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Background/Purpose: Myocarditis is a severe disorder characterized by the inflammation of the heart's muscular walls, thereby leading to sudden death in young adults. Long non-coding RNA X-inactive specific transcripts (LncRNA XIST) are a class of transcripts having a length ˃ 200 nts with the absence of protein-coding abilities. They exert their function of apoptosis in various cancers and inflammatory diseases. background: Myocarditis is a severe disorder characterized by the inflammation of the heart muscular walls leading to the sudden death in young adults. Long non-coding RNA X-inacitve specific transcript (LncRNA XIST) are a class of transcripts having length ˃ 200 nts with absence of protein coding abilities. They exerts its function in apoptosis in various cancers and inflammation diseases. Objective: The current work intended to investigate the impact and mechanism of XIST on inflammation induced by LPS in AC16 cells. objective: The current work intended to investigate the impact and mechanism of XIST in in the inflammation induced by LPS in AC16 cells. Methods: An in vitro inflammatory injury model was established by stimulating AC16 cells with LPS. CCK-8 was used to test AC16 cell viability and FCM to detect apoptosis. The Elisa assay was used to measure the level of IL-8, IL-1β, and TNF-α. The RT-qPCR was used to detect XIST, miR-370-3p, Bax, and Bcl-2 in LPS-stimulated AC16 cells. The Elisa assay was performed to assess the phosphorylation of PI3K, AKT and mTOR in AC16 cells. method: An in vitro inflammatory injury model was established by stimulating AC16 cells with LPS. CCK-8 assay was employed to examine the AC16 cell viability while the cell apoptosis was detected by FCM assay. The level of IL-8, IL-1β, and TNF-α were assessed using Elisa assay. The expression of XIST, miR-370-3p and the mRNA expressions of Bax and Bcl-2 in AC16 cells stimulated with LPS were detected using RT-qPCR. Elisa assay was performed to assess the phosphorylation of PI3K, AKT and mTOR in AC16 cells. Results: Our findings showed LPS exposure to significantly reduce AC16 cell viability while increasing inflammation and apoptosis. Also, XIST expression was reduced in AC16 cells stimulated with LPS. Overexpression of XIST in AC16 cells increased cell survival, inhibited apoptosis, and increased the expressions of Bcl-2, Bax, and inflammatory modulators (IL-8, TNF-α, and IL-1β). Inhibiting XIST in AC16 cells produced opposite outcomes. MiR-370-3p mimics inhibited XIST's effect on inflammation, viability, and apoptosis. Moreover, XIST inhibited the phosphorylation levels of mTOR, AKT, and PI3K in LPS-injured AC16 cells. result: Our results indicated that exposure of LPS significantly decreased the AC16 cell viability while increased the inflammation and apoptosis in AC16 cells. Also, XIST expression was reduced in AC16 cells stimulated with LPS. Overexpression of XIST mitigated the injury induced by LPS in AC16 cells, proved by enhancing the cell viability, inhibiting apoptosis rate and levels of Bcl-2 and Bax and inflammatory modulators (IL-8, TNF-α, and IL-1β) in LPS-stimulated AC16 cells. Besides, opposite results were observed by the inhibition of XIST in AC16 cells. Furthermore, XIST negatively regulated miR-370-3p expression and the impact of XIST overexpression on the inflammation, viability and apoptosis was blocked by miR-370-3p mimic. Moreover, XIST inhibited the phosphorylation level of mTOR, AKT, and PI3K in LPS-injured AC16 cells. Conclusion: The data elucidate lncRNA XIST to exert its anti-inflammatory and anti-apoptotic effects on AC16 cells stimulated by LPS via down-regulating miR-370-3p and inhibiting PI3K/AKT/mTOR pathways. These findings suggest a novel treatment strategy for myocarditis. other: Not applicable

BACKGROUND Azilsartan medoxomil (AZL-M), an angiotensin II receptor blocker, has a well-characterized efficacy and safety profile in patients with hypertension. AZL-M is approved for use in over 40 countries globally; however, it is not yet approved in China. Therefore, a phase 3 registration study to assess the efficacy (antihypertensive effect), safety, and tolerability of AZL-M compared with valsartan in Chinese patients with essential hypertension was undertaken. METHODS This multicenter, double-blind, randomized, 8-week phase 3 study compared AZL-M with valsartan in Chinese patients aged ≥18 years with essential hypertension. Endpoints included change from baseline to week 8 in trough sitting clinic systolic blood pressure (scSBP) and ambulatory blood pressure monitoring parameters. RESULTS Overall, 612 patients (mean age, 57.1 years; 57.5% male) were randomized to AZL-M 80 mg (n = 209), AZL-M 40 mg (n = 199), or valsartan 160 mg (n = 204). Baseline mean scSBP was similar in all groups (157.9-158.5 mm Hg). The mean reduction in trough scSBP from baseline to week 8 was significantly greater with AZL-M 80 mg than with valsartan (-24.2 vs -20.6 mm Hg; P = .010), and noninferior with AZL-M 40 mg versus valsartan (-22.5 vs -20.6 mm Hg; P = .184). Mean reduction in 24-hour mean systolic blood pressure (n = 257) was significantly greater with both AZL-M 80 mg (-17.0 mm Hg; P

Currently, commercial semiconductor-based memories face the problem of static energy consumption caused by leakage currents. Magnetoelectric random access memory (MeRAM), as a type of nonvolatile memory, provides a solution to this problem and can be used to replace the entire memory hierarchy as a universal memory. In contrast to spin transfer torque RAM (STT-RAM), MeRAM uses voltage controlled magnetic anisotropy (VCMA) effect to manipulate the switching of magnetic tunnel junctions (MTJs). MeRAM or VCMA-MTJ technology is more energy efficient and less likely to break down than STT-RAM. However, VCMA-MTJ suffers from serious write problems caused by variations in the VCMA coefficient, the external in-plane magnetic field, and the CMOS process. In this paper, a compact and SPICE-compatible VCMA-MTJ model is proposed. Then, a self-adaptive write circuit is proposed in which the write process is robust to variations in the VCMA coefficient and the external in-plane magnetic field. Finally, two practical methods are proposed to make our proposed self-adaptive write circuit also robust to 3 $\sigma$ CMOS process variations, as demonstrated by Monte Carlo simulations. The proposed self-adaptive write circuit can assist in the design of next-generation high-speed, low-power MeRAM chips.

Since Internet of Things devices should ideally be self-powered, there is great demand for devices with ultra-low operating voltages that can run on energy harvested from a noisy environment. In this paper, a novel all spin logic (ASL) device with voltage controlled magnetic anisotropy (VCMA) effect amplified by negative capacitance (NC) is proposed for the first time. This novel device can operate at a working voltage as low as 1 mV. A three-step pulse scheme is also proposed. Based on simulations of the VCMA effect and the NC effect coupled with the spin modular approach, the feasibility of the proposed ASL device with a 1-mV working voltage and its immunity to variations in device parameters and supply voltage are analyzed.

The high current density required by magnetic tunneling junction (MTJ) switching driven by the spin transfer torque (STT) effect leads to large power consumption and severe reliability issues, hindering the timetable for STT magnetic random access memory to mass market. By utilizing the voltage-controlled magnetic anisotropy (VCMA) effect, the MTJ can be switched by the voltage effect and is postulated to achieve ultralow power (fJ). However, the VCMA coefficient measured in experiments cannot meet the requirement for MTJ with dimensions below 100 nm. And an external in-plane magnetic field usually is demanded for precessional VCMA switching. Here, in this paper, a novel approach for the amplification of the VCMA effect, which borrows ideas from negative capacitance, is proposed. The feasibility of the proposal is proved by physical simulation and in-depth analysis. Since the amplified VCMA effect, the external magnetic field can be eliminated. A three-terminal novel MTJ memory cell is designed with which both low power and high speed can be achieved.

The making use of 2-D material as transistor channel is a rapid growth field since it can provide enough gate controllability for transistors at scaling limit. Among all kinds of 2-D materials, monolayer MoS2 stands out because of its large intrinsic bandgap and moderate mobility at room temperature. Most of the simulation work assumes the source/drain contacts of monolayer MoS2 transistors are Ohmic type, while in experiment the Schottky barrier contacts are more frequently seen. In this paper, the performance of single layer MoS2 double gate transistors with Schottky barrier contacts is evaluated with nonequilibrium Green’s function method. The image force lowering effect, which is crucial for accurate simulation of Schottky barrier, is taken into account. The simulation results reveal that increasing doping concentration is the most effective way to adjust monolayer MoS2 transistor performance. Transistor performance with Schottky barrier contacts can be comparable and even outperforms those with Ohmic contacts. The dependence of subthreshold swing, drain-induced barrier lowering and intrinsic delay on Schottky barrier height, source/drain extension length, and doping concentration in source/drain extension region are also simulated and analyzed. The effect of phonon scattering on performance of monolayer MoS2 transistor with Schottky barrier contacts and Ohmic contacts is also presented.

In this work, a spin torque nano oscillator (STNO) device whose frequency can be tuned by Voltage Controlled Magnetic Anisotropy effect (VCMA) is proposed. The requirement of magnetic bias field in previous STNO devices is eliminated by the introduction of VCMA effect. Based on VCMA-STNO, a novel architecture is proposed which can compose of a modulation/demodulation digital frequency shift keying (DFSK) communication system. The proposed architecture utilizes VCMA-STNO as core devices and is much simpler comparing with its CMOS counterpart. The proposed VCMA-STNO modulation/demodulation architecture will help to design next generation spintronics DFSK communication system.

Curcumin, which is the effective component of turmeric (Curcuma longa), has previously been shown to exert potent antioxidant, antitumor and anti‑inflammatory activities in vitro and in vivo. However, the mechanism underlying the protective effects of curcumin against oxidative damage in endothelial cells remains unclear. The present study aimed to examine the effects of curcumin on hydrogen peroxide (H2O2)‑induced apoptosis and autophagy in EA.hy926 cells, and to determine the underlying molecular mechanism. Cultured EA.hy926 cells were treated with curcumin (5‑20 µmol/l) 4 h prior to and for 4 h during exposure to H2O2 (200 µmol/l). Oxidative stress resulted in a significant increase in the rate of cell apoptosis, which was accompanied by an increase in the expression levels of caspase‑3 and B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax), and a decrease in the expression levels of Bcl‑2. Treatment with curcumin (5 or 20 µmol/l) significantly inhibited apoptosis, and reversed the alterations in caspase‑3, Bcl‑2 and Bax expression. Furthermore, curcumin induced autophagy and microtubule‑associated protein 1A/1B‑light chain 3‑Ⅱ expression, and suppressed the phosphorylation of Akt and mammalian target of rapamycin (mTOR). These results indicated that curcumin may protect cells against oxidative stress‑induced damage through inhibiting apoptosis and inducing autophagy via the Akt/mTOR pathway.

In this paper, we propose an all spin logic device with voltage controlled magnetic anisotropy (VCMA-ASL) and employ negative capacitance (NC) effect as a novel approach to amplify the VCMA effect. A new working strategy of 3-step operation scheme has been proposed, which reduces the energy consumption effectively as well as accelerates switching process.

Blood lipid management is one of the effective strategies for coronary heart disease, and statins are the first-line lipid-lowering drugs. Low density lipoprotein cholesterol (LDL-C) drop brings about cardioprotective effects. Proprotein convertase subtilisin kexin type 9 (PCSK9) is known to increase LDL-C, thus hazarding LDL-C reduction-induced benefits. To date, how PCSK9 responds to various lipid-lowering strategies has not been fully clarified.This study involves patients with stable angina and aims to explore and clarify the short-term impacts of rosuvastatin and ezetimibe, alone or in combination, on circulating PCSK9. A total of 68 patients with stable angina were enrolled and 60 eligible patients were randomly assigned into 3 groups (20 subjects in each). Patients in different groups were treated for a period of 14 days with rosuvastatin 10 mg/d, ezetimibe 10 mg/d, and rosuvastatin 10 mg/d plus ezetimibe 10 mg/d, respectively. Concentrations of blood LDL-C and PCSK9 levels were measured at baseline and at the 14Both rosuvastatin and ezetimibe could reduce the LDL-C levels, and rosuvastatin displayed a stronger cholesterol-lowering effect than ezetimibe. Moreover, when combined, they yielded even greater efficacy in lowering LDL-C, as compared with either rosuvastatin or ezetimibe mono-treatment (P0.05). Rosuvastatin therapy (alone or combined with ezetimibe) caused significant rise in circulating PCSK9. Nevertheless, no significant growth of PCSK9 levels (P=0.558) was observed during ezetimibe treatment. At the 14Rosuvastatin plus ezetimibe therapy is more effective in reducing LDL-C levels as compared with either rosuvastatin or ezetimibe mono-medication. Meanwhile, such combination strategy does not further increase the levels of circulating PCSK9 compared to rosuvastatin mono-intervention, thus maintaining maximal clinical benefits from lipid-lowering.

Purpose: To evaluate the antiseptic effect of caffeoylquinic acid (CA) in in vivo and in vitro models.Methods: In vivo sepsis was produced in rats via cecal ligation and puncture (CLP) method. Four groups of rats were used: control group, untreated CLP group, and two CA groups treated with caffeoylquinic acid (50 and 100 mg/kg, p.o.) for 30 days before the induction of sepsis. Following the induction of sepsis, histological assessment of lung tissue was carried out using hematoxylin and eosin, and isolectin B4 staining. In addition, in vitro tests were performed on RAW264.7 cells in which inflammation and oxidative stress were induced by lipopolysaccharide (LPS).Results: Treatment with CA significantly (p < 0.05) enhanced the survival of lung cells, relative to the CLP group. Lung histopathology revealed that pretreatment with CA did not attenuate the increased infiltration of macrophages in the alveoli. Results from in vitro studies showed that CA attenuated LPS-induced nitric oxide (NO) levels, but had no significant effect on the level of LPS-induced pro-inflammatory cytokines in RAW264.7 cells (p < 0.05).Conclusion: These results reveal that CA attenuates NO and TNF-α levels in LPS-stimulated macrophages, thereby decreasing inflammation-associated sepsis. Thus, CA may have beneficial effects on lung injury as a result of its antioxidant and anti-inflammatory activities.Keywords: Caffeoylquinic acid, Sepsis, Oxidative stress, Cytokines, Cecalligation, Puncture

To investigate whether sodium tanshinone IIA silate (STS) as an add-on therapy to conventional treatment may provide additional benefits for patients with unstable angina pectoris (UAP) and is associated with changes in profiles of serum inflammatory factors.Eighty patients diagnosed with UAP were randomly divided into two groups for the 2-week treatment. The control group received conventional therapy, while the treatment group was given intravenous STS (0.06 mg in 250 mL, once daily) as an add-on therapy to the conventional medications. The therapeutic efficacy and changes in serum levels of several inflammatory cytokines, including monocyte chemotactic protein 1 (MCP-1), tumor necrosis factor alpha (TNF-α), peroxisome proliferator-activated receptor (PPAR-γ), and high-sensitivity C-reactive protein (hs-CRP) from baseline were determined and compared between the two group.The clinical symptoms of all patients in both groups were improved after treatment. The overall rate of effectiveness was 97.5% in the treatment group vs. 80.0% in the control group. Serum levels of MCP-1, TNF-α, and hs-CRP levels were significantly reduced in both groups (P0.01), whereas the reduction was greater in patients receiving additional STS (P0.05). PPAR-γ was significantly elevated in both groups (P0.01).STS in combination with conventional treatment may be associated with better outcomes in patients with UAP.