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15 results on '"T. S., Jacques"'

1. Effective induction therapy for anti-SRP associated myositis in childhood: A small case series and review of the literature

Author

E. L. Binns, E. Moraitis, S. Maillard, S. Tansley, N. McHugh, T. S. Jacques, L. R. Wedderburn, C. Pilkington, S. A. Yasin, K. Nistala, and on behalf of the UK Juvenile Dermatomyositis Research Group (UK and Ireland)

Subjects
Pediatrics, RJ1-570, Diseases of the musculoskeletal system, RC925-935
Abstract

Abstract Background Anti-Signal Recognition Particle associated myopathy is a clinically and histopathologically distinct subgroup of Juvenile Idiopathic Inflammatory Myositis, which is under-recognised in children and fails to respond to conventional first line therapies. We present three cases where remission was successfully induced using combination therapy with intensive rehabilitation. Case presentations Three new patients are reported. All 3 cases presented with profound, rapid-onset, proximal myopathy and markedly raised CK, but no rash. Histology revealed a destructive myopathy characterized by scattered atrophic and necrotic fibres with little or no inflammatory infiltrate. All 3 patients responded to induction with cyclophosphamide, IVIG and rituximab, in conjunction with intensive physiotherapy and methotrexate as the maintenance agent. Our patients regained near-normal strength (MMT > 70/80), in contrast with the current literature where >50% of cases reported severe residual weakness. A literature search on paediatric anti-SRP myositis was performed to June 2016; PubMed was screened using a combination of the following terms: signal recognition particle, autoantibodies, antibodies, myositis, muscular diseases, skeletal muscle, childhood, paediatric, juvenile. Articles in a foreign language were excluded. Nine case studies were found. Conclusion This paper supports the hypothesis that anti-SRP myositis is distinct from other JIIM. It is an important differential to JDM and should be considered where there is severe weakness without rash or if highly elevated muscle enzymes (CK > 10,000 U/l) are found. Early identification is essential to initiate aggressive medical and physical therapy. Greater international collaboration and long-term follow-up data is needed to establish the most effective treatment strategy for this rare group of patients.

Published
2017
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2. SHH pathway inhibition is protumourigenic in adamantinomatous craniopharyngioma

Author

G, Carreno, J K R, Boult, J, Apps, J M, Gonzalez-Meljem, S, Haston, R, Guiho, C, Stache, L S, Danielson, A, Koers, L M, Smith, A, Virasami, L, Panousopoulos, M, Buchfelder, T S, Jacques, L, Chesler, S P, Robinson, and J P, Martinez-Barbera

Subjects
Male, animal structures, Adolescent, tumour, Research, pituitary, SHH, Craniopharyngioma, Disease Models, Animal, Mice, Child, Preschool, embryonic structures, vismodegib, Animals, Humans, Hedgehog Proteins, Pituitary Neoplasms, Child, Cell Proliferation, Signal Transduction
Abstract

Pharmacological inhibition of the sonic hedgehog (SHH) pathway can be beneficial against certain cancers but detrimental in others. Adamantinomatous craniopharyngioma (ACP) is a relevant pituitary tumour, affecting children and adults, that is associated with high morbidity and increased mortality in long-term follow-up. We have previously demonstrated overactivation of the SHH pathway in both human and mouse ACP. Here, we show that this activation is ligand dependent and induced by the expression of SHH protein in a small proportion of tumour cells. We investigate the functional relevance of SHH signalling in ACP through MRI-guided preclinical studies using an ACP mouse model. Treatment with vismodegib, a clinically approved SHH pathway inhibitor, results in a significant reduction in median survival due to premature development of highly proliferative and vascularised undifferentiated tumours. Reinforcing the mouse data, SHH pathway inhibition in human ACP leads to a significant increase in tumour cell proliferation both ex vivo, in explant cultures, and in vivo, in a patient-derived xenograft model. Together, our results demonstrate a protumourigenic effect of vismodegib-mediated SHH pathway inhibition in ACP.

Published
2019

3. Ewing sarcoma.

Author

A., Perry, E., de Álava, C., Haberler, T. S., Jacques, M., Kool, B. A., Orr, S. H., Park, D., Sturm, S., Yip, and A., Yoshida

Published
2021

4. Pleomorphic xanthoastrocytoma.

Author

C., Giannini, D., Capper, D., Figarella-Branger, T. S., Jacques, D. T. W., Jones, D. N., Louis, W., Paulus, and U., Tabori

Published
2021

6. Pilocytic astrocytoma.

Author

T., Tihan, D., Figarella-Branger, C., Giannini, K., Gupta, C. E., Hawkins, T. S., Jacques, D. T. W., Jones, S. M., Pfister, F. J., Rodriguez, U., Tabori, and P., Varlet

Published
2021

8. Editorial

Author

T S, Jacques

Subjects
Histology, Neurology, Physiology (medical), Humans, Neurology (clinical), Neuropathology, Pathology and Forensic Medicine
Published
2018
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9. Abstracts from the 2011 BNOS Conference, June 29 - July 1, 2011, Homerton College, Cambridge

Author

S. Ammoun, L. Zhou, M. Barczyk, D. Hilton, S. Hafizi, C. Hanemann, K. S. Lehnus, L. K. Donovan, G. J. Pilkington, Q. An, I. A. Anderson, S. Thomson, M. Bailey, E. Lekka, J. Law, C. Davis, K. Banfill, C. Loughrey, P. Hatfield, D. Bax, R. Elliott, R. Bishop, K. Taylor, L. Marshall, N. Gaspar, M. Viana-Pereira, R. Reis, J. Renshaw, A. Ashworth, C. Lord, C. Jones, C. Bellamy, L. Shaw, J. Alder, A. Shorrocks, R. Lea, S. Birks, M. Burnet, G. Pilkington, J. D. Bruch, J. Ho, C. Watts, S. J. Price, S. Camp, V. Apostolopoulos, A. Mehta, F. Roncaroli, D. Nandi, B. Clark, M. Mackinnon, N. MacLeod, W. Stewart, A. Chalmers, A. Cole, G. Hanna, K. Bailie, D. Conkey, J. Harney, C. Darlow, S. Chapman, L. Mohsen, S. Price, L. Donovan, H. Dyer, H. Lord, K. Fletcher, R. das Nair, J. MacNiven, S. Basu, P. Byrne, L. Glancz, G. Critchley, M. Grech-Sollars, D. Saunders, K. Phipps, J. Clayden, C. Clark, A. Greco, S. Acquati, S. Marino, S. Hammouche, S. P. Wilkins, T. Smith, A. Brodbelt, S. Clark, A. H. L. Wong, P. Eldridge, J. O. Farah, J. Bruch, G. Lamb, S. Smith, A. James, M. Glegg, T. Jeffcote, S. Boulos, P. Robbins, N. Knuckey, A. Banigo, A. R. Brodbelt, M. D. Jenkinson, J. N. Jeyapalan, M. A. Mumin, T. Forshew, A. R. Lawson, R. G. Tatevossian, T. S. Jacques, D. Sheer, J. Kilday, K. Wright, S. Leavy, J. Lowe, E. Schwalbe, S. Clifford, R. Gilbertson, B. Coyle, R. Grundy, P. Kinsella, M. Clynes, V. Amberger-Murphy, N. Barron, S. R. Lambert, D. Jones, D. Pearson, I. Ichimura, V. Collins, L. Steele, P. Sinha, P. Chumas, J. Tyler, D. Ogawa, E. Chiocca, M. DeLay, A. Bronisz, M. Nowicki, J. Godlewski, S. Lawler, M. K. Lee, M. Javadpour, P. Abel, T. Dawson, B. Lea, C. S.-K. Lim, P. L. Grundy, M. Pendleton, A. Williamson, A. Merve, X. Zhang, S. Miller, H. A. Rogers, P. Lyon, V. Rand, M. Adamowicz-Brice, S. C. Clifford, J. T. Hayden, S. Dyer, S. Pfister, A. Korshunov, M.-A. Brundler, R. G. Grundy, M. Nankivell, P. Mulvenna, R. Barton, P. Wilson, C. Faivre-Finn, C. Pugh, R. Langley, D. Ngoga, D. Tennant, A. Williams, P. Moss, G. Cruickshank, K. Owusu-Agyemang, S. Bell, J. St.George, S. G. Piccirillo, S. Qadri, E. Pirola, M. Jenkinson, R. Rahman, C. Rahman, D. MacArthur, F. Rose, K. Shakesheff, C. Carroll, P. Watson, M. Hawkins, H. Spoudeas, D. Walker, T. Holland, H. Ring, A. Rooney, S. McNamara, M. Fraser, R. Rampling, A. Carson, R. Grant, J. Royds, S. Al Nadaf, A. Ahn, Y.-J. Chen, A. Wiles, D. Jellinek, A. Braithwaite, B. Baguley, M. MacFarlane, N. Hung, T. Slatter, S. Rusbridge, N. Walmsley, S. Griffiths, P. Wilford, J. Rees, D. Ryan, P. Liu, S. Galavotti, M. Shaked-Rabi, E. Tulchinsky, S. Brandner, P. Salomoni, A. Schulte, H. S. Gunther, S. Zapf, S. Riethdorf, M. Westphal, K. Lamszus, S. K. Selvanathan, H. J. Salminen, S. Setua, M. E. Welland, M. Shevtsov, W. Khachatryan, A. Kim, K. Samochernych, A. Pozdnyakov, I. V. Guzhova, I. V. Romanova, B. Margulis, J. Barrow, D. Macarthur, A. Long, Z. Maherally, J. R. Smith, L. Dickson, S. Prabhu, F. Harris, T. J. Snape, M. Sussman, S. Wilne, W. Whitehouse, G. Chow, J.-F. Liu, T. Snape, A. Karakoula, F. Rowther, T. Warr, A. Zisakis, V. Varsos, A. Panteli, O. Karypidou, A. Zampethanis, A. Fotovati, S. Abu-Ali, P.-S. Wang, L. Deleyrolle, C. Lee, J. Triscott, J. Y. Chen, S. Franciosi, Y. Nakamura, Y. Sugita, T. Uchiumi, M. Kuwano, B. R. Leavitt, S. K. Singh, A. Jury, H. Wakimoto, B. A. Reynolds, C. J. Pallen, S. E. Dunn, S. Shepherd, S. Scott, D. Bowyer, L. Wallace, B. Hacking, R. Jena, J. Gillard, M. Verraeult, B. Reynolds, C. Dunham, M. Bally, J. Hukin, S. Singhal, S. Singh, and S. Dunn

Subjects
Cisplatin, Cancer Research, Cell growth, Chemistry, Ascorbic acid, Molecular biology, Abstracts, Oncology, Mechanism of action, Cell culture, medicine, Neurology (clinical), Viability assay, medicine.symptom, Cytotoxicity, IC50, medicine.drug
Abstract

INTRODUCTION: Substituted indoles and related structures have been shown to exhibit potent anticancer activity against breast cancer cell lines. Here, the effects of structurally similar substituted indoles against the human glial cancer cell lines, 1321N1 and U87MG, have been investigated by comparing the effects of these compounds to conventional anti cancer drugs. METHODS: Cell viability in the presence of the test compounds was measured using an MTS assay and corroborated by an ATP cell proliferation assay as well as a Trypan blue exclusion test. The significance of reactive oxygen species (ROS) in the process was determined using an Image-iT® LIVE ROS kit from Invitrogen. RESULTS: Both cell lines were treated with four commercial anticancer drugs and IC50 values were only reached at concentrations of 20 µM for cisplatin and 50 µM for gemcitabine over 48hrs on the 1321N1 cell line. However, the more malignant U87MG cell line was resistant to all the drugs, except for cisplatin where the IC50 value was reached at 300 µM after treatment for 48hrs. Similar studies were carried out with various substituted indoles and the cytotoxicity results on both cell lines showed that the IC50 value was reached within 90 minutes for the most potent compound at a concentration of 600 µM (1321N1) and 800 µM (U87MG). The idea that the mechanism of action of these compounds may work through the generation of ROS was investigated and this was confirmed over a similar time course using a suitable fluorogenic marker. Moreover, it was shown that the addition of an antioxidant (ascorbic acid) abolished the potency of the most active compound. CONCLUSION: Here, it has been demonstrated that certain substituted indoles are able to have a rapid, deleterious effect on the viability of two glioma cell lines and indicated that ROS generation may induce cell death.

Published
2011
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12. LAB-PEDIATRICS LABORATORY RESEARCH

Author

D. Carvalho, L. Bjerke, D. Bax, L. Chen, I. Kozarewa, S. Baker, R. Grundy, A. Ashworth, C. Lord, D. Hargrave, R. M. Reis, C. Jones, S. Bender, W. Feng, D. T. Jones, M. Kool, H. Cin, S. Pleier, S. Hutter, D. Sturm, H.-K. Liu, A. Korshunov, P. Lichter, S. M. Pfister, I. Alimova, D. K. Birks, P. Harris, S. Venkataraman, V. E. Marquez, N. K. Foreman, R. Vibhakar, S. Whiteway, A. Donson, E. Xipell, P. Jauregui, M. Gonzalez, s. tejada-solis, R. Diez-Valle, T. Tunon, I. Zazpe, J. Mora, A. M. Carcaboso, C. Gomez-MAnzano, J. Fueyo, M. Alonso, K. Dorris, M. Sobo, P. Holden, E. Panditharatna, S. Li, A. Margol, C. Stephenson, L. Miles, S. Goldman, S. Asgharzadeh, A. Onar, M. Fouladi, R. Drissi, A. Erdreich-Epstein, X. Ren, H. Zhou, K. Snyder, M. Stamper, J. Perez, J. Nazarian, T. Gershon, A. Crowther, I. Garcia, V. Gama, H. Yuan, S. Chang, M. Deshmukh, M. Hutt, W. Goldstein, A. Price, K. J. Lim, K. Warren, H. Chang, C. G. Eberhart, E. H. Raabe, K. Karakoula, K. P. Phipps, W. Harkness, R. Hayward, D. Thompson, T. S. Jacques, J. L. Darling, T. J. Warr, C. Guldal, C. Potts, R. Rotenberry, A. M. Kenney, V. Amani, A. M. Griesinger, A. M. Donson, L. T. Bemis, S. K. Schittone, M. Morgan, A. Thorburn, J. Mulcahy-Levy, I. Kolkowitz, N. Andor, T. Jensen, A. Banerjee, N. Gupta, C. Petritsch, M. Taylor, R. Hashizume, M. Tom, D. Haas-Kogan, S. Mueller, D. Stearns, N. Ma, R. Levy, D. Gate, J. Rodriguez, J. Breunig, M. Danielpour, and T. Town

Subjects
Cancer Research, medicine.medical_specialty, business.industry, 03 medical and health sciences, Abstracts, 0302 clinical medicine, Oncology, 030220 oncology & carcinogenesis, medicine, Medical physics, Neurology (clinical), Laboratory research, business, 030217 neurology & neurosurgery
Published
2012

13. Ultrastructural and cytochemical study of neurones in the rat dorsal motor nucleus of the vagus after axon crush

Author

V, Navaratnam, T S, Jacques, and J N, Skepper

Subjects
Neurons, Histocytochemistry, Nerve Crush, Vagus Nerve, Axonal Transport, Axons, Rats, Microscopy, Electron, Butyrylcholinesterase, Acetylcholinesterase, Animals, Female, Rats, Wistar, Horseradish Peroxidase
Abstract

The cell populations in the dorsal motor nucleus of the vagus (DMNV) of the rat were studied by light microscopy and transmission electron microscopy, including retrograde labeling with horseradish peroxidase and histochemical demonstration of the distribution of the activity of the enzymes acetylcholinesterase (AcChE) and butyrylcholinesterase (BuChE). Two types of neurones were observed: 1) Larger Type A cells, which stain for both AcChE and BuChE and which project into the vagus nerve trunk, and 2) smaller Type B cells, which stain lightly for AcChE but not for BuChE and which do not project into the vagus nerve. Standardised vagal crush at the mid-cervical level causes loss of cholinesterase activity in Type A neurones within a few days but has no effect on Type B neurones. Changes in nuclear morphology of Type A neurones are pronounced at 10 weeks postinjury, indicating that degeneration is irreversible even by this stage. The number of Type A cells projecting to the vagus nerve reduces as a function of time, presumably as these cells die. Only a small number of Type A neurones persist at 2 years postinjury.

Published
1998

14. Meeting report

Author

T. S. Jacques

Subjects
Histology, Neurology, Physiology (medical), Neurology (clinical), Pathology and Forensic Medicine
Published
2005
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