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Query: UMLS:C0694563 (eds)
 1,062 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Posterior subcapsular cataracts (PSCC) occur in a high percentage of patients treated with long-term systemic corticosteroids (Naumann Gott, Apple DJ, eds: Pathology of the Eye. New York: Springer-Verlag, 1986). Fifteen patients with cystic fibrosis treated at Duke University Medical Center between January 1982 and October 1987 required prednisone for treatment of allergic bronchopulmonary aspergillosis (ABPA). Two of these patients (13.3%) were noted to have PSCC during prednisone therapy. We retrospectively examined factors associated with steroid administration that may have been predictive of the development of PSCC in these patients including: 1) steroid therapy for longer than 2 years, 2) steroid dose of 10 mg/day or greater for longer than 6 months, 3) steroid dose of 40 mg/day or greater for longer than 2 months, and 4) change in linear growth pattern during steroid therapy. None of these factors predicted the risk of developing PSCC. Therefore, we recommend that all patients with cystic fibrosis who receive steroids for the treatment of a concomitant condition such as ABPA should undergo careful examination for opacities of the ocular lens at each clinical visit regardless of the duration or dose of steroids.
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PMID:Risk factors for the development of posterior subcapsular cataracts in patients with cystic fibrosis and allergic bronchopulmonary aspergillosis treated with corticosteroids. 274 22

Inositol phosphate formation in response to cholinergic stimulation was studied in cultured human sweat duct cells, prelabelled with myo-[2-3H]inositol. Formation of inositol mono-, bis-, tris- and tetrakisphosphates was increased after 15 min stimulation by 30 microM carbachol. Formation of inositol 1,3,4-trisphosphate and inositol tetrakisphosphate was significantly increased within 1 min at carbachol concentrations between 10 microM and 100 microM. No detectable increase in inositol 1,4,5-trisphosphate formation was observed at 15 s or 1 min, but an increase was observed after 15 min at a carbachol concentration of 30-100 microM. The data are consistent with an involvement of inositol polyphosphates in the biphasic response of ion transport, to cholinergic stimulation in these cells (see Pederson, P.S. (1986) 6th Professional Conference "Broken Arrow 1986". Genetic and Eptihelial Dysfunction in Cystic Fibrosis (Riordan, J.R. and Buchwalds, M., eds.), Alan Liss, New York and Pedersen, P.S. (1987) Med. Sci. Res. 15, 769-770) and suggest a different pattern of metabolism from exocrine acinar cells.
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PMID:Formation of inositol polyphosphates in cultured human sweat duct cells in response to cholinergic stimulation. 292 Jan 83

It has been assumed in the past that pancreatic acinar cells represent an irreversible end stage in development. Consequently, when there was an increase in structures that had the morphology of ductules, the interpretation was that they were derived from the proliferation of stem cells and/or pre-existing ductular cells. Pancreatitis, however, is regressive in nature [Bockman (1984) In: Pancreatitis: Concepts and Classification. Gyr, K.E., Singer, M.V., Sarles, H., eds. Elsevier, Amsterdam, pp. 11-15]. That is, it is characterized by parenchymal destruction and loss, rather than by expansion of parenchyma. Furthermore, it was assumed that the organization of the pancreatic parenchyma is like bunches of grapes, with spheroidal acini representing the grapes, and the ductules representing the stems. Given this organization, it would be difficult to understand how regressive changes could lead to clusters of ductular structures. Investigations using three-dimensional reconstruction and retrograde injections have altered our idea of pancreatic organization. In addition to spheroidal acini, there also are other shapes, including tubular acini. Moreover, ductules do not necessarily stop when they encounter an acinus. They may emerge on the other side. Combined ductular and acinar lumina may anastomose with each other. It is now clear that pancreatic acini may undergo redifferentiation, taking on the morphology of ductules and forming tubular complexes during pancreatitis, as well as in response to pancreatic cancer, cystic fibrosis, or blockage of the ductal system. With this understanding of pancreatic architecture and morphological plasticity, it is easier to understand the changes one sees with pancreatic diseases.
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PMID:Morphology of the exocrine pancreas related to pancreatitis. 922 Apr 28