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5. Contributors

Author

Adams, Paul C., primary, Albrecht, Helmut, additional, Bajaj, Jasmohan, additional, Baik, Soon Koo, additional, Beuers, Ulrich, additional, Biggins, Scott W., additional, Bismuth, Henri, additional, Boberg, Kirsten Muri, additional, Bonkovsky, Herbert L., additional, Bosch, Jaime, additional, Boyer, Thomas D., additional, Brunt, Elizabeth M., additional, Caselitz, Martin, additional, Caselmann, Wolfgang H., additional, Cave, Matt, additional, Chan, Henry Lik-Yuen, additional, Chang, Kyong-Mi, additional, Ciancio, Alessia, additional, Colombo, Massimo, additional, Conjeevaram, Hari S., additional, Cox, Diane W., additional, Day, Chris P., additional, Doctor, R. Brian, additional, Oude Elferink, Ronald P.J., additional, Elisofon, Scott A., additional, El-Serag, Hashem B., additional, Esmat, Gamal, additional, Everson, Gregory T., additional, Falkner, Keith Cameron, additional, Fallon, Michael B., additional, Feng, Sandy, additional, Fischer, Hans-Peter, additional, Fortune, Brett E., additional, Friedman, Scott L., additional, García-Pagán, J.C., additional, Garcia-Tsao, Guadalupe, additional, Ghishan, Fayez K., additional, Gores, Gregory J., additional, Gruessner, Rainer W., additional, Gupta, Sanjeev, additional, Hammoud, Ghassan M., additional, Heathcote, E.J., additional, Helmke, Steve M., additional, Hirschfield, G.M., additional, Hunt, Douglas, additional, Iavarone, Massimo, additional, Ibdah, Jamal A., additional, Imbert-Bismut, Françoise, additional, Jansen, Peter L.M., additional, Johnson, Benjamin F., additional, F. Jonas, Maureen M., additional, Jones, Dean P., additional, Kamath, Patrick S., additional, Karlsen, Tom H., additional, Kelly, Deirdre, additional, Kettelle, J., additional, Khan, Khalid M., additional, Knolle, Percy, additional, Kramer, David J., additional, Kumar, Manoj, additional, Kumar, Navaneeth C., additional, Lai, Jennifer C., additional, Lapointe, Réal, additional, Lazaridis, Konstantinos N., additional, Lechel, André, additional, Lee, Samuel S., additional, Lencioni, Riccardo, additional, Levy, Cynthia, additional, Lindor, Keith D., additional, Locarnini, Stephen, additional, Lok, Anna S.F., additional, Malhi, Harmeet, additional, Manns, Michael P., additional, Marrero, Jorge A., additional, McClain, Craig, additional, McCuskey, Robert, additional, McGovern, Barbara H., additional, McHutchison, John G., additional, Moradpour, Darius, additional, Navarro, Victor J., additional, Neuberger, James, additional, Nevah R., Moises I., additional, Nevzorova, Yulia A., additional, Patton, Heather M., additional, Penin, François, additional, Perlmutter, David, additional, Plessier, Aurélie, additional, Poynard, Thierry, additional, Puri, Puneet, additional, Rice, Charles, additional, Rizzetto, Mario, additional, Roberts, Eve A., additional, Rockey, Don C., additional, Roy-Chowdhury, Jayanta, additional, Roy-Chowdhury, Namita, additional, Rudolph, K. Lenhard, additional, Russo, Mark W., additional, Saab, Sammy, additional, Sanyal, Arun J., additional, Sarin, S.K., additional, Schrumpf, Erik, additional, Seeff, Leonard B., additional, Seijo, S., additional, Shah, Vijay H., additional, Shedlofsky, Steven I., additional, Shouval, Daniel, additional, Sirlin, Claude B., additional, Smith, Maxwell L., additional, Smorodinsky, Emmanuil, additional, Spengler, Ulrich, additional, Sterling, Richard K., additional, Stewart, Stephen F., additional, Strader, Doris B., additional, Strassburg, Christian P., additional, Stravitz, R. Todd, additional, Sud, Priti, additional, Sulkowski, Mark S., additional, Talwalkar, Jayant A., additional, Terrault, Norah A., additional, Tillmann, Hans L., additional, Trautwein, Christian, additional, Vagefi, Parsia A., additional, Valla, Dominique, additional, Wagner, Siegfried, additional, Warner, Nadia, additional, Wong, Vincent Wai-Sun, additional, and Zayed, Naglaa, additional

Published
2012
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11. Coulomb excitation of neutron-rich beams at REX-ISOLDE

Author

Scheit, H., primary, Niedermaier, O., additional, Bildstein, V., additional, Boie, H., additional, Fitting, J., additional, von Hahn, R., additional, Köck, F., additional, Lauer, M., additional, Pal, U. K., additional, Podlech, H., additional, Repnow, R., additional, Schwalm, D., additional, Alvarez, C., additional, Ames, F., additional, Bollen, G., additional, Emhofer, S., additional, Habs, D., additional, Kester, O., additional, Lutter, R., additional, Rudolph, K., additional, Pasini, M., additional, Thirolf, P. G., additional, Wolf, B. H., additional, Eberth, J., additional, Gersch, G., additional, Hess, H., additional, Reiter, P., additional, Thelen, O., additional, Warr, N., additional, Weisshaar, D., additional, Aksouh, F., additional, Van den Bergh, P., additional, Van Duppen, P., additional, Huyse, M., additional, Ivanov, O., additional, Mayet, P., additional, Van de Walle, J., additional, Äystö, J., additional, Butler, P. A., additional, Cederkäll, J., additional, Delahaye, P., additional, Fynbo, H. O. U., additional, Fraile, L. M., additional, Forstner, O., additional, Franchoo, S., additional, Köster, U., additional, Nilsson, T., additional, Oinonen, M., additional, Sieber, T., additional, Wenander, F., additional, Pantea, M., additional, Richter, A., additional, Schrieder, G., additional, Simon, H., additional, Behrens, T., additional, Gernhäuser, R., additional, Kröll, T., additional, Krücken, R., additional, Münch, M., additional, Davinson, T., additional, Gerl, J., additional, Huber, G., additional, Hurst, A., additional, Iwanicki, J., additional, Jonson, B., additional, Lieb, P., additional, Liljeby, L., additional, Schempp, A., additional, Scherillo, A., additional, Schmidt, P., additional, and Walter, G., additional

Published
2005
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32. Cold fragmentation of 234U and 236U

Author

Quade, U., primary, Rudolph, K., additional, Armbruster, P., additional, Clerc, H. -G., additional, Lang, W., additional, Mutterer, M., additional, Pannicke, J., additional, Schmitt, C., additional, Theobald, J. P., additional, Gönnenwein, F., additional, and Schrader, H., additional

Published
1982
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37. Fusion and transfer around the Coulomb-barrier of the systems 33S + 90,91,92Zr

Author

Corradi, L., primary, Lenz, U., additional, Löbner, K. E. G., additional, Pascholati, P. R., additional, Quade, U., additional, Rudolph, K., additional, Schomburg, W., additional, Skorka, S. J., additional, Thies, H. G., additional, Montagnoli, G., additional, Napoli, D. R., additional, Pengo, R., additional, Scarlassara, F., additional, Stefanini, A. M., additional, Tivelli, A., additional, Beghini, S., additional, and Signorini, C., additional

Published
1988
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42. Werner Syndrome, Telomeres, and Stress Signaling: Implications for Future Therapies?

Author

Rudolph, K. Lenhard, Davis, Terence, and Kipling, David

Abstract

Werner syndrome (WS) is a premature ageing disorder used as a model of normal human ageing. WS individuals have several characteristics of normal ageing, such as cataracts, hair greying, and skin ageing, but manifest these at an early age. Additionally, WS individuals have high levels of infl ammatory diseases such as atherosclerosis and type II diabetes. The in vivo ageing in WS is associated with premature ageing of fi broblasts in culture, and it is thought that WS is a disease of accelerated cell ageing. Normal fi broblasts senesce as a result of telomere erosion and WRNp is known to play a role in telomere maintenance. However, telomeres in WS cells do not appear to show accelerated rates of erosion. Thus the cause of the accelerated senescence is not understood. Several features of WS cells suggest that they are growing under conditions of stress, and low oxygen conditions and antioxidant treatment revert some of the accelerated senescence phenotype. In addition, WS cells have significant levels of genomic instability. Oxidative stress and genomic instability result in the activation of stress kinases such as p38, and the p38-specifi c inhibitor SB203580 essentially prevents the accelerated senescence seen in WS fi broblasts. The recent development of p38 inhibitors with different binding properties, specifi cities, and oral bioavailability, and of new potent and selective inhibitors of other stress kinases such as JNK and MK2, will make it possible to dissect the roles of various kinase pathways in the accelerated senescence of WS cells. If this accelerated senescence is refl ective of WS ageing in vivo, these kinase inhibitors may well form the basis of anti-ageing therapeutics for individuals with WS. [ABSTRACT FROM AUTHOR]

Published
2008
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43. p16INK4a and Stem Cell Ageing: A Telomere-Independent Process?

Author

Rudolph, K. Lenhard and Sharpless, Norman E.

Abstract

Long-lived mammals replace lost or consumed cells at a tremendous pace: an adult human replaces <1% of their many trillion red blood cells every day through de novo synthesis. Similarly, cell division at various rates is at work throughout life to continuously replace lost cells in many epithelial tissues such as the gut, skin, breast, and lung. Moreover, several tissues (e.g., memory T-lymphocytes, pancreatic β-cells) possess a potential for "facultative growth" in the adult; that is, under certain circumstances (e.g., infection, pregnancy), these usually quiescent cells re-enter the cell cycle en masse to increase the mass of a given tissue through controlled proliferation. These forms of tissue replacement and repair require that many adult mammalian tissues contain reservoirs of stem cells capable of generating terminally differentiated effector cell types. The unique cellular property that enables stem cells to maintain such function throughout life is the ability to produce large numbers of differentiated cell types while also self-renewing themselves so that their reserves do not become depleted. In this chapter, I will review some of the evidence to support the notion that certain aspects of mammalian ageing result from an age-dependent decline in the function of self-renewing stem cells, and discuss the relationship of p16INK4a and telomeres with regard to stem cell ageing. [ABSTRACT FROM AUTHOR]

Published
2008
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44. Targeting Telomerase: Therapeutic Options for Cancer Treatment.

Author

Rudolph, K. Lenhard, Keith, W. Nicol, and Bilsland, Alan E.

Abstract

Telomerase is a suitable target for drug development because of its high prevalence, selective expression, and mechanistic importance in many cancer types. Telomerase targeting strategies can be defi ned as immunotherapy, gene therapy, and inhibition either by oligonucleotides or small molecules. However, few published approaches have entered clinical testing. There are advantages and limitations to each approach, and their different mechanisms of action must be taken into account in order to design appropriate preclinical models and identify appropriate endpoints for clinical trials. In this chapter we review the development pipelines for each class of telomerase-directed therapeutics, summarizing future challenges, opportunities, and development gaps. [ABSTRACT FROM AUTHOR]

Published
2008
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45. Telomere Binding Proteins and Disease.

Author

Rudolph, K. Lenhard and Blasco, Maria A.

Abstract

An increasingly growing number of human diseases including cancer and age-related diseases have been associated to telomeric dysfunction. The progressive telemore loss that occurs with aging in humans is proposed to contribute to the pathobiology of age-related diseases. Evidence for this comes from the study of mouse models that reproduce the corresponding full-blown human pathology only when in the setting of critically short telemores. Moreover, telomerase itself, as well as several telomere-binding proteins, has been found altered in human pathologies. Here, we will review recent findings suggesting that the length and function of telomeres are a biological determinant in the development of certain human diseases associated with aging, particularly from the perspective of mouse models for telomere dysfunction. [ABSTRACT FROM AUTHOR]

Published
2008
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46. Telomerase as a Potential Regulator of Tissue Progenitor Cells.

Author

Rudolph, K. Lenhard and Artandi, Steven E.

Abstract

Telomerase, the reverse transcriptase that synthesizes telomeres, comprises two minimal subunits, TERT, the protein subunit, and TERC, the RNA subunit that provides the template for telomere addition (Blackburn 2001, Smogorzewska and de Lange 2004). Telomerase is intimately associated with progenitor cell compartments in vivo and with cancers. This association between telomerase and actively proliferating normal and malignant cells is likely due in part to the need for telomere synthesis to offset the end replication problem. However, recent data implicate telomerase as contributing in a more direct fashion to the proliferation of tissue progenitor cells, and this action of telomerase in facilitating progenitor cell proliferation is independent of its function in adding telomere repeats. [ABSTRACT FROM AUTHOR]

Published
2008
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47. Telomere Shortening Induces Cell Intrinsic Checkpoints and Environmental Alterations Limiting Adult Stem Cell Function.

Author

Rudolph, K. Lenhard, Gutierrez, Luis Guachalla, and Ju, Zhenyu

Abstract

A decline in adult stem cell function is one of the features of ageing, which is associated with impaired tissue maintenance and reduced regenerative capacity. Telomere shortening occurs in the vast majority of human tissues during ageing and is also observed in ageing stem cell compartments. Studies of somatic cells have shown that telomere dysfunction induces DNA damage checkpoints, which lead to cell cycle arrest (senescence) or apoptosis. Whether similar checkpoint responses occur in stem cells in response to telomere shortening and whether this contributes to impaired organ maintenance during ageing remains to be investigated. In addition to the activation of cell intrinsic checkpoints, telomere shortening can also induce cell extrinsic, environmental alterations that limit stem cell function. Understanding of adult stem cell ageing and could ultimately lead to the identification of targets for therapies aiming to improve organ maintenance during ageing. In this chapter we summarize our current knowledge on checkpoint responses and environmental alteration induced by telomere dysfunction. [ABSTRACT FROM AUTHOR]

Published
2008
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48. Senescence Signatures of Human Hematopoietic Stem Cells.

Author

Rudolph, K. Lenhard, Zimmermann, Stefan, and Martens, Uwe M.

Abstract

Hematopoietic stem cells (HSCs) provide the basis for the enormous regenerative capacity of the hematopoietic system. Despite the need for a lifelong production of blood cells, replicative exhaustion seems to affect the HSC pool. Erosion of telomeres, protective structures at the ends of eukaryotic chromosomes, limits the replicative life span of most somatic cells. The expression of telomerase, the enzyme synthesizing telomeres de novo, is restricted to highly proliferative cells like germ line cells and tumor cells. Adult stem cells such as HSCs still exhibit telomerase activity to a certain level. Here, the telomerase activity does not prevent telomere shortening, suggesting a restriction of the proliferative capacity of HSCs. In this review, we discuss the relevance of telomere maintenance, potential functions of telomerase, and possible clinical applications of telomere manipulation in the hematopoietic stem cell compartment. Furthermore, we discuss new insights affecting the aging of the hematopoietic stem cell pool besides replicative exhaustion. [ABSTRACT FROM AUTHOR]

Published
2008
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49. Telomeres, Senescence, Oxidative Stress, and Heterogeneity.

Author

Rudolph, K. Lenhard, Passos, João F., Nelson, Glyn, and von Zglinicki, Thomas

Abstract

Life span heterogeneity is a hallmark of the ageing process. It is also a characteristic feature of telomere-dependent replicative senescence. We review here evidence showing that telomere shortening is heterogeneous between telomeres and between cells, and relate this to cell-to-cell variation in mitochondrial function and production of reactive oxygen species (ROS). Telomere shortening is to a large extent governed by ROS-mediated telomeric DNA damage, and we show here that apparently stochastic variation in mitochondrial ROS production can account for vast differences in replicative potential between individual cell lineages. [ABSTRACT FROM AUTHOR]

Published
2008
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50. Mechanisms of Stem Cell Ageing.

Author

Rudolph, K. Lenhard, Waterstrat, Amanda, Oakley, Erin, Miller, Alison, Swiderski, Carol, Liang, Ying, and Van Zant, Gary

Abstract

There are many definitions of the term "ageing" and perhaps even more theories that seek to explain its causes (Balcombe and Sinclair 2001). From a physiological standpoint, ageing beyond reproductive maturity is often viewed as a progression of multisystem deficits in tissue function. In adult mammals, tissue homeostasis is maintained by stem cell populations that reside in, or migrate between, a variety of adult tissues. These stem cells ensure proper tissue function by generating new cells to replace those lost or damaged over time. Despite the presence of adult stem cells in muscle, nervous, gastrointestinal, hematopoietic, and other tissues, each of these systems exhibit functional decline with age (Edwards et al. 2002, Campisi 2003, Kondo et al. 2003, Penninx et al. 2003, Pinto et al. 2003, Linton and Dorshkind 2004, Balducci and Ershler 2005, Fulle et al. 2005, Kamminga 2005, Bauer et al. 2006, Keller 2006, Theise 2006). It is compelling to consider that functional changes in the stem cell compartment of adult tissues precedes and perhaps contributes to the manifestation of ageing phenotypes. In this chapter we will review literature describing the effects of ageing on the well-characterized stem cells of the hematopoietic system. In this system, ageing is accompanied by immune compromise, anemia, and a dramatic increase in the incidence of malignancy (Edwards et al. 2002, Campisi 2003, Penninx et al. 2003, Pinto et al. 2003, Linton and Dorshkind 2004, Balducci and Ershler 2005). Several studies support the hypothesis that these ageing phenotypes stem from functional changes in hematopoietic stem cells (HSCs). [ABSTRACT FROM AUTHOR]

Published
2008
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