Reconstruction of plasma density profiles by measuring spectra of radiation emitted from oscillating plasma dipoles

We suggest a new method for characterising non-uniform density distributions of plasma by measuring the spectra of radiation emitted from a localised plasma dipole oscillator excited by colliding electromagnetic pulses. The density distribution can be determined by scanning the collision point in space. Two-dimensional particle-in-cell simulations demonstrate the reconstruction of linear and nonlinear density profiles corresponding to laser-produced plasma. The method can be applied to a wide range of plasma, including fusion and low temperature plasmas. It overcomes many of the disadvantages of existing methods that only yield average densities along the path of probe pulses, such as interferometry and spectroscopy

Residual stress measurement in thin films using the semi-destructive ring-core drilling method using Focused Ion Beam

In the present study, residual stress evaluation in thin films was achieved using a semi-destructive trench-cutting method. Focused Ion Beam (FIB) was employed to introduce the strain relief by ring-core milling, i.e. creating a trench around an "island". Either SEM or FIB imaging can be used to record sequences of images for strain change evaluation by Digital Image Correlation (DIC) analysis of micrographs. A regular array of shallow holes was drilled on a thin overlayer of Pt (∼100nm) deposited on to the film prior to patterning and trenching, in order to reduce the damage introduced by the ion beam during imaging and to assist the DIC strain evaluation by adding traceable markers. Finite Element (FE) simulation was also carried out to predict the curves for strain relief as a function of milling depth, and compared with the experimental measurements, which show good agreement with each other. An empirical mathematical description of the curves was proposed that allows efficient residual stress evaluation in thin solid films. © 2011 Published by Elsevier Ltd

Natural killer cells attenuate cytomegalovirus-induced hearing loss in mice

<div><p>Congenital cytomegalovirus (CMV) infection is the most common non-hereditary cause of sensorineural hearing loss (SNHL) yet the mechanisms of hearing loss remain obscure. Natural Killer (NK) cells play a critical role in regulating murine CMV infection via NK cell recognition of the Ly49H cell surface receptor of the viral-encoded m157 ligand expressed at the infected cell surface. This Ly49H NK receptor/m157 ligand interaction has been found to mediate host resistance to CMV in the spleen, and lung, but is much less effective in the liver, so it is not known if this interaction is important in the context of SNHL. Using a murine model for CMV-induced labyrinthitis, we have demonstrated that the Ly49H/m157 interaction mediates host resistance in the temporal bone. BALB/c mice, which lack functional Ly49H, inoculated with mCMV at post-natal day 3 developed profound hearing loss and significant outer hair cell loss by 28 days of life. In contrast, C57BL/6 mice, competent for the Ly49H/m157 interaction, had minimal hearing loss and attenuated outer hair cell loss with the same mCMV dose. Administration of Ly49H blocking antibody or inoculation with a mCMV viral strain deleted for the m157 gene rendered the previously resistant C57BL/6 mouse strain susceptible to hearing loss to a similar extent as the BALB/c mouse strain indicating a direct role of the Ly49H/m157 interaction in mCMV-dependent hearing loss. Additionally, NK cell recruitment to sites of infection was evident in the temporal bone of inoculated susceptible mouse strains. These results demonstrate participation of NK cells in protection from CMV-induced labyrinthitis and SNHL in mice.</p></div

Pathophysiology of acute experimental pancreatitis: Lessons from genetically engineered animal models and new molecular approaches

The incidence of acute pancreatitis is growing and worldwide population-based studies report a doubling or tripling since the 1970s. 25% of acute pancreatitis are severe and associated with histological changes of necrotizing pancreatitis. There is still no specific medical treatment for acute pancreatitis. The average mortality resides around 10%. In order to develop new specific medical treatment strategies for acute pancreatitis, a better understanding of the pathophysiology during the onset of acute pancreatitis is necessary. Since it is difficult to study the early acinar events in human pancreatitis, several animal models of acute pancreatitis have been developed. By this, it is hoped that clues into human pathophysiology become possible. In the last decade, while employing molecular biology techniques, a major progress has been made. The genome of the mouse was recently sequenced. Various strategies are possible to prove a causal effect of a single gene or protein, using either gain-of-function (i.e., overexpression of the protein of interest) or loss-of-function studies (i.e., genetic deletion of the gene of interest). The availability of transgenic mouse models and gene deletion studies has clearly increased our knowledge about the pathophysiology of acute pancreatitis and enables us to study and confirm in vitro findings in animal models. In addition, transgenic models with specific genetic deletion or overexpression of genes help in understanding the role of one specific protein in a cascade of inflammatory processes such as pancreatitis where different proteins interact and co-react. This review summarizes the recent progress in this field. Copyright (c) 2005 S. Karger AG, Basel

Quarkonium dissociation by anisotropy

We compute the screening length for quarkonium mesons moving through an anisotropic, strongly coupled N=4 super Yang-Mills plasma by means of its gravity dual. We present the results for arbitrary velocities and orientations of the mesons, as well as for arbitrary values of the anisotropy. The anisotropic screening length can be larger or smaller than the isotropic one, and this depends on whether the comparison is made at equal temperatures or at equal entropy densities. For generic motion we find that: (i) mesons dissociate above a certain critical value of the anisotropy, even at zero temperature; (ii) there is a limiting velocity for mesons in the plasma, even at zero temperature; (iii) in the ultra-relativistic limit the screening length scales as $(1-v^2)^\epsilon$ with \epsilon =1/2, in contrast with the isotropic result \epsilon =1/4.Comment: 39 pages, 26 figures; v2: minor changes, added reference

An iron-based beverage, HydroFerrate fluid (MRN-100), alleviates oxidative stress in murine lymphocytes in vitro

BackgroundSeveral studies have examined the correlation between iron oxidation and H2O2 degradation. The present study was carried out to examine the protective effects of MRN-100 against stress-induced apoptosis in murine splenic cells in vitro. MRN-100, or HydroFerrate fluid, is an iron-based beverage composed of bivalent and trivalent ferrates.MethodsSplenic lymphocytes from mice were cultured in the presence or absence of MRN-100 for 2 hrs and were subsequently exposed to hydrogen peroxide (H2O2) at a concentration of 25 μM for 14 hrs. Percent cell death was examined by flow cytometry and trypan blue exclusion. The effect of MRN-100 on Bcl-2 and Bax protein levels was determined by Western blot.ResultsResults show, as expected, that culture of splenic cells with H2O2 alone results in a significant increase in cell death (apoptosis) as compared to control (CM) cells. In contrast, pre-treatment of cells with MRN-100 followed by H2O2 treatment results in significantly reduced levels of apoptosis. In addition, MRN-100 partially prevents H2O2-induced down-regulation of the anti-apoptotic molecule Bcl-2 and upregulation of the pro-apoptotic molecule Bax.ConclusionOur findings suggest that MRN-100 may offer a protective effect against oxidative stress-induced apoptosis in lymphocytes

Use of a colonoscope for distal duodenal stent placement in patients with malignant obstruction

Background: Stent placement in the distal duodenum or proximal jejunum with a therapeutic gastroscope can be difficult, because of the reach of the endoscope, loop formation in the stomach, and flexibility of the gastroscope. The use of a colonoscope may overcome these problems. Objective: To report our experience with distal duodenal stent placement in 16 patients using a colonoscope. Methods: Multicenter, retrospective series of patients with a malignant obstruction at the level of the distal duodenum and proximal jejunum and treated by stent placement using a colonoscope. Main outcome measurements are technical success, ability to eat, complications, and survival. Results: Stent placement was technically feasible in 93% (15/16) of patients. Food intake improved from a median gastric outlet obstruction scoring system (GOOSS) score of 1 (no oral intake) to 3 (soft solids) (p = 0.001). Severe complications were not observed. One patient had persistent obstructive symptoms presumably due to motility problems. Recurrent obstructive symptoms were caused by tissue/tumor ingrowth through the stent mesh [n = 6 (38%)] and stent occlusion by debris [n = 1 (6%)]. Reinterventions included additional stent placement [n = 5 (31%)], gastrojejunostomy [n = 2 (12%)], and endoscopic stent cleansing [n = 1 (6%)]. Median survival was 153 days. Conclusion: Duodenal stent placement can effectively and safely be performed using a colonoscope in patients with an obstruction at the level of the distal duodenum or proximal jejunum. A colonoscope has the advantage that it is long enough and offers good endoscopic stiffness, which avoids looping in the stomach

MicroRNAs in pulmonary arterial remodeling

Pulmonary arterial remodeling is a presently irreversible pathologic hallmark of pulmonary arterial hypertension (PAH). This complex disease involves pathogenic dysregulation of all cell types within the small pulmonary arteries contributing to vascular remodeling leading to intimal lesions, resulting in elevated pulmonary vascular resistance and right heart dysfunction. Mutations within the bone morphogenetic protein receptor 2 gene, leading to dysregulated proliferation of pulmonary artery smooth muscle cells, have been identified as being responsible for heritable PAH. Indeed, the disease is characterized by excessive cellular proliferation and resistance to apoptosis of smooth muscle and endothelial cells. Significant gene dysregulation at the transcriptional and signaling level has been identified. MicroRNAs are small non-coding RNA molecules that negatively regulate gene expression and have the ability to target numerous genes, therefore potentially controlling a host of gene regulatory and signaling pathways. The major role of miRNAs in pulmonary arterial remodeling is still relatively unknown although research data is emerging apace. Modulation of miRNAs represents a possible therapeutic target for altering the remodeling phenotype in the pulmonary vasculature. This review will focus on the role of miRNAs in regulating smooth muscle and endothelial cell phenotypes and their influence on pulmonary remodeling in the setting of PAH