Concentration-response curves to acetylcholine (ACh) before/after inhibition of EET formation by PPOH (10 μmol/l) or 17-ODYA (10 μmol/l) in phenylephrine (PE)-preconstricted renal arteries (n = 5).

<p>Incubation with PPOH (A) or 17-ODYA (C) decreased ACh-induced vasodilation in lean and obese Zucker (OZ) rats. But the treatment with PPOH (B) or 17-ODYA (D) resulted in less reduction in OZ rats than in lean control rats. ** P<0.001, *P<0.05.</p

Endothelial dysfunction in renal arcuate arteries of obese Zucker rats: The roles of nitric oxide, endothelium-derived hyperpolarizing factors, and calcium-activated K⁺ channels - Fig 1

<p><b>Body weight (A) and blood glucose (B) data for each age-matched lean and obese Zucker (OZ) rats (n = 5)</b>. Body weight of OZ rats was greater than that in lean control rats (A). Blood glucose level significantly increased as expected in OZ rats at ages of 12 and 20 weeks (B). ** P<0.001, *P<0.05.</p

Concentration-response curves to acetylcholine (ACh) before/after incubation with charybdotoxin (Cha, 1 μmol/l) and apamin (1 μmol/l) in phenylephrine (PE)-preconstricted renal arcuate arteries (n = 5).

<p>The incubation with Cha and apamin decreased vasodilation in lean control rats (A), but no alternation was seen in obese Zucker (OZ) rats (B). Incubation with L-NNA, indomethacin (Indo), Cha, and apamin almost abolished vasodilation induced by ACh in both lean and OZ rats (A and B). NS 1619 elicited a concentration-dependent vasodilation in PE-preconstricted renal arcuate arteries (C). However, the vasodilation induced by 1, 10 and 50 μmol/l was decreased in OZ rats (C). ** P<0.001, *P<0.05.</p

Roles of nitric oxide (NO), endothelium-derived hyperpolarizing factors (EDHF), and calcium-activated K⁺ (K_Ca) channels in renal arcuate arteries.

<p>Acetylcholine (ACh) can induce endothelium-dependent vasodilation by the release of NO (①) and EDHF (②) from endothelial cells in renal arcuate arteries. NO is derived from endothelial NO synthase (eNOS), while prostacyclin (PGI₂) and epoxyeicosatrienoic acids (EETs, as EDHFs) are generated from arachidonic acids by cyclooxygenase (COX), and cytochrome P-450 (CYP) epoxygenase, respectively. EETs facilitate the hyperpolarization of smooth muscle cells and vascular relaxation through K⁺ efflux mediated by the opening of K_Ca channels either in endothelial cells or in smooth muscle cells. The K⁺ released from K_Ca channels of endothelial cells into the subendothelial space (potential connective tissue space beneath the endothelium) subsequently actives inward rectifying K⁺ (K_ir) channels on smooth muscle cells, while producing K⁺ efflux as well. In the present study, the contribution of NO and EDHF to endothelium vasodilation was impaired and the activity of K_Ca channels was downregulated in renal arcuate arteries of obese Zucker (OZ) rats at 20 weeks of age, but PGI₂ had no effect on ACh-elicited vasodilation. Barium chloride, inhibitor of the K_ir channel; Charybdotoxin (Cha)+Apamin, inhibitor of the K_Ca channel; Glibenclamide, inhibitor of the K_ATP channel; Indomethacin, inhibitor of COX; L-NNA, inhibitor of eNOS; NS1619, agonist of the K_Ca channel; and PPOH or 17-ODYA, inhibitors of CYP epoxygenase.</p

Concentration-response curves to acetylcholine (ACh) before/after incubation with L-NNA (10 μmol/l) or L-NNA plus indomethacin (10 μmol/l) in phenylephrine (PE)-preconstricted renal arteries (n = 5).

<p>L-NNA incubation resulted in a significant reduction in vasodilation in response to ACh in obese Zucker (OZ) rats and lean control rats (A), but the reduction was less in OZ rats than in lean rats (B). Combined treatment with L-NNA plus indomethacin did not further enhance the inhibitory effect of L-NNA. The reduction by L-NNA and indomethacin (D) was similar to that by L-NNA alone (B). Fig (C) shows the contribution of EDHF to ACh-induced vasodilation after treatment of L-NNA and indomethacin. The EDHF-mediated vasodilation was decreased in OZ rats. ** P<0.001, *P<0.05.</p

Additional file 2: of Long noncoding RNA AFAP1-AS1 predicts a poor prognosis and regulates non–small cell lung cancer cell proliferation by epigenetically repressing p21 expression

TableS2. mRNAs increased abundance (≥2-fold) in AFAP1-AS1 knockdown A549 cells. (XLS 125 kb

Additional file 1: of Long noncoding RNA AFAP1-AS1 predicts a poor prognosis and regulates non–small cell lung cancer cell proliferation by epigenetically repressing p21 expression

TableS1. The list of primers and the sequence of siRNAs. (XLS 8 kb

Highly Electrically Conductive Polyiodide Ionic Liquid Cathode for High-Capacity Dual-Plating Zinc–Iodine Batteries

Zinc–iodine batteries are one of the most intriguing types of batteries that offer high energy density and low toxicity. However, the low intrinsic conductivity of iodine, together with high polyiodide solubility in aqueous electrolytes limits the development of high-areal-capacity zinc–iodine batteries with high stability, especially at low current densities. Herein, we proposed a hydrophobic polyiodide ionic liquid as a zinc-ion battery cathode, which successfully activates the iodine redox process by offering 4 orders of magnitude higher intrinsic electrical conductivity and remarkably lower solubility that suppressed the polyiodide shuttle in a dual-plating zinc–iodine cell. By the molecular engineering of the chemical structure of the polyiodide ionic liquid, the electronic conductivity can reach 3.4 × 10–3 S cm–1 with a high Coulombic efficiency of 98.2%. The areal capacity of the zinc–iodine battery can achieve 5.04 mAh cm–2 and stably operate at 3.12 mAh cm–2 for over 990 h. Besides, a laser-scribing designed flexible dual-plating-type microbattery based on a polyiodide ionic liquid cathode also exhibits stable cycling in both a single cell and 4 × 4 integrated cell, which can operate with the polarity-switching model with high stability