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Träfflista för sökning "LAR1:gu ;lar1:(lu);srt2:(1990-1994)"

Sökning: LAR1:gu > Lunds universitet > (1990-1994)

  • Resultat 1-6 av 6
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1.
  • Alian, Wael A, 1970, et al. (författare)
  • Laser-induced fluorescence studies of meso-tetra(hydroxyphenyl)chlorin in malignant and normal tissues in rats.
  • 1994
  • Ingår i: British journal of cancer. - : Springer Science and Business Media LLC. - 0007-0920 .- 1532-1827. ; 70:5, s. 880-5
  • Tidskriftsartikel (refereegranskat)abstract
    • meso-Tetra(hydroxyphenyl)chlorin (mTHPC) is an attractive second-generation dihydroporphyrin photosensitiser for use in photodynamic therapy. In this study, 1.3 mg kg-1 body weight mTHPC was administered intravenously, and laser-induced fluorescence was used to characterise and compare its localisation and retention in different rat tissues, including an induced experimental adenocarcinoma, 24 h and 48 h post injection. These studies were performed in an attempt to predict the anatomical locations where mTHPC PDT might be most effective and suggest suitable injection--irradiation intervals in each case. Of particular interest were the intra-abdominal and intrathoracic tissues. The fluorescence was induced at 405 nm and the fluorescence spectrum in the region 450-750 nm was analysed. All collected spectra were dominated by the fluorescence signature of mTHPC with its peak at 652 nm, and all values in this study are in terms of background-free drug-specific fluorescence intensity at that wavelength. The photosensitiser accumulated in high concentrations in the tumour and the reticuloendothelial system. Muscular organs, such as the heart and the abdominal wall, were characterised by a low drug fluorescence signature.
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2.
  • Allwood, Jens, 1947, et al. (författare)
  • Den kognitiva revolutionen
  • 1993
  • Ingår i: Framtider. Institutet för framtidsstudier, Stockholm. ; 12:1
  • Tidskriftsartikel (refereegranskat)
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3.
  • Deshpande, J, et al. (författare)
  • Ultrastructural changes in the hippocampal CA1 region following transient cerebral ischemia: evidence against programmed cell death.
  • 1992
  • Ingår i: Experimental brain research. Experimentelle Hirnforschung. Expérimentation cérébrale. - 0014-4819. ; 88:1, s. 91-105
  • Tidskriftsartikel (refereegranskat)abstract
    • The ultrastructural changes in the pyramidal neurons of the CA1 region of the hippocampus were studied 6 h, 24 h, 48 h, and 72 h following a transient 10 min period of cerebral ischemia induced by common carotid occlusion combined with hypotension. The pyramidal neurons showed delayed neuronal death (DND), i.e. at 24 h and 48 h postischemia few structural alterations were noted in the light microscope, while at 72 h extensive neuronal degeneration was apparent. The most prominent early ultrastructural changes were polysome disaggregation, and the appearance of electron-dense fluffy dark material associated with tubular saccules. Mitochondria and nuclear elements appeared intact until frank neuronal degeneration. The dark material accumulated with extended periods of recirculation in soma and in the main trunks of proximal dendrites, often beneath the plasma membrane, less frequently in the distal dendrites and seldom in spines. Protein synthesis inhibitors (anisomycin, cycloheximide) and an RNA synthesis inhibitor (actinomycin D), administered by intrahippocampal injections or subcutaneously, did not mitigate neuronal damage. Therefore, DND is probably not apoptosis or a form of programmed cell death. We propose that the dark material accumulating in the postischemic period represents protein complexes, possibly aggregates of proteins or internalized plasma membrane fragments, which may disrupt vital cellular structure and functions, leading to cell death.
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4.
  • Ekström, Per, et al. (författare)
  • A calmodulin inhibitor with high specificity, compound 48/80, inhibits axonal transport in frog nerves without disruption of axonal microtubules.
  • 1991
  • Ingår i: Acta physiologica Scandinavica. - 0001-6772. ; 142:2, s. 181-9
  • Tidskriftsartikel (refereegranskat)abstract
    • The calmodulin inhibitor compound 48/80 has previously been shown to arrest axonal transport in vitro in the regenerating frog sciatic nerve. The inhibition was limited to the outgrowth region of nerves, which had been allowed to regenerate in vivo for 6 days after a crush lesion, before they were incubated with or without drugs in vitro overnight. The effects of compound 48/80 on the regenerating nerve were further investigated. A concentration of compound 48/80 (50 micrograms ml-1), which effectively inhibits axonal transport, did not cause observable changes of the microtubules of regenerating axons in the outgrowth region as judged by electron microscopy. Furthermore, it was shown that also a lower concentration (25 micrograms ml-1) inhibited axonal transport. As a measure of possible metabolic effects, the level of ATP was assessed in the regenerating nerve after exposure to compound 48/80. Compound 48/80 at 25 micrograms ml-1 did not change the level of ATP in the nerve. The assembly of bovine brain microtubule proteins in a cell-free system was unaffected by 25 micrograms ml-1 of compound 48/80 and slightly inhibited by 50 micrograms ml-1. At higher concentrations (greater than 100 micrograms ml-1) assembly of microtubules appeared stimulated, and microtubule spirals as well as closely aligned microtubules could be seen. These effects appeared to be unrelated to the transport effects. The present results indicate that compound 48/80 arrests axonal transport via mechanisms other than destruction of axonal microtubules or interference with the energy metabolism. It is possible that these mechanisms involve inhibition of calmodulin-regulated events essential to the transport.
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6.
  • Riise, Gerdt C., 1956, et al. (författare)
  • Circulating cell adhesion molecules in bronchial lavage and serum in COPD patients with chronic bronchitis
  • 1994
  • Ingår i: Eur Respir J. - 0903-1936. ; 7:9, s. 1673-1677
  • Tidskriftsartikel (refereegranskat)abstract
    • The initial phase of inflammation in bronchial asthma appears to be triggered by the expression of leucocyte-endothelial adhesion molecules on endothelial cell surfaces. Cell adhesion molecules (CAMs) cause adhesion of leucocytes to the endothelium prior to their subsequent extravasation into inflamed tissue. We wanted to determine whether circulating intercellular adhesion molecule-1 (cICAM-1) and circulating E-selectin (cE-selectin) could be detected in bronchial lavage fluid and serum in patients with stable chronic obstructive pulmonary disease (COPD) and chronic bronchitis. Bronchoscopy and small volume bronchial lavage was performed in 19 patients with COPD and chronic bronchitis and in 13 control subjects. We found increased mean levels of cICAM-1 both in serum (481 micrograms.l-1) and in bronchial lavage (24 micrograms.l-1) in the COPD patients as compared to the controls (321 micrograms.l-1 in serum, 15 micrograms.l-1 in lavage). We also found higher mean levels of cE-selectin in serum from the COPD patients (86 micrograms.l-1) compared to controls (50 micrograms.l-1). The serum levels of cE-selectin correlated significantly with lung function measured as forced expiratory volume in one second (FEV1) in percentage of predicted. Patients with significant intrabronchial bacterial colonization had increased levels of serum cE-selectin. Our results indicate that cCAMs may reflect an upregulation of CAMs on endothelial and epithelial airway cells in COPD.
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