491 research outputs found
A modified layer-removal method for residual stress measurement in electrodeposited nickel films
Combining the traditional layer-removal method with a cantilever beam model, a modified layer-removal method is developed and used to measure residual stress in single and multi-layer electrodeposited nickel films with thickness of 2.5 μm. The out-of-plane displacement of the free tip of a cantilever beam is measured by the digital speckle correlation method. The results show that residual stress in a single semimat nickel film is compressive, while in a multi-layer system composed of dark, semimat and holophote nickel, residual stress in the surface layer is tensile. Residual stress decreases gradually with the increase of etching depths of single and multi-layer films. These findings are in qualitative agreement with nanoindentation tests, which confirms the reliability of the modified layer-removal method
In vitro shoot induction and plant regeneration from flower buds in Paphiopedilum orchids
Paphiopedilum species are recalcitrant in tissue culture, and no explant from mature plants has been successfully mass propagated in vitro. This study was aimed at inducing shoots and regenerating plants from the flowering plants of a sequentially flowering Paphiopedilum Deperle and a single floral Paphiopedilum Armeni White. By using cross-sectioned flower buds (FBs), we found that in both species, only sections that contained the base tissue of FBs were able to produce shoots and plants. We have also found that sections of FBs between 1.5 and 3.0 cm from Paphiopedilum Deperle were able to produce shoots, but only sections of FBs > 2.5 cm from Paphiopedilum Armeni White were regenerable. Our microscopic observations revealed that the small bract at the FB base harbored a new miniature FB, which further harbored a primitive FB with dome-shaped meristem-like tissues that presumably led to the plant induction. The reiteration of this pattern resulted in a scorpioid cyme inflorescence architecture in the multifloral Paphiopedilum species, and its failure to reiterate resulted in a single flower. The induction rates were 57-75%, and all plants survived in a greenhouse. This method is potentially applicable for the micropropagation and conservation of slipper orchids
Andrographolide Inhibits PI3K/AKT-Dependent NOX2 and iNOS Expression Protecting Mice against Hypoxia/Ischemia-Induced Oxidative Brain Injury
This study aimed to explore the mechanisms by which andrographolide protects against hypoxia-induced oxidative/nitrosative brain injury provoked by cerebral ischemic/reperfusion (CI/R) injury in mice. Hypoxia in vitro was modeled using oxygen-glucose deprivation (OGD) followed by reoxygenation of BV-2 microglial cells. Our results showed that treatment of mice that have undergone CI/R injury with andrographolide (10-100 mu g/kg, i.v.) at 1 h after hypoxia ameliorated CI/R-induced oxidative/nitrosative stress, brain infarction, and neurological deficits in the mice, and enhanced their survival rate. CI/R induced a remarkable production in the mouse brains of reactive oxygen species (ROS) and a significant increase in protein nitrosylation; this primarily resulted from enhanced expression of NADPH oxidase 2 (NOX2), inducible nitric oxide synthase (iNOS), and the infiltration of CD11b cells due to activation of nuclear factor-kappa B (NF-kappa B) and hypoxia-inducible factor 1-alpha (HIF-1 alpha). All these changes were significantly diminished by andrographolide. In BV-2 cells, OGD induced ROS and nitric oxide production by upregulating NOX2 and iNOS via the phosphatidylinositol-3-kinase (PI3K)/AKT-dependent NF-kappa B and HIF-1 alpha pathways, and these changes were suppressed by andrographolide and LY294002. Our results indicate that andrographolide reduces NOX2 and iNOS expression possibly by impairing PI3K/AKT-dependent NF-kappa B and HIF-1 alpha activation. This compromises microglial activation, which then, in turn, mediates andrographolide's protective effect in the CI/R mice
Glial activation involvement in neuronal death by Japanese encephalitis virus infection
Japanese encephalitis is characterized by profound neuronal destruction/dysfunction and concomitant microgliosis/astrogliosis. Although substantial activation of glia is observed in Japanese encephalitis virus (JEV)-induced Japanese encephalitis, the inflammatory responses and consequences of astrocytes and microglial activation after JEV infection are not fully understood. In this study, infection of cultured neurons/glia with JEV caused neuronal death and glial activation, as evidenced by morphological transformation, increased cell proliferation and elevated tumour necrosis factor (TNF)-alpha, interleukin (IL)-1 beta, IL-6 and RANTES (regulated upon activation, normal T-cell expressed and secreted) production. Replication-competent JEV caused all glial responses and neurotoxicity. However, replication-incompetent JEV lost these abilities, except for the ability to change microglial morphology. The bystander damage caused by activated glia also contributed to JEV-associated neurotoxicity. Microglia underwent morphological changes, increased cell proliferation and elevated TNF-alpha, IL-1 beta, IL-6 and RANTES expression in response to JEV infection. In contrast, IL-6 and RANTES expression, but no apparent morphological changes, proliferation or TNF-alpha/IL-1 beta expression, was demonstrated in JEV-infected astrocytes. Supernatants of JEV-infected microglia, but not JEV-infected astrocytes, induced glial activation and triggered neuronal death. Antibody neutralization studies revealed that TNF-alpha and IL-1 beta, but not RANTES or IL-6, released by activated microglia appeared to play roles in JEV-associated neurotoxicity. In conclusion, following JEV infection, neuronal death was accompanied by concomitant microgliosis and astrogliosis, and neurotoxic mediators released by JEV-activated microglia, rather than by JEV-activated astrocytes, had the ability to amplify the microglial response and cause neuronal death
Measurements of the observed cross sections for exclusive light hadron production in e^+e^- annihilation at \sqrt{s}= 3.773 and 3.650 GeV
By analyzing the data sets of 17.3 pb taken at GeV
and 6.5 pb taken at GeV with the BESII detector at the
BEPC collider, we have measured the observed cross sections for 12 exclusive
light hadron final states produced in annihilation at the two energy
points. We have also set the upper limits on the observed cross sections and
the branching fractions for decay to these final states at 90%
C.L.Comment: 8 pages, 5 figur
Search for the Rare Decays J/Psi --> Ds- e+ nu_e, J/Psi --> D- e+ nu_e, and J/Psi --> D0bar e+ e-
We report on a search for the decays J/Psi --> Ds- e+ nu_e + c.c., J/Psi -->
D- e+ nu_e + c.c., and J/Psi --> D0bar e+ e- + c.c. in a sample of 5.8 * 10^7
J/Psi events collected with the BESII detector at the BEPC. No excess of signal
above background is observed, and 90% confidence level upper limits on the
branching fractions are set: B(J/Psi --> Ds- e+ nu_e + c.c.)<4.8*10^-5, B(J/Psi
--> D- e+ nu_e + c.c.) D0bar e+ e- + c.c.)<1.1*10^-5Comment: 10 pages, 4 figure
Measurements of psi(2S) decays to octet baryon-antibaryon pairs
With a sample of 14 million psi(2S) events collected by the BESII detector at
the Beijing Electron Positron Collider (BEPC), the decay channels psi(2S)->p
p-bar, Lambda Lambda-bar, Sigma0 Sigma0-bar, Xi Xi-bar are measured, and their
branching ratios are determined to be (3.36+-0.09+-0.24)*10E-4,
(3.39+-0.20+-0.32)*10E-4, (2.35+-0.36+-0.32)*10E-4, (3.03+-0.40+-0.32)*10E-4,
respectively. In the decay psi(2S)->p p-bar, the angular distribution parameter
alpha is determined to be 0.82+-0.17+-0.04.Comment: 8 pages, 8 figure
Measurements of the observed cross sections for exclusive light hadrons containing at , 3.650 and 3.6648 GeV
By analyzing the data sets of 17.3, 6.5 and 1.0 pb taken,
respectively, at , 3.650 and 3.6648 GeV with the BES-II
detector at the BEPC collider, we measure the observed cross sections for
, , ,
and at the three energy
points. Based on these cross sections we set the upper limits on the observed
cross sections and the branching fractions for decay into these
final states at 90% C.L..Comment: 7 pages, 2 figure
Partial wave analysis of J/\psi \to \gamma \phi \phi
Using events collected in the BESII detector, the
radiative decay is
studied. The invariant mass distribution exhibits a near-threshold
enhancement that peaks around 2.24 GeV/.
A partial wave analysis shows that the structure is dominated by a
state () with a mass of
GeV/ and a width of GeV/. The
product branching fraction is: .Comment: 11 pages, 4 figures. corrected proof for journa
Direct Measurements of Absolute Branching Fractions for D0 and D+ Inclusive Semimuonic Decays
By analyzing about 33 data sample collected at and around 3.773
GeV with the BES-II detector at the BEPC collider, we directly measure the
branching fractions for the neutral and charged inclusive semimuonic decays
to be and , and determine the ratio of the two branching
fractions to be
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