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- Lee, SY, et al.
(författare)
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Effect of magnetized electron cooling on a Hopf bifurcation
- 1996
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Ingår i: PHYSICAL REVIEW E. - : AMER INST PHYSICS. ; 53:1, s. 1287-1290
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Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)abstract
- We have observed longitudinal limit cycle oscillations of a proton beam when a critical threshold in the relative velocity between the proton beam and the cooling electrons has been exceeded. The threshold for the bifurcation of a fixed point into a limit
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- Lernmark, Å, et al.
(författare)
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Heterogeneity of islet pathology in two infants with recent onset diabetes mellitus
- 1995
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Ingår i: Virchows Archiv. - 0945-6317. ; 425:6, s. 631-640
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Tidskriftsartikel (refereegranskat)abstract
- The mechanisms by which the beta cells of pancreatic islets are destroyed in insulin-dependent diabetes mellitus (IDDM) are poorly understood. In this report the pancreatic histo- and immunopathology of two children, both HLA-DR 3/4, DQ 2/8 positive and who both died from cerebral oedema within a day of clinical diagnosis of IDDM, were investigated. Patient 1, a 14-month-old girl, had a 4-week history of polydipsia and polyuria. Patient 2, a 3-year-old boy, had 2 days of illness. Both patients had a similarly severe loss of insulin cells but differed markedly as to the extent of lymphocytic islet infiltration (insulitis). Apart from insulitis, marked islet macrophage infiltration was demonstrated in both patients with the HAM-56 monoclonal antibody. Neither patient showed aberrant expression of HLA class II antigens on insulin-immunoreactive cells, but allele-specific HLA-DQ8 expression was evident on endothelial cells. Glutamic acid decarboxylase immunoreactivity was detected in both insulin- and glucagon-immunoreactive cells. It is concluded that the heterogeneity of islet pathology, especially insulitis, may reflect different dynamics and extent rather than different pathomechanisms of immune destruction of islets in IDDM.
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- Tamás, Markus J., 1970, et al.
(författare)
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Fps1p controls the accumulation and release of the compatible solute glycerol in yeast osmoregulation.
- 1999
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Ingår i: Molecular microbiology. - 0950-382X .- 1365-2958. ; 4, s. 1087-104
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Tidskriftsartikel (refereegranskat)abstract
- The accumulation of compatible solutes, such as glycerol, in the yeast Saccharomyces cerevisiae, is a ubiquitous mechanism in cellular osmoregulation. Here, we demonstrate that yeast cells control glycerol accumulation in part via a regulated, Fps1p-mediated export of glycerol. Fps1p is a member of the MIP family of channel proteins most closely related to the bacterial glycerol facilitators. The protein is localized in the plasma membrane. The physiological role of Fps1p appears to be glycerol export rather than uptake. Fps1 delta mutants are sensitive to hypo-osmotic shock, demonstrating that osmolyte export is required for recovery from a sudden drop in external osmolarity. In wild-type cells, the glycerol transport rate is decreased by hyperosmotic shock and increased by hypo-osmotic shock on a subminute time scale. This regulation seems to be independent of the known yeast osmosensing HOG and PKC signalling pathways. Mutants lacking the unique hydrophilic N-terminal domain of Fps1p, or certain parts thereof, fail to reduce the glycerol transport rate after a hyperosmotic shock. Yeast cells carrying these constructs constitutively release glycerol and show a dominant hyperosmosensitivity, but compensate for glycerol loss after prolonged incubation by glycerol overproduction. Fps1p may be an example of a more widespread class of regulators of osmoadaptation, which control the cellular content and release of compatible solutes.
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