82 research outputs found
The cometary composition of a protoplanetary disk as revealed by complex cyanides
Observations of comets and asteroids show that the Solar Nebula that spawned
our planetary system was rich in water and organic molecules. Bombardment
brought these organics to the young Earth's surface, seeding its early
chemistry. Unlike asteroids, comets preserve a nearly pristine record of the
Solar Nebula composition. The presence of cyanides in comets, including 0.01%
of methyl cyanide (CH3CN) with respect to water, is of special interest because
of the importance of C-N bonds for abiotic amino acid synthesis. Comet-like
compositions of simple and complex volatiles are found in protostars, and can
be readily explained by a combination of gas-phase chemistry to form e.g. HCN
and an active ice-phase chemistry on grain surfaces that advances
complexity[3]. Simple volatiles, including water and HCN, have been detected
previously in Solar Nebula analogues - protoplanetary disks around young stars
- indicating that they survive disk formation or are reformed in situ. It has
been hitherto unclear whether the same holds for more complex organic molecules
outside of the Solar Nebula, since recent observations show a dramatic change
in the chemistry at the boundary between nascent envelopes and young disks due
to accretion shocks[8]. Here we report the detection of CH3CN (and HCN and
HC3N) in the protoplanetary disk around the young star MWC 480. We find
abundance ratios of these N-bearing organics in the gas-phase similar to
comets, which suggests an even higher relative abundance of complex cyanides in
the disk ice. This implies that complex organics accompany simpler volatiles in
protoplanetary disks, and that the rich organic chemistry of the Solar Nebula
was not unique.Comment: Definitive version of the manuscript is published in Nature, 520,
7546, 198, 2015. This is the author's versio
PET/CT Imaging of c-Myc Transgenic Mice Identifies the Genotoxic N-Nitroso-Diethylamine as Carcinogen in a Short-Term Cancer Bioassay
Background: More than 100,000 chemicals are in use but have not been tested for their safety. To overcome limitations in the cancer bioassay several alternative testing strategies are explored. The inability to monitor non-invasively onset and progression of disease limits, however, the value of current testing strategies. Here, we report the application of in vivo imaging to a c-Myc transgenic mouse model of liver cancer for the development of a short-term cancer bioassay. Methodology/Principal Findings: mCT and 18 F-FDG mPET were used to detect and quantify tumor lesions after treatment with the genotoxic carcinogen NDEA, the tumor promoting agent BHT or the hepatotoxin paracetamol. Tumor growth was investigated between the ages of 4 to 8.5 months and contrast-enhanced mCT imaging detected liver lesions as well as metastatic spread with high sensitivity and accuracy as confirmed by histopathology. Significant differences in the onset of tumor growth, tumor load and glucose metabolism were observed when the NDEA treatment group was compared with any of the other treatment groups. NDEA treatment of c-Myc transgenic mice significantly accelerated tumor growth and caused metastatic spread of HCC in to lung but this treatment also induced primary lung cancer growth. In contrast, BHT and paracetamol did not promote hepatocarcinogenesis. Conclusions/Significance: The present study evidences the accuracy of in vivo imaging in defining tumor growth, tumor load, lesion number and metastatic spread. Consequently, the application of in vivo imaging techniques to transgeni
IgE-dependent enhancement of Th2 cell-mediated allergic inflammation in the airways
T helper 2 (Th2) cell-derived cytokines, including interleukin (IL)-4, IL-5 and IL-13, play important roles in causing allergic airway inflammation. In contrast to Th2 cells, however, the role of IgE and mast cells in inducing allergic airway inflammation is not understood fully. In the present study, we addressed this point using transgenic mice expressing trinitrophenyl (TNP)-specific IgE (TNP–IgE mice), which enable us to investigate the role of IgE without the influence of antigen-specific T cell activation and other immunoglobulins. When the corresponding antigen, TNP–BSA, was administered intranasally to TNP–IgE mice, a large number of CD4(+) T cells were recruited into the airways. In contrast, TNP–BSA administration did not induce eosinophil recruitment into the airways or airway hyperreactivity. Furthermore, when ovalbumin (OVA)-specific Th2 cells were transferred to TNP–IgE mice and the mice were challenged with inhaled OVA, TNP–BSA administration increased OVA-specific T cell recruitment and then enhanced Th2 cell-mediated eosinophil recruitment into the airways. These results indicate that IgE-induced mast cell activation principally induces CD4(+) T cell recruitment into the airways and thus plays an important role in enhancing Th2 cell-mediated eosinophilic airway inflammation by recruiting Th2 cells into the site of allergic inflammation
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