LIM domain only 7 negatively controls nonalcoholic steatohepatitis in the setting of hyperlipidemia.

BACKGROUND AND AIMS: Hyperlipidemia has been extensively recognized as a high-risk factor for NASH; however, clinical susceptibility to NASH is highly heterogeneous. The key controller(s) of NASH susceptibility in patients with hyperlipidemia has not yet been elucidated. Here, we aimed to reveal the key regulators of NASH in patients with hyperlipidemia and to explore its role and underlying mechanisms. APPROACH AND RESULTS: To identify the predominant suppressors of NASH in the setting of hyperlipidemia, we collected liver biopsy samples from patients with hyperlipidemia, with or without NASH, and performed RNA-sequencing analysis. Notably, decreased Lineage specific Interacting Motif domain only 7 (LMO7) expression robustly correlated with the occurrence and severity of NASH. Although overexpression of LMO7 effectively blocked hepatic lipid accumulation and inflammation, LMO7 deficiency in hepatocytes greatly exacerbated diet-induced NASH progression. Mechanistically, lysine 48 (K48)-linked ubiquitin-mediated proteasomal degradation of tripartite motif-containing 47 (TRIM47) and subsequent inactivation of the c-Jun N-terminal kinase (JNK)/p38 mitogen-activated protein kinase (MAPK) cascade are required for the protective function of LMO7 in NASH. CONCLUSIONS: These findings provide proof-of-concept evidence supporting LMO7 as a robust suppressor of NASH in the context of hyperlipidemia, indicating that targeting the LMO7-TRIM47 axis is a promising therapeutic strategy for NASH.

UGCG modulates heart hypertrophy through B4GalT5-mediated mitochondrial oxidative stress and the ERK signaling pathway.

Mechanical pressure overload and other stimuli often contribute to heart hypertrophy, a significant factor in the induction of heart failure. The UDP-glucose ceramide glycosyltransferase (UGCG) enzyme plays a crucial role in the metabolism of sphingolipids through the production of glucosylceramide. However, its role in heart hypertrophy remains unknown. In this study, UGCG was induced in response to pressure overload in vivo and phenylephrine stimulation in vitro. Additionally, UGCG downregulation ameliorated cardiomyocyte hypertrophy, improved cardiomyocyte mitochondrial oxidative stress, and reduced the ERK signaling pathway. Conversely, UGCG overexpression in cardiomyocytes promoted heart hypertrophy development, aggravated mitochondrial oxidative stress, and stimulated ERK signaling. Furthermore, the interaction between beta-1,4-galactosyltransferase 5 (B4GalT5), which catalyses the synthesis of lactosylceramide, and UGCG was identified, which also functions as a synergistic molecule of UGCG. Notably, limiting the expression of B4GalT5 impaired the capacity of UGCG to promote myocardial hypertrophy, suggesting that B4GalT5 acts as an intermediary for UGCG. Overall, this study highlights the potential of UGCG as a modulator of heart hypertrophy, rendering it a potential target for combating heart hypertrophy.

ING5 overexpression upregulates miR-34c-5p/Snail1 to inhibit EMT and invasion of lung cancer cells.

ING5 belongs to the inhibitor of growth (ING) candidate tumor suppressor family, which is involved in multiple cellular functions, such as cell cycle regulation, apoptosis, and chromatin remodelling. Previously, we reported that ING5 overexpression inhibits EMT by regulating EMT-related molecules, including Snail1, at the mRNA and protein levels. However, the mechanisms remain unclear. In the current study, we identify that ING5 overexpression induces the upregulation of miR-34c-5p. The expression levels of both ING5 and miR-34c-5p in NSCLC tissues from the TCGA database are decreased compared with that in adjacent tissues. Higher expression levels of both ING5 and miR-34c-5p predict longer overall survival (OS). Snail1 is the target gene of miR-34c-5p, as predicted by an online database, which is further verified by a dual-luciferase reporter assay. The expression level of Snail1 in NSCLC cells is markedly reduced following miR-34c-5p overexpression, leading to the inactivation of the Snail1 downstream TGF-ß/Smad3 signaling pathway. The TGF-ß signaling-specific inhibitor LY2157299 reverses the enhanced EMT, proliferation, migration, and invasion abilities induced by the miR-34c-5p inhibitor. Furthermore, tail vein injection of miR-34c-5p agomir inhibits xenografted tumor metastasis. Overall, this study concludes that miR-34c-5p, induced by ING5 overexpression, is a tumor suppressor that targets Snail1 and mediates the inhibitory effects of ING5 on the EMT and invasion of NSCLC cells. These results provide a novel mechanism mediating the antitumor effects of ING5.

Integrating a Nanowire Laser in an on-Chip Photonic Waveguide.

We report a simple and facile integration strategy of a laser source in passive photonic integrated circuits (PICs) by deterministically embedding semiconductor nanowires (NWs) in waveguides. InP NWs laid on a SiN slab are buried by a polymer layer which also acts as an electron-beam resist. With electron-beam lithography, hybrid polymer-SiN waveguides are formed with precisely embedded NWs. The lasing behavior of the waveguide-embedded NWs is confirmed, and more importantly, the NW lasing mode couples into the hybrid waveguide and forms an in-plane guiding mode. Multiple waveguide-embedded NW lasers are further integrated in complex photonic structures to illustrate that the waveguiding mode supplied by the NW lasers could be manipulated for on-chip signal processing, including power splitting and wavelength-division multiplexing. This integration strategy of an on-chip laser is applicable to other PIC platforms, such as silicon and lithium niobate, and the top cladding layer could be changed by depositing SiN or SiO2, promising its CMOS compatibility.

FGF5 protects heart from sepsis injury by attenuating cardiomyocyte pyroptosis through inhibiting CaMKII/NFκB signaling.

Sepsis accompanied by myocardial injury is an important cause of multiple organ dysfunction, and its underlying molecular mechanism is not fully clear. Although diverse effects of fibroblast growth factor (FGF) in heart have been discovered till now, the specific role of FGF5 in heart remains unclear. Therefore, our study aims to explore the possible impacts of FGF5 on sepsis-induced cardiac injury. Sepsis-induced cardiac injury was established through administration of lipopolysaccharide (LPS). The expression level of FGF5 in sepsis heart was decreased, and injection of FGF5-overexpressing adenovirus attenuated cardiac injury reflected by echocardiographic and pathological findings. Besides, FGF5 overexpression, not only in vivo heart but also in vitro cardiomyocytes, reduced the levels of oxidative stress and pyroptosis resulted from LPS. In addition, overexpression of FGF5 reduced LPS-activated the levels of phosphorylated CaMKII (p-CaMKII), p-NFκB, NLRP3, caspase-1, IL-1ß and IL-18. Furthermore, KN93, the inhibitor of CaMKII, exerted the similarly protective effects on LPS-induced pyroptosis. In summary, our study implied the beneficial effects of FGF5 on LPS-induced cardiac injury, which was at least partially attributed to the inhibition of CaMKII-mediated pyroptotic signaling.

Propagation characteristics of terahertz wave in inductively coupled plasma.

Firstly, the electron density distribution of inductively coupled plasma (ICP) is measured by laser Thomson scattering (TS) method and the features of the ICP under the same experimental conditions are simulated by finite element method (FEM). The simulated results are in good agreement with the experimental results, which verifies the accuracy of the ICP generation simulation model. Secondly, the propagation characteristics of terahertz wave in ICP are measured by terahertz time domain spectroscopy (THz-TDS) and calculated by FEM according to the electron density distribution of ICP simulated in the first step above. The high consistency between the experimental and simulation results of terahertz wave propagation characteristics in ICP further proves the accuracy of terahertz wave transmission model in plasma and the feasibility of joint simulation with ICP generation simulation model.

Coptisine Attenuates Diabetes-Associated Endothelial Dysfunction through Inhibition of Endoplasmic Reticulum Stress and Oxidative Stress.

Coptisine is the major bioactive protoberberine alkaloid found in Rhizoma Coptidis. Coptisine reduces inflammatory responses and improves glucose tolerance; nevertheless, whether coptisine has vasoprotective effect in diabetes is not fully characterized. Conduit arteries including aortas and carotid arteries were obtained from male C57BL/6J mice for ex vivo treatment with risk factors (high glucose or tunicamycin) and coptisine. Some arterial rings were obtained from diabetic mice, which were induced by high-fat diet (45% kcal% fat) feeding for 6 weeks combined with a low-dose intraperitoneal injection of streptozotocin (120 mg/kg). Functional studies showed that coptisine protected endothelium-dependent relaxation in aortas against risk factors and from diabetic mice. Coptisine increased phosphorylations of AMPK and eNOS and downregulated the endoplasmic reticulum (ER) stress markers as determined by Western blotting. Coptisine elevates NO bioavailability and decreases reactive oxygen species level. The results indicate that coptisine improves vascular function in diabetes through suppression of ER stress and oxidative stress, implying the therapeutic potential of coptisine to treat diabetic vasculopathy.

A long-acting isomer of Ac-SDKP attenuates pulmonary fibrosis through SRPK1-mediated PI3K/AKT and Smad2 pathway inhibition.

Idiopathic pulmonary fibrosis (IPF) is a progressive, life-threatening lung disease with a poor prognosis. N-acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a critical negative regulator of fibrosis development. However, it's extremely short half-life greatly limits its applications. Previously, we reported an Ac-SDKP analog peptide in which Asp and Lys residues were replaced with D-amino acids (Ac-SDD KD P). Ac-SDD KD P exhibits better resistance to angiotensin-1-converting enzyme (ACE)-mediated degradation and a longer half-life than Ac-SDKP in rat and human sera. The objective of this study was to explore the potential application of Ac-SDD KD P for the treatment of IPF and to clarify the underlying mechanisms. We found that Ac-SDD KD P exerted similar antifibrotic effects as Ac-SDKP on human fetal lung fibroblast-1 (HFL-1) proliferation, α-smooth muscle actin (α-SMA), collagen I and collagen III expression, and Smad-2 phosphorylation in vitro. In vivo, Ac-SDD KD P exhibited significantly greater protective effects against bleomycin-induced pulmonary fibrosis than Ac-SDKP in mice. α-SMA, CD45, collagen I and collagen III expression, and Smad-2 phosphorylation were significantly decreased in the lungs of Ac-SDD KD P-treated but not Ac-SDKP-treated mice. Furthermore, a pull-down experiment was used to screen for molecules that interact with Ac-SDKP. Co-immunoprecipitation (Co-IP) and computer-based molecular docking experiments demonstrated an interaction between Ac-SDKP or Ac-SDD KD P (Ac-SDKP/Ac-SDD KD P) and serine/arginine-rich protein-specific kinase 1 (SRPK1) that caused inhibition SRPK1-mediated phosphatidylinositol-3 kinase/ serine/threonine kinase (PIK3/AKT) signaling pathway activation and Smad2 phosphorylation and thereby attenuated lung fibrosis. Our data suggest that long-acting Ac-SDD KD P may potentially be an effective drug for the treatment of pulmonary fibrosis. The interacting molecule and antifibrotic mechanism of Ac-SDKP/Ac-SDD KD P were also identified, providing an experimental and theoretical foundation for the clinical application of the drug.

d-amino acid modification protects N-Acetyl-seryl-aspartyl-lysyl-proline from physiological hydroxylation and increases its antifibrotic effects on hepatic fibrosis.

N-Acetyl-seryl-aspartyl-lysyl-proline (Ac-SDKP) is a critical negative regulator of fibrosis development in the liver. However, its extremely short half-life in vivo greatly compromises its potential applications. Here, we report an Ac-SDKP analog peptide with d-amino acid replacement (Ac-SDD KD P). The stability of Ac-SDD KD P and its prevention of liver fibrosis were investigated in vitro and in vivo. The stabilities of Ac-SDKP and Ac-SDD KD P exposed to angiotensin-1-converting enzyme (ACE) and their half-lives in rats and human sera were determined by high-performance liquid chromatography. The inhibitory effects of Ac-SDKP and Ac-SDD KD P on the proliferation and activation of hepatic stellate cells (HSC-T6) were evaluated using the Cell Counting Kit-8, Western blotting, reverse transcription quantitative polymerase chain reaction, and immunofluorescence assays. Finally, the protective effects of Ac-SDKP and Ac-SDD KD P on carbon tetrachloride (CCl4 )-induced liver fibrosis in rats were compared. d-Amino acid replacement significantly enhanced the stability of the peptide to ACE and prolonged the half-life of Ac-SDKP in rats and human sera. The Ac-SDKP-mediated inhibition of HSC-T6 cell proliferation was well preserved, and Ac-SDD KD P exerted inhibitory effects comparable to Ac-SDKP on α-smooth muscle actin (α-SMA), collagen I and III expression, and phosphorylated-Smad-2 expression. After intraperitoneal (i.p.) administration, Ac-SDD KD P exhibited significantly greater protection than Ac-SDKP against CCl4 -induced liver fibrosis in rats. The serum alanine aminotransferase, aspartate aminotransferase, albumin, and total protein levels of the Ac-SDD KD P-treated rats were significantly lower than those of the Ac-SDKP-treated rats. α-SMA, CD45, and collagen I and III expression, as well as Smad-2 phosphorylation were significantly attenuated in the livers of the Ac-SDD KD P-treated rats compared to those of the Ac-SDKP-treated rats. Furthermore, we showed that the Ac-SDD KD P concentration in the rat liver increased to a physiological level of 60 min after i.p. administration, although i.p. administration of Ac-SDKP failed to enhance the peptide concentration in the rat liver. Our findings indicate that d-amino acid replacement is a simple and effective method to enhance the stability of Ac-SDKP. Ac-SDD KD P represents potential application of Ac-SDKP in fibrosis treatment and provides a new potential treatment strategy for liver fibrosis. © 2019 IUBMB Life, 71(9):1302-1312, 2019.

Self-Assembly Growth of In-Rich InGaAs Core-Shell Structured Nanowires with Remarkable Near-Infrared Photoresponsivity.

Understanding the compositional distribution of ternary nanowires is essential to build the connection between nanowire structures and their potential applications. In this study, we grew epitaxial ternary InGaAs nanowires with high In concentration on GaAs {111}B substrates. Our detailed electron microscopy characterizations suggest that the grown ternary InGaAs nanowires have an extraordinary core-shell structure with In-rich cores and Ga-enriched shells, in which both nanowire cores and shells showed compositional gradient. It was found that In-rich nanowire cores are formed due to the Ga-limited growth environment, caused by the competition with the spontaneous InGaAs planar layer growth on the substrate that consumes more Ga than the nominal Ga concentration during the growth. Moreover, the composition gradient in the nanowires cores and shells is a result of strain relaxation between them. Our optoelectronic property measurements from prototype nanowire devices show a remarkable photoresponsivity under the near-infrared illumination. This study provides a new approach for designing and realizing complex nanowire heterostructures for high-efficiency nanowire-based systems and devices.

Visible Light-Assisted High-Performance Mid-Infrared Photodetectors Based on Single InAs Nanowire.

One-dimensional InAs nanowires (NWs) have been widely researched in recent years. Features of high mobility and narrow bandgap reveal its great potential of optoelectronic applications. However, most reported work about InAs NW-based photodetectors is limited to the visible waveband. Although some work shows certain response for near-infrared light, the problems of large dark current and small light on/off ratio are unsolved, thus significantly restricting the detectivity. Here in this work, a novel "visible light-assisted dark-current suppressing method" is proposed for the first time to reduce the dark current and enhance the infrared photodetection of single InAs NW photodetectors. This method effectively increases the barrier height of the metal-semiconductor contact, thus significantly making the device a metal-semiconductor-metal (MSM) photodiode. These MSM photodiodes demonstrate broadband detection from less than 1 µm to more than 3 µm and a fast response of tens of microseconds. A high detectivity of ∼1012 Jones has been achieved for the wavelength of 2000 nm at a low bias voltage of 0.1 V with corresponding responsivity of as much as 40 A/W. Even for the incident wavelength of 3113 nm, a detectivity of ∼1010 Jones and a responsivity of 0.6 A/W have been obtained. Our work has achieved an extended detection waveband for single InAs NW photodetector from visible and near-infrared to mid-infrared. The excellent performance for infrared detection demonstrated the great potential of narrow bandgap NWs for future infrared optoelectronic applications.

Paris Saponin VII Inhibits the Migration and Invasion in Human A549 Lung Cancer Cells.

Metastasis is the main cause of death in lung cancer. Targeting the process of metastasis is a strategy to lung cancer treatment. Trillium tschonoskii Maxim., a traditional Chinese medicine, has been used for treatment of many diseases, including cancer. This study aims to determine the anti-metastatic effect of paris saponin VII (PS VII) which was extracted from T. tschonoskii Maxim. by using human lung cancer cell line A549 cells. Our results showed that PS VII could significantly suppress the viability as well as cell migration and invasion abilities of A549 cells in a concentration-dependent manner. PS VII reduced the activity of matrix metalloproteinase-2 (MMP-2) and MMP-9 by elevating the expression of TIMP1/2. These data indicated that PS VII could reduce the metastatic capability of A549 cells, probably through up-regulating the expression of TIMP1/2. These findings demonstrated a new therapeutic potential for PS VII in anti-metastatic therapy of lung cancer. Copyright © 2015 John Wiley & Sons, Ltd.

Experimental study on mechanical and hydraulic properties of xanthan gum improved low liquid limit silty soil.

The low liquid limit silty soil in the North China plain area is generally unsuitable for direct use as roadbed and slope soil. In order to improve the performance of low liquid limit silty soil, xanthan gum was used as an improver. Through a series of tests, the improvement effect of xanthan gum on low liquid limit silty soil was studied. The test results showed that Xanthan gum as an improver could significantly improve the unconfined compressive strength of silty soil. With the increase in dosage and curing age, the unconfined compressive strength of improved silty soil continued to improve and eventually tended to stabilize. The optimal dosage and curing period were 2% and 7 days, respectively. In addition, Xanthan gum could greatly improve the permeability and disintegration of low liquid limit silty soil. The permeability coefficient of improved silty soil with a content of 0.75% Xanthan gum and a 7-day curing period was 4.73 × 10-4 m·s-1, which was only 1.10% of that of plain silty soil at the same curing period. After immersion in water for 12 h, the soil only experienced slight disintegration. The scanning electron microscope image showed that the gel generated by the hydration reaction of Xanthan gum could improve the compactness and integrity of the soil by filling the voids, thus significantly improving the mechanical and hydraulic properties of the low liquid limit silty soil.

Experimental study on direct tensile fatigue performance of basalt fiber reinforced concrete.

Conducting research on the fatigue performance of concrete materials is of great significance for the anti fatigue design of concrete structures. Currently, indirect tensile or compressive strength tests are commonly used to study the fatigue performance of basalt fiber reinforced concrete, but there is little research on its fatigue performance under direct tensile conditions. Using a fatigue testing machine and a self-developed concrete axial tensile device, direct tensile fatigue tests of basalt fiber reinforced concrete were conducted under different fiber content and stress levels. Based on fatigue test data, the entire fatigue tensile process of basalt fiber reinforced concrete was analyzed, and the effects of fiber content and stress level on the fatigue life of concrete specimens were explored. Strain fatigue life curves of concrete with different fiber content were plotted. The experimental results indicate that the failure mode of basalt fiber reinforced concrete under cyclic loading is brittle failure; with the increase of basalt fiber content, the fatigue life of concrete first increases and then decreases. When the fiber content is 0.3%, the fatigue life of basalt fiber concrete is the highest compared to the benchmark concrete. When the fiber content is the same, the fatigue life of concrete decreases with the increase of stress level. The fatigue deformation process of basalt fiber reinforced concrete can be divided into three stages: the stage of fast strain growth, the stage of uniform strain growth, and the stage of rapid strain growth.

Step by step and combined supporting technique with allowable deformation + limiting shape for soft rock roadway.

Aiming at the difficult problems of the large deformation in weakly cemented soft rock roadways, the reasons of large deformation are analyzed for roadways in Hongqingliang coal mine. On this basis, the principle of step by step combined support technology based on allowable deformation + limiting shape for weakly cemented soft rock roadway is proposed, and the optimal support parameters of step by step combined technology are determined by FLAC3D. Step by step combined support technology includes the primary support of anchor bolt + anchor cable + initial shotcrete and the secondary support of U-shaped steel shed + filling flexible material behind shed + control of key parts. The comparative analysis on the site shows that the deformation rate and final deformation amount of the surrounding rock after the step by step combined support are less than those of the primary support, and the deformation of the surrounding rock can be controlled effectively after the secondary support is added. Step by step combined support is superior to the traditional bolt + anchor cable combined repair in terms of economy and efficiency. The optimal construction period of each working procedure of the step by step combined technology is 28 days after the completion of the first support, and the step by step combined support based on allowable deformation + limiting shape is an effective way to control the surrounding rock of soft rock roadway.

Calculation method and evaluation of surrounding rock pressure of vertical shaft.

The surrounding rock pressure of vertical shafts is one of the basic parameters of shaft lining design. Investigating its calculation methods and applicable scopes has great engineering significance. The paper classifies and compares the calculation methods, discusses the application scopes of various calculation methods, and proposes that the axisymmetric layered method is highly consistent with the field monitoring data for the calculation of surrounding rock pressure of vertical shafts in bedrock sections on the basis of practical engineering examples. On the basis of Terzaghi theory, the calculation formula of surrounding rock pressure of vertical shaft in inclined rock strata with single group joints is derived. The formula can reflect the influence of rock strata dip angle and joints.

Dexmedetomidine mitigates lipopolysaccharide-induced acute lung injury by modulating heat shock protein A12B to inhibit the toll-like receptor 4/nuclear factor-kappa B signaling pathway.

Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS): Life-threatening medical conditions characterized by high morbidity and mortality rates, where the inflammatory process plays a crucial role in lung tissue damage, especially in models induced by lipopolysaccharide (LPS). Heat shock protein A12B (HSPA12B) has strong anti-infammatory properties However, it is unknown whether increased HSPA12B is protective against LPS-induced ALI. And Dexmedetomidine (DEX) is a potent α2-adrenergic receptor (α2-AR) agonist that has been shown to protect against sepsis-induced lung injury, however, the underlying mechanisms of this protection are not fully understood. This study utilized bioinformatics analysis and an LPS-induced ALI model to explore how DEX alleviates lung injury by modulating HSPA12B and inhibiting the Toll-like receptor 4/nuclear factor-kappa B (TLR4/NF-κB) signaling pathway. Results indicate that HSPA12B overexpression and DEX pre-treatment markedly mitigated LPS-induced lung injury, which was evaluated by the deterioration of histopathology, histologic scores, the W/D weight ratio, and total protein expression, tumor necrosis factor-alpha (TNF-α), and interleukin-1ß (IL-1ß) in the BALF, and the levels of NO, MDA,SOD and MPO in the lung. Moreover, HSPA12B overexpression and DEX pre-treatment significantly reduces lung injury and inflammation levels by upregulating HSPA12B and inhibiting the activation of the TLR4/NF-κB signaling pathway. On the contrary, when the expression of HSPA12B is inhibited, the protective effect of DEX pre-treatment on lung tissue is significantly weakened.In summary, our research demonstrated that the increased expression of AAV-mediated HSPA12B in the lungs of mice inhibits acute inflammation and suppresses the activation of TLR4/NF-κB pathway in a murine model of LPS-induced ALI. DEX could enhance HSPA12B and inhibit the initiation and development of inflammation through down-regulating TLR4/NF-κB pathway.These findings highlight the potential of DEX as a therapeutic agent for treating ALI and ARDS, offering new strategies for clinical intervention.

3,4',5-Trimethoxy-trans-stilbene ameliorates hepatic insulin resistance and oxidative stress in diabetic obese mice through insulin and Nrf2 signaling pathways.

Resveratrol has profound benefits against diabetes. However, whether its methylated derivative 3,4',5-trimethoxy-trans-stilbene (3,4',5-TMS) also plays a protective role in glucose metabolism is not characterized. We aimed to study the anti-diabetic effects of 3,4',5-TMS in vitro and in vivo. Insulin-resistant HepG2 cells (IR-HepG2) were induced by high glucose plus dexamethasone whilst six-week-old male C57BL/6J mice received a 60 kcal% fat diet for 14 weeks to establish an obese diabetic model. 3,4',5-TMS did not reduce the cell viability of IR-HepG2 cells at concentrations of 0.5 and 1 µM, which enhanced the capability of glycogen synthesis and glucose consumption in IR-HepG2 cells. Four-week oral administration of 3,4',5-TMS at 10 mg kg-1 day-1 ameliorated insulin sensitivity and glucose tolerance of diet-induced obese (DIO) mice. 3,4',5-TMS activated the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) pathway by inhibiting phosphorylation of insulin receptor substrate (IRS)-1 at Ser307 and increasing the protein levels of IRS-1 and IRS-2 to restore the insulin signaling pathway in diabetes. 3,4',5-TMS also upregulated the phosphorylation of glycogen synthase kinase 3 beta (GSK3ß) at Ser9. 3,4',5-TMS suppressed oxidative stress by increasing the protein levels of nuclear factor erythroid 2-related factor 2 (Nrf2), heme oxygenase-1 (HO-1) and NAD(P)H : quinone oxidoreductase 1 (NQO1) and antioxidant enzyme activity. In summary, 3,4',5-TMS alleviated hepatic insulin resistance in vitro and in vivo, by the activation of the insulin signaling pathway, accomplished by the suppression of oxidative stress.

Excitation of Terahertz Spoof Surface Plasmons on a Roofed Metallic Grating by an Electron Beam.

In this paper, both fundamental SSP modes on a roofed metallic grating and its effective excitation of the bounded SSP mode by an injected electron beam on the structure are numerically examined and investigated in the THz regime. Apart from the bounded SSP mode on the metallic grating with open space, the introduced roofed metallic grating can generate a closed waveguide mode that occupies the dispersion region outside the light line. The closed waveguide mode shifts gradually to a higher frequency band with a decreased gap size, while the bounded SSP mode line becomes lower. The effective excitation of the bounded SSP mode on this roofed metallic grating is also implemented and studied by using a particle-in-cell simulation studio. The output SSP power spectrums with various gap sizes by the same electron beam on this roofed metallic grating are obtained and analyzed. The simulation results reveal that the generated SSP spectra show a slight red shift with a decreased gap size. This work on the excitation of the SSP mode using an electron beam can benefit the development of high-power compact THz radiation sources by utilizing the strong near-field confinement of SSPs on metallic gratings.