Ultra-compact on-chip meta-waveguide phase modulator based on split ring magnetic resonance.

With the development of photonic integration technology, meta-waveguides have become a new research hotspot. They have broken through the theoretical diffraction limit by virtue of the strong electromagnetic manipulation ability of the metasurface and the strong electromagnetic field limitation and guidance ability of the waveguide. However, the reported meta-waveguides lack research on dynamic modulation. Therefore, we analyze the modulation effect of the metasurface on the optical field in the waveguide and design an ultra-compact on-chip meta-waveguide phase modulator using split ring magnetic resonance. It has a very short modulation length of only 3.65 µm, wide modulation bandwidth of 116.8 GHz, and low energy consumption of 263.49 fJ/bit. By optimizing the structure, the energy consumption can be further reduced to 90.69 fJ/bit. Meta-waveguides provide a promising method for the design of integrated photonic devices.

Ultrafast metamaterial all-optical switching based on coherent modulation.

We report a demonstration of an ultrafast all-optical switching with unique light control effects. The all-optical switching consists of a gold film with asymmetric split rings and a silica substrate. The device effectively controls the transmission and absorption of continuous pulses in the communication band (1200-1800 nm) and short pulses with a pulse duration of 80 fs by using the interaction of two coherent beams on nano-metamaterials with a thickness of only 50 nm. The metamaterial can achieve more than 90 % output control under continuous light irradiation. When the pulse duration is 80 fs, the switching contrast ratio is greater than 3 : 1 and the modulation bandwidth is greater than 12.5 THz. Switching time can be on the order of femtosecond. This paper provides a new structure for ultra-high speed optical data processing components in coherent networks.

Multifunctional analysis and verification of lightning-type electromagnetic metasurfaces.

Aiming at the problems that most of the existing electromagnetic metasurfaces have single function and narrow application scope, a highly integrated lightning-type metasurface is proposed in this study. It can realize the functions of circular dichroism (CD), absorption of electromagnetic waves, broadband x-to-y cross polarization conversion (CPC) function, linear-to-circular polarization conversion (LTC-PC) function and asymmetric transmission (AT), and its functions are also analyzed and verified. The designed metasurface consists of the bottom grating structure, the lower SiO2, the middle lightning-type graphene, the upper SiO2, the top graphene and photosensitive silicon. Through numerical calculations, the CD of design can reach more than 85% at 4.22 THz. The function of bimodal absorption is achieved at 4.09 and 8.69 THz. At 7.41∼8.21 THz, the polarization conversion ratio (PCR) of the metasurface reaches more than 99%. Simultaneously, the function of LTC-PC can be formed when PCR is 50%. Finally, when the designed metasurface is in the transmissive state, the AT of design is close to 60% at 7.84 THz. This design provides a new design idea and method for biomedical detection, image processing, modulators, smart switches, optical diodes and other fields.

Rutin alleviates EndMT by restoring autophagy through inhibiting HDAC1 via PI3K/AKT/mTOR pathway in diabetic kidney disease.

BACKGROUND: Diabetic kidney disease (DKD) is a primary microvascular complication of diabetes. However, a complete cure for DKD has not yet been found. Although there is evidence that Rutin can delay the onset of DKD, the underlying mechanism remains unclear. PURPOSE: To investigate the renoprotective effect of Rutin in the process of DKD and to explore its potential molecular mechanisms. METHODS: Db/db mice and high glucose (HG)-induced human renal glomerular endothelial cells (GEnCs) were used as in vivo and in vitro models, respectively. Western blot (WB), Immunohistochemistry (IHC)and Immunofluorescence (IF) staining were used to identify the expression level of proteins associated with endothelial-to-mesenchymal transition (EndMT) and autophagy. Tandem Mass Tag (TMT)-based proteomics analysis was utilized to reveal the mechanism of Rutin in DKD. Transfection with small interfering RNA (siRNA) to reveal the role of histone deacetylase 1 (HDAC1) in HG-induced GEnCs. RESULTS: Following 8 weeks of Rutin administration, db/db mice's kidney function and structure significantly improved. In HG-induced GEnCs, activation of autophagy attenuates cellular EndMT. Rutin could alleviate EndMT and restore autophagy in vivo and in vitro models. Proteomics analysis results showed that HDAC1 significantly downregulated in the 200 mg/kg/d Rutin group compared with the db/db group. Transfection with si-HDAC1 in GEnCs partially blocked HG-induced EndMT and restored autophagy. Furthermore, Rutin inhibits the phosphorylation of the PI3K / AKT/ mTOR pathway. HDAC1 overexpression was suppressed in HG-induced GEnCs after using Rapamycin, a specific mTOR inhibitor, verifying the correlation between mTOR and HDAC1. CONCLUSION: Rutin alleviates EndMT by restoring autophagy through inhibiting HDAC1 via the PI3K/AKT/mTOR pathway in DKD.

Astragaloside IV Improves the Barrier Damage in Diabetic Glomerular Endothelial Cells Stimulated by High Glucose and High Insulin.

Objective: To investigate the protective effect and mechanism of astragaloside IV (AS-IV) on damage in human glomerular endothelial cells (GEnCs) stimulated by high glucose and high insulin. Methods: The transwell method was used to detect the integrity of the cell barrier after AS-IV intervention in a high glucose and high insulin environment for 24 h; immunofluorescence and Western blot methods were used to detect the tight junction protein ZO-1 and claudin-5 expression; intracellular and extracellular 1ß (IL-1ß) and tumor necrosis factor α (TNFα) were determined by ELISA; expression and activation of AKT, p-AKT, GSK3α/ß, and p-GSK3α/ß were evaluated by Western blot. Results: The results showed that AS-IV had a significant protective effect on the cell barrier of GEnCs. High glucose or insulin inhibited cell viability in a concentration-dependent manner. High glucose or insulin significantly inhibited glucose uptake and promoted release of reactive oxygen species in GEnCs. Administration with AS-IV dramatically preserved viability of the cells; moreover, the expression of intracellular tight junction proteins was upregulated, inflammatory cytokines including IL-1ß and TNFα were decreased, and the AKT-GSK3 pathway participated in modulation of AS-IV in GEnCs cells. Conclusion: We found in the present study that AS-IV can preserve filtration barrier integrity in glomerular endothelial cells under diabetic settings, its effects on increasing the cell energy metabolism and cell viability, inhibiting inflammation and oxidative stress damage, and enhancing tight junction between cells play a role in it; and the intracellular signaling pathway AKT-GSK modulated the above function. Our present finding supplied a new understanding towards development of DN and provided an alternative method on ameliorating DN.

Ginsenoside Rg1 attenuates high glucose-induced endothelial barrier dysfunction in human umbilical vein endothelial cells by protecting the endothelial glycocalyx.

Disruption of the endothelial barrier is essential for vascular complications associated with diabetes mellitus, and damage to the endothelial glycocalyx has been demonstrated to participate in this process. Ginsenoside Rg1 (Rg1), the major active component isolated from Panax notoginseng, is widely applied for the protection against vascular injury. The present study aimed to analyze the effect of high glucose on endothelial barrier function and its association with endothelial glycocalyx in human umbilical vein endothelial cells (HUVECs), and explore the potential benefits of Rg1 in protecting endothelial barrier function from high glucose-induced injury. The results indicated that high glucose induced a disorder of the endothelial glycocalyx and increased heparanase mRNA expression in HUVECs, which was reversed by Rg1 treatment. In addition, Rg1 treatment reduced transendothelial electrical resistance and transendothelial albumin passage after high-glucose stimulation. The present study suggested that high glucose caused a disruption in the endothelial glycocalyx and increased heparanase expression, which finally resulted in endothelial barrier dysfunction in HUVECs. Of note, Rg1 has a protective effect on high glucose-induced endothelial barrier dysfunction by attenuating the associated increase in heparanase expression.

Irisin Alleviates Advanced Glycation End Products-Induced Inflammation and Endothelial Dysfunction via Inhibiting ROS-NLRP3 Inflammasome Signaling.

The activation of NLR family pyrin domain containing 3 (NLRP3) inflammasome have been implicated in the initiation or progression of atherosclerosis. Recent research showed that irisin, a newly discovered adipomiokine, alleviates endothelial dysfunction in type 2 diabetes partially via reducing oxidative/nitrative stresses, suggesting that irisin may be a promising candidate for the treatment of vascular complications of diabetes. However, the association between irisin and NLRP3 inflammasome in the pathogenesis of atherosclerosis remains unclear. In the present study, we cultured human umbilical vein endothelial cells (HUVECs) in advanced glycation end products (AGEs) medium; exogenous irisin (0.01, 0.1, 1 µg/ml) were used as an intervention reagent. siRNA and adenoviral vector were constructed to realize silencing and over-expression of NLRP3 gene. Our data showed that irisin significantly reversed AGEs-induced oxidative stress and NLRP3 inflammasome signaling activation (p < 0.05), and increased the endothelial nitric oxide synthase (eNOS) and nitric oxide (NO) production in a dose-dependent manner (p < 0.05). siRNA-mediated knockdown NLRP3 facilitated the irisin-mediated anti-inflammatory and antiatherogenic effects (p < 0.05). However, these irisin-mediated effects were reversed by over-expression NLRP3 (p < 0.05). Taken together, our results reveal that irisin alleviates AGEs-induced inflammation and endothelial dysfunction via inhibiting ROS-NLRP3 inflammasome signaling, suggest a likely mechanism for irisin-induced therapeutic effect in vascular complications of diabetes.

Short-Chain Fatty Acids Inhibit Oxidative Stress and Inflammation in Mesangial Cells Induced by High Glucose and Lipopolysaccharide.

Recently, an connection between Short-chain fatty acids (SCFAs) produced by intestinal microbiota and kidney has been revealed. The aim of this study was to explore whether SCFAs or their specific G protein-coupled receptors 43 (GPR43) agonist inhibit oxidative stress and inflammatory response in glomerular mesangial cells (GMCs) induced by high glucose and lipopolysaccharide (LPS). Our research showed that treatment with SCFAs, especially acetate and butyrate, or GPR43 agonist significantly inhibited GMCs proliferation induced by high glucose and LPS, and then reversed the production of reactive oxygen species (ROS) and malondialdehyde (MDA) but increased levels of antioxidant enzyme superoxide dismutase (SOD). Furthermore, SCFAs or GPR43 agonist obviously increased the protein expression of GPR43 induced by high glucose and LPS, but diminished the expression of adhesion molecule intercellular adhesion molecule-1 (ICAM-1), and then decreased the proinflammatory cytokine monocyte chemoattractant protein (MCP-1) and interleukin-1ß (IL-1ß) release from GMCs stimulated by the high glucose and LPS. These combined results support the hypothesis that SCFAs or GPR43 agonist can inhibit oxidative stress and inflammation of GMCs induced by high glucose and LPS, suggesting that SCFAs induced signaling pathway may act as new therapeutic targets of diabetic nephropathy (DN).

Calycosin Rebalances Advanced Glycation End Products-Induced Glucose Uptake Dysfunction of Hepatocyte In Vitro.

Diabetes mellitus (DM) often accompanies liver dysfunction. Astragali Radix is a traditional Chinese herbal medicine that is widely administrated to ameliorate the symptoms of diabetes as well as liver dysfunction, but its acting mechanism is still not yet fully recognized. Advanced glycation end products (AGEs) play a key role in promoting diabetic organ dysfunction. Both hyperglycemia and AGEs can induce insulin resistance, hepatocyte damage and liver dysfunction. We designed this study to explore the effects of the phytoestrogen Calycosin, a major active component of Astragali Radix, on AGEs-induced glucose uptake dysfunction in the hepatocyte cell line and relevant mechanisms. MTT and BrdU methods were applied to evaluate cell viability. 2-NBDG was used to observe glucose uptake by a live cell imaging system. Immunofluorescence method was carried out to investigate GLUT1, GLUT4, and RAGE protein expressions on cell membrane. cAMP content was determined by an EIA method. We found Calycosin concentration-dependently ameliorated AGEs-induced hepatocyte viability damage. AGEs dramatically reduced basal glucose uptake in hepatocytes, and this reduction could be reversed by Calycosin administration. By immunofluorescence detection, we observed that Calycosin could inhibit AGEs-induced GLUT1 expression down-regulation via estrogen receptor (ER). Furthermore, Calycosin decreased AGEs-promoted RAGE and cAMP elevation in hepatocytes. These findings strongly suggest that Calycosin can ameliorate AGEs-promoted glucose uptake dysfunction in hepatocytes; the protection of cell viability and ER-RAGE and GLUT1 pathways play a significant role in this modulation.

Combined estrogen replacement therapy on metabolic control in postmenopausal women with diabetes mellitus.

Previous studies have shown that the incidence of diabetes is higher when women come to menopause. This study was carried out to examine the effects of combined estrogen replacement therapy (ERT) on diabetes in postmenopausal women. PubMed/MEDLINE was searched for English-language articles published between January 1997 and June 2011. Studies that examined ERT on the incidence of diabetes and randomized clinical trials that evaluated combined ERT (estrogen plus progesterone) on diabetic indices in postmenopausal women were included. Pooled relative risks were calculated using a random- or a fixed-effects model. Sixteen studies comprising 17,971 cases were included. Based on the pooled data, ERT significantly reduced the incidence of diabetes [odds ratio (OR), 0.61; 95% confidence interval (CI), 0.55-0.68, ERT past/current/continuous use vs. never use; OR, 0.57; 95% CI, 0.51-0.65, ERT current/continuous use vs. past/never use]. Women with combined ERT have significantly lower levels of fasting plasma glucose (mean difference, -1.41 mM/L; 95% CI, -2.49 to -0.33 mM/L) and HbA1c (mean difference, -0.73%; 95% CI, from -1.28 to -0.18%) compared with placebo. Furthermore, combined ERT dramatically reduced plasma total cholesterol (mean difference, -0.34 mM/L; 95% CI, from -0.53 to -0.15 mM/L) and low-density lipoprotein (mean difference, -0.43 mM/L; 95% CI, from -0.71 to -0.14 mM/L) but slightly increased high-density lipoprotein (mean difference, 0.02 mM/L; 95% CI, from -0.07 to 0.12 mM/L) levels as compared with placebo control. This systemic review and meta-analysis provides evidence that postmenopausal women taking low-dose combined ERT have a decreased risk of developing diabetes and have better diabetic control.

Calycosin entered HUVECs and ameliorated AGEs-promoted cell apoptosis via the Bcl-2 pathway.

Endothelial cell (EC) apoptosis plays a pivotal role in the progression of diabetic complications. Abundant studies have demonstrated the pivotal role of advanced glycation end products (AGEs) on the development of diabetes. The aim of the present study was to investigate the effect of calycosin, a phytoestrogen, on AGEs-induced human umbilical vein endothelial cell (HUVEC) apoptosis. Fluorescence polarization and fluorescence absorption assays indicated that calycosin interacted with AGEs in a time-dependent manner. Further studies found that calycosin entered the cells as detected by HPLC. The MTT method demonstrated that calycosin ameliorated AGEs-induced HUVEC apoptosis in a dose-dependent manner, and statistical significance was observed at 1 × 10(-8) M of calycosin; this behavior was further demonstrated by acridine orange/ethidium bromide staining in that the presence of calycosin dramatically reduced AGEs-induced red staining in HUVECs. Further studies found that pre-incubation with calycosin at 1 × 10(-8) M dramatically increased anti-apoptotic Bcl-2 while decreased pro-apoptotic Bax and Bad expressions as detected by immunocytochemistry, and the effect of calycosin on rebalancing the ratio of Bcl-2/Bax was more significant than that of its glycoside, calycosin-7-O-ß-D-glucopyranoside (CG). Furthermore, calycosin slightly reversed AGEs-induced cell oxidative stress at 1 × 10(-8) M, but its antioxidative stress effect was less significant than that of CG. The present study strongly indicates that calycosin can enter the cell and modulate endothelial cell dysfunction by ameliorating AGEs-induced cell apoptosis.

[Leaves of Platanus orientalis as the carbon source for denitrification].

Leaching solution from Platanus orientalis fallen leaves was used as the carbon source for denitrification, and organic acid releasing regularity and influencing factors during the dipping process were discussed. The main organic acid was fumarate, and others were citric acid, oxalic acid and malic acid according to the analysis by HPLC. The average nitrate removal rate was 2.19 mg x h(-1), when the leaching solution was used as the carbon source during denitrification, while the rates were 2.29, 2.26 and 1.87 mg x h(-1) respectively with methanol, acetic acid and glucose as the carbon source. The rate with the leaching solution was slightly lower than those with methanol and acetic acid, but higher than that with glucose. The experimental results indicated that 7.5 mg equivalent of COD from the leaching solution of Platanus orientalis fallen leaves were met for 1 mg nitrate reduction and there was no nitrite accumulation during the denitrification.