Technological process optimization and measurement of image quality of the electrically bifocal metalens.

This Letter describes the design procedure and process optimization of the electrically bifocal metalens. In our design, horizontal and vertical polarization is manipulated by applying a suitable voltage to a twisted nematic liquid crystal (TN-LC) cell. Each nanostructure is designed to be a rectangular prism, making different polarizations of light experience various phase delays, thus causing bi-focus.

Time-Effective Simulation Methodology for Broadband Achromatic Metalens Using Deep Neural Networks.

Metasurface has demonstrated potential and novel optical properties in previous research. The prevailing method of designing a macroscale metasurface is based on the local periodic approximation. Such a method relies on the pre-calculated data library, including phase delay and transmittance of the nanostructure, which is rigorously calculated by the electromagnetic simulation.

Ultrawide-angle and high-efficiency metalens in hexagonal arrangement.

Wide-angle optical systems play a vital role in imaging applications and have been researched for many years. In traditional lenses, attaining a wide field of view (FOV) by using a single optical component is difficult because these lenses have crucial aberrations. In this study, we developed a wide-angle metalens with a numerical aperture of 0.

Electrically modulated varifocal metalens combined with twisted nematic liquid crystals.

Focus-tunable lenses are indispensable to optical systems. This paper proposes an electrically modulated varifocal metalens combined with twisted nematic liquid crystals. In our design, a metalens is employed to focus on different points depending on the polarization state of incident light.

NADPH oxidase NOX1 is involved in activation of protein kinase C and premature senescence in early stage diabetic kidney.

Increased oxidative stress and activation of protein kinase C (PKC) under hyperglycemia have been implicated in the development of diabetic nephropathy. Because reactive oxygen species derived from nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, NOX1 accelerate the translocation of PKC isoforms, NOX1 is postulated to play a causative role in the development of diabetic nephropathy. Hyperglycemia was induced in wild-type and Nox1-deficient mice (KO) by two doses of streptozotocin injection.

Molecular detection of trisomy 21 by bicolor competitive fluorescent PCR.

Objective: To develop a reliable and specific method for rapid prenatal diagnosis of Trisomy 21 (Down syndrome).

Methods: We established a dual color competitive fluorescent Polymerase Chain Reaction (PCR) to measure the gene dosage of Down syndrome critical region (DSCR), a single copy sequence in chromosome 21. Another unique single copy sequence located on chromosome 2 (USC2) but not glyceraldehyde-3-phosphate dehydrogenase (GAPDH) was chose as reference gene.

[Detecting Down syndrome with a novel dual-color competitive quantitative fluorescent polymerase chain reaction method].

Objective: To develop a rapid method for the detection of Down syndrome (DS) using dual-color competitive quantitative fluorescent polymerase chain reaction (DCC-QF-PCR), and to assess its feasibility for the prenatal diagnosis of Down syndrome.

Methods: DNA was extracted from peripheral blood of 30 DS patients and 60 normal men, common primers for DSCR and USC2 genes and respective TaqMan probes were designed and synthesized. The results of DCC-QF-PCR were compared with those of QF-PCR which measured the ratio between DSCR and GAPDH.

Activation of Src-ATF1 pathway is involved in upregulation of Nox1, a catalytic subunit of NADPH oxidase, by aldosterone.

In this study, we mainly focused on how aldosterone regulates Nox1, a catalytic subunit of NADPH oxidase (NOX) in vascular smooth muscle cells (VSMC). We found that aldosterone can induce the expression of Nox1, which is upregulated by the activation of the Src and activating transcription factor 1 (ATF1), but can not be suppressed by the inhibitors of the epidermal growth factor receptor (EGFR) or Matrix Metalloproteinase (MMP). Aldosterone triggers ATF1 phosphorylation in dose dependent fashion, but this effect is not blocked by actinomycin D, suggesting a non-genomic effect of aldosterone.

The mitochondria mediate the induction of NOX1 gene expression by aldosterone in an ATF-1-dependent manner.

High aldosterone (Ald) levels can induce hypertrophy of vascular smooth muscle cells (VSMCs), which carries high risks of heart failure. A previous study showed that Ald induces hypertrophy of VSMCs by up-regulating NOX1, a catalytic subunit of NADPH oxidase that produces superoxides. However, the precise mechanism remains unknown.

[A novel deletion mutation in AR gene causes complete androgen insensitivity syndrome in a Chinese family].

Objective: To identify the mutation of the androgen receptor (AR) gene in a complete androgen insensitivity family.

Methods: DNA was extracted from peripheral blood samples from family members in the family. PCR and DNA sequencing were then employed to detect the mutation of AR gene.

Protein kinase C-delta is involved in induction of NOX1 gene expression by aldosterone in rat vascular smooth muscle cells.

In this study, we focused on the relationship between aldosterone and NOX1 expression in vascular smooth muscle cells (VSMCs). For the first time, with the use of specific inhibitors of protein kinase C (PKC), we report that PKCdelta mediates upregulation of NOX1 induced by 10 nM aldosterone in cultured VSMCs. Participation of PKC in the mediation of NOX1 regulation was further confirmed by the effect of diacylglycerol, a PKC agonist, on the NOX1 RNA in A7r5 cells with Northern blot analysis.

Molecular mechanisms underlying PGF2alpha-induced hypertrophy of vascular smooth muscle cells.

The present review focuses primarily on the studies we made in recent years to improve the understanding of the molecular mechanisms of PGF2alpha-induced hypertrophy of Vascular Smooth Muscle Cells (VSMC). In this review, we will summarize the recent findings in the context of the PGF2alpha signaling pathway in three parts: PGF2alpha binding to its receptor, transactivation of EGF receptor, two independent signaling transduction pathways increasing the expression of NOX1 gene.

Synergy of aldosterone and high salt induces vascular smooth muscle hypertrophy through up-regulation of NOX1.

Aldosterone and excessive salt intake are obviously implicated in human arteriosclerosis. Aldosterone activates NADPH oxidase that induces superoxide production and cardiovascular cell hypertrophy. The activity of NADPH oxidase is influenced by the expression of its subunit, through which, vasoactive agents activate in the enzyme.

NOX1/NADPH oxidase negatively regulates nerve growth factor-induced neurite outgrowth.

Reactive oxygen species produced by NADPH oxidase are involved in the neuronal death associated with various neurodegenerative disorders. However, the role of NADPH oxidase in neuronal differentiation has not been well characterized. In nondifferentiated PC12 cells, the mRNA level of NOX1, a catalytic subunit of NADPH oxidase expressed in nonphagocytes, was approximately 10 times higher than that of the phagocyte type subunit, NOX2 (gp91(phox)), while the transcript of another isoform, NOX4, was not detected.

Transactivation of the EGF receptor and a PI3 kinase-ATF-1 pathway is involved in the upregulation of NOX1, a catalytic subunit of NADPH oxidase.

We previously reported that hypertrophy of vascular smooth muscle cells caused by prostaglandin (PG) F2alpha is mediated by the induction of NOX1, a catalytic subunit of NADPH oxidase that generates superoxide. The signal transduction pathway(s) involved in this process, however, remained unresolved. PGF2alpha enhanced the phosphorylation of the epidermal growth factor (EGF) receptor, and a selective inhibitor of EGF receptor kinase, tyrphostin AG1478, significantly suppressed PGF2alpha-induced NOX1 expression.

Essential role of ATF-1 in induction of NOX1, a catalytic subunit of NADPH oxidase: involvement of mitochondrial respiratory chain.

NADPH oxidase is the major source of superoxide production in cardiovascular tissues. We and others reported that PG (prostaglandin) F2alpha, PDGF (platelet-derived growth factor) and angiotensin II cause hypertrophy of vascular smooth muscle cells by induction of NOX1 (NADPH oxidase 1), a catalytic subunit of NADPH oxidase. We found DPI (diphenylene iodonium), an inhibitor of flavoproteins, including NADPH oxidase itself, almost completely suppressed induction of NOX1 mRNA by PGF2alpha or PDGF in a rat vascular smooth muscle cell line, A7r5.

NADPH oxidase is involved in prostaglandin F2alpha-induced hypertrophy of vascular smooth muscle cells: induction of NOX1 by PGF2alpha.

Prostaglandin (PG) F(2alpha), one of the primary prostanoids generated in vascular tissue, is known to cause hypertrophy in vascular smooth muscle cells. To clarify the molecular mechanisms underlying PGF(2alpha)-induced hypertrophy, the involvement of reactive oxygen species was examined in a rat vascular smooth muscle cell line, A7r5. PGF(2alpha) and (+)-fluprostenol, a selective agonist of the PGF receptor, significantly increased intracellular O(2)(-) in A7r5.