| 1. |
- Cao, Jun, et al.
(författare)
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Helicobacter pylori-antigen-binding fragments expressed on the filamentous M13 phage prevent bacterial growth
- 2000
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Ingår i: Biochimica et Biophysica Acta - General Subjects. - 0304-4165 .- 1872-8006. ; 1474:1, s. 107-113
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Tidskriftsartikel (refereegranskat)abstract
- Colonization of the human stomach by Helicobacter pylori is associated with the development of gastritis, duodenal ulcer, mucosa-associated lymphoid tissue (MALT) lymphoma, and gastric cancer. H. pylori-antigen-binding single-chain variable fragments (ScFv) were derived from murine hybridomas producing monoclonal antibodies and expressed as a g3p-fusion protein on a filamentous M13 phage. The recombinant ScFv-phage reacted specifically with a 30-kDa monomeric protein of a H. pylori surface antigen preparation and by means of immunofluorescence microscopy the phage was shown to bind to both the spiral and coccoid forms of the bacterium. In vitro, the recombinant phage exhibited a bacteriocidal effect and inhibited specifically the growth of all the six strains of H. pylori tested. When H. pylori was pretreated with the phage 10 min before oral inoculation of mice, the colonization of the mouse stomachs by the bacterium was significantly reduced (P<0.01). The results suggest that genetic engineering may be used to generate therapy-effective phages.
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| 2. |
- Li, K., et al.
(författare)
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MBE-based SiGe/Si heterojunction multilayer structures
- 2001
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Ingår i: Journal of Crystal Growth. - 0022-0248 .- 1873-5002. ; 227-228, s. 744-748
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Konferensbidrag (övrigt vetenskapligt/konstnärligt)abstract
- In this paper, SiGe/Si multilayer heterostructures prepared by molecular beam epitaxy (MBE) are described with the aim of manufacturing SiGe heterojunction bipolar transistors (HBTs). Based on the simulations made by Medici, device structures have been designed and grown. The quality of the MBE layered structures has been characterized by reflection high-energy electron diffraction, X-ray diffraction, secondary ion mass spectrometry and spreading resistance. Furthermore, SiGe-HBTs have been fabricated. Promising DC and RF results of processed HBT devices have been obtained. © 2001 Elsevier Science B.V.
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| 3. |
- Yuan, Xi Ming, 1959-, et al.
(författare)
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Lysosomal destabilization during macrophage damage induced by cholesterol oxidation products
- 2000
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Ingår i: Free Radical Biology & Medicine. - 0891-5849 .- 1873-4596. ; 28:2, s. 208-218
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Tidskriftsartikel (refereegranskat)abstract
- We have previously shown that oxidized low-density lipoprotein (LDL) induces damage to the macrophage lysosomal membranes, with ensuing leakage of lysosomal contents and macrophage cell death. Cholesterol oxidation products (ChOx) have been reported to be the major cytotoxic components of oxidized LDL/LDL− and also to stimulate cholesterol accumulation in vascular cells. In the present study, we characterized the initial events during macrophage damage induced by cholesterol oxidation products (ChOx). Within 24 h of exposure, ChOx caused lysosomal destabilization, release to the cytosol of the lysosomal marker-enzyme cathepsin D, apoptosis, and postapoptotic necrosis. Enhanced autophagocytosis and chromatin margination was found 12 h after the exposure to ChOx, whereas apoptosis and postapoptotic necrosis was pronounced 24 and 48 h after the exposure. Some lysosomal vacuoles were then filled with degraded cellular organelles, indicating phagocytosis of apoptotic bodies by surviving cells. Because caspase-3 activation was detected in the ChOx-exposed cells, lysosomal destabilization may associate with the leakage of lysosomal enzymes, and activation of the caspase cascade. MnSOD mRNA levels were markedly increased after 24 h of exposure to ChOx, suggesting associated induction of mitochondrial protection repair or turnover. We conclude that ChOx-induced damage to lysosomes and mitochondria are sequelae to the cascade of oxysterol cytotoxic events. The early disruption of lysosomes induced by ChOx, with resultant autophagocytosis may be a critical event in apoptosis and/or necrosis of macrophages/foam cells during the development of atherosclerotic lesions.
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