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A Yilmaz

Publications and source records attributed to A Yilmaz.

At least 73 records · Page 4Linked to original sources
PubMed1998

Effect of reversed light-dark cycle on skin conductance in male rats.

Reversal of light-dark cycle was used to investigate the effect of the circadian changes on skin conductance, a tonic electrodermal activity parameter, in rats. Rats were adapted for 3 wk. to one of two lighting programs. The animals on the normal cycle were illuminated from 08.00-20.00; on the reverse cycle, from 20.00-08.00. Although during Week 1 to Week 3, skin conductance increased gradually in both groups, this increase was more dramatic in rats adapted to light from 20.00 to 08.00 than in the other group. When the animals on the reverse cycle were readjusted to a normal circadian cycle for 3 weeks, skin conductance decreased gradually to initial values. At Weeks 1, 2, 3, and 6, skin conductance was significantly higher in rats on the reverse light-dark cycle than in those on the normal cycle. The present data suggest that changes in normal light-dark conditions affect skin conductance in rats.

Animals↗
PubMed1998

Malignant transformation of simian virus 40-immortalized human milk epithelial cells by chemical carcinogenesis accompanied by loss of heterozygosity on chromosome 1 but not microsatellite instability.

Simian virus 40-immortalized human milk epithelial cells (HuMI) are anchorage dependent and non-tumorigenic but can spontaneously progress to anchorage-independent and tumorigenic cells. To see whether HuMI cells can be transformed into anchorage-independent cells by chemical carcinogens, we treated them with 3-methylcholanthrene (MCA, 10 microg/mL). After 7-8 wk of culture, none of the treated cells grew in soft agar. However, when HuMI cells treated with MCA were cultured with 12-O-tetradecanoylphorbol-13-acetate (TPA, 10 ng/mL), they grew in soft agar; cells treated with TPA alone did not. TPA at this dose was cytotoxic to HuMI cells but not to their tumorigenic subline HuMI-TTu2. The response of the anchorage-independent HuMI-T cells was intermediate. These results indicate that HuMI cells can be transformed by treatment with MCA plus TPA, possibly because TPA selects those cells that are progressing toward malignancy. All five clones from MCA plus TPA-induced transformed cells formed malignant carcinomas in nude mice. When microsatellite changes at 17 loci in HuMI, HuMI-T, HuMI-TTu2, and five MCA plus TPA-transformed cells were examined, none of these cell lines showed instability at any locus, and no change in microsatellite length was found. However, all five MCA plus TPA-transformed cell lines showed loss of heterozigosity at 1q21-23 and 1q42 loci. This region of chromosome 1 is known to contain at least one antiproliferative gene, and our results suggest that inactivation of such a gene may be essential for full transformation of HuMI cells by chemical carcinogens.

Breast↗
PubMed1996

Differential effect of interleukin-4 and transforming growth factor beta 1 on expression of proto-oncogenes and autocrine insulin-like growth factor II in colorectal carcinoma cells.

We have compared the effect of interleukin-4 and transforming growth factor beta 1 on proliferation and gene expression in two colorectal carcinoma cell lines, LS513 and LS1034. Transforming growth factor beta 1 was a potent inhibitor for both cells lines and virtually abolished de novo DNA synthesis. Interleukin-4 inhibited thymidine incorporation up to 60 and 45%, respectively. While both cytokines exerted a comparable cyto-inhibitory activity they displayed differential effects on proto-oncogene expression. Transforming growth factor beta 1 markedly down-regulated c-myc in LS1034 but not in LS513 cells. In contrast, expression of c-fos was induced by interleukin-4 in LS513 but not in LS1034 cells. Interestingly, in agreement with their cyto-inhibitory activity both cytokines suppressed the expression of insulin-like growth factor II in LS1034, which is an autocrine growth factor for these cells.

Cell Division↗
PubMed1996

In vitro NMR proton T1 measurements in peritoneal ascites.

The proton spin-lattice relaxation rate (1/T1) in malignant and non-malignant ascites was measured with an FT NMR spectrometer operating at 60 MHz. The mean relaxation rate in non-malignant ascites was significantly smaller than that of malignant ascites. However, the 1/T1 of malignant ascites overlaps with that of non-malignant ascites over all concentrations of total protein (TP) in samples. The 1/T1 in non-malignant ascites correlates strongly with TP, whilst the 1/T1 in malignant ascites shows only a moderate correlation. T1 measurements before and after addition of ascorbic acid (reductant) suggest that there is a small paramagnetic contribution of ions to the 1/T1 in malignant ascites. The least-squares fitting of 1/T1 versus TP for non-malignant data gives a linear relationship, and suggests that the T1 mechanism in non-malignant ascites is caused by a fast chemical exchange of water molecules between protein-bound water and free water.

Ascites↗
PubMed1996

Comparison of cryopreservation of supernumerary pronuclear human oocytes obtained after intracytoplasmic sperm injection (ICSI) and after conventional in-vitro fertilization.

A comparison was made of pronuclear stage human oocytes obtained either after classical in-vitro fertilization (IVF) or after intracytoplasmic sperm injection (ICSI). After ICSI or IVF, three fertilized oocytes from each patient were kept in culture for a further 24 h before embryo transfer. The surplus oocytes were cryopreserved using the 'open freezing system' and 1,2-propanediol and sucrose as cryoprotectants. A cohort of 817 and 1626 oocytes in pronuclear stage were frozen after IVF and ICSI respectively. Of these, 333 and 744 zygotes have been thawed, of which 78 and 76.5% were morphologically intact zygotes after IVF and ICSI respectively. From the 204 (ICSI) and 89 (IVF) zygote transfers performed, 34 (17%) and 18 (20%) pregnancies were established. Both groups showed a similar abortion rate of approximately 20%. It is concluded that pronuclear stage oocytes resulting from ICSI can be successfully frozen/thawed and the survival and pregnancy rates achieved are comparable to those for zygotes obtained after IVF.

Cryopreservation↗
PubMed1996

Glyoxalase 1 (GLO1) polymorphism in eight geographical regions of Turkey.

The distribution of glyoxalase 1 (GLO1) phenotypes in eight geographical regions of Turkey was studied. The GLO1*1 allele frequency varies from 0.3630 to 0.4118, which is in good agreement with the previously estimated range of variability. Excess numbers of heterozygotes compared to the Hardy-Weinberg equilibrium were observed in all regions. The reason of this requires further investigations.

Alleles↗
PubMed1995

Evolution of glomerular basement membrane changes in chronic rejection.

We have investigated the evolution of chronic glomerular changes in the absence of the recurrence of original disease in an experimental rat model of chronic renal allograft rejection. Using serial graft needle biopsies and serum creatinine levels, we were able to focus on early glomerular changes that are associated with good graft function. The recipient rats were divided into 5 groups, 2 with allogeneic (DA to WF) transplants and 3 with syngeneic (DA to DA) transplants. In the first 2 allogeneic groups, one group received cyclosporine (CsA) for 2 weeks (n = 7) and the other received CsA for 12 weeks (n = 5). In the 2-week treatment group, all allografts developed chronic rejection, compared with none in the 12-week group. Syngeneic controls received CsA for 2 (n = 3) and 12 weeks (n = 3), or no immunosuppression (n = 2) in order to exclude the effects of CsA. The first detectable ultrastructural event was slight deposition of electron lucent material in the glomerular basement membrane. Contrary to previous morphological studies, the initial deposition was not subendothelial, but was within the lamina densa itself. Examination of allogeneic grafts with good graft function and syngeneic grafts showed glomerular alterations that were similar to the early changes preceding chronic rejection. The intensity of changes in optimally immunosuppressed allografts was mild, and they were arrested early in the evolving stage of glomerular basement membrane changes. In the suboptimally immunosuppressed allografts with chronic rejection, the glomerular basement membrane changes became more pronounced and extensive in subsequent biopsies. Thus, all recipients in different groups showed similar glomerular alterations, but to different intensities. These results suggest a common pathogenetic mechanism which might be endothelial damage. In chronic rejection, the endothelial damage might be immunologically mediated by rejection episodes and progressive, whereas in syngeneic grafts and in allografts without chronic rejection, perioperative trauma, ischemia, and graft reperfusion may be responsible for the self-limiting glomerular changes.

Animals↗
PubMed1995

Chronic renal allograft rejection can be predicted by area under the serum creatinine versus time curve (AUCCr).

Acute rejection is the most important single risk factor for chronic renal allograft rejection. Numerical quantitation of rejection episodes does not take into account the intensity and length of these episodes, both of which may contribute to the severity of chronic rejection. We propose a single numerical parameter for the frequency, intensity and length of acute rejections, the "Area Under the Serum Creatinine versus Time Curve" (AUCCr) using renal allografts between inbred rat strains. Twenty-seven renal transplantations were performed from the DA to WF rat strain. The rats were immunosuppressed with 5 mg/kg body weight of CyA injected s.c. for 1, 2, 3 and 12 weeks, resulting in differing numbers (0-4) of biopsy-confirmed acute rejections of varying intensity (s-cre: 100-448 mumol/L) and length (3-24 days), all of which were reversed with additional CyA treatment. The intensity of chronic changes in graft histology was quantitated using the "Chronic Allograft Damage Index" (CADI). End-point transplant function was quantitated as level of serum creatinine at sacrifice. The AUCCr from 0 to 3 weeks (AUCCr0-3), encompassing the recovery period after operation, free of rejections, did not correlate with the CADI (r = 0.230, P = 0.249). All AUCCr from 3 weeks onwards correlated with the CADI. The best correlation with the CADI was obtained with AUCCr from 3 to 12 weeks (AUCCr3-12) (r = 0.922, P = 0.0001). This interval coincides with the timing of all acute rejection episodes. AUCCr3-12 correlated equally well to end-point transplant function (r = 0.890, P = 0.0001).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1995

Interleukin 4 down-regulates expression of c-kit and autocrine stem cell factor in human colorectal carcinoma cells.

Stem cell factor (SCF) is a cytokine which plays an important role in the development of precursor cells. We have investigated the expression of SCF and its receptor, the c-kit proto-oncogene, in human colorectal carcinoma cell lines. Using reverse transcription-PCR, we confirmed the expression of c-kit in two lines (LS174T and LS1034) and of SCF in 9 of 11 cell lines tested. In a Northern blot, a single transcript of 6.6 kb was detected for SCF mRNA. In addition, two lines (LS174T and HT29) synthesized SCF protein, as detected by Western blot analysis. SCF stimulated proliferation and colony formation of LS174T in a dose-dependent manner up to 160%. A half-maximal effect was obtained with about 5.5 ng/ml of SCF under both growth conditions. LS174T cells expressed the M(r) 145,000 c-kit protein on the cell surface and a neutralizing anti-c-kit mAb inhibited colony formation of LS174T by 40%. Interleukin 4 (IL-4) completely inhibited SCF-induced proliferation of LS174T cells. Interestingly, IL-4 induced an almost complete down-regulation of both c-kit and SCF expression in LS174T. Our findings suggest that in LS174T cells, an SCF-mediated autocrine loop is functional and that IL-4 down-regulates the expression of both the receptor and the ligand of this circuit.

Base Sequence↗
PubMed1994

Growth inhibition of human colorectal-carcinoma cells by interleukin-4 and expression of functional interleukin-4 receptors.

The growth-inhibitory effect of interleukin-4 (IL-4) was investigated in a panel of 7 human colorectal-carcinoma cell lines. In 5 cell lines (HT29, WiDr, LS411N, LS513, LS1034) a dose-dependent reduction of proliferation was documented. At 100 U/ml, IL-4 inhibited thymidine incorporation between 45 and 75% and MTT conversion (26 to 41%). The ability of LS513 and WiDr cells to form colonies after IL-4 treatment was reduced by 85 and 62% respectively. LS513 was the most sensitive cell line, with IL-4 inducing half-maximal inhibition at 5 to 6 U/ml. The inhibitory effect of IL-4 was completely neutralized by anti-IL-4 antibodies. Northern-blot analysis revealed the presence of IL-4-receptor (IL-4R) mRNA in all cell lines. The membrane expression of the 130-kDa IL-4R was assessed by FACS, utilizing an anti-IL-4R monoclonal antibody and was confirmed by biotinylated IL-4 binding. Our results attribute an important role for IL-4 as a negative regulator of colorectal-carcinoma cell growth, thus indicating a possible avenue for intervention in this disease.

Blotting, Northern↗
PubMed1994

Blockade of the insulin-like growth-factor-I receptor inhibits growth of human colorectal cancer cells: evidence of a functional IGF-II-mediated autocrine loop.

Insulin-like growth factors (IGFs) are potent proliferation stimulators for numerous tumor cells and often function as autocrine growth factors. We have previously shown that exogenous IGF-I and IGF-II enhance proliferation of colorectal carcinoma cells. The biological signal of both factors is transmitted through the IGF-I receptor (IGF-I-R). This receptor was expressed in 12/12 colorectal carcinoma cell lines tested. alpha IR3, a neutralizing monoclonal antibody (MAb) directed against the human IGF-I-R, inhibited proliferation in 7/12 lines (Caco-2, HT-29, LS411N, LS513, LS1034, WiDr and SW620), as reflected by a reduction of MTT conversion (19 to 42%), a decrease in cell number (39 to 72%) and an increase in doubling time (up to 2-fold). In addition, in 4 cell lines (Caco-2, LS513, LS1034, WiDr) alpha IR3 suppressed colony formation in methylcellulose (40 to 84%). Excess of exogenous IGF completely neutralized alpha IR3-mediated inhibitory effects. Northern blot analysis revealed abundant expression of 2 IGF-II transcripts of 5.0 and 4.3 kb in LS1034 cells. In addition, we observed that growth inhibition by alpha IR3 was correlated with a more differentiated phenotype. Our results suggest that growth of many colorectal carcinoma cell lines is regulated by autocrine IGF-II-mediated stimulation of the IGF-I-R.

Antibodies, Monoclonal↗
PubMed1994

Secretion of bioactive granulocyte-macrophage colony-stimulating factor by human colorectal carcinoma cells.

Secretion of several cytokines by colorectal carcinoma cells has been substantiated. These do not include granulocyte-macrophage colony-stimulating factor (GM-CSF) thus far. We show that the supernatant of two human colorectal carcinoma cell lines, LS1034 and SW480, stimulates proliferation of GM-CSF-dependent M07e cells. The activity was constitutively secreted by LS1034 cells and could be induced by serum-free culture conditions in SW480 cells. Addition of a neutralizing anti-GM-CSF antibody completely inhibited this activity. Preabsorption with anti-GM-CSF antibody removed all M07e growth-stimulating activity from LS1034 and SW480 supernatant. Western blot analysis revealed the presence of GM-CSF in LS1034 supernatant. Our results indicate that human colorectal carcinoma cells secrete indeed biologically active GM-CSF.

Colorectal Neoplasms↗
PubMed1994

Identification of a cell-surface glycoprotein associated with normal mammary and extramammary epithelial cells.

The goal of the study was to identify any normal genes that may become inactivated in malignant cells, with associated modifications or loss of gene products. Consequently, attempts were made to identify such products by generating monoclonal antibodies using an immune tolerisation-immunisation procedure. Using such a technique, a plasma membrane-associated glycoprotein with an apparent molecular weight of 92 kDa was identified. The glycoprotein was termed luminal epithelial antigen (LEA.92). The pattern of expression of LEA.92 was demonstrated by an indirect immunostaining technique. Using an in vitro model system representing various stages of breast oncogenesis, LEA.92 was detected on normal or immortalised mammary epithelial cell (MEC) lines which were dependent on epidermal growth factor (EGF) and anchorage formation for growth and non-tumorigenic in nude mice. In contrast, LEA.92 was undetectable on oncogenically transformed or established lines of mammary carcinoma cell lines which were independent of EGF or anchorage formation for growth and were highly tumorigenic. The results appear to suggest a correlation between the down-regulation of LEA.92 and the development of tumorigenicity in malignant MEC lines. Furthermore, the patterns of expression of LEA.92 on breast cells in tissue mirrored those of breast epithelial cells in cell cultures. LEA.92 was detected on the surface of normal but not malignant epithelial cells, which included breast, cervix, colon, lung, pancreas and stomach. LEA.92 appeared to be distinct from receptor for epidermal growth factor, antigens associated with milk fat globule membrane and the family of epithelium-specific keratins.

Adult↗
PubMed1993

Malignant progression of SV40-immortalised human milk epithelial cells.

A human breast epithelial cell line (Hu-MI), established by microinjecting SV40 DNA into human milk epithelial cells, exhibits the phenotype of luminal epithelial cells and is neither clonogenic nor tumorigenic. From this cell line we have selected two sublines, HuMI-T and HuMI-TTul, reflecting different stages of spontaneous transformation. HuMI-T cells grow anchorage-independently, but do not induce tumours in nude mice. HuMI-TTul cells are clonogenic as well as tumorigenic. Cells from both lines exhibit polymorphic structural and numerical chromosome aberrations. Immortalisation of normal luminal epithelial cells from human mammary gland with SV40 DNA alone may thus cause random genetic changes eventually resulting in tumorigenic cell lines. Since Hu-MI, HuMI-T and HuMI-TTul represent some of the consecutive stages taking place during cellular transformation, they are particularly suited as a novel in vitro model system to study progression of human breast cancer.

Animals↗
PubMed1993

Transhiatal versus transthoracic esophagectomy for esophageal cancer.

We retrospectively analyzed 238 patients with esophageal carcinoma treated between 1983 and 1991; 120 underwent transthoracic esophagectomy, and 118 underwent transhiatal esophagectomy. The two groups were statistically similar in preoperative characteristics, except that upper esophageal cancer was more frequent in the transhiatal esophagectomy group than in the transthoracic esophagectomy group (p < 0.01). The rate of postoperative complications differed significantly in wound infection (21% in patients who underwent transthoracic esophagectomy, 10% in those who underwent transhiatal esophagectomy; p < 0.05) and empyema (11% with transthoracic esophagectomy, 1% with transhiatal esophagectomy; p < 0.01). Pneumothorax was detected in 24% of the transhiatal esophagectomy cases. Intraoperative blood loss was 1340 +/- 490 ml in the transthoracic esophagectomy group and 930 +/- 340 ml in the transhiatal esophagectomy group (p < 0.001). Hospital mortality was 11% in the transthoracic esophagectomy group and 6.7% in the transhiatal esophagectomy group. Late complication rate was lower with transhiatal esophagectomy than with transthoracic esophagectomy (11% and 51%, respectively). There was no significant difference in actuarial survival of patients in both groups. Transhiatal esophagectomy, which can be performed in almost all levels of the esophagus, is the safer of the two operations.

Anastomosis, Surgical↗
PubMed1992

Chronic rejection of rat renal allograft. III. Ultrastructure of vascular and glomerular changes.

The main histological features for 'chronic' rejection of rat renal allograft are ongoing perivascular and interstitial inflammation, vascular intimal hyperplasia and glomerular sclerosis. In this communication we have investigated the ultrastructural features of renal parenchyma by comparing chronically rejecting rat renal allografts immunosuppressed initially with cyclosporine to similarly immunosuppressed syngeneic transplants. Electron microscopy confirmed that the primary arterial change was smooth muscle cell proliferation in media, thickening and focal destruction of the internal elastic lamina, and influx of smooth muscle cells and their proliferation in the intima, leading to a nearly complete occlusion of the lumen. In the glomeruli, the most prominent features were mesangial matrix increase, narrowing of capillary lumen, and basement membrane thickening with a double contour appearance in capillary walls. A thin membrane, similar to lamina densa, appeared beneath the endothelium in some segments. Mesangial interposition, formation of new basement membrane and mesangial widening due to increase of basement membrane-like material was nearly always present. As none of these vascular and glomerular changes were observed in similarly immunosuppressed syngeneic transplants, we consider these ultrastructural alterations characteristic for chronic rejection in a rat renal allograft.

Animals↗