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12
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"Williams, Carol Lynch"
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Glimpse
Living with their mother who earns money as a prostitute, two sisters take care of each other and when the older one attempts suicide, the younger one tries to uncover the reason.
Book
A-317491, a novel potent and selective non-nucleotide antagonist of P2X3 and P2X2/3 receptors, reduces chronic inflammatory and neuropathic pain in the rat
P2X 3 and P2X 2/3 receptors are highly localized on peripheral and central processes of sensory afferent nerves, and activation of these channels contributes to the pronociceptive effects of ATP. A-317491 is a novel non-nucleotide antagonist of P2X 3 and P2X 2/3 receptor activation. A-317491 potently blocked recombinant human and rat P2X 3 and P2X 2/3 receptor-mediated calcium flux ( K i = 22–92 nM) and was highly selective (IC 50 >10 μM) over other P2 receptors and other neurotransmitter receptors, ion channels, and enzymes. A-317491 also blocked native P2X 3 and P2X 2/3 receptors in rat dorsal root ganglion neurons. Blockade of P2X 3 containing channels was stereospecific because the R -enantiomer (A-317344) of A-317491 was significantly less active at P2X 3 and P2X 2/3 receptors. A-317491 dose-dependently (ED 50 = 30 μmol/kg s.c.) reduced complete Freund's adjuvant-induced thermal hyperalgesia in the rat. A-317491 was most potent (ED 50 = 10–15 μmol/kg s.c.) in attenuating both thermal hyperalgesia and mechanical allodynia after chronic nerve constriction injury. The R -enantiomer, A-317344, was inactive in these chronic pain models. Although active in chronic pain models, A-317491 was ineffective (ED 50 >100 μmol/kg s.c.) in reducing nociception in animal models of acute pain, postoperative pain, and visceral pain. The present data indicate that a potent and selective antagonist of P2X 3 and P2X 2/3 receptors effectively reduces both nerve injury and chronic inflammatory nociception, but P2X 3 and P2X 2/3 receptor activation may not be a major mediator of acute, acute inflammatory, or visceral pain.
Journal Article
Messenger
\"Evie Messenger, who can see and talk to ghosts, tries to solve the mystery of a teenage ghost who is following her\"-- Provided by publisher.
Book
Erratum: Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease
Nat. Genet. 41, 1088–1093 (2009); published online 6 September 2009; corrected after print 9 May 2013 In the version of this article initially published, Reinhard Heun was not included in the author list. This has been corrected in the HTML and PDF versions of the article.
Journal Article
Signed, Skye Harper
In 1972, while her idol, Mark Spitz, is in Germany competing in the Olympics, fifteen-year-old Winston, her Nanny, and her crush, Steve, head to Las Vegas in Steve's parents' motorhome to reconnect with Winston's mother, who left ten years before to become a star.
Book
Erratum: Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease
Nat. Genet. 41, 1088–1093 (2009); published online 6 September; corrected after print 28 September 2009 In the version of this article initially published, the name of the first author of reference 12 was stated incorrectly in the reference list. The correct reference is: “Lambert, J.-C. et al. Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease.
Journal Article
Human Subjects Research Regulation
The current framework for the regulation of human subjects research emerged largely in reaction to the horrors of Nazi human experimentation, revealed at the Nuremburg trials, and the Tuskegee syphilis study, conducted by U.S. government researchers from 1932 to 1972. This framework, combining elements of paternalism with efforts to preserve individual autonomy, has remained fundamentally unchanged for decades. Yet, as this book documents, it has significant flaws -- including its potential to burden important research, overprotect some subjects and inadequately protect others, generate inconsistent results, and lag behind developments in how research is conducted. Invigorated by the U.S. government's first steps toward change in over twenty years,Human Subjects Research Regulationbrings together the leading thinkers in this field from ethics, law, medicine, and public policy to discuss how to make the system better. The result is a collection of novel ideas -- some incremental, some radical -- for the future of research oversight and human subject protection.After reviewing the history of U.S. research regulations, the contributors consider such topics as risk-based regulation; research involving vulnerable populations (including military personnel, children, and prisoners); the relationships among subjects, investigators, sponsors, and institutional review boards; privacy, especially regarding biospecimens and tissue banking; and the possibility of fundamental paradigm shifts.ContributorsAdam Braddock, Alexander Morgan Capron, Ellen Wright Clayton, I. Glenn Cohen, Susan Cox, Amy L. Davis, Hilary Eckert, Barbara J. Evans, Nir Eyal, Heidi Li Feldman, Benjamin Fombonne, Elisa A. Hurley, Ana S. Iltis, Gail H. Javitt, Greg Koski, Nicole Lockhart, Holly Fernandez Lynch, Michael McDonald, Michelle N. Meyer, Osagie K. Obasogie, Efthimios Parasidis, Govind Persad, Rosamond Rhodes, Suzanne M. Rivera, Zachary M. Schrag, Seema K. Shah, Jeffrey Skopek, Laura Stark, Patrick Taylor, Anne Townsend, Carol Weil, Brett A. Williams, Leslie E. Wolf
eBook
Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer's disease, and shows evidence for additional susceptibility genes
We undertook a two-stage genome-wide association study of Alzheimer's disease involving over 16,000 individuals. In stage 1 (3,941 cases and 7,848 controls), we replicated the established association with the APOE locus (most significant SNP: rs2075650, p= 1.8×10−157) and observed genome-wide significant association with SNPs at two novel loci: rs11136000 in the CLU or APOJ gene (p= 1.4×10−9) and rs3851179, a SNP 5′ to the PICALM gene (p= 1.9×10−8). Both novel associations were supported in stage 2 (2,023 cases and 2,340 controls), producing compelling evidence for association with AD in the combined dataset (rs11136000: p= 8.5×10−10, odds ratio= 0.86; rs3851179: p= 1.3×10−9, odds ratio= 0.86). We also observed more variants associated at p< 1×10−5 than expected by chance (p=7.5×10−6), including polymorphisms at the BIN1, DAB1 and CR1 loci.
Journal Article