysis. The alloy possesses a superior yield strength up to ∼4 GPa, primarily due to its hierarchical microstructure including column nanograins, preferred orientation, a high density of planar defects and the presence of the hexagonal close packed (HCP) phase. While the yield strength of the alloy has shown size-independency, the deformation behaviour was strongly dependent on the sample size. Specifically, with decreasing the pillar diameters, the dominant deformation mode changed from highly localized and catastrophic shear banding to apparently homogeneous deformation with appreciable plasticity. This transition is believed to be governed by the size-dependent critical stress required for a shear band traversing the pillar and mediated by the competition between shear-induced softening and subsequent hardening mechanisms. In addition, an unexpected phase transformation from HCP to face-centered cubic (FCC) was observed in the highly localized deformation zones, leading to strain softening that contributed to accommodating plasticity. These findings provide insights into the criticality of sample dimensions in influencing mechanical behaviors of nanostructured metallic materials used for nanoelectromechanical systems.

CeO2-x coatings were deposited under variable oxygen flow ratios (%fO2) onto Si substrates by reactive magnetron sputtering. Nanoindentation testing revealed an increase in the hardness, elastic modulus, H/E and H3/E2 ratio with increasing oxygen flow ratio, which in turn increased the adhesion and tribological performance of the coatings. Scratch testing yielded the highest critical load (LC2 = 28.8 N) and CPRS = 103 for the coating deposited with the highest oxygen flow ratio (57 %fO2). Cracking events during scratch testing were initiated by tensile forces behind the scratch stylus, which led to the formation of semi-circular ring cracks. As the normal load increased, transverse cracks emerged extending outwards from the scratch track towards the edge causing the exposure of substrate. Beyond LC2, severe spallation of the CeO2-x coatings led to coating failure. Furthermore, the specific wear rates of the CeO2-x coatings were determined to be within the ~10−15 m3/Nm range influenced by three-body abrasive wear. In-depth analyses from scratch and wear data indicates that these coatings possess good adhesion and durability.

Adaptations to stress can occur through epigenetic processes and may be a conduit for informing offspring of environmental challenge. We employed ChIP-sequencing for H3K4me3 to examine effects of early maternal deprivation (peer-rearing, PR) in archived rhesus macaque hippocampal samples (male, n = 13). Focusing on genes with roles in stress response and behavior, we assessed the effects of rearing on H3K4me3 binding by ANOVA. We found decreased H3K4me3 binding at genes critical to behavioral stress response, the most robust being the oxytocin receptor gene OXTR, for which we observed a corresponding decrease in RNA expression. Based on this finding, we performed behavioral analyses to deter mine whether a gain-of-function nonsynonymous OXTR SNP inter acted with early stress to influence relevant behavioral stress reactivity phenotypes (n = 194), revealing that this SNP partially rescued the PR phenotype. PR infants exhibited higher levels of separation anxiety and arousal in response to social separation, but infants carrying the alternative OXTR allele did not exhibit as great a separation response. These data indicate that the oxytocin system is involved in social-separation response and suggest that epigenetic down-modulation of OXTR could contribute to behavior al differences observed in PR animals. Epigenetic changes at OXTR may represent predictive adaptive responses that could impart readiness to respond to environmental challenge or maintain proximity to a caregiver but also contribute to behavioral pathology. Our data also demonstrate that OXTR polymorphism can permit animals to partially overcome the detrimental effects of early maternal deprivation, which could have translational implications for human psychiatric disorders., Funding Agencies|Intramural Research Program of the National Institute on Alcohol Abuse and Alcoholism, NIH

Recent studies have suggested an association between alcoholism and DNA methylation, a mechanism that can mediate long-lasting changes in gene transcription. Here, we examined the contribution of DNA methylation to the long-term behavioral and molecular changes induced by a history of alcohol dependence. In search of mechanisms underlying persistent rather than acute dependence-induced neuroadaptations, we studied the role of DNA methylation regulating medial prefrontal cortex (mPFC) gene expression and alcohol-related behaviors in rats 3 weeks into abstinence following alcohol dependence. Postdependent rats showed escalated alcohol intake, which was associated with increased DNA methylation as well as decreased expression of genes encoding synaptic proteins involved in neurotransmitter release in the mPFC. Infusion of the DNA methyltransferase inhibitor RG108 prevented both escalation of alcohol consumption and dependence-induced downregulation of 4 of the 7 transcripts modified in postdependent rats. Specifically, RG108 treatment directly reversed both downregulation of synaptotagmin 2 (Syt2) gene expression and hypermethylation on CpG#5 of its first exon. Lentiviral inhibition of Syt2 expression in the mPFC increased aversion-resistant alcohol drinking, supporting a mechanistic role of Syt2 in compulsive-like behavior. Our findings identified a functional role of DNA methylation in alcohol dependence-like behavioral phenotypes and a candidate gene network that may mediate its effects. Together, these data provide novel evidence for DNA methyltransferases as potential therapeutic targets in alcoholism.

Recent studies have suggested an association between alcoholism and DNA methylation, a mechanism that can mediate long-lasting changes in gene transcription. Here, we examined the contribution of DNA methylation to the long-term behavioral and molecular changes induced by a history of alcohol dependence. In search of mechanisms underlying persistent rather than acute dependence-induced neuroadaptations, we studied the role of DNA methylation regulating medial prefrontal cortex (mPFC) gene expression and alcohol-related behaviors in rats 3 weeks into abstinence following alcohol dependence. Postdependent rats showed escalated alcohol intake, which was associated with increased DNA methylation as well as decreased expression of genes encoding synaptic proteins involved in neurotransmitter release in the mPFC. Infusion of the DNA methyltransferase inhibitor RG108 prevented both escalation of alcohol consumption and dependence-induced downregulation of 4 of the 7 transcripts modified in postdependent rats. Specifically, RG108 treatment directly reversed both downregulation of synaptotagmin 2 (Syt2) gene expression and hypermethylation on CpG#5 of its first exon. Lentiviral inhibition of Syt2 expression in the mPFC increased aversion-resistant alcohol drinking, supporting a mechanistic role of Syt2 in compulsive-like behavior. Our findings identified a functional role of DNA methylation in alcohol dependence-like behavioral phenotypes and a candidate gene network that may mediate its effects. Together, these data provide novel evidence for DNA methyltransferases as potential therapeutic targets in alcoholism.

Recent studies have suggested an association between alcoholism and DNA methylation, a mechanism that can mediate long-lasting changes in gene transcription. Here, we examined the contribution of DNA methylation to the long-term behavioral and molecular changes induced by a history of alcohol dependence. In search of mechanisms underlying persistent rather than acute dependence-induced neuroadaptations, we studied the role of DNA methylation regulating medial prefrontal cortex (mPFC) gene expression and alcohol-related behaviors in rats 3 weeks into abstinence following alcohol dependence. Postdependent rats showed escalated alcohol intake, which was associated with increased DNA methylation as well as decreased expression of genes encoding synaptic proteins involved in neurotransmitter release in the mPFC. Infusion of the DNA methyltransferase inhibitor RG108 prevented both escalation of alcohol consumption and dependence-induced downregulation of 4 of the 7 transcripts modified in postdependent rats. Specifically, RG108 treatment directly reversed both downregulation of synaptotagmin 2 (Syt2) gene expression and hypermethylation on CpG#5 of its first exon. Lentiviral inhibition of Syt2 expression in the mPFC increased aversion-resistant alcohol drinking, supporting a mechanistic role of Syt2 in compulsive-like behavior. Our findings identified a functional role of DNA methylation in alcohol dependence-like behavioral phenotypes and a candidate gene network that may mediate its effects. Together, these data provide novel evidence for DNA methyltransferases as potential therapeutic targets in alcoholism.

Recent studies have suggested an association between alcoholism and DNA methylation, a mechanism that can mediate long-lasting changes in gene transcription. Here, we examined the contribution of DNA methylation to the long-term behavioral and molecular changes induced by a history of alcohol dependence. In search of mechanisms underlying persistent rather than acute dependence-induced neuroadaptations, we studied the role of DNA methylation regulating medial prefrontal cortex (mPFC) gene expression and alcohol-related behaviors in rats 3 weeks into abstinence following alcohol dependence. Postdependent rats showed escalated alcohol intake, which was associated with increased DNA methylation as well as decreased expression of genes encoding synaptic proteins involved in neurotransmitter release in the mPFC. Infusion of the DNA methyltransferase inhibitor RG108 prevented both escalation of alcohol consumption and dependence-induced downregulation of 4 of the 7 transcripts modified in postdependent rats. Specifically, RG108 treatment directly reversed both downregulation of synaptotagmin 2 (Syt2) gene expression and hypermethylation on CpG#5 of its first exon. Lentiviral inhibition of Syt2 expression in the mPFC increased aversion-resistant alcohol drinking, supporting a mechanistic role of Syt2 in compulsive-like behavior. Our findings identified a functional role of DNA methylation in alcohol dependence-like behavioral phenotypes and a candidate gene network that may mediate its effects. Together, these data provide novel evidence for DNA methyltransferases as potential therapeutic targets in alcoholism.

Recent studies have suggested an association between alcoholism and DNA methylation, a mechanism that can mediate long-lasting changes in gene transcription. Here, we examined the contribution of DNA methylation to the long-term behavioral and molecular changes induced by a history of alcohol dependence. In search of mechanisms underlying persistent rather than acute dependence-induced neuroadaptations, we studied the role of DNA methylation regulating medial prefrontal cortex (mPFC) gene expression and alcohol-related behaviors in rats 3 weeks into abstinence following alcohol dependence. Postdependent rats showed escalated alcohol intake, which was associated with increased DNA methylation as well as decreased expression of genes encoding synaptic proteins involved in neurotransmitter release in the mPFC. Infusion of the DNA methyltransferase inhibitor RG108 prevented both escalation of alcohol consumption and dependence-induced downregulation of 4 of the 7 transcripts modified in postdependent rats. Specifically, RG108 treatment directly reversed both downregulation of synaptotagmin 2 (Syt2) gene expression and hypermethylation on CpG#5 of its first exon. Lentiviral inhibition of Syt2 expression in the mPFC increased aversion-resistant alcohol drinking, supporting a mechanistic role of Syt2 in compulsive-like behavior. Our findings identified a functional role of DNA methylation in alcohol dependence-like behavioral phenotypes and a candidate gene network that may mediate its effects. Together, these data provide novel evidence for DNA methyltransferases as potential therapeutic targets in alcoholism.

Impulsivity, describing action without foresight, is an important feature of several psychiatric diseases, suicidality and violent behaviour. The complex origins of impulsivity hinder identification of the genes influencing it and the diseases with which it is associated. Here we perform exon-focused sequencing of impulsive individuals in a founder population, targeting fourteen genes belonging to the serotonin and dopamine domain. A stop codon in HTR2B was identified that is common (minor allele frequency > 1%) but exclusive to Finnish people. Expression of the gene in the human brain was assessed, as well as the molecular functionality of the stop codon, which was associated with psychiatric diseases marked by impulsivity in both population and family-based analyses. Knockout of Htr2b increased impulsive behaviours in mice, indicative of predictive validity. Our study shows the potential for identifying and tracing effects of rare alleles in complex behavioural phenotypes using founder populations, and indicates a role for HTR2B in impulsivity.

Three different functionally graded amorphous carbon (a-C) thin films were deposited on to aluminium substrates using a closed-field unbalanced magnetron sputtering ion plating method. The closed-field configuration prohibits the loss of secondary electrons and consequently enhances the plasma density significantly. The functional gradient of the a-C films was achieved by varying the bias voltage linearly during deposition. Three graded a-C systems possessing different variations in Young's modulus were deposited with the highest Young's modulus at the (i) top surface, (ii) interface or (iii) middle of the film. Of the three systems investigated, the one with the highest Young's modulus at the middle of the film thickness was found to exhibit significantly lower levels of cracking at higher indentation depths. Finite element models that included an embedded ring crack controlled by cohesive zone elements were developed to clarify the effect of ring cracks on the deformation of the films. This study provides guidance for the design of functionally graded coatings against contact damage.

Three different functionally graded amorphous carbon (a-C) thin films were deposited on to aluminium substrates using a closed-field unbalanced magnetron sputtering ion plating method. The closed-field configuration prohibits the loss of secondary electrons and consequently enhances the plasma density significantly. The functional gradient of the a-C films was achieved by varying the bias voltage linearly during deposition. Three graded a-C systems possessing different variations in Young's modulus were deposited with the highest Young's modulus at the (i) top surface, (ii) interface or (iii) middle of the film. Of the three systems investigated, the one with the highest Young's modulus at the middle of the film thickness was found to exhibit significantly lower levels of cracking at higher indentation depths. Finite element models that included an embedded ring crack controlled by cohesive zone elements were developed to clarify the effect of ring cracks on the deformation of the films. This study provides guidance for the design of functionally graded coatings against contact damage.

SCOPUS: le.j, info:eu-repo/semantics/published

SCOPUS: le.j, info:eu-repo/semantics/published

Akhter, R., Zhou, Z., Xie, Z., & Munroe, P. (2021). Enhancing the adhesion strength and wear resistance of nanostructured NiCrN coatings. Applied Surface Science, 541, article 148533. https://doi.org/10.1016/j.apsusc.2020.148533

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Developmental nicotine exposure causes persistent changes in cortical neuron morphology and in behavior. We used microarray screening to identify master transcriptional or epigenetic regulators mediating these effects of nicotine and discovered increases in Ash2lmRNA, encoding a component of a histone methyltransferase complex. We therefore examined genome-wide changes in trimethylation of histone H3 on Lys4 (H3K4me3), a mark induced by the Ash2l complex associated with increased gene transcription. A large proportion of regulated promoter sites were involved in synapse maintenance. We found that Mef2c interacts with Ash2l and mediates changes in H3K4me3. Knockdown of Ash2l or Mef2c abolished nicotine-mediated alterations of dendritic complexity in vitro and in vivo, and attenuated nicotine-dependent changes in passive avoidance behavior. In contrast, overexpression mimicked nicotine-mediated alterations of neuronal structure and passive avoidance behavior. These studies identify Ash2l as a target induced by nicotinic stimulation that couples developmental nicotine exposure to changes in brain epigenetic marks, neuronal structure and behavior.

Developmental nicotine exposure causes persistent changes in cortical neuron morphology and in behavior. We used microarray screening to identify master transcriptional or epigenetic regulators mediating these effects of nicotine and discovered increases in Ash2lmRNA, encoding a component of a histone methyltransferase complex. We therefore examined genome-wide changes in trimethylation of histone H3 on Lys4 (H3K4me3), a mark induced by the Ash2l complex associated with increased gene transcription. A large proportion of regulated promoter sites were involved in synapse maintenance. We found that Mef2c interacts with Ash2l and mediates changes in H3K4me3. Knockdown of Ash2l or Mef2c abolished nicotine-mediated alterations of dendritic complexity in vitro and in vivo, and attenuated nicotine-dependent changes in passive avoidance behavior. In contrast, overexpression mimicked nicotine-mediated alterations of neuronal structure and passive avoidance behavior. These studies identify Ash2l as a target induced by nicotinic stimulation that couples developmental nicotine exposure to changes in brain epigenetic marks, neuronal structure and behavior.