Robert A. James

Newcastle upon Tyne Hospitals NHS Foundation Trust

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Petros Perros

Newcastle University

Sue McGinty

James Cook University

Yvonne Cadet‐James

James Cook University

Russell McGregor

James Cook University

Richard Quinton

Imperial College London

William M. Wood

University of Connecticut

David F. Gordon

University of Oxford

Bijay Vaidya

Royal Devon and Exeter Hospital

E. Chester Ridgway

University of Colorado Denver

M Boskovic

Loma Linda University

Cooperative Institutions

University College London

Newcastle University

University of Minnesota

Centre National de la Recherche Scientifique

Technical University of Denmark

University of Birmingham

Royal Victoria Infirmary

École Nationale Vétérinaire de Toulouse

Université Claude Bernard Lyon 1

Newcastle upon Tyne Hospitals NHS Foundation Trust

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Reversal of severe cognitive impairment following medical treatment of cystic invasive giant prolactinoma

Endocrinology Diabetes and Metabolism Case Reports (2016)

Jakub Bukowczan K. Lois Monika Mathiopoulou Ashley Grossman Robert A. James

Giant prolactinomas are rare tumours of the pituitary, which typically exceed 40 mm in their largest dimension. Impairment of higher cognitive function has been noted post-operatively after transcranial surgery and as a long-term consequence of the radiotherapy treatment. However, there has been little that is reported on such disturbances in relation to the tumour per se, and to our knowledge, there has been none in terms of responsivity to dopamine agonist therapy and shrinkage in these tumours. We present a case of successful restoration of severely impaired cognitive functions achieved safely after significant adenoma involution with medical treatment alone.Giant prolactinomas can be present with profound cognitive defects.Dopamine agonists remain in the mainstay first-line treatment of giant prolactinomas.Mechanisms of the reversible cognitive impairment associated with giant prolactinoma treatment appear to be complex and remain open to further studies.Young patients with giant prolactinomas mandate genetic testing towards familial predisposition.

Prolactinoma

Cognitive Decline

10.1530/edm-15-0111

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Citations (2)

Loss of vision? Clear as crystal!

The Lancet (2010)

Ranjeet Pandit William Innes Nick Strong Robert A. James

Fundus (uterus)

10.1016/s0140-6736(09)61911-5

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Citations (2)

Generation of Missiles by Tornadoes

Robert A. James Edwin G. Burdette Changning Sun

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The Effect of Thyroid Hormone and a Long-Acting Somatostatin Analogue on TtT-97 Murine Thyrotropic Tumors

Thyroid (2000)

Whitney W. Woodmansee David F. Gordon Janet M. Dowding Barbara Stolz Ricardo V. Lloyd

Thyroid hormone inhibits thyrotropin (TSH) production and thyrotrope growth. Somatostatin has been implicated as a synergistic factor in the inhibition of thyrotrope function. We have previously shown that pharmacological doses of thyroid hormone (levothyroxine [LT4]) inhibit growth of murine TtT-97 thyrotropic tumors in association with upregulation of somatostatin receptor type 5 (sst5) mRNA and somatostatin receptor binding. In the current study, we examined the effect of physiological thyroid hormone replacement alone or in combination with the long-acting somatostatin analogue, Sandostatin LAR®, on thyrotropic tumor growth, thyrotropin growth factor-β (TSH-β), and sst5 mRNA expression, as well as somatostatin receptor binding sites. Physiological LT4 replacement therapy resulted in tumor shrinkage in association with increased sst5 mRNA levels, reduced TSH-β mRNA levels and enhanced somatostatin receptor binding. Sandostatin LAR® alone had no effect on any parameter measured. However, Sandostatin LARρ combined with LT4 synergistically inhibited TSH-β mRNA production and reduced final tumor weights to a greater degree. In this paradigm, Sandostatin LAR® required a euthyroid status to alter thyrotrope parameters. These data suggest an important interaction between the somatostatinergic system and thyroid hormone in the regulation of thyrotrope cell structure and function.

Levothyroxine

10.1089/thy.2000.10.533

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Citations (10)

Progesterone Regulated Expression of Flavin-Containing Monooxygenase 5 by the B-Isoform of Progesterone Receptors: Implications for Tamoxifen Carcinogenicity

The Journal of Clinical Endocrinology & Metabolism (1997)

Marilyn M. Miller Robert A. James Jennifer K. Richer David F. Gordon William M. Wood

Progesterone is a key developmental, proliferative, and differentiative hormone in the breast and endometrium, and it can accelerate carcinogenesis in the mammary gland epithelium. In the breast and uterus, progesterone acts through two coexpressed isoforms of progesterone receptors, the B- and A-receptors. To study the function of each isoform in isolation, we previously constructed two breast cancer cell lines that stably and independently express either B-receptors (YB cells) or A-receptors (YA cells). In the present study, YA or YB cells were left untreated, or were treated with the synthetic progestin R5020, and the messages present in each cell line under the two conditions were analyzed by differential display. Two message species are described that are regulated only by B-receptors. One of these is regulated in a ligand-independent manner. A third set of messages, encoding flavin-containing monooxygenase 5 (FMO5), was induced by R5020 only in YB cells. A-receptors appear to be inhibitory. FMOs are involved in the metabolic activation of drugs and xenobiotic compounds, including the antiestrogen tamoxifen, to carcinogenic intermediates. It is possible, therefore, that by upregulating the levels of FMO5, progesterone enhances the carcinogenicity of tamoxifen in target tissues that overexpress progesterone B-receptors.

Progesterone receptor

Antiestrogen

10.1210/jcem.82.9.4239

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Citations (24)

Changes on the stations

Yvonne Cadet‐James Robert A. James Sue McGinty Russell McGregor

The power imbalance in favour of the pastoralists slowly diminished as alternatives to cattle station employment began to emerge. Aboriginal people began to exercise agency in new ways, taking advantage of newly available employment options. For Gugu Badhun people, it took them towards engagement with the wider society and economy away from their traditional land, their protective but confining stations and sometimes from the control of the Act. This chapter focuses on these changing circumstances and the choices which emerged in the first half-century since invasion and 'letting in', from the time of the First World War through much of the twentieth century.

Pastoralism

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Life under the Act

Yvonne Cadet‐James Robert A. James Sue McGinty Russell McGregor

Under Queensland Aboriginal legislation from 1897 until the 1970s, Aboriginal people lived under the constant threat of being removed from their place of residence and sent to one of the many reserves and institutions scattered around the state.

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CT SCAN CAD/CAM SUBPERIOSTEAL IMPLANT

Australian Dental Journal (1994)

Robert A. James

10.1111/j.1834-7819.1994.tb05549.x

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Implant-tissue interface: a case history.

PubMed (1989)

J M Whittaker Daniel J. GaRey Robert A. James

Interface (matter)

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Association Analysis of the Cytotoxic T Lymphocyte Antigen-4 (CTLA-4) and Autoimmune Regulator-1 (AIRE-1) Genes in Sporadic Autoimmune Addison’s Disease¹

The Journal of Clinical Endocrinology & Metabolism (2000)

Bijay Vaidya Helen Imrie D. R. Geatch Petros Perros Steve Ball

Although autoimmune Addison's disease (AAD) may occur as a component of the monogenic autoimmune polyendocrinopathy type 1 syndrome (APS1), it is most commonly found as an isolated disorder or associated with the autoimmune polyendocrinopathy type 2 syndrome (APS2). It is likely that sporadic (non-APS1) AAD is inherited as a complex trait; however, apart from the major histocompatibility complex, the susceptibility genes remain unknown. We have examined polymorphisms at two non-major histocompatibility complex candidate susceptibility loci in sporadic (non-APS1) AAD: the cytotoxic T lymphocyte antigen-4 (CTLA-4) gene and the autoimmune regulator (AIRE-1) gene. DNA samples from AAD subjects (n = 90) and local controls (n = 144 for CTLA-4; n = 576 for AIRE-1) were analyzed for the CTLA-4A/G polymorphism in exon 1 of the CTLA-4 gene and for the common mutant AIRE-1 allele (964del13) in United Kingdom subjects with APS1, by using the restriction enzymes Bst71I and BsrBI, respectively. There was an association of the G allele at CTLA-4A/G in AAD subjects (P = 0.008 vs. controls), which was stronger in subjects with AAD as a component of APS2 than in subjects with isolated AAD. In contrast, the mutant AIRE-1 964del13 allele was carried in one each of the 576 (0.2%) control subjects and the 90 (1.1%) AAD subjects as a heterozygote (P = 0.254, not significant), suggesting that this common AIRE-1 gene abnormality does not have a major role in sporadic (non-APS1) AAD.

Autoimmune regulator

CTLA-4

10.1210/jcem.85.2.6369

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Citations (103)