A Novel High-Isolation Dual-Polarized Patch Antenna with Two In-Band Transmission Zeros.

In this study, we present a novel dual-polarized patch antenna that exhibits high isolation and two in-band transmission zeros (TZs). The design consists of a suspended metal patch, two feeding probes connected to an internal neutralization line (I-NL), and a T-shaped decoupling network (T-DN). The I-NL is responsible for generating the first TZ, and its decoupling principles are explained through an equivalent circuit model. Rigorous design formulas are also derived to aid in the construction of the feeding structure. The T-DN realizes the second TZ, resulting in further improvement of the decoupling bandwidth. Simulation and experimental results show that the proposed antenna has a wide operating bandwidth (2.5-2.7 GHz), high port isolation (>30 dB), and excellent efficiency (>85%).

Simulation Study of High Sensitivity Fiber SPR Temperature Sensor with Liquid Filling.

In this paper, a high sensitivity fiber temperature sensor based on surface plasmon resonance is designed and studied. In the simulation, the single mode fiber is polished to remove most of the cladding, and then gold and silver films are added. Finally, it is embedded in the heat shrinkable tube filled with a thermo-optic coefficient liquid for curing. The numerical simulation results show that the sensing characteristics are sensitive to the remaining cladding thickness of the fiber, the thickness of the gold film and the thickness of the silver film. When the thermo-optic coefficient of the filling liquid is -2.8 × 10-4/°C, the thickness of the gold film, the thickness of the silver film and the thickness of the remaining cladding of the fiber are 30 nm, 20 nm and 1 µm, respectively. The sensitivity of the sensor designed in this paper can reach -6 nm/°C; this result is slightly higher than that of similar research in recent years. It will have a promising application prospect in flexible wearable temperature sensors, smart cities and other fields.

Fiber-integrated optical tweezers for ballistic transport and trapping yeast cells.

Due to their unique operational flexibility and ability to facilitate functional integration, the fascinating application of optical fibers has recently attracted significant attention in the field of optical tweezers and optical manipulation. The traditional optical fiber tweezers (OFTs) can easily trap microparticles in the front or side of the trapping tool, instead of behind. Herein, we propose and demonstrate a novel capillary optical fiber tweezer (COFT) to break the limitation of the optical trapping direction and extend the spatial range of optical trapping. The device consists of a cascade structure of single-mode fiber and capillary optical fiber (COF), which was used to excite higher-order modes in the COF. A COF taper tip was introduced to converge the multimode field, which created a focused output beam, realizing the ballistic transport of multi-yeast cells at the surface of the COF taper tip and their trapping by multiple optical potential wells of the focused output beam. The experimental results showed that the maximum transport length and speed of the cells were greater than 150 µm and 10 µm s-1, respectively, and at least three cells could be trapped simultaneously. The simulation results showed that the trap stiffness of COFT in several potential wells was in the range of 10-40 pN µm-1 W-1, which indicates that COFT has a good trap performance. Therefore, COFT greatly expands the region of the optical potential well, thus guiding and trapping microparticles distributed on the entire surface of the COF taper tip. This device can also greatly improve the optical trapping ability of single or multiple microparticles, providing a new tool for researchers committed to research on micro-nano objects and cells, which is expected to be widely used in the fields of targeted drug delivery, cell dynamic analysis, microfluidic chip driving, etc.

Coronary flow velocity reserve is improved by PPAR-α agonist fenofibrate in patients with hypertriglyceridemia.

INTRODUCTION: Fenofibrate, an agonist of peroxisome proliferator-activated receptor-α (PPAR-α), has a vascular protective effect. AIMS: We investigated the effect of the PPAR-α agonist on coronary artery endothelial function in patients with hypertriglyceridemia. METHODS: Fifty-eight patients with hypertriglyceridemia were divided into two groups: control (no treatment; n = 23) and fenofibrate treatment (n = 35), 200 mg/d, for 6 months. The patients had undergone rest and adenosine treatment to induce hyperemia for quantification of coronary flow velocity reserve (CFVR) by noninvasive Doppler echocardiography before treatment and at 6-month follow-up. Pulse wave velocity (PWV) was measured before treatment and at 6-month follow-up. RESULTS: CFVR was significantly improved with fenofibrate treatment as compared with baseline level and control group (3.14 ± 0.36 vs. 2.80 ± 0.58 and 2.79 ± 0.65, P < 0.01 and 0.05, respectively), with no difference between baseline levels and untreated controls. In addition, at 6 months, plasma level of homocysteine was significantly increased with fenofibrate treatment as compared with at baseline and control group (median 18.13 [range 14.46-22.02]µmol/L vs. 14.09 [12.01-18.81] and 13.34 [9.69-17.06]µmol/L, P < 0.001 and 0.01, respectively). Furthermore, at 6 months, PWV was significantly decreased with fenofibrate treatment as compared with control group (1446 ± 136 cm/s vs. 1570 ± 203 cm/s, P < 0.05). CONCLUSIONS: Treatment with PPAR-α agonist fenofibrate significantly improved CFVR and arterial stiffness in patients with hypertriglyceridemia. This endothelial protective effect may be reduced in part by the side effect of increasing homocysteine.

Ascorbate in aqueous humor augments nitric oxide production by macrophages.

Immunosuppressive molecules within the aqueous humor (AqH) are thought to preserve ocular immune privilege by inhibiting proinflammatory NO production by macrophages (MΦs). Consistent with previous observations, we observed that although MΦs stimulated in the presence of AqH expressed NO synthase 2 (NOS2) protein, nitrite concentrations in culture supernatants, an indirect measure of NO production, did not increase. Interestingly, NOS2 enzymatic activity, as measured by the conversion of L-arginine (L-Arg) into L-citrulline, was augmented in lysates of MΦs stimulated in the presence of AqH. These data suggested that intracellular L-Arg may have been limited by AqH. However, we observed increased mRNA expression of the L-Arg transporter, cationic amino acid transporter 2B, and increased L-Arg uptake in MΦs stimulated in the presence of AqH. Arginases were expressed by stimulated Ms, but competition for L-Arg with NOS2 was excluded. Expression of GTP cyclohydrolase, which produces tetrahydrobiopterin (H(4)B), an essential cofactor for NOS2 homodimerization, increased after M stimulation in the presence or absence of AqH and NOS2 homodimers formed. Taken together, these data provided no evidence for inhibited NOS2 enzymatic activity by AqH, suggesting that a factor within AqH may have interfered with the measurement of nitrite. Indeed, we observed that nitrite standards were not measurable in the presence of AqH, and this effect was due to ascorbate in AqH. Controlling for interference by ascorbate revealed that AqH augmented NO production in MΦs via ascorbate, which limited degradation of H(4)B. Therefore, AqH may augment NO production in macrophages by stabilizing H(4)B and increasing intracellular L-Arg.

PPAR-α Agonist Fenofibrate Upregulates Tetrahydrobiopterin Level through Increasing the Expression of Guanosine 5'-Triphosphate Cyclohydrolase-I in Human Umbilical Vein Endothelial Cells.

Tetrahydrobiopterin (BH4) is an essential cofactor for endothelial nitric oxide (NO) synthase. Guanosine 5'-triphosphate cyclohydrolase-I (GTPCH-I) is a key limiting enzyme for BH4 synthesis. In the present in vitro study, we investigated whether peroxisome proliferator-activated receptor α (PPAR-α) agonist fenofibrate could recouple eNOS by reversing low-expression of intracellular BH4 in endothelial cells and discussed the potential mechanisms. After human umbilical vein endothelial cells (HUVECs) were treated with lipopolysaccharide (LPS) for 24 hours, the levels of cellular eNOS, BH4 and cell supernatant NO were significantly reduced compared to control group. And the fluorescence intensity of intracellular ROS was significantly increased. But pretreated with fenofibrate (10 umol/L) for 2 hours before cells were induced by LPS, the levels of eNOS, NO, and BH4 were significantly raised compared to LPS treatment alone. ROS production was markedly reduced in fenofibrate group than LPS group. In addition, our results showed that the level of intracellular GTPCH-I detected by western blot was increased in a concentration-dependent manner after being treated with fenofibrate. These results suggested that fenofibrate might help protect endothelial function and against atherosclerosis by increasing level of BH4 and decreasing production of ROS through upregulating the level of intracellular GTPCH-I.

Homocysteine impairs coronary artery endothelial function by inhibiting tetrahydrobiopterin in patients with hyperhomocysteinemia.

Hyperhomocysteinemia (HHcy) has been associated with impaired vascular endothelial function. Our previous study demonstrated significantly higher secretion of the chemokine monocyte chemoattractant protein-1 from monocytes in response to lipopolysaccharide in patients with HHcy. In the present study, we investigated whether coronary endothelial function was damaged in patients with chronic HHcy (plasma level of homocysteine >15 µmol/l) and, if so, whether this impaired endothelial function is induced by the uncoupling of endothelial nitric oxide synthase (eNOS). When tetrahydrobiopterin levels are inadequate, eNOS is no longer coupled to l-arginine oxidation, which results in reactive oxygen species rather than nitric oxide production, thereby inducing vascular endothelial dysfunction. The 71 participants were divided into two groups, control (n = 50) and HHcy (n = 21). Quantification of coronary flow velocity reserve (CFVR) was after rest and after adenosine administration done by noninvasive Doppler echocardiography. Plasma levels of nitric oxide and tetrahydrobiopterin were significantly lower in patients with HHcy than in controls (99.54 ± 32.23 vs. 119.50 ± 37.68 µmol/l and 1.43 ± 0.46 vs. 1.73 ± 0.56 pmol/ml, all P < 0.05). Furthermore, CFVR was significantly lower in the HHcy than the control group (2.76 ± 0.49 vs. 3.09 ± 0.52, P < 0.05). In addition, plasma level of homocysteine was negatively correlated with CFVR. Chronic HHcy may contribute to coronary artery disease by inducing dysfunction of the coronary artery endothelium. The uncoupling of eNOS induced by HHcy in patients with chronic HHcy may explain this adverse effect in part.