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Träfflista för sökning "WFRF:(Palmblad J) srt2:(1995-1999)"

Sökning: WFRF:(Palmblad J) > (1995-1999)

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  • Johansson, J, et al. (författare)
  • Pulmonary surfactant: emerging protein analogues
  • 1999
  • Ingår i: BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy. - : Springer Science and Business Media LLC. - 1173-8804. ; 11:2, s. 71-77
  • Tidskriftsartikel (refereegranskat)
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  • Johansson, J, et al. (författare)
  • Synthetic surfactant protein analogues
  • 1998
  • Ingår i: Biology of the neonate. - : S. Karger AG. - 0006-3126. ; 7474 Suppl 1, s. 9-14
  • Tidskriftsartikel (refereegranskat)abstract
    • Surfactant preparations for the treatment of respiratory distress syndrome (RDS) that contain phospholipids and small amounts of the two hydrophobic proteins, SP-B and SP-C, are presently obtained from animal lungs. Since structural information about SP-B and SP-C is available, it appears possible to design analogues that can replace the native proteins in synthetic surfactants. SP-C contains a single helix, but analogues with the poly-Val sequence of the native molecule do not fold into a native-like α-helical conformation. However, replacement of all Val with Leu yields efficient folding into a helical structure and Leu-based SP-C analogues effectively accelerate spreading of surfactant lipids and exhibit some physiological activity in animal models of RDS. The inferior in vivo activity of synthetic surfactants containing SP-C only compared to that of surfactant preparations derived from natural sources may be caused by a lack of covalently linked palmitoyl groups in the analogues and/or absence of SP-B. SP-B is significantly larger than SP-C and has a tertiary fold of several amphipathic helices in a dimeric structure. A single simplified amphipathic helical peptide containing only Leu and Lys does not mimic the surface properties of SP-B in vitro. These circumstances make the design of SP-B analogues from solely structural considerations less likely to be successful than in the case of SP-C.
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  • LERNER, R, et al. (författare)
  • Development and characterization of essential fatty acid deficiency in human endothelial cells in culture
  • 1995
  • Ingår i: Proceedings of the National Academy of Sciences of the United States of America. - : Proceedings of the National Academy of Sciences. - 0027-8424. ; 92:4, s. 1147-1151
  • Tidskriftsartikel (refereegranskat)abstract
    • We induced an essential fatty acid deficiency (EFAD) in human umbilical vein endothelial cells by culture in medium with 20% (vol/vol) delipidated fetal calf serum. EFAD, reflected by decreased cellular linoleic acid (18:2 omega 6) and arachidonic acid (20:4 omega 6) and emergence of the oleic acid derivative 5,8,11-eicosatrienoic acid (20:3 omega 9; Mead's acid), was evident after 1 week of culture and became pronounced after 2 weeks. Beyond that time point, control cells (cultured in 20% normal fetal calf serum) grew deficient of 18:2 omega 6, and EFAD cells died. 18:2 omega 6 addition to EFAD cells resulted in dose-dependent increases of 18:2 omega 6 and 20:4 omega 6. 20:4 omega 6 or 5,8,11,14,17-eicosapentaenoic acid (20:5 omega 3) additions resulted in normalization of these acids, and conversion of 20:5 omega 3 to 4,7,10,13,16,19-docosahexaenoic acid (22:6 omega 3) was noted. Agonist-induced increases in concentrations of prostacycline (prostaglandin I2; PGI2) and cytosolic Ca2+, [Ca2+]i, were reduced in EFAD cells and not restored by 18:2 omega 6 or 20:4 omega 6 additions. Change of the medium in EFAD cultures 1 day before the experiments decreased 20:3 omega 9 and normalized the PGI2 production and [Ca2+]i changes, whereas addition of 20:3 omega 9 to control cells impaired the [Ca2+]i response, indicating a suppressive effect of 20:3 omega 9. Thus, EFAD in endothelial cells is associated with abnormalities of eicosanoid and second-messenger production partly attributable to 20:3 omega 9 accumulation. Moreover, the gradual emergence of 18:2 omega 6 deficiency in regularly grown control cells underlines the need for careful analysis of fatty acids in long-term cell cultures.
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  • Leusen, JHW, et al. (författare)
  • Disturbed interaction of p21-rac with mutated p67-phox causes chronic granulomatous disease
  • 1996
  • Ingår i: The Journal of experimental medicine. - : Rockefeller University Press. - 0022-1007 .- 1540-9538. ; 184:4, s. 1243-1249
  • Tidskriftsartikel (refereegranskat)abstract
    • Chronic granulomatous disease (CGD) is characterized by the failure of phagocytic leukocytes to generate superoxide, needed for the intracellular killing of microorganisms. This is caused by mutations in any one of the four subunits of the nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. In a rare, autosomal recessive form of CGD, a 67-kD cytosolic component of this enzyme (p67-phox) is missing. We here report on a patient with a mutation in the p67-phox gene that leads to expression of a nonfunctional p67-phox protein. The purified granulocytes of this patient failed to produce superoxide and contained about half of the normal amount of p67-phox. Analysis of the cDNA and genomic DNA of this patient showed that the patient is a compound heterozygote for a triplet nucleotide deletion in the p67-phox gene, predicting an in-frame deletion of lysine 58 in the p67-phox protein and a larger deletion of 11-13 kb in the other allele. Interestingly, the 58Lys deletion in p67-phox disrupts the interaction with p21-rac1, a ras-related protein involved in the activation of the NADPH oxidase. In contrast to normal neutrophils, in which p47-phox and p67-phox translocate to the plasma membrane upon cell activation, the cells of the patient did not show this translocation, indicating that an interaction between p67-phox and p21-rac1 is essential for translocation of these cytosolic proteins and activation of the NADPH oxidase. Moreover, this CGD patient represents the first case of disease caused by a disturbed binding of a ras-related protein to its target protein.
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  • Palmblad, J, et al. (författare)
  • [Chronic neutropenia]
  • 1996
  • Ingår i: Nordisk medicin. - 0029-1420. ; 111:9, s. 304-7
  • Tidskriftsartikel (refereegranskat)
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  • Palmblad, J (författare)
  • Drug-induced neutropenias: now and then
  • 1999
  • Ingår i: Archives of internal medicine. - : American Medical Association (AMA). - 0003-9926. ; 159:22, s. 2745-2745
  • Tidskriftsartikel (övrigt vetenskapligt/konstnärligt)
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  • Palmblad, J, et al. (författare)
  • Host defence mechanisms and ageing
  • 1998
  • Ingår i: BAILLIERES CLINICAL INFECTIOUS DISEASES. - 1071-6564. ; 5:1, s. 1-15
  • Forskningsöversikt (övrigt vetenskapligt/konstnärligt)
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