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11. Stoffwerte

Author

Hecker, E., Koch, W., List, P. H., Arnold, H., Walter, W., Baer, H. H., Weil-Malherbe, H., Eberhagen, D., Benson, A. A., Riedl, W., Hepding, L., Blackburn, G. M., Cameron, D. W., Reuber, R., Martius, C., Bosshardt, H.-P., Siedel, W., Pfleiderer, Wolfgang, Gompper, R., Jerchel, D., Stauffacher, D., Huber, G., Wallhäusser, K. H., Schäfer, W., Kofrányi, E., Debuch, H., Asselineau, J., Trösken, O., Rittel, W., Schwyzer, R., Werle, E., Schievelbein, H., Beckmann, S., Freyschlag, H., Zechmeister, L., Schulte, K. E., Reisch, J., Snatzke, G., Friedrich, W., Zahn, R. K., Hoffmann-Ostenhof, O., Kreil-Kiss, G., Heide, K., Granzer, E., Hochstrafter, K., Hannig, K., Bielig, H.-J., Möllinger, H., Dell, H.-D., Klingmüller, V., Neugebauer, F. A., Simon, H., Müllhofer, G., Otting, W., and Rauen, H. M., editor

Published
1964
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12. Endogenous factor VIII synthesis from the intron 22-inverted F8 locus may modulate the immunogenicity of replacement therapy for hemophilia A

Author

Pandey, GS, Yanover, C, Miller-Jenkins, LM, Garfield, S, Cole, SA, Curran, JE, Moses, EK, Rydz, N, Simhadri, V, Kimchi-Sarfaty, C, Lillicrap, D, Viel, KR, Przytycka, TM, Pierce, GF, Howard, TE, Sauna, ZE, Lusher, J, Chitlur, M, Ameri, A, Natarajan, K, Iyer, RV, Thompson, AA, Watts, RG, Kempton, CL, Kessler, C, Barrett, JC, Martin, EJ, Key, N, Kruse-Jarres, R, Lessinger, C, Pratt, KP, Josephson, N, McRedmond, K, Withycombe, J, Walsh, C, Matthews, D, Mahlangu, J, Krause, A, Schwyzer, R, Thejpal, R, Rapiti, N, Goga, Y, Coetzee, M, Stones, D, Mann, K, Butenas, S, Almasy, L, Blangero, J, Carless, M, Raja, R, and Reed, E

Subjects
congenital, hereditary, and neonatal diseases and abnormalities, hemic and lymphatic diseases
Abstract

Neutralizing antibodies (inhibitors) to replacement factor VIII (FVIII, either plasma derived or recombinant) impair the effective management of hemophilia A. Individuals with hemophilia A due to major deletions of the FVIII gene (F8) lack antigenically cross-reactive material in their plasma ("CRM-negative"), and the prevalence of inhibitors in these individuals may be as high as 90%. Conversely, individuals with hemophilia A caused by F8 missense mutations are CRM-positive, and their overall prevalence of inhibitors is

Published
2013
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14. Union Schweizerischer Gesellschaften für experimentelle Biologie Berichte der 2. Jahresversammlung: Fribourg, 23.–24. Mai 1970

Author

Akert, K., Kawana, E., Pfenninger, K., Moor, H., Sandri, C., Arczynska, W., Held, D. R., Haab, P., Boudry, J. F., Rioch-Ramel, F., Burri, P. H., Weibel, E. R., Cerretelli, P., di Prampero, P. E., Piiper, J., Chinet, A., Farber, J. P., Bloom, D. A., Farhi, L. E., Chmouliovsky, M., Churchill, P. C., Dolivo, M., Koelle, G. B., Geelhaar, A., Robert, M., Handwerker, H. O., Wettstein, A., Hösli, L., TebĒcis, A. K., Schönwetter, H. P., Andrès, P. F., Hösli, E., Jirounek, P., Straub, R. W., Kalix, P., Kelly, J. S., Dreifuss, J. J., Jéquier, E., Krayenbühl, H. P., Mehmel, H., Rutishauser, W., Meier, R. E., Dalderup, J., Cuénod, M., Perisic, M., Niemeyer, G., Forssmann, W. G., Oetliker, H., McGuigan, J. A. S., Parmeggiani, P. L., Franzini, C., Scheid, P., Roch-Ramel, F., Jotterand, N., Scherrer, M., Bitterli, J., Siegwart, B., Steiner, C. A., Tomori, Z., Trachtenberg, M. C., Kornblith, P., Häuptli, J., Braun, R., Zellweger, A., Bron, Th., Rous, S., Chmelar, M., Chmelarova, M., Favarger, P., Cueni, L., Schoenenberger, G. A., Allgöwer, M., Schonbach, J., Exton, J. H., Miller, Jr., T. B., Park, C. R., Fellay, G., Portmann, P., GonÇalves, J., Honegger, C. G., Schardt, M., Hecker, H., Marx, W., Shoyab, M., Murer, H., Schatzmann, H. J., Schenker, T. M., von Wartburg, J. P., Schindler, R., Schaer, J. C., Grieder, A., Stauffacher, W., Amherdt, M., Cameron, D., Burr, I., Balant, L., Orci, L., Stucki, J. W., Walter, P., Touabi, M., Jeanrenaud, B., Wacker, H., Lehky, P., Stein, E., Anabitarte, M., Winterhalter, K. H., Tuchschmid, P., Briehl, R. W., Brunori, M., Amiconi, G., Antonini, E., Wyman, J., Anner, Béatrice, Ferrero, J., Schorderet, M., Burkard, W. P., Lengsfeld, H., Gey, K. F., Haefely, W., Corthay, J., Benakis, A., Glasson, B., Haeusler, G., Somlyo, A. V., Somlyo, A. P., Heinrich, U., Langemann, H., Lichtensteiger, W., Iynedjian, P. B., Peters, G., Jalfre, M., Monachon, M. A., Lazáry, S., Stähelin, H., Minder, R., Bickel, M. H., Müller, A. H., Brunner, H., Pletscher, A., Da Prada, M., Berneis, K. H., Thomasset, M., Black, L. W., Ahmad-Zadeh, C., Dubochet, J., Ducommun, M., Kellenberger, E., Wacher, Ph., Tesi, D., Daldrup, J., Gautier, A., Schreyer, M., Cogliati, R., Gautschi, J. R., Goodman, H. M., Billeter, M. A., Hindley, J., Weissmann, C., Granboulan, P., Hess, M. W., Sordat, B., Cottier, H., Joel, D. D., Kellenberger-van der Kamp, C., Kolakofsky, D., Mechler, B., Mach, B., Mira-Moser, F., Schiller, P., Schwyzer, R., Scholl, A., Eppenberger, H. M., Séchaud, J., Staehelin, M., Wehrli, W., Yanagida, M., and Ahmad-Zadeh, G.

Published
1970
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21. LIST OF PARTICIPANTS

Author

TUN-KYI, AUNG, primary, BAJUSZ, S., additional, BEYERMAN, H.C., additional, BEZAS, B., additional, BODANSZKY, M., additional, BOISSONNAS, R.A., additional, BOTVINIK, M.M., additional, BRENNER, M., additional, BRICAS, E., additional, BRUCKNER, V., additional, COSMATOS, A., additional, COSTOPANAGIOTIS, A., additional, CRAIG, L.C., additional, DANE, E., additional, DETERMANN, H., additional, DILARIS, I., additional, DRABAREK, S., additional, ELLIOTT, D.F., additional, FAWCETT, C.P., additional, GHELIS, N., additional, GREVEN, H.M., additional, GUTTMANN, ST., additional, HARTMANN, A., additional, HOFER, W., additional, ISELIN, B.M., additional, IVANOV, V.T., additional, JOŠT, K., additional, KENNER, G.W., additional, KERLING, K.E.TH., additional, KISFALUDY, L., additional, LAW, H.D., additional, LEDERER, E., additional, MANTZOS, H., additional, MEDZIHRADSZKY, K., additional, MEIENHOFER, J., additional, MORLEY, J.S., additional, NESVADBA, H., additional, NIVARD, R.J.F., additional, OKUDA, T., additional, PATCHORNIK, A., additional, PHOTAKI, I., additional, PROX, A., additional, RIDGE, B., additional, ROCCHI, R., additional, RUDINGER, J., additional, RYDON, H.N., additional, SCHNABEL, E., additional, SCOFFONE, E., additional, SCHRÖDER, E., additional, SCHWYZER, R., additional, SELA, M., additional, SHEEHAN, J.C., additional, SHEMYAKIN, M.M., additional, SIEBER, P., additional, SIEDEL, W., additional, SMYTH, D.G., additional, SOUCHLERIS, I., additional, STELAKATOS, G.C., additional, STUDER, R.O., additional, TASCHNER, E., additional, TESSER, G.I., additional, THEODOROPOULOS, D.M., additional, WADE, R., additional, WALEY, S.G., additional, WEYGAND, F., additional, WIELAND, TH., additional, WITKOP, B., additional, WÜNSCH, E., additional, YOUNG, G.T., additional, ZERVAS, L., additional, ZIOUDROU, C., additional, ZIPP, O., additional, and ZUBER, H., additional

Published
1966
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22. Erratum to: Stoffwerte

Author

Hecker, E., primary, Koch, W., additional, List, P. H., additional, Arnold, H., additional, Walter, W., additional, Baer, H. H., additional, Weil-Malherbe, H., additional, Eberhagen, D., additional, Benson, A. A., additional, Riedl, W., additional, Hepding, L., additional, Blackburn, G. M., additional, Cameron, D. W., additional, Reuber, R., additional, Martius, C., additional, Bosshardt, H.-P., additional, Siedel, W., additional, Pfleiderer, Wolfgang, additional, Gompper, R., additional, Jerchel, D., additional, Stauffacher, D., additional, Huber, G., additional, Wallhäusser, K. H., additional, Schäfer, W., additional, Kofrányi, E., additional, Debuch, H., additional, Asselineau, J., additional, Kofrinyi, E., additional, Trösken, O., additional, Rittel, W., additional, Schwyzer, R., additional, Werle, E., additional, Schievelbein, H., additional, Beckmann, S., additional, Freyschlag, H., additional, Zechmeister, L., additional, Schulte, K. E., additional, Reisch, J., additional, Snatzke, G., additional, Friedrich, W., additional, Zahn, R. K., additional, Hoffmann-Ostenhof, O., additional, Kreil-Kiss, G., additional, Heide, K., additional, Hannig, K., additional, Granzer, E., additional, Hochstrafter, K., additional, Bielig, H.-J., additional, Möllinger, H., additional, Dell, H.-D., additional, Klingmüller, V., additional, Neugebauer, F. A., additional, Simon, H., additional, Müllhofer, G., additional, and Otting, W., additional

Published
1964
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27. Endogenous factor VIII synthesis from the intron 22-inverted F8 locus may modulate the immunogenicity of replacement therapy for hemophilia A

Author

Pandey, G., Yanover, C., Miller-Jenkins, L., Garfield, S., Cole, S., Curran, J., Moses, Eric, Rydz, N., Simhadri, V., Kimchi-Sarfaty, C., Lillicrap, D., Viel, K., Przytycka, T., Pierce, G., Howard, T., Sauna, Z., Lusher, J., Chitlur, M., Ameri, A., Natarajan, K., Iyer, R., Thompson, A., Watts, R., Kempton, C., Kessler, C., Barrett, J., Martin, E., Key, N., Kruse-Jarres, R., Lessinger, C., Pratt, K., Josephson, N., McRedmond, K., Withycombe, J., Walsh, C., Matthews, D., Mahlangu, J., Krause, A., Schwyzer, R., Thejpal, R., Rapiti, N., Goga, Y., Coetzee, M., Stones, D., Mann, K., Butenas, S., Almasy, L., Blangero, J., Carless, M., Raja, R., Reed, E., Pandey, G., Yanover, C., Miller-Jenkins, L., Garfield, S., Cole, S., Curran, J., Moses, Eric, Rydz, N., Simhadri, V., Kimchi-Sarfaty, C., Lillicrap, D., Viel, K., Przytycka, T., Pierce, G., Howard, T., Sauna, Z., Lusher, J., Chitlur, M., Ameri, A., Natarajan, K., Iyer, R., Thompson, A., Watts, R., Kempton, C., Kessler, C., Barrett, J., Martin, E., Key, N., Kruse-Jarres, R., Lessinger, C., Pratt, K., Josephson, N., McRedmond, K., Withycombe, J., Walsh, C., Matthews, D., Mahlangu, J., Krause, A., Schwyzer, R., Thejpal, R., Rapiti, N., Goga, Y., Coetzee, M., Stones, D., Mann, K., Butenas, S., Almasy, L., Blangero, J., Carless, M., Raja, R., and Reed, E.

Abstract

Neutralizing antibodies (inhibitors) to replacement factor VIII (FVIII, either plasma derived or recombinant) impair the effective management of hemophilia A1. Individuals with hemophilia A due to major deletions of the FVIII gene (F8) lack antigenically cross-reactive material in their plasma (“CRM-negative”), and the prevalence of inhibitors in these individuals may be as high as 90%. Conversely, individuals with hemophilia A caused by F8 missense mutations are CRM-positive, and their overall prevalence of inhibitors is <10% (ref. 2). Individuals with the F8 intron 22 inversion (found in ~50% of individuals with severe hemophilia A) have been grouped with the former on the basis of their genetic defect and CRM-negative status. However, only ~20% of these individuals develop inhibitors3. Here we demonstrate that the levels of F8 mRNA and intracellular FVIII protein in B lymphoblastoid cells and liver biopsies from individuals with the intron 22 inversion are comparable to those in healthy controls. These results support the hypothesis that most individuals with the intron 22 inversion are tolerized to FVIII and thus do not develop inhibitors. Furthermore, we developed a new pharmacogenetic algorithm that permits the stratification of inhibitor risk for individuals and subpopulations by predicting the immunogenicity of replacement FVIII using, as input, the number of putative T cell epitopes in the infused protein and the competence of major histocompatibility complex class II molecules to present such epitopes. This algorithm showed statistically significant accuracy in predicting the presence of inhibitors in 25 unrelated individuals with the intron 22 inversion.

Published
2013

29. Lipid-induced secondary structures and orientations of (Leu5)-enkephalin: Helical and crystallographic double-bend conformers revealed by IRATR and molecular modelling

Author

Schwyzer, R. Moutevelis-Minakakis, P. Kimura, S. Gremlich, H.-U.

Abstract

Lipid-induced secondary structures and orientations of the two enantiomeric [Leu5]-enkephalins, L-Tyr-Gly-Gly-L-Phe-L-Leu, and D-Tyr-Gly-Gly-D-Phe-D-Leu, on flat multi-bilayers of 1-palmitoyl-2-oleoyl-sn-glycero-3-phosphocholine (POPC) were examined with polarized attenuated total reflection IR (IRATR) spectroscopy and molecular mechanics procedures. The membrane-bound peptides showed identical IR spectra in the amide I and II band regions that indicated membrane-induced secondary structures and specific orientations of the non-zwitterionic molecules. A Lorentzian band shape analysis based on second derivatives of the original curves and the observed band polarizations suggested the presence of helical structures (βIII·-and α-turns), oriented more or less perpendicular to the membrane surface. Other folded structures, e.g. βI- and γ turns, were not excluded. Molecular modelling of non-zwitterionic [Leu5]-enkephalin with two βIII-turns or an α-turn resulted in essentially four low-energy conformers containing (i) two βIII-turns, (ii) one α-turn, (iii) a βIII-turn fused to an α-turn, and (iv) a βIII-turn fused to a βI-turn as in the crystallographic molecular conformation described by Aubry et al. [Biopolymers 28, 27-40 (1989)]. Zwitterionic [Leu5]-enkephalin with two βIII-tums collapsed to a C13 turn (a distorted α-turn) bridged by a γI-turn (v). The alignment of the amide I oscillators within the helical structures, (i), (ii) and (iii), and the double-bend structures, (iv) and (v), explained the observed amide I and II polarizations. Differences between these and other lipid-induced [Leu5]-enkephalin conformers reported in the literature may be caused by the lipid polymorphism of the model membranes used. Possible implications of the new conformers for the molecular mechanism of opioid receptor selection are discussed in terms of the membrane compartments theory.

Published
1997

35. Compound heterozygous sickle cell disease and β0- thalassaemia: An interesting case.

Author

von Fintel, R., Schwyzer, R., Poole, J., and Alli, N. A.

Subjects
*SICKLE cell anemia, *HEMOGLOBINS, *VOMITING in animals, *ABDOMINAL pain in children, *JAUNDICE, *PHOTOTHERAPY
Abstract

Haemoglobinopathies are a group of inherited disorders caused by structural variations of the haemoglobin molecule. We report the case of a 5-year-old girl suffering from chronic haemolytic anaemia. A diagnosis of compound heterozygous sickle cell disease (SCD) and β0-thalassaemia was established using haemoglobin sub-fractionation studies and parental screening. The latter revealed the father and mother to have heterozygous SCD and heterozygous β-thalassaemia, respectively. Evaluation of children with a haemolytic anaemia requires a thorough history and physical examination, appropriate laboratory testing and careful interpretation of the results. [ABSTRACT FROM AUTHOR]

Published
2013
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