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14 results on '"Gladish, D."'

3. Genome screen in familial intracranial aneurysm

Author

Foroud, T, Sauerbeck, L, Brown, R, Anderson, C, Woo, D, Kleindorfer, D, Flaherty, ML, Deka, R, Hornung, R, Meissner, I, Bailey-Wilson, JE, Langefeld, C, Rouleau, G, Connolly, ES, Lai, D, Koller, DL, Huston, J, Broderick, JP, Fisher, W, Forson, H, Mee, E, Howe, C, Vos, S, Hankey, G, Knuckey, N, Laidlaw, J, Reilly, P, Dorsch, N, Morgan, M, Besser, M, Rosenfeld, J, Athanasiadis, K, Claxton, A, Dunne, V, Griffith, J, Davidson, J, Pope, S, Froelich, A, Day, A, Brach, R, Zuccarello, M, Ringer, A, Yeh, H, Franklin, K, Ramussen, P, Andrews-Hinders, D, Wheeler, T, Sacco, R, Lamonica, D, Lewis, SB, Royster, A, Payner, T, Miracle, N, Murphy, K, Kohler, B, Ogilvy, C, Buckley, D, Manansala, J, Ferguson, G, Mayer, C, Peacock, J, Desjarlais, A, Aldrich, EF, Aldrich, C, Byard, C, Brown, RD, Jaeger, L, Morgenstern, L, Concannon, M, Qureshi, AI, Harris-Lane, P, Batjer, H, Joven, G, Thompson, S, Richard, MT, Hopper, A, Kassam, AB, Lee, K, Johnston, C, Katsura, K, Giannotta, S, Fishback, D, Steinberg, G, Luu, D, Coburn, M, Malkoff, M, Wojner, A, Kassel, N, Worrall, B, Radakovic, G, Tirschwell, D, Tanzi, P, Derdeyn, C, Catanzaro, M, Kaufmann, A, Gladish, D, Foroud, T, Sauerbeck, L, Brown, R, Anderson, C, Woo, D, Kleindorfer, D, Flaherty, ML, Deka, R, Hornung, R, Meissner, I, Bailey-Wilson, JE, Langefeld, C, Rouleau, G, Connolly, ES, Lai, D, Koller, DL, Huston, J, Broderick, JP, Fisher, W, Forson, H, Mee, E, Howe, C, Vos, S, Hankey, G, Knuckey, N, Laidlaw, J, Reilly, P, Dorsch, N, Morgan, M, Besser, M, Rosenfeld, J, Athanasiadis, K, Claxton, A, Dunne, V, Griffith, J, Davidson, J, Pope, S, Froelich, A, Day, A, Brach, R, Zuccarello, M, Ringer, A, Yeh, H, Franklin, K, Ramussen, P, Andrews-Hinders, D, Wheeler, T, Sacco, R, Lamonica, D, Lewis, SB, Royster, A, Payner, T, Miracle, N, Murphy, K, Kohler, B, Ogilvy, C, Buckley, D, Manansala, J, Ferguson, G, Mayer, C, Peacock, J, Desjarlais, A, Aldrich, EF, Aldrich, C, Byard, C, Brown, RD, Jaeger, L, Morgenstern, L, Concannon, M, Qureshi, AI, Harris-Lane, P, Batjer, H, Joven, G, Thompson, S, Richard, MT, Hopper, A, Kassam, AB, Lee, K, Johnston, C, Katsura, K, Giannotta, S, Fishback, D, Steinberg, G, Luu, D, Coburn, M, Malkoff, M, Wojner, A, Kassel, N, Worrall, B, Radakovic, G, Tirschwell, D, Tanzi, P, Derdeyn, C, Catanzaro, M, Kaufmann, A, and Gladish, D

Abstract

Background: Individuals with 1st degree relatives harboring an intracranial aneurysm (IA) are at an increased risk of IA, suggesting genetic variation is an important risk factor. Methods: Families with multiple members having ruptured or unruptured IA were recruited and all available medical records and imaging data were reviewed to classify possible IA subjects as definite, probable or possible IA or not a case. A 6 K SNP genome screen was performed in 333 families, representing the largest linkage study of IA reported to date. A 'narrow' (n = 705 definite IA cases) and 'broad' (n = 866 definite or probable IA) disease definition were used in multipoint model-free linkage analysis and parametric linkage analysis, maximizing disease parameters. Ordered subset analysis (OSA) was used to detect gene × smoking interaction. Results: Model-free linkage analyses detected modest evidence of possible linkage (all LOD < 1.5). Parametric analyses yielded an unadjusted LOD score of 2.6 on chromosome 4q (162 cM) and 3.1 on chromosome 12p (50 cM). Significant evidence for a gene × smoking interaction was detected using both disease models on chromosome 7p (60 cM; p ≤ 0.01). Our study provides modest evidence of possible linkage to several chromosomes. Conclusion: These data suggest it is unlikely that there is a single common variant with a strong effect in the majority of the IA families. Rather, it is likely that multiple genetic and environmental risk factors contribute to the susceptibility for intracranial aneurysms.

Published
2009

4. Unruptured intracranial aneurysms--risk of rupture and risks of surgical intervention

Author

Wiebers, D., Whisnant, J., Forbes, G., Meissner, I., Brown, R., Piepgras, D., Huston, J., Nichols, D., O Fallon, W., Peacock, J., Jaeger, L., Kassell, N., Kongable-Beckman, G., Torner, J., Rajput, M., Drake, C., Kurtzke, J., Marler, J., Walker, M., Meyer, F., Atkinson, J., Marsh, W., Thielen, K., Ferguson, G., Barr, H., Lownie, S., Hachinski, V., Fox, A., Sahjpaul, R., Parrent, A., Mayer, C., Lindsay, K., Teasdale, E., Bone, I., Fatukasi, J., Lindsay, M., Cail, W., Sagher, O., Davis, M., Sengupta, R., Bates, D., Gholkar, A., Murdy, J., Wilson, S., Praharaj, S., Partridge, G., Reynolds, C., Hind, N., Ogilvy, C., Crowell, R., Gress, D., Schaefer, P., Choi, I., Buckley, D., Sloan, K., King, D., Giannotta, S., Ameriso, S., Teitelbaum, T., Thomson, E., Fishback, D., Vajda, J., Nyary, I., Czirjak, S., Horvath, M., Szikora, I., Pasztor, E., Varady, P., Erdos, A., Edner, G., Wahlgren, N., Lindqvist, M., Antonsson, A., Da Pian, R., Pasqualin, A., Chioffi, F., Beltramello, A., Zampieri, G., Benati, A., Rossi, G., Ronkainen, A., Hernesniemi, J., Vapalahti, M., Rinne, J., Luukkonen, M., Vihavainen, M., Savolainen, S., Koivisto, T., Leivo, S., Helin, K., Steinberg, G., Marks, M., Vanefsky, M., Norbash, A., Thompson, R., Bell, T., Marcellus, M., Meyer, A., Kerr, R., Adams, C., Molyneux, A., Vinden, S., Bacon, F., Shrimpton, J., Parker, S., Day, A., Nadeau, S., Stachniak, J., Friedman, W., Fessler, R., Peters, K., Jacob, R., Roper, S., Smith, A., Lafrentz, P., Howard, M., Loftus, C., Adams, H., Crosby, D., Rogers, M., Broderick, J., Tew, J., Brott, T., Loveren, H., Yeh, H., Zuccarello, M., Tomsick, T., Gaskill-Shipley, M., Minneci, L., Mcmahon, N., Castel, J., Orgogozo, J., Loiseau, H., Bourgeois, P., Berge, J., Dousset, V., Cuny, E., Richard, M., Agbi, C., Hugenholtz, H., Benoit, B., Morrish, W., Wee, R., Grahovac, S., Pratt, L., Mortensen, M., Andreoli, A., Testa, C., Comani, V., Trevisan, C., Limoni, P., Carlucci, F., Leonardi, M., Sturiale, C., Pendl, G., Eder, H., Klein, G., Eder, M., Leber, K., Horner, T., Leipzig, T., Payner, T., Denardo, A., Scott, J., Redelman, K., Fisher, W., Rosner, M., Vitek, G., Hand, M., Flack, Wf, Sichez, J., Pertuiset, B., Fohanno, D., Marsault, C., Casasco, A., Biondi, A., Capelle, L., Duffau, H., Winn, H., Grady, M., Newell, D., Longstreth, W., Thompson, P., Bybee, H., Jones, D., Findlay, J., Petruk, K., Steinke, D., Ashforth, R., Stenerson, P., Schindel, D., Vanderhoven, H., Neves, J., Zager, E., Flamm, E., Raps, E., Hurst, R., Parrott, S., Sellers, M., Torchia, M., Anderson, B., West, M., Fewer, D., Hill, N., Sutherland, G., Ross, I., Mcclarty, B., Brownstone, R., Williams, O., Narotam, P., Christane, L., Mcginn, G., Gladish, D., Kirkpatrick, P., Pickard, J., Antoun, N., Simpson, D., Higgins, N., Turner, C., Tebbs, S., Holness, R., Malloy, D., Phillips, S., Maloney, W., Molina-De-Orozco, V., Baxter, B., Connolly-Campbell, K., Macdougall, A., Gentili, F., Wallace, M., Ter Brugge, K., Willinsky, R., Tymianski, M., Rickards, L., Tucker, W., Lambert, C., Montanera, W., Rychlewski, C., Flood, C., Villani, R., Sganzerla, E., Tomei, G., Bettinelli, A., Ceccarelli, G., Righini, A., Bello, L., Marras, C., Nelson, R., Lewis, T., Renowden, C., Clarke, Y., Varian, L., Chyatte, D., Sila, C., Perl, J., Masaryk, T., Porterfield, R., Shaw, M., Foy, P., Nixon, T., Dunn, L., Clitheroe, N., Smith, T., Eldridge, P., Humphrey, P., Wiseman, J., Hawkins, K., Owen, L., Ost, K., Saminaden, S., Mohr, G., Schondorf, R., Carlton, J., Maleki, M., Just, N., Brien, S., Entis, S., Tampieri, D., Simons, N., Mooij, J., Metzemackers, J., Hew, J., Beks, J., Veen, A., Bosma, I., Sprengers, M., Rinkel, G., Gijn, J., Ramos, L., Tulleken, C., Greebe, P., Vliet, F., Borgesen, S., Jespersen, B., Boge-Rasmussen, T., Willumsen, L., Homer, D., Eller, T., Carpenter, J., Meyer, J., Munson, R., Small, B., Nussbaum, E., Heros, R., Latchaw, R., Camarata, P., Lundgren, J., Mattsen, N., Whittle, I., Sellar, R., O Sullivan, M., Steers, A., Statham, P., Malcolm, G., Price, R., Hoffman, B., Yonas, H., Wechsler, L., Thompson-Dobkin, J., Jungreis, C., Kassam, A., Kirby, L., Parent, A., Lewis, A., Azordegan, P., Smith, R., Alexander, L., Gordon, D., Russell, W., Benashvili, G., Perry, R., Scalzo, D., Mandybur, G., Morgan, C., Karanjia, P., Madden, K., Kelman, D., Gallant, T., Vanderspek, H., Choucair, A., Neal, J., Mancl, K., Saveland, H., Brandt, L., Holtas, S., Trulsson, B., Macdonald, R., Weir, B., Mojtahedi, S., Amidei, C., Vermeulen, M., Bosch, D., Hulsmans, F., Albrecht, K., Roos, Y., Vet, A., Gorissen, A., Mechielsen, M., Martin, N., Gobin, Y., Saver, J., Vinuela, F., Duckwiler, G., Kelly, D., Frazee, J., Da Graca, R., Gravori, T., Illingworth, R., Richards, P., Wade, J., Colquhoun, I., Bashir, E., Shortt, S., Weaver, J., Fisher, M., Stone, B., Chaturvedi, S., Davidson, R., Davidson, K., Giombini, S., Solero, C., Boiardi, A., Cimino, C., Valentini, S., Antonio Silvani, Alberts, M., Friedman, A., Gentry, A., Hoffman, K., Hughes, R., Lillihei, K., Earnest, M., Nichols, J., Kindt, G., Anderson, A., Levy, S., Breeze, R., Noonan, V., Dowd, C., Vanwestrop, J., Wilson, C., Berger, M., Hannegan, L., Marcos, J., Ugarte, L., Kitchen, N., Taylor, W., Kumar, M., Grieve, J., Durity, F., Boyd, M., Fairholm, D., Griesdale, D., Honey, C., Redekop, G., Toyota, B., Turnbull, I., Woodhurst, W., Zwimpfer, T., Teal, P., Grabe, D., Brevner, A., Piepgras, A., Schmiedek, P., Schwartz, A., Weber, T., Biller, J., Brem, S., Cybulski, G., Chadwick, L., Bronstein, K., Pietila, T., Brock, M., Krug, D., Krznaric, I., and Kivisaari, R.

Subjects
Adult, Male, medicine.medical_specialty, International Subarachnoid Aneurysm Trial, Adolescent, Rupture rate, Aneurysm, Ruptured, Risk Factors, Intervention (counseling), Unruptured cerebral aneurysm, Medicine, Humans, Prospective Studies, Aged, Probability, Retrospective Studies, Aged, 80 and over, Rupture, Spontaneous, business.industry, Age Factors, Intracranial Aneurysm, General Medicine, Middle Aged, Subarachnoid Hemorrhage, Emergency medicine, Female, business, Vascular Surgical Procedures
Abstract

The management of unruptured intracranial aneurysms requires knowledge of the natural history of these lesions and the risks of repairing them.A total of 2621 patients at 53 participating centers in the United States, Canada, and Europe were enrolled in the study, which had retrospective and prospective components. In the retrospective component, we assessed the natural history of unruptured intracranial aneurysms in 1449 patients with 1937 unruptured intracranial aneurysms; 727 of the patients had no history of subarachnoid hemorrhage from a different aneurysm (group 1), and 722 had a history of subarachnoid hemorrhage from a different aneurysm that had been repaired successfully (group 2). In the prospective component, we assessed treatment-related morbidity and mortality in 1172 patients with newly diagnosed unruptured intracranial aneurysms.In group 1, the cumulative rate of rupture of aneurysms that were less than 10 mm in diameter at diagnosis was less than 0.05 percent per year, and in group 2, the rate was approximately 11 times as high (0.5 percent per year). The rupture rate of aneurysms that were 10 mm or more in diameter was less than 1 percent per year in both groups, but in group 1, the rate was 6 percent the first year for giant aneurysms (or =25 mm in diameter). The size and location of the aneurysm were independent predictors of rupture. The overall rate of surgery-related morbidity and mortality was 17.5 percent in group 1 and 13.6 percent in group 2 at 30 days and was 15.7 percent and 13.1 percent, respectively, at 1 year. Age independently predicted surgical outcome.The likelihood of rupture of unruptured intracranial aneurysms that were less than 10 mm in diameter was exceedingly low among patients in group 1 and was substantially higher among those in group 2. The risk of morbidity and mortality related to surgery greatly exceeded the 7.5-year risk of rupture among patients in group 1 with unruptured intracranial aneurysms smaller than 10 mm in diameter.

Published
1998

8. DISTRIBUTION AND HABITAT USE OF THE MISSOURI RIVER AND LOWER YELLOWSTONE RIVER BENTHIC FISHES FROM 1996 TO 1998: A BASELINE FOR FISH COMMUNITY RECOVERY.

Author

Wildhaber, M. L., Gladish, D. W., and Arab, A.

Abstract

ABSTRACT Past and present Missouri River management practices have resulted in native fishes being identified as in jeopardy. In 1995, the Missouri River Benthic Fishes Study was initiated to provide improved information on Missouri River fish populations and how alterations might affect them. The study produced a baseline against which to evaluate future changes in Missouri River operating criteria. The objective was to evaluate population structure and habitat use of benthic fishes along the entire mainstem Missouri River, exclusive of reservoirs. Here we use the data from this study to provide a recent-past baseline for on-going Missouri River fish population monitoring programmes along with a more powerful method for analysing data containing large percentages of zero values. This is carried out by describing the distribution and habitat use of 21 species of Missouri River benthic fishes based on catch-per-unit area data from multiple gears. We employ a Bayesian zero-inflated Poisson model expanded to include continuous measures of habitat quality (i.e. substrate composition, depth, velocity, temperature, turbidity and conductivity). Along with presenting the method, we provide a relatively complete picture of the Missouri River benthic fish community and the relationship between their relative population numbers and habitat conditions. We demonstrate that our single model provides all the information that is often obtained by a myriad of analytical techniques. An important advantage of the present approach is reliable inference for patterns of relative abundance using multiple gears without using gear efficiencies. Copyright © 2011 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Published
2012
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12. Changes in growth and structure of pea primary roots (Pisum sativum L. cv. Alaska) as a result of sudden flooding.

Author

Niki T and Gladish DK

Subjects
Apoptosis physiology, Cell Nucleus metabolism, Cell Nucleus ultrastructure, Disasters, Mitosis physiology, Mitotic Index, Pisum sativum cytology, Plant Root Cap cytology, Vacuoles metabolism, Vacuoles ultrastructure, Water metabolism, Pisum sativum growth & development, Plant Root Cap growth & development
Abstract

Pea (Pisum sativum L. cv. Alaska) primary roots were exposed to flooding after growth for 4 or 5 d at 25 degrees C under relatively dry conditions. Flooding after 4 d growth reduced, but did not stop, primary root growth, and cavities caused by degradation of central vascular cells were typically found from 10-60 mm from the tips. Flooding after 5 d stopped primary root growth and caused cell death in the tips, and vascular cavities formed that typically were 20-60 mm from the tips of the roots. Degradation of root tip cells in 5-day-roots was very rapid and began in the elongation zone and later in the apical zone. Root tips discolored, narrowed or curled before growth arrest. The mitotic indices of 5-day-root tips were suppressed by the flooding treatment. A few mitotic figures were observed in roots treated with flooding after 4 d growth. Affected cells had condensed nuclei, but cytoplasms appeared to be normal in the early stages of cell degradation. Later these cells became very vacuolated. The relationship of flooding to root growth, vascular cavity formation, and the morphology of pea primary roots is described with regard to the ability to resist flooding stress.

Published
2001
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13. Regeneration of tissue following cavity formation in the vascular cylinders of Pisum sativum (Fabaceae) primary roots.

Author

Niki T, Rost T, and Gladish D

Abstract

The reorganization of vascular cylinders of pea (Pisum sativum, cv. Alaska) primary roots following the formation of vascular cavities was examined by light and electron microscopy. Cavities usually began forming ~20 mm from the root tip and were continuous to ~90 mm from the tips in roots 150 mm long, where they began filling with specialized parenchyma cells (SP cells). SP cells were usually produced by enlargement of parenchymous cells of the primary xylem at cavity margins. Depending on the extent and shape of the cavity, they were also sometimes produced by primary phloem parenchyma and early derivatives of the vascular cambium. Enlargement and some divisions of SP cells continued until a cavity was completely filled by them. SP cells proceeded through a series of cytoplasmic changes as they developed. First the cytoplasmic layer became thicker and more electron dense than surrounding cells. As SP cells enlarged there was an increase in vesicular traffic and the cytoplasm became less electron dense. Ultimately the cytoplasm thinned further, organelles degenerated, and the tonoplast sometimes broke down. SP cells did not form secondary walls. X-ray microanalysis revealed that SP cells accumulated potassium and rubidium to the same degree as cortical and xylem parenchyma cells and to a greater degree than immature secondary and late-maturing tracheary elements.

Published
1998

14. Botulinum toxin injection for cervicogenic headache.

Author

Hobson DE and Gladish DF

Subjects
Adult, Female, Headache etiology, Humans, Neck, Whiplash Injuries complications, Anti-Dyskinesia Agents therapeutic use, Botulinum Toxins therapeutic use, Headache therapy
Abstract

We report a 28-year-old woman with a 5-year history of cervicogenic headache following a whiplash injury. Her unilateral neck pain, if aggravated by exertion, would create a predictable sequence of events leading to a hemicephalgia. She proved medically refractory to usual therapies, but had a striking response to a single botulinum toxin Injection in her symptomatic trapezius muscle. Repeated Injections every 3 months have been required to maintain this benefit. The Implications of this observation are discussed.

Published
1997
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