Colossal Magnetoresistive Switching Induced by d0 Ferromagnetism of MgO in a Semiconductor Nanochannel Device with Ferromagnetic Fe/MgO Electrodes.

Exploring potential spintronic functionalities in resistive switching (RS) devices is of great interest for creating new applications, such as multifunctional resistive random-access memory and novel neuromorphic computing devices. In particular, the importance of the spin-triplet state of cation vacancies in oxide materials, which is induced by localized and strong O-2p on-site Coulomb interactions, in RS devices has been overlooked. d0 ferromagnetism sometimes appears due to the spin-triplet state and ferromagnetic Zener's double exchange interactions between cation vacancies, which are occasionally strong enough to make nonmagnetic oxides ferromagnetic. Here, for the first time, anomalous and colossal magneto-RS (CMRS) with very high magnetic field dependence is demonstrated by utilizing an unconventional RS device composed of a Ge nanochannel with all-epitaxial single-crystalline Fe/MgO electrodes. The device shows colossal and unusual behavior as the threshold voltage and ON/OFF ratio strongly depend on a magnetic field, which is controllable with an applied voltage. This new phenomenon is attributed to the formation of d0-ferromagnetic filaments by attractive Mg vacancies due to the spin-triplet states with ferromagnetic double exchange interactions and the ferromagnetic proximity effect of Fe on MgO. The findings will allow the development of energy-efficient CMRS devices with multifield susceptibility.

Insight into Scattering Mechanisms and Transport Properties of AgCuS for Flexible Thermoelectric Applications.

The development of flexible thermoelectric devices requires materials possessing ductility and high thermoelectric performance at room temperature. However, only a few existing materials meet both criteria. In this study, the ductile properties, electronic structure, and transport properties of the low-temperature phase α-AgCuS were elucidated using first-principles calculations combined with Boltzmann transport theory. With a layered zigzag structure similar to the well-known ductile semiconductor Ag2S, AgCuS is determined to have good metal-like ductility. Through consideration of various intrinsic scattering mechanisms, we found that electron-polar optical phonon interactions have the most significant impact on the transport behavior of AgCuS. The predominance of this type of interaction is also disclosed by the covalent-ionic bonding nature of the Ag-S and Cu-S bonds. Therefore, weakening this interaction via doping or alloying could optimize the thermoelectric performance of the system. At room temperature, a maximum dimensionless figure of merit ZT of up to 0.592 could be achieved under a tuning of hole concentration to 2 × 1019 cm-3, suggesting that α-AgCuS could be a promising p-type candidate for flexible thermoelectric applications.

Ferromagnetism and giant magnetoresistance in zinc-blende FeAs monolayers embedded in semiconductor structures.

Material structures containing tetrahedral FeAs bonds, depending on their density and geometrical distribution, can host several competing quantum ground states ranging from superconductivity to ferromagnetism. Here we examine structures of quasi two-dimensional (2D) layers of tetrahedral Fe-As bonds embedded with a regular interval in a semiconductor InAs matrix, which resembles the crystal structure of Fe-based superconductors. Contrary to the case of Fe-based pnictides, these FeAs/InAs superlattices (SLs) exhibit ferromagnetism, whose Curie temperature (TC) increases rapidly with decreasing the InAs interval thickness tInAs (TC ∝ tInAs-3), and an extremely large magnetoresistance up to 500% that is tunable by a gate voltage. Our first principles calculations reveal the important role of disordered positions of Fe atoms in the establishment of ferromagnetism in these quasi-2D FeAs-based SLs. These unique features mark the FeAs/InAs SLs as promising structures for spintronic applications.

Correction: Intrinsic defect formation and the effect of transition metal doping on transport properties in a ductile thermoelectric material α-Ag2S: a first-principles study.

Correction for 'Intrinsic defect formation and the effect of transition metal doping on transport properties in a ductile thermoelectric material α-Ag2S: a first-principles study' by Ho Ngoc Nam et al., Phys. Chem. Chem. Phys., 2021, DOI: .

Intrinsic defect formation and the effect of transition metal doping on transport properties in a ductile thermoelectric material α-Ag2S: a first-principles study.

In this paper, the electronic structure and transport properties of a ductile thermoelectric material α-Ag2S are examined using first-principles calculations combined with the Boltzmann transport equation within a constant relaxation-time approximation. The use of the exchange-correlation functional SCAN + rVV10 successfully describes the geometric and electronic structure of α-Ag2S with a direct bandgap value of 0.99 eV, which is consistent with the previous experimental observations. Based on the calculations of the formation energy of typical intrinsic defects, it is found that intrinsic defect formation greatly affects the conductivity of the system where silver vacancy and interstitial silver act as p-type and n-type defects, respectively. Large Seebeck coefficients at room-temperature, of around -760 µV K-1 for n-type and 1400 µV K-1 for p-type, are realized. It is also suggested that the doping of fully filled d-block elements such as Cu and Au not only maintained the Seebeck coefficients at high values but also improved electrical conductivity by more than 1.4 times, leading to the improvement of the power factor by up to 40% compared to the non-doped sample at low carrier concentration.

Hole-mediated ferromagnetism in a high-magnetic moment material, Gd-doped GaN.

As an exotic material in spintronics, Gd-doped GaN is known as a room- temperature ferromagnetic material that possesses a large magnetic moment (4000 µBper Gd ion). This paper theoretically proposes that the large magnetic moment and room-temperature ferromagnetism observed in Gd-doped GaN is caused by N 2p holes based on the assumption that Ga-vacancies (VGa) result from the introduction of Gd ions via the volume compensation effect. This causes that the too large magnetic moment is estimated for Gd ions if only Gd ions contributed the magnetic moment.

Computational materials design of defect-induced ferrimagnetic MnO.

We present a computational materials design for defect-induced ferrimagnetic MnO. The magnetic properties of MnO containing Mn vacancies were investigated using first-principle calculations. For these electronic structure calculations, we employed a pseudo-self-interaction-corrected local density approximation (PSIC-LDA). We used the Korringa-Kohn-Rostoker coherent potential approximation (KKR-CPA) to create a random distribution of atoms at the assigned sites. Having described the magnetic properties with a classic Heisenberg model, we calculated the effective exchange coupling constants by applying the magnetic force theorem to two magnetic sites embedded in the CPA medium. We estimated the Curie temperatures from the calculated exchange interactions. This study found that the Mn vacancies induced ferrimagnetic ground states in MnO, and that the Curie temperature could reach room temperature at Mn vacancy concentrations above 20%. These findings suggest a new route for designing ferrimagnetic materials from anti-ferromagnetic host materials.

Neurodynamics of cognitive set shifting in monkey frontal cortex and its causal impact on behavioral flexibility.

Flexible behavior depends on the ability to shift an internal cognitive set as soon as external demand changes. According to neuropsychological studies in human and nonhuman primates, selective lesion to the PFC impairs flexible behavioral shifting. Our previous fMRI study demonstrated that the prefrontal regions showed transient activation related to set shifting in humans and monkeys. To investigate the underlying neural processing, we recorded single-unit activities while monkeys performed a cognitive-set-shifting task, which required shifting between shape-matching and color-matching behaviors. We identified a group of neurons in the inferior arcuate region that exhibited selective activity when the monkeys were required to shift their cognitive set. These shift-related neurons were localized in the focal area along the posterior bank of the inferior arcuate sulcus. Reversible inactivation of this area ipsilateral to the response hand with a small volume of muscimol (even with 0.5 µl) selectively impaired the performance of behavioral shifting. Moreover, this selective behavioral impairment strongly correlated with the dose of muscimol. These results demonstrated localized neural processing for cognitive set shifting and its causal role for behavioral flexibility in primates.

Neuronal signal dynamics during preparation and execution for behavioral shifting in macaque posterior parietal cortex.

Cognitive flexibility arises from our ability to shift behaviors depending on demand changes. Behavioral shifting recruits both a preparatory process for an upcoming behavior and an execution process for the actual behavior. Although neuroimaging studies have shown that several brain regions, including posterior parietal cortex (PPC) participated in each component process, it remains unresolved how such processes are implemented at the single-cell level or even whether these processes are distinctively carried out across microstructures in such regions. By recording single-unit activity from PPC of two monkeys performing an analog of the Wisconsin Card Sorting Test, we found that, in the execution process, two types of neurons exhibited activity modulation depending on whether shift was (shift trial) or was not required (nonshift trial): one type showing larger activity and the other showing smaller activity in the shift trial than in the nonshift trial. In the preparatory process, in contrast, the population activity of both types became larger in the shift trial than in the nonshift trial. The majority of both types exhibited shift-related activity modulation in both processes, whereas the remaining was specialized in the execution process. The former and the latter neurons were spatially intermingled within PPC. Significantly, when the animals performed set shifting spontaneously in prospect of a demand change, the shift-related activity modulation still emerged in both processes. We suggest that both execution and preparation signals are represented within PPC, and that these signals reflect behavioral shifting mechanisms that can be driven by either internal or external triggers.

Cognitive set reconfiguration signaled by macaque posterior parietal neurons.

When faced with problems, we can flexibly change our ways of thinking or our point of view. Our cognitive flexibility arises from this ability of shifting cognitive sets. To elucidate how this dynamic process is implemented in the primate brain, single-unit activity was recorded from the posterior parietal cortex (PPC) of two monkeys performing analogs of the Wisconsin Card Sorting Test, which is most commonly used to test cognitive flexibility in humans. We successfully trained the monkeys to promptly perform set shifting, mostly within a single trial, and found shift-related activity: PPC neurons were transiently activated when the monkeys shifted from one cognitive set to another, but not when they shifted in the opposite direction. This shift-related activity emerged about 4 s before the actual behavioral responses, and it well predicted whether the cognitive set would be successfully shifted. These results provide insights into single-unit level mechanisms of cognitive flexibility.

The relationship between CA/C ratio and individual differences in dynamic accommodative responses while viewing stereoscopic images.

The oculomotor synergy as expressed by the CA/C and AC/A ratios was investigated to examine its influence on our previous observation that whereas convergence responses to stereoscopic images are generally stable, some individuals exhibit significant accommodative overshoot. Using a modified video refraction unit while viewing a stereoscopic LCD, accommodative and convergence responses to balanced and unbalanced vergence and focal stimuli (BVFS and UBVFS) were measured. Accommodative overshoot of at least 0.3 D was found in 3 out of 8 subjects for UBVFS. The accommodative response differential (RD) was taken to be the difference between the initial response and the subsequent mean static steady-state response. Without overshoot, RD was quantified by finding the initial response component. A mean RD of 0.11 +/- 0.27 D was found for the 1.0 D step UBVFS condition. The mean RD for the BVFS was 0.00 +/- 0.17 D. There was a significant positive correlation between CA/C ratio and RD (r = +0.75, n = 8, p < 0.05) for only UBVFS. We propose that inter-subject variation in RD is influenced by the CA/C ratio as follows: an initial convergence response, induced by disparity of the image, generates convergence-driven accommodation commensurate with the CA/C ratio; the associated transient defocus subsequently decays to a balanced position between defocus-induced and convergence-induced accommodations.

Induction of human adiponectin gene transcription by telmisartan, angiotensin receptor blocker, independently on PPAR-gamma activation.

Adiponectin, an adipose tissue-specific plasma protein, has been shown to ameliorate insulin resistance and inhibit the process of atherosclerosis. Recently, several reports have stated that angiotensin type 1 receptor blockers (ARBs), increase adiponectin plasma level, and ameliorate insulin resistance. Telmisartan, a subclass of ARBs, has been shown to be a partial agonist of the peroxisome proliferator-activated receptor (PPAR)-gamma, and to increase the plasma adiponectin level. However, the transcriptional regulation of the human adiponectin gene by telmisartan has not been determined yet. To elucidate the effect of telmisartan on adiponectin, the stimulatory regulation of human adiponectin gene by telmisartan was investigated in 3T3-L1 adipocytes, utilizing adenovirus-mediated luciferase reporter gene-transferring technique. This study indicates that telmisartan may stimulate adiponectin transcription independent of PPAR-gamma.

Evidence for the role of small ubiquitin-like modifier 4 as a general autoimmunity locus in the Japanese population.

CONTEXT: Recently, an association of a single nucleotide polymorphism, 163A>G encoding M55V, in the gene SUMO4, which has been shown to be a negative feedback regulator for nuclear factor kappaB, has been reported in type 1 diabetes. OBJECTIVE: To establish whether SUMO4 locus contributes to the genetic susceptibility to other autoimmune disorders, a case-control analysis was carried out using genomic DNA from type 1 diabetes, autoimmune thyroid disease (AITD), rheumatoid arthritis (RA), and primary Sjögren's syndrome. SUBJECTS: A total of 1480 samples, including 929 cases (411 patients with type 1 diabetes, 292 AITD, 172 RA, and 54 primary Sjögren's syndrome) and 551 healthy control subjects of Japanese origin participated in the study. METHODS: The 163A>G (rs237025, M55V) polymorphism of SUMO4 was genotyped. RESULTS: SUMO4 M55V variant was associated not only with type 1 diabetes [odds ratio (OR), 1.42; 95% confidence interval (CI), 1.09-1.84; P = 0.0072], but also with increased risk of other autoimmune diseases, AITD (OR, 1.52; 95% CI, 1.14-2.03; P = 0.0041) and RA without amyloidosis (OR, 1.53; 95% CI, 1.65-2.24; P = 0.027), but not primary Sjögren's syndrome. Furthermore, the association of SUMO4 M55V variant was stronger in type 1 diabetic patients complicated with AITD (OR, 1.62; 95% CI, 1.06-2.47; P = 0.023) and in patients who have neither type 1 diabetes-susceptible class II HLA, DRB1*0405 nor DRB1*0901 (OR, 2.28; 95% CI, 1.34-3.87; P = 0.0018). CONCLUSIONS: These results indicate that the SUMO4 is a more common autoimmune disease gene and a supplementary risk factor to type 1 diabetes in conjunction with class II HLA.

Hepatitis B-related polyarteritis nodosa presenting necrotizing vasculitis in the hepatobiliary system successfully treated with lamivudine, plasmapheresis and glucocorticoid.

A 64-year-old man was admitted for alithiasic cholecystitis. Necrotizing vasculitis was detected in a gallbladder obtained at the cholecystectomy. Slight elevation of transaminases, HBe antigens and hepatitis B-DNA (HBV-DNA) were detected in the patient. Intrahepatic necrotizing vasculitis was also detected in the liver biopsy specimen, and he also suffered from peripheral neuropathy of suddenly onset. Based on the diagnosis of hepatitis B-related polyarteritis nodosa, lamivudine was initially administered, followed by plasmapheresis and glucocorticoid steroid therapy. These treatments brought satisfactory improvement of polyarteritis nodosa without exacerbation of liver function.

Identification of the promoter region required for human adiponectin gene transcription: Association with CCAAT/enhancer binding protein-beta and tumor necrosis factor-alpha.

Adiponectin, an adipose tissue-specific plasma protein, is involved in insulin sensitizing and has anti-atherosclerotic properties. Plasma levels of adiponectin are decreased in obese individuals and patients with type 2 diabetes with insulin resistance. Tumor necrosis factor-alpha (TNF-alpha) decreases the expression of adiponectin in adipocytes. The aims of the present study were: (1) to identify the promoter region responsible for basal transcription of the human adiponectin gene, and (2) to investigate the mechanism by which adiponectin was regulated by TNF-alpha. The human adiponectin promoter (2.1kb) was isolated and used for luciferase reporter analysis by transient transfection into 3T3-L1 adipocytes. Deletion analysis demonstrated that the promoter region from -676 to +41 was sufficient for basal transcriptional activity. Mutation analysis of putative response elements for sterol regulatory element binding protein (SREBP) (-431 to -423) and CCAAT/enhancer binding protein (C/EBP) (-230 to -224) showed that both elements were required for basal promoter activity. Adiponectin transcription was increased 3-fold in cells that over-expressed constitutively active C/EBP-beta. Electrophoretic mobility shift assay, using nuclear extract from 3T3-L1 cells and the -258 to -199 region as a probe, demonstrated specific DNA-protein binding, which was abolished by TNF-alpha treatment. The present data indicate that the putative response elements for SREBP and C/EBP are required for human adiponectin promoter activity, and that suppression by TNF-alpha may, at least in part, be associated with inactivation of C/EBP-beta.

Rapid inhibition of leptin signaling by glucocorticoids in vitro and in vivo.

Elevated secretion of glucocorticoids (GCs) or hypersensitivity to GCs has a permissive effect on the development of obesity and leads to abnormalities of body fat distribution. Recent studies demonstrated GCs act as antagonists of leptin in rodents. However, little is known about the interaction between GCs and leptin signaling. In the present study, we investigated the effects of GCs on leptin action in vitro and in vivo. GCs rapidly inhibited the leptin-induced STAT3 phosphorylation in a dose- and time-dependent manner, as assayed by Western blotting using anti-phosphospecific-STAT3 in human hepatoma cell lines (Huh7) transiently expressing long form leptin receptor. GCs also inhibited the leptin-induced JAK2 tyrosine phosphorylation but unaltered the specific binding of (125)I-leptin to the cells. Parallel experiments, however, demonstrated that the inhibitory effects of GCs were not observed in either IL-6- or LIF-induced STAT3 phosphorylation. Furthermore, we examined the feeding behavior and hypothalamic leptin signaling following intracerebroventricular (icv) infusion of GCs prior to icv leptin infusion in Sprague-Dawley rats. The food intake after 24 h of icv leptin injection increased 3-fold in GCs-treated animals. In addition, central infusion of GCs resulted in a marked reduction of hypothalamic STAT3 phosphorylation in response to icv infusion of leptin. To clarify the molecular mechanism by which GCs rapidly reduce leptin-induced JAK/STAT signaling, we examined the intracellular signal transduction pathway potentially mediated by GCs. PD98059, a specific MEK inhibitor, blocked the inhibitory effects of GCs on leptin-induced JAK/STAT activation in Huh7 cells. These results suggest GCs antagonize leptin action by a rapid inhibition of the leptin-induced JAK/STAT pathway partly via MAPK cascade.

Association between IL-18 gene promoter polymorphisms and CTLA-4 gene 49A/G polymorphism in Japanese patients with type 1 diabetes.

Interleukin-18 (IL-18) is a potent proinflammatory cytokine which is strongly associated with the development of diabetes in NOD mice. To test the putative involvement of IL-18 gene polymorphism in predisposition to human type 1 diabetes, the SNPs at position -607 (C/A) and -137 (G/C) in the promoter region of IL-18 gene were analyzed by sequence-specific PCR in 116 patients with type 1 diabetes and 114 normal controls. A linkage disequilibrium found only three of the four possible haplotypes defined by these SNPs. The distribution of the IL-18 gene genotypes at position -607 was significantly different between patients with type 1 diabetes and normal controls (P=0.023). Furthermore, there was a significant increase in haplotype 1 (-607C/-137G) in the patients compared with controls (P=0.006). The association study of the susceptible CTLA-4 genotype (GG at nucleotide position 49 in exon 1) or HLA-DR4-DQB1*0401 and type 1 diabetes showed that the predisposing IL-18 gene haplotype modulates the risk on CTLA-4 GG genotype, but not on HLA-DR4-DQB1*0401 haplotype. Among subjects carrying the CTLA-4 GG genotype, the frequency of IL-18 haplotype 1 in patients with type 1 diabetes was significantly higher than that in controls (91% vs. 71%, P=0.012). However, IL-18 haplotype 1 was not frequent in patients who do not exhibit the CTLA-4 high-risk genotype. These results suggest that the IL-18 gene polymorphism is associated with a type 1 diabetes susceptibility, and there might be a gene-gene interaction between IL-18 gene with susceptible CTLA-4 gene.

Prefrontal neuronal activity encodes spatial target representations sequentially updated after nonspatial target-shift cues.

We examined prefrontal neuronal activity while monkeys performed a sequential target-shift task, in which, after a positional cue indicated the initial saccade target among 8 peripheral positions, the monkeys were required to internally shift the target by one position on every flash of a target-shift cue. The target-shift cue appeared in the center 0 to 3 times within a single trial and was always the same in shape, size, and color. We found selective neuronal activity related to the target position: when the target-shift cue implied the target shift to particular peripheral positions, neurons exhibited early-dominant and late-dominant activity during the following delay period. The early-dominant target-selective activity emerged early in the delay just after the presentation of the target-shift cue, whereas the late-dominant activity gradually built up toward the end of the delay. Because the target-shift cue was not related to any specific target location, the early-dominant target-selective activity could not be a mere visual response to the target-shift cue. We suggest that the early-dominant activity reflects the transitory representation for the saccade target that was triggered by the nonspatial target-shift cue, whereas the late-dominant activity reflects the target representation in the spatial working memory or the preparatory set for the possible impending saccade, being repeatedly updated during sequential target shifts.

Stromal cell-derived factor-1 chemokine gene variant in patients with type 1 diabetes and autoimmune thyroid disease.

Type 1 diabetes is a heterogenous autoimmune disease and is frequently associated with other organ-specific autoimmune diseases, including autoimmune thyroid disease (AITD). Type 1 diabetic patients with AITD are known to have clinical and immunological features distinct from patients without AITD. This study investigated whether stromal cell-derived factor (SDF)-1 gene polymorphism is associated with susceptibility to type 1 diabetes and AITD. SDF-1 is a powerful chemokine that upregulates T-cell migration and activation, and the gene for SDF-1 is located near type 1 diabetes susceptibility locus IDDM10. The SDF1-3'A variant (801 G to A in the 3'-untranslated region) was determined by the PCR-RFLP technique in 54 type 1 diabetic patients with AITD, 75 type 1 diabetic patients without AITD, 137 nondiabetic patients with AITD, and 106 healthy subjects in a case-control study. No significant differences on the allele and genotype frequencies of the SDF1 gene polymorphism were found, not only in type 1 diabetic patients with AITD compared with normal controls but also between nondiabetic patients with AITD and healthy control subjects. These results suggest that the SDF1-3'A variant is not associated with genetic susceptibility to type 1 diabetic patients and AITD.

Interleukin-10 gene promoter region polymorphisms in patients with type 1 diabetes and autoimmune thyroid disease.

Type 1 diabetes is a heterogeneous autoimmune disease and is frequently associated with other organ-specific autoimmune diseases, including autoimmune thyroid disease (AITD). Type 1 diabetic patients with AITD are known to show distinct clinical and immunological features from patients without AITD. This study investigated whether interleukin-10 (IL-10) gene promoter region polymorphisms are associated with susceptibility to type 1 diabetes and AITD. The frequency of -1082G/A, -819C/T, and -592C/A polymorphisms was analyzed in 54 type 1 diabetic patients with AITD, 74 type 1 diabetic patients without AITD, 124 nondiabetic patients with AITD, and 107 healthy subjects in a case-control study. No significant differences on the allele and genotype frequencies of three polymorphisms were found not only in type 1 diabetic patients with AITD compared with normal controls, but also between nondiabetic patients with AITD and healthy controls. The distribution of IL-10 gene haplotypes was also similar between both patient groups and normal controls. These results suggest that IL-10 gene promoter region polymorphisms are not associated with genetic susceptibility to type 1 diabetes and AITD.