955 research outputs found
Monitoring of lung edema by microwave reflectometry during lung ischemia-reperfusion injury in vivo
It is still unclear whether lung edema can be monitored by microwave reflectometry and whether the measured changes in lung dry matter content (DMC) are accompanied by changes in PaO(2) and in pro-to anti-inflammatory cytokine expression (IFN-gamma and IL-10). Right rat lung hili were cross-clamped at 37 degrees C for 0, 60, 90 or 120 min ischemia followed by 120 min reperfusion. After 90 min (DMC: 15.9 +/- 1.4%; PaO(2): 76.7 +/- 18 mm Hg) and 120 min ischemia (DMC: 12.8 +/- 0.6%; PaO(2): 43 +/- 7 mm Hg), a significant decrease in DMC and PaO(2) throughout reperfusion compared to 0 min ischemia (DMC: 19.5 +/- 1.11%; PaO(2): 247 +/- 33 mm Hg; p < 0.05) was observed. DMC and PaO(2) decreased after 60 min ischemia but recovered during reperfusion (DMC: 18.5 +/- 2.4%; PaO(2) : 173 +/- 30 mm Hg). DMC values reflected changes on the physiological and molecular level. In conclusion, lung edema monitoring by microwave reflectometry might become a tool for the thoracic surgeon. Copyright (c) 2006 S. Karger AG, Basel
First identification of large electric monopole strength in well-deformed rare earth nuclei
Excited states in the well-deformed rare earth isotopes Sm and
Er were populated via ``safe'' Coulomb excitation at the Munich MLL
Tandem accelerator. Conversion electrons were registered in a cooled Si(Li)
detector in conjunction with a magnetic transport and filter system, the
Mini-Orange spectrometer. For the first excited state in Sm at
1099 keV a large value of the monopole strength for the transition to the
ground state of could be extracted. This confirms the interpretation of the lowest
excited state in Sm as the collective -vibrational
excitation of the ground state. In Er the measured large electric
monopole strength of clearly identifies the state at 1934 keV to be the
-vibrational excitation of the ground state.Comment: submitted to Physics Letters
Radioactive decays at limits of nuclear stability
The last decades brought an impressive progress in synthesizing and studying
properties of nuclides located very far from the beta stability line. Among the
most fundamental properties of such exotic nuclides, usually established first,
is the half-life, possible radioactive decay modes, and their relative
probabilities. When approaching limits of nuclear stability, new decay modes
set in. First, beta decays become accompanied by emission of nucleons from
highly excited states of daughter nuclei. Second, when the nucleon separation
energy becomes negative, nucleons start to be emitted from the ground state.
Here, we present a review of the decay modes occurring close to the limits of
stability. The experimental methods used to produce, identify and detect new
species and their radiation are discussed. The current theoretical
understanding of these decay processes is overviewed. The theoretical
description of the most recently discovered and most complex radioactive
process - the two-proton radioactivity - is discussed in more detail.Comment: Review, 68 pages, 39 figure
Microevolution of Helicobacter pylori during prolonged infection of single hosts and within families
Our understanding of basic evolutionary processes in bacteria is still very limited. For example, multiple recent dating estimates are based on a universal inter-species molecular clock rate, but that rate was calibrated using estimates of geological dates that are no longer accepted. We therefore estimated the short-term rates of mutation and recombination in Helicobacter pylori by sequencing an average of 39,300 bp in 78 gene fragments from 97 isolates. These isolates included 34 pairs of sequential samples, which were sampled at intervals of 0.25 to 10.2 years. They also included single isolates from 29 individuals (average age: 45 years) from 10 families. The accumulation of sequence diversity increased with time of separation in a clock-like manner in the sequential isolates. We used Approximate Bayesian Computation to estimate the rates of mutation, recombination, mean length of recombination tracts, and average diversity in those tracts. The estimates indicate that the short-term mutation rate is 1.4×10−6 (serial isolates) to 4.5×10−6 (family isolates) per nucleotide per year and that three times as many substitutions are introduced by recombination as by mutation. The long-term mutation rate over millennia is 5–17-fold lower, partly due to the removal of non-synonymous mutations due to purifying selection. Comparisons with the recent literature show that short-term mutation rates vary dramatically in different bacterial species and can span a range of several orders of magnitude
An unusual cause of granulomatous disease
BACKGROUND: Chronic granulomatous disease (CGD) is an inherited disorder of phagocytic cells caused by an inability to generate active microbicidal oxygen species required kill certain types of fungi and bacteria. This leads to recurrent life-threatening bacterial and fungal infections with tissue granuloma formation. CASE PRESENTATION: We describe a case of X-linked Chronic granulomatous disease (CGD) diagnosed in an 18-year-old male. He initially presented with granulomatous disease mimicking sarcoidosis and was treated with corticosteroids. He subsequently developed Burkholderia cepacia complex pneumonia and further investigation confirmed a diagnosis of CGD. CONCLUSION: Milder phenotypes of CGD are now being recognised. CGD should be considered in patients of any age with granulomatous diseases, especially if there is a history of recurrent or atypical infection
Protection from pulmonary ischemia-reperfusion injury by adenosine A2A receptor activation
<p>Abstract</p> <p>Background</p> <p>Lung ischemia-reperfusion (IR) injury leads to significant morbidity and mortality which remains a major obstacle after lung transplantation. However, the role of various subset(s) of lung cell populations in the pathogenesis of lung IR injury and the mechanisms of cellular protection remain to be elucidated. In the present study, we investigated the effects of adenosine A<sub>2A </sub>receptor (A<sub>2A</sub>AR) activation on resident lung cells after IR injury using an isolated, buffer-perfused murine lung model.</p> <p>Methods</p> <p>To assess the protective effects of A<sub>2A</sub>AR activation, three groups of C57BL/6J mice were studied: a sham group (perfused for 2 hr with no ischemia), an IR group (1 hr ischemia + 1 hr reperfusion) and an IR+ATL313 group where ATL313, a specific A<sub>2A</sub>AR agonist, was included in the reperfusion buffer after ischemia. Lung injury parameters and pulmonary function studies were also performed after IR injury in A<sub>2A</sub>AR knockout mice, with or without ATL313 pretreatment. Lung function was assessed using a buffer-perfused isolated lung system. Lung injury was measured by assessing lung edema, vascular permeability, cytokine/chemokine activation and myeloperoxidase levels in the bronchoalveolar fluid.</p> <p>Results</p> <p>After IR, lungs from C57BL/6J wild-type mice displayed significant dysfunction (increased airway resistance, pulmonary artery pressure and decreased pulmonary compliance) and significant injury (increased vascular permeability and edema). Lung injury and dysfunction after IR were significantly attenuated by ATL313 treatment. Significant induction of TNF-α, KC (CXCL1), MIP-2 (CXCL2) and RANTES (CCL5) occurred after IR which was also attenuated by ATL313 treatment. Lungs from A<sub>2A</sub>AR knockout mice also displayed significant dysfunction, injury and cytokine/chemokine production after IR, but ATL313 had no effect in these mice.</p> <p>Conclusion</p> <p>Specific activation of A<sub>2A</sub>ARs provides potent protection against lung IR injury via attenuation of inflammation. This protection occurs in the absence of circulating blood thereby indicating a protective role of A<sub>2A</sub>AR activation on resident lung cells such as alveolar macrophages. Specific A<sub>2A</sub>AR activation may be a promising therapeutic target for the prevention or treatment of pulmonary graft dysfunction in transplant patients.</p
- …