James M. Cannon to Senator James O. Eastland, 8 July 1976

Typed letter signed dated 8 July 1976 from James M. Cannon, Assistant to the President for Domestic Affairs, to Eastland, re: Section 404 of the Federal Water Pollution Control Act. Attached: copy White House press release dated 2 July 1976, re: above topic.https://egrove.olemiss.edu/joecorr_g/1077/thumbnail.jp

Forest diagrams for elements of Thompson's group F

We introduce forest diagrams to represent elements of Thompson's group F. These diagrams relate to a certain action of F on the real line in the same way that tree diagrams relate to the standard action of F on the unit interval. Using forest diagrams, we give a conceptually simple length formula for elements of F with respect to the {x_0,x_1} generating set, and we discuss the construction of minimum-length words for positive elements. Finally, we use forest diagrams and the length formula to examine the structure of the Cayley graph of F.Comment: 44 pages, 70 figure

Interoperability in the GENESIS 3.0 Software Federation : the NEURON Simulator as an Example

© 2013 Cornelis et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.Poster presented at CNS 2013Non peer reviewe

Retrotransposition-Competent Human LINE-1 Induces Apoptosis in Cancer Cells With Intact p53

Retrotransposition of human LINE-1 (L1) element, a major representative non-LTR retrotransposon in the human genome, is known to be a source of insertional mutagenesis. However, nothing is known about effects of L1 retrotransposition on cell growth and differentiation. To investigate the potential for such biological effects and the impact that human L1 retrotransposition has upon cancer cell growth, we examined a panel of human L1 transformed cell lines following a complete retrotransposition process. The results demonstrated that transposition of L1 leads to the activation of the p53-mediated apoptotic pathway in human cancer cells that possess a wild-type p53. In addition, we found that inactivation of p53 in cells, where L1 was undergoing retrotransposition, inhibited the induction of apoptosis. This suggests an association between active retrotransposition and a competent p53 response in which induction of apoptosis is a major outcome. These data are consistent with a model in which human retrotransposition is sensed by the cell as a “genetic damaging event” and that massive retrotransposition triggers signaling pathways resulting in apoptosis

Dwarf Cepheids in the Carina Dwarf Spheroidal Galaxy

We have discovered 20 dwarf Cepheids (DC) in the Carina dSph galaxy from the analysis of individual CCD images obtained for a deep photometric study of the system. These short-period pulsating variable stars are by far the most distant (~100 kpc) and faintest (V ~ 23.0) DCs known. The Carina DCs obey a well-defined period-luminosity relation, allowing us to readily distinguish between overtone and fundamental pulsators in nearly every case. Unlike RR Lyr stars, the pulsation mode turns out to be uncorrelated with light-curve shape, nor do the overtone pulsators tend towards shorter periods compared to the fundamental pulsators. Using the period-luminosity (PL) relations from Nemec et al. (1994 AJ, 108, 222) and McNamara (1995, AJ, 109, 1751), we derive (m-M)_0 = 20.06 +/- 0.12, for E(B-V) = 0.025 and [Fe/H] = -2.0, in good agreement with recent, independent estimates of the distance/reddening of Carina. The error reflects the uncertainties in the DC distance scale, and in the metallicity and reddening of Carina. The frequency of DCs among upper main sequence stars in Carina is approximately 3%. The ratio of dwarf Cepheids to RR Lyr stars in Carina is 0.13 +/- 0.10, though this result is highly sensitive to the star-formation history of Carina and the evolution of the Horizontal Branch. We discuss how DCs may be useful to search effectively for substructure in the Galactic halo out to Galactocentric distances of ~100 kpc.Comment: 20 pages of text, 7 figure

Increased risk for other cancers in individuals with Ewing sarcoma and their relatives.

BackgroundThere are few reports of the association of other cancers with Ewing sarcoma in patients and their relatives. We use a resource combining statewide genealogy and cancer reporting to provide unbiased risks.MethodsUsing a combined genealogy of 2.3 million Utah individuals and the Utah Cancer Registry (UCR), relative risks (RRs) for cancers of other sites were estimated in 143 Ewing sarcoma patients using a Cox proportional hazards model with matched controls; however, risks in relatives were estimated using internal cohort-specific cancer rates in first-, second-, and third-degree relatives.ResultsCancers of three sites (breast, brain, complex genotype/karyotype sarcoma) were observed in excess in Ewing sarcoma patients. No Ewing sarcoma patients were identified among first-, second-, or third-degree relatives of Ewing sarcoma patients. Significantly increased risk for brain, lung/bronchus, female genital, and prostate cancer was observed in first-degree relatives. Significantly increased risks were observed in second-degree relatives for breast cancer, nonmelanoma eye cancer, malignant peripheral nerve sheath cancer, non-Hodgkin lymphoma, and translocation sarcomas. Significantly increased risks for stomach cancer, prostate cancer, and acute lymphocytic leukemia were observed in third-degree relatives.ConclusionsThis analysis of risk for cancer among Ewing sarcoma patients and their relatives indicates evidence for some increased cancer predisposition in this population which can be used to individualize consideration of potential treatment of patients and screening of patients and relatives

No evidence of BRCA2 mutations in chromosome 13q-linked Utah high-risk prostate cancer pedigrees

<p>Abstract</p> <p>Background</p> <p>Germline mutations in the <it>BRCA2 </it>gene have been suggested to account for about 5% of familial prostate cancer; mutations have been reported in 2% of early onset (i.e., ≤ 55 years) prostate cancer cases and a segregating founder mutation has been identified in Iceland (999del5). However, the role of <it>BRCA2 </it>in high risk prostate cancer pedigrees remains unclear.</p> <p>Findings</p> <p>We examined the potential involvement of <it>BRCA2 </it>in a set offive high-risk prostate cancer pedigrees in which all prostate cases were no more distantly related than two meioses from another case, and the resulting cluster contained at least four prostate cancer cases. We selected these five pedigrees from a larger dataset of 59 high-risk prostate cancer pedigrees analyzed in a genome-wide linkage screen. Selected pedigrees showed at least nominal linkage evidence to the <it>BRCA2 </it>region on chromosome 13q. We mutation screened all coding regions and intron/exon boundaries of the <it>BRCA2 </it>gene in the youngest prostate cancer case who carried the linked 13q segregating haplotype, as well as in a distantly related haplotype carrier to confirm any segregation. We observed no known protein truncating <it>BRCA2 </it>deleterious mutations. We identified one non-segregating <it>BRCA2 </it>variant of uncertain significance, one non-segregating intronic variant not previously reported, and a number of polymorphisms.</p> <p>Conclusion</p> <p>In this set of high-risk prostate cancer pedigrees with at least nominal linkage evidence to <it>BRCA2</it>, we saw no evidence for segregating <it>BRCA2 </it>protein truncating mutations in heritable prostate cancer.</p