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Biomedical subjects

G Erdos

Publications and source records attributed to G Erdos.

At least 19 recordsLinked to original sources
PubMed2005

Hearts and mouths: perceptions of oral hygiene by at-risk heart surgery patients.

OBJECTIVE: To assess and use the attitudes of patients who are placed at risk after valvular heart surgery due to the connection between poor oral hygiene, valvular heart disease/surgery and the risk of developing infective endocarditis. DESIGN: A qualitative (focus group) design based study carried out on subjects three months post heart surgery. METHOD: There were five focus groups of five participants each convened by an experienced moderator. RESULTS: These portrayed an apparent pressing desire by most patients to talk about their experiences. However, patients did not accept the link between their oral health and their general health. Oral hygiene practices were not necessarily oral health related. CONCLUSIONS: The importance of the study in understanding the reasons for a patient's behaviour is evident when there is a clear need to modify the behaviour patterns of the patients effectively. Clinical trials can now be developed based on these results.

Adult↗
PubMed2005

Cassini magnetometer observations during Saturn orbit insertion.

Cassini's successful orbit insertion has provided the first examination of Saturn's magnetosphere in 23 years, revealing a dynamic plasma and magnetic environment on short and long time scales. There has been no noticeable change in the internal magnetic field, either in its strength or its near-alignment with the rotation axis. However, the external magnetic field is different compared with past spacecraft observations. The current sheet within the magnetosphere is thinner and more extended, and we observed small diamagnetic cavities and ion cyclotron waves of types that were not reported before.

Journal Article↗
PubMed2001

Direct transfection and activation of human cutaneous dendritic cells.

Gene therapy techniques can be important tools for the induction and control of immune responses. Antigen delivery is a critical challenge in vaccine design, and DNA-based immunization offers an attractive method to deliver encoded transgenic protein antigens. In the present study, we used a gene gun to transfect human skin organ cultures with a particular goal of expressing transgenic antigens in resident cutaneous dendritic cells. Our studies demonstrate that when delivered to human skin, gold particles are observed primarily in the epidermis, even when high helium delivery pressures are used. We demonstrate that Langerhans cells resident in the basal epidermis can be transfected, and that biolistic gene delivery is sufficient to stimulate the activation and migration of skin dendritic cells. RT-PCR analysis of dendritic cells, which have migrated from transfected skin, demonstrates the presence of transgenic mRNA, indicating direct transfection of cutaneous dendritic cells. Importantly, transfected epidermal Langerhans cells can efficiently present a peptide derived from the transgenic melanoma antigen MART-1 to a MART-1-specific CTL. Taken together, our results demonstrate direct transfection, activation, and antigen-specific stimulatory function of in situ transduced human Langerhans cells.

Biolistics↗
PubMed1998

DQAsomes: a novel potential drug and gene delivery system made from Dequalinium.

PURPOSE: Dequalinium, a drug known for over 30 years, is a dicationic amphiphile compound resembling bolaform electrolytes. The purpose of our work was to determine the state of aggregation of dequalinium in aqueous medium and to investigate both, its ability to bind DNA and its potential to serve as a novel non-viral transfection vector. METHODS: The form of aggregation was determined employing electron microscopic techniques. The DNA binding capacity of dequalinium was assayed using SYBR Green I stain. For in vitro cell transfection experiments plasmid DNA encoding for firefly luciferase was used. RESULTS: Dequalinium forms in aqueous medium liposome-like aggregates, which we term DQAsomes. These dequalinium vesicles bind DNA and they are able to transfect cells in vitro with an efficiency comparable to Lipofectin. CONCLUSIONS: Based on the intrinsic properties of dequalinium such as the in vivo selectivity for carcinoma cells and selective accumulation in mitochondria we propose DQAsomes as a novel and unique drug and gene delivery system.

Animals↗
PubMed1998

[Molecular effects of a microbicidal substance on relevant microorganisms: electron microscopic and biochemical studies on povidone-iodine].

The microbicidal activity of the broad spectrum antimicrobial agent povidone-iodine is due to the strong oxidizing effects of free iodine on functional groups of amino acids, nucleotides and double bonds of unsaturated fatty acids. While the chemical mechanism of action of PVP-iodine is well understood, the actual sequence of events on the cellular and molecular level that causes rapid cell death has not been fully understood. The aim of this study was to elucidate effects of povidone-iodine on cell ultrastructure by electron microscopy and to monitor changes in enzyme activity and nucleotide efflux. Staphylococcus aureus, E. coli and C. albicans, medically relevant gram-positive, gram-negative and yeast micro-organisms, served as models. In the presence of povidone-iodine, rapid partitioning of the cytoplasm and pronounced coagulation of nuclear material was noted. Especially C. albicans exhibited a rapid, dose-dependent "loosening" of the cell wall; cells remained intact without lysis, rupture or wall breakage. Changes in beta-galactosidase and nucleotide concentrations were measured in E. coli. A rapid and dose-dependent loss of cellular beta-galactosidase activity was found, with no increase in the supernatant; loss of cellular nucleotides corresponded with an increase in the supernatant. Electron microscopy and biochemical observations support the conclusion that povidone-iodine interacts with cell walls of micro-organisms causing pore formation or generating solid-liquid interfaces at the lipid membrane level which lead to loss of cytosol material, in addition to enzyme denaturation. The chemical mechanism of action explains the fact that povidone-iodine does never generate resistance in micro-organisms.

Anti-Infective Agents, Local↗
PubMed1997

Molecular effects of povidone-iodine on relevant microorganisms: an electron-microscopic and biochemical study.

The aim of this study was to elucidate the effects of povidone-iodine (PVP-I) on cell ultrastructure by electron microscopy and to monitor changes in enzyme activity and nucleotide efflux. Staphylococcus aureus, Escherichia coli and Candida albicans, medically relevant gram-positive, gram-negative and yeast microorganisms, served as models. In the presence of PVP-I, rapid partitioning of the cytoplasm and pronounced coagulation of nuclear material was noted. E. coli and S. aureus showed no major structural wall damage. C. albicans exhibited a rapid, dose-dependent 'loosening' of the cell wall; cells remained intact without lysis, rupture or wall breakage. Changes in beta-galactosidase and nucleotide concentrations were measured in E. coli. A rapid and dose-dependent loss of cellular beta-galactosidase activity was found, with no increase in the supernatant; loss of cellular nucleotides corresponded with an increase in the supernatant. Electron-microscopic and biochemical observations support the conclusion that PVP-I interacts with cell walls of microorganisms causing pore formation or generating solid-liquid interfaces at the lipid membrane level which lead to loss of cytosol material, in addition to enzyme denaturation.

Anti-Infective Agents, Local↗
PubMed1996

Hypoglycemia-induced AP-1 transcription factor and basic fibroblast growth factor gene expression in multidrug resistant human breast carcinoma MCF-7/ADR cells.

We investigated the effect of hypoglycemic treatment on the activation of the AP-1 transcription factors and the regulation of basic fibroblast growth factor (bFGF) gene expression in multidrug resistant human breast carcinoma MCF-7/ADR cells. Northern blot and gel mobility shift assays showed that hypoglycemic treatment induced c-jun and c-fos gene expression, AP-1 binding activity, as well as bFGF gene expression. Moreover, transfected cells expressing high levels of abnormal c-Jun protein exhibited a reduction in the bFGF protein levels compared to parental cells. A potent protein kinase C (PKC) inhibitor, H-7 (60 micrograms/ml) suppressed the stress-induced bFGF gene expression. Our study also demonstrated that H-7 did not facilitate the decay of bFGF mRNA. Thus, the suppression of bFGF gene expression by treatment with H-7 was due to the effect of the drug on the synthesis of bFGF mRNA rather than the stability of bFGF mRNA. Our data suggest that hypoglycemia-induced bFGF gene expression is mediated through the activation of PKC and the AP-1 transcription factors.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1995

Effect of ionizing radiation on AP-1 binding activity and basic fibroblast growth factor gene expression in drug-sensitive human breast carcinoma MCF-7 and multidrug-resistant MCF-7/ADR cells.

We studied the effect of ionizing radiation on the activation of the AP-1 transcription factors and the regulation of basic fibroblast growth factor (bFGF) gene expression in drug-sensitive human breast carcinoma (MCF-7) cells and its drug-resistant variant (MCF-7/ADR) cells. Northern blot and gel mobility shift assays showed that 135 cGy of ionizing radiation induced c-jun and c-fos gene expression, AP-1 binding activity, as well as bFGF gene expression in MCF-7/ADR cells. In MCF-7 cells, however, we observed little/no induction of bFGF gene expression and AP-1 binding activity after the stress. Nevertheless, MCF-7 cells transfected with plasmids containing c-jun gene contain high levels of bFGF protein. H-7 (60 micrograms/ml), a potent protein kinase C (PKC) inhibitor, inhibited the stress-induced AP-1 binding activity and bFGF gene expression in MCF-7/ADR cells. Corroborating this observation, overexpression of PKC alpha induced bFGF gene expression in MCF-7 cells. Taken together, these results suggest that stress-induced bFGF gene expression is mediated through the activation of PKC and AP-1 transcription factors. Differences in the levels of PKC activity and AP-1 binding factors may be responsible for differential expression of bFGF among breast cancer cell lines. Although there are large differences in response to ionizing radiation between MCF-7 and MCF-7/ADR cell lines, we observed no significant differences in radiocytotoxicity between them.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1995

Differential effect of 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) on alpha B-crystallin and hsp70 gene expression in murine cell lines.

We studied the effect of isoquinolinesulfonamide derivatives (H-7, H-8, and HA1004) on the expression of two heat shock genes (alpha beta-crystallin and hsp70) in NIH 3T3 and Swiss 3T3 cells after heat shock at 45 degrees for 10 min. Western blots and northern blots showed that H-7 effectively suppressed the accumulation of HSP70 and alpha B-crystallin mRNA as well as the synthesis of their proteins. The degree of suppression was dependent upon the concentration of the drug. Moreover, the expression of the hsp genes was differentially suppressed by H-7. The expression of the alpha B-crystallin gene was more effectively inhibited than that of the hsp70 gene by H-7. Nuclear run-on assay demonstrates that this difference was due to the differential effect of H-7 on the elongation of transcription of different hsp genes.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Effect of 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7) on HSP70 and HSP28 gene expression and thermotolerance development in human colon carcinoma cells.

The effect of 1-(5-isoquinolinesulfonyl)-2-methylpiperazine (H-7), a potent protein kinase C (PKC) inhibitor, on the development of thermotolerance and expression of heat shock genes (HSP70 and HSP28) was investigated in human colon carcinoma HT-29 cells. After acute heating at 45 degrees for 15 min, cells became resistant to a challenge heat shock. The development of thermotolerance was suppressed by adding H-7 after heat shock. Northern blots show that the levels of HSP70 and HSP28 mRNA increased rapidly and reached maximal values within 6 hr. H-7 suppressed the accumulation of HSP70 and HSP28 mRNA as well as their protein synthesis, and the level of suppression was concentration dependent. However, little effect was observed if the drug was added 1 hr before and during heat shock. These results suggest that PKC is involved in the regulation of heat shock gene expression after acute heat shock.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Mechanism of quercetin-induced suppression and delay of heat shock gene expression and thermotolerance development in HT-29 cells.

Previous studies have shown that a combination of low pH and quercetin (QCT) treatment following heat shock markedly suppresses and delays the expression of heat shock protein genes, particularly the HSP70 gene (Lee et al., Biochem. Biophys. Res. Commun., 186:1121-1128, 1992). The possible mechanism for alteration of gene expression by treatment with QCT at low pH was investigated in human colon carcinoma cells. Cells were heated at 45 degrees C for 15 min and then incubated at 37 degrees C for various times (0-12 h) with QCT (0.05-0.2 mM) at pH 7.4 or 6.5. Gel mobility-shift analysis of whole cell extracts from heated cells showed the formation of the heat shock transcription factor (HSF)-heat shock element (HSE) complex. Dissociation of HSF from the HSE of the human HSP70 promotor occurred within 4 h under both pH conditions. The kinetics of recovery were not affected by treatment with 0.1% dimethyl sulfoxide (DMSO). However, the dissociation of HSF-HSE complex was markedly delayed during treatment with a combination of low pH and QCT. In addition, in vitro transcription assays showed a suppression of initiation and elongation of HSP70 mRNA. These results may explain why the combination of low pH and QCT treatment suppresses and delays the HSP70 gene expression as well as thermotolerance development.

Base Sequence↗
PubMed1994

Regulation of HSP70 and HSP28 gene expression: absence of compensatory interactions.

We have previously reported the lack of HSP28 gene expression during acute and chronic thermotolerance development in L929 cells (J Cell Physiol 152: 118-125, 1992; Cancer Res 52: 5787, 1992). In contrast to HSP28, an extremely high level of inducible HSP70 synthesis was observed. These results led us to investigate the possibility of compensatory interactions between HSP70 and HSP28. To test the hypothesis, L929 cells were transfected with the human HSP28 gene contained in plasmid pCMV27. Data from Western blot and two-dimensional gel electrophoresis of [3H] leucine and [32P] orthophosphate-labeled proteins showed the synthesis and phosphorylation of HSP28 in transfected cells after heating at 45 degrees C for 10 min. However, the expression of constitutive and inducible HSP70 genes, along with the synthesis of their proteins, was not decreased after heat shock. These results suggest an independent regulation of HSP28 and HSP70 gene expression.

Animals↗
PubMed1994

Effect of staurosporine on the transcription of HSP70 heat shock gene in HT-29 cells.

We have investigated the effects of staurosporine (STP), an inhibitor of PKC, on the expression of the HSP70 gene in human colon carcinoma HT-29 cells. Cells were heated at 45 degrees C for 15 min and incubated at 37 degrees C for up to 6 hr with or without STP. When STP (5 micrograms/ml) was added during 37 degrees C incubation, the accumulation of HSP70 mRNA was suppressed. The suppression of the mRNA accumulation was due to the decrease in initiation and elongation activity of the HSP70 gene. Our study also demonstrated that the effect of STP on the elongation and accumulation of HSP70 mRNA appeared to be selective and the drug did not influence the elongation and accumulation of the house keeping gene, beta-actin mRNA. In addition, the drug did not alter the early response of heat shock gene expression, the heat-induced HSF binding activity. These results suggest that STP affects the late response of the transcriptional regulatory system of HSP genes.

Actins↗
PubMed1994

Effect of isoquinolinesulfonamides on heat shock gene expression during heating at 41 degrees C in human carcinoma cell lines.

The possible involvement of PKC in the regulation of heat shock genes expression was investigated with three isoquinolinesulfonamide derivatives (H-7, H-8, and HA1004) in DUT-145, MCF-7, and MCF-7/ADR cells. The drug was added 1 hr before and during heating at 41 degrees C. Northern blots show that the levels of HSP70 and HSP28 mRNA increased rapidly and reached maximal values within 4-8 hr and 8-12 hr, respectively. H-7 and H-8 which are potent PKC inhibitors selectively suppressed the accumulation of HSP70 mRNA as well as the synthesis of HSP70. In contrast, HA1004 which is a potent PKA inhibitor but a weak PKC inhibitor did not affect HSP70 gene expression. These results suggest that PKC rather than PKA plays an important role in the regulation of heat shock gene expression.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1993

Homoharringtonine induces heat protection and facilitates dissociation of heat shock transcription factor and heat shock element complex.

We investigated the effects of combined treatment with homoharringtonine (HHT) and hyperthermia on cytotoxicity and transcriptional regulation of heat shock genes in human colon carcinoma (HT-29) cells. The drug (100 ng/ml) which inhibited protein synthesis by 93% protected cells from killing at 43 degrees C. For example, treatment with HHT 2 hr before and during heating produced a 9-fold increase in survival from 3.7 x 10(-2) to 3.2 x 10(-1) after 10 hr at 43 degrees C. Little or no protection was observed if the drug was added only during heating. Interestingly, adding the drug (100 ng/ml) 2 hr before and during heat facilitated the dissociation of heat shock transcription factor-heat shock element (HSF-HSE) complex during continuous heating at 43 degrees C. These findings related to the literature suggest that the free pool of HSC70 is increased by inhibiting protein synthesis. An increase in the level of free HSC70 may more effectively protect or repair thermolabile targets and consequently affect regulation of heat shock response.

Antineoplastic Agents, Phytogenic↗
PubMed1993

Effect of staurosporine on suppression of heat shock gene expression and thermotolerance development in HT-29 cells.

Staurosporine, an inhibitor of protein kinase C (PKC), was selected to determine the effect of drug on the development of thermotolerance and the expression of heat shock protein genes. Experiments were carried out with human colon carcinoma HT-29 cells. Heat shock induction consisted of 45 degrees C for 15 min and subsequent incubation at 37 degrees C for 6 h. Thermotolerance developed rapidly, reached its maximum at 6 h after heat shock, and decayed gradually. At maximal thermal resistance, thermotolerance ratio at 10% isosurvival was 3.8. The development of thermotolerance was markedly inhibited by treatment with staurosporine (0.1-5.0 micrograms/ml). Exposure to 1.0 and 5.0 micrograms/ml staurosporine reduced thermotolerance ratio to 1.8 and 1.1 respectively. Further, the levels of heat shock protein genes (HSP 28 and 70) encoding mRNA were equally reduced by the drug treatment. These results suggest that PKC is involved in the regulation of heat shock gene expression and development of thermotolerance.

Alkaloids↗
PubMed1993

Immunogold localization of porcine oviductal secretory proteins within the zona pellucida, perivitelline space, and plasma membrane of oviductal and uterine oocytes and early embryos.

The objectives of the present study were to develop an antibody probe to the porcine estrogen-dependent oviductal glycoproteins and to determine, by use of immunogold electron microscopy, whether these glycoproteins become associated with oviductal and uterine oocytes and early embryos. Polyclonal antibody, prepared using the M(r) 75,000-85,000 glycoprotein, separated from other proteins by two-dimensional SDS-PAGE, specifically recognized all three estrogen-dependent glycoproteins (acidic 75,000-85,000 M(r); acidic 100,000 M(r); basic 100,000 M(r)). In ampullary tissue collected from ovariectomized and estrogen-treated gilts and from gilts at Day 1 of estrus, gold particles were clustered over putative secretory granules restricted to the apical region of secretory epithelial cells. While follicular oocytes did not react with immunoreactive colloidal gold, oviductal and uterine unfertilized oocytes were found to be densely and uniformly labeled by colloidal gold throughout the zona pellucida, associated with flocculent material in the perivitelline space, and associated with microvilli and vitelline membrane. Similarly, in oviductal (1-4-cell) and unhatched uterine (4-cell/blastocyst) embryos, colloidal gold particles were distributed throughout the zona pellucida, heavily associated with flocculent material in the perivitelline space, and associated with the plasma membrane of the blastomeres. Immunoreactive colloidal gold remained detectable within Day 7 hatched uterine embryos, but not with embryos from later days. These results further support the proposal that porcine estrogen-dependent oviductal glycoproteins are released into the oviductal lumen, become associated with oviductal and uterine oocytes and early embryos, and are retained by oocytes and early embryos in the uterus.

Animals↗