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- Thomas, R. D., et al.
(author)
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Hot Water from Cold. The Dissociative Recombination of Water Cluster Ions
- 2010
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In: Journal of Physical Chemistry A. - : American Chemical Society (ACS). - 1089-5639 .- 1520-5215. ; 114:14, s. 4843-4846
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Journal article (peer-reviewed)abstract
- Dissociative recombination of the Zundel cation D(5)O(2)(+) almost exclusively produces D + 2 D(2)O with a maximum kinetic energy release of 5.1 eV. An imaging technique is used to investigate the distribution of the available reaction energy among these products. Analysis shows that as much as 4 eV can be stored internally by the molecular fragments, with a preference for producing highly excited molecular fragments, and that the deuteron shows a nonrandom distribution of kinetic energies. A possible mechanism and the implications for these observations are addressed.
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| 2. |
- Thomas, Richard D., et al.
(author)
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Dissociative recombination of LiH2
- 2014
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In: Physical Review A. Atomic, Molecular, and Optical Physics. - 1050-2947 .- 1094-1622. ; 89:5, s. 050701-
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Journal article (peer-reviewed)abstract
- In this paper, we report results regarding how LiH2+ fragments as a result of a low-energy collision with an electron (dissociative recombination), a reaction that contains only elements and particles created during the very first phase of the universe. The collision-energy-dependent reaction rate and cross sections show detailed structures, more so than predicted by theory, suggesting significant rovibrational coupling in the ion and a complex reaction surface. From the structure of the molecule, the reaction predominantly results in the formation of Li + H-2. However, 23% of the reaction flux leads to more interesting products, with 17% producing Li + 2H and 6% producing LiH + H. These last two channels break the strongest molecular bond in the system and, in the case of the latter channel, form a significantly weaker ionic bond. Possible reasons behind this interesting behavior are discussed, together with the interaction between the available reaction channels.
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| 5. |
- Lau, Nga M., et al.
(author)
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Markers of Celiac Disease and Gluten Sensitivity in Children with Autism
- 2013
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In: PLOS ONE. - : Public Library of Science (PLoS). - 1932-6203. ; 8:6, s. e66155-
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Journal article (peer-reviewed)abstract
- Objective: Gastrointestinal symptoms are a common feature in children with autism, drawing attention to a potential association with celiac disease or gluten sensitivity. However, studies to date regarding the immune response to gluten in autism and its association with celiac disease have been inconsistent. The aim of this study was to assess immune reactivity to gluten in pediatric patients diagnosed with autism according to strict criteria and to evaluate the potential link between autism and celiac disease. Methods: Study participants included children (with or without gastrointestinal symptoms) diagnosed with autism according to both the Autism Diagnostic Observation Schedule (ADOS) and the Autism Diagnostic Interview, Revised (ADIR) (n = 37), their unaffected siblings (n = 27), and age-matched healthy controls (n = 76). Serum specimens were tested for antibodies to native gliadin, deamidated gliadin, and transglutaminase 2 (TG2). Affected children were genotyped for celiac disease associated HLA-DQ2 and -DQ8 alleles. Results: Children with autism had significantly higher levels of IgG antibody to gliadin compared with unrelated healthy controls (p<0.01). The IgG levels were also higher compared to the unaffected siblings, but did not reach statistical significance. The IgG anti-gliadin antibody response was significantly greater in the autistic children with gastrointestinal symptoms in comparison to those without them (p<0.01). There was no difference in IgA response to gliadin across groups. The levels of celiac disease-specific serologic markers, i.e., antibodies to deamidated gliadin and TG2, did not differ between patients and controls. An association between increased anti-gliadin antibody and presence of HLA-DQ2 and/or -DQ8 was not observed. Conclusions: A subset of children with autism displays increased immune reactivity to gluten, the mechanism of which appears to be distinct from that in celiac disease. The increased anti-gliadin antibody response and its association with GI symptoms points to a potential mechanism involving immunologic and/or intestinal permeability abnormalities in affected children.
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| 6. |
- Moeller, Sina, et al.
(author)
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Lack of association between autism and anti-GM1 ganglioside antibody
- 2013
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In: Neurology. - 0028-3878 .- 1526-632X. ; 81:18, s. 1640-1641
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Journal article (other academic/artistic)abstract
- Forty of 54 children with autism were reported to have an elevated antibody response to GM1 ganglioside that correlated with disease severity.1 Antiganglioside autoantibodies, especially those directed at GM1, are known to be associated with and play a pathogenic role in some immune-mediated peripheral neuropathies.2,3 The presumed link between autism and anti-GM1 antibodies, therefore, implies that testing may identify a sizable subset of patients who would benefit from immunomodulatory therapy. To evaluate the proposed association between autism and anti-GM1 antibodies, serum samples from children diagnosed with autism by strict clinical criteria and those without autism were analyzed using a standard, validated immunoassay protocol.
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| 7. |
- Schmees, Christian, et al.
(author)
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Macropinocytosis of the PDGF β-receptor promotes fibroblast transformation by H-RasG12V
- 2012
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In: Molecular Biology of the Cell. - 1059-1524 .- 1939-4586. ; 23:13, s. 2571-2582
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Journal article (peer-reviewed)abstract
- Receptor tyrosine kinase (RTK) signaling is frequently increased in tumor cells, sometimes as a result of decreased receptor down-regulation. To what extent the endocytic trafficking routes can contribute to such RTK hyper-activation is unclear. Here, we show for the first time that fibroblast transformation by H-RasG12V induces the internalization of platelet-derived growth factor β-receptor (PDGFRβ) by macropinocytosis, enhancing its signaling activity and increasing anchorage-independent proliferation. H-RasG12V transformation and PDGFRβ activation synergized in stimulating PI 3-kinase activity, leading to receptor macropinocytosis. PDGFRβ macropinocytosis was both necessary and sufficient for enhanced receptor activation. Blocking macropinocytosis by inhibition of phosphatidylinositol (PI) 3-kinase prevented the increase in receptor activity in transformed cells. Conversely, increasing macropinocytosis by Rabankyrin-5 overexpression was sufficient to enhance PDGFRβ activation in non-transformed cells. Simultaneous stimulation with PDGF-BB and epidermal growth factor (EGF) promoted macropinocytosis of both receptors and increased their activation in non-transformed cells. We propose that H-Ras transformation promotes tumor progression by enhancing growth factor receptor signaling as a result of increased receptor macropinocytosis.
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