109 research outputs found
Few-photon single ionization of cold rubidium in the over-the-barrier regime
Photoionization of the rubidium (Rb) atoms cooled in a magneto-optical trap,
characterized by the coexistence of the ground 5 and the excited
5 states, is investigated experimentally and theoretically with the
400 nm femtosecond laser pulses at intensities of W/cm -
W/cm. Recoil-ion momentum distribution (RIMD) of Rb
exhibits rich ring-like structures and their energies correspond to one-photon
ionization of the 5 state, two-photon and three-photon ionizations of
the 5 state, respectively. With the increasing of , we find that
experimental signals near zero-momentum (NZM) in RIMDs resulted from the
5 state enhance dramatically and its peaked Rb momenta dwindle
obviously while that from the 5 state is maintained. Meanwhile, the
ion-yield ratio of the 5 over the 5 states varies from to
as increases. These features indicate a transition from
perturbative ionization to strong-perturbative ionization for the 5
state. Numerical simulations by solving the time-dependent Schr\"odinger
equation (TDSE) can qualitatively explain the measurements of RIMD, photoion
angular distributions, as well as ion-yield ratio. However, some discrepancies
still exist, especially for the NZM dip, which could stem from the
electron-electron correlation that is neglected in the present TDSE simulations
since we have adopted the single-active-electron approximation
Ellipticity-dependent sequential over-barrier ionization of cold rubidium
We perform high-resolution measurements of momentum distribution on Rb
recoil ions up to charge state , where laser-cooled rubidium atoms are
ionized by femtosecond elliptically polarized lasers with the pulse duration of
35 fs and the intensity of 3.310 W/cm in the over-barrier
ionization (OBI) regime. The momentum distributions of the recoil ions are
found to exhibit multi-band structures as the ellipticity varies from the
linear to circular polarizations. The origin of these band structures can be
explained quantitatively by the classical OBI model and dedicated classical
trajectory Monte Carlo simulations with Heisenberg potential. Specifically,
with back analysis of the classical trajectories, we reveal the ionization time
and the OBI geometry of the sequentially released electrons, disentangling the
mechanisms behind the tilted angle of the band structures. These results
indicate that the classical treatment can describe the strong-field multiple
ionization processes of alkali atoms
Phosphine-catalyzed activation of cyclopropenones: a versatile C3 synthon for (3+2) annulations with unsaturated electrophiles
We herein report a phosphine-catalyzed (3 + 2) annulation of cyclopropenones with a wide variety of electrophilic π systems, including aldehydes, ketoesters, imines, isocyanates, and carbodiimides, offering products of butenolides, butyrolactams, maleimides, and iminomaleimides, respectively, in high yields with broad substrate scope. An α-ketenyl phosphorous ylide is validated as the key intermediate, which undergoes preferential catalytic cyclization with aldehydes rather than stoichiometric Wittig olefinations. This phosphine-catalyzed activation of cyclopropenones thus supplies a versatile C3 synthon for formal cycloadditon reactions
Three-dimensional controlled growth of monodisperse sub-50 nm heterogeneous nanocrystals
The ultimate frontier in nanomaterials engineering is to realize their composition control with atomic scale precision to enable fabrication of nanoparticles with desirable size, shape and surface properties. Such control becomes even more useful when growing hybrid nanocrystals designed to integrate multiple functionalities. Here we report achieving such degree of control in a family of rare-earth-doped nanomaterials. We experimentally verify the co-existence and different roles of oleate anions (OA-) and molecules (OAH) in the crystal formation. We identify that the control over the ratio of OA- to OAH can be used to directionally inhibit, promote or etch the crystallographic facets of the nanoparticles. This control enables selective grafting of shells with complex morphologies grown over nanocrystal cores, thus allowing the fabrication of a diverse library of monodisperse sub-50 nm nanoparticles. With such programmable additive and subtractive engineering a variety of three-dimensional shapes can be implemented using a bottom-up scalable approach
Novel Swine Influenza Virus Reassortants in Pigs, China
During swine influenza virus surveillance in pigs in China during 2006–2009, we isolated subtypes H1N1, H1N2, and H3N2 and found novel reassortment between contemporary swine and avian panzootic viruses. These reassortment events raise concern about generation of novel viruses in pigs, which could have pandemic potential
Protective effects of fentanyl preconditioning on cardiomyocyte apoptosis induced by ischemia-reperfusion in rats
Noise Filtering Strategies of Adaptive Signaling Networks: The Case of E. Coli Chemotaxis
Two distinct mechanisms for filtering noise in an input signal are identified
in a class of adaptive sensory networks. We find that the high frequency noise
is filtered by the output degradation process through time-averaging; while the
low frequency noise is damped by adaptation through negative feedback. Both
filtering processes themselves introduce intrinsic noises, which are found to
be unfiltered and can thus amount to a significant internal noise floor even
without signaling. These results are applied to E. coli chemotaxis. We show
unambiguously that the molecular mechanism for the Berg-Purcell time-averaging
scheme is the dephosphorylation of the response regulator CheY-P, not the
receptor adaptation process as previously suggested. The high frequency noise
due to the stochastic ligand binding-unbinding events and the random ligand
molecule diffusion is averaged by the CheY-P dephosphorylation process to a
negligible level in E.coli. We identify a previously unstudied noise source
caused by the random motion of the cell in a ligand gradient. We show that this
random walk induced signal noise has a divergent low frequency component, which
is only rendered finite by the receptor adaptation process. For gradients
within the E. coli sensing range, this dominant external noise can be
comparable to the significant intrinsic noise in the system. The dependence of
the response and its fluctuations on the key time scales of the system are
studied systematically. We show that the chemotaxis pathway may have evolved to
optimize gradient sensing, strong response, and noise control in different time
scalesComment: 15 pages, 4 figure
Docosahexaenoic Acid-Derived Neuroprotectin D1 Induces Neuronal Survival via Secretase- and PPARγ-Mediated Mechanisms in Alzheimer's Disease Models
Neuroprotectin D1 (NPD1) is a stereoselective mediator derived from the omega-3 essential fatty acid docosahexaenoic acid (DHA) with potent inflammatory resolving and neuroprotective bioactivity. NPD1 reduces Aβ42 peptide release from aging human brain cells and is severely depleted in Alzheimer's disease (AD) brain. Here we further characterize the mechanism of NPD1's neurogenic actions using 3xTg-AD mouse models and human neuronal-glial (HNG) cells in primary culture, either challenged with Aβ42 oligomeric peptide, or transfected with beta amyloid precursor protein (βAPP)sw (Swedish double mutation APP695sw, K595N-M596L). We also show that NPD1 downregulates Aβ42-triggered expression of the pro-inflammatory enzyme cyclooxygenase-2 (COX-2) and of B-94 (a TNF-α-inducible pro-inflammatory element) and apoptosis in HNG cells. Moreover, NPD1 suppresses Aβ42 peptide shedding by down-regulating β-secretase-1 (BACE1) while activating the α-secretase ADAM10 and up-regulating sAPPα, thus shifting the cleavage of βAPP holoenzyme from an amyloidogenic into the non-amyloidogenic pathway. Use of the thiazolidinedione peroxisome proliferator-activated receptor gamma (PPARγ) agonist rosiglitazone, the irreversible PPARγ antagonist GW9662, and overexpressing PPARγ suggests that the NPD1-mediated down-regulation of BACE1 and Aβ42 peptide release is PPARγ-dependent. In conclusion, NPD1 bioactivity potently down regulates inflammatory signaling, amyloidogenic APP cleavage and apoptosis, underscoring the potential of this lipid mediator to rescue human brain cells in early stages of neurodegenerations
Bone Marrow Derived Mesenchymal Stem Cells Inhibit Inflammation and Preserve Vascular Endothelial Integrity in the Lungs after Hemorrhagic Shock
Hemorrhagic shock (HS) and trauma is currently the leading cause of death in young adults worldwide. Morbidity and mortality after HS and trauma is often the result of multi-organ failure such as acute lung injury (ALI) and acute respiratory distress syndrome (ARDS), conditions with few therapeutic options. Bone marrow derived mesenchymal stem cells (MSCs) are a multipotent stem cell population that has shown therapeutic promise in numerous pre-clinical and clinical models of disease. In this paper, in vitro studies with pulmonary endothelial cells (PECs) reveal that conditioned media (CM) from MSCs and MSC-PEC co-cultures inhibits PEC permeability by preserving adherens junctions (VE-cadherin and β-catenin). Leukocyte adhesion and adhesion molecule expression (VCAM-1 and ICAM-1) are inhibited in PECs treated with CM from MSC-PEC co-cultures. Further support for the modulatory effects of MSCs on pulmonary endothelial function and inflammation is demonstrated in our in vivo studies on HS in the rat. In a rat “fixed volume” model of mild HS, we show that MSCs administered IV potently inhibit systemic levels of inflammatory cytokines and chemokines in the serum of treated animals. In vivo MSCs also inhibit pulmonary endothelial permeability and lung edema with concurrent preservation of the vascular endothelial barrier proteins: VE-cadherin, Claudin-1, and Occludin-1. Leukocyte infiltrates (CD68 and MPO positive cells) are also decreased in lungs with MSC treatment. Taken together, these data suggest that MSCs, acting directly and through soluble factors, are potent stabilizers of the vascular endothelium and inflammation. These data are the first to demonstrate the therapeutic potential of MSCs in HS and have implications for the potential use of MSCs as a cellular therapy in HS-induced lung injury
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