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23 results on '"Walsh, S. V."'

1. Synbiotic therapy (bifidobacterium longum/synergy 1) initiates resolution of inflammation in patients with active ulcerative colitis: a randomised controlled pilot trial

Author

Furrie, E, Macfarlane, S, Kennedy, A, Cummings, J H, Walsh, S V, O'Neil D A, and Macfarlane, G T

Subjects
Ulcerative colitis -- Care and treatment, Ulcerative colitis -- Drug therapy, Ulcerative colitis -- Research, Saccharomyces -- Observations, Probiotics -- Analysis, Probiotics -- Research, Lactobacillus -- Analysis, Lactobacillus -- Observations, Escherichia coli -- Observations, Bifidobacterium -- Analysis, Bifidobacterium -- Observations, Antibiotics -- Drug therapy, Antibiotics -- Research, Health
Published
2005

4. Irish Society of Gastroenterology: Proceedings of Winter Meeting held November, 1994 in Dublin

Author

Neelamakam, P. K., Brazil, E., Attwood, S., Traynor, O., Yaqoob, J., Khan, M. I., O’Toole, D., Noonan, N., Carey, C., Kelleher, D., Weir, D. G., Keeling, P. W. N., Monahan, D., Cogan, L., Willoughby, R., Jackson, J., Whelan, A., Weir, D. G., Feighery, C., Kaminski, G. Z., Conroy, A., Dooley, S., Parfrey, N. A., McEneaney, P., O’Morain, C., McGrath, J. P., Stuart, R. C., Hill, J., Byrne, P. J., Timon, C., Chung, S. C. S., VanHasselt, A., Hennessy, T. P. J., Hamilton, D., Mulcahy, D., Walsh, D., Farrely, C., Tormey, W., Fielding, J., Watson, G., Conroy, A., Kaminski, G. Z., Dooley, S., Parfrey, N. A., Khan, M. I., Yaqoob, J., Cherukuri, A., Maloney, M., Toole, D. O., Corcoran, M., Noonan, N., Weir, D. G., Keeling, P. W. N., Coffey, J., Butt, F., McAvinchey, D., Delaney, P. V., Burke, G. J., Feighery, C., Youngprapakorn, S., Srinivasan, U., Willoughby, R., Leonard, N., O’Farrelly, C., Morain, C. O., Weir, D. G., Whelan, C. A., Barry, E., Collins, C., Costello, P., Willoughby, R., Feighery, C., O’Herlihy, C., O’Donoghue, D. P., O’Farrelly, C., Yaqoob, J., Khan, M. I., Corcoran, M., Clabby, C., Toole, D. O., Noonan, N., Kelleher, D., Weir, D. G., Keeling, P. W. N., McCarthy, J., Kenny-Walsh, E., Whelton, M. J., Morrin, M., Khan, F., Delaney, P., O’Keeffe, J., Mills, K., Willoughby, R., Feighery, C., Bennett, M. A., Kay, E. W., Mulcahy, H., O’Donoghue, D. P., Leader, M., Croke, D. T., Yaqoob, J., Fan, X. G., Khan, I., Toole, D. O., Noonan, N., Carey, C., Kelleher, D., Weir, D. G., Keeling, P. W. N., Keating, S., Morrison, C., Buckley, M., O’Morain, C., O’Reilly, F. M., Darby, C., Courtney, M. G., Murphy, G. M., Fielding, J. F., O’Boyle, C. J., Boyle, T. J., Costello, P., Mulhall, K., Kerin, M. J., Courtney, D., Quill, D. S., Given, H. F., Kehoe, S., Boyle, T. J., Quirke, R., Stephens, R. B., Norris, S., Costello, P., Collins, C., Traynor, O., McEntee, G., Hegarty, J., Farrelly, C., Thottaparambil, D., Thomas, R., Houghton, G., Sachithanandan, S., Geoghegan, A., Leader, M., Doyle, S., McGrath, J. P., McCaul, C., Byrne, P. J., Walsh, T. N., Hennessy, T. P. J., Khan, M. I., Yaqoob, J., Farrell, R., Gusau, B., Toole, D. O., Carey, C., Noonan, N., Kelleher, D., Keeling, P. W. N., Courtney, M. G., O’Mahoney, M. S., AlBloushi, S., Sachithanandan, J., Walshe, J., Carmody, M., Donohoe, J., Shattock, A. G., Parfrey, N., Fielding, J. F., Collins, C., Lynch, S., Madrigal, L., Norris, S., McEntee, J., Traynor, O., Hegarty, J., O’Farrelly, C., Khan, M. I., Yaqoob, J., Murphy, R., Ahmed, Z., Ryan, M., Montwill, C., Morgan, A., Smith, P., Walker, F., Murphy, A., Moloney, M., McGrath, S., Kelleher, D., Taraneweh, E., Bhatia, A. K., O’Keeffe, D., McCarthy, P., Rajan, E., Albloushi, S., Farrell, B. O’, Shattock, A., Courtney, M. G., Fielding, J. F., Buckley, M., Kearney, D., Lee, J., Gleeson, F., Khan, M. I., Yaqoob, J., Murphy, R., Ahmed, Z., Montwill, C., Ryan, M., Morgan, A., Smith, P., Walker, F., McNamara, B., Cuffe, J., O’Sullivan, G. C., Harvey, B. J., Curran, B., Bennett, M. A., Croke, D. T., Mulcahy, H., Kay, E., Leader, M., O’Donoghue, D. P., Yaqoob, J., Khan, M. I., Corcoran, M., Clabby, C., O’Toole, D., Noonan, N., Weir, D. G., Keeling, P. W. N., Lawler, L., Attwood, S. E. A., Bourke, G., Hyland, J., Owens, W. A., Loughrey, C. M., McAleer, J. A., McManus, K. G., Dillon, J. F., Wong, F. C., Lo, T. C. N., Chan, K. H., Plevris, J. N., Finlayson, N. D. C., Miller, J. D., Bouchier, I. A. D., Hayes, P. C., Walsh, S. V., Egan, L. J., Connolly, C. E., Stevens, F. M., Egan, E. L., McCarthy, C. F., Ma, Q. Y., Magee, G. D., Ardill, J. E., Buchanan, K. D., Rowlands, B. J., McGettigan, P., Chan, R., Shea, B. O’, McManus, J., Feely, J., Donoghue, J., Fanning, N., Mathias, J., Gillen, P., Tanner, W. A., Keane, F. B. V., Campbell, D. M., Donnelly, V., O’Connell, D., Behan, M., O’Herlihy, C., O’Connell, P. R., Ko, C. S., Mealy, K., Walsh, T. N., Hennessy, T. P. J., Gusau, B. M., O’Toole, D., Farrell, R., Noonan, N., Maloney, M., Goggins, M., Yakoub, J., Keeling, P. W. N., Farrell, R. J., Goggins, M., Kelleher, D., Weir, D. G., Keeling, P. W. N., Mahmud, N., Weir, D. G., and Kelleher, D.

Published
1995
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5. The Yeast Genome Directory

Author

Goffeau, A., Aert, R., Agostini-Carbone, M. L., Ahmed, A., Aigle, M., Alberghina, L., Albermann, K., Albers, M., Aldea, M., Alexandraki, D., Aljinovic, G., Allen, E., Alt-Mörbe, J., André, B., Andrews, S., Ansorge, W., Antoine, G., Anwar, R., Aparicio, A., Araujo, R., Arino, J., Arnold, F., Arroyo, J., Aviles, E., Backes, U., Baclet, M. C., Badcock, K., Bahr, A., Baladron, V., Ballesta, J. P. G., Bankier, A. T., Banrevi, A., Bargues, M., Baron, L., Barreiros, T., Barrell, B. G., Barthe, C., Barton, A. B., Baur, A., Bécam, A.-M., Becker, A., Becker, I., Beinhauer, J., Benes, V., Benit, P., Berben, G., Bergantino, E., Bergez, P., Berno, A., Bertani, I., Biteau, N., Bjourson, A. J., Blöcker, H., Blugeon, C., Bohn, C., Boles, E., Bolle, P. A., Bolotin-Fukuhara, M., Bordonné, R., Boskovic, J., Bossier, P., Botstein, D., Bou, G., Bowman, S., Boyer, J., Brandt, P., Brandt, T., Brendel, M., Brennan, T., Brinkman, R., Brown, A., Brown, A. J. P., Brown, D., Brückner, M., Bruschi, C. V., Buhler, J. M., Buitrago, M. J., Bussereau, F., Bussey, H., Camasses, A., Carcano, C., Carignani, G., Carpenter, J., Casamayor, A., Casas, C., Castagnoli, L., Cederberg, H., Cerdan, E., Chalwatzis, N., Chanet, R., Chen, E., Chéret, G., Cherry, J. M., Chillingworth, T., Christiansen, C., Chuat, J.-C., Chung, E., Churcher, C., Churcher, C. M., Clark, M. W., Clemente, M. L., Coblenz, A., Coglievina, M., Coissac, E., Colleaux, L., Connor, R., Contreras, R., Cooper, J., Copsey, T., Coster, F., Coster, R., Couch, J., Crouzet, M., Cziepluch, C., Daignan-Fornier, B., Dal Paro, F., Dang, D. V., D’Angelo, M., Davies, C. J., Davis, K., Davis, R. W., De Antoni, A., Dear, S., Dedman, K., Defoor, E., De Haan, M., Delaveau, Th., Del Bino, S., Delgado, M., Delius, H., Delneri, D., Del Rey, F., Demolder, J., Démolis, N., Devlin, K., de Wergifosse, P., Dietrich, F. S., Ding, H., Dion, C., Dipaolo, T., Doignon, F., Doira, C., Domdey, H., Dover, J., Du, Z., Dubois, E., Dujon, B., Duncan, M., Durand, P., Düsterhöft, A., Düsterhus, S., Eki, T., El Bakkoury, M., Eide, L. G., Entian, K.-D., Eraso, P., Erdmann, D., Erfle, H., Escribano, V., Esteban, M., Fabiani, L., Fabre, F., Fairhead, C., Fartmann, B., Favello, A., Faye, G., Feldmann, H., Fernandes, L., Feroli, F., Feuermann, M., Fiedler, T., Fiers, W., Fleig, U. N., Flöth, M., Fobo, G. M., Fortin, N., Foury, F., Francingues-Gaillard, M. C., Franco, L., Fraser, A., Friesen, J.D., Fritz, C., Frontali, L., Fukuhara, H., Fulton, L., Fuller, L. J., Gabel, C., Gaillardin, C., Gaillon, L., Galibert, F., Galisson, F., Galland, P., Gamo, F.-J., Gancedo, C., Garcia-Cantalejo, J. M., García-Gonzalez, M. I., Garcia-Ramirez, J. J., García-Saéz, M., Gassenhuber, H., Gatius, M., Gattung, S., Geisel, C., Gent, M. E., Gentles, S., Ghazvini, M., Gigot, D., Gilliquet, V., Glansdorff, N., Gómez-Peris, A., Gonzaléz, A., Goulding, S. E., Granotier, C., Greco, T., Grenson, M., Grisanti, P., Grivell, L. A., Grothues, D., Gueldener, U., Guerreiro, P., Guzman, E., Haasemann, M., Habbig, B., Hagiwara, H., Hall, J., Hallsworth, K., Hamlin, N., Hand, N. J., Hanemann, V., Hani, J., Hankeln, T., Hansen, M., Harris, D., Harris, D. E., Hartzell, G., Hatat, D., Hattenhorst, U., Hawkins, J., Hebling, U., Hegemann, J., Hein, C., Hennemann, A., Hennessy, K., Herbert, C. J., Hernandez, K., Hernando, Y., Herrero, E., Heumann, K., Heuss- Neitzel, D., Hewitt, N., Hiesel, R., Hilbert, H., Hilger, F., Hillier, L., Ho, C., Hoenicka, J., Hofmann, B., Hoheisel, J., Hohmann, S., Hollenberg, C. P., Holmstrøm, K., Horaitis, O., Horsnell, T. S., Huang, M.-E., Hughes, B., Hunicke-Smith, S., Hunt, S., Hunt, S. E., Huse, K., Hyman, R. W., Iborra, F., Indge, K. J., Iraqui Houssaini, I., Isono, K., Jacq, C., Jacquet, M., Jacquier, A., Jagels, K., Jäger, W., James, C. M., Jauniaux, J. C., Jia, Y., Jier, M., Jimenez, A., Johnson, D., Johnston, L., Johnston, M., Jones, M., Jonniaux, J.-L., Kaback, D. B., Kallesøe, T., Kalman, S., Kalogeropoulos, A., Karpfinger-Hartl, L., Kashkari, D., Katsoulou, C., Kayser, A., Kelly, A., Keng, T., Keuchel, H., Kiesau, P., Kirchrath, L., Kirsten, J., Kleine, K., Kleinhans, U., Klima, R., Komp, C., Kordes, E., Korol, S., Kötter, P., Krämer, C., Kramer, B., Kreisl, P., Kucaba, T., Kuester, H., Kurdi, O., Laamanen, P., Lafuente, M. J., Landt, O., Lanfranchi, G., Langston, Y., Lashkari, D., Latreille, P., Lauquin, G., Le, T., Legrain, P., Legros, Y., Lepingle, A., Lesveque, H., Leuther, H., Lew, H., Lewis, C., Li, Z. Y., Liebl, S., Lin, A., Lin, D., Logghe, M., Lohan, A. J. E., Louis, E. J., Lucchini, G., Lutzenkirchen, K., Lyck, R., Lye, G., Maarse, A. C., Maat, M. J., Macri, C., Madania, A., Maftahi, M., Maia e Silva, A., Maillier, E., Mallet, L., Mannhaupt, G., Manus, V., Marathe, R., Marck, C., Marconi, A., Mardis, E., Martegani, E., Martin, R., Mathieu, A., Maurer, C. T. C., Mazón, M. J., Mazzoni, C., McConnell, D., McDonald, S., McKee, R. A., McReynolds, A. D. K., Melchioretto, P., Menezes, S., Messenguy, F., Mewes, H. W., Michaux, G., Miller, N., Minenkova, O., Miosga, T., Mirtipati, S., Möller-Rieker, S., Möstl, D., Molemans, F., Monnet, A., Monnier, A-L., Montague, M. A., Moro, M., Mosedale, D., Möstl, D., Moule, S., Mouser, L., Murakami, Y., Müller-Auer, S., Mulligan, J., Murphy, L., Muzi Falconi, M., Naitou, M., Nakahara, K., Namath, A., Nasr, F., Navas, L., Nawrocki, A., Nelson, J., Nentwich, U., Netter, P., Neu, R., Newlon, C. S., Nhan, M., Nicaud, J.-M., Niedenthal, R. K., Nombela, C., Noone, D., Norgren, R., Nußbaumer, B., Obermaier, B., Odell, C., Öfner, P., Oh, C., Oliver, K., Oliver, S. G., Ouellette, B. F., Ozawa, M., Paces, V., Pallier, C., Pandolfo, D., Panzeri, L., Paoluzi, S., Parle-Mcdermott, A. G., Pascolo, S., Patricio, N., Pauley, A., Paulin, L., Pearson, B. M., Pearson, D., Peluso, D., Perea, J., Pérez-Alonso, M., Pérez-Ortin, J. E., Perrin, A., Petel, F. X., Pettersson, B., Pfeiffer, F., Philippsen, P., Piérard, A., Piravandi, E., Planta, R. J., Plevani, P., Poch, O., Poetsch, B., Pohl, F. M., Pohl, T. M., Pöhlmann, R., Poirey, R., Portetelle, D., Portillo, F., Potier, S., Proft, M., Prydz, H., Pujol, A., Purnelle, B., Puzos, V., Rajandream, M. A., Ramezani Rad, M., Rasmussen, S. W., Raynal, A., Rechmann, S., Remacha, M., Revuelta, J. L., Rice, P., Richard, G-F., Richterich, P., Rieger, M., Rifken, L., Riles, L., Rinaldi, T., Rinke, M., Roberts, A. B., Roberts, D., Rodriguez, F., Rodriguez-Belmonte, E., Rodriguez-Pousada, C., Rodriguez-Torres, A. M., Rose, M., Rossau, R., Rowley, N., Rupp, T., Ruzzi, M., Saeger, W., Saiz, J. E., Saliola, M., Salom, D., Saluz, H. P., Sánchez-Perez, M., Santos, M. A., Sanz, E., Sanz, J. E., Saren, A.-M., Sartorello, F., Sasanuma, M., Sasanuma, S-I., Scarcez, T., Schaaf-Gerstenschläger, I., Schäfer, B., Schäfer, M., Scharfe, M., Scherens, B., Schroff, N., Sen-Gupta, M., Shibata, T., Schmidheini, T., Schmidt, E. R., Schneider, C., Scholler, P., Schramm, S., Schreer, A., Schröder, M., Schwager, C., Schwarz, S., Schwarzlose, C., Schweitzer, B., Schweizer, M., Sdicu, A-M., Sehl, P., Sensen, C., Sgouros, J. G., Shogren, T., Shore, L., Shu, Y., Skala, J., Skelton, J., Slonimski, P. P., Smit, P. H. M., Smith, V., Soares, H., Soeda, E., Soler-Mira, A., Sor, F., Soriano, N., Souciet, J. L., Soustelle, C., Spiegelberg, R., Stateva, L. I., Steensma, H. Y., Stegemann, J., Steiner, S., Stellyes, L., Sterky, F., Storms, R. K., St. Peter, H., Stucka, R., Taich, A., Talla, E., Tarassov, I., Tashiro, H., Taylor, P., Teodoru, C., Tettelin, H., Thierry, A., Thireos, G., Tobiasch, E., Tovan, D., Trevaskis, E., Tsuchiya, Y., Tzermia, M., Uhlen, M., Underwood, A., Unseld, M., Urbanus, J. H. M., Urrestarazu, A., Ushinsky, S., Valens, M., Valle, G., Van Broekhoven, A., Vandenbol, M., Van Der Aart, Q. J. M., Van Der Linden, C. G., Van Dyck, L., Vanoni, M., Van Vliet-Reedijk, J. C., Vassarotti, A., Vaudin, M., Vaughan, K., Verhasselt, P., Vetter, I., Vierendeels, F., Vignati, D., Vilela, C., Vissers, S., Vleck, C., Vo, D. T., Vo, D. H., Voet, M., Volckaert, G., Von Wettstein, D., Voss, H., Vreken, P., Wagner, G., Walsh, S. V., Wambutt, R., Wang, H., Wang, Y., Warmington, J. R., Waterston, R., Watson, M. D., Weber, N., Wedler, E., Wedler, H., Wei, Y., Whitehead, S., Wicksteed, B. L., Wiemann, S., Wilcox, L., Wilson, C., Wilson, R., Winant, A., Winnett, E., Winsor, B., Wipfli, P., Wölfl, S., Wohldman, P., Wolf, K., Wolfe, K. H., Wright, L. F., Wurst, H., Xu, G., Yamasaki, M., Yelton, M. A., Yokohama, K., Yoshikawa, A., Yuping, S., Zaccaria, P., Zagulski, M., Zimmermann, F. K., Zimmermann, J., Zimmermann, M., Zhong, W-W., Zollner, A., and Zumstein, E.

Published
1997
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9. Synbiotic therapy (Bifidobacterium Iongum/Synergy 1) initiates resolution of inflammation in patients with active ulcerative colitis: a randomised controlled pilot trial.

Author

Furrie, E., Macfarlane, S., Kennedy, A., Cummings, J. H., Walsh, S. V., O'neil, D. A., and Macfarlane, G. T.

Subjects
INFLAMMATORY bowel diseases, ULCERATIVE colitis, INFLAMMATION, CYTOKINES, MUCOUS membranes, COLONOSCOPY
Abstract

Background and aims: Ulcerative colitis (UC) is an acute and chronic inflammatory disease of the large bowel with unknown aetiology. The immune response against normal commensal microorganisms is believed to drive inflammatory processes associated with UC. Therefore, modulation of bacterial communities on the gut mucosa, through the use of probiotics and prebiotics, may be used to modify the disease state. Methods: A synbiotic was developed for use in UC patients combining a probiotic, Bifidobacterium longum, isolated from healthy rectal epithelium, and a prebiotic (Synergy 1), a preferential immunoligofructose growth substrate for the probiotic strain. Treatment was employed in a double blinded randomised controlled trial using 18 patients with active UC for a period of one month. Clinical status was scored and rectal biopsies were collected before and after treatment, and transcription levels of epithelium related immune markers were measured. Results: Sigmoidoscopy scores (scale 0-6) were reduced in the test group (start 4.5 (1.4), end 3.1 (2.5)) compared with placebo (start 2.6 (2.1), end 3.2 (2.2)) (p = 0.06). mRNA levels for human beta defensins 2, 3, and 4, which are strongly upregulated in active UC, were significantly reduced in the test group after treatment (p = 0.016, 0.038, and 0.008, respectively). Tumour necrosis factor a and interleukin 1 a, which are inflammatory cytokines that drive inflammation and induce defensin expression, were also significantly reduced after treatment (p =0.018 and 0.023, respectively). Biopsies in the test group had reduced inflammation and regeneration of epithelial tissue. Conclusions: Short term synbiotic treatment of active UC resulted in improvement of the full clinical appearance of chronic inflammation in patients receiving this therapy. [ABSTRACT FROM AUTHOR]

Published
2005
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13. BARRETT'S OESOPHAGUS IN YOUNG ADULTS: NO INCREASE IN THE PUTATIVE BARRETT'S PRECURSOR, "MULTILAYERED EPITHELIUM"; RAISED LAMINA PROPRIA EOSINOPHILS IDENTIFIED.

Author

Tiam, R., Abouda, G., Dillon, J., and Walsh, S. V.

Subjects
ESOPHAGUS diseases, YOUNG adults, CHILDREN, EPITHELIUM, MUCOUS membranes, INFLAMMATION
Abstract

The article presents a study on Barrett's oesophagus in young adults. Barrett's oesophagus may occur in children and young adults. "Multilayered epithelium" (ME) has been recently described as a precursor to Barrett's oesophagus, however, it has not been studied in young adults. In addition, little attention has been paid to inflammatory cells of Barrett's mucosa in this group. In this study, ME was rarely identified in either patient groups and no difference in the prevalence of ME was identified between younger and older patients. Therefore, the role of ME as a precursor lesion must remain uncertain.

Published
2004

14. Groove pancreatitis: a case series and review of the literature.

Author

Latham J, Sanjay P, Watt DG, Walsh SV, and Tait IS

Subjects
Alcohol Drinking, Humans, Male, Middle Aged, Pancreaticoduodenectomy, Pancreatitis, Chronic diagnostic imaging, Pancreatitis, Chronic pathology, Pancreatitis, Chronic surgery, Radiography, Pancreatitis, Chronic diagnosis
Abstract

Introduction: Groove pancreatitis is a form of chronic pancreatitis affecting the space surrounded by the pancreatic head, duodenum and common bile duct. The clinical findings can conflict with pancreatic cancer causing diagnostic dilemma preoperatively., Case Series: We describe two patients with a history of alcohol excess, who presented with a few months history of upper abdominal pain associated with weight loss and vomiting. Endoscopic and radiological investigations related duodenal narrowing, biliary dilatation and multiple pseudocysts around the head of the pancreas and duodenum. A Whipple's pancreaticoduodenectomy was carried out in both patients. Histopathology report demonstrated cystic areas in both medial and lateral walls of the duodenum microscopically consistent with groove pancreatitis., Conclusion: The diagnosis of groove pancreatitis should be considered in patients with duodenal stenosis and cystic lesions around the head of the pancreas associated with history of alcohol excess. Differentiation from pancreatic cancer is difficult preoperatively.

Published
2013
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15. Neutrophil transmigration in inflammatory bowel disease is associated with differential expression of epithelial intercellular junction proteins.

Author

Kucharzik T, Walsh SV, Chen J, Parkos CA, and Nusrat A

Subjects
Adherens Junctions metabolism, Adherens Junctions pathology, Cadherins metabolism, Cell Adhesion Molecules metabolism, Chronic Disease, Claudin-1, Cytoskeletal Proteins metabolism, Down-Regulation, Epithelial Cells metabolism, Epithelial Cells pathology, Epithelium metabolism, Gene Expression Regulation, Humans, Immunoblotting, Inflammatory Bowel Diseases genetics, Inflammatory Bowel Diseases metabolism, Intercellular Junctions metabolism, Intestinal Mucosa metabolism, Intestinal Mucosa pathology, Junctional Adhesion Molecules, Membrane Proteins genetics, Membrane Proteins metabolism, Neutrophil Infiltration, Occludin, Phosphoproteins metabolism, Proteins genetics, RNA genetics, RNA metabolism, Tight Junctions metabolism, Tight Junctions pathology, Zonula Occludens-1 Protein, beta Catenin, Epithelium pathology, Inflammatory Bowel Diseases pathology, Intercellular Junctions pathology, Neutrophils pathology, Proteins metabolism, Trans-Activators
Abstract

Inflammatory bowel disease (IBD) consisting of ulcerative colitis (UC) and Crohn's (CD) typically displays a waxing and waning course punctuated by disease flares that are characterized by transepithelial migration of neutrophils (PMN) and altered barrier function. Since epithelial barrier function is primarily regulated by the apical most intercellular junction referred to as the tight junction (TJ), our aim was to examine expression of TJ and adherens junction (AJ) proteins in relation to PMN infiltration in mucosal tissue samples from patients with active IBD. Expression of epithelial intercellular TJ proteins (occludin, ZO-1, claudin-1, and JAM) and subjacent AJ (beta-catenin and E-cadherin) proteins were examined by immunoflourescence/confocal microscopy, immunohistochemistry, and Western blotting. Colonic mucosa from patients with UC revealed dramatic, global down-regulation of the key TJ transmembrane protein occludin in regions of actively transmigrating PMN and in quiescent areas in the biopsy samples. Significant decreases in occludin expression were observed at the protein and mRNA levels by Western and Northern blotting. In contrast, expression of other TJ and AJ proteins such as ZO-1, claudin-1, JAM, beta-catenin, and E-cadherin were down-regulated only in epithelial cells immediately adjacent to transmigrating PMN. Analysis of inflamed mucosa from Crohn's disease patients mirrored the results obtained with UC patients. No change in TJ and AJ protein expression was observed in colonic epithelium from patients with collagenous colitis or lymphocytic colitis that are respectively characterized by a thickened subepithelial collagen plate and increased intraepithelial lymphocytes. These results suggest that occludin expression is diminished in IBD by mechanisms distinct from those regulating expression of other intercellular junction proteins. We speculate that down-regulation of epithelial occludin may play a role in enhanced paracellular permeability and PMN transmigration that is observed in active inflammatory bowel disease.

Published
2001
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16. Rho kinase regulates tight junction function and is necessary for tight junction assembly in polarized intestinal epithelia.

Author

Walsh SV, Hopkins AM, Chen J, Narumiya S, Parkos CA, and Nusrat A

Subjects
Actins metabolism, Adherens Junctions chemistry, Adherens Junctions enzymology, Amides pharmacology, Caco-2 Cells, Cadherins analysis, Cell Membrane Permeability physiology, Cell Polarity physiology, Cells, Cultured, Detergents, Electrophysiology, Enzyme Inhibitors pharmacology, Epithelial Cells enzymology, Epithelial Cells ultrastructure, Humans, Intestinal Absorption physiology, Intracellular Signaling Peptides and Proteins, Membrane Proteins analysis, Mutagenesis physiology, Occludin, Octoxynol, Phosphoproteins analysis, Protein Serine-Threonine Kinases antagonists & inhibitors, Protein Serine-Threonine Kinases genetics, Pyridines pharmacology, Solubility, Tight Junctions chemistry, Transfection, Zonula Occludens-1 Protein, rho-Associated Kinases, Intestinal Mucosa cytology, Intestinal Mucosa enzymology, Protein Serine-Threonine Kinases metabolism, Tight Junctions enzymology
Abstract

Background & Aims: Tight junctions are crucial determinants of barrier function in polarized intestinal epithelia and are regulated by Rho guanosine triphosphatase. Rho kinase (ROCK) is a downstream effector of Rho., Methods: A specific inhibitor of ROCK, Y-27632, was used to examine the role of ROCK in the regulation of tight junctions in model intestinal (T84) cells by electrophysiologic, biochemical, morphologic, and molecular biologic approaches., Results: ROCK inhibition induced reorganization of apical F-actin structures and enhanced paracellular permeability but did not alter the distribution or detergent solubility of tight junction proteins. Confocal microscopy showed colocalization of a subpool of ROCK with the tight junction protein zonula occludens 1. Inhibition of ROCK function by a dominant negative mutant of ROCK also produced reorganization of apical F-actin structures without disruption of tight junctions. ROCK inhibition in calcium switch assays showed that ROCK is necessary for the assembly of tight and adherens junctions. Upon calcium repletion, occludin, zonula occludens 1, and E-cadherin failed to redistribute to the intercellular junctions; assembly of the apical F-actin cytoskeleton was prevented; and barrier function failed to recover., Conclusions: We suggest that ROCK regulates intact tight junctions via its effects on the F-actin cytoskeleton. ROCK is also critical for assembly of the apical junctional proteins and the F-actin cytoskeleton organization during junctional formation.

Published
2001
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17. P53 and beta catenin expression in chronic ulcerative colitis--associated polypoid dysplasia and sporadic adenomas: an immunohistochemical study.

Author

Walsh SV, Loda M, Torres CM, Antonioli D, and Odze RD

Subjects
Adenoma surgery, Adenomatous Polyposis Coli pathology, Adult, Aged, Aged, 80 and over, Chronic Disease, Colitis, Ulcerative surgery, Colonic Neoplasms chemistry, Colonic Neoplasms surgery, Colonic Polyps chemistry, Colonic Polyps surgery, Female, Humans, Immunohistochemistry, Male, Middle Aged, beta Catenin, Adenoma pathology, Colitis, Ulcerative pathology, Colonic Neoplasms pathology, Colonic Polyps pathology, Cytoskeletal Proteins analysis, Gene Expression Regulation, Neoplastic, Trans-Activators, Tumor Suppressor Protein p53 analysis
Abstract

In patients with chronic ulcerative colitis (CUC), polypoid dysplastic lesions (PDLs) are morphologically similar to sporadic adenomas (SAs), but may be biologically distinct from them and are managed differently. p53 mutations have been shown to occur at an earlier phase in the progression of CUC-associated neoplasia when compared with sporadic colon carcinogenesis. In contrast, APC gene mutations are common and occur at an earlier stage in the development of SA. beta catenin is a cell membrane protein that accumulates in the nucleus of colon cancer cells in response to APC gene mutations. This study was performed to test the hypothesis that CUC-associated PDLs have a different molecular profile than do CUC-associated SAs and therefore may be distinguished on this basis. Mucosal biopsy specimens of 38 benign polypoid epithelial neoplasms (17 CUC-associated PDLs and 21 CUC-associated SAs) from 33 patients with CUC and 13 SAs from patients without CUC (controls) were immunohistochemically stained for p53 and beta catenin and graded as follows: 0 = no staining, 1+ = <50% of cells positive, and 2+ = > or =50% of cells positive. The results were correlated with the clinical and histologic features and compared between the two CUC-associated polyp subgroups. Overall, six (16%) polyps were p53-positive, of which five were CUC-associated PDLs (one 1+ and four 2+) and one was a CUC-associated SA (1+) (p = 0.05). Strong (2+) p53 positivity was detected, however, in only CUC-associated PDLs (4 of 5; 80%). Nine of 32 polyps evaluated for beta catenin were positive and included 1 (8%) of 12 CUC-associated PDLs and 8 (40%) of 20 CUC-associated SAs (p = 0.06). Two of the nine beta catenin polyps were strongly positive, and both were CUC-associated SAs. Non-CUC-associated (control) SAs were positive for p53 and beta catenin in 2 (15%) of 13 and 6 (46%) of 13 cases, but none in a strong (2+) fashion. No differences were observed in p53 or beta catenin staining, between CUC-associated and non-CUC-associated SAs. Neither p53 nor beta catenin expression correlated with any clinical or pathologic features, including size and degree of dysplasia of the polyps. CUC-associated PDLs and CUC-associated SAs may have a different molecular genotype. In patients with CUC, the combination of strong p53 expression and absent or weak beta catenin expression is evidence in favor of a CUC-associated PDL in diagnostically difficult lesions. Furthermore, CUC-associated and non-CUC-associated SAs have a similar P53 and beta catenin immunophenotype and thus provide evidence that they are pathogenetically related neoplasms regardless of the presence or absence of colitis.

Published
1999
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18. Allergic esophagitis in children: a clinicopathological entity.

Author

Walsh SV, Antonioli DA, Goldman H, Fox VL, Bousvaros A, Leichtner AM, and Furuta GT

Subjects
Child, Child, Preschool, Eosinophilia immunology, Eosinophilia pathology, Eosinophilia therapy, Eosinophils pathology, Esophagitis immunology, Esophagitis therapy, Esophagus metabolism, Esophagus pathology, Female, Gastroesophageal Reflux immunology, Gastroesophageal Reflux pathology, Gastroesophageal Reflux therapy, Humans, Hydrogen-Ion Concentration, Hypersensitivity immunology, Hypersensitivity therapy, Male, Monitoring, Physiologic, Retrospective Studies, Esophagitis pathology, Hypersensitivity pathology
Abstract

Infiltration of esophageal epithelium by eosinophils is seen in reflux esophagitis and allergic gastroenteritis. This study was performed to identify differences between patients with acid reflux esophagitis and those with non-acid reflux, possibly allergic, esophagitis. Intraepithelial eosinophils were demonstrated in posttherapy esophageal biopsy specimens in 28 children treated for gastroesophageal reflux disease (GERD). These patients were divided into three groups based on their response to treatment and the results of esophageal pH probe monitoring. Eleven patients (Group A) had incomplete clinical response and normal pH probe monitoring results. Ten patients (Group B) had incomplete response but did not have pH probe monitoring. These two groups formed the index population. Seven patients (Group C) had clinical improvement with GERD therapy and abnormal pH probe monitoring characteristic of GERD; they constituted the control population. Clinical, laboratory, and pathologic features were evaluated to detect differences between index and control populations. Dysphagia, food impaction, failure to thrive, peripheral eosinophilia, and abnormal allergen skin test results were detected only in Group A and B patients. Biopsy specimens of the distal 9 cm of the esophagus, after GERD therapy, contained larger numbers of eosinophils in Groups A and B than in Group C as shown on high-power fields (HPF) (A: 31/HPF +/- 19.5; B: 28/HPF +/-23.7; versus C: 5/HPF +/-6.7; p = 0.009). Eosinophil aggregates were identified only in Groups A and B (p = 0.07). Eosinophils located preferentially in the superficial layers of the squamous epithelium were noted only in Groups A and B (p = 0.02). Group A and B patients demonstrated clinical improvement when given antiallergic therapy. The authors identified a group of pediatric patients characterized by an allergic history, lack of adequate response to GERD therapy, normal esophageal pH probe monitoring results, and large numbers of eosinophils in esophageal biopsy specimens obtained after GERD treatment. On the basis of these features, the authors propose that these patients represent examples of allergic esophagitis.

Published
1999
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19. Protothecosis: an unusual cause of chronic subcutaneous and soft tissue infection.

Author

Walsh SV, Johnson RA, and Tahan SR

Subjects
Chronic Disease, Female, Humans, Male, Middle Aged, Soft Tissue Infections complications, Soft Tissue Infections microbiology, Soft Tissue Infections pathology, Prototheca isolation & purification, Skin Diseases, Infectious complications, Skin Diseases, Infectious microbiology, Skin Diseases, Infectious pathology
Abstract

Protothecosis of subcutaneous and soft tissues is a rare occurrence in humans. We present two patients with chronic subcutaneous protothecosis affecting the elbow and foot respectively. Both patients had been treated with local corticosteroid injections and had recent exposure to water. The diagnosis was made histopathologically in both cases and confirmed by culture in one case. Histopathology showed typical Protothecal sporangia with surrounding mixed inflammatory infiltrate including necrotizing granulomas. Organisms stained positively with periodic acid-schiff, Gomori's methenamine silver, and Gridley fungus stains. In one case, intravenous chemotherapy was required to eliminate the pathogens. Histopathologic identification of the organisms is vital to ensure adequate therapy and avoid chronic smoldering infection.

Published
1998
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20. Inflammatory myofibroblastic tumor of the pancreaticobiliary region: morphologic and immunocytochemical study of three cases.

Author

Walsh SV, Evangelista F, and Khettry U

Subjects
Actins analysis, Adult, Aged, Bile Duct Diseases metabolism, Bile Duct Diseases virology, Biomarkers analysis, Diagnosis, Differential, Fatal Outcome, Female, Granuloma, Plasma Cell metabolism, Granuloma, Plasma Cell virology, Herpesvirus 4, Human isolation & purification, Humans, Immunohistochemistry, In Situ Hybridization, Lung Diseases pathology, Male, Middle Aged, Pancreatic Diseases metabolism, Pancreatic Diseases virology, RNA, Viral analysis, Bile Duct Diseases pathology, Granuloma, Plasma Cell pathology, Liver Diseases pathology, Pancreatic Diseases pathology
Abstract

Inflammatory myofibroblastic tumor (IMT) is a rare tumor of the pancreaticobiliary region. The etiology and biologic behavior of IMTs at this site are unknown. We present three patients with IMT of the pancreaticobiliary region, each with long-term follow-up. In all three cases a second tumor developed. Grossly these tumors mimicked a malignant process. Microscopically, all were composed of an admixture of spindle cells and chronic inflammatory cells, including plasma cells, lymphocytes, eosinophils, and macrophages. The spindle cells stained positively for smooth muscle actin and vimentin but were negative for S-100, cytokeratin, CD35, and latent membrane protein. Results of in situ hybridization with EBER probes were negative in all cases. In addition to carcinoma, the differential diagnosis of these tumors includes follicular dendritic cell tumor and inflammatory fibrosarcoma. The importance of extensive pathologic examination to prevent misdiagnosis and the need for long-term follow-up are emphasized. This subset of IMT does not appear to be related to Epstein-Barr virus.

Published
1998
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21. Massive thymic hemorrhage in a neonate: an entity revisited.

Author

Walsh SV, Cooke R, Mortimer G, and Loftus BG

Subjects
Anemia, Neonatal etiology, Erythroblastosis, Fetal complications, Fatal Outcome, Fetal Distress complications, Humans, Infant, Newborn, Lymphatic Diseases etiology, Male, Respiratory Distress Syndrome, Newborn etiology, Hemorrhage etiology, Thymus Gland
Abstract

The authors describe a case of early neonatal death of a full-term infant who had respiratory distress and anemia after fetal distress during labor. Postmortem examination disclosed mediastinal compression by a large fresh hemorrhage into the left lobe of the thymus. Massive thymic hemorrhage is an extremely rare but sometimes lethal occurrence; it may represent a manifestation of early-onset hemorrhagic disease of the newborn.

Published
1996
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22. Enteropathy-associated T-cell lymphoma in the West of Ireland: low-frequency of Epstein-Barr virus in these tumors.

Author

Walsh SV, Egan LJ, Connolly CE, Stevens FM, Egan EL, and McCarthy CF

Subjects
Antigens, CD analysis, Cell Nucleus chemistry, Cytoplasm chemistry, Gastrointestinal Neoplasms epidemiology, Gastrointestinal Neoplasms pathology, Herpesvirus 4, Human genetics, Humans, Immunophenotyping, In Situ Hybridization, Ireland, Ki-1 Antigen analysis, Lymphoma, T-Cell epidemiology, RNA, Viral analysis, RNA, Viral genetics, Retrospective Studies, Viral Matrix Proteins analysis, Celiac Disease complications, Gastrointestinal Neoplasms virology, Herpesvirus 4, Human isolation & purification, Lymphoma, T-Cell virology
Abstract

The Epstein-Barr virus has been implicated in the etiology of endemic Burkitt's lymphoma, post-transplant lymphoma, large-cell anaplastic CD30 (Ki-1)-positive lymphoma, and in many T-cell lymphomas. A recent report has found Epstein-Barr virus genome in association with 4 of 11 cases (36%) of enteropathy-associated T-cell lymphoma. In a retrospective study, we have characterized 22 consecutive cases of enteropathy-associated T-cell lymphoma from the West of Ireland where celiac disease is endemic. All cases were immunophenotyped with T- and B-cell markers including the anaplastic large-cell lymphoma marker CD30 or Ki-1. Nineteen cases were studied for latent membrane protein expression and 16 for Epstein-Barr virus small RNAs by in situ hybridization using EBER oligonucleotides on routinely processed sections. Only 1 of 16 cases (6%) showed Epstein-Barr virus in tumor cells and no cases stained with latent membrane protein. Eight of 22 cases (36%) including the EBER-positive case were positive for CD30. These results suggest that the Epstein-Barr virus does not commonly play a role in the pathogenesis of enteropathy-associated T-cell lymphoma from this area.

Published
1995

23. Celiac-associated lymphoma. A single institution experience of 30 cases in the combination chemotherapy era.

Author

Egan LJ, Walsh SV, Stevens FM, Connolly CE, Egan EL, and McCarthy CF

Subjects
Adult, Aged, Antineoplastic Combined Chemotherapy Protocols therapeutic use, Female, Humans, Intestinal Neoplasms drug therapy, Intestinal Neoplasms mortality, Lymphoma drug therapy, Lymphoma mortality, Male, Middle Aged, Survival Rate, Celiac Disease complications, Intestinal Neoplasms etiology, Lymphoma etiology
Abstract

Celiac sprue (CS) is frequently complicated by malignancy, most commonly small intestinal lymphoma. Our study was performed in an area with a high prevalence of CS to define the clinical features, response to treatment, and outcome of this tumor. Of a total of 31 lymphomas complicating CS identified, 30 case records and 24 tumor specimens were reviewed. Overall 1-year survival was 9 of 29 (31%) and 5-year survival 3 of 27 (11%). Seven previously diagnosed celiac patients developed lymphoma; length on gluten-free diet ranged from 12 to 252 months (median 44 months). In this group, presentation was nonspecific, diagnosis difficult, and survival poor (lymphoma diagnosed in life in four of seven, mean survival 2.25 months). Twenty-three patients had CS and lymphoma diagnosed during the same illness. In this group, 14 of 23 presented with a surgical emergency and were treated with tumor resection and chemotherapy. Nine are disease-free and alive or died of another cause after 10-196 months (mean 74 follow-up). Celiac-associated lymphoma is a frequent, difficult to diagnose, and commonly fatal complication of CS. An aggressive diagnostic approach, including laparoscopy, is recommended. Long-term survival can be expected in a significant number of these patients and in our series was almost exclusively confined to those treated with chemotherapy.

Published
1995

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