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- Evertsson, Sofia, 1972-, et al.
(författare)
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Apoptosis in relation to proliferating cell nuclear antigen and Dukes' stage in colorectal adenocarcinoma
- 1999
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Ingår i: International Journal of Oncology. - 1019-6439 .- 1791-2423. ; 15:1, s. 53-58
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Tidskriftsartikel (refereegranskat)abstract
- Colorectal cancer is a disease that is associated with default in the balance of apoptotic regulation. In the present study apoptosis was examined in 158 colorectal adenocarcinomas using the terminal deoxynucleotidyl transferase mediated digoxigenin nick end labeling (TUNEL) method. The median apoptotic index (AI) was 0.95% (range 0-6. 68%). Eighty-two tumours exhibited AI 0.95%. We revealed a positive correlation between apoptosis and proliferation determined as the expression of proliferating cell nuclear antigen (PCNA, p=0.002). The frequency of apoptosis increased from Dukes' stage A, B, C to D (p=0.01). No correlations were found between apoptosis and the patients' sex, age, tumour location, growth pattern, differentiation, prognosis, bcl-2, p53 or K-ras. Our findings suggest that we should further investigate the relationship between apoptosis and cellular proliferative activity in colorectal cancer to evaluate whether this might provide additional information in the selection of patients for effective adjuvant therapy.
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| 2. |
- Fang, Hong, et al.
(författare)
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Detection of imipenem-resistant and metronidazole-resistant Bacteroides fragilis group strains in fecal samples
- 1999
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Ingår i: Clinical Microbiology and Infection. - : Elsevier BV. - 1198-743X .- 1469-0691. ; 5:12, s. 753-758
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Tidskriftsartikel (refereegranskat)abstract
- Objective: To investigate the imipenem and metronidazole resistance profiles of Bacteroides fragilis group strains in fecal samples and to detect the resistance genes (ccrA and nim) coding for imipenem and metronidazole resistance in B. fragilis group strains. Methods: In total, 925 fecal samples, 729 from consecutive diarrhea patients and 196 from healthy controls, were collected at Huddinge University Hospital in 1997. A modified disk diffusion method was employed to screen for imipenem-resistant and metronidazole-resistant B. fragilis group strains. In strains considered resistant by the modified disk diffusion method, the minimum inhibitory concentrations (MICs) were further determined by the agar dilution method. PCR assays were used to detect the carbapenem-hydrolyzing metallo-P-lactamase gene (ccrA) and the 5-nitroimidazole resistance genes (nim) in pure cultures (purePCR), directly from fecal samples through direct broth enrichment (dirPCR) and by immunomagnetic separation (imsPCR). Results: Two imipenem-resistant B. fragilis strains, one of which was simultaneously resistant to metronidazole, and two B. fragilis group strains with MICs near the breakpoint for metronidazole resistance, were isolated from the fecal samples of diarrhea patients. The ccrA gene was identified in all the imipenem-resistant B. fragilis strains by purePCR, dirPCR and imsPCR. The nim genes were also detectable by these PCR assays. Conclusions: The incidences of imipenem-resistant and metronidazole-resistant B. fragilis group strains were low in the investigated diarrhea patients. Simultaneous resistance to imipenem and metronidazole is of great concern in clinical medicine, and the proposed PCR assays may be useful in epidemiologic studies of distribution of resistance genes in the fecal microflora.
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| 4. |
- Hong, J., et al.
(författare)
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Plasma chemistries for high density plasma etching of SiC
- 1999
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Ingår i: Journal of Electronic Materials. - Charlottesville, VA, USA. - 0361-5235 .- 1543-186X. ; 28:3, s. 196-201
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Tidskriftsartikel (refereegranskat)abstract
- A variety of different plasma chemistries, including SF6, Cl2, ICI, and IBr, have been examined for dry etching of 6H-SiC in high ion density plasma tools (inductively coupled plasma and electron cyclotron resonance). Rates up to 4500 angstroms·min-1 were obtained for SF6 plasmas, while much lower rates (≀800 angstroms·min-1) were achieved with Cl2, ICI, and IBr. The F2-based chemistries have poor selectivity for SiC over photoresist masks (typically 0.4-0.5), but Ni masks are more robust, and allow etch depths ≥10 Όm in the SiC. A micromachining process (sequential etch/deposition steps) designed for Si produces relatively low etch rates (<2,000 angstroms·min-1) for SiC.
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| 5. |
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| 6. |
- Sun, Xiao-Feng, et al.
(författare)
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Heat shock protein 72/73 in relation to cytoplasmic p53 expression and prognosis in colorectal adenocarcinomas
- 1997
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Ingår i: International Journal of Cancer. - : John Wiley and Sons, Ltd. - 0020-7136 .- 1097-0215. ; 74:6, s. 600-604
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Tidskriftsartikel (refereegranskat)abstract
- Heat shock proteins (hsp) are molecular chaperones that are increased by various environmental and patho-physiological stimuli. Hsp can bind to mutant/wild-type p53 in tumors and, consequently, could not only regulate p53 accumulation or localization but also modulate its biological effects on cells. However, there is little information available on the significance of hsp expression in colorectal cancer. The aim of our study was to investigate the relationship of hsp to p53 expression, clinico-pathological factors and prognosis in a series of 256 patients with colorectal adenocarcinomas, using immuno-histochemistry. Seventy-five cases exhibited hsp expression in the cytoplasm, with 11 presenting both cytoplasmic and nuclear staining. Hsp expression was related positively to cytoplasmic p53 expression but not to nuclear p53 expression. In the subgroup of rectal tumors, hsp over-expression appeared to predict unfavorable survival, though its prognostic value diminished using multivariate analysis. There were no significant relationships of hsp with patient sex or age, tumor site, Duke's stage, growth pattern or differentiation.
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| 7. |
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| 8. |
- Zhang, Hong, 1957-
(författare)
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Alloxan Toxicity to macrophages and Insulinoma Cells
- 1995
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Doktorsavhandling (övrigt vetenskapligt/konstnärligt)abstract
- Alloxan induces damage and death of pancreatic islet B-cells in severalexperimental animal models, thus causing insulin-dependent diabetes mellitus (IDDM or type I diabetes). This unique cytotoxicity of alloxan has been studied for more than fifty years. The mechanisms behind the cytotoxicity of alloxan have, however, never been fully understood, although an increasing number of authors now suggest formation of reactive oxygen species, targeting the plasma membrane, mitochondria and DNA. In the present study, we have investigated: (i) the production of superoxide and hydrogen peroxide during reactions between alloxan and reducing agents such as cysteine, reduced glutathione, and ascorbic acid; (ii) the cytotoxic effects of alloxan in the absence of reducing agents, on model systems of cultured macrophages and insulinoma cells; (iii) the cytotoxicity of alloxan together with the reducing agents on these cultured cells; (iv) the cytotoxicity of hydrogen peroxide, used at concentrations similar to those formed during the reactions of alloxan with reducing agents; (v) the influence of iron and the iron-chelator, desferrioxamine, on the alloxan-induced cytotoxicity; and (vi) the influence of starvation-induced autophagocytosis on the sensitivity of cells to hydrogen peroxide-induced oxidative stress. Cell viability was estimated by a delayed trypan blue dye exclusion test and plasma membrane permeability by a modified microfluorometric combined fluorescein diacetate-propidium iodide staining technique. Lysosomal membrane stability was microfluorometrically assayed by acridine orange and neutral red relocalization techniques. The intracellular amounts of iron, reduced glutathione, antioxidant enzymes, and ATP were biochemically and cytochemically studied under a variety of conditions. The results showed that: (i) superoxide artion radicals and hydrogen peroxide were produced by reactions between alloxan and several reducing agents (e.g. cysteine, reduced glutathione and ascorbic acid). Hydrogen peroxide readily diffused through cellular membranes into the lysosomes if it was not previously degraded by the cellular antioxidative defence systems. Hydroxyl radicals might be produced by intralysosornal Fenton reactions, if reactive iron was present, resulting in lysosomal membrane damage followed by a leakage of lysosomal lytic enzymes with ensuing cell degeneration and eventually cell death. (ii) If iron was adsorbed to plasma membranes, extracellularly produced superoxide anion radicals and hydrogen peroxide might cause the plasma membrane damage due to Fenton reactions. (iii) Preincubation with desferrioxamine, or the presence of catalase inhibited the cytotoxicity induced by alloxan and reducing agents. (iv) The antioxidative defence activity of insulinoma cells was low. (v) Starvation in PBS enhanced the sensitivity of both macrophages and insulinoma cells to oxidative stress induced by hydrogen peroxide mediated through increased activity of autophagocytotosis. Thus, the amount of intralysosomal reactive iron consequently resulted from the degradation of various iron-containing metallo-proteins. We conclude that the exposure of cells to alloxan together with a reducing agent created cellular oxidative stress through extracellular formation of superoxide anion radicals and hydrogen peroxide. The latter compound easily penetrated plasma and lysosomal membranes, reaching the lysosomal interior. If enough reactive iron was present within lysosomes and the hydrogen peroxide was not degraded by catalase or glutathione peroxidase before entering the acidic vacuolar apparatus hydroxyl radicals could be produced via intralysosomal Fenton reactions.The hydroxyl radicals, in turn, would attack and damage the lysosomalmembranes, causing a leakage of lysosomal enzymes to the cytosol and eventually leading to cell death. The sensitivity of cells to alloxan-induced cytotoxicity in the presence of reducing agents was therefore a function of (i) the rate of hydrogen peroxide production, (ii) the cellular antioxidative defence systems, (iii) the lysosomal amount of reactive iron, and (iv) the capacity of autophagocytosis.
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