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11 results on '"Hoist, J. J."'

2. Abstracts from the sixth meeting of the international association of pancreatology, November 2–4, 1994, Chicago, IL

Author

Burdick, Michael, Hollingsworth, Tony, Gansauge, S., Gansauge, F., Link, K. H., Schoenberg, M. H., Poch, B., Beger, H. G., Wagner, A. C. C., Steffen, H., Göke, B., Gaisano, H. Y., Sheu, L., Foskett, J. K., Trimble, W. S., Lee, Y. L., Kwon, H. Y., Park, H. S., Lee, S. M., Park, H. J., aguchi, S., Green, G. M., Mitamura, K., Komatsu, Y., Arai, I., Yamaura, H., Wang, OJ, Adrian, TE, Teyssen, S., Niebel, W., Niebergall, E., Singer, M. V., Umehara, K, Ohara, T, Kataoka, K, Okamura, H, Kato, M, Sakagami, J, Ohta, A, Murase, M, Hosoda, M, Yamane, Y, Kashima, K, Ibata, Y, Balthazar, Emil J., Banks, P. A., Garzof, S. G., Langevin, R. E., Silverman, S. G., Sica, G. T., Bassi, C., Benini, A., Muner, A., Falconi, M., Abbas, H., Pederzoli, P., Salvia, R., Minelli, E. Bertazzoni, Shaskar, S. Shanmuga, Shearer, M. G., Imrie, C. W., Brodmerkel, G. J., Reed, P. A., Carr-Locke, DL, Musa, A, Lichtenstein, DR, Dam, J Van, Banks, PA, Eisele, S., Schoenberg, M. H., Böchjer, M., Beger, H. G., Foitzik, Th., Fern’andez-del Castillo, C., Rattner, D. W., Ferraro, M. J., Warshaw, A. L., Foitzik, Th., Schmidt, J., Hotz, H., Warshaw, A. L., Buhr, H. J., Klar, E., Heinisch, A., Kadow, R., Bioss, U., Schölmerich, J., Zimgibl, H., Leser, H. -G., Manes, G., Rabitti, P. G., Laccetti, M., Cavallera, A., Paceili, L., Gagiione, G., Uomo, G., Marinqhini, A., Zinsmeister, A. R., Melton, L. J., DiMagno, E. P., Marotta, F., Chui, D. H., Barbi, G., Zhong, G. G., Marotta, F., Chui, D. H., Tajiri, H., Bellini, O., Zhong, G. G., Barbi, G., McKay, C, Baxter, J. N., Imrie, C. W., Mithöfer, K., Fern’andez-delCastillo, C., Frick, T. W., Lewandrowski, K., Rattner, D. W., Warshaw, A. L., Pezzilli, R., Billi, P., Miniero, R., Gullo, L., Barakat, B., Migliuli, M., Rau, B., Schad, M., Schoenberg, M., Beger, H. G., Richter, F., Matthias, R., Sakagami, J, Kataoka, K, Ohta, A, Umehara, K, Imoto, M, Murase, M, Hosoda, M, Yamane, Y, Kato, M, Kashima, K, Ashihara, T, Schofield, D, Sharer, NM, Heywood, KM, Waters, HM, Braganza, JM, Scott, P, Sharer, NM, Bilton, D, Deardon, D, Lee, S, Taylor, PM, McCloy, RF, Braganza, JM, Shen, J., Shao, H., Wu, Z. P., Jin, J. J., Shiel, N, Cassidy, O, Sharma, H, Braganza, J. M., Soöckmann, F., Ahrens, J., Leonhardt, U., Otto, J., Ritzel, U., Ramadori, G., Tian, Fuzhou, Hu, JZ, Huang, DR, Wang, XH, Lian, HW, Zhang, BY, Miao, JG, Li, Xu, Zhou, HT, Uomo, G., Rabitti, P. G., Laccetti, M., Manes, G., Esposico, P., Perrocti, F., Visconci, M., Vaccaro, M. I., Dagrosa, M. A., Mora, M. I., Sordelli, D. O., Vogt, W., MeOmann, H., Heinisch, A., Linseis, A., Holstege, A., Schölmerich, J., Leser, H. -G., Weiser, M. R., Gibbs, S. A. L., Hechcman, H. B., Moore, F. D., Worthington, H. V., Runt, L. P., HcCloy, R. F., KacLennan, I. A., Braqanza, J. M., Heath, D, Alexander, D, Wilson, C, Larvin, M, Imrie, CW, McMahon, MJ, Larvin, M, Ward, J, Robinson, PJ, Chalmers, AG, McMahon, MJ, Apte, M, Wilson, J, McCaughan, G, Korsten, M, Norton, I, Piroia, R, Bimmler, D., Frick, T. W., Scheele, G. A., Bockman, Dale E., Büchler, Markus, Beger, Hans G., Cavallini, G., Brunori, M. P., Rigo, L., Bovo, P., Filippini, M., Vaona, B., Di Francesco, V., Frulloni, L., Marcori, M., Farri, P. C., Laardini, M. T., Pederzoli, P., Chowdhury, Riaz, Ochi, Koji, Mizushima, Takaaki, Tsurumi, Tetsuya, Harada, Hideo, Laver, P., Hoist, J. J., Ohe, M. v. d., Goebell, H., Mi Zumoto, A., Sarr, M. G., DiMagno, E. P., Moore, R., Frey, C. F., Debas, H. T., Mulvihill, S. J., Onizuka, S., Kuroda, H., Kuroda, Y., Hongo, H., Matsuzaki, S., Ito, M., Sekine, L., Tsunoda, T., Pap, ’A., Hrisztov, V., Pap, ’A., Marosi, E., Simon, K., Tak’acs, T., Pederzoli, P., Falconi, M., Bassi, C., Bonora, A., Talamini, G., Saivia, R., Benini, L., Caldiron, E., Vesentini, S., Cavallini, G., Raijman, Isaac, Kortan, Paul, Haber, Gregory B., Ramesh, H, Varghese, CJ, Schofield, D, Kay, PM, Bottiglieri, T, Uden, S, Bilton, D, Braganza, JM, Gut, A, Segal, I, Snehalatha, C, Mohan, V, Braganza, JM, Silva, E., Ceneviva, R., Velludo, M. A. L., Silvan, E., Ruebner, B., Ceneviva, R., Velludo, M. A. L., Roselino, J. E. S., Foss, M. C., Talaraini, G., Falcaoi, M., Frmlltai, L, K Fraacesca, V., Maxwi, M., Vaosa, B., Baro, P., Baxu, C., Pedercoli, P., Cavalliai, G., Taiamini, G., Iacano, C., Faicsai, M., Frulloni, L., Rige, L., Castagnisi, A., Marcori, M., Angelini, G., Bassi, C., Bom, P., Vaoss, B., Vantini, I., Sen, G., Pederzali, P., Cavallini, G., Štimee, B, Bulajič, M, Milosavljevi’c, T, Krsti’c, R, Markovi’c, M, Korneti, V, Ugljcš’c, M, Abruzzesse, IL, Evans, DB, Larry, L, King, T, Raijman, I, Roubein, L, Frazier, M, lacono, C., Faca, E., Falezza, G., Bonora, E., Aurola PP, Serio, G., lacono, C., Nicoli, N., Mansueto, G. C., Zicari, M., Marchiori, L., Mangiante, G., Seno, G., Imarnura, M., Yamauchi, H., Inoue, M., Onda, M., UchlDa, E., Almqtq, T., Yamanaka, Y., Kqbayashi, T., Yokqyama, T., Aida, K., Sasajima, K., Tajiri, T., Egami, K., Yamashita, K., Naitq, Z., Asano, G., Lewandrowski, K. B., Kirby, R. E., Southern, J. F., Compton, C. C., Warshaw, A. L., Lip, J, Strömmer, L, Permert, J, Larsson, J, Adrian, TE, Loftus, E. V., Adkins, M. C., Olivares-Pakzad, B., Batts, K. P., Stephens, D. H., Farnell, M. B., Sarr, H. G., Thompson, G. B., van Heerden, J. A., Kelly, D. G., Miller, L. J., Pearson, R. K., Clain, J. E., Petersen, B. T., DiMagno, E. P., Matsumoto, Cancer S., Chowdhury, R., Mizushima, T., Ochi, K., Harada, H., Miki, H., Ozkan, Hnsan, Saisho, Hiromitsu, Yarnaguchi, Taketo, Ishihara, Takeshi, Kikuchi, Yasuharu, Tsuyuguchi, Toshio, Ohto, Masao, Pasqual, C., Sperti, C., Liesai, G., Guido, M., Pedrazzoli, S., Sperti, C., Pasquali, C., Khajeturian, E., Guolo, P., Pedrazzoli, S., Tadokoro, H., Watanabe, S., Moriyoshi, Y., Yoshida, K., Shiratori, K., Takeuchi, T., Uchida, E., Onda, M., Tajiri, T., Egami, K., Yamashita, K., Aida, K., Yamanaka, Y., Kobayashi, T., Aimoto, T., Yokoyama, T., Inoue, M., Naito, Z., Asano, G., Valentich, M. A., Monis, B., Barotto, N. N., and Herrera, P.

Published
1994
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4. Modeling of the transient mobility in disordered organic semiconductors with a Gaussian density of states.

Author

Germs, W. Chr., van der Hoist, J. J. M., van Mensfoort, S. L. M., Bobbert, P. A., and Coehoorn, R.

Subjects
*SEMICONDUCTORS, *CONDUCTION electrons, *GAUSSIAN distribution, *MONTE Carlo method, *COPOLYMERS
Abstract

The charge-carrier mobility in organic semiconductors is often studied using non-steady-state experiments. However, energetic disorder can severely hamper the analysis due to the occurrence of a strong time dependence of the mobility caused by cartier relaxation. The multiple-trapping model is known to provide an accurate description of this effect. However, the value of the conduction level energy and the hopping attempt rate, which enter the model as free parameters, are not a priori known for a given material. We show how for the case of a Gaussian density of states both parameters can be deduced from the parameter values used to describe the measured dc current-voltage characteristics within the framework of the extended Gaussian disorder model. The approach is validated using three-dimensional Monte Carlo modeling. In the analysis, the charge-density dependence of the time-dependent mobility is included. The model is shown to successfully predict the low-frequency differential capacitance of sandwich-type devices based on a polyfluorene copolymer. [ABSTRACT FROM AUTHOR]

Published
2011
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5. Nutrient-stimulated GLP-2 release and crypt cell proliferation in experimental short bowel syndrome.

Author

Martin, G. R., Wallace, L. E., Hartmann, B., Hoist, J. J., Demchyshyn, L., Toney, K., and Sigalet, D. L.

Subjects
GASTROINTESTINAL hormones, PEPTIDE hormones, GASTROINTESTINAL system, INTESTINAL surgery, SMALL intestine, CELL proliferation
Abstract

Glucagon-like peptide-2 (GLP-2) is an enteroendocrine peptide that is released in response to luminal nutrients and has unique trophic actions in the gastrointestinal tract. These features suggest GLP-2 may be important in controlling intestinal adaptation. We examined the relationship over time of GLP-2 production and adaptation to intestinal resection, the effects of resection-induced malabsorption on GLP-2 production, and the correlation of endogenous serum GLP-2 levels with adaptation as measured by crypt-cell proliferation (CCP). We initially examined the effect of nutrient malabsorption, induced by a 90% resection of the proximal intestine studied on day 4, on the time course and levels of GLP-2 release. Secondly, the degree of malabsorption was varied by performing intestinal transection or 50, 75, or 90% resection of proximal small intestine. Finally, the relationship of GLP-2 levels over time with adaptation to a 90% resection was examined by determining GLP-2 levels on days 7, 14, and 28, and correlating this with intestinal adaptation, as assessed by morphology and CCP rate. A 90% resection significantly increased basal and postprandial GLP-2 levels, with a net increase in nutrient-stimulated exposure over 90 min; GLP-2 exposure (integrated levels vs. time) increased 12.7-fold in resected animals (P < 0.001). Basal and postprandial GLP-2 levels significantly correlated with the magnitude of intestinal resection (r² = 0.71; P < 0.001), CCP (r² = 0.48; P < 0.005), and nutrient malabsorption (protein, P < 0.001; fat, P < 0.005). The increase in CCP was maintained to 28 days after small bowel resection and was associated with an ongoing elevation in GLP-2 release. These findings suggest that GLP-2 is important in initiating and maintaining the small intestinal adaptive response to resection. [ABSTRACT FROM AUTHOR]

Published
2005
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9. Publisher's Note: Modeling of the transient mobility in disordered organic semiconductors with a Gaussian density of states [Phys. Rev. B 84, 165210 (2011)].

Author

Germs, W. Chr., van der Hoist, J. J. M., van Mensfoort, S. L. M., Bobbert, E A., and Coehoonl, R.

Subjects
*ORGANIC semiconductors
Abstract

A correction to the article "Modeling of the Transient Mobility in Disordered Organic Semiconductors With a Gaussian Density of States" that was published in the November 4, 2011 issue is presented.

Published
2011
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10. Tachykinin NK1 receptors mediate atropine-resistant net aboral propulsive complexes in porcine ileum.

Author

Schmidt PT and Hoist JJ

Subjects
Animals, Ileum physiology, In Vitro Techniques, Peristalsis physiology, Receptors, Tachykinin physiology, Substance P physiology, Swine, Atropine pharmacology, Ileum drug effects, Muscarinic Antagonists pharmacology, Peristalsis drug effects, Receptors, Tachykinin antagonists & inhibitors
Abstract

Background: We studied the effects of tachykinin receptor antagonists on fluid-induced, spontaneous net aboral propulsive complexes in isolated, vascularly perfused porcine ileal segments., Methods: Fluid was instilled at a constant rate into the proximal opening of the segment, resulting in regular, rapidly propagating propulsive complexes along the entire ileal segment in the aboral direction., Results: NKI, NK2 or NK3 receptor antagonists (CP99994, SR48968 and SR 142801 all at 10(-6) M) had no effect on the frequency of propulsive complexes. Atropine (10(-6) M) abolished the propulsive complexes for 15.0 +/- 1.3 min (n = 18). In spite of continued atropine infusion, the propulsive complexes reappeared. Infusion of the NK1 receptor antagonist CP99994 (10(-6) M) during continued atropine infusion blocked net aboral propulsive complexes in 5 experiments for 12.2 +/- 2.4 min and resulted in motor paralysis in 2 experiments. SP release, measured in the venous effluent, was significantly increased in relation to propulsive complexes during atropine infusion., Conclusion: We conclude that, in the porcine ileum, tachykinins mediate atropine-resistant net aboral propulsive complexes acting on NKI receptors.

Published
2002
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11. Deficiency of the intestinal growth factor, glucagon-like peptide 2, in the colon of SCID mice with inflammatory bowel disease induced by transplantation of CD4+ T cells.

Author

Schmidt PT, Hartmann B, Bregenholt S, Hoist JJ, and Claesson MH

Subjects
Animals, CD4-Positive T-Lymphocytes, Colon pathology, Disease Models, Animal, Glucagon-Like Peptide 2, Glucagon-Like Peptides, Inflammatory Bowel Diseases etiology, Inflammatory Bowel Diseases pathology, Mice, Mice, SCID, Glucagon deficiency, Growth Substances deficiency, Inflammatory Bowel Diseases metabolism, Peptide Fragments deficiency
Abstract

Background: Glucagon-like peptide 2 (GLP-2) is produced in endocrine L-cells of the intestinal mucosa. Recently, GLP-2 was found to stimulate intestinal mucosal growth. Our objective was to study the content of GLP-2 in the large intestine in a murine model of T-cell-induced inflammatory bowel disease., Methods: Inflammation was induced by adoptive transfer of CD4+ blast T cells from BALB/c mice to SCID mice. The amount of GLP-2 (1-33) was measured with a specific, NH2-terminally directed radioimmunoassay in tissue extracts from the large intestine of transplanted mice developing colitis and from BALB/c and SCID control mice., Results: In the middle and descending colon segments showing the most severe signs of inflammatory lesions in the CD4+ T-cell-transplanted mice, the amount of GLP-2 was significantly lower than in similar colon segments in both untransplanted SCID mice and normal BALB/c mice (P = 0.0013 and 0.0033). In the descending colon the amount of GLP-2 was 6.7 +/- 1.0 pmol/g protein in the CD4+ transplanted mice compared with 68.4 +/- 20.3 and 42.7 +/- 4.3 in the two groups of control mice. Similar findings were made with regard to the contents of the two other proglucagon-derived intestinal peptides, glicentin and GLP-1., Conclusion: The amount of GLP-2 is markedly reduced in the colon of mice with a T-cell-induced inflammatory bowel disease histopathologically resembling both Crohn disease and ulcerative colitis. This observation may provide a pathophysiologic rationale for administration of GLP-2 as a trophic factor in inflammatory bowel disease.

Published
2000
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