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Institution

St Bartholomew's Hospital

HealthcareLondon, United Kingdom
About: St Bartholomew's Hospital is a healthcare organization based out in London, United Kingdom. It is known for research contribution in the topics: Population & Cancer. The organization has 11054 authors who have published 13229 publications receiving 501102 citations. The organization is also known as: St. Bartholomew's Hospital & The Royal Hospital of St Bartholomew.


Papers
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Journal ArticleDOI
01 Sep 1982-Brain
TL;DR: The potential value of muscle biopsy in the diagnosis of unusual and otherwise unexplained cerebral syndromes in man, even in the absence of muscle weakness, is illustrated.
Abstract: We describe two patients with mitochondrial myopathies who presented with complex multisystem diseases predominantly affecting the central nervous system. In both cases the disease ran a fluctuating clinical course, eventually leading to profound impairment of intellectual function. In Case 1 dementia was associated with optic atrophy, absent pupillary responses, impaired eye movements and generalized dystonic rigidity without evidence of weakness or loss of muscle bulk. In Case 2 myoclonus preceded the onset of ataxia, generalized weakness and mental confusion by several years. Biochemical studies on isolated muscle mitochondria revealed defects in the mitochondrial respiratory chain which were located at NADH-CoQ reductase in Case 1, and at cytochrome b in Case 2. This study illustrates the potential value of muscle biopsy in the diagnosis of unusual and otherwise unexplained cerebral syndromes in man, even in the absence of muscle weakness.

189 citations

Journal ArticleDOI
TL;DR: A combined study of clinical and anatomical material employing standardized definitions of the neurovascular relationships in both groups confirms that vascular compression of the fifth cranial nerve is an anatomical abnormality specific to trigeminal neuralgia.
Abstract: Neurovascular decompression is a widely practiced technique for the treatment of trigeminal neuralgia, and yet there is still debate as to whether the beneficial effect results from relieving the nerve of compression by an anatomically abnormal vessel or from the manipulation and trauma the nerve undergoes during the procedure. The development of this operation has been hampered by the lack of adequate anatomical studies in normal controls. The authors present a combined study of clinical and anatomical material employing standardized definitions of the neurovascular relationships in both groups. Detailed simulations of the operative procedure were carried out on fresh cadavers matched for age, sex, and side, and a technique of in situ blood vessel perfusion was developed that enabled the normal neurovascular arrangement to be observed post mortem at physiological pressures. Neurovascular compression, typified by a large vessel distorting and creating a groove in the fifth cranial nerve, was found in 37 of the 41 cases of trigeminal neuralgia; recurrence of pain did not relate to the site of compression. A follow-up study was carried out for a median of 53 months (range 12 to 103 months). No distortion was found in a total of 50 normal cadaveric dissections; however, on perfusion to physiological pressures, the percentage of nerves with vessels adjacent or in simple contact increased from 16% to 40%. This study using this new technique confirms that vascular compression of the fifth cranial nerve is an anatomical abnormality specific to trigeminal neuralgia.

188 citations

Journal ArticleDOI
TL;DR: The receptor present on the endothelium responsible for the release of nitric oxide in response to the ET/SX peptides is most probably different from that present on smooth muscle that mediates BQ‐123‐insensitive contractions.
Abstract: 1. We have compared the receptors mediating the contractions of rings of rat thoracic aorta or rabbit pulmonary artery and rat stomach strips in response to the endothelin/sarafotoxin (ET/SX) family of peptides and to those mediating endothelium-dependent vasodilations within the isolated perfused mesentery of the rat. To discriminate ETA receptors from ETB receptors we have used the criteria that ET-1 is more active than SX6c on ETA receptors, and that the ET/SX peptides are equiactive on ETB receptors. We have also assessed the effects of the ETA receptor-selective antagonist BQ-123, and the non-selective ET receptor antagonist PD 142893 on the responses of each preparation to the ET/SX peptides. 2. ET-1-induced constrictions of the rat thoracic aorta (EC50 3 x 10(-10) M), a prototypic ETA receptor-mediated response, or isolated perfused mesentery of the rat were antagonized by BQ-123 (10(-5) M) or PD 142893 (10(-5) M). SX6c did not constrict either the rat isolated perfused mesentery or the rat thoracic aorta. Thus, ETA receptors mediate these constrictions. 3. ET-1 and SX6c were approximately equipotent in constricting rabbit pulmonary artery rings (EC50S 3-6 x 10(-10) M). Neither BQ-123 (10(-5) M) nor PD 142893 antagonized the contractions induced by ET-1. These effects suggest mediation by ETB receptors but PD 142893 (10(-5) M) did give a 3 fold antagonism of constrictions induced by SX6c. 4. SX6c was more potent than ET-1 in contracting the rat stomach strip (threshold concentrations 10(-10) and 3 x 10(-10) M).(ABSTRACT TRUNCATED AT 250 WORDS)

188 citations

Journal ArticleDOI
TL;DR: It is indicated that human PMNs contain and/or release neutral proteases, which can both rapidly produce and degrade ET-1, an observation which may have important (patho)physiologic implications.

188 citations

Journal ArticleDOI
TL;DR: Comparison of synaptic and non-synaptic mitochondria by rate-zonal separation confirmed the distinct identity of the two mitochondrial populations.
Abstract: A method has been developed whereby a fraction of rat brain mitochondria (synaptic mitochondria) was isolated from synaptosomes. This brain mitochondrial fraction was compared with the fraction of "free" brain mitochondria (non-synaptic) isolated by the method of Clark & Nicklas (1970). (J. Biol. Chem. 245, 4724-4731). Both mitochondrial fractions are shown to be relatively pure, metabolically active and well coupled. 2. The oxidation of a number of substrates by synaptic and non-synaptic mitochondria was studied and compared. Of the substrates studied, pyruvate plus malate was oxidized most rapidly by both mitochondrial populations. However, the non-synaptic mitochondria oxidized glutamate plus malate almost twice as rapidly as the synaptic mitochondria. 3. The activities of certain tricarboxylic acid-cycle and related enzymes in synaptic and non-synaptic mitochondria were determined. Citrate synthase (EC 4.1.3.7), isocitrate dehydrogenase (EC 1.1.1.41) and malate dehydrogenase (EC 1.1.1.37) activities were similar in both fractions, but pyruvate dehydrogenase (EC 1.2.4.1) activity in non-synaptic mitochondria was higher than in synaptic mitochondria and glutamate dehydrogenase (EC 1.4.1.3) activity in non-synaptic mitochondria was lower than that in synaptic mitochondria. 4. Comparison of synaptic and non-synaptic mitochondria by rate-zonal separation confirmed the distinct identity of the two mitochondrial populations. The non-synaptic mitochondria had higher buoyant density and evidence was obtained to suggest that the synaptic mitochondria might be heterogeneous. 5. The results are also discussed in the light of the suggested connection between the heterogeneity of brain mitochondria and metabolic compartmentation.

187 citations


Authors

Showing all 11065 results

NameH-indexPapersCitations
Philippe Froguel166820118816
Geoffrey Burnstock141148899525
Michael A. Kamm12463753606
David Scott124156182554
Csaba Szabó12395861791
Roger Williams122145572416
Derek M. Yellon12263854319
Walter F. Bodmer12157968679
John E. Deanfield12049761067
Paul Bebbington11958346341
William C. Sessa11738352208
Timothy G. Dinan11668960561
Bruce A.J. Ponder11640354796
Alexandra J. Lansky11463254445
Glyn Lewis11373449316
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Performance
Metrics
No. of papers from the Institution in previous years
YearPapers
20232
202216
2021390
2020354
2019307
2018257