Oytun Portakal

Coenzyme Q10 concentrations and antioxidant status in tissues of breast cancer patients.

OBJECTIVES An increasing amount of experimental and epidemiological evidence implicates the involvement of oxygen derived radicals in the pathogenesis of cancer development. Oxygen derived radicals are able to cause damage to membranes, mitochondria, and macromolecules including proteins, lipids and DNA. Accumulation of DNA damages has been suggested to contribute to carcinogenesis. It would, therefore, be advantageous to pinpoint the effects of oxygen derived radicals in cancer development. DESIGN AND METHODS In the present study, we investigated the relationship between oxidative stress and breast cancer development in tissue level. Breast cancer is the most common malignant disease in Western women. Twenty-one breast cancer patients, who underwent radical mastectomy and diagnosed with infiltrative ductal carcinoma, were used in the study. We determined coenzyme Q10 (Q) concentrations, antioxidant enzyme activities (mitochondrial and total superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), catalase), and malondialdehyde (MDA) levels in tumor and surrounding tumor-free tissues. RESULTS Q concentrations in tumor tissues significantly decreased as compared to the surrounding normal tissues (p < 0.001). Higher MDA levels were observed in tumor tissues than noncancerous tissues (p < 0.001). The activities of MnSOD, total SOD, GSH-Px and catalase in tumor tissues significantly increased (p < 0.001) compared to the controls. CONCLUSIONS These findings may support that reactive oxygen species increased in malignant cells, and may cause overexpression of antioxidant enzymes and the consumption of coenzyme Q10. Increased antioxidant enzyme activities may be related with the susceptibility of cells to carcinogenic agents and the response of tumor cells to the chemotherapeutic agents. Administration of coenzyme Q10 by nutrition may induce the protective effect of coenzyme Q10 on breast tissue.

Effects of pentoxifylline and coenzyme Q10 in hepatic ischemia/reperfusion injury.

OBJECTIVES We examined whether pentoxifylline (PTX) and coenzyme Q10 (Q) pretreatment affect ischemia-reperfusion damage in the rat liver. DESIGN AND METHODS Twenty minutes of reflow following 30 min of ischemia was performed. Before the experiment, rats were treated PTX 50 mg/kg, IP or PTX 50 mg/kg IP + Q10 mg/kg, intragastric, or untreated. Rats were divided into four groups: control (C), ischemia-reperfusion (IR), PTX-treated (P), and Q+PTX-treated (QP) groups. Hepatic glutathione (GSH) and malondialdehyde (MDA) levels and catalase, superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and reductase (GSSGR) activities were measured. RESULTS In IR group GSH levels decreased (p<0.01), conversely MDA levels increased (p<0.01). PTX pretreatment did not affect GSH and MDA values, but Q+PTX pretreatment improved of those (p<0.01). It was shown that catalase and GSH-Px activities increased during ischemia-reperfusion (p<0.01, both of), but PTX pretreatment did not significantly ameliorate those activities. GSSGR activity was higher in IR group than in basal levels (p<0.01). The decrease GSSGR activity that was observed in P group was not significant compared to IR group. During ischemia/reperfusion also SOD activity increased as compared with controls (p<0.05). In PTX-treated group, SOD activity was significantly higher than control and ischemia/reperfusion groups (p<0.01, both of). Q+PTX treatment ameliorated those enzyme activities to the control values. CONCLUSIONS Short-term hepatic ischemia-reperfusion diminished GSH, increased MDA levels and induced some antioxidant enzyme activities. Q+PTX pretreatment was useful in hepatic ischemia-reperfusion injury, but treatment of PTX alone did not cause beneficial effect in the present study.

Efficacy of new leukocyte parameters versus serum C-reactive protein, procalcitonin, and interleukin-6 in the diagnosis of neonatal sepsis.

The aim of this study was to investigate and compare the efficacy of the new leukocyte parameters mean neutrophil and monocyte volume (MNV, MMV), conductivity (MNC, MMC), scattering (MNS, MMS) and volume distribution width (NDW, MDW) with serum C‐reactive protein (CRP), procalcitonin (PC) and interleukin (IL)‐6 in the diagnosis of neonatal sepsis.

Comparison of the efficacy of new leukocyte parameters with serum C‐reactive protein, procalcitonin, interleukin‐6 levels in the diagnosis of neonatal sepsis

The aim of this study was to investigate and compare the efficacy of the new leukocyte parameters mean neutrophil and monocyte volume (MNV, MMV), conductivity (MNC, MMC), scattering (MNS, MMS) and volume distribution width (NDW, MDW) with serum C‐reactive protein (CRP), procalcitonin (PC) and interleukin (IL)‐6 in the diagnosis of neonatal sepsis.

Erythrocyte Agglutination in a Child with Neuroblastoma

Neuroblastoma is the most common extracranial solid tumor in children. Here we present a 4- year-old boy diagnosed with neuroblastoma, showing erythrocyte agglutination on blood smear six days after intensive chemotherapy. Total blood count showed a significant discrepancy between hemoglobin and hematocrit values. Mean corpuscular hemoglobin (MCH) and mean corpuscular volume (MCV) values were elevated. Erythrocyte agglutination was disappeared after the sample was warmed at 37 0 C. Cold agglutination reaction was found to be positive whereas direct Coombs test was found to be negative. Follow-up total blood counts were back to reference range after cyclophosphamide, etoposide and cisplatin therapy. To our knowledge, this is the first report in the literature in which erythrocyte (red blood cell) agglutination due to cold agglutinins was detected in a child diagnosed with neuroblastoma.

Extremely high parathyroid hormone concentrations associated with pityriasis rubra pilaris and monoclonal gammopathy of unknown significance: A clinical dilemma

We present a case with extremely high parathyroid hormone (PTH) concentrations in the order of hundred thousands accompanied by dermatological and hematological diseases. After several diagnostic interventions, no malignancy could be demonstrated except monoclonal gammopathy of unknown significance. The dermatological findings were taken to be manifestations of the hematological disease. Since the first serum intact PTH concentration of the patient was found to be higher than 2500 pg/ml, dilution study was performed and found to be 215,977 pg/ml. The high concentration of serum PTH was taken to be falsely high due to assay interference. This concentration was checked from three different paths; a test for linear dilution was performed, the test was repeated with another method and the sample was treated to remove or inhibit interfering substances. The results were compatible with endogenous antibody interference, presumed to be a result of monoclonal gammopathy. The extremely high PTH concentrations were not only due to assay interference, but also secondary hyperparathyroidism, which was evident by the decrease in PTH concentrations with calcium and vitamin D treatments.

An automated image analysis system can be beneficial in preclassification of leucocytes in children with hematological disease.

This study was aimed to evaluate the analytical performance of an automated image analysis system (a pilot model of Diff Master™ Octavia) for the preclassification of leucocytes in children with hematological disease. Manual microscopy performed by pediatric hematologists was used as the reference method. Five mature cell class and blasts were evaluated. Diff Master Octavia correctly preclassified 87.4% of all leucocytes with a high reproducibility. The overall accuracy was found to be 93.0%. Clinical sensitivity was 97.7% and specificity was 76.0%. The average time per slide for Diff Master™ Octavia was 2.3 min lower than that of manual method. Our results indicated that the Diff Master™ Octavia can detect and preclassify leucocytes accurately; therefore, it can be used as an efficient and fast method in pediatric hematology routine. J. Clin. Lab. Anal. 25:71–75, 2011.