Appendix 2-5: Rejected ecotox bibliography for Chlorpyrifos



Download 6.25 Mb.
Page114/151
Date conversion04.02.2017
Size6.25 Mb.
1   ...   110   111   112   113   114   115   116   117   ...   151
Bis-I, U0126, lead, methylmercury, and amphetamine), while trans-Retinoic acid decreased cell viability but not neurite outgrowth. Valproic acid was without effect. The sensitivity of the two models was chemical specific: NS-1 cells were more sensitive to Bis-I, methylmercury and trans-Retinoic acid, while CGC were more sensitive to U0126, lead, and amphetamine. For every chemical (except trans-Retinoic acid), neurite outgrowth was equal to or more sensitive than cell viability. In comparison, out of seven chemicals without prior evidence for effects on neurite outgrowth, only one decreased neurite outgrowth (diphenhydramine in CGC). These findings demonstrate that the effects of chemicals on neurite outgrowth may be cell type specific. Published by Elsevier Inc.
Keywords: Neurite growth, Chemical screening, High content analysis, Neuronal cell
ISI Document Delivery No.: 560DF

1091. Raevskii, O. A.; Razdol'skii, A. N.; Tonkopii, V. D.; Iofina, I. V., and Zagrebin, A. O. Classificatory and Quantitative Models of the Relationship Between the Structures of Chemical Compounds and Their Toxicity for Daphnia magna. 2008; 42, (6): 329-334.


Rec #: 1260
Keywords: NO CONC,QSAR
Call Number: NO CONC (ADC,AMSV,AMYOH,ATN,CBF,CHT,CPY,CYP,DCA,DDVP,DM,DMT,DZ,ETHN,FNT,FNV,FPP,MCRE,MLO,MOL,NCTN,PCP,PMR,PPNOL,PPX,RSM,SMT,STCH,TCF,nBUT), NO QSAR (ADC,AMSV,AMYOH,ATN,CBF,CHT,CPY,CYP,DCA,DDVP,DM,DMT,DZ,ETHN,FNT,FNV,FPP,MCRE,MLO,MOL,NCTN,PCP,PMR,PPNOL,PPX,RSM,SMT,STCH,TCF,nBUT)
Notes: Chemical of Concern: 24DC,2BE,3CE,ADC,AMSV,AMYOH,AN,ATN,BNZ,C6OH,CBF,CHT,CPY,CTC,CYP,DCA,DDVP,DM,DMT,DZ,EGY,EPRN,ETHN,FNT,FNV,FPP,HPT,MCRE,MLO,MOL,NCTN,PCP,PL,PMR,PPNOL,PPX,PRN,RSM,SMT,STCH,TCF,TEPP,nBUT

1092. Rafalska-Metcalf, I. U.; Powers, S. L.; Joo, L. M.; Leroy, G., and Janicki, S. M. Single Cell Analysis of Transcriptional Activation Dynamics.


Rec #: 50589
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: Nucleic Acids Res. 1992 Jan 25;20(2):273-8 (medline /1311071)
COMMENTS: Cites: J Cell Sci. 2007 Jul 15;120(Pt 14):2301-7 (medline /17606985)
COMMENTS: Cites: Nature. 1989 Jul 6;340(6228):66-8 (medline /2662015)
COMMENTS: Cites: Mol Cell Biol. 1995 Jul;15(7):3685-96 (medline /7791775)
COMMENTS: Cites: EMBO J. 1994 Oct 17;13(20):4807-15 (medline /7957049)
COMMENTS: Cites: Cell. 1998 Jan 9;92(1):105-16 (medline /9489704)
COMMENTS: Cites: Cell. 1999 Apr 30;97(3):299-311 (medline /10319811)
COMMENTS: Cites: Science. 2000 Feb 18;287(5456):1262-5 (medline /10678832)
COMMENTS: Cites: Nature. 2000 Apr 6;404(6778):604-9 (medline /10766243)
COMMENTS: Cites: Microbiol Mol Biol Rev. 2000 Jun;64(2):435-59 (medline /10839822)
COMMENTS: Cites: Cell Growth Differ. 2000 Aug;11(8):417-24 (medline /10965846)
COMMENTS: Cites: Nature. 2000 Sep 28;407(6803):471-5 (medline /11028991)
COMMENTS: Cites: Genes Dev. 2000 Oct 15;14(20):2551-69 (medline /11040209)
COMMENTS: Cites: Cell. 2000 Nov 10;103(4):667-78 (medline /11106736)
COMMENTS: Cites: Nat Cell Biol. 2000 Dec;2(12):871-8 (medline /11146650)
COMMENTS: Cites: Science. 2001 Feb 2;291(5505):843-7 (medline /11225636)
COMMENTS: Cites: EMBO J. 2001 May 1;20(9):2224-35 (medline /11331588)
COMMENTS: Cites: J Cell Biol. 2001 Jul 9;154(1):33-48 (medline /11448988)
COMMENTS: Cites: Cell. 2002 Feb 22;108(4):439-51 (medline /11909516)
COMMENTS: Cites: Mol Cell Biol. 2002 Jun;22(11):3794-802 (medline /11997514)
COMMENTS: Cites: J Biol Chem. 2002 Nov 29;277(48):46043-50 (medline /12297514)
COMMENTS: Cites: Cell. 2002 Nov 1;111(3):381-92 (medline /12419248)
COMMENTS: Cites: Nat Struct Mol Biol. 2007 Sep;14(9):796-806 (medline /17676063)
COMMENTS: Cites: Nat Struct Mol Biol. 2007 Nov;14(11):1025-40 (medline /17984965)
COMMENTS: Cites: Mol Cell Biol. 2008 Feb;28(3):926-38 (medline /18025106)
COMMENTS: Cites: Mol Cell. 2007 Dec 28;28(6):978-90 (medline /18158896)
COMMENTS: Cites: Mol Cell. 2008 Apr 11;30(1):51-60 (medline /18406326)
COMMENTS: Cites: Cell. 2008 May 16;133(4):581-4 (medline /18485867)
COMMENTS: Cites: Dev Dyn. 2008 Jun;237(6):1636-44 (medline /18498094)
COMMENTS: Cites: Methods. 2008 Jul;45(3):233-41 (medline /18586105)
COMMENTS: Cites: J Cell Biol. 2009 Apr 6;185(1):87-100 (medline /19349581)
COMMENTS: Cites: J Virol. 2010 Jan;84(1):76-87 (medline /19846528)
COMMENTS: Cites: Science. 2002 Nov 22;298(5598):1623-6 (medline /12446911)
COMMENTS: Cites: Mol Cell. 2003 Feb;11(2):353-63 (medline /12620224)
COMMENTS: Cites: Mol Cell. 2003 Feb;11(2):365-76 (medline /12620225)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2003 Jul 22;100(15):8758-63 (medline /12840145)
COMMENTS: Cites: Mol Cell Biol. 2003 Sep;23(17):6229-42 (medline /12917344)
COMMENTS: Cites: Mol Cell. 2004 Jan 16;13(1):33-43 (medline /14731392)
COMMENTS: Cites: Cell. 2004 Mar 5;116(5):683-98 (medline /15006351)
COMMENTS: Cites: Nat Rev Mol Cell Biol. 2004 May;5(5):403-10 (medline /15122353)
COMMENTS: Cites: Mol Cell. 2004 Jun 4;14(5):657-66 (medline /15175160)
COMMENTS: Cites: Curr Biol. 2004 Jun 22;14(12):1112-6 (medline /15203006)
COMMENTS: Cites: Science. 2004 Jun 18;304(5678):1797-800 (medline /15205532)
COMMENTS: Cites: Genes Dev. 2004 Oct 15;18(20):2437-68 (medline /15489290)
COMMENTS: Cites: Biochem J. 2005 Apr 1;387(Pt 1):257-69 (medline /15548137)
COMMENTS: Cites: Nat Biotechnol. 2004 Dec;22(12):1567-72 (medline /15558047)
COMMENTS: Cites: Mol Cell. 2005 Aug 19;19(4):523-34 (medline /16109376)
COMMENTS: Cites: Mol Cell. 2005 Aug 19;19(4):535-45 (medline /16109377)
COMMENTS: Cites: Mol Biol Cell. 2006 Feb;17(2):814-23 (medline /16339075)
COMMENTS: Cites: Science. 2006 Feb 10;311(5762):844-7 (medline /16469925)
COMMENTS: Cites: Mol Cell. 2006 Aug 4;23(3):297-305 (medline /16885020)
COMMENTS: Cites: J Virol. 2006 Nov;80(21):10772-86 (medline /16928766)
COMMENTS: Cites: Nature. 2006 Aug 31;442(7106):1050-3 (medline /16929308)
COMMENTS: Cites: Nat Rev Mol Cell Biol. 2006 Aug;7(8):557-67 (medline /16936696)
COMMENTS: Cites: J Virol. 2006 Sep;80(18):8909-19 (medline /16940503)
COMMENTS: Cites: Mol Cell Biol. 2007 Feb;27(3):937-48 (medline /17130237)
COMMENTS: Cites: Cell. 2007 Feb 23;128(4):693-705 (medline /17320507)
COMMENTS: Cites: J Biol Chem. 2007 May 4;282(18):13141-5 (medline /17329240)
COMMENTS: Cites: Nature. 2007 May 24;447(7143):407-12 (medline /17522673)
COMMENTS: Cites: J Cell Biol. 2007 Jun 18;177(6):957-67 (medline /17576795)
COMMENTS: Cites: Science. 1990 Aug 31;249(4972):1046-9 (medline /2144363)
ABSTRACT: BACKGROUND: Gene activation is thought to occur through a series of temporally defined regulatory steps. However, this process has not been completely evaluated in single living mammalian cells.
ABSTRACT: METHODOLOGY/PRINCIPAL FINDINGS: To investigate the timing and coordination of gene activation events, we tracked the recruitment of GCN5 (histone acetyltransferase), RNA polymerase II, Brd2 and Brd4 (acetyl-lysine binding proteins), in relation to a VP16-transcriptional activator, to a transcription site that can be visualized in single living cells. All accumulated rapidly with the VP16 activator as did the transcribed RNA. RNA was also detected at significantly more transcription sites in cells expressing the VP16-activator compared to a p53-activator. After alpha-amanitin pre-treatment, the VP16-activator, GCN5, and Brd2 are still recruited to the transcription site but the chromatin does not decondense.
ABSTRACT: CONCLUSIONS/SIGNIFICANCE: This study demonstrates that a strong activator can rapidly overcome the condensed chromatin structure of an inactive transcription site and supercede the expected requirement for regulatory events to proceed in a temporally defined order. Additionally, activator strength determines the number of cells in which transcription is induced as well as the extent of chromatin decondensation. As chromatin decondensation is significantly reduced after alpha-amanitin pre-treatment, despite the recruitment of transcriptional activation factors, this provides further evidence that transcription drives large-scale chromatin decondensation.
MESH HEADINGS: Alpha-Amanitin/pharmacology
MESH HEADINGS: Binding Sites
MESH HEADINGS: Cell Line, Tumor
MESH HEADINGS: *Chromatin Assembly and Disassembly
MESH HEADINGS: *Cytological Techniques
MESH HEADINGS: Etoposide/metabolism
MESH HEADINGS: Humans
MESH HEADINGS: Nuclear Proteins/metabolism
MESH HEADINGS: Protein Transport
MESH HEADINGS: Protein-Serine-Threonine Kinases/metabolism
MESH HEADINGS: RNA Polymerase II/metabolism
MESH HEADINGS: Time Factors
MESH HEADINGS: Transcription Factors/metabolism
MESH HEADINGS: Transcriptional Activation/*genetics
MESH HEADINGS: p300-CBP Transcription Factors/metabolism eng

1093. Raffaele, K. C.; Rowland, J.; May, B.; Makris, S. L.; Schumacher, K., and Scarano, L. J. The use of developmental neurotoxicity data in pesticide risk assessments. 2010; 32, (5): 563-572.


Rec #: 67269
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: Following the passage of the Food Quality Protection Act, which mandated an increased focus on evaluating the potential toxicity of pesticides to children, the number of guideline developmental neurotoxicity (DNT) studies (OPPTS 870.6300) submitted to the U.S. Environmental Protection Agency (EPA) Office of Pesticide Programs (OPP) was greatly increased. To evaluate the impact of available DNT studies on individual chemical risk assessments, the ways in which data from these studies are being used in pesticide risk assessment were investigated. In addition, the neurobehavioral and neuropathological parameters affected at the lowest observed adverse effect level (LOAEL) for each study were evaluated to ascertain whether some types of endpoints were consistently more sensitive than others. As of December 2008, final OPP reviews of DNT studies for 72 pesticide chemicals were available; elimination of studies with major deficiencies resulted in a total of 69 that were included in this analysis. Of those studies, 15 had been used to determine the point of departure for one or more risk assessment scenarios, and an additional 13 were determined to have the potential for use as a point of departure for future risk assessments (selection is dependent upon review of the entire database available at the time of reassessment). Analysis of parameters affected at the study LOAELs indicated that no single parameter was consistently more sensitive than another. Early assessment time points (e.g., postnatal day (PND) 11/21) tended to be more sensitive than later time points (e.g., PND 60). These results demonstrate that data generated using the current guideline DNT study protocol are useful in providing points of departure for risk assessments. The results of these studies also affirm the importance of evaluating a spectrum of behavioral and neuropathological endpoints, in both young and adult animals, to improve the detection of the potential for a chemical to cause developmental neurotoxicity. Published by Elsevier Inc.
Keywords: Developmental neurotoxicity testing, DNT, Risk assessment, Pesticides
ISI Document Delivery No.: 651PT

1094. Rafiq, K.; Nakano, D.; Ihara, G.; Hitomi, H.; Fujisawa, Y.; Ohashi, N.; Kobori, H.; Nagai, Y.; Kiyomoto, H.; Kohno, M., and Nishiyama, A. Effects of Mineralocorticoid Receptor Blockade on Glucocorticoid-Induced Renal Injury in Adrenalectomized Rats.


Rec #: 50319
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: ABSTRACT: OBJECTIVES: Aldosterone is well recognized as the selective physiological ligand for mineralocorticoid receptor in epithelia. However, in-vitro studies have demonstrated that the affinity of aldosterone and glucocorticoids for mineralocorticoid receptor is similar. We hypothesized that glucocorticoids are involved in the development of renal injury through an mineralocorticoid receptor-dependent mechanism.
ABSTRACT: METHODS AND RESULTS: Uninephrectomized (UNX) rats were treated with 1% NaCl and divided into three groups: vehicle, bilateral adrenalectomy (ADX) + hydrocortisone (HYDRO; 5 mg/kg/day, s.c.), ADX + HYDRO + eplerenone (0.125% in chow). HYDRO-treated UNX-ADX rats showed increased blood pressure and urinary albumin-to-creatinine ratio with an increase in the expression of the mineralocorticoid receptor target genes, serum and glucocorticoid-regulated kinases-1 and Na+/H+ exchanger isoform-1, in renal tissues. HYDRO treatment induced morphological changes in the kidney, including glomerulosclerosis and podocyte injury. Treatment with eplerenone markedly decreased the gene expression and reduced the albuminuria and renal morphological changes. In contrast, dexamethasone (0.2 mg/kg per day, s.c.) + UNX + ADX induced hypertension and albuminuria in different groups of rats. Eplerenone failed to ameliorate these changes.
ABSTRACT: CONCLUSIONS: Our findings indicate that chronic glucocorticoid excess could activate mineralocorticoid receptor and, in turn, induce the development of renal injury.
MESH HEADINGS: Adrenalectomy
MESH HEADINGS: Animals
MESH HEADINGS: Base Sequence
MESH HEADINGS: DNA Primers/genetics
MESH HEADINGS: Dexamethasone/toxicity
MESH HEADINGS: Gene Expression/drug effects
MESH HEADINGS: Glucocorticoids/*toxicity
MESH HEADINGS: Hydrocortisone/*toxicity
MESH HEADINGS: Hypertension/etiology/genetics/physiopathology
MESH HEADINGS: Kidney/*drug effects/injuries/pathology/physiopathology
MESH HEADINGS: Male
MESH HEADINGS: *Mineralocorticoid Receptor Antagonists/pharmacology
MESH HEADINGS: RNA, Messenger/genetics/metabolism
MESH HEADINGS: Rats
MESH HEADINGS: Rats, Inbred WKY
MESH HEADINGS: Receptors, Mineralocorticoid/genetics
MESH HEADINGS: Spironolactone/analogs &
MESH HEADINGS: derivatives/pharmacology eng

1095. Ragas, Ad Mj; Oldenkamp, R; Preeker, N L; Wernicke, J ; Schlink, U, and Ragas, Ad MJ. Cumulative Risk Assessment of Chemical Exposures in Urban Environments. 2011 Jul; 37, (5): 872-881.


Rec #: 43259
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: We performed a cumulative risk assessment for people living in a hypothetical urban environment, called Urbania. The main aims of the study were to demonstrate how a cumulative risk assessment for a middle-sized European city can be performed and to identify the bottlenecks in terms of data availability and knowledge gaps. The assessment focused on five air pollutants (i.e., PM10, benzene, toluene, nonane and naphthalene) and six food pesticides (i.e., acetamiprid, carbendazim, chlorpyrifos, diazinon, imidacloprid and permethrin). Exposure predictions showed that PM10, benzene and naphthalene exposure frequently exceeded the standards, and that the indoor environment contributed more than the outdoor environment. Effect predictions showed that mixture and interaction effects were generally limited. However, model calculations indicated potential synergistic effects between naphthalene and benzene and between chlorpyrifos, diazinon and toluene. PM10 dominated the health impact expressed in Disability Adjusted Life Years (DALYs). We conclude that measures to reduce the health impact of environmental pollution should focus on the improvement of indoor air quality and the reduction of PM10 emissions. Cumulative risk assessment can be improved by (1) the development of person-oriented exposure models that can simulate the cumulative exposure history of individuals, (2) a better mechanistic understanding of the effects of cumulative stressors, and (3) the development of instruments to prioritize stressors for inclusion in cumulative risk assessments.
Keywords: Risk assessment
Keywords: P 0000:AIR POLLUTION
Keywords: Toluene
Keywords: Naphthalene
Keywords: Benzene
Keywords: Risk Abstracts; Pollution Abstracts; Environment Abstracts
Keywords: Chlorpyrifos
Keywords: Air pollution
Keywords: Pesticides
Keywords: Emissions
Keywords: Diazinon
Keywords: R2 23010:General: Models, forecasting
Keywords: ENA 01:Air Pollution
Date revised - 2011-08-01
Language of summary - English
Pages - 872-881
ProQuest ID - 885050556
SubjectsTermNotLitGenreText - Air pollution; Chlorpyrifos; Risk assessment; Toluene; Pesticides; Emissions; Naphthalene; Diazinon; Benzene
Last updated - 2012-03-29
British nursing index edition - Environment International [Environ. Int.]. Vol. 37, no. 5, pp. 872-881. Jul 2011.
Corporate institution author - Ragas, Ad MJ; Oldenkamp, R; Preeker, N L; Wernicke, J; Schlink, U
DOI - 69baf3b8-a89f-4215-ad6bcsaobj201; 14892193; 0160-4120 English

1096. Rahimi, F.; Shanmugam, A., and Bitan, G. Structure-Function Relationships of Pre-Fibrillar Protein Assemblies in Alzheimer's Disease and Related Disorders.


Rec #: 51239
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: COMMENTS: Cites: Brain Res Bull. 2000 Nov 1;53(4):389-97 (medline /11136994)
COMMENTS: Cites: Trends Neurosci. 2001 Apr;24(4):219-24 (medline /11250006)
COMMENTS: Cites: J Cell Biol. 2001 Jun 11;153(6):1151-60 (medline /11402060)
COMMENTS: Cites: Biochemistry. 2001 Jul 3;40(26):7812-9 (medline /11425308)
COMMENTS: Cites: Cell Mol Neurobiol. 2001 Feb;21(1):1-13 (medline /11440193)
COMMENTS: Cites: J Biol Chem. 2001 Sep 14;276(37):35176-84 (medline /11441003)
COMMENTS: Cites: J Mol Biol. 2001 Aug 10;311(2):325-40 (medline /11478864)
COMMENTS: Cites: J Biotechnol. 2006 Mar 23;122(2):186-97 (medline /16233926)
COMMENTS: Cites: J Biol Chem. 2005 Dec 30;280(52):42669-75 (medline /16246845)
COMMENTS: Cites: J Physiol. 2006 Apr 15;572(Pt 2):477-92 (medline /16469784)
COMMENTS: Cites: Neurobiol Aging. 2006 Apr;27(4):570-5 (medline /16481071)
COMMENTS: Cites: Curr Opin Pharmacol. 2006 Apr;6(2):214-20 (medline /16483845)
COMMENTS: Cites: Protein Pept Lett. 2006;13(3):247-54 (medline /16515452)
COMMENTS: Cites: Nature. 2006 Mar 16;440(7082):352-7 (medline /16541076)
COMMENTS: Cites: FEBS J. 2006 May;273(10):2206-22 (medline /16649997)
COMMENTS: Cites: J Struct Biol. 2006 Jul;155(1):104-10 (medline /16650774)
COMMENTS: Cites: Biochemistry. 2006 Jul 4;45(26):8143-51 (medline /16800639)
COMMENTS: Cites: FASEB J. 2006 Sep;20(11):1916-7 (medline /16818470)
COMMENTS: Cites: Am J Physiol Endocrinol Metab. 2006 Dec;291(6):E1317-24 (medline /16849627)
COMMENTS: Cites: Biochemistry. 2006 Aug 8;45(31):9496-508 (medline /16878984)
COMMENTS: Cites: J Neurosci. 2006 Aug 2;26(31):8160-7 (medline /16885229)
COMMENTS: Cites: Mol Cell Neurosci. 2006 Nov;33(3):274-82 (medline /16962789)
COMMENTS: Cites: Curr Opin Psychiatry. 2006 Nov;19(6):555-63 (medline /17012931)
COMMENTS: Cites: Methods Enzymol. 2006;413:199-217 (medline /17046398)
COMMENTS: Cites: J Mol Biol. 2006 Dec 15;364(5):853-62 (medline /17046788)
COMMENTS: Cites: Nature. 2006 Oct 19;443(7113):774-9 (medline /17051203)
COMMENTS: Cites: Neuron. 2006 Nov 9;52(3):403-7 (medline /17088207)
COMMENTS: Cites: J Pept Sci. 2007 Feb;13(2):94-9 (medline /17103463)
COMMENTS: Cites: J Pept Sci. 2006 Dec;12(12):823-8 (medline /17131295)
COMMENTS: Cites: Biochemistry. 2006 Dec 26;45(51):15157-67 (medline /17176037)
COMMENTS: Cites: Ann Neurol. 2006 Dec;60(6):668-76 (medline /17192927)
COMMENTS: Cites: Biopolymers. 2007 May;86(1):23-31 (medline /17216631)
COMMENTS: Cites: FEBS J. 2007 Feb;274(4):990-1000 (medline /17227385)
COMMENTS: Cites: J Neurosci. 2007 Jan 24;27(4):751-61 (medline /17251414)
COMMENTS: Cites: Biochemistry. 2007 Feb 13;46(6):1503-10 (medline /17279615)
COMMENTS: Cites: Protein Sci. 2007 Apr;16(4):723-32 (medline /17327396)
COMMENTS: Cites: Semin Pediatr Neurol. 2007 Mar;14(1):15-25 (medline /17331880)
COMMENTS: Cites: J Neurosci. 2007 Mar 14;27(11):2866-75 (medline /17360908)
COMMENTS: Cites: Mol Cell Neurosci. 2007 Jun;35(2):183-93 (medline /17368908)
COMMENTS: Cites: Neurosci Res. 2007 May;58(1):1-5 (medline /17379343)
COMMENTS: Cites: Trends Biochem Sci. 2007 May;32(5):204-6 (medline /17419062)
COMMENTS: Cites: Ann Med. 2007;39(3):200-7 (medline /17457717)
COMMENTS: Cites: IUBMB Life. 2007 Apr-May;59(4-5):332-45 (medline /17505973)
COMMENTS: Cites: J Am Chem Soc. 2007 Jun 20;129(24):7517-22 (medline /17518465)
COMMENTS: Cites: J Mol Biol. 2007 Jul 6;370(2):372-84 (medline /17521669)
COMMENTS: Cites: Chem Phys Lipids. 2007 Sep-Oct;149(1-2):28-39 (medline /17603032)
COMMENTS: Cites: J Biol Chem. 1992 Aug 25;267(24):17082-6 (medline /1512246)
COMMENTS: Cites: Science. 1992 Apr 10;256(5054):184-5 (medline /1566067)
COMMENTS: Cites: Arch Biochem Biophys. 1992 May 1;294(2):630-8 (medline /1567217)
COMMENTS: Cites: Ann Neurol. 1991 Oct;30(4):572-80 (medline /1789684)
COMMENTS: Cites: Nature. 1970 Aug 15;227(5259):680-5 (medline /5432063)
COMMENTS: Cites: J Immunol Methods. 1983 Nov 25;64(3):313-20 (medline /6199426)
COMMENTS: Cites: J Immunol Methods. 1983 Dec 16;65(1-2):55-63 (medline /6606682)
COMMENTS: Cites: Biochemistry. 1983 Apr 26;22(9):2193-202 (medline /6860660)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1993 Nov 15;90(22):10573-7 (medline /7504270)
COMMENTS: Cites: Exp Neurol. 1995 Nov;136(1):22-31 (medline /7589331)
COMMENTS: Cites: Neurodegeneration. 1995 Mar;4(1):23-32 (medline /7600183)
COMMENTS: Cites: Biochemistry. 1995 Apr 18;34(15):5191-200 (medline /7711039)
COMMENTS: Cites: J Biol Chem. 1995 Apr 21;270(16):9564-70 (medline /7721886)
COMMENTS: Cites: Curr Opin Biotechnol. 1993 Aug;4(4):403-11 (medline /7763970)
COMMENTS: Cites: Trends Biotechnol. 1994 May;12(5):149-53 (medline /7764895)
COMMENTS: Cites: Mol Pharmacol. 1994 Mar;45(3):373-9 (medline /8145724)
COMMENTS: Cites: Annu Rev Neurosci. 1994;17:341-71 (medline /8210179)
COMMENTS: Cites: J Neurochem. 1993 Nov;61(5):1916-26 (medline /8229002)
COMMENTS: Cites: Amyloid. 2005 Jun;12(2):88-95 (medline /16011984)
COMMENTS: Cites: Nat Neurosci. 2005 Aug;8(8):1051-8 (medline /16025111)
COMMENTS: Cites: J Mol Biol. 2005 Sep 16;352(2):282-98 (medline /16095615)
COMMENTS: Cites: J Neurochem. 2005 Nov;95(3):834-47 (medline /16135089)
COMMENTS: Cites: Chem Phys Lipids. 2005 Oct;137(1-2):52-61 (medline /16140289)
COMMENTS: Cites: J Am Chem Soc. 2005 Oct 5;127(39):13472-3 (medline /16190691)
COMMENTS: Cites: J Biol Chem. 2006 Jan 20;281(3):1599-604 (medline /16282321)
COMMENTS: Cites: J Neurochem. 1993 Nov;61(5):1965-8 (medline /8229004)
COMMENTS: Cites: Biophys J. 1993 Dec;65(6):2383-95 (medline /8312477)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1993 Jan 15;90(2):567-71 (medline /8380642)
COMMENTS: Cites: Biophys J. 1995 Aug;69(2):640-51 (medline /8527678)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1996 Feb 6;93(3):1125-9 (medline /8577726)
COMMENTS: Cites: Neurosci Lett. 1995 Nov 17;200(2):105-8 (medline /8614555)
COMMENTS: Cites: Biochem Biophys Res Commun. 1996 Jun 25;223(3):592-7 (medline /8687441)
COMMENTS: Cites: J Biol Chem. 1996 Aug 23;271(34):20631-5 (medline /8702810)
COMMENTS: Cites: Nat Med. 1996 Aug;2(8):864-70 (medline /8705854)
COMMENTS: Cites: Mt Sinai J Med. 1996 Jan;63(1):16-23 (medline /8935845)
COMMENTS: Cites: Brain Res. 1997 Jan 2;744(1):7-14 (medline /9030407)
COMMENTS: Cites: J Biol Chem. 1997 Mar 21;272(12):7977-82 (medline /9065468)
COMMENTS: Cites: J Neurochem. 1997 May;68(5):2092-7 (medline /9109537)
COMMENTS: Cites: Chem Biol. 1997 Feb;4(2):119-25 (medline /9190286)
COMMENTS: Cites: Biophys J. 1997 Jul;73(1):67-75 (medline /9199772)
COMMENTS: Cites: J Struct Biol. 1997 Jun;119(1):59-71 (medline /9216088)
COMMENTS: Cites: J Biol Chem. 1997 Aug 29;272(35):22364-72 (medline /9268388)
COMMENTS: Cites: Methods Enzymol. 1997;289:3-13 (medline /9353714)
COMMENTS: Cites: Curr Opin Struct Biol. 1998 Feb;8(1):101-6 (medline /9519302)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1998 Apr 14;95(8):4224-8 (medline /9539718)
COMMENTS: Cites: J Biol Chem. 1998 May 29;273(22):13379-82 (medline /9593665)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1998 May 26;95(11):6448-53 (medline /9600986)
COMMENTS: Cites: J Mol Biol. 1998 Jul 10;280(2):245-58 (medline /9654449)
COMMENTS: Cites: Amyloid. 1998 Jun;5(2):121-42 (medline /9686307)
COMMENTS: Cites: Biochemistry. 1998 Nov 3;37(44):15247-53 (medline /9799484)
COMMENTS: Cites: Nephrol Dial Transplant. 1998;13 Suppl 7:33-40 (medline /9870435)
COMMENTS: Cites: Am J Pathol. 1999 Jan;154(1):271-9 (medline /9916941)
COMMENTS: Cites: EMBO J. 1999 Feb 15;18(4):815-21 (medline /10022824)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3590-4 (medline /10097081)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1999 Mar 30;96(7):3688-93 (medline /10097098)
COMMENTS: Cites: Scand J Immunol. 1999 Mar;49(3):219-23 (medline /10102637)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 1999 May 25;96(11):6020-4 (medline /10339534)
COMMENTS: Cites: Biochemistry. 1999 Jul 13;38(28):8972-80 (medline /10413470)
COMMENTS: Cites: J Neurosci Res. 1999 Aug 15;57(4):458-66 (medline /10440895)
COMMENTS: Cites: Biochemistry. 1999 Aug 24;38(34):11189-96 (medline /10460176)
COMMENTS: Cites: J Biol Chem. 1999 Sep 3;274(36):25945-52 (medline /10464339)
COMMENTS: Cites: Methods Enzymol. 1999;309:429-59 (medline /10507039)
COMMENTS: Cites: J Neurosci. 1999 Oct 15;19(20):8876-84 (medline /10516307)
COMMENTS: Cites: Biochim Biophys Acta. 2000 Jan 3;1476(1):93-102 (medline /10606771)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2000 Jan 18;97(2):571-6 (medline /10639120)
COMMENTS: Cites: Biochemistry. 2000 Mar 14;39(10):2552-63 (medline /10704204)
COMMENTS: Cites: J Mol Biol. 2000 Mar 17;297(1):73-87 (medline /10704308)
COMMENTS: Cites: J Biol Chem. 2000 Jun 16;275(24):18495-502 (medline /10764800)
COMMENTS: Cites: Biochem J. 2000 May 15;348 Pt 1:137-44 (medline /10794724)
COMMENTS: Cites: J Mol Biol. 2000 May 19;298(5):833-40 (medline /10801352)
COMMENTS: Cites: J Neurosci. 2000 Jun 1;20(11):3993-4001 (medline /10818134)
COMMENTS: Cites: J Neurosci. 2000 Jun 1;20(11):4050-8 (medline /10818140)
COMMENTS: Cites: FASEB J. 2000 Jun;14(9):1233-43 (medline /10834945)
COMMENTS: Cites: Annu Rev Neurosci. 2000;23:649-711 (medline /10845078)
COMMENTS: Cites: Biochim Biophys Acta. 2000 Jul 26;1502(1):16-30 (medline /10899428)
COMMENTS: Cites: Biophys J. 2000 Aug;79(2):1053-65 (medline /10920035)
COMMENTS: Cites: Microsc Res Tech. 2000 Aug 15;50(4):305-15 (medline /10936885)
COMMENTS: Cites: J Struct Biol. 2000 Jun;130(2-3):109-22 (medline /10940219)
COMMENTS: Cites: J Struct Biol. 2000 Jun;130(2-3):130-41 (medline /10940221)
COMMENTS: Cites: J Struct Biol. 2000 Jun;130(2-3):217-31 (medline /10940227)
COMMENTS: Cites: Biochemistry. 2000 Sep 5;39(35):10831-9 (medline /10978169)
COMMENTS: Cites: Nat Struct Biol. 2000 Dec;7(12):1095-9 (medline /11101888)
COMMENTS: Cites: J Biol Chem. 2004 Nov 5;279(45):46363-6 (medline /15385542)
COMMENTS: Cites: J Pept Sci. 2004 Oct;10(10):612-21 (medline /15526710)
COMMENTS: Cites: Nat Neurosci. 2005 Jan;8(1):79-84 (medline /15608634)
COMMENTS: Cites: Science. 2005 Jan 14;307(5707):262-5 (medline /15653506)
COMMENTS: Cites: Protein Expr Purif. 2005 Mar;40(1):183-9 (medline /15721787)
COMMENTS: Cites: Neurobiol Dis. 2005 Apr;18(3):459-65 (medline /15755672)
COMMENTS: Cites: Trends Neurosci. 2005 Apr;28(4):182-7 (medline /15808352)
COMMENTS: Cites: Nat Neurosci. 2001 Sep;4(9):859-60 (medline /11528409)
COMMENTS: Cites: Nat Neurosci. 2001 Sep;4(9):887-93 (medline /11528419)
COMMENTS: Cites: J Mol Biol. 2001 Oct 5;312(5):1103-19 (medline /11580253)
COMMENTS: Cites: FASEB J. 2001 Nov;15(13):2433-44 (medline /11689468)
COMMENTS: Cites: J Neurochem. 2001 Nov;79(3):595-605 (medline /11701763)
COMMENTS: Cites: Protein Sci. 2001 Dec;10(12):2541-7 (medline /11714922)
COMMENTS: Cites: Biochemistry. 2001 Dec 11;40(49):14736-43 (medline /11732892)
COMMENTS: Cites: J Neurosci. 2002 Mar 15;22(6):2153-64 (medline /11896155)
COMMENTS: Cites: Biochemistry. 2002 Apr 9;41(14):4595-602 (medline /11926821)
COMMENTS: Cites: Nature. 2002 Apr 4;416(6880):535-9 (medline /11932745)
COMMENTS: Cites: Biochemistry. 2002 May 14;41(19):6115-27 (medline /11994007)
COMMENTS: Cites: Curr Opin Neurobiol. 2002 Apr;12(2):211-6 (medline /12015239)
COMMENTS: Cites: Brain Res Brain Res Rev. 2002 Jun;39(1):29-54 (medline /12086707)
COMMENTS: Cites: Peptides. 2002 Jul;23(7):1215-28 (medline /12128079)
COMMENTS: Cites: Peptides. 2002 Jul;23(7):1311-5 (medline /12128087)
COMMENTS: Cites: Science. 2002 Jul 19;297(5580):353-6 (medline /12130773)
COMMENTS: Cites: J Biol Chem. 2002 Oct 25;277(43):41032-7 (medline /12171927)
COMMENTS: Cites: Protein Sci. 2002 Sep;11(9):2067-79 (medline /12192063)
COMMENTS: Cites: Biochem Soc Trans. 2002 Aug;30(4):552-7 (medline /12196135)
COMMENTS: Cites: J Neurosci Res. 2002 Sep 1;69(5):567-77 (medline /12210822)
COMMENTS: Cites: Biochemistry. 2002 Sep 24;41(38):11338-43 (medline /12234175)
COMMENTS: Cites: Trends Biochem Sci. 2002 Oct;27(10):527-33 (medline /12368089)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2002 Dec 10;99(25):16052-7 (medline /12456886)
COMMENTS: Cites: J Biol Chem. 2003 Mar 28;278(13):11612-22 (medline /12499373)
COMMENTS: Cites: Exp Gerontol. 2003 Apr;38(4):347-51 (medline /12670620)
COMMENTS: Cites: Science. 2003 Apr 18;300(5618):486-9 (medline /12702875)
COMMENTS: Cites: J Protein Chem. 2003 Jan;22(1):31-40 (medline /12739896)
COMMENTS: Cites: Ultramicroscopy. 2003 Oct-Nov;97(1-4):73-9 (medline /12801659)
COMMENTS: Cites: J Biol Chem. 2003 Sep 12;278(37):34882-9 (medline /12840029)
COMMENTS: Cites: Neurobiol Dis. 2003 Aug;13(3):177-90 (medline /12901832)
COMMENTS: Cites: J Mol Med (Berl). 2003 Nov;81(11):678-99 (medline /12942175)
COMMENTS: Cites: J Mol Biol. 2003 Sep 26;332(4):795-808 (medline /12972252)
COMMENTS: Cites: Biochemistry. 2003 Sep 23;42(37):10971-7 (medline /12974632)
COMMENTS: Cites: Ageing Res Rev. 2003 Oct;2(4):343-56 (medline /14522239)
COMMENTS: Cites: J Mol Biol. 2003 Nov 14;334(1):129-41 (medline /14596805)
COMMENTS: Cites: J Am Chem Soc. 2003 Dec 17;125(50):15359-65 (medline /14664580)
COMMENTS: Cites: Curr Opin Rheumatol. 2004 Jan;16(1):67-75 (medline /14673392)
COMMENTS: Cites: Biochemistry. 2003 Dec 30;42(51):15078-83 (medline /14690417)
COMMENTS: Cites: J Am Chem Soc. 2004 Feb 25;126(7):1992-2005 (medline /14971932)
COMMENTS: Cites: J Neurosci. 2004 Apr 14;24(15):3801-9 (medline /15084661)
COMMENTS: Cites: J Biol Chem. 2004 Jul 23;279(30):31374-82 (medline /15133040)
COMMENTS: Cites: Neuropathol Appl Neurobiol. 2004 Jun;30(3):215-24 (medline /15175075)
COMMENTS: Cites: J Neurosci. 2004 Jul 28;24(30):6799-809 (medline /15282285)
COMMENTS: Cites: Neurosci Lett. 2004 Aug 19;366(3):320-5 (medline /15288443)
COMMENTS: Cites: J Org Chem. 2004 Oct 29;69(22):7776-8 (medline /15498016)
COMMENTS: Cites: J Neurosci. 2004 Nov 10;24(45):10191-200 (medline /15537891)
COMMENTS: Cites: FASEB J. 2005 Mar;19(3):437-9 (medline /15604358)
COMMENTS: Cites: Exp Neurol. 2005 Feb;191 Suppl 1:S17-27 (medline /15629758)
COMMENTS: Cites: J Am Chem Soc. 2005 Feb 23;127(7):2075-84 (medline /15713083)
COMMENTS: Cites: J Biol Chem. 2005 Apr 29;280(17):17294-300 (medline /15722360)
COMMENTS: Cites: Nat Rev Mol Cell Biol. 2005 Mar;6(3):197-208 (medline /15738986)
COMMENTS: Cites: J Neurosci. 2005 Mar 9;25(10):2455-62 (medline /15758153)
COMMENTS: Cites: J Struct Biol. 2005 May;150(2):180-9 (medline /15866741)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2005 May 17;102(20):7115-20 (medline /15883377)
COMMENTS: Cites: Protein Sci. 2005 Jun;14(6):1581-96 (medline /15930005)
COMMENTS: Cites: Methods Mol Biol. 2005;305:101-14 (medline /15939995)
COMMENTS: Cites: Methods Mol Biol. 2005;299:153-74 (medline /15980600)
COMMENTS: Cites: FASEB J. 2005 Aug;19(10):1344-6 (medline /15919759)
COMMENTS: Cites: Protein Expr Purif. 2005 Jul;42(1):200-10 (medline /15939307)
COMMENTS: Cites: Methods Mol Biol. 2005;299:3-9 (medline /15980591)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2005 Jul 26;102(30):10427-32 (medline /16020533)
COMMENTS: Cites: Nature. 2005 Jul 28;436(7050):554-8 (medline /16049488)
COMMENTS: Cites: Peptides. 2006 Jan;27(1):95-104 (medline /16139931)
COMMENTS: Cites: Biochemistry. 2005 Sep 13;44(36):12113-9 (medline /16142909)
COMMENTS: Cites: Curr Drug Discov Technol. 2004 Oct;1(3):229-42 (medline /16472250)
COMMENTS: Cites: J Mol Biol. 2006 Apr 21;358(1):106-19 (medline /16499926)
COMMENTS: Cites: J Comb Chem. 2006 Mar-Apr;8(2):213-20 (medline /16529516)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2006 Mar 28;103(13):5161-6 (medline /16549764)
COMMENTS: Cites: Annu Rev Biochem. 2006;75:333-66 (medline /16756495)
COMMENTS: Cites: J Struct Biol. 2006 Aug;155(2):146-53 (medline /16806970)
COMMENTS: Cites: J Mol Biol. 2006 Aug 25;361(4):785-95 (medline /16875699)
COMMENTS: Cites: Trends Mol Med. 2006 Sep;12(9):395-6 (medline /16880006)
COMMENTS: Cites: Science. 2006 Aug 25;313(5790):1093-7 (medline /16931756)
COMMENTS: Cites: Methods Enzymol. 2006;413:20-33 (medline /17046389)
COMMENTS: Cites: Methods Enzymol. 2006;413:217-36 (medline /17046399)
COMMENTS: Cites: Behav Genet. 2007 Jan;37(1):79-100 (medline /17072762)
COMMENTS: Cites: J Gen Physiol. 2006 Dec;128(6):637-47 (medline /17101816)
COMMENTS: Cites: J Neurochem. 2007 Jan;100(1):23-35 (medline /17116235)
COMMENTS: Cites: Biochem Biophys Res Commun. 2007 Feb 9;353(2):443-9 (medline /17184733)
COMMENTS: Cites: FEBS J. 2006 Dec;273(24):5598-611 (medline /17212777)
COMMENTS: Cites: Nat Rev Mol Cell Biol. 2007 Feb;8(2):101-12 (medline /17245412)
COMMENTS: Cites: J Neurosci. 2007 Jan 24;27(4):796-807 (medline /17251419)
COMMENTS: Cites: J Biol Chem. 2007 Apr 13;282(15):11590-601 (medline /17308309)
COMMENTS: Cites: Diabetes. 2007 May;56(5):1324-32 (medline /17353506)
COMMENTS: Cites: Scand J Clin Lab Invest. 2007;67(2):179-90 (medline /17365997)
COMMENTS: Cites: J Mol Biol. 2007 May 18;368(5):1448-57 (medline /17397862)
COMMENTS: Cites: Neurodegener Dis. 2007;4(1):13-27 (medline /17429215)
COMMENTS: Cites: Nature. 2007 May 24;447(7143):453-7 (medline /17468747)
COMMENTS: Cites: Biochemistry. 2007 Jun 19;46(24):7079-87 (medline /17521170)
COMMENTS: Cites: Biochemistry. 2007 Jun 19;46(24):7107-18 (medline /17530780)
COMMENTS: Cites: J Am Chem Soc. 2001 Aug 22;123(33):8141-2 (medline /11506581)
COMMENTS: Cites: Cell Mol Neurobiol. 2001 Jun;21(3):255-84 (medline /11569537)
COMMENTS: Cites: J Pept Sci. 2001 Sep;7(9):488-94 (medline /11587187)
COMMENTS: Cites: Neurosci Lett. 2001 Nov 16;314(3):115-8 (medline /11704297)
COMMENTS: Cites: Eur J Biochem. 2001 Nov;268(22):5930-6 (medline /11722581)
COMMENTS: Cites: Brain Res. 2002 Jan 11;924(2):133-40 (medline /11750898)
COMMENTS: Cites: Nature. 2002 Apr 4;416(6880):507-11 (medline /11932737)
COMMENTS: Cites: Biochem Biophys Res Commun. 2002 Apr 12;292(4):931-6 (medline /11944904)
COMMENTS: Cites: J Biol Chem. 2002 Aug 30;277(35):32046-53 (medline /12058030)
COMMENTS: Cites: Nature. 2002 Jul 18;418(6895):291 (medline /12124613)
COMMENTS: Cites: Peptides. 2002 Jul;23(7):1265-70 (medline /12128083)
COMMENTS: Cites: Biochemistry. 2002 Aug 13;41(32):10209-17 (medline /12162735)
COMMENTS: Cites: Neurochem Int. 2002 Nov;41(5):345-52 (medline /12176077)
COMMENTS: Cites: J Biol Chem. 2002 Oct 25;277(43):40173-6 (medline /12198111)
COMMENTS: Cites: J Biol Chem. 2002 Nov 8;277(45):43243-6 (medline /12215440)
COMMENTS: Cites: J Mol Biol. 2002 Oct 4;322(5):1089-102 (medline /12367530)
COMMENTS: Cites: J Mol Biol. 2003 Jan 3;325(1):135-48 (medline /12473457)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2003 Jan 7;100(1):330-5 (medline /12506200)
COMMENTS: Cites: Annu Rev Neurosci. 2003;26:267-98 (medline /12704221)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2003 May 27;100(11):6370-5 (medline /12750461)
COMMENTS: Cites: Am J Physiol Cell Physiol. 2003 Oct;285(4):C873-80 (medline /12814914)
COMMENTS: Cites: Proc Natl Acad Sci U S A. 2003 Sep 2;100(18):10417-22 (medline /12925731)
COMMENTS: Cites: Int J Biol Macromol. 2003 Sep;32(3-5):173-7 (medline /12957314)
COMMENTS: Cites: J Mol Neurosci. 2003;20(3):305-13 (medline /14501013)
COMMENTS: Cites: Biochemistry. 2003 Nov 11;42(44):12749-60 (medline /14596589)
COMMENTS: Cites: Biochemistry. 2003 Dec 9;42(48):14092-8 (medline /14640676)
COMMENTS: Cites: Neurobiol Dis. 2003 Dec;14(3):567-78 (medline /14678772)
COMMENTS: Cites: Exp Eye Res. 2004 Feb;78(2):243-56 (medline /14729357)
COMMENTS: Cites: J Mol Biol. 2004 May 14;338(5):943-57 (medline /15111058)
COMMENTS: Cites: Neurobiol Aging. 2004 May-Jun;25(5):569-80 (medline /15172732)
COMMENTS: Cites: Acc Chem Res. 2004 Jun;37(6):357-64 (medline /15196045)
ABSTRACT: Several neurodegenerative diseases, including Alzheimer's, Parkinson's, Huntington's and prion diseases, are characterized pathognomonically by the presence of intra- and/or extracellular lesions containing proteinaceous aggregates, and by extensive neuronal loss in selective brain regions. Related non-neuropathic systemic diseases, e.g., light-chain and senile systemic amyloidoses, and other organ-specific diseases, such as dialysis-related amyloidosis and type-2 diabetes mellitus, also are characterized by deposition of aberrantly folded, insoluble proteins. It is debated whether the hallmark pathologic lesions are causative. Substantial evidence suggests that these aggregates are the end state of aberrant protein folding whereas the actual culprits likely are transient, pre-fibrillar assemblies preceding the aggregates. In the context of neurodegenerative amyloidoses, the proteinaceous aggregates may eventuate as potentially neuroprotective sinks for the neurotoxic, oligomeric protein assemblies. The pre-fibrillar, oligomeric assemblies are believed to initiate the pathogenic mechanisms that lead to synaptic dysfunction, neuronal loss, and disease-specific regional brain atrophy. The amyloid beta-protein (Abeta), which is believed to cause Alzheimer's disease (AD), is considered an archetypal amyloidogenic protein. Intense studies have led to nominal, functional, and structural descriptions of oligomeric Abeta assemblies. However, the dynamic and metastable nature of Abeta oligomers renders their study difficult. Different results generated using different methodologies under different experimental settings further complicate this complex area of research and identification of the exact pathogenic assemblies in vivo seems daunting. Here we review structural, functional, and biological experiments used to produce and study pre-fibrillar Abeta assemblies, and highlight similar studies of proteins involved in related diseases. We discuss challenges that contemporary researchers are facing and future research prospects in this demanding yet highly important field.
MESH HEADINGS: Alzheimer Disease/*pathology
MESH HEADINGS: Amyloid beta-Peptides/*chemistry/*ultrastructure
MESH HEADINGS: Animals
MESH HEADINGS: Humans
MESH HEADINGS: Peptide Fragments/*chemistry/ultrastructure
MESH HEADINGS: *Protein Conformation
MESH HEADINGS: Protein Folding
MESH HEADINGS: Structure-Activity Relationship eng

1097. Rahman, M F; Mahboob, M; Grover, P, and Rahman, M F. In Vitro Acetylcholinesterase Inhibition and Cytotoxic Effect of Some Organophosphorus Pesticides in Human Erythrocytes and Hepg2 Cells. 2008 Jun; 15, (1): 49-55.


Rec #: 45909
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: Abstract: In vitro effects of some novel organophosphates like RPR-II, RPR-V, chlorpyrifos, dimethoate and monocrotophos (MCP) were studied in human erythrocytes with special reference to acetylcholinesterase (AChE) and mitochondrial function (MTT assay) in HepG2 cell lines. The purpose of the present study was to quantify "in vitro" effect by means of the 50 percent inhibition (IC sub(50) using acetylthiocholine iodide as substrate in human RBC in the presence of different concentrations of pesticides. Our study indicated dose dependent AChE inhibition by all the OP compounds tested. The IC sub(50) observed for RPR-II, RPR-V and chlorpyrifos was greater than 10 mM, whereas dimethoate and MCP showed 1.60 and 2.38 mM respectively showing dimethoate 1.48 times more potent than MCP. The kinetic constant (Vmax and Km) showed the trend of decreasing with all the compounds assayed indicating non-competative inhibition. Similarly, the cell viability (MTT) also decreased by all the tested five OP compounds. RPR-II and RPR-V were found to be least toxic and IC sub(50) observed was greater than 10 mM, whereas IC sub(50) observed for chlorpyrifos, dimethoate and MCP were 0.835, 0.850 and 0.576 mM respectively. These results indicated dose dependent cytotoxic effect by all these OP compounds on HepG2 cell lines and relatively MCP was most potent in comparison to other compounds tested. From the present study, it can be concluded that the in vitro AChE and MTT assays are sensitive assays and can be used as biochemical marker for the exposure of organophosphates.
Keywords: Pesticides (organophosphorus)
Keywords: Biochemical markers
Keywords: Acetylcholinesterase
Keywords: Environmental Studies--Toxicology And Environmental Safety
Keywords: Erythrocytes
Keywords: monocrotophos
Keywords: Mitochondria
Keywords: organophosphates
Keywords: Chlorpyrifos
Keywords: Cytotoxicity
Keywords: Kinetics
Keywords: Dimethoate
Keywords: X 24330:Agrochemicals
Keywords: Toxicology Abstracts
Date revised - 2008-11-01
Language of summary - English
Pages - 49-55
ProQuest ID - 290259603
SubjectsTermNotLitGenreText - Dimethoate; Chlorpyrifos; Acetylcholinesterase; Erythrocytes; organophosphates; Cytotoxicity; Mitochondria; Kinetics; Biochemical markers; monocrotophos; Pesticides (organophosphorus)
Last updated - 2011-10-26
Corporate institution author - Rahman, M F; Mahboob, M; Grover, P
DOI - OB-MD-0008492379; 8508039; 0971-6580 English

1098. Raina, R.; Hall, P., and Sun, L. N. Occurrence and Relationship of Organophosphorus Insecticides and Their Degradation Products in the Atmosphere in Western Canada Agricultural Regions. 2010; 44, (22): 8541-8546.


Rec #: 67299
Keywords: FATE
Notes: Chemical of Concern: CPY
Abstract: Abstract: This paper presents the atmospheric occurrence and seasonal variations of the most frequently detected organophosphorus insecticides (OPs) and their OP oxon degradation products at Brats Lake, Saskatchewan in the Canadian Prairies (April 2003 to March 2004, January-December, 2005) and at Abbotsford in the Lower Frazer Valley (LFV) of British Columbia from May 2004 to December, 2005. During 2005 there were 10 OPs, 8 OP oxons, and 6 other OP degradation products measured. The most frequently detected OPs were chlorpyrifos, malathion, and diazinon. At Bratt's Lake the highest atmospheric concentrations were observed for chlorpyrifos, with maximum concentrations observed during July and August in 2003 showing much higher concentrations than those from 2005. This was related to its usage for grasshopper control in the province. At Abbotsford, diazinon and malathion were observed in much higher atmospheric concentrations than chlorpyrifos. Concentrations reached maximum in spring for diazinon and summer for malathion. This study is the first reported study of seasonal variations of OP oxons with their parent OP. Chlorpyrifos axon concentrations during July were generally low, indicating strong local source contributions. The chlorpyrifos oxon/chlorpyrifos ratio and diazinon oxon/diazinon ratio showed a strong seasonal variation with increasing ratio from spring to summer which was attributed to increasing sunlight hours. Malathion oxon/mathion at both sites was similar and relatively constant throughout the year. The oxon/thion ratio represents a good indicator of age of source or contributions from local versus regional atmospheric sources.
Keywords: CURRENT-USE PESTICIDES, GAS-CHROMATOGRAPHY, MASS-SPECTROMETRY, AIR
ISI Document Delivery No.: 680QA

1099. Raina, Renata; Hall, Patricia, and Raina, Renata. Field Evaluation of Solid Sorbents for Ambient Air Sampling of Pesticides. 2010; 3, 57-66.


Rec #: 44259
Keywords: CHEM METHODS
Notes: Chemical of Concern: CPY
Abstract: Abstract: Seven solid sorbents including Amberlite registered XAD-2 and XAD-4, Tenax-TA registered , Anasorb-747, Chromosorb 102, 108, and 750 were evaluated for the collection of the gas phase fraction of pesticides under field conditions at an agricultural site, Bratt's Lake, SK, located in the Canadian prairies. The polyurethane foam (PUF)/sorbent cartridge consists of two PUF layers which sandwich the solid sorbent and each layer was analyzed separately to determine which portion of the PUF/solid sorbent retained the pesticides and the extent of breakthrough. The pesticides that had high detection frequency throughout the study and ambient air concentrations well above MDL were triallate, trifluralin, ethalfluralin, and chlorpyrifos. All sorbents had improved collection efficiency as compared to a standard 7.6 cm PUF and the improvement varied with each pesticide. The most effective sorbents for trapping gas phase fraction of pesticides were XAD-2, XAD-4, Tenax-TA, and Chromosorb 108. The only sorbent not recommended for use is Chromosorb 750. For selected sampling periods when ambient concentrations were above detection limits a number of other organochlorine and organophosphorus pesticides also showed more efficient collection with PUF/solid sorbent cartridges as compared to PUF cartridge. Shorter sample collection periods of 4-days improved detection frequency of pesticides.
Keywords: Soil
Keywords: Chlorpyrifos
Keywords: Prairies
Keywords: Lakes
Keywords: Sorbents
Keywords: Organochlorine compounds
Keywords: P 0000:AIR POLLUTION
Keywords: Pollution Abstracts; Environment Abstracts; Aqualine Abstracts; Water Resources Abstracts; ASFA 3: Aquatic Pollution & Environmental Quality
Keywords: Pesticides
Keywords: Air sampling
Keywords: Trifluralin
Keywords: ENA 01:Air Pollution
Date revised - 2012-10-01
Language of summary - English
Pages - 57-66
ProQuest ID - 1093467038
SubjectsTermNotLitGenreText - Soil; Chlorpyrifos; Prairies; Lakes; Sorbents; Organochlorine compounds; Pesticides; Air sampling; Trifluralin
Last updated - 2012-11-20
British nursing index edition - Air, Soil and Water Research. Vol. 3, pp. 57-66. 2010.
Corporate institution author - Raina, Renata; Hall, Patricia
DOI - 39ce2dce-51eb-44b8-b02fmfgefd101; 17174673; 1178-6221 English

1100. Rajasekaran, D.; Subbaraghavalu, G., and Jayapandian, P. Guillain-Barre Syndrome Due to Organophosphate Compound Poison.


Rec #: 77829
Keywords: HUMAN HEALTH
Notes: Chemical of Concern: CPY
Abstract: ABSTRACT: Acute manifestations of Organophosphate Compound (OPC) poison are due to effect cholinergic excess. Others are intermediate syndrome [IMS], organophosphate induced delayed neuropathy [OPIND] and chronic organophosphate induced neuropsychiatric disorder [COPIND]. All these manifestation have specific period of occurrence and duration. There are very sparse reports of toxic demylination due to OPC poisoning. We report a case of Guillain-Barre Syndrome (GBS) due to toxic demyelination following OPC poison.
MESH HEADINGS: Adult
MESH HEADINGS: Atropine/therapeutic use
MESH HEADINGS: Chlorpyrifos/*poisoning
MESH HEADINGS: Cholinesterase Inhibitors/therapeutic use
MESH HEADINGS: Cholinesterase Reactivators/therapeutic use
MESH HEADINGS: Gastric Lavage
MESH HEADINGS: Guillain-Barre Syndrome/*chemically induced/drug therapy/therapy
MESH HEADINGS: Humans
MESH HEADINGS: Insecticides/*poisoning
MESH HEADINGS: Male
MESH HEADINGS: Methylprednisolone/therapeutic use
MESH HEADINGS: Neuroprotective Agents/therapeutic use
MESH HEADINGS: Parasympatholytics/therapeutic use
MESH HEADINGS: Plasmapheresis
MESH HEADINGS: Pralidoxime Compounds/therapeutic use eng

1101. Raju, M. B.; Rao, C. N.; Kumar, G. V. R.; Rao, B. T.; Krishna, P. M.; Sreenivasulu, V.; Prasad, K., and Venkateswarlu, P. METHOD FOR THE DETERMINATION OF ORGANOPHOSPHORUS PESTICIDE RESIDUES IN OKRA (ABLEMOSCHUS ESCULENTUS) BY LIQUID CHROMATOGRAPHY-TANDEM MASS SPECTROMETRY. 2012; 35, (1-4): 375-384.


Rec #: 67329
Keywords: CHEM METHODS
Notes: Chemical of Concern: CPY
Abstract: Abstract: A method basing on liquid chromatography-mass spectrometry (LC-MS/MS) was developed for sensitive determination of Organophosphorus pesticides namely Monochrotophos, Quinalphos and Chlorpyrifos in okra in Andhra Pradesh (South India). The method involves extraction of 10 g of homogenized okra samples (2 g of Sodium chloride + 8 g of Magnesium sulfate) with 10 mL of acetonitrile later cleaned up by dispersive solid phase extraction with the combination of primary secondary amine (PSA), graphitized carbon black (GCB), C18, and anhydrous magnesium sulfate. Final analysis was performed by liquid chromatography-dear() spray ionization-tandem mass spectrometry operated in the multiple reaction monitoring (MRM) mode, acquiring two specific precursor-production transitions per target compound. The average recoveries measured at 10 mu g/kg were in the range 81-106% for all of the compounds tested with relative standard deviations below 14%. The methodology has been proven to be highly efficient and robust and thus the method is highly suitable for monitoring the Maximum Residue Limits (MRL) compliance of the pesticides.
Keywords: LC-MS/MS, matrix effect, okra, pesticide residues, QuEChERS method,
ISI Document Delivery No.: 901LG

1102. Ramani, Vimal. Effect of pesticides on phosphate solubilization by Bacillus sphaericus and Pseudomonas cepacia. 2011 Mar; 99, (3): 232-236.


Rec #: 3560
Keywords: BACTERIA
Notes: Chemical of Concern: CPY
Abstract: Intensive screening of phosphate solubilizing bacteria with genetic potential for increased tolerance to high salt, high pH and high temperature could enhance production of food and forage in semi-arid regions. Emphasizing particularly on this hypothesis 165 phosphate solubilizing bacteria was isolated. Among these, two cultures Bacillus sphaericus and Pseudomonas cepacia were selected on the basis of salt tolerance property and PS activity with different forms of phosphates. In the present investigation both these culture were assessed for the effect of six different pesticides, to confirm its successful realistic application as microbial inoculants in actual farm conditions. Both cultures showed better phosphate solubilizing activity with phosphate containing pesticides. Among these two isolates P. cepacia was a better performer in terms of phosphate solubilizing activity with different pesticides. It may be due to its well documented extra ordinary, versatile metabolic activity. The present study may prove them to be potential candidates to be used as microbial inoculants. Phosphate solubilization/ Pesticides/ Microbial inoculants/ Phosphate solubilizing bacteria/ Bacillus sphaericus/ Pseudomonas cepacia

1103. Ramon-Azcon, J.; Sanchez-Baeza, F.; Sanvicens, N., and Marco, M. P. Development of an Enzyme-Linked Immunosorbent Assay for Determination of the Miticide Bromopropylate. 2009; 57, (2): 375-384.


Rec #: 67349
Keywords: IN VITRO
Notes: Chemical of Concern: CPY
Abstract: Abstract: This paper reports for the first time the development of an immunoassay for the analysis of the miticide bromopropylate (BP). The chemical structure of the immunizing haptens was designed to maximize the recognition of the bis-bromophenyl group of BP. Thus, the assay uses polyclonal antibodies raised against 2,2-bis(4-bromophenyl)-N-2-hydroxyacetamide-butanoic acid (hapten 2) conjugated to keyhole
1   ...   110   111   112   113   114   115   116   117   ...   151


The database is protected by copyright ©dentisty.org 2016
send message

    Main page