73 research outputs found
Magnetic properties and giant magnetoresistance in melt-spun CoCu alloys
Magnetic, structural, and transport properties of as quenched and annealed Co10Cu90 samples have been investigated using x¿ray diffraction and a SQUID magnetometer. The largest value of MR change was observed for the as¿quenched sample annealed at 450°C for 30 min. The magnetic and transport properties closely correlate with the microstructure, mainly with Co magnetic particle size and its distribution. For thermal annealing the as quenched samples below 600°C, the Co particle diameters increase from 4.0 to 6.0 nm with a magnetoresistance (MR) drop from 33.0% to 5.0% at 10 K. Comparison with the theory indicates that the interfacial electron spin¿dependent scattering mechanism correlates with GMR for Co particle diameters up to about 6.0 nm
Reconstructive Neuron Pruning for Backdoor Defense
Deep neural networks (DNNs) have been found to be vulnerable to backdoor
attacks, raising security concerns about their deployment in mission-critical
applications. While existing defense methods have demonstrated promising
results, it is still not clear how to effectively remove backdoor-associated
neurons in backdoored DNNs. In this paper, we propose a novel defense called
\emph{Reconstructive Neuron Pruning} (RNP) to expose and prune backdoor neurons
via an unlearning and then recovering process. Specifically, RNP first unlearns
the neurons by maximizing the model's error on a small subset of clean samples
and then recovers the neurons by minimizing the model's error on the same data.
In RNP, unlearning is operated at the neuron level while recovering is operated
at the filter level, forming an asymmetric reconstructive learning procedure.
We show that such an asymmetric process on only a few clean samples can
effectively expose and prune the backdoor neurons implanted by a wide range of
attacks, achieving a new state-of-the-art defense performance. Moreover, the
unlearned model at the intermediate step of our RNP can be directly used to
improve other backdoor defense tasks including backdoor removal, trigger
recovery, backdoor label detection, and backdoor sample detection. Code is
available at \url{https://github.com/bboylyg/RNP}.Comment: Accepted by ICML2
Develop a 3D Neurological Disease Model of Human Cortical Glutamatergic Neurons Using Micropillar-Based Scaffolds
Establishing an effective three-dimensional (3D) in vitro culture system to better model human neurological diseases is desirable, since the human brain is a 3D structure. Here, we demonstrated the development of a polydimethylsiloxane (PDMS) pillar-based 3D scaffold that mimicked the 3D microenvironment of the brain. We utilized this scaffold for the growth of human cortical glutamatergic neurons that were differentiated from human pluripotent stem cells. In comparison with the 2D culture, we demonstrated that the developed 3D culture promoted the maturation of human cortical glutamatergic neurons by showing significantly more MAP2 and less Ki67 expression. Based on this 3D culture system, we further developed an in vitro disease-like model of traumatic brain injury (TBI), which showed a robust increase of glutamate-release from the neurons, in response to mechanical impacts, recapitulating the critical pathology of TBI. The increased glutamate-release from our 3D culture model was attenuated by the treatment of neural protective drugs, memantine or nimodipine. The established 3D in vitro human neural culture system and TBI-like model may be used to facilitate mechanistic studies and drug screening for neurotrauma or other neurological diseases
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Association of cluster determinant 36, scavenger receptor class B type 1, and major facilitator superfamily domain containing the 2a genetic polymorphism with serum lipid profile in aging population with type 2 diabetes mellitus
Background
Lipid metabolism disorder commonly happens in subjects with Type 2 diabetes mellitus (T2DM) which may be linked to genetic variants of lipid metabolism-related genes. However, few studies have explored the relationship between lipid metabolism-related gene polymorphism and serum lipid profile in aging subjects with T2DM. The present study was designed to explore the impact of genetic polymorphism of cluster determinant 36 (CD36) (rs1049673, rs1054516, rs2151916), scavenger receptor class B type 1 (SCARB1) (rs5888), and major facilitator superfamily domain containing the 2a (MFSD2A) (rs12083239, rs4233508, rs12072037) on the relationship between circulating lipids in aging subjects with T2DM.
Methods
205 T2DM patients and 205 age and gender matched control subjects were recruited. Information on demographic characteristics was collected by using a self-administered questionnaire. Fasting venous blood samples were taken for lipid-related gene genotyping and serum lipid profile measurement. The Chi-square test was used to compare percentage differences and to calculate P-value for Hardy-Weinberg equilibrium. Logistic regression and multiple linear regression were used to explore the risk or correlation between variables, and general linear model (GLM) was used to compare the means of serum lipids between the groups.
Results
In T2DM group, CD36 rs1054516 and MFSD2A rs12072037 were correlated with serum TC level. In control group, CD36 rs1049673 was correlated with serum HDL-C level. Meanwhile, T2DM subjects with MFSD2A rs12083239 (CG), MFSD2A rs4233508 (TT), and MFSD2A rs12072037 (AA) had higher TG level than control subjects. T2DM subjects with CD36 rs1049673 (CG, GG), CD36 rs1054516 (CT), CD36 rs2151916 (TT, CT), SCARB1 rs5888 (GG), MFSD2A rs12083239 (GG, CG), MFSD2A rs4233508 (TT), and MFSD2A rs12072037 (CA, AA) had lower HDL-C level than control subjects. T2DM subjects with MFSD2A rs12072037 (AA) had lower LDL-C level than control subjects. In dominant model, major genotype (GG) of SCARB1 gene was associated with the risk of T2DM (OR = 0.636, P = 0.032).
Conclusion
The genetic polymorphism of CD36 (rs1049673, rs1054516, rs2151916), SCARB1 (rs5888), and MFSD2A (rs12083239, rs4233508, rs12072037) were associated with serum lipids in T2DM subjects. The SCARB1 rs5888 major genotype (GG) was a protective factor for T2DM. Large scale cohort study is required to determine the relationship between lipid metabolism-related gene polymorphism, serum lipid profile and T2DM in aging subjects
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Gender-specific association of SLC19A1 and MTHFR genetic polymorphism with oxidative stress biomarkers and plasma folate levels in older adults
Background
Plasma folate levels are closely related to antioxidant capacity and are regulated by folate pathway gene polymorphism. However, few studies have explored the gender-specific association of folate pathway gene polymorphism with oxidative stress biomarkers. The present study was designed to explore the gender-specific independent and combined impacts of solute carrier family 19 member 1 (SLC19A1) and methylenetetrahydrofolate reductase (MTHFR) genetic polymorphisms on oxidative stress biomarkers in older adults.
Methods
A total of 401 subjects were recruited, including 145 males and 256 females. Demographic characteristics of the participants were collected by using a self-administered questionnaire. Fasting venous blood samples were taken for folate pathway gene genotyping, circulating lipids parameters and erythrocyte oxidative stress biomarkers measurement. The difference of genotype distribution and the Hardy-Weinberg equilibrium was calculated by the Chi-square test. The general linear model was applied to compare the plasma folate levels and erythrocyte oxidative stress biomarkers. Multiple linear regression was used to explore the correlation between genetic risk scores and oxidative stress biomarkers. Logistic regression was used to explore the association of genetic risk scores of folate pathway gene with folate deficiency.
Results
The male subjects have lower plasma folate and HDL-C levels than the female ones, and the male carrying MTHFR rs1801133 (CC) or MTHFR rs2274976 (GA) genotypes have higher erythrocyte SOD activity. The plasma folate levels, erythrocyte SOD and GSH-PX activities were negatively correlated with genetic risk scores in the male subjects. A positive correlation between the genetic risk scores and folate deficiency was observed in the male subjects.
Conclusions
There was association between folate pathway gene polymorphism of Solute Carrier Family 19 Member 1 (SLC19A1) and Methylenetetrahydrofolate Reductase (MTHFR) with erythrocyte SOD and GSH-PX activities, and folate levels in male but not in female aging subjects. Genetic variant of genes involved in folate metabolism has strong impact on plasma folate levels in the male aging subjects. Our data demonstrated that there was a potential interaction of gender and its genetic background in affecting the body's antioxidant capacity and the risk of folate deficiency in aging subjects
Current-driven magnetization switching in a van der Waals ferromagnet Fe3GeTe2
The recent discovery of ferromagnetism in two-dimensional (2D) van der Waals
(vdW) materials holds promises for novel spintronic devices with exceptional
performances. However, in order to utilize 2D vdW magnets for building
spintronic nanodevices such as magnetic memories, key challenges remain in
terms of effectively switching the magnetization from one state to the other
electrically. Here, we devise a bilayer structure of Fe3GeTe2/Pt, in which the
magnetization of few-layered Fe3GeTe2 can be effectively switched by the
spin-orbit torques (SOTs) originated from the current flowing in the Pt layer.
The effective magnetic fields corresponding to the SOTs are further
quantitatively characterized using harmonic measurements. Our demonstration of
the SOT-driven magnetization switching in a 2D vdW magnet could pave the way
for implementing low-dimensional materials in the next-generation spintronic
applications
Tripterine Treatment Improves Endothelial Progenitor Cell Function via Integrin-Linked Kinase
PgtE Enzyme of Salmonella enterica Shares the Similar Biological Roles to Plasminogen Activator (Pla) in Interacting With DEC-205 (CD205), and Enhancing Host Dissemination and Infectivity by Yersinia pestis
Yersinia pestis, the cause of plague, is a newly evolved Gram-negative bacterium. Through the acquisition of the plasminogen activator (Pla), Y. pestis gained the means to rapidly disseminate throughout its mammalian hosts. It was suggested that Y. pestis utilizes Pla to interact with the DEC-205 (CD205) receptor on antigen-presenting cells (APCs) to initiate host dissemination and infection. However, the evolutionary origin of Pla has not been fully elucidated. The PgtE enzyme of Salmonella enterica, involved in host dissemination, shows sequence similarity with the Y. pestis Pla. In this study, we demonstrated that both Escherichia coli K-12 and Y. pestis bacteria expressing the PgtE-protein were able to interact with primary alveolar macrophages and DEC-205-transfected CHO cells. The interaction between PgtE-expressing bacteria and DEC-205-expressing transfectants could be inhibited by the application of an anti-DEC-205 antibody. Moreover, PgtE-expressing Y. pestis partially re-gained the ability to promote host dissemination and infection. In conclusion, the DEC-205-PgtE interaction plays a role in promoting the dissemination and infection of Y. pestis, suggesting that Pla and the PgtE of S. enterica might share a common evolutionary origin.Peer reviewe
The Persistent Circulation of Enterovirus 71 in People's Republic of China: Causing Emerging Nationwide Epidemics Since 2008
Emerging epidemics of hand-foot-and-mouth disease (HFMD) associated with enterovirus 71 (EV71) has become a serious concern in mainland China. It caused 126 and 353 fatalities in 2008 and 2009, respectively. The epidemiologic and pathogenic data of the outbreak collected from national laboratory network and notifiable disease surveillance system. To understand the virological evolution of this emerging outbreak, 326 VP1 gene sequences of EV71 detected in China from 1987 to 2009 were collected for genetic analyses. Evidence from both traditional and molecular epidemiology confirmed that the recent HFMD outbreak was an emerging one caused by EV71 of subgenotype C4. This emerging HFMD outbreak is associated with EV71 of subgenotype C4, circulating persistently in mainland China since 1998, but not attributed to the importation of new genotype. Originating from 1992, subgenotype C4 has been the predominant genotype since 1998 in mainland China, with an evolutionary rate of 4.6∼4.8×10−3 nucleotide substitutions/site/year. The phylogenetic analysis revealed that the majority of the virus during this epidemic was the most recent descendant of subgenotype C4 (clade C4a). It suggests that the evolution might be one of the potential reasons for this native virus to cause the emerging outbreak in China. However, strong negative selective pressure on VP1 protein of EV71 suggested that immune escape might not be the evolving strategy of EV71, predicting a light future for vaccine development. Nonetheless, long-term antigenic and genetic surveillance is still necessary for further understanding
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