Origin of blue photoluminescence from colloidal silicon nanocrystals fabricated by femtosecond laser ablation in solution.

We present a detailed investigation into the origin of blue emission from colloidal silicon (Si) nanocrystals (NCs) fabricated by femtosecond laser ablation of Si powder in 1-hexene. High resolution transmission electron microscopy and Raman spectroscopy observations confirm that Si NCs with average size 2.7 nm are produced and well dispersed in 1-hexene. Fourier transform infrared spectrum and x-ray photoelectron spectra have been employed to reveal the passivation of Si NCs surfaces with organic molecules. On the basis of the structural characterization, UV-visible absorption, temperature-dependent photoluminescence (PL), time-resolved PL, and PL excitation spectra investigations, we deduce that room-temperature blue luminescence from colloidal Si NCs originates from the following two processes: (i) under illumination, excitons first form within colloidal Si NCs by direct transition at the X or Γ (Γ25 → Γ'2) point; (ii) and then some trapped excitons migrate to the surfaces of colloidal Si NCs and further recombine via the surface states associated with the Si-C or Si-C-H2 bonds.

High levels of glucose promote the activation of hepatic stellate cells via the p38-mitogen-activated protein kinase signal pathway.

The relationship between the p38-mitogen-activated protein kinase (p38-MAPK) signal pathway and high glucose-induced hepatic stellate cell (HSC) activation was investigated in this study. Sixty human HSC samples were randomly selected and used in the control (cultured normally), high-glucose (cultured in the presence of high glucose), and blocking (cultured under high-glucose conditions in the presence of the p38-MAPK inhibitor, SB203580) groups. The cells were incubated for 120 h and subsequently analyzed for morphological changes by inverted microscopy and for a-smooth muscle actin (a-SMA) expression (to determine the degree of HSC activation) by the method of streptavidin-biotin complex and western blot. Phospho-p38-MAPK protein expression was analyzed by western blotting. a-SMA and phospho-p38-MAPK expression was significantly upregulated in HSCs cultured under high-glucose conditions, compared to the HSCs cultured normally (P < 0.01). On the other hand, phospho-p38-MAPK and a-SMA protein levels were significantly lower in the blocking group compared to the high-glucose group (P < 0.01). Based on these results, we concluded that high-glucose levels induce HSC activation mediated by phospho-p38-MAPK. Therefore, blocking the p38-MAPK signal pathway could inhibit this effect.

Glucagon-like peptide-1 receptor agonists inhibit hepatic stellate cell activation by blocking the p38 MAPK signaling pathway.

We investigated the effects of glucagon-like peptide-1 receptor (GLP-1R) agonists on p38 mitogen-activated protein kinase (MAPK) signaling during inhibition of hepatic stellate cell (HSC) activity. Human HSCs were cultured and morphologically identified. HSC samples were collected and randomly divided into three groups (N = 20 samples per group): a control group treated with high glucose (final concentration 25 mM); a GLP-1R agonist group treated with liraglutide (final concentration 5 mM); and a p38-blocked group treated with the p38 MAPK inhibitor SB203580 (final concentration 14 µM). All cells were cultured for 120 h followed by detection of phosphorylated p38 MAPK (p-p38 MAPK) and α-smooth muscle actin (α-SMA, a measure of HSC activation) by western blot. p-p38 MAPK and α-SMA expression levels were both significantly lower in HSCs in the GLP-1R agonist and p38-blocked groups compared with the control group (all P < 0.01). GLP-1R agonists may inhibit the activation of HSCs by blocking the p38 MAPK signaling pathway.

A comparison of an anti-CD25 immunotoxin, Ontak and anti-CD25 microbeads for their ability to deplete alloreactive T cells in vitro.

Ex vivo depletion of alloreactive CD25(+) T cells from a stem cell transplant (SCT) can reduce the incidence of graft-versus-host disease (GVHD) while preserving antimicrobial and perhaps antileukemia activity. However, the most effective methods for allodepleting T cells prior to transplant have not been determined. In this study, we have compared three agents that deplete CD25(+) activated, alloreactive T cells. These included Ontak (Denileukin Diftitox), an IL-2 fusion toxin, anti-CD25 microbeads (MACS), an anti-CD25 immunotoxin (IT) and a combination of the IT and MACS. Peripheral blood mononuclear cells (PBMCs) activated in a primary mixed lymphocyte reaction (MLR) were allodepleted using optimal amounts of each agent, and the cells were then analyzed by flow cytometry. The treated cells were examined both for remaining alloreactivity and for the preservation of third party reactivity by testing them in a secondary MLR. Our data demonstrate that both the anti-CD25 IT and the anti-CD25 MACS were equally effective in depleting CD4(+)CD25(+) cells and in sparing T cells that were reactive with third party cells. The anti-CD25 IT was, however, superior in depleting alloreactive CD8(+)CD25(+) cells. In contrast, Ontak did not eliminate alloreactive cells and the Ontak-treated cells retained significant reactivity against the original stimulator cells.

Self-instability of finite sized solid-liquid interfaces.

In solid-liquid systems, macroscopic solids lose their equilibrium and melt in a manner that results in overall movement of the solid-liquid interface. This phenomenon occurs when they are subjected to temperature gradients or external stress, for example. However, many experiments suggest that the melting of nano- and micro-sized metallic nuclei follows a different process not described by traditional melting theory. In this paper, we demonstrate through simulation that the melting of solid nuclei of these sizes occurs via random breaches at the interfaces. Moreover, this breaching process occurs at the exact solid-liquid equilibrium temperature and in the absence of any external disturbance, which suggests the name "self-instability" for this melting process. We attribute this spontaneous instability to the curvature of the samples; based on the relationship between the sample's instability and its curvature, we propose a destabilizing model for small systems. This model fits well with experimental results and leads to new insights into the instability behavior of small-sized systems; these insights have broad implications for research topics ranging from dendrite self-fragmentation to nanoparticle instability.

[Pharmacological localization of Horner's syndrome. Case report].

Horner's syndrome is derived from an interruption of the sympathetic pathway at any point along its course between the hypothalamus and the orbit. This pathway is generally considered to consist of three neurons. It had been suggested that the pupillary response to various pharmacologic agents will aid in localizing the lesioned neuron in the sympathetic pathway. We had the opportunity to observe a patient who developed Horner's syndrome as a consequence of pulmonary apex adenocarcinoma. Clinical, radiologic and pharmacologic studies are presented. The methods of pharmacologic localization are discussed.