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1. Current-induced nanogap formation and graphitization in boron-doped diamond films

Author

Seshan, V., Arroyo, C. R., Castellanos-Gomez, A., Prins, F., Perrin, M. L., Janssens, S. D., Haenen, K., Nesládek, M., Sudhölter, E. J. R., de Smet, L. C. P. M., van der Zant, H. S. J., and Dulic, D.

Subjects
Condensed Matter - Mesoscale and Nanoscale Physics, Condensed Matter - Materials Science
Abstract

A high-current annealing technique is used to fabricate nanogaps and hybrid diamond/graphite structures in boron-doped nanocrystalline diamond films. Nanometer-sized gaps down to 1 nm are produced using a feedback-controlled current annealing procedure. The nanogaps are characterized using scanning electron microscopy and electronic transport measurements. The structural changes produced by the elevated temperature, achieved by Joule heating during current annealing, are characterized using Raman spectroscopy. The formation of hybridized diamond/graphite structure is observed at the point of maximum heat accumulation., Comment: 14 pages 4 figures + 1 supplemental figure

Published
2012
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3. Book reviews

Author

Meister, Richard, Wall, W. D., Bohnsack, Fritz, Nel, B. F., Meyer-Bothling, Helmut, Roucek, Joseph S., Prins, F. W., Möckelmann, Hans, and Dallmer, H. J.

Published
1961
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5. Primary cilia organization reflects polarity in the growth plate and implies loss of polarity and mosaicism in osteochondroma

Author

Andrea, C.E. de, Wiweger, M., Prins, F., Bovee, J.V.M.G., Romeo, S., and Hogendoorn, P.C.W.

Subjects
bone tumor cartilage cell polarity growth plate hereditary multiple exostoses osteochondroma smooth-muscle-cells endochondral ossification intraflagellar transport electron-microscopy mice lacking cartilage chondrocytes expression bone differentiation
Abstract

Primary cilia are specialized cell surface projections found on most cell types. Involved in several signaling pathways, primary cilia have been reported to modulate cell and tissue organization. Although they have been implicated in regulating cartilage and bone growth, little is known about the organization of primary cilia in the growth plate cartilage and osteochondroma. Osteochondromas are bone tumors formed along the growth plate, and they are caused by mutations in EXT1 or EXT2 genes. In this study, we show the organization of primary cilia within and between the zones of the growth plate and osteochondroma. Using confocal and electron microscopy, we found that in both tissues, primary cilia have a similar formation but a distinct organization. The shortest ciliary length is associated with the proliferative state of the cells, as confirmed by Ki-67 immunostaining. Primary cilia organization in the growth plate showed that non-polarized chondrocytes (resting zone) are becoming polarized (proliferating and hypertrophic zones), orienting the primary cilia parallel to the longitudinal axis of the bone. The alignment of primary cilia forms one virtual axis that crosses the center of the columns of chondrocytes reflecting the polarity axis of the growth plate. We also show that primary cilia in osteochondromas are found randomly located on the cell surface. Strikingly, the growth plate-like polarity was retained in sub-populations of osteochondroma cells that were organized into small columns. Based on this, we propose the existence of a mixture ('mosaic') of normal lining (EXT+/- or EXTwt/wt) and EXT-/- cells in the cartilaginous cap of osteochondromas. Laboratory Investigation (2010) 90, 1091-1101; doi:10.1038/labinvest.2010.81; published online 26 April 2010

Published
2010

8. Vanggewas aardappel in de praktijk 2006

Author

Hoek, J. and Prins, F.

Subjects
plant protection, ondergewassen, aardappelen, gewasbescherming, globodera pallida, cultural control, globodera rostochiensis, catch crops, ziektebestrijdende teeltmaatregelen, PPO Arable Farming, Multifunctional Agriculture and Field Production of Vegetables, ASG Facilities, Staff & Services, arable farming, nematodenbestrijding, nematode control, solanum tuberosum, nematoda, potatoes, akkerbouw, PPO Akkerbouw, Groene Ruimte en Vollegrondsgroente
Abstract

PPO en Agrifirm zijn via een enquête onder een aantal telers nagegaan hoe men de teelt heeft uitgevoerd en welke teeltproblemen zich hebben voorgedaan. Daarnaast hebben telers suggesties gedaan voor verbetering van de regelgeving

Published
2007

10. Invertebrate animals as a component of the traditional medicine trade in KwaZulu-Natal, South Africa

Author

Herbert, D.G., Hamer, M.L., Mander, M., Mkhize, N., and Prins, F.

Subjects
Biodiversity, Taxonomy
Abstract

Herbert, D.G., Hamer, M.L., Mander, M., Mkhize, N., Prins, F., . (2003): Invertebrate animals as a component of the traditional medicine trade in KwaZulu-Natal, South Africa. African Invertebrates 44 (2): 1-18, DOI: http://doi.org/10.5281/zenodo.7666422, {"references":["ALINO, P. M., CAJIPE, G. J. B., GANZON- FORTES, E. T., LICUANAN, W. R. Y., MONTANO, N. E. & TUPAS, L. M. 1990. The use of marine organisms in folk medicine and horticulture: a preliminary study. Philippines: Seaweed Information Centre, Leaflet 1.","ARNOLD, H-J. & GULUMIAN, M. 1984. Pharmacopoeia of traditional medicine in Venda. Journal of Ethnopharmacology 12: 35-74.","BERGLUND, A-I. 1976. Zulu thought-patterns and symbolism. Cape Town: David Philip, for Swedish Institute of Missionary Research, Uppsala.","BERLIN, B. 1973. Folk systematics in relation to biological classification and nomenclature. Annual Review of Ecology and Systematics. 4: 259-271.","BERLIN, B. 1992. Ethnobiological classification. Princeton: Princeton University Press.","BENTLEY,A. C. & COCKCROFT,A. C. 1995. Sand dollar (Echinodiscus bisperforatus) distribution and abundance in South Africa:Implications for conservation and legislation. South African Journal of Science 91: 38-40.","BOSSARD, E. 1996. La medecine traditionelle au centre et a l'ouest de l'Angola. Lisbon: Instituto de Investigacao Cientifica Tropical.","BRANCH, G. M., GRIFFITHS, C. L., BRANCH, M. L. & BECKLEY, L. E. 1994. Two Oceans. A guide to the marine life of southern Africa. Cape Town: David Philip.","BRYANT, A. T. 1966. Zulu medicine and medicine-men. Cape Town: Struik.","CHUNG, P-R., PARK, G-M., JUNG, Y., YONG, T-S., IM, K-I. & SOH, C-T. 2000. Medicinal molluscs in Korea. Korean Journal of Malacology 16 (1-2): 55-60.","CLARE, A. S. 1996. Marine natural product antifoulants: status and potential. Biofouling 9: 211-229.","CLARK, T., CROUCH, N. & NGWENYA, A. 1996. Ibhungezi - the Afro-Spanish fly. Africa Environment and Wildlife 4 (5): 8.","CUNNINGHAM,A.B. & ZONDI, A. S. 1991. Use of animal parts for the commercial trade in traditional medicines. Pietermaritzburg: Institute of Natural Resources. (working paper No. 76).","DAVIES- COLEMAN, M. 1996. Marine invertebrate bioprospecting in South Africa. SANCOR Newsletter 145: 4-5.","DERWENT, S. & MANDER, M. 1997. Twitchers bewitched: The use of birds in traditional healing. Africa: Birds & Birding 2 (1): 22-25.","FINGERMAN, M. & NAGABHUSHANAM, R. 2001. eds, Bio-organic compounds: chemistry and biomedical applications. Recent Advances in marine Biotechnology 6.","FOURIE, T. G., SWART, I. & SNYCKERS, F. O. 1992. Folk medicine: a viable starting point for pharmaceutical research. South African Journal of Science 88: 190-193.","HAMMOND- TOOKE, D. 1989. Rituals and medicines. Johannesburg: Ad. Donker.","HIGA, T., TANAKA, J., OHTANI, I. I., MUSMAN, M., ROY, M. C. & KURODA, I. 2001. Bioactive compounds from coral reef invertebrates. Pure and Applied Chemistry 73 (3): 589-593.","ICZN 1999. International Code of Zoological Nomenclature. Fourth ed'n London: International Trust for Zoological Nomenclature.","IRELAND, C. M., ROLL, D. M., MOLINSKI, T. F., MCKEE, T.C., ZABRISKIE, T.M. & SWERSEY, J. J. 1988. Uniqueness of the marine chemical environment: categories of marine natural products from invertebrates. In: Fautin. D. G. ed., Biomedical importance of marine organisms. San Francisco: California Academy of Sciences, pp. 41-52.","JUNOD, H. A. 1927. The life of a South African tribe. Vol. II. Mental Life. London: Macmillan (reprinted 1962. New York: University Books).","KALK, M. 1995. Sea meadows and sand banks on the subtidal fringe. In: Kalk, M. ed., A natural history of Inhaca Island Mozambique. Johannesburg: Witwatersrand University Press, pp. 247-275.","KYLE, R., PEARSON, B., FIELDING, P. J., ROBERTSON, W. D. & BIRNIE, S. L. 1997.Subsistence shellfish harvesting in the Maputaland marine reserve in northern KwaZulu-Natal, South Africa: rocky shore organisms. Biological Conservation 82: 183-192.","MACDONALD, I. A. W. 1984. Witchdoctors versus wildlife in South Africa. African Wildlife 38 (1): 2-9.","MANDER, M. 1998. Marketing of indigenous medicinal plants in South Africa. Rome: FAO.","MAYER, A. M. S. 1999. Marine pharmacology in 1998: antitumor and cytotoxic compounds. The Pharmacologist 41 (4): 159-164.","MCKEAN, S. G. 1995. A directory of animal species used for traditional medicine in KwaZulu-Natal. Pietermaritzburg: Natal Parks Board internal report.","NGUBANE, H. 1977. Body and mind in Zulu medicine. London: Academic Press.","OLIVERA, B. M. & CRUZ, L. J. 2001. Conotoxins in retrospect. Toxicon 39 (1): 7-14.","PEMBERTON, R. W. 1999. Insects and other arthropods used as drugs in Korean traditional medicine. Journal of Ethnopharmacology 65: 207-216.","PLUG, I. 1987. An analysis of witchdoctor diving sets. Research Natco Museum 1 (3): 48-67.","SCHEUER, P. J. 1988. Ethno-natural historical leads. In: Fautin, D. G. ed. Biomedical importance of marine organisms. San Francisco: California Academy of Sciences, pp. 37-40.","SIMELANE, T. S. 1996.The traditional use of indigenous vertebrates. MSc thesis, University of Port Elizabeth.","SIMELANE, T. S. & KERLEY, G. I. H. 1998. Conservation implications of the use of vertebrates by Xhosa traditional healers in South Africa. South African Journal of Wildlife Research 28 (4): 121-126.","TANG, W. 1987. Chinese medicinal materials from the sea. Abstracts of Chinese Medicines 1 (4): 571-600.","WYNBERG, R. & LAIRD, S. 1997. The scramble for genes. Biodiversity prospecting in South Africa. Africa: Environment & Wildlife 5 (3): 53-59."]}

Published
2003
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11. Qualitative alterations in laminin expression in experimental lupus nephritis

Author

Kootstra, C. J., Bergijk, E. C., Veninga, A., Prins, F. A., de Heer, E., Abrahamson, D. R., and Bruijn, J. A.

Subjects
Kidney Glomerulus, Antibodies, Monoclonal, Graft vs Host Disease, Immunohistochemistry, Lupus Nephritis, Peptide Fragments, Mice, Inbred C57BL, Epitopes, Mice, Mice, Inbred DBA, Animals, Female, Tissue Distribution, Laminin, Microscopy, Immunoelectron, Research Article
Abstract

Previous studies have revealed quantitative alterations in laminin-1 expression at the mRNA and protein levels during the development of glomerulonephritis and glomerulosclerosis in chronic graft-versus-host disease in mice, a model for lupus nephritis. We have now studied the qualitative alterations in laminin expression with two monoclonal antibodies that recognize epitopes on either the E8 or the P1 fragment of laminin-1. Both of these fragments are involved in cell-matrix and matrix-matrix interactions. In normal glomeruli these laminin epitopes are present only in the mesangial matrix; during embryogenesis, however, they are also present in the glomerular basement membrane. The distribution of laminin epitopes was first studied by using immunofluorescence in kidneys of mice with graft-versus-host disease at different points in time after disease induction. Reflection contrast and immunoelectron microscopy were performed after in vivo injection of the horseradish peroxidase-coupled monoclonal antibodies. In glomeruli of mice 8 weeks after disease induction, both injected antibodies bound specifically in electron-dense immune deposits in the mesangium and subepithelially along the glomerular basement membrane as well as in the expanded mesangial matrix. At 11 and 12 weeks after disease induction, when focal and segmental glomerulosclerosis had developed, the antibodies additionally bound in the matrix subendothelially along the glomerular basement membrane and at the periphery of end-stage sclerotic lesions. To study changes in the distribution of laminin epitopes over time, mice were injected with either monoclonal antibody before induction of graft-versus-host disease. The antibodies were detected 8 and 12 weeks later in the mesangial matrix of mice with lupus nephritis. Once segmental glomerulosclerosis had developed, the antibodies were additionally detected within the thickened glomerular capillary wall. The specific binding of anti-laminin monoclonal antibodies in electron-dense immune deposits further substantiates the hypothesis that anti-laminin autoantibodies participate in glomerular immune complex formation in this model, as suggested by earlier studies. Furthermore, our results show that the distribution of glomerular laminin epitopes in the matrix is altered during the development of glomerular disease. These changes in the structure of the glomerular basement membrane may contribute to the abnormal cell-matrix and matrix-matrix interactions during the development of glomerular disease in this model for lupus nephritis.

Published
1995

13. Conference Reports

Author

Nicolich, Rinaldo, primary, Yoshida, Masaru, additional, Kehelpannala, K. V. Wilbert, additional, Davies, T. C., additional, Prins, F. Winkler, additional, Danelian, Taniel, additional, BAUDIN, François, additional, and Weissert, Helmut, additional

Published
2003
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19. Kupffer cell depletion in vivo results in clearance of large-sized IgA aggregates in rats by liver endothelial cells.

Author

Bogers, W. M. J. M., Stad, R. K., Janssen, D. J., Prins, F. A., van Rooijen, N., van Es, L. A., and Daha, M. R.

Subjects
KUPFFER cells, IMMUNOGLOBULIN A, DIPHOSPHONATES, MACROPHAGES, PHOSPHONATES, LABORATORY rats
Abstract

We investigated the clearance kinetics and tissue distribution of different sized IgA in normal and macrophage-depleted rats. Rats were injected iv with liposomes containing dichloromethylcne diphosphonate (DMDP). DMDP treatment resulted in complete depletion of liver macrophages 24-48 h after administration. Normal and macrophage depleted rats were injected intravenously with monomeric, dimetic, polymeric or aggregated polymeric IgA (AIgA) and assessed for blood clearance and tissue distribution. In normal rats, clearance of IgA was size dependent, i.e. a faster clearance with increasing size. No differences in clearance kinetics were observed of the different sized IgA between normal and DMDP-treated rats. TCA non-precipitable radioactivity, a measure for degradation of IgA. was found in the circulation of normal and DMDP-treated rats after AIgA administration. The liver was the main organ responsible for the clearance of IgA in normal and DMDP-treated rats. Immunofluorescenee studies on liver biopsies indicated that AIgA was associated with Kupffer cells in normal rats. Electronmicroscopical studies revealed that the AIgA was internalized and located in vesicles in Kupffer cells. In DMDP-treated rats the AIgA was associated with endothelial cells and electron microscopy studies showed that this AIgA was taken up by endothelial cells. These data show that rat liver endothelial cells are able to bind, internalize and degrade AIgA in situations where Kupffer cells are absent, and that these cells may play an important role in the handling of AIgA and IgA-immune complexes. [ABSTRACT FROM AUTHOR]

Published
1991

20. Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

Author

PRINS, F. A. DE, HILL, D. J., FEKETE, M., ROBSEN, D. J., FIELLER, N. R. J., ASSCHE, F. A. VAN, and MILNER, R. D. G.

Abstract

In this study, the experimental model of Wigglesworth was used to limit the maternal blood supply to the rat fetus and induce intrauterine growth retardation. The associated changes in plasma somatomedin activity, insulin, glucose, and cartilage metabolic activity are reported. The mean body weight ( ± SEM) of 108 fetuses in ligated uterine horns was significantly lower than that of 146 control fetuses (ligated, 2820 ± 50 mg; control, 3180 ± 50 mg; p< 0.001), as was mean nose-tail tip length (ligated, 55.6 ± 0.4 mm; control, 59.4 ± 0.3 mm; p< 0.001) and mean liver weight (ligated, 222 ± 5 mg; control, 274 ± 5 mg; p< 0.001). The uptake of [35S]sulfate by fetal costal cartilage in basal culture medium was significantly lower in growth-retarded fetuses than in controls. Plasma somatomedin activity measured by fetal rat cartilage bioas-say was significantly lower in growth-retarded than in control fetuses (p< 0.001). The growth-retarded fetuses were relatively hypoinsulinemic and hypoglycemic compared to control animals. These studies suggest that nutrient supply may become a limiting factor in the release of insulin and the circulating levels of somatomedin activity in the rat fetus, and hence in its growth.

Published
1984

21. Reduced Plasma Somatomedin Activity and Costal Cartilage Sulfate Incorporation Activity during Experimental Growth Retardation in the Fetal Rat

Author

De Prins, F A, Hill, D J, Fekete, M, Robsen, D J, Fieller, N R J, Van Assche, F A, and Milner, R D G

Abstract

ABSTRACT. In this study, the experimental model of Wigglesworth was used to limit the maternal blood supply to the rat fetus and induce intrauterine growth retardation. The associated changes in plasma somatomedin activity, insulin, glucose, and cartilage metabolic activity are reported. The mean body weight ( ± SEM) of 108 fetuses in ligated uterine horns was significantly lower than that of 146 control fetuses (ligated, 2820 ± 50 mg; control, 3180 ± 50 mg; p < 0.001), as was mean nose-tail tip length (ligated, 55.6 ± 0.4 mm; control, 59.4 ± 0.3 mm; p < 0.001) and mean liver weight (ligated, 222 ± 5 mg; control, 274 ± 5 mg; p < 0.001). The uptake of [35S]sulfate by fetal costal cartilage in basal culture medium was significantly lower in growth-retarded fetuses than in controls. Plasma somatomedin activity measured by fetal rat cartilage bioas-say was significantly lower in growth-retarded than in control fetuses (p < 0.001). The growth-retarded fetuses were relatively hypoinsulinemic and hypoglycemic compared to control animals. These studies suggest that nutrient supply may become a limiting factor in the release of insulin and the circulating levels of somatomedin activity in the rat fetus, and hence in its growth.

Published
1984
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23. A histologic study of the extracellular matrix during the development of glomerulosclerosis in murine chronic graft-versus-host disease

Author

Ec, Bergijk, Munaut C, Hans baelde, Prins F, Jm, Foidart, Pj, Hoedemaeker, and Ja, Bruijn

Subjects
Glomerulosclerosis, Focal Segmental, Kidney Glomerulus, Graft vs Host Disease, Capillaries, Extracellular Matrix, Mice, Inbred C57BL, Mice, Microscopy, Electron, Mice, Inbred DBA, Immunoglobulin G, Chronic Disease, Animals, Collagen, Laminin, Microscopy, Immunoelectron, Research Article
Abstract

The development of glomerulosclerosis was studied in murine chronic graft-versus-host disease (GvHD), which is a model for human systemic lupus erythematosus. The authors investigated the distribution patterns of six components of the extracellular matrix (ECM), i.e., laminin, fibronectin, collagen types I, III, IV, and VI during the course of the disease. All of these ECM components except collagen type I were found in the glomeruli of normal mice, where all of them were intrinsic constituents of the mesangium. Laminin, fibronectin, and collagen type IV were also found in the glomerular capillary walls. Starting 6 weeks after the induction of GvHD and continuing at week 8, the onset of an expansion of the mesangial matrix was observed. At the same time, the amounts of laminin, fibronectin, and collagen types IV and VI increased. Ten weeks after the onset of the disease, glomerulosclerosis developed. Traces of the interstitial collagen type I were found in sclerotic glomeruli. The levels of four ECM components, i.e., collagens III, IV, VI, and laminin were markedly decreased in the sclerotic glomeruli as compared with week 8. In contrast, the amount of fibronectin in the sclerotic glomeruli increased dramatically. Immunoelectron microscopic examination showed fibronectin in the sclerotic lesions, in contrast to laminin, collagen type I, and collagen type IV. It is concluded that the sclerotic lesions in murine chronic GvHD contain fibronectin. The small amounts of the ECM components laminin, as well as collagens III, IV, and VI in the sclerotic glomeruli in GvHD, might represent remnants of mesangial material and collapsed capillary walls. These components are probably replaced by increased production and/or accumulation of collagen type I and fibronectin.

25. Ticagrelor in patients with diabetes and stable coronary artery disease with a history of previous percutaneous coronary intervention (THEMIS-PCI): a phase 3, placebo-controlled, randomised trial

Author

Deepak L Bhatt, Philippe Gabriel Steg, Shamir R Mehta, Lawrence A Leiter, Tabassome Simon, Kim Fox, Claes Held, Marielle Andersson, Anders Himmelmann, Wilhelm Ridderstråle, Jersey Chen, Yang Song, Rafael Diaz, Shinya Goto, Stefan K James, Kausik K Ray, Alexander N Parkhomenko, Mikhail N Kosiborod, Darren K McGuire, Robert A Harrington, Vladimir Santos, Ashit Jain, Irina Lendel, Michael Russo, W H Haught, Manuel Bouza, Harinder Gogia, Supratim Banerjee, George Kichura, Louis Kantaros, Francisco Padron, Rakesh Passi, Jay Stone, Michael Pursley, Michael D'Urso, Timothy Gardner, James Bennett, Khaled Nour, Satinder Saini, Wenwu Zhang, Dharam Kumbhani, Dustin Thomas, Dominick Angiolillo, Barry Bertolet, Amaury Roman-Miranda, Robert Black, Ramin Manshadi, Carlos Vaca, Antonio Blanco, Mark Napoli, David Brabham, Ayim Akyea-Djamson, Pratik Desai, Sudhir Prasada, Ajit Khaira, Leslie Forgosh, Ira Lieber, Guillermo Umpierrez, Dinesh Singal, Juan Londono, Neil Fraser, Jose Ruiz, Damaris Vega, Lilia Rodriguez, Christopher Brown, Faizullah Syed, Guarav Aggarwala, William Eaves, Michael Foster, Dinesh Gupta, David Avino, Wail Asfour, Glen Tonnessen, Xue-Qiao Zhao, Narendra Singh, Andrew Brockmyre, Norman Lepor, Nicolas Shammas, David Blick, Steven Hearne, John Prodafikas, Edgar Carell, Mark Izzo, Amin Karim, Bosh Zakhary, Mahmoud Atieh, Steven Leichter, Charles Meadows, David Hotchkiss, Mazen Abu-Fadel, Alan Wiseman, Jeffrey Bander, Mahesh Shah, Subhash Banerjee, Ricky Ganim, Karen Sopko, Misal Khan, Ramon Lloret, Troy Weirick, Rajendra Mehta, Udho Thadani, Anuj Bhargava, Mikhail Kosiborod, Jaynier Moya, Cezar Staniloae, Yamirka D Guerra, Anil Chhabra, Douglas Kosmicki, Wassim Shaheen, Akber Mohammed, J'Cinda Bitters, Jan Pattanayak, Julian Javier, Sunny Srivastava, Roland Phillips, Jessie Al-Amin, Michael Lillestol, Patrick Simpson, Lydie Hazan, Amit Amin, Gopi Shah, Denes Korpas, Bruce Platt, Jim Dickert, Orlando Puente, Louis Hiotis, Timothy Doyle, Raj Rajan, Alan Meholick, Christian Gring, Elie Hage-Korban, Robert Feldman, Harry Colfer, Samuel Butman, Malcolm Foster, Terence Hart, Randall Huling, Shervin Eshaghian, Ofsman Quintana, Deanna Cheung, Franklin Handel, Mara Rodriguez, David Suh, Paul Gordon, Gregg Pressman, Michael Bauer, William French, Mark Barettella, Sridhar Chatrathi, Damodhar Suresh, Ronald Goldberg, Mark Huth, Liwa Younis, Aref Rahman, Richard Mascolo, Michelle Welch, Randeep Suneja, Stephen Smith, Scott Shurmur, John Agaiby, Ahmad Jingo, Janice Johnston, Mary Beth, Anthony Vlastaris, Susan Kemp, Hamid Taheri, Edward Pereira, Michael Deyoung, Zafir Hawa, Ray Smith, Thomas Galski, Samer Garas, M Reddy, Susheel Sharma, Joeseph Hargrove, Charles Treasure, Ronald Emerson, Tariq Haddad, Kathryn Rohr, Larry Levinson, Raul Gaona, Barry Uretsky, Hiralal Maheshwari, Denny Lee, Stephanie Kinnaman, Robert Singal, Jeffrey Geohas, Osvaldo Gigliotti, Ajit Raisinghani, Charanjit Khurana, Brent Hella, Michael Kelberman, Steven Voyce, Sanjay Singh, Eric Lo, Pradeep Singh, Ross Goodfellow, Stuart Fischer, Richard Lorraine, Traci Turner, Jeffrey Shanes, Robert Busch, Robert Broker, Michelle Zaniewski, Kevin Pounds, Giselle Debs-Perez, Stephen Ong, Brad Frandsen, Douglas Fullington, Naseem Jaffrani, Ahtaram Khan, Marcus Lee, Joe Pouzar, George Revtyak, Julian Gonzalez, Samer Nakhle, Abel Murillo, Douglas Young, Sashi Makam, Mushtaq Syed, Kevin Woolf, Paul Grena, Sarab Alfata, Sharan Mahal, David Hoffman, Tinoy Kizhakekuttu, Joseph Deering, Janak Bhavsar, Scott Mikesell, William Wilson, Vance Wilson, Salah El, Francis Spinale, Vinod Kannarkat, Sunder Rao, Lenita Hanson, John Bertsch, Elena Gonzalez-Ortiz, Norma Severino, John Willis, Joel Schock, Ladan Bakhtari, Raul Gazmuri, Saadat Ansari, Jason Hall, Arvind Mehta, Neal Shealy, Stuart Zarich, Deovrat Singh, Kishor Vora, Nabil Andrawis, Darron Molter, David Maron, Jose Cardona, Ronald D'Agostino, Tamjeed Arshad, Rodney Samaan, David Jones, Dale Presser, John Heath, Sandy Green, George Bittar, Sheldon Henry, David Korn, John Schmedtje, Venkatesh Nadar, Bruce Graham, Ajay Labroo, Leonardo Clavijo, Hal Roseman, Gilbert Ledesma, Robert Rosen, Isaac Dor, William Kirby, Jennefer Sutton, Frank Eder, Bruce Iteld, Jose Gomez-Cortes, Maurice Buchbinder, Joseph Kasper, Antonio Terrelonge, Gustavo Torres, Ted Jagielo, Jose Alvarez, Yehuda Handelsman, Mario Guillen, Randall Richwine, Lorena Lewy-Alterbaum, Clinton Corder, Moogali Arvind, David Bolshoun, Magdy Mikhail, Stephen Minton, Odilon Alvarado, J Abbott, Brett Cauthen, Ryan Welter, Randy Mintz, John Cox, Annette Quick, Melvin Weiss, Johnny Dy, James Zebrack, Glenn Gandelman, Vinayak Hegde, Marc Silver, Michele DeGregorio, William Lawson, Christopher Paa, Anna Bortnick, Merrill Krolick, Rodolfo Sotolongo, Jorge Cheirif, Priya Kumar, Preetham Jetty, Ambar Patel, Mariusz Kruk, Iwona Kobielusz-Gembala, Barbara Rewerska, Adam Madrzejewski, Krzysztof Milewski, Jerzy Cygler, Joanna Petryka-Mazurkiewicz, Waldemar Jastrzebski, Janusz Korecki, Wojciech Fil, Janusz Prokopczuk, Anna Bochenek, Marek Wujkowski, Robert Witek, Piotr Konczakowski, Pawel Miekus, Marcin Szczasny, Wlodzimierz Musial, Krzysztof Cymerman, Jacek Lampart, Jacek Mikosinski, Slawomir Szynal, Issa Fares, Grzegorz Opolski, Stanislaw Mazur, Beata Wozakowska-Kaplon, Renata Bijata-Bronisz, Lukasz Wierucki, Beata Losa, Grzegorz Drelich, Marek Konieczny, Pawel Starczewski, Lidia Pawlowicz, Pawel Jesionowski, Jaroslaw Jurowiecki, Jacek Gniot, Mariusz Czyzycki, Karol Stania, Izabela Kucharczyk-Bauman, Benita Busz-Papiez, Agnieszka Karczmarczyk, Wanda Sudnik, Alina Koszek, Piotr Kolodziej, Bartosz Skwarna, Nicolás Jaramillo, Maciej Jankowski, Wojciech Czochra, Leszek Kinasz, Beata Miklaszewicz, Teresa Stasinska, Wladyslaw Pluta, Marcin Basiak, Teresa Rusicka, Izabela Niedbal-Yahfouf, Grazyna Popenda, Romuald Korzeniak, Agnieszka Mirek, Rafal Mariankowski, Lukasz Wojnowski, Marek Korol, Jacek Baszak, Piotr Podolec, Wojciech Piesiewicz, Aleksander Zurakowski, Carlos Luengas, Marek Skura, Piotr Pilecki, Piotr Majchrzak, Ewa Krzyzagórska, Marcin Drozd, Barbara Kaczmarek, Teresa Sliwinska, Katarzyna Zelazowska, Rafal Sztembis, Katarzyna Landa, Lidia Matyszczak-Toniak, Krzysztof Strojek, Marek Piepiorka, Robert Malinowski, Maria Górska, Edyta Stolarczyk-Sowa, Leszek Romanowski, Elzbieta Zinka, Zygfryd Reszka, Joanna Skierkowska, Anna Uzunow, Ewa Laskowska-Derlaga, Ekaterina Puntus, Elena D Kosmacheva, Natalia Koziolova, Prokhor Pavlov, Tatiana Supryadkina, Yury Didenko, Philipp Kopylov, Andrei Kazakov, Sergei Aksentiev, Elena Vishneva, Alexey Repin, Olga Smolenskaya, Olga Mantserova, Oleg Khrustalev, Elena Privalova, Vladimir Konstantinov, Svetlana Boldueva, Andrey Ezhov, Alexander Chernyavsky, Gadel Kamalov, Albert Galyavich, Galina Zubeeva, Galina Nechaeva, Sergey Shustov, Nino Dzhaiani, Tatiana Treshkur, Nataliya Osokina, Alexey Panov, Elena Shutemova, Valeriy Makukhin, Tatiana Kropotina, Larisa Tsyba, Yuri Karpov, J M Sizova, Marina Ballyuzek, Nikolay Tarasov, Elena Demchenko, Olga Barbarash, Valentin Moiseev, Valentin Markov, Vadim Kuznetsov, Inna Viktorova, Igor Sergienko, Lyudmila Ermoshkina, Niyaz Khasanov, Tatiana Khlevchuk, Andrey Baglikov, Sergey Shalaev, Elena Zonova, Elena Reznik, Larisa Haisheva, Tatyana Morugova, Nikita Lomakin, Alexander Vishnevsky, Yuri Shvarts, Olga Magnitskaya, Marina Mikhailusova, Elena Pavlysh, Igor Libov, Anna Zateyschikova, Victor Kostenko, Anton Edin, Yaroslava Khovaeva, Konstantin Zakharov, Raisa Stryuk, Vladimir Khirmanov, Sergey Kanorskiy, Sergey Yakushin, Anna Barabashkina, Hongwei Li, Qiang Zhao, Jian Zhang, Jianhua Ma, Yong He, Ming Luo, Aidong Zhang, Ningru Zhang, Yingru Chai, Genshan Ma, Hao Wang, Zhigang Liu, Lanjie He, Zhifang Song, Xiaolin Dong, Liang Tao, Zhanquan Li, Xi Su, Xiangqing Kong, Heping Niu, Junbo Ge, Zhurong Luo, Wenjun Huang, Daoquan Peng, Zuyi Yuan, Maria Milanova, Doncho Tenev, Antoni Gogov, Dimitar Karageorgiev, Todor Kolchev, Nikolay Rusev, Nikolina Georgieva, Rumen Kondov, Veselin Rusinov, Ivo Petrov, Georgi Stanchev, Mariana Konteva, Adriana Dincheva, Zdravka Yaneva, Ralitsa Vatova, Katya Ilieva, Nikolai Runev, Borislav Kolomanov, Ivan Petrov, Nikolay Iliev, Snezhanka Tisheva, Boryana Chompalova, Maria Tokmakova, Dimitar Raev, Kolyo Byanov, Dimitar Markov, Lenko Mihov, Atanas Mihov, Nora Milcheva, Milen Minchev, Mihail Mollov, Borislav Borisov, Tihomir Tihchev, Venelin Karakolev, Bojidar Dimov, Svetoslav Georgiev, Lachezar Smilov, Bon K Koo, Taehoon Ahn, Soon J Hong, Junghan Yoon, Seok K Oh, Myung H Jeong, Doo-Il Kim, Kiyuk Chang, Weon Kim, Joo-Yong Hahn, Kwang S Cha, Jung-Hee Lee, Si-Wan Choi, Chang-Wook Nam, In-Ho Chae, Yong H Park, Seung-Jea Tahk, Won-Yong Shin, Jei-Keon Chae, Byung J Kim, Jang-Whan Bae, Woo J Park, Seung W Rha, Young J Choi, Jin-Yong Hwang, Hun S Park, Luciano Baracioli, Fabio Guimaraes, Eduardo Vasconcellos, José Saraiva, Adamastor Pereira, Queulla Santos, Paulo Rossi, Lilia Maia, Miguel Madeira, Marcio Pereira, Roberto Botelho, Gilmar Reis, Freddy Eliaschewitz, Joao Borges, Carlos Nascimento, Jose A Fortes, Weimar de Souza, Pedro Pimentel, Miguel Hissa, Marcos Franchetti, Dalton Precoma, Costantino Ortiz, Mauro Hernandes, Wladmir Saporito, Fabio R dos Santos, Adrian Kormann, Fernando Neuenschwander, Oscar Dutra, Nelson Rassi, Luiz Tanajura, Juliana Souza, Delcio S Junior, Paulo Leaes, Adriana Forte, Teresa C Bonansea, Jose Marin, Bruno Machado, Maria J Cerqueira, Frederico Silva, Yorghos Michalaros, Euler Manenti, Cintia Cercato, Estevao Figueiredo, Ming-En Liu, Yi-Chih Wang, Tsung-Ming Lee, Chih Fang, Yen-Wen Wu, Kwo-Chang Ueng, Huey-Herng Sheu, Wen T Lai, I-Chang Hsieh, Zhih-Cherng Chen, Mu-Jang Lee, Chern Chiang, Kou-Gi Shyu, Chien-Hsun Hsia, Guang-Yuan Mar, Shih-Hung Chan, Chih-Cheng Wu, Wei-Kung Tseng, Kuan-Cheng Chang, Hung-I Yeh, Ji-Hung Wang, Charles Hou, Inna Sorokina, Maryna Dolzhenko, Olha Horoshko, Oleksandr Karpenko, Leonid Rudenko, Igor Vakaliuk, Anna Kulyk, Olena Levchenko, Oleksandr Prokhorov, Dmytro Reshotko, Mykhaylo Sorokivskyy, Nataliia Velichko, Valentyn Maslovskyi, Zinaida Teliatnikova, Sergiy Dotsenko, Olena Krakhmalova, Igor Kraiz, Viktoria Zharinova, Larysa Bula, Igor Kaydashev, Valeriy Molodtsov, Lesya Rasputina, Viktoriya Pidlisna, Olena Lysunets, Anatoliy Kravchenko, Liubomyr Glushko, Tetyana Khomazyuk, Yevgeniya Svyshchenko, Oleksandr Parkhomenko, Boris Mankovsky, Orest Abrahamovych, Andriy Yagensky, Mykola Stanislavchuk, Larisa Vasilyeva, Liubov Sokolova, Oleg Sychov, Vira Tseluyko, Igor Kyrychenko, Mykola Rishko, Sergiy Furkalo, Richard Gallo, Olivier Bertrand, Shamir Mehta, Christian Constance, Bruce Sussex, Remo Zadra, Simon Kouz, Raja Chehayeb, Amritanshu Pandey, Danielle Dion, Gordon Bailey, Laurie Hill, Krishnan Ramanathan, Micha Dorsch, Alykhan Nanji, Mohan Babapulle, Martine Montigny, Gilbert Gosselin, Payam Dehghani, Dennis Rupka, Michel Le May, Francis Pichette, Francois St-Maurice, Patrick Teefy, Samer Mansour, Saleem Kassam, Stephen Cheung, Anthony D Siega, Dennis O'Keefe, Eric Sabbah, Alan Bell, Guy Chouinard, Brian Wong, Mark Miller, Daniel Gaudet, Pierre Lachance, Iqbal Bata, Robert Petrella, Denis Gossard, Richard Dumas, Douglas Ing, Hagop Boyrazian, Ricardo Bessoudo, Thao T Huynh, Randy Hart, Jasmin Belle-Isle, Dinkar Shukla, Allan Kelly, Giuseppe Mazza, James Cha, Sam Henein, Andre Frechette, Saul Vizel, Joanne F Liutkus, Michael O'Mahony, Frank Halperin, Jacobus Kooy, John Graham, Allan Bailey, Ronald Wojcik, Igor Wilderman, Tibor Turi, Ákos Motyovszki, Béla Merkely, Csaba Király, Péter Andrássy, Zsolt Sárszegi, Tibor Fülöp, Zsolt Zilahi, István Édes, Andras Papp, Gábor Müller, Anna Czigány, Szilárd Zólyomi, László Korányi, János Takács, Ferenc Juhász, Bela Benczur, Sándor Kancz, András Földi, András C Nagy, Judit Bakai, István Greschik, László Püski, László Nagy, Róbert Kirschner, Roman Kuchar, Petr Hajek, Ladislav Busak, Daniel Michalik, Ivo Matyasek, Ivana Marusincova, Dusan Kucera, Ondrej Jerabek, Michaela Honkova, Vratislav Dedek, Ivan Rihacek, Pavel Kos, Josef Slaby, Martina Machkova, Eva Zidkova, Lubomir Elbl, Hana Grunfeldova, Jiri Carda, Vladimir Mrozek, Jiri Maly, Richard Milkovic, Jan Malecha, Hana Skalicka, Ivo Oral, Eva Krcova, Libor Lisa, Jan Belohlavek, Roman Miklik, Ondrej Cermak, Jana Bednarova, Zdenek Peroutka, Jindrich Spinar, Andreas Wilke, Karl-Friedrich Appel, Jens Taggeselle, Andreas Förster, Nicole Toursarkissian, Ekkehard Schmidt, Jochen Bott, Ayham Al-Zoebi, Dirk Hennig, Sabine Fischer, Norbert Schön, Joachim Sauter, Gregor Simonis, Ruth Nischik, Werner Rieker, Isabelle Schenkenberger, Thomas Behnke, Gerhard Klausmann, Michael Jeserich, Dietmar Trenk, Ingo Weigmann, Hannes Reuter, Reinhard Rummel, Candy von Münchhausen, Charlotte von Engelhardt, Eishun Horibe, Taro Shibasaki, Tomohiko Sato, Tsunekazu Kakuta, Ichiro Michishita, Michinao Tan, Ryoji Ishiki, Takahiko Aoyama, Shinichi Higashiue, Yawara Niijima, Akira Idogaki, Toru Hasegawa, Arihiro Kiyosue, Yoshiaki Tomobuchi, Katsunori Kawamitsu, Satsuki Kawasaki, Yoshiki Hata, Kazuki Fukui, Kozaburo Seki, Takashi Takenaka, Mitsuru Abe, Noriaki Utsu, Atsuyuki Oono, Kazuhisa Mitsuo, Atsushi Sueyoshi, Atsushi Hirohata, Mitsuru Tsujimoto, Osamu Ueda, Shinichi Takase, Masahiro Suzuki, Satoru Sakuragi, Fumi Yamamoto, Noritaka Fujimoto, Shigeo Kakinoki, Tatsushi Sugiura, Hiroshi Sugino, Toshihiro Nakamura, Toshiaki Kadokami, Hiroki Uehara, Masahiro Ono, Koichi Yokoya, Akihiro Koike, Sei Komatsu, Masahiro Sonoda, Hideki Ueno, Tomofumi Doi, Yuichiro Takagi, Kazuteru Fujimoto, Yutaka Eki, Munenori Okubo, Kenichiro Sasaki, Martijn van Eck, Eelko Ronner, Salem The, Ruud van de Wal, Pieter Nierop, Cornelis de Nooijer, Henri Werner, Iris Westendorp, Coen van der Zwaan, Hendrikus Crijns, Jan H Cornel, Sipke Strikwerda, Robert Bos, Edwin de Melker, Adrianus Kuijper, Hans Louwerenburg, Jacobus Plomp, Jan-Melle Dantzig, Francisco Prins, Henricus van Kesteren, Frank Willems, Giovanni Amoroso, Gabriela Carnero, Ernesto Duronto, Diego Besada, Carolina Chacon, Pedro Zangroniz, Silvana Solis, Alberto Liberman, Virginia Sernia, Andres Alvarisqueta, Laura Maffei, Oscar G Vilamajo, Celso García, Maximiliano Sicer, Juan Muntaner, Anselmo Bordonava, Juan Albisu, Alejandra Zanini, Lucas Rista, Miguel Hominal, José N Estrada, Aldo Prado, Diego M Gosparini, Beatriz Schiavi, Armando G Castillo, José G Ruíz, Guillermo R Martinez, Víctor G López, Enrique L Rosas, Gabriel R Lopez, Elias G Cantu, Manuel de los Ríos Ibarra, Francisco P Padilla, Jose P Carrasco, Luis V Carrillo, Joel D García, Alfredo N Askar, Carlos A Salinas, Marco A Gamba, Carlos G Sanchez, Arnulfo G Cantú, Raul V Sánchez, Jaime C Madrigal, Rafael H Urbano, Andrés Í Romo, José R González Juanatey, Paolo Racugno, Angel C Fillat, José M de la Torre Hernández, Juan A Peláez, Jorge B Cortada, Pablo G Pavia, Manuel J Navarro, Roberto M Asenjo, Francisco F Díaz, Eduard B Peligero, Fernando A Manterola, Antonio F Ortiz, Juan D Mediavilla García, Francisco M Ortuño, Tomás R Vera, Alfonso S González, Jaime A Viñas, Francisco J Fernández Portales, Petra S Mayordomo, Francisco B Ojeda, Antonio R Domínguez, Rosa S González, Diego B Guerrero, Juan M Ruiz Nodar, Xavier G Marimon, José G Margáez, Roberto M Aguilera, José F Díaz Fernández, José L Zamorano Gómez, Vicente B González, Bruno G del Blanco, Ignacio P Pérez, Mercé R Moreno, Ainhoa R Ereño, José A García Lledó, Juan Prieto, Alex Villablanca, Carlos Raffo, Christian Pincetti, Carlos Conejeros, Oscar Roman, Manuel Rodriguez, Paola Varleta, Cindy Goldberg, Jorge Sandoval, German Arriagada, Lucio Leon, Sergio Potthoff, Jorge Cobos, Christian Figueroa, Ellen Makotoko, Nyda Fourie, Lesley Burgess, Hendrik Nortje, Rust Theron, Perumal Pillai, Naresh Ranjith, Julien Trokis, Soobramoney Pillay, Jeevren Reddy, Theema Nunkoo, Cornelia Kapp, Dorothea Urbach, Lawrence Distiller, Adrian Horak, Louis van Zyl, Kathleen Coetzee, Zelda Punt, Junaid Bayat, Saleem Dawood, Ismail Mitha, Trevenesan Padayachee, Farzana Hoosen, Anthony Dalby, null Prabhavathi, Prakash Gowdaiah, Vimal Mehta, Milan Chag, Milind Gadkari, Kannaiyan Ramamurthee, Asit Das, Jitendra S Sawhney, Suvro Banerjee, Prachee Sathe, Srilakshmi Adhyapak, Tuan Nguyen, Vinh Pham, Huan Do, Anh Nguyen, Hien Nguyen, Binh Truong, Shahnaz Jamil-Copley, Chim Lang, Alastair Pell, Azfar Zaman, Robert Storey, Neil Swanson, Simon Smith, David Sharman, Denise Braganza, Peter Hammond, Andrew Moriarty, Stephen Bain, Maurice Pye, Andrew Sharp, Mark Blagden, Harpal Randeva, Timothy Myhill, Girish Viswanathan, Philip Keeling, Piers Clifford, Manish Saxena, Kristopher Lyons, John McMurray, Feeroz Jaafar, Clare Murphy, Simon Cartwright, Kamal Abouglila, Lubomir Antalik, Peter Krajci, Miroslav Urban, Frantisek Fazekas, Daniel Pella, Daniel Koleny, Tatiana Vykoukalova, Vladimir Macek, Daniela Vinanska, Livia Jamriskova, Slavomir Such, Peter Fulop, Stefan Farsky, Viliam Bugan, Jaroslava Strbova, Karol Micko, Juraj Palka Jr, Vladimir Sivak, Dalby Kristensen, Jens Refsgaard, Lene Holmvang, Ulrik Dixen, Henrik Nielsen, Kenneth Egstrup, Lisette O Jensen, Roman Sykulski, Ole Rasmussen, Alin Andries, Anders Luckow, Gitte Nielsen, Torben Sørensen, Chaiyasith Wongvipaporn, Noppadol Chamnarnphol, Suphot Srimahachota, Nakarin Sansanayudh, Srun Kuanprasert, Damras Tresukosol, Bancha Sookananchai, Mehmet Kanadasi, Turkay Ozcan, Murathan Kucuk, Zeki Ongen, Ertugrul Okuyan, Alev Arat, Sadik Acikel, Ahmet Yalcin, Umit Guray, Ceyhun Ceyhan, Necla Ozer, Sakir Arslan, Oskar Angerås, Nina Johnston, Ann-Charlotte Weiderman, Stellan Bandh, Ole Hansen, Hans Larnefeldt, Dawid Kusiak, Carl-Johan Lindholm, Anders Hedman, David Erlinge, Dan Curiac, Pia Lundman, Roberto Zucconi-Mazzini, Layth Aladellie, Jens Jensen, Jan Verwerft, Mathias Vrolix, Dirk Faes, Harry Striekwold, Peter Sinnaeve, Patrick Timmermans, Antoine Guedes, Marc Delforge, Jan Nimmegeers, Francis Stammen, Ian Buysschaert, Etienne Hoffer, Geert Hollanders, Geert Vervoort, Patrick Coussement, Stefan de Maeseneire, Luc Janssens, Stein A Gravdal, Knut Risberg, Lars Gullestad, Ola D Hofseth, Dennis Nilsen, Knut T Lappegård, Christian van den Heuvel, Charlotte Gibbs, Alamdar Khusrawi, Satish Arora, Tadeusz Tomala, Thorbjørn Kjærnli, Jan Berg-Johansen, Robert Hagemeier, Gunnar Skjelvan, David Colquhoun, John Amerena, Claire Morbey, Christopher Hammett, Anthony Dart, Ronald Lehman, Andrew Hamilton, Matthew Worthley, Peter Purnell, Alan Whelan, Richard MacIsaac, Ktut Arya, Sultan Linjawi, Joseph Proietto, Lakshman Prasad, Aldo Rodriguez, Armando Godoy, Victor Rodriguez, Percy Berrospi, Carlos Chavez, Sandra Negron, Javier Heredia, Felix Medina, Helard Manrique, Walter Cabrera, Fernando Cordova, Trinidad Quinteros, Jaime M Haro, Susana Regalado, Javier Guitton, Hugo Arbanil, Michel Pansieri, Eric Decoulx, Pascal Goube, Axel de Labriolle, Jean N Labeque, Gregoire Range, Yves Cottin, Gilles Montalescot, Guillaume Cayla, Nicolas Danchin, Denis Angoulvant, Emile Ferrario, Meyer Elbaz, Olivier Dubreuil, Philippe G Steg, Caroline Fontaine, Emmanuel Sorbets, Hafiz Omer, Shukri Al-Saif, Hussam Al-Faleh, Abdullah Al-Shehri, Halia Alshehri, Rasha Bazari, Pak Hei, Man Ying, Michael Chan, Michelle Wong, Ronald Ma, Shing C Siu, Chiu C Tsang, Maurizio Ferrario, Emilio Assanelli, Michele Senni, Piermarco Piatti, Paolo Calabrò, Stefano Urbinati, Massimo Michisanti, Ferdinando Varbella, Salvatore de Cosmo, Roberto Trevisan, Sandro Bellotti, Giuseppe Di Pasquale, Angelo S Bongo, Massimo Uguccioni, Edoardo Mannucci, Ciro Mauro, Mauro Ragonese, Claudio Fresco, Maurizio Turturo, Rossella Marcucci, Manuel J Lievano Triana, Camilo Arana, Jose Accini, Rodrigo Botero, Marlena Muzyk-Osikowicz, Fredy T Dada, Gregorio S Vallejo, Fernando Manzur, Daniel Isaza, Dora Molina, Juan G Mesa, Alvaro Quintero, Kai Nyman, Jyrki Mäkelä, Jorma Strand, Sakari Nieminen, Jyrki Taurio, Matti Kuusela, Timo Valle, Mikko Pietilä, Sakari Kekki, Timo Strandberg, Marc Klutstein, Gabriel Greenberg, Yoseph Rozenman, Ehud Chorin, Ariel Roguin, Basil Lewis, Amir Bashkin, Edgar Tan, Jose P Prado, Arthur Ferrolino, Noe Babilonia, Benny Barbas, Generoso Matiga, Raul M Coching, Heinz Drexel, Helmut Brath, Christoph Schnack, Ursula Hanusch, Evelyn Fließer-Görzer, Bernhard Paulweber, Christoph Ebenbichler, Rudolf Prager, Kurt Huber, Michael Wolzt, Johann Auer, Rudolf Berger, Gerit-Holger Schernthaner, Gabriela Stanciulescu, Mihai Creteanu, Marilena Spiridon, Viorica Dobreanu, Dragos Vinereanu, Laura C Iosipescu, Octavian Istratoaie, Ioan Coman, Constantin Militaru, Mircea Cinteza, Peter R Sinnaeve, José C Nicolau, José F Kerr Saraiva, Ramón Corbalán, Petr Widimský, Steen D Kristensen, Juha Hartikainen, Harald Darius, Hung F Tse, Robert G Kiss, Prem Pais, Eli Lev, Leonardo de Luca, Gabriel A Ramos López, Frederic Kontny, Noe A Babilonia, Dmitry A Zateyshchikov, Mikhail Ruda, Omer Elamin, František Kovář, Anthony J Dalby, Héctor Bueno, Chern-En Chiang, Alexander Parkhomenko, Tuan Q Nguyen, Maria Leonsson-Zachrisson, Herrada, Anthony, Brigham & Women’s Hospital [Boston] (BWH), Harvard Medical School [Boston] (HMS), AP-HP - Hôpital Bichat - Claude Bernard [Paris], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Laboratoire de Recherche Vasculaire Translationnelle (LVTS (UMR_S_1148 / U1148)), Université Paris 13 (UP13)-Université Paris Diderot - Paris 7 (UPD7)-Institut National de la Santé et de la Recherche Médicale (INSERM), Royal Brompton Hospital, McMaster University [Hamilton, Ontario], Keenan Research Centre of the Li Ka Shing Knowledge Institute [Toronto], St. Michael's Hospital, University of Toronto, Service de Pharmacologie médicale = service de pharmacologie - Dosage de médicaments [CHU Saint-Antoine], CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU), Sorbonne Université (SU), National Heart and Lung Institute [London] (NHLI), Imperial College London-Royal Brompton and Harefield NHS Foundation Trust, Uppsala University Hospital, Uppsala Universitet [Uppsala], AstraZeneca, Tokai University, Uppsala University, Imperial College London, Saint Luke's Mid America Heart Institute, University of Missouri [Kansas City] (UMKC), University of Missouri System, University of New South Wales [Sydney] (UNSW), University of Texas Southwestern Medical Center [Dallas], Stanford University, Centre Hospitalier Universitaire de Nîmes (CHU Nîmes), Université de Montpellier (UM), Bhatt, D, Steg, P, Mehta, S, Leiter, L, Simon, T, Fox, K, Held, C, Andersson, M, Himmelmann, A, Ridderstrale, W, Chen, J, Song, Y, Diaz, R, Goto, S, James, S, Ray, K, Parkhomenko, A, Kosiborod, M, Mcguire, D, Harrington, R, Santos, V, Jain, A, Lendel, I, Russo, M, Haught, W, Bouza, M, Gogia, H, Banerjee, S, Kichura, G, Kantaros, L, Padron, F, Passi, R, Stone, J, Pursley, M, D'Urso, M, Gardner, T, Bennett, J, Nour, K, Saini, S, Zhang, W, Kumbhani, D, Thomas, D, Angiolillo, D, Bertolet, B, Roman-Miranda, A, Black, R, Manshadi, R, Vaca, C, Blanco, A, Napoli, M, Brabham, D, Akyea-Djamson, A, Desai, P, Prasada, S, Khaira, A, Forgosh, L, Lieber, I, Umpierrez, G, Singal, D, Londono, J, Fraser, N, Ruiz, J, Vega, D, Rodriguez, L, Brown, C, Syed, F, Aggarwala, G, Eaves, W, Foster, M, Gupta, D, Avino, D, Asfour, W, Tonnessen, G, Zhao, X, Singh, N, Brockmyre, A, Lepor, N, Shammas, N, Blick, D, Hearne, S, Prodafikas, J, Carell, E, Izzo, M, Karim, A, Zakhary, B, Atieh, M, Leichter, S, Meadows, C, Hotchkiss, D, Abu-Fadel, M, Wiseman, A, Bander, J, Shah, M, Ganim, R, Sopko, K, Khan, M, Lloret, R, Weirick, T, Mehta, R, Thadani, U, Bhargava, A, Moya, J, Staniloae, C, Guerra, Y, Chhabra, A, Kosmicki, D, Shaheen, W, Mohammed, A, Bitters, J, Pattanayak, J, Javier, J, Srivastava, S, Phillips, R, Al-Amin, J, Lillestol, M, Simpson, P, Hazan, L, Amin, A, Shah, G, Korpas, D, Platt, B, Dickert, J, Puente, O, Hiotis, L, Doyle, T, Rajan, R, Meholick, A, Gring, C, Hage-Korban, E, Feldman, R, Colfer, H, Butman, S, Hart, T, Huling, R, Eshaghian, S, Quintana, O, Cheung, D, Handel, F, Rodriguez, M, Suh, D, Gordon, P, Pressman, G, Bauer, M, French, W, Barettella, M, Chatrathi, S, Suresh, D, Goldberg, R, Huth, M, Younis, L, Rahman, A, Mascolo, R, Welch, M, Suneja, R, Smith, S, Shurmur, S, Agaiby, J, Jingo, A, Johnston, J, Beth, M, Vlastaris, A, Kemp, S, Taheri, H, Pereira, E, Deyoung, M, Hawa, Z, Smith, R, Galski, T, Garas, S, Reddy, M, Sharma, S, Hargrove, J, Treasure, C, Emerson, R, Haddad, T, Rohr, K, Levinson, L, Gaona, R, Uretsky, B, Maheshwari, H, Lee, D, Kinnaman, S, Singal, R, Geohas, J, Gigliotti, O, Raisinghani, A, Khurana, C, Hella, B, Kelberman, M, Voyce, S, Singh, S, Lo, E, Singh, P, Goodfellow, R, Fischer, S, Lorraine, R, Turner, T, Shanes, J, Busch, R, Broker, R, Zaniewski, M, Pounds, K, Debs-Perez, G, Ong, S, Frandsen, B, Fullington, D, Jaffrani, N, Khan, A, Lee, M, Pouzar, J, Revtyak, G, Gonzalez, J, Nakhle, S, Murillo, A, Young, D, Makam, S, Syed, M, Woolf, K, Grena, P, Alfata, S, Mahal, S, Hoffman, D, Kizhakekuttu, T, Deering, J, Bhavsar, J, Mikesell, S, Wilson, W, Wilson, V, El, S, Spinale, F, Kannarkat, V, Rao, S, Hanson, L, Bertsch, J, Gonzalez-Ortiz, E, Severino, N, Willis, J, Schock, J, Bakhtari, L, Gazmuri, R, Ansari, S, Hall, J, Mehta, A, Shealy, N, Zarich, S, Singh, D, Vora, K, Andrawis, N, Molter, D, Maron, D, Cardona, J, D'Agostino, R, Arshad, T, Samaan, R, Jones, D, Presser, D, Heath, J, Green, S, Bittar, G, Henry, S, Korn, D, Schmedtje, J, Nadar, V, Graham, B, Labroo, A, Clavijo, L, Roseman, H, Ledesma, G, Rosen, R, Dor, I, Kirby, W, Sutton, J, Eder, F, Iteld, B, Gomez-Cortes, J, Buchbinder, M, Kasper, J, Terrelonge, A, Torres, G, Jagielo, T, Alvarez, J, Handelsman, Y, Guillen, M, Richwine, R, Lewy-Alterbaum, L, Corder, C, Arvind, M, Bolshoun, D, Mikhail, M, Minton, S, Alvarado, O, Abbott, J, Cauthen, B, Welter, R, Mintz, R, 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Conejeros, C, Roman, O, Varleta, P, Goldberg, C, Sandoval, J, Arriagada, G, Corbalan, R, Leon, L, Potthoff, S, Cobos, J, Figueroa, C, Makotoko, E, Fourie, N, Burgess, L, Nortje, H, Theron, R, Pillai, P, Ranjith, N, Trokis, J, Pillay, S, Reddy, J, Nunkoo, T, Kapp, C, Urbach, D, Distiller, L, Horak, A, van Zyl, L, Coetzee, K, Punt, Z, Bayat, J, Dawood, S, Mitha, I, Padayachee, T, Hoosen, F, Dalby, A, Prabhavathi, Gowdaiah, P, Mehta, V, Chag, M, Gadkari, M, Ramamurthee, K, Das, A, Sawhney, J, Sathe, P, Adhyapak, S, Nguyen, T, Pham, V, Do, H, Nguyen, A, Nguyen, H, Truong, B, Jamil-Copley, S, Lang, C, Pell, A, Zaman, A, Storey, R, Swanson, N, Sharman, D, Braganza, D, Hammond, P, Moriarty, A, Bain, S, Pye, M, Sharp, A, Blagden, M, Randeva, H, Myhill, T, Viswanathan, G, Keeling, P, Clifford, P, Saxena, M, Lyons, K, Mcmurray, J, Jaafar, F, Murphy, C, Cartwright, S, Abouglila, K, Antalik, L, Krajci, P, Urban, M, Fazekas, F, Pella, D, Koleny, D, Vykoukalova, T, Macek, V, Vinanska, D, Jamriskova, L, Such, S, Fulop, P, Farsky, S, Bugan, V, Strbova, J, Micko, K, Palka Jr, J, Sivak, V, Kristensen, D, Refsgaard, J, Holmvang, L, Dixen, U, Nielsen, H, Egstrup, K, Jensen, L, Sykulski, R, Rasmussen, O, Andries, A, Luckow, A, Nielsen, G, Sorensen, T, Wongvipaporn, C, Chamnarnphol, N, Srimahachota, S, Sansanayudh, N, Kuanprasert, S, Tresukosol, D, Sookananchai, B, Kanadasi, M, Ozcan, T, Kucuk, M, Ongen, Z, Okuyan, E, Arat, A, Acikel, S, Yalcin, A, Guray, U, Ceyhan, C, Ozer, N, Arslan, S, Angeras, O, Johnston, N, Weiderman, A, Bandh, S, Hansen, O, Larnefeldt, H, Kusiak, D, Lindholm, C, Hedman, A, Erlinge, D, Curiac, D, Lundman, P, Zucconi-Mazzini, R, Aladellie, L, Jensen, J, Verwerft, J, Vrolix, M, Faes, D, Striekwold, H, Sinnaeve, P, Timmermans, P, Guedes, A, Delforge, M, Nimmegeers, J, Stammen, F, Buysschaert, I, Hoffer, E, Hollanders, G, Vervoort, G, Coussement, P, de Maeseneire, S, Janssens, L, Gravdal, S, Risberg, K, Gullestad, L, Hofseth, O, Nilsen, D, Lappegard, K, van den Heuvel, 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Mannucci, E, Mauro, C, Ragonese, M, Fresco, C, Turturo, M, Marcucci, R, Lievano Triana, M, Arana, C, Accini, J, Botero, R, Muzyk-Osikowicz, M, Dada, F, Vallejo, G, Manzur, F, Isaza, D, Molina, D, Mesa, J, Quintero, A, Nyman, K, Makela, J, Strand, J, Nieminen, S, Taurio, J, Kuusela, M, Valle, T, Pietila, M, Kekki, S, Strandberg, T, Klutstein, M, Greenberg, G, Rozenman, Y, Chorin, E, Roguin, A, Lewis, B, Bashkin, A, Tan, E, Prado, J, Ferrolino, A, Babilonia, N, Barbas, B, Matiga, G, Coching, R, Drexel, H, Brath, H, Schnack, C, Hanusch, U, Fliesser-Gorzer, E, Paulweber, B, Ebenbichler, C, Prager, R, Huber, K, Wolzt, M, Auer, J, Berger, R, Schernthaner, G, Stanciulescu, G, Creteanu, M, Spiridon, M, Dobreanu, V, Vinereanu, D, Iosipescu, L, Istratoaie, O, Coman, I, Militaru, C, Cinteza, M, Nicolau, J, Kerr Saraiva, J, Widimsky, P, Kristensen, S, Hartikainen, J, Darius, H, Tse, H, Pais, P, Lev, E, de Luca, L, Ramos Lopez, G, Kontny, F, Zateyshchikov, D, Ruda, M, Elamin, O, Kovar, F, Bueno, H, Leonsson-Zachrisson, M, Université Paris Diderot - Paris 7 (UPD7)-Université Paris 13 (UP13)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de pharmacologie - Dosage de médicaments [CHU Saint-Antoine], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-CHU Saint-Antoine [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Sorbonne Université (SU)-Sorbonne Université (SU), and Royal Brompton and Harefield NHS Foundation Trust-Imperial College London

Subjects
Male, Platelet Aggregation Inhibitors/therapeutic use, THEMIS Steering Committee and Investigators, medicine.medical_treatment, Vascular damage Radboud Institute for Health Sciences [Radboudumc 16], 030204 cardiovascular system & hematology, Coronary Angiography, Stroke/epidemiology, Coronary artery disease, DOUBLE-BLIND, 0302 clinical medicine, Hemorrhage/chemically induced, acetylsalicylic acid, antidiabetic agent, placebo, ticagrelor, Secondary Prevention, Medicine, 030212 general & internal medicine, Myocardial infarction, Coronary Artery Bypass, Cardiovascular Diseases/mortality, 11 Medical and Health Sciences, OUTCOMES, Aspirin, [SDV.MHEP] Life Sciences [q-bio]/Human health and pathology, General Medicine, Middle Aged, Clopidogrel, 3. Good health, Ticagrelor/therapeutic use, DRUG-ELUTING STENTS, CLOPIDOGREL, Cardiology, PLATELET INHIBITION, Drug Therapy, Combination, Female, Life Sciences & Biomedicine, Ticagrelor, TIMI, medicine.drug, Coronary Artery Disease/complications, medicine.medical_specialty, Hypoglycemic Agents/therapeutic use, POOLED ANALYSIS, 03 medical and health sciences, Medicine, General & Internal, Percutaneous Coronary Intervention, Double-Blind Method, General & Internal Medicine, Internal medicine, Myocardial Infarction/epidemiology, Humans, Aged, Science & Technology, ANTIPLATELET THERAPY, business.industry, Diabetes Mellitus, Type 2/complications, ELEVATION MYOCARDIAL-INFARCTION, RIVAROXABAN, Percutaneous coronary intervention, medicine.disease, ASPIRIN, Coronary Stenosis/diagnostic imaging, Aspirin/therapeutic use, Conventional PCI, business, [SDV.MHEP]Life Sciences [q-bio]/Human health and pathology
Abstract

Contains fulltext : 215333.pdf (Publisher’s version ) (Closed access) BACKGROUND: Patients with stable coronary artery disease and diabetes with previous percutaneous coronary intervention (PCI), particularly those with previous stenting, are at high risk of ischaemic events. These patients are generally treated with aspirin. In this trial, we aimed to investigate if these patients would benefit from treatment with aspirin plus ticagrelor. METHODS: The Effect of Ticagrelor on Health Outcomes in diabEtes Mellitus patients Intervention Study (THEMIS) was a phase 3 randomised, double-blinded, placebo-controlled trial, done in 1315 sites in 42 countries. Patients were eligible if 50 years or older, with type 2 diabetes, receiving anti-hyperglycaemic drugs for at least 6 months, with stable coronary artery disease, and one of three other mutually non-exclusive criteria: a history of previous PCI or of coronary artery bypass grafting, or documentation of angiographic stenosis of 50% or more in at least one coronary artery. Eligible patients were randomly assigned (1:1) to either ticagrelor or placebo, by use of an interactive voice-response or web-response system. The THEMIS-PCI trial comprised a prespecified subgroup of patients with previous PCI. The primary efficacy outcome was a composite of cardiovascular death, myocardial infarction, or stroke (measured in the intention-to-treat population). FINDINGS: Between Feb 17, 2014, and May 24, 2016, 11 154 patients (58% of the overall THEMIS trial) with a history of previous PCI were enrolled in the THEMIS-PCI trial. Median follow-up was 3.3 years (IQR 2.8-3.8). In the previous PCI group, fewer patients receiving ticagrelor had a primary efficacy outcome event than in the placebo group (404 [7.3%] of 5558 vs 480 [8.6%] of 5596; HR 0.85 [95% CI 0.74-0.97], p=0.013). The same effect was not observed in patients without PCI (p=0.76, pinteraction=0.16). The proportion of patients with cardiovascular death was similar in both treatment groups (174 [3.1%] with ticagrelor vs 183 (3.3%) with placebo; HR 0.96 [95% CI 0.78-1.18], p=0.68), as well as all-cause death (282 [5.1%] vs 323 [5.8%]; 0.88 [0.75-1.03], p=0.11). TIMI major bleeding occurred in 111 (2.0%) of 5536 patients receiving ticagrelor and 62 (1.1%) of 5564 patients receiving placebo (HR 2.03 [95% CI 1.48-2.76], p

Published
2019

26. Controlling light emission by a thermalized ensemble of colloidal quantum dots with a metasurface.

Author

Monin H, Loirette-Pelous A, De Leo E, Rossinelli AA, Prins F, Norris DJ, Bailly E, Hugonin JP, Vest B, and Greffet JJ

Abstract

We report an experimental and theoretical study of light emission by a patterned ensemble of colloidal quantum dots (cQDs). This system modifies drastically the emission spectrum and polarization as compared to a planar layer of cQDs. It exhibits bright, directional and polarized emission including a degree of circular polarization in some directions. We introduce a model of light emission based on a local Kirchhoff law which reproduces accurately all the features of the experiment. The model provides a figure of merit to assess quantitatively the emitted power. This work paves the way to the systematic design of efficient ultrathin light emitting metasurfaces with controlled polarization, spectrum and directivity.

Published
2023
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27. Exciton diffusion in two-dimensional metal-halide perovskites.

Author

Seitz M, Magdaleno AJ, Alcázar-Cano N, Meléndez M, Lubbers TJ, Walraven SW, Pakdel S, Prada E, Delgado-Buscalioni R, and Prins F

Abstract

Two-dimensional layered perovskites are attracting increasing attention as more robust analogues to the conventional three-dimensional metal-halide perovskites for both light harvesting and light emitting applications. However, the impact of the reduced dimensionality on the optoelectronic properties remains unclear, particularly regarding the spatial dynamics of the excitonic excited state within the two-dimensional plane. Here, we present direct measurements of exciton transport in single-crystalline layered perovskites. Using transient photoluminescence microscopy, we show that excitons undergo an initial fast diffusion through the crystalline plane, followed by a slower subdiffusive regime as excitons get trapped. Interestingly, the early intrinsic diffusivity depends sensitively on the choice of organic spacer. A clear correlation between lattice stiffness and diffusivity is found, suggesting exciton-phonon interactions to be dominant in the spatial dynamics of the excitons in perovskites, consistent with the formation of exciton-polarons. Our findings provide a clear design strategy to optimize exciton transport in these systems.

Published
2020
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28. Long-Term Stabilization of Two-Dimensional Perovskites by Encapsulation with Hexagonal Boron Nitride.

Author

Seitz M, Gant P, Castellanos-Gomez A, and Prins F

Abstract

Metal halide perovskites are known to suffer from rapid degradation, limiting their direct applicability. Here, the degradation of phenethylammonium lead iodide (PEA 2 PbI 4 ) two-dimensional perovskites under ambient conditions was studied using fluorescence, absorbance, and fluorescence lifetime measurements. It was demonstrated that the long-term stability of two-dimensional perovskites could be achieved through the encapsulation with hexagonal boron nitride. While un-encapsulated perovskite flakes degraded within hours, the encapsulated perovskites were stable for at least three months. In addition, encapsulation considerably improved the stability under laser irradiation. The environmental stability, combined with the improved durability under illumination, is a critical ingredient for thorough spectroscopic studies of the intrinsic optoelectronic properties of this material platform.

Published
2019
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29. The disappearing San of southeastern Africa and their genetic affinities.

Author

Schlebusch CM, Prins F, Lombard M, Jakobsson M, and Soodyall H

Subjects
Africa, Southern, Archaeology, Fossils, Genetic Variation, Haplotypes, Humans, Phylogeny, Anthropology methods, Black People genetics, DNA, Mitochondrial genetics, Genetics, Population
Abstract

Southern Africa was likely exclusively inhabited by San hunter-gatherers before ~2000 years ago. Around that time, East African groups assimilated with local San groups and gave rise to the Khoekhoe herders. Subsequently, Bantu-speaking farmers, arriving from the north (~1800 years ago), assimilated and displaced San and Khoekhoe groups, a process that intensified with the arrival of European colonists ~350 years ago. In contrast to the western parts of southern Africa, where several Khoe-San groups still live today, the eastern parts are largely populated by Bantu speakers and individuals of non-African descent. Only a few scattered groups with oral traditions of Khoe-San ancestry remain. Advances in genetic research open up new ways to understand the population history of southeastern Africa. We investigate the genomic variation of the remaining individuals from two South African groups with oral histories connecting them to eastern San groups, i.e., the San from Lake Chrissie and the Duma San of the uKhahlamba-Drakensberg. Using ~2.2 million genetic markers, combined with comparative published data sets, we show that the Lake Chrissie San have genetic ancestry from both Khoe-San (likely the ||Xegwi San) and Bantu speakers. Specifically, we found that the Lake Chrissie San are closely related to the current southern San groups (i.e., the Karretjie people). Duma San individuals, on the other hand, were genetically similar to southeastern Bantu speakers from South Africa. This study illustrates how genetic tools can be used to assess hypotheses about the ancestry of people who seemingly lost their historic roots, only recalling a vague oral tradition of their origin., Competing Interests: Compliance with ethical standards Ethical approval All procedures performed in studies involving human participants were in accordance with the ethical standards of the institutional and/or national research committee and with the 1964 Helsinki declaration and its later amendments or comparable ethical standards. Conflict of interest On behalf of all authors, the corresponding author states that there is no conflict of interest.

Published
2016
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30. Defective postreperfusion metabolic recovery directly associates with incident delayed graft function.

Author

Wijermars LG, Schaapherder AF, de Vries DK, Verschuren L, Wüst RC, Kostidis S, Mayboroda OA, Prins F, Ringers J, Bierau J, Bakker JA, Kooistra T, and Lindeman JH

Subjects
Allografts metabolism, Biopsy, Cohort Studies, Delayed Graft Function epidemiology, Delayed Graft Function etiology, Delayed Graft Function pathology, Female, Humans, Incidence, Kidney drug effects, Kidney metabolism, Kidney pathology, Male, Middle Aged, Mitochondria drug effects, Mitochondria metabolism, Oligopeptides therapeutic use, Reperfusion Injury drug therapy, Reperfusion Injury metabolism, Reperfusion Injury pathology, Allografts pathology, Delayed Graft Function metabolism, Graft Survival, Kidney Transplantation adverse effects, Mitochondria pathology, Reperfusion Injury complications
Abstract

Delayed graft function (DGF) following kidney transplantation affects long-term graft function and survival and is considered a manifestation of ischemia reperfusion injury. Preclinical studies characterize metabolic defects resulting from mitochondrial damage as primary driver of ischemia reperfusion injury. In a comprehensive approach that included sequential establishment of postreperfusion arteriovenous concentration differences over the human graft, metabolomic and genomic analysis in tissue biopsies taken before and after reperfusion, we tested whether the preclinical observations translate to the context of clinical DGF. This report is based on sequential studies of 66 eligible patients of which 22 experienced DGF. Grafts with no DGF immediately recovered aerobic respiration as indicated by prompt cessation of lactate release following reperfusion. In contrast, grafts with DGF failed to recover aerobic respiration and showed persistent adenosine triphosphate catabolism indicated by a significant persistently low post reperfusion tissue glucose-lactate ratio and continued significant post-reperfusion lactate and hypoxanthine release (net arteriovenous difference for lactate and hypoxanthine at 30 minutes). The metabolic data for the group with DGF point to a persistent post reperfusion mitochondrial defect, confirmed by functional (respirometry) and morphological analyses. The archetypical mitochondrial stabilizing peptide SS-31 significantly preserved mitochondrial function in human kidney biopsies following simulated ischemia reperfusion. Thus, development of DGF is preceded by a profound post-reperfusion metabolic deficit resulting from severe mitochondrial damage. Strategies aimed at preventing DGF should be focused on safeguarding a minimally required post-reperfusion metabolic competence., (Copyright © 2016 International Society of Nephrology. Published by Elsevier Inc. All rights reserved.)

Published
2016
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31. The tumor area occupied by Tbet+ cells in deeply invading cervical cancer predicts clinical outcome.

Author

Gorter A, Prins F, van Diepen M, Punt S, and van der Burg SH

Subjects
Adult, Aged, Aged, 80 and over, Cell Proliferation, Disease-Free Survival, Female, Forkhead Transcription Factors metabolism, Humans, Immunohistochemistry, Interferon-gamma metabolism, Leukocyte Common Antigens metabolism, Lymphocytes cytology, Middle Aged, Neoplasm Invasiveness, Neoplasm Metastasis, Papillomavirus Infections metabolism, Prognosis, Proportional Hazards Models, Treatment Outcome, Uterine Cervical Neoplasms diagnosis, T-Lymphocytes, Regulatory cytology, Uterine Cervical Neoplasms pathology
Abstract

Background: Deep invasion of the normal surrounding tissue by primary cervical cancers is a prognostic parameter for postoperative radiotherapy and relatively worse survival. However, patients with tumor-specific immunity in the blood at the time of surgery displayed a much better disease free survival. Here we analyzed if this was due to a more tumor-rejecting immune population in the tumor., Methods: Tumor sections from a group of 58 patients with deep normal tissue-invading cervical tumors were stained for the presence of immune cells (CD45), IFNγ-producing cells (Tbet) and regulatory T cells (Foxp3) by immunohistochemistry. The slides were scanned and both the tumor area and the infiltration of the differently stained immune cells were objectively quantified using computer software., Results: We found that an increased percentage of tumor occupied by CD45+ cells was strongly associated with an enhanced tumor-infiltration by Tbet+ cells and Foxp3+ cells. Furthermore, the area occupied by CD45+ immune cells, Tbet+ cells but not Foxp3+ cells within the tumor were, in addition to the lymph node status of patients, associated with a longer disease free survival and disease specific survival. Moreover, interaction analyses between these immune parameters and lymph node status indicated an independent prognostic effect of tumor infiltrating Tbet+ cells. This was confirmed in a multivariate Cox analysis., Conclusions: The area occupied by a preferentially type I oriented CD45+ cell infiltrate forms an independent prognostic factor for recurrence-free and disease-specific survival on top of the patient's lymph node status.

Published
2015
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32. Replication of Plasmodium in reticulocytes can occur without hemozoin formation, resulting in chloroquine resistance.

Author

Lin JW, Spaccapelo R, Schwarzer E, Sajid M, Annoura T, Deroost K, Ravelli RB, Aime E, Capuccini B, Mommaas-Kienhuis AM, O'Toole T, Prins F, Franke-Fayard BM, Ramesar J, Chevalley-Maurel S, Kroeze H, Koster AJ, Tanke HJ, Crisanti A, Langhorne J, Arese P, Van den Steen PE, Janse CJ, and Khan SM

Subjects
Animals, Artemisinins chemistry, Artesunate, Cytoplasm metabolism, Female, Gene Deletion, Genes, Reporter, Malaria parasitology, Male, Mice, Mice, Inbred BALB C, Mutation, Reticulocytes metabolism, Antimalarials chemistry, Chloroquine chemistry, Drug Resistance, Erythrocytes parasitology, Hemeproteins chemistry, Hemoglobins metabolism, Plasmodium berghei cytology, Reticulocytes parasitology
Abstract

Most studies on malaria-parasite digestion of hemoglobin (Hb) have been performed using P. falciparum maintained in mature erythrocytes, in vitro. In this study, we examine Plasmodium Hb degradation in vivo in mice, using the parasite P. berghei, and show that it is possible to create mutant parasites lacking enzymes involved in the initial steps of Hb proteolysis. These mutants only complete development in reticulocytes and mature into both schizonts and gametocytes. Hb degradation is severely impaired and large amounts of undigested Hb remains in the reticulocyte cytoplasm and in vesicles in the parasite. The mutants produce little or no hemozoin (Hz), the detoxification by-product of Hb degradation. Further, they are resistant to chloroquine, an antimalarial drug that interferes with Hz formation, but their sensitivity to artesunate, also thought to be dependent on Hb degradation, is retained. Survival in reticulocytes with reduced or absent Hb digestion may imply a novel mechanism of drug resistance. These findings have implications for drug development against human-malaria parasites, such as P. vivax and P. ovale, which develop inside reticulocytes., (© 2015 Lin et al.)

Published
2015
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33. Preeclampsia is associated with the presence of transcriptionally active placental fragments in the maternal lung.

Author

Buurma AJ, Penning ME, Prins F, Schutte JM, Bruijn JA, Wilhelmus S, Rajakumar A, Bloemenkamp KW, Karumanchi SA, and Baelde HJ

Subjects
Adult, Chorionic Gonadotropin metabolism, Chromosomes, Human, Y metabolism, Female, Humans, Pregnancy, RNA, Messenger metabolism, Transcription, Genetic, Trophoblasts metabolism, Uterus metabolism, Vascular Endothelial Growth Factor Receptor-1 genetics, Lung metabolism, Placenta metabolism, Pre-Eclampsia metabolism, Vascular Endothelial Growth Factor Receptor-1 metabolism
Abstract

Preeclampsia is associated with increased levels of the circulating antiangiogenic factor sFlt-1 and with an excessive shedding of placenta-derived multinucleated syncytial aggregates into the maternal circulation. However, it remains unclear whether these aggregates are transcriptionally active in the maternal organs and can, therefore, contribute to the systemic manifestations of preeclampsia. In this study, we measured placental soluble fms-like tyrosine kinase-1 (sFlt-1) mRNA levels in preeclamptic- and control placentas and performed RNA in situ hybridization to localize the main placental expression site of sFlt-1 mRNA. Because the maternal lung is the first capillary bed that circulating syncytial aggregates traverse, we studied the presence and persistence of placental material in lungs of preeclamptic and control subjects. To confirm the placental origin of these aggregates in maternal lungs, immunohistochemistry for the placenta-specific marker hCG (human chorionic ghonadotropin) and Y chromosome in situ hybridization were performed. Using human placental tissue, we found that syncytial knots are the principal site of expression of the antiangiogenic factor sFlt-1. In addition, autopsy material obtained from women with preeclampsia (n=9) showed significantly more placenta-derived syncytial aggregates in the lungs than in control subjects (n=26). Importantly, these aggregates still contained the antiangiogenic factor sFlt-1 after their entrapment in the maternal lungs. The current study confirms the important role of syncytial knots in placental sFlt-1 mRNA production. In addition, it shows a significant association between preeclampsia and larger quantities of sFlt-1 containing syncytial aggregates in maternal lungs, suggesting that the transfer of syncytial aggregates to the maternal compartment may contribute to the systemic endothelial dysfunction that characterizes preeclampsia.

Published
2013
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34. In situ transmission electron microscopy imaging of electromigration in platinum nanowires.

Author

Rudneva M, Gao B, Prins F, Xu Q, van der Zant HS, and Zandbergen HW

Abstract

In situ transmission electron microscopy was performed on the electromigration in platinum (Pt) nanowires (14 nm thick, 200 nm wide, and 300 nm long) with and without feedback control. Using the feedback control mode, symmetric electrodes are obtained and the gap usually forms at the center of the Pt nanowire. Without feedback control, asymmetric electrodes are formed, and the gap can occur at any position along the wire. The three-dimensional gap geometries of the electrodes in the Pt nanowire were determined using high-angle annular dark-field scanning transmission electron microscopy; the thickness of the nanowire is reduced from 14 nm to only a few atoms at the edge with a gap of about 5-10 nm.

Published
2013
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35. Role of protein biomarkers in the detection of high-grade disease in cervical cancer screening programs.

Author

Brown CA, Bogers J, Sahebali S, Depuydt CE, De Prins F, and Malinowski DP

Abstract

Since the Pap test was introduced in the 1940s, there has been an approximately 70% reduction in the incidence of squamous cell cervical cancers in many developed countries by the application of organized and opportunistic screening programs. The efficacy of the Pap test, however, is hampered by high interobserver variability and high false-negative and false-positive rates. The use of biomarkers has demonstrated the ability to overcome these issues, leading to improved positive predictive value of cervical screening results. In addition, the introduction of HPV primary screening programs will necessitate the use of a follow-up test with high specificity to triage the high number of HPV-positive tests. This paper will focus on protein biomarkers currently available for use in cervical cancer screening, which appear to improve the detection of women at greatest risk for developing cervical cancer, including Ki-67, p16(INK4a), BD ProEx C, and Cytoactiv HPV L1.

Published
2012
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36. IGF1R signaling in Ewing sarcoma is shaped by clathrin-/caveolin-dependent endocytosis.

Author

Martins AS, Ordóñez JL, Amaral AT, Prins F, Floris G, Debiec-Rychter M, Hogendoorn PC, and de Alava E

Subjects
Apoptosis drug effects, Caveolin 1 antagonists & inhibitors, Cell Line, Tumor, Cell Proliferation drug effects, Clathrin antagonists & inhibitors, Humans, Microscopy, Confocal, Models, Biological, Phosphorylation drug effects, Protein Kinase Inhibitors pharmacology, Proteome metabolism, Receptor, IGF Type 1 antagonists & inhibitors, Sarcoma, Ewing pathology, Caveolin 1 metabolism, Clathrin metabolism, Endocytosis drug effects, Receptor, IGF Type 1 metabolism, Sarcoma, Ewing metabolism, Signal Transduction
Abstract

Receptor endocytosis is critical for cell signaling. IGF1R mediates an autocrine loop that is de-regulated in Ewing Sarcoma (ES) cells. Here we study the impact of IGF1R internalization, mediated by clathrin and caveolin-1 (CAV1), in ES signaling. We used clathrin and CAV1-siRNA to interfere in clathrin- and caveolin-dependent endocytosis. Chlorpromazine (CPMZ) and methyl-beta-cyclo-dextrin (MCD) were also used in order to inhibit clathrin- and caveolin-dependent endocytosis, respectively. We analyzed IGF1R internalization and co-localization with clathrin and CAV1 upon ligand binding, as well as the status of the IGF1R pathway, cellular proliferation, and the apoptosis of interfered and inhibited ES cells. We performed a high-throughput tyrosine kinase phosphorylation assay to analyze the effects of combining the IGF1R tyrosine kinase inhibitor AEW541 (AEW) with CPMZ or MCD on the intracellular phospho-proteome. We observed that IGF1R is internalized upon ligand binding in ES cells and that this process is dependent on clathrin or CAV1. The blockage of receptor internalization inhibited AKT and MAPK phosphorylation, reducing the proliferative rate of ES cells and increasing the levels of apoptosis. Combination of AEW with CPMZ or MCD largely enhanced these effects. CAV1 and clathrin endocytosis controls IGF1R internalization and signaling and has a profound impact on ES IGF1R-promoted survival signaling. We propose the combination of tyrosine-kinase inhibitors with endocytosis inhibitors as a new therapeutic approach to achieve a stronger degree of receptor inhibition in this, or other neoplasms dependent on IGF1R signaling.

Published
2011
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37. Charge transport in a zinc-porphyrin single-molecule junction.

Author

Perrin ML, Martin CA, Prins F, Shaikh AJ, Eelkema R, van Esch JH, van Ruitenbeek JM, van der Zant HS, and Dulić D

Abstract

We have investigated charge transport in ZnTPPdT-Pyr (TPPdT: 5,15-di(p-thiolphenyl)-10,20-di(p-tolyl)porphyrin) molecular junctions using the lithographic mechanically controllable break-junction (MCBJ) technique at room temperature and cryogenic temperature (6 K). We combined low-bias statistical measurements with spectroscopy of the molecular levels in the form of I(V) characteristics. This combination allows us to characterize the transport in a molecular junction in detail. This complex molecule can form different junction configurations, having an observable effect on the trace histograms and the current-voltage (I(V)) measurements. Both methods show that multiple, stable single-molecule junction configurations can be obtained by modulating the interelectrode distance. In addition we demonstrate that different ZnTPPdT-Pyr junction configurations can lead to completely different spectroscopic features with the same conductance values. We show that statistical low-bias conductance measurements should be interpreted with care, and that the combination with I(V) spectroscopy represents an essential tool for a more detailed characterization of the charge transport in a single molecule.

Published
2011
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38. Primary cilia organization reflects polarity in the growth plate and implies loss of polarity and mosaicism in osteochondroma.

Author

de Andrea CE, Wiweger M, Prins F, Bovée JV, Romeo S, and Hogendoorn PC

Subjects
Adolescent, Bone Neoplasms genetics, Bone Neoplasms metabolism, Cell Proliferation, Child, Child, Preschool, Female, Growth Plate metabolism, Humans, Kinesins metabolism, Male, Mosaicism, Osteochondroma genetics, Osteochondroma metabolism, Young Adult, Bone Neoplasms pathology, Cell Polarity, Cilia ultrastructure, Growth Plate pathology, Osteochondroma pathology
Abstract

Primary cilia are specialized cell surface projections found on most cell types. Involved in several signaling pathways, primary cilia have been reported to modulate cell and tissue organization. Although they have been implicated in regulating cartilage and bone growth, little is known about the organization of primary cilia in the growth plate cartilage and osteochondroma. Osteochondromas are bone tumors formed along the growth plate, and they are caused by mutations in EXT1 or EXT2 genes. In this study, we show the organization of primary cilia within and between the zones of the growth plate and osteochondroma. Using confocal and electron microscopy, we found that in both tissues, primary cilia have a similar formation but a distinct organization. The shortest ciliary length is associated with the proliferative state of the cells, as confirmed by Ki-67 immunostaining. Primary cilia organization in the growth plate showed that non-polarized chondrocytes (resting zone) are becoming polarized (proliferating and hypertrophic zones), orienting the primary cilia parallel to the longitudinal axis of the bone. The alignment of primary cilia forms one virtual axis that crosses the center of the columns of chondrocytes reflecting the polarity axis of the growth plate. We also show that primary cilia in osteochondromas are found randomly located on the cell surface. Strikingly, the growth plate-like polarity was retained in sub-populations of osteochondroma cells that were organized into small columns. Based on this, we propose the existence of a mixture ('mosaic') of normal lining (EXT(+/-) or EXT(wt/wt)) and EXT(-/-) cells in the cartilaginous cap of osteochondromas.

Published
2010
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39. Human leukocyte antigen class I, MHC class I chain-related molecule A, and CD8+/regulatory T-cell ratio: which variable determines survival of cervical cancer patients?

Author

Jordanova ES, Gorter A, Ayachi O, Prins F, Durrant LG, Kenter GG, van der Burg SH, and Fleuren GJ

Subjects
Adult, Aged, Aged, 80 and over, CD8-Positive T-Lymphocytes immunology, Female, Fluorescent Antibody Technique, Humans, Kaplan-Meier Estimate, Middle Aged, Polymerase Chain Reaction, Prognosis, T-Lymphocytes, Regulatory immunology, Uterine Cervical Neoplasms immunology, Uterine Cervical Neoplasms metabolism, Biomarkers, Tumor analysis, HLA-A Antigens biosynthesis, Histocompatibility Antigens Class I biosynthesis, Lymphocytes, Tumor-Infiltrating immunology, Uterine Cervical Neoplasms mortality
Abstract

Purpose: To investigate the effect of intraepithelial tumor-infiltrating lymphocytes (ieTIL) and their ligands expressed by cervical tumor cells on the outcome of cervical cancer patients., Experimental Design: The prognostic value of ieTILs was investigated in 115 cases of cervical cancer. T-cell subsets, CD57(+) cells, and regulatory T cells (Treg) were enumerated. The associations of these different ieTIL subtypes with human leukocyte antigen (HLA) class I and MHC class I chain-related molecule A (MICA) expression were determined in relation to clinical variables and patient survival., Results: Survival analysis showed that a high number of intraepithelial Treg (FoxP3(+)), a low CD8(+)/regulatory T-cell ratio, and a weak HLA-A expression were all associated with worse survival (P=0.034, 0.025, and 0.033, respectively, log-rank test). Further stratification of patient groups based on HLA-A-MICA expression and HLA-A-MICA-CD8(+)/Treg ratio revealed an even poorer survival (P=0.005). In a multivariate Cox analysis, low CD8(+)/Treg ratio (P=0.047), weak HLA-A-MICA expression (P=0.003), and weak HLA-A-MICA expression combined with low CD8(+)/Treg ratio (P=0.002) were all found to be independent unfavorable prognostic predictors in cervical carcinoma (hazard ratios, 2.7, 4.0, and 4.9, respectively)., Conclusion: Weak HLA-A-MICA expression combined with low CD8(+)/Treg ratio reveals a patient group with the poorest survival in cervical cancer. As a single variable, low CD8(+)/Treg ratio was a significant independent unfavorable prognostic factor.

Published
2008
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40. Distinct subcellular expression of endogenous polycystin-2 in the plasma membrane and Golgi apparatus of MDCK cells.

Author

Scheffers MS, Le H, van der Bent P, Leonhard W, Prins F, Spruit L, Breuning MH, de Heer E, and Peters DJ

Subjects
Animals, Blotting, Western, Calcium Channels metabolism, Calcium-Binding Proteins metabolism, Cell Line, Cell Membrane metabolism, Dogs, Haplorhini, Humans, Kidney cytology, Membrane Proteins immunology, Microscopy, Confocal, Microscopy, Fluorescence, Microscopy, Immunoelectron, Rabbits, Swine, TRPP Cation Channels, Transfection, Golgi Apparatus metabolism, Kidney metabolism, Membrane Proteins metabolism, Polycystic Kidney, Autosomal Dominant metabolism
Abstract

Polycystin-2 is a predicted integral membrane protein with non-selective cation channel activity. The protein is encoded by the PKD2 gene, which is mutated in approximately 15% of patients with autosomal dominant polycystic kidney disease (ADPKD). Polycystin-2 can interact with the transmembrane protein polycystin-1, the product of the PKD1 gene. However, endoplasmic reticulum (ER) localization was reported for (heterologously expressed) polycystin-2 in cultured cells and baso-lateral localization has been reported in renal tissues. Using two polyclonal antisera raised against polycystin-2 we demonstrated distinct expression of the endogenous protein in the Golgi apparatus and the plasma membrane of MDCK cells. In contrast, most of the heterologously expressed polycystin-2 (PC2-EGFP) remained in the ER, substantially overlapping with the staining pattern of protein-disulfide isomerase (PDI), a marker for the ER. Only in a small subset of these cells weak plasma membrane signals were observed. Membrane staining was also suggested by immunoelectron microscopy and was confirmed by subcellular fractionation on sucrose density gradients. The plasma membrane staining disappeared following extraction with a buffer containing Triton X-100, whereas signals for polycystin-1 and E-cadherin remained visible, suggesting that polycystin-2 is neither tightly bound to the Triton X-100 insoluble cytoskeleton, nor to these proteins. We conclude that endogenous polycystin-2 is transported via the Golgi apparatus to the plasma membrane and has a broader membrane localization than polycystin-1. These data suggest that polycystin-2 can move freely in certain regions of the membrane where it probably functions as a channel, activated by, or in complex with, polycystin-1.

Published
2002
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41. Polycystin-1, the product of the polycystic kidney disease 1 gene, co-localizes with desmosomes in MDCK cells.

Author

Scheffers MS, van der Bent P, Prins F, Spruit L, Breuning MH, Litvinov SV, de Heer E, and Peters DJ

Subjects
Animals, Antibodies immunology, Cadherins analysis, Calcium metabolism, Calcium pharmacology, Cell Adhesion drug effects, Cell Line, Cytoplasm chemistry, Cytoplasm drug effects, Cytoplasm metabolism, Cytoplasm ultrastructure, Cytoskeletal Proteins metabolism, Desmoplakins, Desmosomes drug effects, Desmosomes ultrastructure, Dogs, Fluorescent Antibody Technique, Microscopy, Immunoelectron, Precipitin Tests, Proteins chemistry, Proteins genetics, Proteins immunology, TRPP Cation Channels, Desmosomes chemistry, Desmosomes metabolism, Polycystic Kidney Diseases genetics, Proteins metabolism
Abstract

Polycystin-1 is a novel protein predicted to be a large membrane-spanning glycoprotein with an extracellular N-terminus and an intracellular C-terminus, harboring several structural motifs. To study the subcellular localization, antibodies raised against various domains of polycystin-1 and against specific adhesion complex proteins were used for two-color immunofluorescence staining. In Madine Darby canine kidney (MDCK) cells, polycystin-1 was detected in the cytoplasm as well as co-localizing with desmosomes, but not with tight or adherens junctions. Using confocal laser scanning and immunoelectron microscopy we confirmed the desmosomal localization. By performing a calcium switch experiment, we demonstrated the sequential reassembly of tight junctions, subsequently adherens junctions and finally desmosomes. Polycystin-1 only stained the membrane after incorporation of desmoplakin into the desmosomes, suggesting that membrane-bound polycystin-1 may be important for cellular signaling or cell adhesion, but not for the assembly of adhesion complexes.

Published
2000
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42. Epithelial cell adhesion molecule (Ep-CAM) modulates cell-cell interactions mediated by classic cadherins.

Author

Litvinov SV, Balzar M, Winter MJ, Bakker HA, Briaire-de Bruijn IH, Prins F, Fleuren GJ, and Warnaar SO

Subjects
Animals, Antigens, Neoplasm genetics, Cell Adhesion Molecules genetics, Cell Aggregation, Cell Line, Cytoskeleton metabolism, Epithelial Cell Adhesion Molecule, Epithelial Cells, Humans, Mice, Protein Binding, Recombinant Proteins metabolism, Structure-Activity Relationship, Tumor Cells, Cultured, Antigens, Neoplasm metabolism, Cadherins metabolism, Cell Adhesion Molecules metabolism, Intercellular Junctions
Abstract

The contribution of noncadherin-type, Ca2+-independent cell-cell adhesion molecules to the organization of epithelial tissues is, as yet, unclear. A homophilic, epithelial Ca2+-independent adhesion molecule (Ep-CAM) is expressed in most epithelia, benign or malignant proliferative lesions, or during embryogenesis. Here we demonstrate that ectopic Ep-CAM, when expressed in cells interconnected by classic cadherins (E- or N-cadherin), induces segregation of the transfectants from the parental cell type in coaggregation assays and in cultured mixed aggregates, respectively. In the latter assay, Ep-CAM-positive transfectants behave like cells with a decreased strength of cell-cell adhesion as compared to the parental cells. Using transfectants with an inducible Ep-CAM-cDNA construct, we demonstrate that increasing expression of Ep-CAM in cadherin-positive cells leads to the gradual abrogation of adherens junctions. Overexpression of Ep-CAM has no influence on the total amount of cellular cadherin, but affects the interaction of cadherins with the cytoskeleton since a substantial decrease in the detergent-insoluble fraction of cadherin molecules was observed. Similarly, the detergent-insoluble fractions of alpha- and beta-catenins decreased in cells overexpressing Ep-CAM. While the total beta-catenin content remains unchanged, a reduction in total cellular alpha-catenin is observed as Ep-CAM expression increases. As the cadherin-mediated cell-cell adhesions diminish, Ep-CAM-mediated intercellular connections become predominant. An adhesion-defective mutant of Ep-CAM lacking the cytoplasmic domain has no effect on the cadherin-mediated cell-cell adhesions. The ability of Ep-CAM to modulate the cadherin-mediated cell-cell interactions, as demonstrated in the present study, suggests a role for this molecule in development of the proliferative, and probably malignant, phenotype of epithelial cells, since an increase of Ep-CAM expression was observed in vivo in association with hyperplastic and malignant proliferation of epithelial cells.

Published
1997
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44. Qualitative alterations in laminin expression in experimental lupus nephritis.

Author

Kootstra CJ, Bergijk EC, Veninga A, Prins FA, de Heer E, Abrahamson DR, and Bruijn JA

Subjects
Animals, Antibodies, Monoclonal, Epitopes, Female, Graft vs Host Disease etiology, Graft vs Host Disease metabolism, Immunohistochemistry, Kidney Glomerulus metabolism, Laminin immunology, Lupus Nephritis etiology, Mice, Mice, Inbred C57BL, Mice, Inbred DBA, Microscopy, Immunoelectron, Peptide Fragments immunology, Tissue Distribution, Laminin metabolism, Lupus Nephritis metabolism
Abstract

Previous studies have revealed quantitative alterations in laminin-1 expression at the mRNA and protein levels during the development of glomerulonephritis and glomerulosclerosis in chronic graft-versus-host disease in mice, a model for lupus nephritis. We have now studied the qualitative alterations in laminin expression with two monoclonal antibodies that recognize epitopes on either the E8 or the P1 fragment of laminin-1. Both of these fragments are involved in cell-matrix and matrix-matrix interactions. In normal glomeruli these laminin epitopes are present only in the mesangial matrix; during embryogenesis, however, they are also present in the glomerular basement membrane. The distribution of laminin epitopes was first studied by using immunofluorescence in kidneys of mice with graft-versus-host disease at different points in time after disease induction. Reflection contrast and immunoelectron microscopy were performed after in vivo injection of the horseradish peroxidase-coupled monoclonal antibodies. In glomeruli of mice 8 weeks after disease induction, both injected antibodies bound specifically in electron-dense immune deposits in the mesangium and subepithelially along the glomerular basement membrane as well as in the expanded mesangial matrix. At 11 and 12 weeks after disease induction, when focal and segmental glomerulosclerosis had developed, the antibodies additionally bound in the matrix subendothelially along the glomerular basement membrane and at the periphery of end-stage sclerotic lesions. To study changes in the distribution of laminin epitopes over time, mice were injected with either monoclonal antibody before induction of graft-versus-host disease. The antibodies were detected 8 and 12 weeks later in the mesangial matrix of mice with lupus nephritis. Once segmental glomerulosclerosis had developed, the antibodies were additionally detected within the thickened glomerular capillary wall. The specific binding of anti-laminin monoclonal antibodies in electron-dense immune deposits further substantiates the hypothesis that anti-laminin autoantibodies participate in glomerular immune complex formation in this model, as suggested by earlier studies. Furthermore, our results show that the distribution of glomerular laminin epitopes in the matrix is altered during the development of glomerular disease. These changes in the structure of the glomerular basement membrane may contribute to the abnormal cell-matrix and matrix-matrix interactions during the development of glomerular disease in this model for lupus nephritis.

Published
1995

45. Subcellular localization of the bcl-2 protein in malignant and normal lymphoid cells.

Author

de Jong D, Prins FA, Mason DY, Reed JC, van Ommen GB, and Kluin PM

Subjects
3,3'-Diaminobenzidine analysis, Chromosomes, Human, Pair 14, Chromosomes, Human, Pair 18, Humans, Intracellular Membranes chemistry, Mitochondria chemistry, Nuclear Envelope chemistry, Proto-Oncogene Proteins c-bcl-2, Translocation, Genetic, Leukemia, Lymphocytic, Chronic, B-Cell, Lymphocytes chemistry, Proto-Oncogene Proteins analysis
Abstract

The bcl-2 oncogene is expressed in lymphoid and myeloid cells as well as in neurons and several types of epithelial cells and inhibits programmed cell death (apoptosis). Deregulation by the t(14;18) translocation in lymphoid malignancies induces inappropriate cell survival and serves as one of the steps toward a fully malignant behavior. Using pre- and postembedding immunoelectron microscopy in normal and neoplastic lymphocytes, we demonstrate bcl-2 immunoreactivity to the mitochondrial outer circumference and the nuclear envelope and to a lesser degree to the cell membrane. Mitochondrial staining was patchy, reminiscent of mitochondrial contact zones. Additionally, there was a suggestion of association with nuclear pores. In these regions, transmembrane transport is mediated. This may suggest that bcl-2 exerts its function in this process.

Published
1994

46. A histologic study of the extracellular matrix during the development of glomerulosclerosis in murine chronic graft-versus-host disease.

Author

Bergijk EC, Munaut C, Baelde JJ, Prins F, Foidart JM, Hoedemaeker PJ, and Bruijn JA

Subjects
Animals, Capillaries metabolism, Capillaries ultrastructure, Chronic Disease, Collagen classification, Collagen metabolism, Immunoglobulin G metabolism, Kidney Glomerulus blood supply, Laminin metabolism, Mice, Mice, Inbred C57BL, Mice, Inbred DBA, Microscopy, Electron, Microscopy, Immunoelectron, Extracellular Matrix ultrastructure, Glomerulosclerosis, Focal Segmental pathology, Graft vs Host Disease pathology
Abstract

The development of glomerulosclerosis was studied in murine chronic graft-versus-host disease (GvHD), which is a model for human systemic lupus erythematosus. The authors investigated the distribution patterns of six components of the extracellular matrix (ECM), i.e., laminin, fibronectin, collagen types I, III, IV, and VI during the course of the disease. All of these ECM components except collagen type I were found in the glomeruli of normal mice, where all of them were intrinsic constituents of the mesangium. Laminin, fibronectin, and collagen type IV were also found in the glomerular capillary walls. Starting 6 weeks after the induction of GvHD and continuing at week 8, the onset of an expansion of the mesangial matrix was observed. At the same time, the amounts of laminin, fibronectin, and collagen types IV and VI increased. Ten weeks after the onset of the disease, glomerulosclerosis developed. Traces of the interstitial collagen type I were found in sclerotic glomeruli. The levels of four ECM components, i.e., collagens III, IV, VI, and laminin were markedly decreased in the sclerotic glomeruli as compared with week 8. In contrast, the amount of fibronectin in the sclerotic glomeruli increased dramatically. Immunoelectron microscopic examination showed fibronectin in the sclerotic lesions, in contrast to laminin, collagen type I, and collagen type IV. It is concluded that the sclerotic lesions in murine chronic GvHD contain fibronectin. The small amounts of the ECM components laminin, as well as collagens III, IV, and VI in the sclerotic glomeruli in GvHD, might represent remnants of mesangial material and collapsed capillary walls. These components are probably replaced by increased production and/or accumulation of collagen type I and fibronectin.

Published
1992

47. The pathophysiology of protein-overload proteinuria.

Author

Weening JJ, Van Guldener C, Daha MR, Klar N, van der Wal A, and Prins FA

Subjects
Animals, Capillaries pathology, Capillary Permeability, Female, Horseradish Peroxidase metabolism, Immunoglobulin G metabolism, Immunoglobulin M metabolism, Kidney Glomerulus blood supply, Kidney Glomerulus pathology, Metabolic Clearance Rate, Proteinuria etiology, Proteinuria pathology, Rats, Rats, Inbred Strains, Serum Albumin metabolism, Serum Albumin, Bovine metabolism, Proteinuria metabolism
Abstract

Alterations in glomerular function and structure were studied in protein-overload nephrosis in the rat induced by intraperitoneal administration of bovine serum albumin (BSA). Fractional clearance (C/GFR) studies using inulin and tracer proteins of different molecular size and charge revealed in proteinuric rats 1) unchanged glomerular filtration rate and renal plasma flow; 2) a 34-fold increase in C/GFR of rat serum albumin, reaching values similar to BSA; 3) a 2-fold increase in C/GFR for anionic horse radish peroxidase (HRP), but normal values for neutral and cationic HRP, and 4) an 11- and 3-fold increase for heterologous IgG and IgM, respectively. Glomerular epithelial cells showed degenerative changes, but the distribution of anionic sites in the glomerular basement membrane was found to be unaltered, as determined by polyethyleneimine binding studies. In summary, an elevation of serum albumin concentration resulted in an increased transcapillary albumin transport. This was found to lead to degenerative changes of glomerular epithelial cells with development of large pore defects, which were completely reversible.

Published
1987

48. Cytokeratin and neurofilament in lung carcinomas.

Author

van Muijen GN, Ruiter DJ, van Leeuwen C, Prins FA, Rietsema K, and Warnaar SO

Subjects
Adenocarcinoma metabolism, Adenocarcinoma, Bronchiolo-Alveolar metabolism, Antibodies, Monoclonal, Carcinoma, Small Cell metabolism, Carcinoma, Squamous Cell metabolism, Histocytochemistry, Humans, Neurofilament Proteins, Intermediate Filament Proteins metabolism, Keratins metabolism, Lung Neoplasms metabolism, Neoplasm Proteins metabolism
Abstract

Three monoclonal antibodies, one directed against cytokeratin (clone 80) and two directed against neurofilament (clones 2F11 and 3G6), were used in the study of a series of 77 lung carcinomas by immunohistochemical staining. The anti-cytokeratin antibody, a very broadly reacting antibody directed against an antigenic determinant common to a great number of cytokeratins, was applicable on frozen sections. The two anti-neurofilament antibodies, directed against the 70 kD protein (clone 2F11) and the 160 kD and 200 kD proteins (clone 3G6) of neurofilament, were applicable on both frozen sections and paraffin sections. The staining results on the lung carcinomas indicate that all types of tumors studied, including small-cell anaplastic carcinoma, are markedly positive for cytokeratin. Frozen sections of five and formalin-fixed and paraffin-embedded sections of six other small-cell anaplastic carcinomas were negative with both anti-neurofilament monoclonal antibodies. One poorly differentiated squamous cell carcinoma positive with anti-neurofilament clone 2F11 but negative with clone 3G6. This distribution of cytoskeletal proteins demonstrates the epithelial differentiation of all types of lung carcinomas. Neuroendocrine differentiation of lung carcinomas as found in the small-cell anaplastic types does not result in expression of neurofilament proteins.

Published
1984

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