[Care of the dying].
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Biomedical subjects
Publications and source records attributed to C Saunders.
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A study of 96 high-risk, but uneventful pregnancies was performed. Overt hyperglycemia was excluded after 24 weeks of gestation by fasting serum glucose >110 mg, serum glucose of >140 mg two hours after a large breakfast (group 1, 44 subjects) or >140 mg two hours after a standard glucose load (group 2, 52 subjects). A significant linear correlation between the two-hour postprandial serum glucose and birth weight was found in group 1 (r = 0.29, p > 0.05). There was a random correlation (r = -0.002, p < 0.4) in group 2. It is suggested that the dietary habits were an important variable.
We describe two patients with osteomyelitis due to Candida spp. treated with fluconazole, a new triazole antifungal. One patient had extensive involvement of ribs and costochondral regions of the anterior chest, and the other had vertebral infection. Both were cured with courses of 10 and 14 months, with greater than or equal to 1 year of follow-up after fluconazole was discontinued. Fluconazole is an attractive agent for the treatment of Candida osteomyelitis and deserves to be studied more extensively for this indication.
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Localization of receptors in discrete cellular microdomains undoubtedly contributes to their interaction with particular effectors and receptor targets. For G protein-coupled receptors, virtually nothing is known about the mechanisms and structural features responsible for their targeting to and retention in varying surface domains. We have shown that the Gi/ Go-coupled alpha 2A-adrenergic receptor (alpha 2AAR) is directly targeted to the lateral subdomain of MDCK II cells. Mutational analysis has revealed that regions in or near the bilayer are likely critical for alpha 2AAR targeting, whereas endofacial domains contribute to alpha 2AAR retention on the lateral surface. Although the alpha 2BAR also is enriched on the lateral subdomain at steady-state, its polarization occurs after initial random delivery to both apical and basolateral surfaces followed by a selective accumulation on the lateral subdomain. The alpha 2CAR also is expressed on the lateral subdomain and achieves its localization via direct delivery to the basolateral surface; however, the alpha 2CAR also exists in an as yet not fully characterized intracellular compartment. Interestingly, another Gi/Go-coupled receptor, the A1 adenosine receptor, is enriched on the apical surface of MDCK II calls and achieves this localization by direct apical delivery. These findings indicate that receptor delivery to polarized surfaces is not determined by receptor coupling to a specific subpopulation of G proteins.
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The classification of inflammatory muscle disorders is at best confusing owing to the wide spectrum of clinical, histological and serological findings within this group of patients. Although it is generally agreed that most cases reflect an autoimmune disorder with skeletal muscle as the primary target tissue, additional features of the more common form of the disease in juvenile patients, dermatomyositis, have suggested that it may differ in aetiology and pathogenesis from other forms of inflammatory muscle disease. Some adults may also be included within this category. In this study, we have divided patients with inflammatory muscle disease into two groups, 8 adult patients with 'pure' polymyositis and 13 children with dermatomyositis, and compared their in vitro lymphocyte function. Abnormal proliferative responses to T-cell mitogens were shown by peripheral blood mononuclear cells (PBM) from adult patients. PBM from the children gave values similar to normal control children. In vitro immunoglobulin production by cells from adult patients was comparable with appropriate controls both in the presence and absence of pokeweed mitogen. Childhood controls responded similarly to normal adults. PBM from the juvenile patients with dermatomyositis, however, produced significantly elevated levels of immunoglobulin spontaneously, with little or no increase for most patients following mitogen stimulation. This defective response was shown to be a consequence of activated T- and B-cells present in their peripheral blood and was not related to clinical parameters or drug therapy.
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