Search

Your search keyword '"Koeller, M."' showing total 90 results
Start Over Author "Koeller, M."
90 results on '"Koeller, M."'

8. Untersuchungen zur Biokompatibilität und Interaktion von Silber-Nanopartikeln mit humanen mesenchymalen Stammzellen (hMSCs)

Author

Greulich, C., Kittler, S., Epple, M., Köller, M., Buhr, H. J., editor, Hölscher, A., editor, Izbicki, J. R., editor, Jauch, K. W., editor, Post, S., editor, Allgayer, H., editor, Bartsch, D. K., editor, Fries, H., editor, Ghadimi, B. M., editor, Habermann, J. K., editor, Kalthoff, H., editor, Schackert, H. K., editor, Bruns, C. J., editor, Duda, D. N., editor, Fändrich, F., editor, Heberer, M., editor, Nüssler, A. K., editor, Stark, G. B., editor, Brückner, U. B., editor, Ertel, W., editor, Faist, E., editor, Heidecke, C. D., editor, Kalff, J. C., editor, Menger, M. D., editor, Schade, U. F., editor, Vollmar, B., editor, Bechstein, W. O., editor, Klar, E., editor, Klempnauer, J., editor, Minor, T., editor, Neuhaus, P., editor, Schmidt, J., editor, Langer, S., editor, Laschke, M. W., editor, Machens, H. G., editor, Steinau, H. U., editor, Südkamp, N., editor, Vogt, P., editor, Berger, D., editor, Klinge, U., editor, Schachtrupp, A., editor, Schilling, M. K., editor, Schumpelick, V., editor, Altendorf-Hofmann, A., editor, Bollschweiler, E., editor, Bruch, H. -P., editor, Lehnert, T., editor, Lorenz, W., editor, Neugebauer, E., editor, Ohmann, C., editor, Seiler, C. M., editor, Becker, H., editor, Betzler, M., editor, Bittner, R., editor, Broelsch, C., editor, Büchler, M. W., editor, Bumm, R., editor, Dralle, H., editor, Friess, H., editor, Frilling, A., editor, Germer, C. T., editor, Hopt, U., editor, Jonas, S., editor, Jost, J., editor, Markus, B., editor, Raab, H. R., editor, Reith, H. B., editor, Schlag, P. M., editor, Teichmann, W., editor, Uhl, W., editor, Wenisch, H., editor, and Zornig, C., editor

Published
2009
Full Text
View/download PDF

20. Untersuchung der Biokompatibilität von zellbesiedeltem Nickeltitan unter dynamischer Belastung

Author

Habijan, T., Glogowski, T., Kühn, S., Pohl, M., Muhr, G., Köller, M., Buhr, H. J., editor, Hölscher, A., editor, Izbicki, J. R., editor, Jauch, K. W., editor, Post, S., editor, Allgayer, H., editor, Bartsch, D. K., editor, Fries, H., editor, Ghadimi, B. M., editor, Habermann, J. K., editor, Kalthoff, H., editor, Schackert, H. K., editor, Bruns, C. J., editor, Duda, D. N., editor, Fändrich, F., editor, Heberer, M., editor, Nüssler, A. K., editor, Stark, G. B., editor, Brückner, U. B., editor, Ertel, W., editor, Faist, E., editor, Heidecke, C. D., editor, Kalff, J. C., editor, Menger, M. D., editor, Schade, U. F., editor, Vollmar, B., editor, Bechstein, W. O., editor, Klar, E., editor, Klempnauer, J., editor, Minor, T., editor, Neuhaus, P., editor, Schmidt, J., editor, Langer, S., editor, Laschke, M. W., editor, Machens, H. G., editor, Steinau, H. U., editor, Südkamp, N., editor, Vogt, P., editor, Berger, D., editor, Klinge, U., editor, Schachtrupp, A., editor, Schilling, M. K., editor, Schumpelick, V., editor, Altendorf-Hofmann, A., editor, Bollschweiler, E., editor, Bruch, H. -P., editor, Lehnert, T., editor, Lorenz, W., editor, Neugebauer, E., editor, Ohmann, C., editor, Seiler, C. M., editor, Becker, H., editor, Betzler, M., editor, Bittner, R., editor, Broelsch, C., editor, Büchler, M. W., editor, Bumm, R., editor, Dralle, H., editor, Friess, H., editor, Frilling, A., editor, Germer, C. T., editor, Hopt, U., editor, Jonas, S., editor, Jost, J., editor, Markus, B., editor, Raab, H. R., editor, Reith, H. B., editor, Schlag, P. M., editor, Teichmann, W., editor, Uhl, W., editor, Wenisch, H., editor, and Zornig, C., editor

Published
2009
Full Text
View/download PDF

26. Free Papers

Author

Cerny, V., Zivny, P., Dostal, P., Zabka, L., Griffiths, R. D., Palmer, T. E. A., Jones, C., Atkinson, S., Sieffert, E., Bihari, D., Morlion, B. J., Siedhoff, H. P., Fürst, P., Puchstein, C., Sultan, F., Lagrange, D., Boisset, M., Malewiak, M. -I., Braga, M., Gianotti, L., Cestari, A., Vignali, A., Pellegatta, F., Di Carlo, V., Michel, I., Dive, A., Stoffel, M., Galanti, L., Jamart, J., Installé, Et., Chiolero, R., Cayeux, C., Schneiter, Ph., Schwarz, J. M., Tappy, L., Kourias, E., Theodosopoulos, Th., Datsis, A., Vassiliou, J., Smyrniotis, B., Weimann, A., Bastian, L., Bischoff, W. E., Grotz, M., Bode-Böger, S., Hansel, M., Lotz, J., Regel, G., Senkal, M., Kernen, M., Eickhoff, U., Mumme, A., Zumtobel, V., Kollig, E., Wachtler, P., Koeller, M., Wolfram, G., and Guy’s Hospital Intensive Care Group, Guy’s Hospital, London UK

Published
1996
Full Text
View/download PDF

29. Interannual to multidecadal variability and predictability of North Atlantic circulation in a coupled earth system model with parametrized hydraulics

Author

Koeller, M., Kaese, R., and Herrmann, P.

Subjects
Atmospheric Science, Oceanography
Abstract

Several 1000 yr runs of the University of Victoria Earth System Climate Model (UVic ESCM) with a hydraulically controlled overflow in the Denmark Strait are used to analyse the effects of NAO-like variations of the wind stress localized in the subpolar North Atlantic. The focus is laid on improving the representation of the Atlantic meridional overturning circulation (AMOC), the sea surface temperatures in the Nordic Seas and the sea ice coverage without increasing the resolution of the global model. We show that by implementing hydraulic control in the Denmark Strait Overflow the AMOC can be enhanced at depths between 1000 and 3000 m by up to 7 Sverdrup (Sv) towards more realistic values. The stability of the Deep Western Boundary Current is considerably enhanced. The expansion of sea ice into the Nordic Seas in the standard run is pushed back from about 65 degrees N to 75 degrees N when hydraulic parametrization is switched on. In this case sea ice variations at 75 degrees N and Northern Europe air temperatures exhibit a lag of 9 yr to variations in the wind stress curl.

Published
2010

30. Effect of interleukin-6 receptor inhibition with tocilizumab in patients with rheumatoid arthritis (OPTION study): a double-blind, placebo-controlled, randomised trial

Author

Smolen, Js, Beaulieu, A, Rubbert Roth, A, Ramos Remus, C, Rovensky, J, Alecock, E, Woodworth, T, Alten, R, Tate, G, Maldonado Cocco JA, Scali, J, Taylor, A, Hanrahan, P, Nash, P, Smith, M, Smolen, J, Koeller, M, Eberl, G, Dunky, A, Zamani, O, Simon, Jc, Scheinberg, Ma, Yaneva, D, Oparanov, B, Karastatev, D, Atkins, C, Bell, M, Haraoui, B, Marin, L, Thorne, Jc, Zummer, M, Khraishi, M, Mckendry, Rj, Pandith, V, Mccarthy, T, Lau, Cs, Li, E, Mok, Cc, Kahan, A, Wendling, D, Bardin, T, Nguyen, M, Claudepierre, P, Berenbaum, F, Puechal, X, Fiehn, C, Heilig, B, Hellmich, B, Lange, U, Lorenz, Hm, Wendler, J, Czirijak, L, Hodinka, L, Szekanecz, Z, Molad, Y, Nahir, M, Rosner, I, Rubinow, A, Abu Shakra, M, Elkayam, O, Marcolongo, R, Bagnato, G, Triolo, G, Trotta, F, DE VITA, Salvatore, Lugo, Ge, Abud Mendoza, C, Pineca, C, de la Torre IG, Pacheco, C, Leong, Kh, Koh, Dr, Dudler, J, Villiger, P, Lothrenoo, W, Asavatanabodee, P, Nilganuwong, S, and Totemchokchaiyakarn, K.

Subjects
rheumatoid arthritis, interleukin-6
Published
2008

31. Markers of bone turnover do not predict bone metastases in breast cancer

Author

Markus J Seibel, Koeller M, Van der Velden B, and Diel I

Subjects
Adult, Bone Neoplasms, Breast Neoplasms, Middle Aged, Postmenopause, Osteogenesis, Predictive Value of Tests, Case-Control Studies, Odds Ratio, Humans, Female, Bone Remodeling, Prospective Studies, Bone Resorption, Biomarkers, Aged, Follow-Up Studies
Abstract

Markers of bone turnover are often elevated in patients with prevalent bone metastases (BM). To test whether bone markers may be used as early indicators of developing BM, we prospectively studied 113 women with primary breast cancer. At the time of study inclusion, none of the women had BM, skeletal disease or was on bone active drugs. During follow-up (8-52, median 30 mo.), pt. were seen every 3 mo. and blood/urine specimens were obtained. Eleven patients developed BM (BM+) and each of them was matched to 4 women remaining free of BM (BM-). Markers were serum (s) calcium, sTAP, sBAP, sOC, sPICP, sNTX, sCTX and urinary (u) PYD, uDPD, uNTX, uCTX. All analyses were done in single batches after study end. At any given point in time, marker levels in the BM+ group did not differ from those in the BM- group. Levels at baseline did not predict later BM (OR 0.14-1.01, all ns). 93% of all changes in bone markers were below the least significant change, as defined in an independent group of similar patients. The remaining 7% of values could not be associated in a consistent pattern with the occurrence of BM. We conclude that in patients with primary breast cancer, biochemical markers of bone turnover can not be used to predict or diagnose incident BM. This lack in diagnostic validity is mainly attributable to the high overall and long-term variability of the currently used bone markers.

Published
2002

32. Simulation based parameterization for process monitoring of machining operations

Author

Denkena, Berend, Koeller, M., Denkena, Berend, and Koeller, M.

Abstract

Process monitoring can prevent machine and tool failure in metal-cutting. A successful process monitoring of cutting processes depends on reliable monitoring limits for the process. In industrial applications these limits have to be generated in a learning phase during a ramp-up process. In order to enable process monitoring for single batch production without a learning phase, this paper describes a simulation based approach for generating reference data to set process limits. As a foundation for calculation of monitoring limits a position-based process simulation has to be established. In a first step an approach of modeling material removal is evaluated to check whether it fits the application for parameterizing the process monitoring. In this context the potentials of a process simulation for calculating process limits are clarified. Additionally the quality of data generated by this kind of simulation is discussed. In a second step a method is described to implement machine properties by a virtual machine tool within a simulation of material removal. For that purpose a method to use actual data of axis position and tool within the simulation of material removal is necessary. With these data a way-based simulation of material removal can generate reference parameters for monitoring limits instead of using data from a learning phase during the ramp-up process. By using position data of a virtual machine tool a reliable source for the actual position of all axes enables the position-based simulation to perform material removal in a more accurate way.

Published
2013

41. ANTERIOR PITUITARY FUNCTION IN PATIENTS WITH NEWLY DIAGNOSED RHEUMATOID ARTHRITIS.

Author

TEMPL, E., KOELLER, M., RIEDL, M., WAGNER, O., GRANINGER, W., and LUGER, A.

Abstract

SUMMARY Hormonal dysfunction involving the hypothalamic-pituitary-adrenal (HPA) axis, prolactin (PRL) secretion and sex hormone status has been supposed to contribute to the development or persistence of rheumatoid arthritis (RA). In addition, a reduced number of glucocorticoid receptors on circulating lymphocytes has been found in patients with RA. However, so far most studies have been performed in pre-treated patients. A combined test for total anterior pituitary reserve was performed in 10 patients with newly diagnosed untreated RA. Before and after stimulation with the respective hypothalamic releasing hormones, RA patients showed no difference in plasma concentrations of adrenocorticotrophic hormone (ACTH), cortisol, prolactin (PRL) and thyroid-stimulating hormone (TSH) when compared to healthy controls. In contrast, the growth hormone (GH) response to growth hormone-releasing hormone (GHRH) was blunted in RA patients. The hypothalamic-pituitary-thyroid/gonadal and adrenal axes seem to be unaltered in RA. However, if one considers the presence of chronic inflammation, normal plasma ACTH and cortisol concentrations must be considered as inappropriately low. The observed blunted GH release could be mediated by cytokines (e.g. IL-1), which are known to be elevated in RA. [ABSTRACT FROM PUBLISHER]

Published
1996
Full Text
View/download PDF

42. DESTRUCTIVE LYMPHADENOPATHY AND T-LYMPHOCYTE ACTIVATION IN ADULT-ONSET STILL’S DISEASE.

Author

KOELLER, M., KIENER, H., SIMONITSCH, I., ARINGER, M., STEINER, C. W., MACHOLD, K., and GRANINGER, W.

Abstract

Recurrent arthritis, fever and lymphadenopathy are symptoms of adult onset of Still's disease (AOSD). Differential diagnosis requires the exclusion of infections or malignant lymphomas. We report on a case of AOSD showing destructive lymphadenopathy, immunophenotyping of peripheral blood leucocytes revealed strong activation of T-lymphocytes. Bone marrow biopsy also showed an increase of lymphopoietic cells to 23%. Analysis of peripheral blood lymphocytes (PBL) after remission showed no remaining signs of activation. Analysis of lymphocyte activation by flow cytometry correlated with disease activity. [ABSTRACT FROM PUBLISHER]

Published
1995
Full Text
View/download PDF

43. Isolation of a cDNA encoding a novel member of the transglutaminase gene family from human keratinocytes. Detection and identification of transglutaminase gene products based on reverse transcription-polymerase chain reaction with degenerate primers.

Author

Aeschlimann, D, Koeller, M K, Allen-Hoffmann, B L, and Mosher, D F

Abstract

We developed a method using a single set of degenerate oligonucleotide primers for amplification of the conserved active site of transglutaminases by reverse transcription-polymerase chain reaction (RT-PCR) and identification of the PCR products by cleavage with diagnostic restriction enzymes. We demonstrate amplification of tissue transglutaminase (TGC), keratinocyte transglutaminase (TGK), prostate transglutaminase (TGP), the a-subunit of factor XIII, and band 4.2 protein from different human cells or tissues. Analysis of normal human keratinocytes revealed expression of a transglutaminase different from the expected and characterized transglutaminase gene products. A full-length cDNA for the novel transglutaminase (TGX) was obtained by anchored PCR. The deduced amino acid sequence encoded a protein with 720 amino acids and a molecular mass of approximately 81 kDa. A comparison of TGX to the other members of the gene family revealed that the domain structure and the residues required for enzymatic activity and Ca2+ binding are conserved and showed an overall sequence identity of about 35%. Two transcripts with an apparent size of 2.2 and 2.8 kilobases were detected with a specific probe for TGX on Northern blots of human foreskin keratinocyte mRNA, indicating the presence of alternatively spliced mRNAs. cDNA sequencing revealed a shorter TGX transcript lacking the sequence homologous to that encoded by exon III of other transglutaminase genes. TGX expression increased severalfold when keratinocyte cultures were induced to differentiate by suspension or growth to postconfluency, suggesting that TGX contributes to the formation of the cornified envelope.

Published
1998

47. Long-term variability of bone turnover markers in patients with non-metastatic breast cancer

Author

Markus J Seibel, Koeller M, Van der Velden B, and Diel I

Subjects
Adult, Reproducibility of Results, Breast Neoplasms, Middle Aged, Alkaline Phosphatase, Collagen Type I, Postmenopause, Humans, Calcium, Female, Bone Remodeling, Collagen, Prospective Studies, Peptides, Biomarkers, Aged, Follow-Up Studies
Abstract

Variability of bone marker measurements is a major problem in their clinical application. Most studies on marker variability have been performed in healthy subjects and over relatively short intervals of time. We prospectively evaluated the long-term variability of bone markers in 102 postmenopausal women diagnosed with primary breast cancer. During follow up (8-48, median 30 mo.), no patient developed bone metastases or other skeletal disease. Patients were seen every 3 months and exactly timed blood/urine specimens were obtained. All analyses were performed after study end by the same technician, using a single batch of reagents per analyte. The coefficient of variation was calculated as CV (%) = square root(sigma(CVi2)/n) (CVi = SD/mean x 100; n = n of CVi). The least significant change (LSC) was then LSC (%) = Z x CV x square root(2). Z = 1.96 for a 95% confidence interval (LSC-95). In a subset of n = 10 patients with no potential interference during follow-up, lowest CVs were recorded for serum (s) calcium (5%), sTAP (12%) and sBAP (14%). The LSC-95 for these markers were 14%, 33% and 39%, respectively. Highest CVs were seen with urine (56%) and serum (42%) CTX (LSC-95: 155%, 117% resp.). We conclude that in breast cancer patients without bone metastases, long-term variability varied greatly between markers. For certain markers, the LSC seems considerably higher than previously reported.

Catalog

Books, media, physical & digital resources
See catalog results