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: Dezba: Woman of the Desert . Gladys A. Reichard

John Adair
1940 American Anthropologist  
REICHARD (xxvi, 161 pp, 56 photographs by the author and Lilian J. Reichard. $3.00. New York: J. J. Augustin, 1939).  ...  Reichard has written a book which is both readable and accurate.  ... 
doi:10.1525/aa.1940.42.3.02a00090 fatcat:x4rm4bg3mvhuxna64qtn2bobpm

Aging and Personality, par SUZANNE REICHARD, FLORINE LIVSON et PAUL-G. PETERSON. Un vol., 6 p. x 9¼, relié, 237 pages. — JOHN WILEY & SONS INC., 440 Fourth Avenue, New York 16, N.Y., 1962. ($7.95)

A. P.
1963 L'Actualité Economique  
Aging and Personality, par SUZANNE REICHARD, FLORINE LIVSON et PAUL-G. PETERSON. Un vol., 6 p. x 9¼, relié, 237 pages. -JOHN WILEY & SONS INC., 440 Fourth Avenue, New York 16, N.Y. ).  ... 
doi:10.7202/1001920ar fatcat:nqk24ct4ufbefc3jz552zdjq5e

Effects of arsenic exposure on DNA methylation and epigenetic gene regulation

John F Reichard, Alvaro Puga
2010 Epigenomics  
Arsenic is a nonmutagenic human carcinogen that induces tumors through unknown mechanisms. A growing body of evidence suggests that its carcinogenicity results from epigenetic changes, particularly in DNA methylation. Changes in gene methylation status, mediated by arsenic, have been proposed activate oncogene expression or silence tumor suppressor genes, leading to long-term changes in activity of genes controlling cell transformation. Mostly descriptive, and often contradictory, studies have
more » ... emonstrated that arsenic exposure is associated with both hypo-and hyper-methylation at various genetic loci in vivo or in vitro. This ambiguity has made it difficult to assess whether the changes induced by arsenic are causally involved in the transformation process or are simply a reflection of the altered physiology of rapidly dividing cancer cells. Here, we discuss the evidence supporting changes in DNA methylation as a cause of arsenic carcinogenesis and highlight the strengths and limitations of these studies, as well areas where consistencies and inconsistencies exist. Arsenic is an element of major health concern because substantial epidemiologic evidence links inorganic arsenic exposure to a variety of human cancers [201, 202] . Chronic low-dose dietary arsenic exposure is causally linked to cancers of the skin, bladder, liver and lung [1] [2] [3] [4] , and human exposures during gestation are associated with elevated incidence of lung and bladder cancer decades later during adulthood [4] [5] [6] . It is estimated that over 100 million people worldwide are exposed to carcinogenic levels of arsenic [201], the vast majority owing to the consumption of drinking water taken from arsenic contaminated aquifers. Populations affected by arsenic-contaminated drinking water span the globe with significant exposures identified in Bangladesh, India, Taiwan, China, Mexico, Argentina, Chile, Europe and regions of North America. The mechanism by which arsenic mediates carcinogenesis remains a subject of debate, with evidence supporting several plausible etiologies, including disruption of signaling cascades [7], elevated levels of oxidative stress [8, 9] , chromosomal aberrations [10] and epigenetic
doi:10.2217/epi.09.45 pmid:20514360 pmcid:PMC2877392 fatcat:y4xyyeqvnrew3jcwvx62awdnjm

BACH1 Is a Specific Repressor ofHMOX1That Is Inactivated by Arsenite

John F. Reichard, Maureen A. Sartor, Alvaro Puga
2008 Journal of Biological Chemistry  
Intracellular heme is a redox active molecule that can be detrimental to cells at high concentrations or under oxidizing conditions. To prevent accumulation, the inducible enzyme heme oxygenase-1 (HMOX1) catalyzes degradation of heme. In the absence of elevated intracellular heme or oxidative stress, the basic region leucine zipper transcriptional regulator BACH1 binds HMOX1 antioxidant response elements and represses transcription. Conversely, increased intracellular heme or sulfhydryl
more » ... n inactivate BACH1, permitting transcriptional induction of HMOX1. Here, we investigate the effect of BACH1 inactivation on the induction of HMOX1 and as a mechanism for broader gene induction. We show that BACH1 is inactivated at low micromolar arsenite concentrations and that BACH1 inactivation is necessary and sufficient for transcriptional induction of HMOX1. Because BACH1 is thought to interact with antioxidant response element motifs, we further examined the role of BACH1 as a regulator of inducible antioxidant gene expression by assessing the global profile of gene expression following BACH1 knockdown using small interfering RNA. The loss of BACH1 function in human keratinocytes results almost exclusively in HMOX1 induction, suggesting that BACH1 may function as a rheostat regulating levels of intracellular free heme.
doi:10.1074/jbc.m801784200 pmid:18550526 pmcid:PMC2504887 fatcat:hfiixgdjczf4dmqmzfaxi3qzca

Microspectrophotometric analysis of yellow polyester fiber dye loadings with chemometric techniques

Eric J. Reichard, Edward G. Bartick, Stephen L. Morgan, John V. Goodpaster
2017 Forensic Chemistry  
Microspectrophotometry is a quick, accurate, and reproducible method to compare colored fibers for forensic purposes. Applying chemometric techniques to spectroscopic data can provide valuable information, especially when looking at a complex dataset. In this study, background subtracted and normalized visible spectra from ten yellow polyester exemplars dyed with different concentrations of the same dye ranging from 0.1-3.5% (w/w), were analyzed by agglomerative hierarchical clustering (AHC),
more » ... incipal component analysis (PCA), and discriminant analysis (DA). Systematic changes in the wavelength of maximum absorption, peak shape and signal-to-background ratio were noted as dye loading increased. In general, classifying the samples into ten groups (one for each exemplar) had poor accuracy (i.e., 51%). However, classification was much more accurate (i.e., 96%) using three classes of fibers that were identified by AHC as having low (0.10 -0.20 wt%), medium (0.40 -0.75 wt%), and high (1.5 -3.5 wt%) dye loadings. An external validation with additional fibers and data generated by independent analysts confirmed these findings. Lastly, it was also possible to discriminating pairs of exemplars with small differences in dye loadings as a simulation of questioned (Q) versus known (K) comparisons. . Microspectrophotometric analysis of yellow polyester fiber dye loadings with chemometric techniques. Forensic Chemistry, 3, 21-27. https://doi.
doi:10.1016/j.forc.2016.11.001 fatcat:k33koltz5fbj5gwwvhbrfeddcq

Heme oxygenase-1 induction by NRF2 requires inactivation of the transcriptional repressor BACH1

John F. Reichard, Gregory T. Motz, Alvaro Puga
2007 Nucleic Acids Research  
Oxidative stress activates the transcription factor NRF2, which in turn binds cis-acting antioxidant response element (ARE) enhancers and induces expression of protective antioxidant genes. In contrast, the transcriptional repressor BACH1 binds ARE-like enhancers in cells naïve to oxidative stress and antagonizes NRF2 binding until it becomes inactivated by pro-oxidants. Here, we describe the dynamic roles of BACH1 and NRF2 in the transcription of the heme oxygenase-1 (HMOX1) gene. HMOX1
more » ... on, elicited by arsenite-mediated oxidative stress, follows inactivation of BACH1 and precedes activation of NRF2. BACH1 repression is dominant over NRF2-mediated HMOX1 transcription and inactivation of BACH1 is a prerequisite for HMOX1 induction. In contrast, thioredoxin reductase 1 (TXNRD1) is regulated by NRF2 but not by BACH1. By comparing the expression levels of HMOX1 with TXNRD1, we show that nuclear accumulation of NRF2 is not necessary for HMOX1 induction; rather, BACH1 inactivation permits NRF2 already present in the nucleus at low basal levels to bind the HMOX1 promoter and elicit HMOX1 induction. Thus, BACH1 confers an additional level of regulation to ARE-dependent genes that reveals a new dimension to the oxidative stress response.
doi:10.1093/nar/gkm638 pmid:17942419 pmcid:PMC2175339 fatcat:22pzrubzdbdv5mgss2ip53e3ra

Long term low-dose arsenic exposure induces loss of DNA methylation

John F. Reichard, Michael Schnekenburger, Alvaro Puga
2007 Biochemical and Biophysical Research Communications - BBRC  
Arsenic ranks as the number one toxic environmental contaminant. In humans, arsenic exposure is associated with various forms of cancer, cardiovascular and skin diseases, neuropathies of the central nervous system, and genotoxic and immunotoxic effects. Although a well recognized human carcinogen, arsenic itself is not a potent mutagen and has been thought to act through epigenetic mechanisms that modify DNA methylation patterns, perhaps in conjunction with DNA-damaging agents. To develop
more » ... inary support for a more thorough examination of this hypothesis, we have measured the effect of submicromolar and low-micromolar concentrations of arsenite on the methylation status of DNA and the biochemical reactions that regulate it. We find that arsenic causes the depletion of S-adenosylmethionine, the main cellular methyl donor, and represses the expression of the DNA methyltransferase genes DNMT1 and DNMT3A. Possibly as a consequence of these two complementary mechanisms, long-term exposure to arsenic results in DNA hypomethylation.
doi:10.1016/j.bbrc.2006.11.001 pmid:17107663 pmcid:PMC1866367 fatcat:a67m7p6bkbfavax4yuhlar63za

Arsenic Toxicology: Translating between Experimental Models and Human Pathology

J. Christopher States, Aaron Barchowsky, Iain L. Cartwright, John F. Reichard, Bernard W. Futscher, R. Clark Lantz
2011 Environmental Health Perspectives  
Accumulating evidence indicates that arsenic is an environmental toxicant that can mediate epi genetic changes (Reichard et al. 2007; Ren et al. 2011b ).  ...  Because arsenicals inhibit activity of DNA methyltransferases DNMT1 and DNMT3a (Reichard et al. 2007 ), this effect may contribute to overall decreased lev els of DNA methylation.  ... 
doi:10.1289/ehp.1103441 pmid:21684831 pmcid:PMC3230447 fatcat:shlpu2rsbjdtxgs3jpmnxuibcq

Integrative Lincs (Ilincs): Connecting Diseases, Drugs And Mechanisms Of Actions

Marcin Pilarczyk, Mehdi Fazel Najafabadi, Michal Kouril, Naim Mahi, Nicholas Clark, Shana White, Mark Bennett, Wen Niu, John Reichard, Juozas Vasiliauskas, Jarek Meller, Mario Medvedovic
2016 Zenodo  
iLINCS (Integrative LINCS) is an integrative web platform for analysis of omics data and signatures of cellular perturbations. The portal consists of biologists-friendly user interfaces for finding and analyzing datasets and signatures, backend databases with a large collection of datasets (>3,000), pre-computed signatures (>200,000) and their connections (>2*10^9). The portal integrates R analytical engine via several R tools for web-computing (rserve, opencpu, shiny, rgl) and other public
more » ... in web tools and open-source applications (e.g., FTreeView, Enrichr, L1000CDS2) into a coherent web platform for omics data analysis. Analytical tools are organized into three interconnected analytical workflows. The "Dataset" workflow facilitates comprehensive analysis of primary omics datasets. In a typical use case, the user starts with an omics dataset of interest (e.g., GEO dataset corresponding to a disease of interest), performs differential gene expression analysis to construct the signature of the disease. Performs enrichment, pathway and network analysis of differentially expressed genes. Identifies "connected" drug signatures that can implicate a potential therapeutic agent for the disease. The "Signatures" workflow facilitates "connectivity analysis" with a large collection of pre-computed signatures that include LINCS drug perturbation signatures, ENCODE transcription factor binding signatures and a library of "disease related signatures" extracted from public domain omics datasets. User can either select one or more pre-computed signatures, or upload their own signatures to use in the analysis. One of the use-cases involves uploading a custom disease signature, identifying the connected LINCS chemical perturbagen signatures which can then provide putative agents for treating the disease. The "Genes" workflow starts with a user supplied list of genes which are then used to query and analyze primary data and pre-computed signatures. The portal can be accessed freely and does not require user registrati [...]
doi:10.5281/zenodo.167645 fatcat:pb555d6jwrcvhpmtst3is66tp4

Improving the confidence of "questioned versus known" fiber comparisons using microspectrophotometry and chemometrics

Georgina Sauzier, Eric Reichard, Wilhelm van Bronswijk, Simon W. Lewis, John V. Goodpaster
2016 Forensic Chemistry  
Microspectrophotometry followed by chemometric data analysis was conducted on pairs of visually similar blue acrylic fibers, simulating the "questioned versus known" scenarios often encountered in forensic casework. The relative similarity or dissimilarity of each pair was determined by employing principal component analysis, discriminant analysis and Fisher's exact test. Comparison of fibers from within each set resulted in a correct inclusion result in 10 out of 11 scenarios, with the one
more » ... e exclusion attributed to a lack of reproducibility in the spectra. Comparison of fibers from different sets resulted in a correct exclusion result in 108 of 110 scenarios, with two sets that shared identical dye combinations being indistinguishable. Although the presented methods are not infallible, they may nonetheless provide a path forward for forensic fiber examiners that has a more scientifically rigorous basis on which to support their findings in a court of law.
doi:10.1016/j.forc.2016.08.001 fatcat:4jyjgmuqtneodczg625m37lxhm

Threat of Foreign Arthropod-Borne Pathogens to Livestock in the United States

Ralph A. Bram, John E. George, Robert E. Reichard, Walter J. Tabachnick
2002 Journal of medical entomology  
Despite considerable research, there is no vaccine for ASF and affected countries have employed ambitious and costly programs based on depopulation of large swine populations to eradicate the disease (Reichard  ... 
doi:10.1603/0022-2585-39.3.405 pmid:12061432 fatcat:unp47jnf3vd27b3lgumbeufmna

Salmonella typhi, the causative agent of typhoid fever, is approximately 50,000 years old

Claire Kidgell, Ulrike Reichard, John Wain, Bodo Linz, Mia Torpdahl, Gordon Dougan, Mark Achtman
2002 Infection, Genetics and Evolution  
doi:10.1016/s1567-1348(02)00089-8 pmid:12797999 fatcat:6mehltxm7jbclpgpu4q7gwvrn4

N-cadherin and integrins: Two receptor systems that mediate neuronal process outgrowth on astrocyte surfaces

Kevin J. Tomaselli, Karla M. Neugebauer, John L. Bixby, Jack Lilien, Louis F. Reichard
1988 Neuron  
doi:10.1016/0896-6273(88)90207-3 pmid:2856086 fatcat:jffk27zr2fgojh26vbudarfgcm

Induction of Oxidative Stress Responses by Dioxin and other Ligands of the Aryl Hydrocarbon Receptor

John F. Reichard, Timothy P. Dalton, Howard G. Shertzer, Alvaro Puga
2005 Dose-Response  
Reichard et al. Dose-Response: An International Journal, Vol. 3 [2014],Iss. 4, Art. 5 J. F. Reichard et al.  ...  Reichard et al. Dose-Response: An International Journal, Vol. 3 [2014],Iss. 4, Art. 5 J. F. Reichard et al.  ... 
doi:10.2203/dose-response.003.03.003 pmid:18648615 pmcid:PMC2475945 fatcat:ypkcrinnxzbmlooc6acxyqe7qu

CD10 expression in peripheral T-cell lymphomas complicated by a proliferation of large B-cells

Kaaren K Reichard, Erich J Schwartz, John P Higgins, Balasubramanian Narasimhan, Roger A Warnke, Yasodha Natkunam
2006 Modern Pathology  
(f) CD10 immunostain showing positive staining of neoplastic T cells.CD10 in peripheral T-cell lymphoma KK Reichard et al .  ...  (f) CD10 immunostain showing positive staining of neoplastic T cells.CD10 in peripheral T-cell lymphoma KK Reichard et al nodal architecture by atypical lymphoid cells with clear cytoplasm, increased vascularity  ... 
doi:10.1038/modpathol.3800536 pmid:16400325 fatcat:h3qtztmkzrhvvogflhgiitqmlm
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