Room-temperature magnetoresistance in an all-antiferromagnetic tunnel junction.

Antiferromagnetic spintronics1-16 is a rapidly growing field in condensed-matter physics and information technology with potential applications for high-density and ultrafast information devices. However, the practical application of these devices has been largely limited by small electrical outputs at room temperature. Here we describe a room-temperature exchange-bias effect between a collinear antiferromagnet, MnPt, and a non-collinear antiferromagnet, Mn3Pt, which together are similar to a ferromagnet-antiferromagnet exchange-bias system. We use this exotic effect to build all-antiferromagnetic tunnel junctions with large nonvolatile room-temperature magnetoresistance values that reach a maximum of about 100%. Atomistic spin dynamics simulations reveal that uncompensated localized spins at the interface of MnPt produce the exchange bias. First-principles calculations indicate that the remarkable tunnelling magnetoresistance originates from the spin polarization of Mn3Pt in the momentum space. All-antiferromagnetic tunnel junction devices, with nearly vanishing stray fields and strongly enhanced spin dynamics up to the terahertz level, could be important for next-generation highly integrated and ultrafast memory devices7,9,16.

Tunneling Magnetoresistance in Noncollinear Antiferromagnetic Tunnel Junctions.

Antiferromagnetic (AFM) spintronics has emerged as a subfield of spintronics driven by the advantages of antiferromagnets producing no stray fields and exhibiting ultrafast magnetization dynamics. The efficient method to detect an AFM order parameter, known as the Néel vector, by electric means is critical to realize concepts of AFM spintronics. Here, we demonstrate that noncollinear AFM metals, such as Mn_{3}Sn, exhibit a momentum dependent spin polarization which can be exploited in AFM tunnel junctions to detect the Néel vector. Using first-principles calculations, we predict a tunneling magnetoresistance (TMR) effect as high as 300% in AFM tunnel junctions with Mn_{3}Sn electrodes, where the junction resistance depends on the relative orientation of their Néel vectors and exhibits four nonvolatile resistance states. We argue that the spin-split band structure and the related TMR effect can also be realized in other noncollinear AFM metals like Mn_{3}Ge, Mn_{3}Ga, Mn_{3}Pt, and Mn_{3}GaN. Our work provides a robust method for detecting the Néel vector in noncollinear antiferromagnets via the TMR effect, which may be useful for their application in AFM spintronic devices.

A Case of Syncope in a Child due to the Large Segment of Myocardial Bridge.

We report a child with an unusual coronary bridge crossing over the left anterior descending (LAD), circumflex (CX), and right coronary artery (RCA). The bridges range from 0.8-1.2 mm depth. The patient presented with exercise-induced syncope and myocardial infarction (MI). She exhibited no syncope after medicine and exercise control.

LncRNA Expression Profile of Human Thoracic Aortic Dissection by High-Throughput Sequencing.

BACKGROUND/AIMS: In this study, the long non-coding RNA (lncRNA) expression profile in human thoracic aortic dissection (TAD), a highly lethal cardiovascular disease, was investigated. METHODS: Human TAD (n=3) and normal aortic tissues (NA) (n=3) were examined by high-throughput sequencing. Bioinformatics analyses were performed to predict the roles of aberrantly expressed lncRNAs. Quantitative real-time polymerase chain reaction (qRT-PCR) was applied to validate the results. RESULTS: A total of 269 lncRNAs (159 up-regulated and 110 down-regulated) and 2, 255 mRNAs (1 294 up-regulated and 961 down-regulated) were aberrantly expressed in human TAD (fold-change> 1.5, P< 0.05). QRT-PCR results of five dysregulated genes were consistent with HTS data. A lncRNA-mRNA coexpression analysis showed positive correlations between the up-regulated lncRNA (ENSG00000269936) and its adjacent up-regulated mRNA (MAP2K6, R=0.940, P< 0.01), and between the down-regulated lncRNA_1421 and its down-regulated mRNAs (FBLN5, R=0.950, P< 0.01; ACTA2, R=0.96, P< 0.01; TIMP3, R=0.96, P< 0.05). The lncRNA-miRNA-mRNA network indicated that the up-regulated lncRNA XIST and p21 had similar sequences targeted by has-miR-17-5p. The results of luciferase assay and fluorescence immuno-cytochemistry were consistent with that. And qRT-PCR results showed that lncRNA XIST and p21 were expressed at a higher level and has-miR-17-5p was expressed at a lower level in TAD than in NA. The predicted binding motifs of three up-regulated lncRNAs (ENSG00000248508, ENSG00000226530, and EG00000259719) were correlated with up-regulated RUNX1 (R=0.982, P< 0.001; R=0.967, P< 0.01; R=0.960, P< 0.01, respectively). CONCLUSIONS: Our study revealed a set of dysregulated lncRNAs and predicted their multiple potential functions in human TAD. These findings suggest that lncRNAs are novel potential therapeutic targets for human TAD.

Magnetostriction, piezomagnetism and domain nucleation in a Kagome antiferromagnet.

Whenever the elastic energy of a solid depends on magnetic field, there is a magnetostrictive response. Field-linear magnetostriction implies piezomagnetism and vice versa. Here, we show that Mn3Sn, a non-collinear antiferromanget with Weyl nodes, hosts a large and almost perfectly linear magnetostriction even at room temperature. The longitudinal and transverse magnetostriction, with opposite signs and similar amplitude are restricted to the kagome planes and the out-of-plane response is negligibly small. By studying four different samples with different Mn:Sn ratios, we find a clear correlation between the linear magnetostriction, the spontaneous magnetization and the concentration of Sn vacancies. The recently reported piezomagnetic data fits in our picture. We show that linear magnetostriction and piezomagnetism are both driven by the field-induced in-plane twist of spins. A quantitative account of the experimental data requires the distortion of the spin texture by Sn vacancies. We find that the field-induced domain nucleation within the hysteresis loop corresponds to a phase transition. Within the hysteresis loop, a concomitant mesoscopic modulation of local strain and spin twist angles, leading to twisto-magnetic stripes, arises as a result of the competition between elastic and magnetic energies.

Prognostic Value of ß1 Adrenergic Receptor Autoantibody and Soluble Suppression of Tumorigenicity-2 in Patients With Acutely Decompensated Heart Failure.

BACKGROUND: Both ß1 adrenergic receptor autoantibody (ß1-AA) and soluble suppression of tumorigenicity-2 (sST2) take a role in the pathological remodeling of heart failure. However, limited studies investigated the correlation between the expression of ß1-AA and sST2 in patients with acutely decompensated heart failure (ADHF). OBJECTIVE: To explore the correlation between ß1-AA and sST2, and evaluate their prognostic value in patients with ADHF. METHODS: Patients who were admitted for ADHF were included. The N-terminal pro-brain natriuretic peptide (NT-proBNP), sST2, and ß1-AA in blood samples were tested at hospital admission and then followed up for assessing the outcomes. Pearson correlation analysis was used to explore the correlation between ß1-AA and sST2. The effects of ß1-AA, sST2, or the combination of them on the all-cause mortality of patients with ADHF were assessed by Multivariate Cox regression analysis. RESULTS: There were 96 patients with ADHF and 96 control populations enrolled. The ß1-AA was significantly higher in ADHF than in the control group (0.321 ± 0.06 vs. 0.229 ± 0.04, P = 0.000). Pearson correlation analysis showed that ß1-AA was positively correlated with sST2 (r = 0.593), NT-proBNP (r = 0.557), Procalcitonin (r = 0.176), and left ventricular end-diastolic diameter (r = 0.315), but negatively correlated with triglycerides (r = -0.323), and left ventricular ejection fraction (r = -0.430) (all P < 0.05) in ADHF. Patients with ADHF, complicated with both high ß1-AA and sST2, showed the highest all-cause mortality during an average of 25.5 months of follow-up. Multivariate Cox regression showed the combination of both high ß1-AA and sST2 independently correlated with the all-cause mortality after adjustment for other risk factors (hazard ratio 3.348, 95% CI 1.440 to 7.784, P = 0.005). After adding with ß1-AA and sST2, the area under the curves for the prognostic all-cause mortality could increase from 0.642 to 0.748 (P = 0.011). CONCLUSION: The ß1-AA is positively correlated with sST2 in patients with ADHF. Elevated plasma ß1-AA and sST2 level in patients with ADHF are associated with poorer prognoses.

Association Between Fasting Hyperglycemia and New-Onset Atrial Fibrillation in Patients With Acute Myocardial Infarction and the Impact on Short- and Long-Term Prognosis.

Background: The relationship between fasting hyperglycemia (FHG) and new-onset atrial fibrillation (AF) in patients with acute myocardial infarction (AMI) is unclear, and whether their co-occurrence is associated with a worse in-hospital and long-term prognosis than FHG or AF alone is unknown. Objective: To explore the correlation between FHG and new-onset AF in patients with AMI, and their impact on in-hospital and long-term all-cause mortality. Methods: We performed a retrospective cohort study comprising 563 AMI patients. The patients were divided into the FHG group and the NFHG group. The incidence of new-onset AF during hospitalization was compared between the two groups and sub-groups under different Killip grades. Logistic regression was used to assess the association between FHG and new-onset AF. In-hospital mortality and long-term all-cause mortality were compared among patients with FHG, AF, and with both FHG and AF according to 10 years of follow-up information. Results: New-onset AF occurred more frequently in the FHG group than in the NFHG group (21.6 vs. 9.2%, p < 0.001). This trend was observed for Killip grade I (16.6 vs. 6.5%, p = 0.002) and Grade II (17.1 vs. 6.9%, p = 0.005), but not for Killip grade III-IV (40 vs. 33.3%, p = 0.761). Logistic regression showed FHG independently correlated with new-onset AF (OR, 2.56; 95% CI, 1.53-4.30; P < 0.001), and 1 mmol/L increased in fasting glucose was associated with a 5% higher rate of new-onset AF, after adjustment for traditional AF risk factors. AMI patients complicated with both fasting hyperglycemia and AF showed the highest in-hospital mortality and long-term all-cause mortality during an average of 11.2 years of follow-up. Multivariate Cox regression showed FHG combined with AF independently correlated with long-term all-cause mortality after adjustment for other traditional risk factors (OR = 3.13, 95% CI 1.64-5.96, p = 0.001), compared with the group with neither FHG nor new-onset AF. Conclusion: FHG was an independent risk factor for new-onset AF in patients with AMI. AMI patients complicated with both FHG and new-onset AF showed worse in-hospital and long-term all-cause mortality than with FHG or AF alone.

An interesting implantable cardioverter defibrillator treatment for lethal ventricular arrhythmias caused by coronary artery spasm: A case report.

RATIONALE: Coronary artery spasm (CAS) could cause serious lethal ventricular arrhythmias. While implantable cardioverter defibrillators (ICDs) have been recommend for secondary prevention of sudden cardiac death related to lethal ventricular arrhythmias. However, in resuscitated sudden cardiac death caused by CAS, the effect of ICD is still not well clear. PATIENT CONCERNS: A 60-year-old male presented with 2 episodes of syncope. Coronary angiography showed normal coronary arteries. Twenty-four hour Holter electrocardiograms revealed that there were repeatedly transient marked ST segment elevation in the all leads except avR lead, junctional rhythm, and subsequently nonsustained ventricular tachycardia. DIAGNOSES: Ischemic-induced lethal ventricular arrhythmias caused by CAS. INTERVENTIONS: Both calcium channel blocker (diltiazem, 180 mg twice daily) and nitrate (isosorbide dinitrate 40 mg twice daily) were initially administrated, and ICD was subsequently implanted as a secondary prevention. OUTCOMES: In the early stage of CAS, ICD therapy terminated the lethal ventricular arrhythmias. Conversely, after the administration of epinephrine, ICD therapy, even combined with external defibrillation, failed in resuscitating sudden cardiac death. LESSONS: For the sudden cardiac death related to lethal ventricular arrhythmias caused by CAS, ICD therapy is an efficient secondary prevention base on administrating coronary vasodilators. Furthermore, administration of epinephrine should be avoided during cardiorespiratory resuscitation of sudden cardiac death caused by CAS.

In vitro biocompatibility evaluation of bioresorbable copolymers prepared from L-lactide, 1, 3-trimethylene carbonate, and glycolide for cardiovascular applications.

PLLA-TMC-GA terpolymer was prepared by ring-opening polymerization of L-lactide, 1, 3-trimethylene carbonate (TMC), and glycolide (GA). The biocompatibility of terpolymer was evaluated in comparison with PLLA and PLLA-TMC with the aim of assessing their potential in the development of bioresorbable cardiovascular stents. Various aspects of in vitro biocompatibility were considered, including MTT assay, hemolytic test, dynamic clotting time, platelet adhesion, platelet activation, protein adsorption, plasma recalcification time and release of cytokines. The results revealed that the terpolymer presents good cytocompatibility and hemocompatibility. Moreover, no significant increase in the release of cytokines was detected. It is thus concluded that these polymers, in particular PLLA-TMC-GA terpolymer present good biocompatibility for cardiovascular applications.

[Drug-eluting stent implantation for unprotected left main coronary artery disease: immediate and long-term outcomes].

OBJECTIVE: To evaluate the safety and efficacy of drug-eluting stent (DES) implantation in selective patients with left main coronary artery disease. METHOD: From October 2002 to November 2007, 44 consecutive patients underwent percutaneous coronary interventions (PCI) on left main coronary artery lesions, including 5 patients with concurrent left ventricular dysfunction (ejection fraction<40%), 2 with chronic respiratory dysfunction and 5 with chronic renal failure. The findings in coronary angiography, procedural success rate, severe complications and the follow-up results of the patients were analyzed. RESULTS: The immediate procedural success rate was 100% in these patients without any severe complications. No non-fatal acute myocardial infarction or emergency coronary artery bypass grafting (CABG) was performed and death occurred in none of the cases during hospitalization. In the follow-up period for 14.2-/+9.3 (6-65) months after PCI, no subacute or late thromboses were found. One patient died from heart failure 4 months after PCI, and 6 patients (13.6%) experienced recurrent angina. Thirty-seven patients (84.1%) were free of any major cardiovascular events (MACE) after the procedure. A repeat coronary angiography was performed in 35 patients (79.5%) within 6 months after PCI, and 3 (8.6%) of them were confirmed to have restenosis, including 1 patient with distal bifurcation restenosis who were subsequently treated with CABG and two patients with side-branch ostium restenosis managed with cutting balloon dilation. CONCLUSIONS: Implantation of drug-eluting stents is safe and effective for management of left main coronary artery disease with good immediate and long-term outcomes.