[Treatment of pupillary blockage in aphakia by vitrectomy].
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Biomedical subjects
Publications and source records attributed to A Robin.
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New psychiatric out-patients were offered immediate or delayed appointments (average delay 12 weeks) in random order. The two groups thus formed, comprising 234 patients, were shown to be comparable in some important respects. Immediate appointments were taken up significantly more frequently than delayed appointments, and 12 per cent of immediate and 22 per cent of delayed patients did not receive any psychiatric service. No evidence was found that delay increased other medical services supplied. Non-attenders were presumed to suffer from "neurosis" and "personality problem". Initial attenders used more services than those who failed to keep their first appointment but came later. A waiting list is proposed as a screening device to limit out-patient referrals.
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A case report on a young man who developed after cranial trauma a typical opsoclonus and neurological symptoms dominated by left sensory hemiparesis of the thalamic type; this deficit affected all sensory modalities and involved the whole of the left side, with disturbances of motility caused by impairment of sensation. A general review of opsoclonus is presented and supported by various neurological tables. The discussion on aetiology takes into account the frequent benign causes (encephalitic syndromes, ataxic forms of poliomyelitis), but also the possibility of serious lesions developing in the cerebellum and cerebrum; and finally there remain a number of cases of unknown aetiology. Clinical observations of opsoclonus are rare, and anatomical data is still less; this is why physiopathological interpretations, the object of interesting discussions, are only reached with wisdom.
Gluconate-resistant mutants were isolated from Escherichia coli strain DF 1070 deficient in phosphogluconate dehydrogenase (EC 1.1.1.44) and in phosphogluconate dehydrogenase (EC 4.2.1.12) which is inhibited by gluconate. Among the resistant mutants, AR 13 has been identified as a gluconate kinase (EC 2.7.1.12)-deficient strain. This mutant exhibits an inducible gluconate transport system capable of concentrating gluconate in the cytoplasm against a concentration gradient. The accumulated gluconate is subject to permanent turnover, and is not chemically modified. The kinetics of induction and deinduction indicate a single inducible component, rate limiting for the transport function, and the distribution of transport capacity among non-induced progeny of induced parents indicates that the inducible protein is membrane bound.
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