Publications by authors named "Aditya Agrahari"

2 Publications

  • Page 1 of 1

Crystal structure of 9-methacryloylanthracene.

Acta Crystallogr E Crystallogr Commun 2015 Apr 11;71(Pt 4):357-9. Epub 2015 Mar 11.

Department of Chemistry, University of Akron, Akron OH 44325, USA.

In the title compound, C18H14O, with systematic name 1-(anthracen-9-yl)-2-methyl-prop-2-en-1-one, the ketonic C atom lies 0.2030 (16) Å out of the anthryl-ring-system plane. The dihedral angle between the planes of the anthryl and methacryloyl moieties is 88.30 (3)° and the stereochemistry about the Csp (2)-Csp (2) bond in the side chain is transoid. In the crystal, the end rings of the anthryl units in adjacent mol-ecules associate in parallel-planar orientations [shortest centroid-centroid distance = 3.6320 (7) Å]. A weak hydrogen bond is observed between an aromatic H atom and the O atom of a mol-ecule displaced by translation in the a-axis direction, forming sheets of parallel-planar anthryl groups packing in this direction.
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http://dx.doi.org/10.1107/S2056989015004090DOI Listing
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4438842PMC
April 2015

The role of trace elements, thiamin (e) and transketolase in autism and autistic spectrum disorder.

Front Biosci (Elite Ed) 2015 Jan 1;7:229-41. Epub 2015 Jan 1.

Department of Chemistry, Cleveland State University, Cleveland OH USA.

Although there has been much research into autism or autistic spectrum disorder (ASD), there is room for considerable conjecture regarding the etiology of these developmental brain disorders. ASD is marked by a complex interaction between environmental factors and genetic predisposition, including epistasis. This manuscript argues that changes in oxidative metabolism, thiamine homeostasis, heavy metal deposition and cellular immunity have a role in the etiopathogenesis of autism and ASD. Recent findings from our group and others provide evidence for abnormal thiol metabolism, marked by significant alteration in the deposition of several trace heavy metal species. Together with these, we find differences in thiamine homeostasis in ASD patients, which can be corrected by supplementation. We hypothesize that altered thiol metabolism from heavy metal toxicity, one of the key mechanisms for oxidative stress production, may be responsible for the biochemical alterations in transketolase, dysautonomia and abnormal thiamine homeostasis. Although it is unknown why these particular metals accumulate, we suspect that children with ASD and forms of autism may have particular trouble excreting thiol-toxic heavy metal species, many of which exist as divalent cations. We maintain mercury accumulation is evidence of altered clearance. Together with concomitant oxidative stress, these findings may offer an intriguing component or possible mechanism for oxidative stress-mediated neurodegeneration in ASD patients. Regardless of the exact cause, these factors may be more important to the etiology of this symptomatically diverse disease spectrum. Here, we offer insight into new avenues of exploration as well as the development of novel treatment approaches for these growing and devastating diseases.
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http://dx.doi.org/10.2741/730DOI Listing
January 2015