Search

Your search keyword '"Mellon S"' showing total 323 results
Start Over Author "Mellon S"
323 results on '"Mellon S"'

54. Circulating hematopoietic progenitor cell number is associated with prefrontal cortical thickness, white matter integrity and PTSD duration in combat-exposed veterans

Author

Aschbacher, K., primary, Mellon, S., additional, Sinclair, E., additional, Marmar, C.R., additional, Henn-Haase, C., additional, Abu-Amara, D., additional, Yehuda, R., additional, Flory, J., additional, Bierer, L., additional, Wolkowitz, O.M., additional, and Mueller, S., additional

Published
2015
Full Text
View/download PDF

56. Pregnane X receptor (PXR) activation: A mechanism for neuroprotection in a mouse model of Niemann-Pick C disease

Author

Walkley, S. U., Langmade, S. J., Schaffer, J. E., Suzuki, K., Ory, D. S., Mohri, I., Frolov, A., Covey, D. F., Gale, S. E., and Mellon, S. H.

Subjects
endocrine system, surgical procedures, operative, hemic and immune systems, chemical and pharmacologic phenomena, lipids (amino acids, peptides, and proteins)
Abstract

Niemann–Pick type C1 (NPC1) disease is a fatal neurodegenerative disease characterized by neuronal lipid storage and progressive Purkinje cell loss in the cerebellum. We investigated whether therapeutic approaches to bypass the cholesterol trafficking defect in NPC1 disease might delay disease progression in the npc1−/− mouse model. We show that the neurosteroid allopregnanolone (ALLO) and T0901317, a synthetic oxysterol ligand, act in concert to delay onset of neurological symptoms and prolong the lifespan of npc1−/− mice. ALLO and T0901317 therapy preserved Purkinje cells, suppressed cerebellar expression of microglial-associated genes and inflammatory mediators, and reduced infiltration of activated microglia in the cerebellar tissue. To establish whether the mechanism of neuroprotection in npc1−/− mice involves GABAA receptor activation, we compared treatment of natural ALLO and ent-ALLO, a stereoisomer that has identical physical properties of natural ALLO but is not a GABAA receptor agonist. ent-ALLO provided identical functional and survival benefits as natural ALLO in npc1−/− mice, strongly supporting a GABAA receptor-independent mechanism for ALLO action. On the other hand, the efficacy of ALLO, ent-ALLO, and T0901317 therapy correlated with the ability of these compounds to activate pregnane X receptor-dependent pathways in vivo. These findings suggest that treatment with pregnane X receptor ligands may be useful clinically in delaying the progressive neurodegeneration in human NPC disease.

Published
2006
Full Text
View/download PDF

58. The Expeditionary Mind

Author

MARINE CORPS COMMAND AND STAFF COLL QUANTICO VA, Mellon, S. M., MARINE CORPS COMMAND AND STAFF COLL QUANTICO VA, and Mellon, S. M.

Abstract

The Marine Corps must remain focused on its amphibious roots and enhance its expeditionary mindset if it is to remain a "versatile, fast-moving and hard-hitting..." force to meet the demands of the American people and those of the world. As an amphibious force in expeditionary readiness, the Marine Corps must take the time to re-evaluate its role providing rapid response to regions in the "Arc of Instability" and other similar littorals throughout the world. Logistically mature theaters of operation as seen in the current operating environment (COE) will not exist in the future. To enhance expeditionary capability and to prepare for operations beyond the COE, the Marine Corps must reduce the weight of it equipment and the weight of the individual Marine's combat load, return to the basics by educating and training the Marine Corps on the logistics of amphibious operations, and finally, focus the efforts of logisticians within the MAGTF to provide right time logistics support from ship to shore., EWS Contemporary Issues Paper.

Published
2008

62. Muscle disorders * 111. The impact of fatigue in patients with idiopathic inflammatory myopathy: a mixed method study

Author

Campbell, R., primary, Hofmann, D., additional, Hatch, S., additional, Gordon, P., additional, Lempp, H., additional, Das, L., additional, Blumbergs, P., additional, Limaye, V., additional, Vermaak, E., additional, McHugh, N., additional, Edwards, M. H., additional, Jameson, K., additional, Sayer, A. A., additional, Dennison, E., additional, Cooper, C., additional, Salvador, F. B., additional, Huertas, C., additional, Isenberg, D., additional, Jackson, E. J., additional, Middleton, A., additional, Churchill, D., additional, Walker-Bone, K., additional, Worsley, P. R., additional, Mottram, S., additional, Warner, M., additional, Morrissey, D., additional, Gadola, S., additional, Carr, A., additional, Stokes, M., additional, Srivastava, R. N., additional, Sanghi, D., additional, Elbaz, A., additional, Mor, A., additional, Segal, G., additional, Drexler, M., additional, Norman, D., additional, Peled, E., additional, Rozen, N., additional, Goryachev, Y., additional, Debbi, E. M., additional, Haim, A., additional, Wolf, A., additional, Debi, R., additional, Cohen, M. S., additional, Igolnikov, I., additional, Bar Ziv, Y., additional, Benkovich, V., additional, Bernfeld, B., additional, Collins, J., additional, Moots, R. J., additional, Clegg, P. D., additional, Milner, P. I., additional, Ejtehadi, H. D., additional, Nelson, P. N., additional, Wenham, C., additional, Balamoody, S., additional, Hodgson, R., additional, Conaghan, P., additional, Wilkie, R., additional, Blagojevic, M., additional, Jordan, K. P., additional, Mcbeth, J., additional, Peffers, M. J., additional, Beynon, R. J., additional, Thornton, D. J., additional, Chapman, R., additional, Chapman, V., additional, Walsh, D., additional, Kelly, S., additional, Hui, M., additional, Zhang, W., additional, Doherty, S., additional, Rees, F., additional, Muir, K., additional, Maciewicz, R., additional, Doherty, M., additional, Snelling, S., additional, Davidson, R. K., additional, Swingler, T., additional, Price, A., additional, Clark, I., additional, Stockley, E., additional, Hathway, G., additional, Faas, H., additional, Auer, D., additional, Hirsch, G., additional, Hale, E., additional, Kitas, G., additional, Klocke, R., additional, Abraham, A., additional, Pearce, M. S., additional, Mann, K. D., additional, Francis, R. M., additional, Birrell, F., additional, Tucker, M., additional, Mellon, S. J., additional, Jones, L., additional, Price, A. J., additional, Dieppe, P. A., additional, Gill, H. S., additional, Ashraf, S., additional, Walsh, D. A., additional, McCollum, D., additional, McCabe, C., additional, Grieve, S., additional, Shipley, J., additional, Gorodkin, R., additional, Oldroyd, A. G., additional, Evans, B., additional, Greenbank, C., additional, Bukhari, M., additional, Rajak, R., additional, Bennett, C., additional, Williams, A., additional, Martin, J. C., additional, Abdulkader, R., additional, MacNicol, C., additional, Brixey, K., additional, Stephenson, S., additional, Clunie, G., additional, Andrews, R. N., additional, Clark, E. M., additional, Gould, V. C., additional, Carter, L., additional, Morrison, L., additional, Tobias, J. H., additional, Pye, S. R., additional, Vanderschueren, D., additional, O'Neill, T. W., additional, Lee, D. M., additional, Jans, I., additional, Billen, J., additional, Gielen, E., additional, Laurent, M., additional, Claessens, F., additional, Adams, J. E., additional, Ward, K. A., additional, Bartfai, G., additional, Casanueva, F., additional, Finn, J. D., additional, Forti, G., additional, Giwercman, A., additional, Han, T. S., additional, Huhtaniemi, I., additional, Kula, K., additional, Lean, M. E., additional, Pendleton, N., additional, Punab, M., additional, Wu, F. C., additional, Boonen, S., additional, Mercieca, C., additional, Webb, J., additional, Bhalla, A., additional, Fairbanks, S., additional, Moss, K. E., additional, Collins, C., additional, Sedgwick, P., additional, Parker, J., additional, Harvey, N. C., additional, Cole, Z. A., additional, Crozier, S. R., additional, Ntani, G., additional, Mahon, P. A., additional, Robinson, S. M., additional, Inskip, H. M., additional, Godfrey, K. M., additional, Dennison, E. M., additional, Bridges, M., additional, Ruddick, S., additional, Holroyd, C. R., additional, Mahon, P., additional, Godfrey, K., additional, McNeilly, T., additional, McNally, C., additional, Beringer, T., additional, Finch, M., additional, Coda, A., additional, Davidson, J., additional, Walsh, J., additional, Fowlie, P., additional, Carline, T., additional, Santos, D., additional, Patil, P., additional, Rawcliffe, C., additional, Olaleye, A., additional, Moore, S., additional, Fox, A., additional, Sen, D., additional, Ioannou, Y., additional, Nisar, S., additional, Rankin, K., additional, Birch, M., additional, Finnegan, S., additional, Rooney, M., additional, Gibson, D. S., additional, Malviya, A., additional, Ferris, C. M., additional, Rushton, S. P., additional, Foster, H. E., additional, Hanson, H., additional, Muthumayandi, K., additional, Deehan, D. J., additional, Birt, L., additional, Poland, F., additional, MacGregor, A., additional, Armon, K., additional, Pfeil, M., additional, McErlane, F., additional, Beresford, M. W., additional, Baildam, E. M., additional, Thomson, W., additional, Hyrich, K., additional, Chieng, A., additional, Gardner-Medwin, J., additional, Lunt, M., additional, Wedderburn, L., additional, Newell, K., additional, Evans, A., additional, Manning, G., additional, Scaife, C., additional, McAllister, C., additional, Pennington, S. R., additional, Duncan, M., additional, Moore, T., additional, Pericleous, C., additional, Croca, S. C., additional, Giles, I., additional, Alber, K., additional, Yong, H., additional, Midgely, A., additional, Rahman, A., additional, Rzewuska, M., additional, Mallen, C., additional, Strauss, V. Y., additional, Belcher, J., additional, Peat, G., additional, Byng-Maddick, R., additional, Wijendra, M., additional, Penn, H., additional, Roddy, E., additional, Muller, S., additional, Hayward, R., additional, Kamlow, F., additional, Pakozdi, A., additional, Jawad, A., additional, Green, D. J., additional, Hider, S. L., additional, Singh Bawa, S., additional, Bawa, S., additional, Turton, A., additional, Palmer, M., additional, Lewis, J., additional, Moss, T., additional, Goodchild, C. E., additional, Tang, N., additional, Scott, D., additional, Salkovskis, P., additional, Selvan, S., additional, Williamson, L., additional, Thalayasingam, N., additional, Higgins, M., additional, Saravanan, V., additional, Rynne, M., additional, Hamilton, J. D., additional, Heycock, C., additional, Kelly, C., additional, Norton, S., additional, Sacker, A., additional, Done, J., additional, Young, A., additional, Smolen, J. S., additional, Fleischmann, R. M., additional, Emery, P., additional, van Vollenhoven, R. F., additional, Guerette, B., additional, Santra, S., additional, Kupper, H., additional, Redden, L., additional, Kavanaugh, A., additional, Keystone, E. C., additional, van der Heijde, D., additional, Weinblatt, M. E., additional, Mozaffarian, N., additional, Liu, S., additional, Zhang, N., additional, Wilkinson, S., additional, Riaz, M., additional, Ostor, A. J., additional, Nisar, M. K., additional, Burmester, G., additional, Mariette, X., additional, Navarro-Blasco, F., additional, Oezer, U., additional, Kary, S., additional, Unnebrink, K., additional, Jobanputra, P., additional, Maggs, F., additional, Deeming, A., additional, Carruthers, D., additional, Rankin, E., additional, Jordan, A., additional, Faizal, A., additional, Goddard, C., additional, Pugh, M., additional, Bowman, S., additional, Brailsford, S., additional, Nightingale, P., additional, Tugnet, N., additional, Cooper, S. C., additional, Douglas, K. M., additional, Edwin Lim, C. S., additional, Bee Lian Low, S., additional, Joy, C., additional, Hill, L., additional, Davies, P., additional, Mukherjee, S., additional, Cornell, P., additional, Westlake, S. L., additional, Richards, S., additional, Rahmeh, F., additional, Thompson, P. W., additional, Breedveld, F., additional, Keystone, E., additional, Landewe, R., additional, McIlraith, M., additional, Dharmapalaiah, C., additional, Shand, L., additional, Rose, G., additional, Watts, R., additional, Eldashan, A., additional, Dasgupta, B., additional, Borg, F. A., additional, Bell, G. M., additional, Anderson, A. E., additional, Harry, R. A., additional, Stoop, J. N., additional, Hilkens, C. M., additional, Isaacs, J., additional, Dickinson, A., additional, McColl, E., additional, Banik, S., additional, Smith, L., additional, France, J., additional, Rutherford, A., additional, Scott Russell, A., additional, Smith, J., additional, Jassim, I., additional, Withrington, R., additional, Bacon, P., additional, De Lord, D., additional, McGregor, L., additional, Morrison, I., additional, Stirling, A., additional, Porter, D. R., additional, Saunders, S. A., additional, Else, S., additional, Semenova, O., additional, Thompson, H., additional, Ogunbambi, O., additional, Kallankara, S., additional, Baguley, E., additional, Patel, Y., additional, Alzabin, S., additional, Abraham, S., additional, Taher, T. E., additional, Palfeeman, A., additional, Hull, D., additional, McNamee, K., additional, Pathan, E., additional, Kinderlerer, A., additional, Taylor, P., additional, Williams, R. O., additional, Mageed, R. A., additional, Iaremenko, O., additional, Mikitenko, G., additional, Ferrari, M., additional, Kamalati, T., additional, Pitzalis, C., additional, Pearce, F., additional, Tosounidou, S., additional, Obrenovic, K., additional, Erb, N., additional, Packham, J., additional, Sandhu, R., additional, White, C., additional, Cardy, C. M., additional, Justice, E., additional, Frank, M., additional, Li, L., additional, Lloyd, M., additional, Ahmed, A., additional, Readhead, S., additional, Ala, A., additional, Fittall, M., additional, Manson, J., additional, Sibilia, J., additional, Marc Flipo, R., additional, Combe, B., additional, Gaillez, C., additional, Le Bars, M., additional, Poncet, C., additional, Elegbe, A., additional, Westhovens, R., additional, Hassanzadeh, R., additional, Mangan, C., additional, Fleischmann, R., additional, van Vollenhoven, R., additional, Huizinga, T. W. J., additional, Goldermann, R., additional, Duncan, B., additional, Timoshanko, J., additional, Luijtens, K., additional, Davies, O., additional, Dougados, M., additional, Hewitt, J., additional, Owlia, M., additional, Schiff, M., additional, Alten, R., additional, Kaine, J. L., additional, Nash, P. T., additional, Delaet, I., additional, Qi, K., additional, Genovese, M. C., additional, Clark, J., additional, Kardash, S., additional, Wong, E., additional, Hull, R., additional, McCrae, F., additional, Shaban, R., additional, Thomas, L., additional, Young-Min, S., additional, Ledingham, J., additional, Covarrubias Cobos, A., additional, Leon, G., additional, Mysler, E. F., additional, Keiserman, M. W., additional, Valente, R. M., additional, Abraham Simon Campos, J., additional, Porawska, W., additional, Box, J. H., additional, Legerton, C. W., additional, Nasonov, E. L., additional, Durez, P., additional, Pappu, R., additional, Teng, J., additional, Edwards, C. J., additional, Arden, N., additional, Campbell, J., additional, van Staa, T., additional, Housden, C., additional, Sargeant, I., additional, Choy, E., additional, McAuliffe, S., additional, Roberts, K., additional, Sarzi-Puttini, P., additional, Andrianakos, A., additional, Sheeran, T. P., additional, Choquette, D., additional, Finckh, A., additional, Desjuzeur, M.-L., additional, Gemmen, E. K., additional, Mpofu, C., additional, Gottenberg, J.-E., additional, Shah, P., additional, Cox, M., additional, Nye, A., additional, O'Brien, A., additional, Jones, P., additional, Jones, G. T., additional, Paudyal, P., additional, MacPherson, H., additional, Sim, J., additional, Ernst, E., additional, Fisken, M., additional, Lewith, G., additional, Tadman, J., additional, Macfarlane, G. J., additional, Bertin, P., additional, Arendt, C., additional, Terpstra, I., additional, VanLunen, B., additional, de Longueville, M., additional, Zhou, H., additional, Cai, A., additional, Lacy, E., additional, Kay, J., additional, Matteson, E., additional, Hu, C., additional, Hsia, E., additional, Doyle, M., additional, Rahman, M., additional, Shealy, D., additional, Scott, D. L., additional, Ibrahim, F., additional, Abozaid, H., additional, Hassell, A., additional, Plant, M., additional, Walker, D., additional, Simpson, G., additional, Kowalczyk, A., additional, Prouse, P., additional, Brown, A., additional, George, M., additional, Kumar, N., additional, Mackay, K., additional, Marshall, S., additional, Ludivico, C. L., additional, Murthy, B., additional, Corbo, M., additional, Samborski, W., additional, Berenbaum, F., additional, Ambrugeat, J., additional, Bennett, B., additional, Burkhardt, H., additional, Bykerk, V., additional, Roman Ivorra, J., additional, Wollenhaupt, J., additional, Stancati, A., additional, Bernasconi, C., additional, Scott, D. G. I., additional, Claydon, P., additional, Ellis, C., additional, Buchan, S., additional, Pope, J., additional, Bingham, C. O., additional, Massarotti, E. M., additional, Coteur, G., additional, Weinblatt, M., additional, Ball, C., additional, Ainsworth, T., additional, Kermik, J., additional, Woodham, J., additional, Haq, I., additional, Quesada-Masachs, E., additional, Carolina Diaz, A., additional, Avila, G., additional, Acosta, I., additional, Sans, X., additional, Alegre, C., additional, Marsal, S., additional, McWilliams, D., additional, Kiely, P. D., additional, Bolce, R., additional, Wang, J., additional, Ingham, M., additional, Dehoratius, R., additional, Decktor, D., additional, Rao, V., additional, Pavlov, A., additional, Klearman, M., additional, Musselman, D., additional, Giles, J., additional, Bathon, J., additional, Sattar, N., additional, Lee, J., additional, Baxter, D., additional, McLaren, J. S., additional, Gordon, M.-M., additional, Thant, K. Z., additional, Williams, E. L., additional, Earl, S., additional, White, P., additional, Williams, J., additional, Jan, A. K., additional, Bhatti, A. I., additional, Stafford, C., additional, Carolan, M., additional, and Ramakrishnan, S. A., additional

Published
2012
Full Text
View/download PDF

77. Whole-genome DNA methylation status associated with clinical PTSD measures of OIF/OEF veterans

Author

Hammamieh, R, Chakraborty, N, Gautam, A, Muhie, S, Yang, R, Donohue, D, Kumar, R, Daigle, B J, Zhang, Y, Amara, D A, Miller, S-A, Srinivasan, S, Flory, J, Yehuda, R, Petzold, L, Wolkowitz, O M, Mellon, S H, Hood, L, Doyle, F J, Marmar, C, and Jett, M

Abstract

Emerging knowledge suggests that post-traumatic stress disorder (PTSD) pathophysiology is linked to the patients’ epigenetic changes, but comprehensive studies examining genome-wide methylation have not been performed. In this study, we examined genome-wide DNA methylation in peripheral whole blood in combat veterans with and without PTSD to ascertain differentially methylated probes. Discovery was initially made in a training sample comprising 48 male Operation Enduring Freedom (OEF)/Operation Iraqi Freedom (OIF) veterans with PTSD and 51 age/ethnicity/gender-matched combat-exposed PTSD-negative controls. Agilent whole-genome array detected ~5600 differentially methylated CpG islands (CpGI) annotated to ~2800 differently methylated genes (DMGs). The majority (84.5%) of these CpGIs were hypermethylated in the PTSD cases. Functional analysis was performed using the DMGs encoding the promoter-bound CpGIs to identify networks related to PTSD. The identified networks were further validated by an independent test set comprising 31 PTSD+/29 PTSD− veterans. Targeted bisulfite sequencing was also used to confirm the methylation status of 20 DMGs shown to be highly perturbed in the training set. To improve the statistical power and mitigate the assay bias and batch effects, a union set combining both training and test set was assayed using a different platform from Illumina. The pathways curated from this analysis confirmed 65% of the pool of pathways mined from training and test sets. The results highlight the importance of assay methodology and use of independent samples for discovery and validation of differentially methylated genes mined from whole blood. Nonetheless, the current study demonstrates that several important epigenetically altered networks may distinguish combat-exposed veterans with and without PTSD., Version of Record

Published
2017
Full Text
View/download PDF

86. Concerns and recommendations regarding inherited cancer risk: the perspectives of survivors and female relatives.

Author

Mellon S, Berry-Bobovski L, Gold R, Levin N, Tainsky MA, Mellon, Suzanne, Berry-Bobovski, Lisa, Gold, Robin, Levin, Nancy, and Tainsky, Michael A

Abstract

Background: Little research is available comparing differences in cancer risk perceptions between cancer survivors and family members at risk for hereditary breast/ovarian cancer.Methods: Qualitative focus groups with survivor-female relative dyads (N = 39) were conducted.Results: Important differences exist between the concerns of survivors and family members relevant to their cancer risk. Survivors focused on their own concerns from a personal perspective, whereas family members focused on the survivors' health and tended to suppress their own fears of cancer. Specific recommendations for inclusion of family members in cancer risk education are provided.Conclusions: Addressing family member differences is critical to tailor specific risk information inclusive of the entire family. [ABSTRACT FROM AUTHOR]

Published
2007
Full Text
View/download PDF

88. The Whittier Narrows, California Earthquake of October 1, 1987 -- Damage to State Highway Bridges.

Author

Gates, J. H., Mellon, S., and Klein, G.

Abstract

Damage to state highway bridges was confined primarily to one bridge. Shear damage, classified as moderate, occurred to the columns of one bent. The bridge was shored up and opened to traffic in less than 22 hours. Minor damage also occurred at bearings and other locations on sixteen other bridges. Evidence of movement was also noted on seven other bridges.

Published
1988
Full Text
View/download PDF

92. Analysis by immunocytochemistry and in situ hybridization of renin and its mRNA in kidney, testis, adrenal, and pituitary of the rat.

Author

Deschepper, C F, Mellon, S H, Cumin, F, Baxter, J D, and Ganong, W F

Abstract

Renin gene expression in cells and tissues of the rat was examined by in situ hybridization histochemistry and immunocytochemistry. By using a mouse cDNA probe, hybridization histochemistry revealed renin mRNA in the renal juxtaglomerular cells, testicular Leydig cells, adrenal zona glomerulosa cells, the intermediate lobe of the pituitary, and scattered cells of the anterior lobe of the pituitary. With four separate antisera to mouse submaxillary renin, there was immunoreactivity in the renal juxtaglomerular cells. However, only one of the antisera stained the Leydig cells, a second stained the adrenal zona glomerulosa, a third stained the intermediate lobe of the pituitary, and a fourth stained scattered cells of the anterior lobe of the pituitary that were identified as gonadotrophs. The variations with the different antisera in detecting extrarenal renin are unexplained but could imply that posttranslational proteolysis or glycosylation of preprorenin varies in different tissues with consequent variations in immunoreactivity. The finding of renin mRNA and renin-like immunoreactivity in these tissues supports the notion that these tissues are sites for production of renin.

Published
1986
Full Text
View/download PDF

94. Molecular variants in the P450c11AS gene as determinants of aldosterone synthase activity in the Dahl rat model of hypertension.

Author

Cover, C M, Wang, J M, St Lezin, E, Kurtz, T W, and Mellon, S H

Abstract

Dahl salt-sensitive (S) and salt-resistant (R) rats are widely used to study genetic determinants of salt-sensitive hypertension. Differences in blood pressure under a high sodium diet in these two strains may be due to differences in the synthesis of 18-OH-11-deoxycorticosterone (18-OH DOC). This difference in 18-OH-DOC synthesis is due to mutations in the Dahl R rat's gene for P450c11 beta (11 beta-hydroxylase), an adrenal enzyme involved in the synthesis of both corticosterone and 18-OH DOC from 11-deoxycorticosterone. Aldosterone/renin ratios in plasma and in the adrenals are greater in Dahl S than R rats, suggesting an altered physiologic relationship between the renin-angiotensin and aldosterone systems between these strains. We demonstrate that the mRNA for P450c11AS, (aldosterone synthase), an enzyme required for aldosterone synthesis, is identical in the Dahl S rat and in normotensive Sprague-Dawley rats, but that P450c11AS mRNA from the Dahl R rat contains 7 mutations that result in two amino acid substitutions. These two changes result in a form of P450c11AS that has a greater apparent Vmax and lower apparent Km, resulting in an enzyme that catalyzes the conversion of 11-deoxycorticosterone to aldosterone at a greater rate in Dahl R rats than the P450c11AS in Dahl S rats or Sprague-Dawley rats. Although plasma and adrenal renin are lower in Dahl S versus R rats, the regulation of P450c11AS mRNA expression in rats fed a low and high salt diet are identical in these strains. The current findings may explain both the reduced aldosterone concentrations and increased aldosterone/renin ratios previously reported in the Dahl S versus Dahl R rat.

Published
1995

95. Interaction of a tissue-specific factor with an essential rat growth hormone gene promoter element

Author

West, B L, Catanzaro, D F, Mellon, S H, Cattini, P A, Baxter, J D, and Reudelhuber, T L

Abstract

Rat growth hormone (rGH) gene expression is normally restricted to the anterior pituitary. As a model of this tissue specificity, we compared the transient expression of an rGH-chloramphenicol acetyltransferase (CAT) hybrid gene in rGH-producing rat pituitary tumor (GC) cells and in non-rGH-producing rat fibroblast (rat-2) cells. Deletion analysis of the rGH portion of this hybrid gene demonstrated that DNA sequences within 140 base pairs 5' to the rGH gene were sufficient for correct cell type-specific expression. Deletion of an additional 35 base pairs of the rGH 5'-flanking DNA resulted in a loss of expression of the transfected hybrid gene and correlated with the interaction of a putative trans-acting factor with this region of the rGH promoter. This factor was detectable by DNase I footprinting in a crude nuclear extract from GC cells but not from rat-2 cells. Site-directed mutagenesis of the footprint region caused complete loss of expression of a hybrid gene containing 530 base pairs 5' to the rGH gene. Thus, the interaction of this factor, which we term GC2, is likely to be essential for the tissue-specific expression of the rGH gene.

Published
1987
Full Text
View/download PDF

96. cAMP regulates P450scc gene expression by a cycloheximide-insensitive mechanism in cultured mouse Leydig MA-10 cells.

Author

Mellon, S H and Vaisse, C

Abstract

Mouse MA-10 Leydig tumor cells synthesize and secrete progesterone in response to human chorionic gonadotropin, luteinizing hormone, and cAMP but may not synthesize androgens. Maximal doses of human chorionic gonadotropin, ovine luteinizing hormone, forskolin, or 8-bromoadenosine 3',5'-cyclic monophosphate, stimulated cytochrome P450scc mRNA accumulation 1.5- to 3-fold and progesterone secretion 10- to 100-fold in MA-10 cells. P450scc mRNA increased by 2 hr and was maximal by 8 hr; polymerase run-on experiments showed this was due to increased P450scc gene transcription. MA-10 cells are a hormonally homogeneous population, as all cells expressed P450scc mRNA and responded to cAMP equally. cAMP-stimulated accumulation of P450scc mRNA continued in the presence of cycloheximide. Gonadotropins stimulated testicular steroidogenesis by coordinate cAMP-induced increases in P450scc gene transcription, mRNA accumulation, and P450scc activity. We cloned rat P450c17 cDNA and showed it detected no P450c17 mRNA in control or cAMP-stimulated MA-10 cells by RNA transfer blots or RNase protection assays. Similarly, HPLC detected no 17 alpha-hydroxyprogesterone or testosterone synthesis in MA-10 cells. Thus MA-10 cells, unlike untransformed Leydig cells, do not express detectable amounts of P450c17 mRNA or P450c17 activity.

Published
1989
Full Text
View/download PDF

97. P450c11B3 mRNA, transcribed from a third P450c11 gene, is expressed in a tissue-specific, developmentally, and hormonally regulated fashion in the rodent adrenal and encodes a protein with both 11-hydroxylase and 18-hydroxylase activities.

Author

Mellon, S H, Bair, S R, and Monis, H

Abstract

The rat genome contains four P450c11 genes. One of these (CYP11B1) encodes P450c11 beta, which is the steroid 11 beta-hydroxylase found solely in the adrenal zona fasciculata/reticularis, and is responsible for the conversion of 11-deoxycorticosterone to corticosterone. A second P450c11 gene (CYP11B2) encodes P450c11AS, which is the aldosterone synthase found solely in the adrenal zona glomerulosa. P450c11AS has three activities, 11 beta-hydroxylase, 18-hydroxylase, and 18-oxidase, and is responsible for the conversion of 11-deoxycorticosterone to aldosterone. Recently, two more rat P450c11 genes, P450c11B3 and P450c11B4, were cloned. P450c11B4 appears to be a pseudogene, as two exons are replaced by unrelated DNA. P450c11B3 closely resembles P450c11 beta in mRNA and encoded amino acid sequences, predicting a protein of 498 amino acids. However, the expression of this mRNA and protein have not been demonstrated to date. We now demonstrate that this P450c11B3 mRNA is expressed in the adrenal gland several days after birth and is not expressed during fetal development or in the adult rat adrenal. Like P450c11 beta mRNA, P450c11B3 mRNA is expressed in the zona fasciculata/reticularis and not in the zona glomerulosa. However, the regulation of P450c11B3 mRNA expression is different from that of P450c11 beta mRNA, in that its abundance is decreased by ACTH in a sex-dependent fashion. Transfection of eukaryotic cells with a vector expressing P450c11B3 shows that this form of P450c11 can convert 11-deoxycorticosterone (DOC) to corticosterone and thus has the same enzymatic activity as P450c11 beta. In addition, P450c11B3 can convert DOC to 18-OH DOC and corticosterone to 18-OH corticosterone and thus has 18-hydroxylase activity similar to P450c11AS, but it lacks detectable 18-oxidase activity. Thus, P450c11B3 catalyzes 11 beta- and 18-hydroxylation and thus has a spectrum of activities midway between P450c11 beta and P450c11AS.

Published
1995

98. KELT-6b: A Transiting Mildly-Inflated Saturn with a Metal-Poor Host

Author

Collins, Karen A., Siverd, R., Thomas Beatty, Eastman, J., Gaudi, B. S., Pepper, J., Stassun, K., Latham, D. W., Bieryla, A., Manner, M., Jensen, E. L., Kielkopf, J. F., Gregorio, J., Fulton, B. J., Buchhave, L. A., Penev, K., Crepp, J. R., Cargile, P., Mack, C. E., Oberst, T. E., Avril, R. L., Mellon, S., Mcleod, K. K., Dhital, S., Stefanik, R. P., Calkins, M. L., Esquerdo, G., Berlind, P. L., Street, R., Zambelli, R., Mao, Q., Richert, A. J., Gould, A., Depoy, D. L., Marshall, J. L., Pogge, R. W., Trueblood, M., and Trueblood, P.

100. Constraining the period of the ringed secondary companion to the young star J1407 with photographic plates

Author

Mentel R., Kenworthy M., Cameron D., Scott E., Mellon S., Hudec R., Birkby J., Mamajek E., Schrimpf A., Reichart D., Haislip J., Kouprianov V., Hambsch F., Tan T., Hills K., Grindlay J., Rodriguez J., Lund M., Kuhn R., Mentel R., Kenworthy M., Cameron D., Scott E., Mellon S., Hudec R., Birkby J., Mamajek E., Schrimpf A., Reichart D., Haislip J., Kouprianov V., Hambsch F., Tan T., Hills K., Grindlay J., Rodriguez J., Lund M., and Kuhn R.

Abstract

© ESO 2018. Context. The 16 Myr old star 1SWASP J140747.93-394542.6 (V1400 Cen) underwent a series of complex eclipses in May 2007, interpreted as the transit of a giant Hill sphere filling debris ring system around a secondary companion, J1407b. No other eclipses have since been detected, although other measurements have constrained but not uniquely determined the orbital period of J1407b. Finding another eclipse towards J1407 will help determine the orbital period of the system, the geometry of the proposed ring system and enable planning of further observations to characterize the material within these putative rings. Aims. We carry out a search for other eclipses in photometric data of J1407 with the aim of constraining the orbital period of J1407b. Methods. We present photometry from archival photographic plates from the Harvard DASCH survey, and Bamberg and Sonneberg Observatories, in order to place additional constraints on the orbital period of J1407b by searching for other dimming and eclipse events. Using a visual inspection of all 387 plates and a period-folding algorithm we performed a search for other eclipses in these data sets. Results. We find no other deep eclipses in the data spanning from 1890 to 1990, nor in recent time-series photometry from 2012-2018. Conclusions. We rule out a large fraction of putative orbital periods for J1407b from 5 to 20 yr. These limits are still marginally consistent with a large Hill sphere filling ring system surrounding a brown dwarf companion in a bound elliptical orbit about J1407. Issues with the stability of any rings combined with the lack of detection of another eclipse, suggests that J1407b may not be bound to J1407.

Catalog

Books, media, physical & digital resources
See catalog results