67 research outputs found
Visually quantifying single-qubit quantum memory
To store quantum information, quantum memory plays a central intermediate
ingredient in a network. The minimal criterion for a reliable quantum memory is
the maintenance of the entangled state, which can be described by the
non-entanglement-breaking (non-EB) channel. In this work, we show that all
single-qubit quantum memory can be quantified without trusting input state
generation. In other words, we provide a semi-device-independent approach to
quantify all single-qubit quantum memory. More specifically, we apply the
concept of the two-qubit quantum steering ellipsoids to a single-qubit quantum
channel and define the channel ellipsoids. An ellipsoid can be constructed by
visualizing finite output states within the Bloch sphere. Since the
Choi-Jamio{\l}kowski state of a channel can all be reconstructed from geometric
data of the channel ellipsoid, a reliable quantum memory can be detected.
Finally, we visually quantify the single-qubit quantum memory by observing the
volume of the channel ellipsoid.Comment: 9 pages, 5 figure
Cyclosporine A combined with medium/low dose prednisone in progressive IgA nephropathy
AbstractThe aim of the present study was to evaluate the efficacy of cyclosporine A (CsA) combined with medium/low dose prednisone in the treatment of progressive immunoglobulin A nephropathy (IgAN). Ninety-six patients who satisfied the inclusion criteria were enrolled in a prospective controlled clinical study. They were assigned into two groups and initially given either 0.6–0.8 mg/kg/day prednisone (maximum 40 mg/day) plus 3 mg/kg/day CsA (CsA group), or 1 mg/kg/day prednisone (maximum 60 mg/day) alone (steroid group). During therapy, the dose of prednisone was reduced in both groups and the dose of CsA was gradually tailed off over the first 3 months and maintained at 2 mg/kg/day in the CsA group. Urinary protein excretion, serum biochemical indexes, clinical efficacy and side effects of CsA were assayed. A significant decline in mean 24-hour urinary protein excretion (p < 0.05) was observed 1 month after treatment in patients in the CsA group, which was observed 2 months after treatment in the steroid group. The decline in mean 24-hour urinary protein excretion in the CsA group was more significant than in the steroid group. Serum albumin level increased significantly in the CsA group 2 months after therapy (p < 0.05). Moreover, at the end of the course, a higher remission rate was observed in patients with Lee’s Grade III IgAN after combined treatment with prednisone and CsA (p < 0.05). No significant difference in clinical efficacy was observed in patients with Lee’s Grade IV and Grade V IgAN between the two groups (p > 0.05). CsA at a dose of 2–3 mg/kg/day in combination with medium/low dose prednisone was effective in inducing remission of IgAN, especially for patients with Lee's Grade III IgAN, and is a safe and effective choice for short-term treatment of patients with progressive IgAN
Berberine improves kidney function in diabetic mice via AMPK activation.
Diabetic nephropathy is a major cause of morbidity and mortality in diabetic patients. Effective therapies to prevent the development of this disease are required. Berberine (BBR) has several preventive effects on diabetes and its complications. However, the molecular mechanism of BBR on kidney function in diabetes is not well defined. Here, we reported that activation of AMP-activated protein kinase (AMPK) is required for BBR-induced improvement of kidney function in vivo. AMPK phosphorylation and activity, productions of reactive oxygen species (ROS), kidney function including serum blood urea nitrogen (BUN), creatinine clearance (Ccr), and urinary protein excretion, morphology of glomerulus were determined in vitro or in vivo. Exposure of cultured human glomerulus mesangial cells (HGMCs) to BBR time- or dose-dependently activates AMPK by increasing the thr172 phosphorylation and its activities. Inhibition of LKB1 by siRNA or mutant abolished BBR-induced AMPK activation. Incubation of cells with high glucose (HG, 30 mM) markedly induced the oxidative stress of HGMCs, which were abolished by 5-aminoimidazole-4-carboxamide ribonucleoside, AMPK gene overexpression or BBR. Importantly, the effects induced by BBR were bypassed by AMPK siRNA transfection in HG-treated HGMCs. In animal studies, streptozotocin-induced hyperglycemia dramatically promoted glomerulosclerosis and impaired kidney function by increasing serum BUN, urinary protein excretion, and decreasing Ccr, as well as increased oxidative stress. Administration of BBR remarkably improved kidney function in wildtype mice but not in AMPKα2-deficient mice. We conclude that AMPK activation is required for BBR to improve kidney function in diabetic mice
Visually quantifying single-qubit quantum memory
To store quantum information, quantum memory plays a central intermediate ingredient in a network. The minimal criterion for a reliable quantum memory is the maintenance of the entangled state, which can be described by the non-entanglement-breaking (non-EB) channel. In this work, we show that all single-qubit quantum memory can be quantified without trusting input state generation. In other words, we provide a semi-device-independent approach to quantify all single-qubit quantum memory. More specifically, we apply the concept of the two-qubit quantum steering ellipsoids to a single-qubit quantum channel and define the channel ellipsoids. An ellipsoid can be constructed by visualizing finite output states within the Bloch sphere. Since the Choi-Jamiołkowski state of a channel can all be reconstructed from geometric data of the channel ellipsoid, a reliable quantum memory can be detected. Finally, we visually quantify the single-qubit quantum memory by observing the volume of the channel ellipsoid
AMPK upregulations by AICAR or gene overexpression attenuate HG-induced oxidative stress in cultured HGMCs.
<p>(<b>A</b>) HGMCs were incubated with D-glucose (30 mM) in presence or absence of AICAR (2 mM) for 12 hours. ROS productions were detected by DHE fluorescence. N is 5 in each group. <sup>*</sup><i>P</i><0.05 vs. control, <sup>#</sup><i>P</i><0.05 vs HG alone. (<b>B</b>) HGMCs infected with Ad-GFP or Ad-AMPK-CA for 48 hours were incubated with HG for 12 hours. ROS productions were detected by DHE fluorescence. The picture is a representative from 3 independent experiments. <sup>*</sup><i>P</i><0.05 vs. control GFP. NS indicates no significance.</p
BBR-induced AMPK activation in cultured HGMCs is LKB1-dependent.
<p>(<b>A</b>) HGMCs were transfected with control siRNA or LKB1 siRNA for 48 h. Then cells were treated with BBR (100 µM) for 2 hours. AMPK thr172 phosphorylation in total cell lysate was detected by western blot. The blot is a representative of three blots from three independent experiments. *<i>P</i><0.05 VS control. NS indicates no significance. (<b>B</b>) HGMCs were infected with adenovirus containing LKB1-WT, LKB1-S428A or LKB1-S307A for 48 h. The infected cells were then treated with BBR (100 µM) for 2 hours. AMPK-Thr172 phosphorylation was detected by Western blot. The blot is a representative blot from three independent experiments. *<i>P</i><0.05 VS ad-GFP. NS indicates no significance.</p
BBR prevents hyperglycemia-induced renal dysfunction in <i>WT</i> but not in <i>AMPKα2<sup>-/-</sup></i> mice.
<p>Permanent hyperglycemia in <i>WT</i> and <i>AMPKα2<sup>-/-</sup></i> mice was induced by a low-dose STZ induction. All mice were received with or without BBR administration (200 mg/kg body weight daily) for 8 weeks after the stable diabetic model was established. At the end of experiments, mice were sacrificed. (<b>A</b>) Blood glucose in all mice. 5–10 mice in each group. <sup>*</sup><i>P</i><0.05 vs. WT alone, <sup>#</sup><i>P</i><0.05 vs STZ plus WT. NS indicates no significance. (<b>B</b>) Morphological and quantitative analysis of glomerulus by HE staining. a, WT; b, WT + STZ; c, WT + STZ + BBR; d, <i>AMPKα2<sup>-/-</sup></i> + STZ; e, <i>AMPKα2<sup>-/-</sup></i> + STZ + BBR. (<b>C</b>) Serum BUN, (<b>D</b>) creatine clearance rate (Ccr), and (<b>E</b>) urinary protein excretion were assayed. 5–10 mice in each group. <sup>*</sup><i>P</i><0.05 vs. control, <sup>#</sup><i>P</i><0.05 vs DM in WT. NS indicates no significance.</p
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