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  • 11
    Electronic Resource
    Electronic Resource
    Detection of group C adenovirus DNA in small-cell lung cancer with the nested polymerase chain reaction (1997)
    Springer
    Journal of cancer research and clinical oncology 123 (1997), S. 377-382 
    Details
    ISSN: 1432-1335
    Keywords: Key words Adenovirus ; Small-cell lung cancer ; Polymerase chain reaction ; In situ hybridization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Group C adenovirus is latent in human tissues and can malignantly transform cells. The purpose of this study was to investigate the association between this virus and lung cancer. We investigated latent adenoviral infection using the nested polymerase chain reaction and in situ hybridization in transbronchial biopsy specimens from patients with small-cell lung cancer and non-small-cell lung cancer. The polymerase chain reaction was performed on DNA extracts with two sets of primers directed at a 261-base-pair target sequence of the E1A region of the adenoviral genome. In situ hybridization was performed on histological sections using DNA representing the entire adenovirus type 5 genome. E1A target DNA was present in 11 (31%) of 35 cases of small-cell lung cancer but in none of the 40 cases of non-small-cell lung cancer (P〈0.01). Of the 11 cases found positive by PCR, 8 were positive for adenovirus DNA by in situ hybridization. Adenovirus was prominent in tumor cells in 5 of the 8 cases, and in normal epithelial cells in the 3 remaining cases. Adenovirus DNA was not detected by in situ hybridization in specimens in which E1A DNA was not detected by the polymerase chain reaction. Small-cell lung cancer has mutations or deletions in the p53 and retinoblastoma genes more frequently than are found in non-small-cell lung cancer. Therefore, we speculate that adenovirus infection might participate in the pathogenesis of SCLC by producing mutation in these genes, rather than by inhibiting the function of these proteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01240120
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  • 12
    Electronic Resource
    Electronic Resource
    Case report 812 (1993)
    Springer
    Skeletal radiology 22 (1993), S. 549-551 
    Details
    ISSN: 1432-2161
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00209109
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  • 13
    Electronic Resource
    Electronic Resource
    A deletion in the sapA homologue cluster is responsible for the loss of the S-layer in Campylobacter fetus strain TK (1997)
    Springer
    Archives of microbiology 167 (1997), S. 196-201 
    Details
    ISSN: 1432-072X
    Keywords: Key wordsCampylobacter fetus ; sapA Homologues ; Promoter ; Chi sequence ; Antigenic variation ; Surface layer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Abstract The surface array protein (SAP) of Campylobacter fetus strain TK is encoded by seven homologous sapA genes clustered on the chromosomal DNA. The spontaneously arising variant strain TK(SAP–) produces no SAP and carries an approximately 10-kb chromosomal deletion. To elucidate the mechanism underlying the loss of SAP synthesis, we analyzed the region containing the sapA homologues and the deletion. We constructed a physical map of the sapA cluster region by aligning the clones that contain sapA homologues. These analyses demonstrated that all sapA homologues were located within a limited region of about 50 kb of chromosomal DNA of strain TK. The TK(SAP–) deletion was located within this cluster and was 13.3 kb in size. The deletion occurred between two sapA homologues and resulted in the formation of a chimeric sapA homologue in the variant strain. Sequence analysis of the upstream regions and the conserved regions of all sapA homologues revealed a high degree of similarity. However, only one sapA homologue contained a putative promoter sequence. This promoter sequence was located in the deleted region. Thus, the deletion of the promoter appears to be responsible for the loss of SAP expression in TK(SAP–).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s002030050435
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  • 14
    Electronic Resource
    Electronic Resource
    Effects of gastric distension and prostaglandin on acid ethanol-induced mucosal lesions in the rat (1988)
    Springer
    Digestive diseases and sciences 33 (1988), S. 1569-1577 
    Details
    ISSN: 1573-2568
    Keywords: ethanol ; gastric lesions ; gastric distension ; prostaglandin ; mucosal fold ; cytoprotection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of gastric distension on the morphology of acidified ethanol (AE) -induced mucosal lesions and on the protective action of 16,16-dm PGE2 were investigated in rats. AE (50% ethanol in 150 mM HCl) was given by gavage in the intact stomach or through a fistula prepared in the forestomach in the pylorus-ligated stomach. AE produced elongated bands of hemorrhagic necrosis within 1 hr in the former, while in the pylorus-ligated stomach the shape of lesions varied depending upon the volume of irritant. One milliliter produced bandlike lesions, whereas 2 ml or more induced widespread lesions; such volumes were observed to remove the mucosal folds. 16,16-dm PGE2 (0.3–10 μg/kg, subcutaneous) dose dependently reduced bandlike lesions in the intact stomach, but had no or little effect on non-band-like lesions in the pylorus-ligated stomach. This agent (10 μg/kg) had a slight effect on the reduction of PD caused by 10-min exposure of the stomach to AE (2 ml) in the intact stomach, while such effects were not apparent in the pylorus-ligated stomach. Oral gentian violet (2 ml, 0.3% w/v) produced bandlike staining of the mucosa in intact rats, but the effect was blocked by pyloric ligation. 16,16-dm PGE2 also significantly prevented the localized staining pattern seen in intact rats. These results suggest that (1) the bandlike pattern of AE-induced injury is dependent on the presence of mucosal folds (distending the stomach abolishes mucosal folds and widespread injury results); (2) 16,16-dm PGE2 prevented the fold-related, bandlike lesions and bandlike staining of the mucosa, but failed to abolish the generalized lesions; and (3) PG cytoprotection appears associated with the formation of bandlike lesions which are dependent on the presence of mucosal folds.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01535948
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  • 15
    Electronic Resource
    Electronic Resource
    An inhibitor of cyclic AMP-dependent protein kinase enhances the superoxide production of human neutrophils stimulated by N-formyl-methionyl-leucyl-phenylalanine (1995)
    Springer
    Molecular and cellular biochemistry 145 (1995), S. 19-24 
    Details
    ISSN: 1573-4919
    Keywords: human neutrophils ; respiratory burst ; cyclic AMP-dependent protein kinase ; calcium ion
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract Intact human neutrophils produced superoxide (O2 −) by the stimulation with N-formyl-methionyl-leucyl-phenylalanine (fMLP) even when the extracellular Ca2+ was absent (0.56±0.13 nmol/min per 106 cells). The production by fMLP was enhanced more than twice in the presence of the extracellular Ca2+. Moreover, the O2 − production by fMLP in the presence of extracellular Ca2+ was enhanced nearly three times by the treatment of cells with H-89, an inhibitor of cyclic AMP-dependent protein kinase (PKA). The enhancement was not observed when the extracellular Ca2+ was depleted from the reaction mixture. In addition, H-89 did not enhance fMLP-induced O2 − production of electropermeabilized neutrophils in which the intracellular Ca2+ concentration was fixed to about 100 nM. These observations suggest that not only Ca2+ influx but the inhibition of PKA is necessary for the maximum O2 − production by fMLP and that the O2 − production is partially suppressed by the activation of PKA induced by fMLP.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00925708
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  • 16
    Electronic Resource
    Electronic Resource
    Release of nitric oxide and expression of constitutive nitric oxide synthase of human endothelial cells: Enhancement by a 14-membered ring macrolide (1998)
    Springer
    Molecular and cellular biochemistry 181 (1998), S. 157-161 
    Details
    ISSN: 1573-4919
    Keywords: human endothelial cells ; erythromycin ; calcium ion ; nitric oxide ; constitutive nitric oxide synthase ; cyclic AMP-dependent protein kinase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology , Medicine
    Notes: Abstract A 14-membered ring macrolide, erythromycin, acts not only as an antibacterial but also as an anti-inflammatory agent. We have previously reported that erythromycin modulates neutrophil functions and ameliorates neutrophil-induced endothelial cell damage through the action of cyclic AMP-dependent protein kinase (PKA) and nitric oxide (NO). We investigated the effect of erythromycin on human endothelial cell functions. Erythromycin enhanced intracellular calcium ion concentration ([Ca2+]i) of endothelial cells and NO release from endothelial cells. The enhancement of NO release from endothelial cells by erythromycin was abolished by addition of EGTA in the medium and was partially reduced by addition of H-89, an inhibitor of PKA. These results suggest that erythromycin enhances NO release from endothelial cells through the action of PKA and [Ca2+]i. In addition, constitutive NO synthase (cNOS) protein expression of endothelial cells was dose-dependently enhanced by treatment with erythromycin, which might also contribute to the enhancement of NO release from endothelial cells by erythromycin. The effect of erythromycin as an anti-inflammatory agent might be partially mediated through the enhancement of NO release from endothelial cells and the drug might be a useful tool for the investigation of cNOS of endothelial cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006894301389
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  • 17
    Electronic Resource
    Electronic Resource
    Granulocyte-colony stimulating factor promotes invasion by human lung cancer cell lines in vitro (1996)
    Springer
    Clinical & experimental metastasis 14 (1996), S. 351-357 
    Details
    ISSN: 1573-7276
    Keywords: granulocyte-colony stimulating factor ; invasion ; invasion assay ; lung cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: The effects of exogenous and endogenous granulocyte colony-stimulating factor (G-CSF) on invasion by cancer cells were studied, using lung cancer cell lines that produce G-CSF (NCI-H157) and lines that do not (PC-9 and NCI-H23). The invasive capacity of NCI-H157 cells was 26- to 27-fold higher than that of PC-9 and NCI-H23 cells. The invasiveness of PC-9 cells was stimulated by exogenous G-CSF, while that of NCI-H157 cells was not. Antibodies against G-CSF blocked the stimulation of PC-9 cell invasiveness by exogenous G-CSF. Anti G-CSF antibodies also inhibited invasion by NCI-H157 cells in the absence of exogenous G-CSF. These results suggest that endogenous and exogenous G-CSF both stimulate invasion by lung cancer cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00123394
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  • 18
    Electronic Resource
    Electronic Resource
    G-CSF increases secretion of urokinase-typeplasminogen activator by human lung cancer cells (1998)
    Springer
    Clinical & experimental metastasis 16 (1998), S. 551-558 
    Details
    ISSN: 1573-7276
    Keywords: G-CSF ; invasion ; lung cancer ; uPA
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We reported previously that granulocyte colony-stimulating factor (G-CSF) can promote the invasion ofhuman lung cancer cell lines in vitro. However, the exact mechanism of its stimulatory effect on invasionremains to be elucidated. In the present study we mainly focused our attention on the components of theplasminogen activation system in human lung cancer cell lines, because of the central role that plasminogenactivators play in regulating extracellular proteolysis. We showed that G-CSF induced a dose-dependentincrease in the urokinase-type plasminogen activator (uPA) activity in the conditioned medium of a PC-9lung cancer cell line. When the amounts of uPA activity were quantitated by densitometry, we found thateven at a concentration of 0.01 mg/ml, G-CSF had a stimulatory effect on the uPA release, while highconcentrations caused a 3.6-fold increase at a maximum concentration of 1 mg/ml. A Western blot analysisof the conditioned medium confirmed the findings observed in a zymographic analysis. The observed increasein uPA protein was paralleled by a significant increase in the uPA mRNA levels after treatment withG-CSF. However, our experiments failed to identify any alteration in the plasminogen activator inhibitor(PAI) secretion caused by G-CSF. In addition, we also found the expression of G-CSF receptor by PC-9cells, suggesting the possible pathway activated by G-CSF.©Kluwer Academic Publishers
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006546402703
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