Designing plasmonic exceptional points by transformation optics.

Exceptional points (EPs) have been shown to be useful in bringing about sensitive optical properties based on non-Hermitian physics. For example, they have been applied in plasmonics to realize nano-sensing with extreme sensitivity. While the exceptional points are conventionally constructed by considering parity-time symmetric or anti-parity-time symmetric media, we theoretically demonstrate the possibility of generating a series of non-Hermitian systems by transforming a seed system with conventional parity-time symmetry within the transformation optics framework. The transformed systems do not possess PT-symmetry with a conventional parity operator after a spatial operation, i.e. hidden from conventional sense, but are equipped with exceptional points and phase transitions, hinting an alternative method to design non-Hermitian plasmonic systems with sensitive spectra or eigenmodes.

Nonreciprocal field transformation with active acoustic metasurfaces.

Field transformation, as an extension of the transformation optics, provides a unique means for nonreciprocal wave manipulation, while the experimental realization remains a substantial challenge as it requires stringent material parameters of the metamaterials, e.g., purely nonreciprocal bianisotropic parameters. Here, we develop and demonstrate a nonreciprocal field transformation in a two-dimensional acoustic system, using an active metasurface that can independently control all constitutive parameters and achieve purely nonreciprocal Willis coupling. The field-transforming metasurface enables tailor-made field distribution manipulation, achieving localized field amplification by a predetermined ratio. The metasurface demonstrates the self-adaptive capability to various excitation conditions and can be extended to other geometric shapes. The metasurface also achieves nonreciprocal wave propagation for internal and external excitations, demonstrating a one-way acoustic device. The nonreciprocal field transformation not only extends the framework of the transformation theory for nonreciprocal wave manipulation but also holds great potential in applications such as ultrasensitive sensors and nonreciprocal communication.

Quercetin Attenuates Ethanol-Induced Iron Uptake and Myocardial Injury by Regulating the Angiotensin II-L-Type Calcium Channel.

SCOPE: Increased iron deposition in the myocardium in alcoholics may lead to increased risk of cardiac dysfunction. Quercetin has been demonstrated to quench production of intracellular free iron-induced -OH, but the effect of quercetin in ethanol-induced cardiac damage remains unclear. This study aims to explore whether quercetin attenuates ethanol-induced iron uptake and myocardial injury by regulating angiotensin II-L-type voltage-dependent Ca2+ channel (Ang II-LTCC). METHODS AND RESULTS: Adult male C57BL/6J mice are isocalorically pair-fed either a regular or ethanol-containing Lieber De Carli liquid diets supplemented with either quercetin (100 mg kg-1  bw) or desferrioxamine mesylate (DFO, 100 mg kg-1 bw) for 15 weeks. Quercetin alleviated ethanol-induced histopathological changes, creatine kinase isoenzyme release, Ang II secretion, ROS generation, total cardiac iron, and labile iron level. Ethanol exposure or quercetin intervention fails to regulate traditional iron transporters except LTCC. LTCC is upregulated by ethanol and inhibited by quercetin. In H9C2 cell, LTCC is increased by ethanol (100 mm) and/or Ang II (1 µm) concomitant with iron disorders and oxidative stress. This effect is partially normalized by quercetin (50 µm), nifedipine (LTCC inhibitor, 15 µm), or losartan (Ang II receptor antagonist, 100 µm). CONCLUSION: Alcohol-induced cardiac injury is associated with excessive NTBI uptake mediated by Ang II-LTCC activation which may be mediated by quercetin against ethanol cardiotoxicity.

Low shear stress regulates monocyte adhesion to oxidized lipid-induced endothelial cells via an IkappaBalpha dependent pathway.

In regions of a vessel that experience low shear stress and reversing flow patterns, early features in the pathogenesis of atherosclerosis include the accumulation of oxidized LDL (OxLDL) and adhesion of monocytes to endothelial cells (EC). Here we investigated the hypothesis that low shear stress (2 dyn/cm2) and OxLDL are synergistic for enhanced expression of vascular cell adhesion molecule (VCAM-1) and human aortic endothelial cell (HAEC)-monocyte adhesion. This study shows low shear stress can significantly reduce IkappaBalpha levels, activate NF-kappaB, increase the expression of VCAM-1 in HAEC and binding of monocytes. OxLDL itself cannot significantly increase the expression of VCAM-1 in HAEC and binding of monocytes, but through activation of NF-kappaB and degradation of IkappaBalpha induced by low shear stress it can significantly enhance VCAM-1 expression and monocyte adhesion, over that in unmodified LDL or control. These results suggest that low shear stress can regulate monocyte adhesion to oxidized lipid-induced endothelial cells via an IkappaBalpha-dependent pathway, and that low shear stress together with OxLDL may likely play an important role in atherogenesis.

[Overexpression of TGF beta 1 increases elastin expression and adhesion of smooth muscle cells].

This study was conducted to examine the effectiveness of a gene transfer of human TGF beta 1 gene into smooth muscle cells and whether the TGF beta 1 can increase elastin expression of smooth muscle cells. With the help of DOTAP, smooth muscle cells were transfected with pMAMneoTGF beta 1. The positive cell clones were selected with G418. The stable transfection and expression of TGF beta 1 in the smooth muscle cells were determined by immunofluorescence analysis. The expression of elastin in the transfected and untransfected cells were determined by in situ hybridization. The adhesion force between smooth muscle cells and matrix was detected by micropipette system. The results showed abundant TGF beta 1 stable expression in smooth muscle cells. TGF beta 1 gene can increase two-three times elastin expression and increase the adhesion between smooth muscle cells and matrix. TGF beta 1 can be used in vascular tissue engineering to increase smooth muscle cells adhesion.

Neuroprotective effects of a standardized flavonoid extract from Diospyros kaki leaves.

ETHNOPHARMACOLOGICAL RELEVANCE: Flavonoids, extracted from the leaves of Diospyros kaki, are the main therapeutic components of NaoXingQing (NXQ), a potent and patented Chinese herbal remedy widely used in China for the treatment of apoplexy syndrome. AIM OF THE STUDY: To investigate the neuroprotective effects of FLDK-P70, a standardized flavonoid extract, using in vivo rat models of both focal ischemia/reperfusion (I/R) injury induced by middle cerebral artery occlusion (MCAO) and on transient global brain ischemia induced by four-vessel occlusion (4-VO). We also aim to examine the effects of FLDK-P70 on glutamate-induced cell injury of hippocampal neurons as well as on hypoxia-induced injury of cortical neurons in primary cell culture. MATERIALS AND METHODS AND RESULTS: Administration of FLDK-P70 for 12 days (40, 80 mg/kg body weight, p.o., 5 days before and 7 days after 4-VO) increased the survival of hippocampal CA1 pyramidal neurons after transient global brain ischemia. Similarly, administration of FLDK-P70 for 7 days (40, 80 mg/kg body weight, p.o., 3 days before and 4 days after MCAO) significantly reduced the lesion of the insulted brain hemisphere and improved the neurological behavior of rats. In primary rat hippocampal neuronal cultures, pretreatment with FLDK-P70 (5, 10 microg/ml) protected neurons from glutamate-induced excitotoxic neuronal death in a dose-dependent manner. In primary rat cerebral cortical neuronal culture, pretreatment with FLDK-P70 (25, 100 microg/ml) also reduced hypoxia-reoxygen induced neuronal death and apoptosis in a dose-dependent manner. CONCLUSIONS: These in vivo and in vitro results suggest that FLDK-P70 significantly protects rats from MCAO and 4-VO ischemic injury in vivo and protects hippocampal neurons from glutamate-induced excitotoxic injury as well as cortical neurons from hypoxia-induced injury in vitro. The mechanisms of these effects may be due to the antioxidative activity of the flavonoids. These results convincingly demonstrate that FLDK-P70 may be useful for the prevention and treatment of ischemia/reperfusion injury and other related neurodegenerative diseases.

Aging changes of the angioarchitecture and arterial morphology of the spinal cord in rats.

BACKGROUND: It is well known that vascular myelopathy increases with age, however, there are no systematic reports on the quantitative capillary density in the spinal cord and no reports concerning the age-related changes of vascularity and capillary density of the spinal cord. OBJECTIVE: Age-related changes of vascularity and capillary density of the spinal cord and the morphology of the ventral spinal artery were observed and measured so as to provide reference to study the microcirculation of the spinal cord. METHODS: Three different age groups of Wistar rats (1-2, 6-7 and >22 months old) were studied by ink-gelatin injection, corrosion casts, biological stereological technique, image analysis and transmission electron microscope. RESULTS: The number of central arteries per centimeter of the spinal cord decreased significantly with age; the ventral spinal artery and central arteries often became tortuous in the >22 month group. Capillary density in the anterior horn was significantly higher than that in the posterior horn. Capillary density in the gray matter decreased significantly with age. These aging changes of the ventral spinal artery in the rat included that the folds of internal elastic membrane were reduced, the internal elastic membrane thinned and disrupted, the endothelial cells degenerated and broke away from the wall, and smooth muscle cells in the tunica media degenerated and protruded to the lumen. The relative content of the elastic fibers decreased significantly with age, while the relative content of the collagenic fibers and the ratio of the C/E increased significantly with age. CONCLUSIONS: The difference between capillary density in gray and white matter in the spinal cord has shown that the need of metabolization is adapted to the function of the neurons, and the anterior horn is more sensitive than the posterior horn to anoxia and is easily damaged during ischemia in the spinal cord. Aging changes of capillary density and arterial morphology of the spinal cord may be important contributory factors in vascular myelopathy.