Off-diagonal long-range order in Laughlin's states for particles obeying fractional statistics.
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Biomedical subjects
Publications and source records attributed to N Read.
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A proportion of superficial capillaries in joint synovium are known to be fenestrated. The specialized functions of these fenestrated capillaries are unknown. We report the finding of fenestrae in tenosynovial capillaries from rabbit peroneal tendon sheaths. Fenestrations occupied 0.66% of the endothelial surface. Fenestrated capillaries appear to be a general feature of synovium, rather than a specific feature of joint tissue.
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Antigen-induced arthritis in the rabbit (AIAR) provides the closest experimental equivalent to human rheumatoid arthritis in terms of infiltration of synovial tissue by lymphoid cells. A method is described for quantitative histological analysis of AIAR. Measurements of total cell numbers, lymphocyte and polymorphonuclear leucocyte infiltration, and thickness of infiltrated synovium were obtained for ranges of antigen dosage and duration of arthritis. The method has been devised as part of a system for the analysis of joint swelling, synovial fluid biochemistry and cytology, cartilage proteoglycan chemistry and synovial histology on the same specimen.
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The effect of dexamethasone on bradykinin-induced release of eicosanoids from isolated lungs of guinea-pigs exposed to pure oxygen (O2) is described. Pathological changes were induced in the lungs of guinea-pigs exposed to pure O2 for 72 and 96 h. Bradykinin-induced release of 6-oxo-PGF1 alpha and thromboxane B2 (TXB2) was increased in lungs from guinea-pigs exposed to 72 and 96 h of O2. Removal of PGI2 and PGE2 was not affected by the exposure to O2, but the removal of bradykinin was significantly reduced after 96 h of O2 exposure. Dexamethasone did not reduce bradykinin-induced release of eicosanoids from lungs of control animals, but it did inhibit the release from lungs of guinea-pigs exposed to O2. Dexamethasone had no effect on the metabolism of Bk by the inflamed lungs.
The invasion of leukocytes into and around a myocardial infarct was studied in chloralose-anesthetized dogs subjected to 1-hr occlusion of the left anterior descending coronary artery and reperfused for periods up to 5 hr. Polymorphonuclear leukocytes adhering to the endothelium of blood vessels within the ischemic area are evident at the end of the occlusion period. During reperfusion, the leukocytes migrate into the myocardium and large groups of cells can be observed "streaming" toward the irreversibly damaged area after 5 hr reperfusion. Infarcted tissue produces 10 times more 12-hydroxyeicosatetraenoic acid (a metabolite attributed to the invading leukocytes) from arachidonic acid than adjacent "normal" areas of the ventricle. BW755C (10 mg/kg-1 i.v.), which inhibits both the lipoxygenase and cyclooxygenase pathways of arachidonic metabolism, attenuates leukocyte infiltration into the infarcted myocardium, prevents 12-hydroxyeicosatetraenoic acid formation and significantly reduces infarct size (P less than .005). BW755C also significantly diminishes the incidence of cardiac arrhythmias during infarction. In animals where circulating white cells are reduced 60% by treatment with hydroxyurea (20 mg/kg-1 i.v./day for 5 days), there is also a smaller infarct (P less than .01). Indomethacin (5 mg/kg-1 i.v.) and dexamethasone (0.2 mg/kg-1 i.v.), which do not affect leukocyte migration into the ischemic myocardium, do not reduce infarct size. It is proposed that migrating leukocytes contribute to the tissue injury accompanying myocardial ischemia, possibly by the release of proinflammatory mediators such as lipoxygenase products, free radicals (oxygen metabolites) and hydrolytic enzymes. Drugs which reduce the migration and/or activation of leukocytes may be useful in reducing infarct size.
Using the mutant strain Aspergillus awamori 66A producing a recombinant Ca2+-dependent photosensitive protein aequorin, the dynamics of Ca2+ was studied for the first time in the cytosol of the micromycetes exposed to stressful factors, such as an increase in extracellular Ca2+ to 50 mM, hypoosmotic shock, and mechanical shock. Cell response to stress proved to involve an increase in the Ca2+ concentration in the cytosol, which was determined from the amplitude of aequorin luminescence and the time of the amplitude enhancement and relaxation. The level of Ca2+ response depended on the physiological stimulus. Inhibitory analysis with various agents that block Ca2+ channels and with agonists that specifically enhance the activity of the channels suggested that (1) the level of Ca2+ in the cytosol of micromycetes increases in response to stress because of the ion influx from both the growth medium and intracellular reservoirs and (2) the potential-dependent transport systems play the major role in the Ca2+ influx into the cytosol of the micromycete cells.
General hospital mental health programs in large inner city communities face challenges in developing responsive services for populations facing high rates of serious mental illness, substance abuse, homelessness, and poverty. In addition provincial political pressures such as Mental Health Reform and hospital restructuring have caused general hospital mental health programs to reevaluate how services are delivered and resources are allocated. This paper describes how one inner city mental health service in a university teaching setting developed successful strategies to respond to these pressures. Strategies included: (a) merging two general hospital mental health services to pool resources; (b) allocating resources to innovative care delivery models consistent with provincial reforms and community needs; (c) fostering staff role changes, job transitions, and the development of new professional competencies to complement the innovative care delivery models; and (d) developing processes to evaluate the effects of these changes on client.