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314 results on '"Prendiville, J"'

6. Leprosy Masked By Steroids

Author

Prendiville, J. S., Cream, J. J., Rose, F. Clifford, Scott, J. T., Woodrow, D. F., and Waters, M. F. R.

Published
1984

11. Intracerebral large artery disease in Aicardi-Goutières syndrome implicates SAMHD1 in vascular homeostasis

Author

Ramesh, V, Bernardi, B, Stafa, A, Garone, Caterina, Franzoni, E, Abinun, M, Mitchell, P, Mitra, D, Friswell, M, Nelson, J, Shalev, Sa, Rice, Gi, Gornall, H, Szynkiewicz, M, Aymard, F, Ganesan, V, Prendiville, J, Livingston, Jh, Crow, Yj, Ramesh V, Bernardi B, Stafa A, Garone C, Franzoni E, Abinun M, Mitchell P, Mitra D, Friswell M, Nelson J, Shalev SA, Rice GI, Gornall H, Szynkiewicz M, Aymard F, Ganesan V, Prendiville J, Livingston JH, and Crow YJ

Subjects
Male, DNA Mutational Analysis, Infant, Proteins, Phosphoproteins, SAM Domain and HD Domain-Containing Protein 1, Exodeoxyribonucleases, Child, Preschool, Homeostasis, Humans, Point Mutation, Carotid Stenosis, Female, Cerebral Arterial Diseases, Child, Monomeric GTP-Binding Proteins
Abstract

AIM: To describe a spectrum of intracerebral large artery disease in Aicardi-Goutières syndrome (AGS) associated with mutations in the AGS5 gene SAMHD1. METHOD: We used clinical and radiological description and molecular analysis. RESULTS: Five individuals (three males, two females) were identified as having biallelic mutations in SAMHD1 and a cerebral arteriopathy in association with peripheral vessel involvement resulting in chilblains and ischaemic ulceration. The cerebral vasculopathy was primarily occlusive in three patients (with terminal carotid occlusion and basal collaterals reminiscent of moyamoya syndrome) and aneurysmal in two. Three of the five patients experienced intracerebral haemorrhage, which was fatal in two individuals. Post-mortem examination of one patient suggested that the arteriopathy was inflammatory in origin. INTERPRETATION: Mutations in SAMHD1 are associated with a cerebral vasculopathy which is likely to have an inflammatory aetiology. A similar disease has not been observed in patients with mutations in AGS1 to AGS4, suggesting a particular role for SAMHD1 in vascular homeostasis. Our report raises important questions about the management of patients with mutations in SAMHD1

Published
2010

12. Book reviews

Author

Mooney, David, Maurer, Brian, Prendiville, J. B., Reid, Stephen, Cantwell, D. F., Martin, Edward A., Mooney, David J., McNicholl, B., McCarthy, C. F., and Walsh, Noel

Published
1975
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13. Book reviews

Author

Fennelly, J. J., Greally, John, Powell, David, Heffernan, S., Swallow, Michael, Drury, M. I., Walsh, J. H., McKenna, John, and Prendiville, J. B.

Published
1974
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14. Proceedings of The Irish Association for Cancer Research Meeting: Universiiy College, Galway, 21St September, 1984

Author

Corridan, J. P., Moran, M. A., Herity, B., Hilliard, N., Moriarty, M., Fennelly, J., McCambridge, M. M., Casey, M., Quigley, M., Moriarty, M., Hunt, S., Gordon, Lynn, Lowry, W. S., Moriarty, M., Prendiville, J., Raftery, H., Blake, P., Herity, B., Robinson, A., Conroy, R., Pomeroy, M., Herity, Bernadette, Murphy, J. F., Daly, Leslie, Atkinson, R. J., Pomeroy, M., Kelly, D., McCabe, M., Fennelly, J. J., Moriarty, M., Duffy, G., Duff, F., Robinson, A., Duffy, J., Reynolds, Maura, McCann, S. R., Keeling, P., Byrne, P. J., Mealy, K., Whelan, A., Feighery, C., Hennessy, T. P. J., Mealy, K., Keeling, P., Byrne, P. J., Whelan, A., Feighery, C., Hennessy, T. P. J., Duffy, M. J., O’Connell, M., Cantwell, B., Fennelly, J., O’Siorain, L., Conroy, R., Duffy, M. J., O’Ccnnel, M., Fennelly, J., O’Siorain, L., Conroy, R., Simon, J., Harrington, M. G., O’Siorain, Li, O’Briain, S., McDonnell, S., Moriarty, M., Clynes, M., Seymour, C. B., Mothersill, C., Byrne, P., Hennessy, T. P. J., Moriarty, M., Lavelle, S. M., Lomhair, M. Mac, O’Reilly, D., Mullins, E., Canty, S., Collins, J. K., Davis, J., Conroy, J., Collins, J. K., Keatinge, M. B., Collins, P. B., Duignan, J. P., Dickson, B., Johnson, A. H., McCann, A., Seymour, C., Mothersill, C., Long, A., Moriarty, M., O’Donoghue, D., Mulgrew, S., Seymour, C., Mothersill, C., Moriarty, M., Conere, T. J., Church, S. W., Lowry, Sidney, Earls, B., and Russell, R. J.

Published
1985
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15. Book reviews

Author

Martin, Edward A., Fennelly, J. J., Lanigan, John, McCollum, Stanley T., O’Malley, Eoin, McNulty, James G., Kelly, W. Doyle, Baker, R. S. W., O’Brien, Brendan, Browne, Alan D. H., O’Halloran, M. J., Hargadon, O. P., Sheehan, Patricia M. E., Prendiville, J. B., and Breathnacht, C. S.

Published
1971
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16. Book reviews

Author

O’Brien, B., O’Connell, L., Prendiville, J., Fitzgerald, O., Quinlan, H., Davys, R., Hickey, M., O’Farrell, P. T., Bradshaw, T., Coakley, J. B., McVey, H., R.H.M., Towers, R., O’Donovan, D. K., O’Malley, E., and Gavin, E. L.

Published
1958
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18. Book reviews

Author

Carroll, Robert, Beckett, P. G. S., Prendiville, J. B., Bourke, Geoffrey J., Coonan, Miss K., Drury, M. I., Breathnach, C. S., O'Dea, James ST. L., Walsh, A., Stokes, B. M., Guinan, P. M., Quinn, Catherine A., Smith, G. S., and Barnes, J.

Published
1972
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19. Book reviews

Author

Prendiville, J. B., Whelton, M. J., Regan, Brian F., Breathnach, C. S., Holland, P. D. J., O’Brien, M. A., Hurley, Pierse, Fitzgerald, M. J. T., Hartigan, P. J., and Mulcahy, R.

Published
1976
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21. Book reviews

Author

MacConaill, M. A., Erskine, C. A., Micks, R. H., Prendiville, J. B., Fleetwood, J., Boland, S. J., and Mehigan, J. A.

Published
1957
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22. Book reviews

Author

Murphy, Edward L., O’Brien, B., Doolin, M., Donovan, F., Fleming, John, and Prendiville, J. B.

Published
1959
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23. SLC29A3 gene is mutated in pigmented hypertrichosis with insulin-dependent diabetes mellitus syndrome and interacts with the insulin signaling pathway.

Author

Cliffe, S.T., Kramer, J.M., Hussain, K., Robben, J.H., Jong, E.K. de, Brouwer, A.P.M. de, Nibbeling, E., Kamsteeg, E.J., Wong, M., Prendiville, J., James, C., Padidela, R., Becknell, C., Bokhoven, J.H.L.M. van, Deen, P.M.T., Hennekam, R.C.M., Lindeman, R., Schenck, A., Roscioli, T., Buckley, M.F., Cliffe, S.T., Kramer, J.M., Hussain, K., Robben, J.H., Jong, E.K. de, Brouwer, A.P.M. de, Nibbeling, E., Kamsteeg, E.J., Wong, M., Prendiville, J., James, C., Padidela, R., Becknell, C., Bokhoven, J.H.L.M. van, Deen, P.M.T., Hennekam, R.C.M., Lindeman, R., Schenck, A., Roscioli, T., and Buckley, M.F.

Abstract

Contains fulltext : 81613.pdf (publisher's version ) (Closed access), Pigmented hypertrichotic dermatosis with insulin-dependent diabetes (PHID) syndrome is a recently described autosomal recessive disorder associated with predominantly antibody negative, insulin-dependent diabetes mellitus. In order to identify the genetic basis of PHID and study its relationship with glucose metabolism, we performed homozygosity mapping in five unrelated families followed by candidate gene sequencing. Five loss-of-function mutations were identified in the SLC29A3 gene which encodes a member of a highly conserved protein family that transports nucleosides, nucleobases and nucleoside analogue drugs, hENT3. We show that PHID is allelic with a related syndrome without diabetes mellitus, H syndrome. The interaction of SLC29A3 with insulin signaling pathways was then studied using an established model in Drosophila melanogaster. Ubiquitous knockdown of the Drosophila ortholog of hENT3, dENT1 is lethal under stringent conditions; whereas milder knockdown induced scutellar bristle phenotypes similar to those previously reported in the knockdown of the Drosophila ortholog of the Islet gene. A cellular growth assay showed a reduction of cell size/number which could be rescued or enhanced by manipulation of the Drosophila insulin receptor and its downstream signaling effectors, dPI3K and dAkt. In summary, inactivating mutations in SLC29A3 cause a syndromic form of insulin-dependent diabetes in humans and in Drosophila profoundly affect cell size/number through interactions with the insulin signaling pathway. These data suggest that further investigation of the role of SLC29A3 in glucose metabolism is a priority for diabetes research.

Published
2009

24. Clinical and molecular phenotype of Aicardi-Goutieres syndrome.

Author

Rice, G., Patrick, T., Parmar, R, Taylor, C.F., Aeby, A., Aicardi, J., Artuch, R., Montalto, S.A., Bacino, C.A., Borroso, B., Baxter, P., Benko, W.S., Bergmann, C., Bertini, E., Biancheri, R., Blair, E., Blau, N., Bonthron, D.T., Briggs, T., Brueton, L., Brunner, H.G., Burke, C.J., Carr, I., Carvalho, D.R., Chandler, K.E., Christen, H.J., Corry, P.C., Cowan, F.M., Cox, H., D'Arrigo, S., Dean, J., Laet, C.E. de, Praeter, C.M. de, Dery, C., Ferrie, C.D., Flintoff, K., Frints, S.G., Garcia-Cazorla, A., Gener, B., Goizet, C., Goutieres, F., Green, A.J., Guet, A., Hamel, B.C.J., Hayward, B.E., Heiberg, A., Hennekam, R.C.M., Husson, M., Jackson, A.P., Jayatunga, R., Jiang, Y.H., Kant, S., Kao, A., King, M., Kingston, H., Klepper, J., Knaap, M.S. van der, Kornberg, A.J., Kotzot, D., Kratzer, W., Lacombe, D., Lagae, L., Landrieu, P.G., Lanzi, G., Leitch, A., Lim, M.J., Livingston, J.H., Lourenco, C.M., Lyall, E.G.H., Lynch, S.A., Lyons, M.J., Marom, D., McClure, J.P., McWilliam, R., Melancon, S.B., Mewasingh, L.D., Moutard, M.L., Nischal, K.K., Ostergaard, J.R., Prendiville, J., Rasmussen, M., Rogers, R.C., Roland, D., Rosser, E.M., Rostasy, K., Roubertie, A., Sanchis, A, Schiffmann, R., Scholl-Burgi, S., Seal, S., Shalev, S.A., Corcoles, C.S., Sinha, G.P., Soler, D., Spiegel, R., Stephenson, J.B., Tacke, U., Tan, T.Y., Willemsen, M.A.A.P., Rice, G., Patrick, T., Parmar, R, Taylor, C.F., Aeby, A., Aicardi, J., Artuch, R., Montalto, S.A., Bacino, C.A., Borroso, B., Baxter, P., Benko, W.S., Bergmann, C., Bertini, E., Biancheri, R., Blair, E., Blau, N., Bonthron, D.T., Briggs, T., Brueton, L., Brunner, H.G., Burke, C.J., Carr, I., Carvalho, D.R., Chandler, K.E., Christen, H.J., Corry, P.C., Cowan, F.M., Cox, H., D'Arrigo, S., Dean, J., Laet, C.E. de, Praeter, C.M. de, Dery, C., Ferrie, C.D., Flintoff, K., Frints, S.G., Garcia-Cazorla, A., Gener, B., Goizet, C., Goutieres, F., Green, A.J., Guet, A., Hamel, B.C.J., Hayward, B.E., Heiberg, A., Hennekam, R.C.M., Husson, M., Jackson, A.P., Jayatunga, R., Jiang, Y.H., Kant, S., Kao, A., King, M., Kingston, H., Klepper, J., Knaap, M.S. van der, Kornberg, A.J., Kotzot, D., Kratzer, W., Lacombe, D., Lagae, L., Landrieu, P.G., Lanzi, G., Leitch, A., Lim, M.J., Livingston, J.H., Lourenco, C.M., Lyall, E.G.H., Lynch, S.A., Lyons, M.J., Marom, D., McClure, J.P., McWilliam, R., Melancon, S.B., Mewasingh, L.D., Moutard, M.L., Nischal, K.K., Ostergaard, J.R., Prendiville, J., Rasmussen, M., Rogers, R.C., Roland, D., Rosser, E.M., Rostasy, K., Roubertie, A., Sanchis, A, Schiffmann, R., Scholl-Burgi, S., Seal, S., Shalev, S.A., Corcoles, C.S., Sinha, G.P., Soler, D., Spiegel, R., Stephenson, J.B., Tacke, U., Tan, T.Y., and Willemsen, M.A.A.P.

Abstract

Contains fulltext : 52556.pdf (publisher's version ) (Closed access)

Published
2007

25. A phase-I study of intravenous bryostatin-1 in patients with advanced cancer

Author

Prendiville, J., Crowther, D., Thatcher, N., Woll, P.J., Fox, B.W., McGown, A., Testa, N., Stern, P., McDermott, R., Potter, M., and Pettit, G.R.

Abstract

Bryostatin 1 is a novel antitumour agent derived from Bugula neritina of the marine phylum\ud Ectoprocta. Nineteen patients with advanced solid tumours were entered into a phase I study to evaluate the\ud toxicity and biological effects of bryostatin 1. Bryostatin 1 was given as a one hour intravenous infusion at the\ud beginning of each 2 week treatment cycle. A maximum of three treatment cycles were given. Doses were\ud escalated in steps from 5 to 65 jig m-2 in successive patient groups. The maximum tolerated dose was\ud 50 fig m2. Myalgia was the dose limiting toxicity and was of WHO grade 3 in all three patients treated at\ud 65 fig m-2. Flu-like symptoms were common but were of maximum WHO grade 2. Hypotension, of maximum\ud WHO grade 1, occurred in six patients treated at doses up to and including 20 jig m 2 and may not have been\ud attributable to treatment with bryostatin 1. Cellulitis and thrombophlebitis occurred at the bryostatin I\ud infusion site of patients treated at all dose levels up to 50 jig m-2, attributable to the 60% ethanol diluent in\ud the bryostatin 1 infusion. Subsequent patients treated at 50 and 65 jig m-2 received treatment with an\ud intravenous normal saline flush and they did not develop these complications. Significant decreases of the\ud platelet count and total leucocyte, neutrophil and lymphocyte counts were seen in the first 24 h after treatment\ud at the dose of 65 jig m2. Immediate decreases in haemoglobin of up to 1.9g dl-' were also noted in patients\ud treated with 65 iLg m2, in the absence of clinical evidence of bleeding or haemodynamic compromise. No\ud effect was observed on the incidence of haemopoietic progenitor cells in the marrow. Some patients'\ud neutrophils demonstrated enhanced superoxide radical formation in response to in vitro stimulation with\ud opsonised zymosan (a bacterial polysaccharide) but in the absence of this additional stimulus, no bryostatin 1\ud effect was observed. Lymphocyte natural killing activity was decreased 2 h after treatment with bryostatin 1,\ud but the effect was not consistently seen 24 h or 7 days later. With the dose schedule examined no antitumour\ud effects were observed. We recommend that bryostatin 1 is used at a dose of 35 to 50 jg m-2 two weekly in\ud phase II studies in patients with malignancies including lymphoma, leukaemia, melanoma or hypernephroma,\ud for which pre-clinical investigations suggest antitumour activity.\ud

Published
1993

27. Phase III trial comparing paclitaxel poliglumex vs docetaxel in the second-line treatment of non-small-cell lung cancer

Author

Paz-Ares, L, primary, Ross, H, additional, O'Brien, M, additional, Riviere, A, additional, Gatzemeier, U, additional, Von Pawel, J, additional, Kaukel, E, additional, Freitag, L, additional, Digel, W, additional, Bischoff, H, additional, García-Campelo, R, additional, Iannotti, N, additional, Reiterer, P, additional, Bover, I, additional, Prendiville, J, additional, Eisenfeld, A J, additional, Oldham, F B, additional, Bandstra, B, additional, Singer, J W, additional, and Bonomi, P, additional

Published
2008
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30. Screening for psychosocial dysfunction in pediatric dermatology practice

Author

Murphy Jm, Michael S. Jellinek, Prendiville J, Lawrence A. Schachner, M. Goshko, Ronald C. Hansen, Nancy B. Esterly, Sandra J. Bishop, and Paula K. Rauch

Subjects
Counseling, Male, Pediatrics, medicine.medical_specialty, Primary care, Skin Diseases, 03 medical and health sciences, 0302 clinical medicine, 030225 pediatrics, Surveys and Questionnaires, medicine, Humans, Mass Screening, Pediatric dermatology, Child, business.industry, Social Behavior Disorders, United States, Pediatric Symptom Checklist, Screening questionnaire, El Niño, Social Class, Pediatrics, Perinatology and Child Health, Female, Complication, business, Psychosocial, Psychopathology
Abstract

The Pediatric Symptom Checklist, a brief psychosocial screening questionnaire, was used in a multi-center study of pediatric dermatology clinics (n=377). Overall rates of positive screening indicated that approximately 13% of patients screened positive, a rate similar to findings in primary care pediatric settings. Examining the sample in greater detail demonstrated that children whose dermatologic disorder is perceived to have a greater impact on their appearance are at higher risk for psychosocial dysfunction.

Published
1991

32. Book reviews

Author

Dean, G., Fitzgerald, P., Powell, M., Prendiville, J. B., O’Driscoll, K., and Bofin, P. J.

Published
1975
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33. Book reviews

Author

Malone, John P., Prendiville, J. B., Canning, B. St. J., Buckley, M. P., and McNulty, James G.

Published
1970
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34. Book reviews

Author

Prendiville, J. B., Tomkin, Gerald H., Chapman, T. T., Kane, Frank, and Kelly, W. Doyle

Published
1968
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44. A randomised trial investigating the dose intensity of primary chemotherapy in patients with ovarian carcinoma: A comparison of chemotherapy given every four weeks with the same chemotherapy given at three week intervals

Author

Wrigley, E., primary, Weaver, A., additional, Jayson, G., additional, Ranson, M., additional, Renninson, J., additional, Prendiville, J., additional, Dobson, M., additional, Collins, C.D., additional, Swindell, R., additional, Buckley, C.H., additional, Radford, J.A., additional, and Crowther, D., additional

Published
1996
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