High-Efficiency Arbitrary Quantum Operation on a High-Dimensional Quantum System.

The ability to manipulate quantum systems lies at the heart of the development of quantum technology. The ultimate goal of quantum control is to realize arbitrary quantum operations (AQUOs) for all possible open quantum system dynamics. However, the demanding extra physical resources impose great obstacles. Here, we experimentally demonstrate a universal approach of AQUO on a photonic qudit with the minimum physical resource of a two-level ancilla and a log_{2}d-scale circuit depth for a d-dimensional system. The AQUO is then applied in a quantum trajectory simulation for quantum subspace stabilization and quantum Zeno dynamics, as well as incoherent manipulation and generalized measurements of the qudit. Therefore, the demonstrated AQUO for complete quantum control would play an indispensable role in quantum information science.

Neuroprotective effects of α-lipoic acid on long-term experimental autoimmune encephalomyelitis.

OBJECTIVE: Experimental autoimmune encephalomyelitis (EAE) is an animal model commonly used in research on the acute phase of multiple sclerosis (MS), but studies on the pathology and pathogenesis of EAE with a long disease course are seldom conducted. Besides its antioxidant properties, the comprehensive mechanisms through which α-lipoic acid (LA) affects EAE remain obscure. We here conducted the study to explore the possible mechanisms. MATERIALS AND METHODS: In this study, the following methods were used for investigating the effects of LA on long-term EAE: hematoxylin-eosin staining (HE) and electron microscopic examinations of pathological changes; Western blotting of ß-amyloid precursor protein (ß-APP) and myelin basic protein (MBP); Enzyme-linked immunosorbent assay (ELISA) of tumor necrosis factor-α (TNF-α), transforming growth factor-ß (TGF-ß), superoxide dismutase (SOD), malondialdehyde (MDA) as well as flow cytometry of CD4+CD25+FoxP3+ regulatory T cells (Tregs). RESULTS: The results showed: (1) diverse pathological features of long-term relapsing-remitting EAE; (2) relatively increased MBP and reduced ß-APP expression in LA recipients 180 days after onset; (3) down-regulated TNF-α and up-regulated TGF-ß levels in LA recipients 7 days after onset; (4) lower MDA and higher SOD levels in LA recipients 180 days after onset; (5) increased Treg levels in LA recipients 7 days after onset. CONCLUSIONS: Aside from oxidative stress, LA possessed anti-inflammatory and immunomodulatory effects on EAE. LA might be a promising candidate for MS treatment.

Alpha-Synuclein affects neurite morphology, autophagy, vesicle transport and axonal degeneration in CNS neurons.

Many neuropathological and experimental studies suggest that the degeneration of dopaminergic terminals and axons precedes the demise of dopaminergic neurons in the substantia nigra, which finally results in the clinical symptoms of Parkinson disease (PD). The mechanisms underlying this early axonal degeneration are, however, still poorly understood. Here, we examined the effects of overexpression of human wildtype alpha-synuclein (αSyn-WT), a protein associated with PD, and its mutant variants αSyn-A30P and -A53T on neurite morphology and functional parameters in rat primary midbrain neurons (PMN). Moreover, axonal degeneration after overexpression of αSyn-WT and -A30P was analyzed by live imaging in the rat optic nerve in vivo. We found that overexpression of αSyn-WT and of its mutants A30P and A53T impaired neurite outgrowth of PMN and affected neurite branching assessed by Sholl analysis in a variant-dependent manner. Surprisingly, the number of primary neurites per neuron was increased in neurons transfected with αSyn. Axonal vesicle transport was examined by live imaging of PMN co-transfected with EGFP-labeled synaptophysin. Overexpression of all αSyn variants significantly decreased the number of motile vesicles and decelerated vesicle transport compared with control. Macroautophagic flux in PMN was enhanced by αSyn-WT and -A53T but not by αSyn-A30P. Correspondingly, colocalization of αSyn and the autophagy marker LC3 was reduced for αSyn-A30P compared with the other αSyn variants. The number of mitochondria colocalizing with LC3 as a marker for mitophagy did not differ among the groups. In the rat optic nerve, both αSyn-WT and -A30P accelerated kinetics of acute axonal degeneration following crush lesion as analyzed by in vivo live imaging. We conclude that αSyn overexpression impairs neurite outgrowth and augments axonal degeneration, whereas axonal vesicle transport and autophagy are severely altered.

Erythropoietin increases circulating endothelial progenitor cells and reduces the formation and progression of cerebral aneurysm in rats.

Endothelial dysfunction triggers early pathological changes in vessel walls, potentially leading to the formation of cerebral aneurysm (CA). Endothelial progenitor cells (EPCs) are critical in repairing damaged endothelium and could prevent or slow CA formation. We hypothesize that erythropoietin (EPO) stimulates EPCs mobilization, could alter the rate of CA formation and progression. The hypothesis was tested in a rat model of CA. CAs were induced in male Sprague-Dawley rats and treated with s.c. administration of EPO. Circulating EPCs and serum vascular endothelial grow factor (VEGF) were measured be flow cytometry and ELISA, respectively. mRNAs for inducible nitric oxide synthase (iNOS), endothelial nitric oxide synthase (eNOS), matrix metalloproteinase-2 (MMP-2), and MMP-9 in aneurysm tissue were quantified by Real-time PCR. The size, internal elastic lamina (IEL), and media thickness of CAs were evaluated 1 and 3 months after aneurysm induction. Circulating EPCs were significantly lower in CA rats as compared to non-surgical controls. EPO increased levels of circulating EPCs and VEGF. It also decreased iNOS, MMP-2, and MMP-9 mRNA levels, while increased eNOS mRNA in aneurysm tissue. The changes in EPCs and biochemical markers are associated with suppression of new CA formation and prevention of preexisting CA progression. We have shown a close association among circulating EPCs, biochemical markers related to vascular remodeling, and the rate of CA formation and progression. Changes in patterns of cerebral blood flow and hypertension induced by surgical ligations of selected arteries exert significant hemodynamic stress to weaken vessel walls, primarily at sites of basilar bifurcation. The surgical stress also reduced circulating EPCs and slowed vascular repairs. EPO mobilizes EPCs from the bone marrow and promotes their homing. These results suggest that EPCs may serve as a marker for CA progression and EPO a promising candidate for the clinical management of CA.

Fabrication of Anti-human Cardiac Troponin I Immunogold Nanorods for Sensing Acute Myocardial Damage.

A facile, rapid, solution-phase method of detecting human cardiac troponin I for sensing myocardial damage has been described using gold nanorods-based biosensors. The sensing is demonstrated by the distinct change of the longitudinal surface plasmon resonance wavelength of the gold nanorods to specific antibody-antigen binding events. For a higher sensitivity, the aspect ratio of gold nanorods is increased up to ca 5.5 by simply adding small amount of HCl in seed-mediated growth solution. Experimental results show that the detecting limit of the present method is 10 ng/mL. Contrast tests reveal that these gold nanorods-based plasmonic biosensors hold much higher sensitivity than that of conventionally spherical gold nanoparticles.

Diagnosis of gastric intestinal metaplasia with confocal laser endomicroscopy in vivo: a prospective study.

BACKGROUND AND STUDY AIMS: Gastric intestinal metaplasia (GIM) is a risk factor for development of intestinal-type gastric cancer. We aimed to assess the usefulness of confocal laser endomicroscopy (CLE) in diagnosing GIM. PATIENTS AND METHODS: 28 patients with known GIM underwent CLE, and CLE criteria for diagnosis of GIM were developed. In addition, 53 consecutive patients with known or suspected GIM were prospectively evaluated. RESULTS: GIM was identified if any of the following three features were present in an image field: goblet cells, columnar absorptive cells and brush border, and villiform foveolar epithelium. GIM was then classified as complete or incomplete according to the shape of the goblet cells, the presence of absorptive cells or brush border, and the architecture of vessels and crypts. In a prospective study, a total of 13 670 CLE images were obtained. Among 267 sites from 53 patients, 160 from 36 patients were diagnosed histopathologically as GIM. The sensitivities of conventional endoscopy and CLE for GIM were 36.88 % vs. 98.13 %, and the specificities were 91.59 % vs. 95.33 %, respectively. The kappa value for the correlation with histological findings was 0.25 for conventional endoscopy vs. 0.94 for CLE. The sensitivity and specificity of CLE were 68.03 % and 89.66 %, respectively, for the diagnosis of complete GIM, and 68.42 % and 83.41 %, respectively, for incomplete GIM; the kappa value for the correspondence between CLE and histological findings was 0.67. CONCLUSION: CLE is a useful and potentially important method for the diagnosis and classification of GIM in vivo.