PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7645
Browse
3 results
Search Results
Conference Object Citation - WoS: 24Effect of pH and Hydration on the Normal and Lateral Interaction Forces Between Alumina Surfaces(2006) Polat, Mehmet; Sato, Kimiyasu; Nagaoka, Takaaki; Watari, KojiNormal and lateral interaction forces between alumina surfaces were measured using Atomic Force Microscopy-Colloid Probe Method at different pH. The normal force curves exhibit a well-defined repulsive barrier and an attractive minimum at acidic pH and the DLVO theory shows excellent agreement with the data. The normal forces are always repulsive at basic pH and the theory fails to represent the measurements. Lateral forces are almost an order of magnitude smaller in the basic solutions. These differences, which have important implications in the study of stability and rheology, are attributed to the hydration of the alumina surface at basic pH. © 2013 Elsevier B.V., All rights reserved.Article Tc-99m Erythromycin Lactobionate Inhalation Scintigraphy in Parenchymal Lung Diseases(Elsevier Science inc, 1999) Durak, H; Aktogu, S; Degirmenci, B; Sayit, E; Ertay, T; Dereli, SWe have investigated Technetium 99m erythromycin lactobionate (Tc 99m EL) clearance from the lungs after inhalation, in the presence of an alveolitis. Eighteen patients (6 sarcoidosis, 7 idiopathic fibrosis, and 5 miliary tuberculosis) were imaged after the patients inhaled 1,110 MBq of Tc 99m EL. Clearance half time for the first 45 min, for 24 h, and retention at 24 h correlated with percentage of lymphocytes in bronchoalveolar lavage fluid (BAL) (r =.729, r =.883, and r =.826, respectively). There was a positive correlation between peripheral penetration (PP) and forced expiratory volume in 1 s (FEV1) (r =.806) and forced vital capacity (FVC) (r =.781). Retention was more marked in sarcoidosis compared with tuberculosis (0.025 < p less than or equal to 0.05). Radioaerosol lung imaging may reflect the pulmonary function impairment in parenchymal lung diseases. Retention of Tc 99m EL may be related to number of BAL cells or presence of a lymphocytic alveolitis. Long residency time of Tc 99m EL in the lungs implies that erythromycin can also be administered by inhalation for therapeutic purposes. NUCL MED BIOL 26;6:695-698, 1999. (C) 1999 Elsevier Science Inc. All rights reserved.Article Citation - WoS: 37Mechanisms of Cellular Resistance To Imatinib in Human Chronic Myeloid Leukemia Cells(Taylor and Francis Ltd., 2007) Baran, Yusuf; Ural, Ali Uğur; Gündüz, UfukA major advancement in the treatment of chronic myeloid leukemia (CML) has been the development of imatinib, which has shown striking activity in the chronic phase and the accelerated phase, but less so in the blast phase of the disease. Despite high rates of hematologic and cytogenetic responses to therapy, the emergence of resistance to imatinib has been recognized as a major problem in the treatment of patients with CML. Various cellular mechanisms may be involved in the nature of cellular resistance. Increased amount of target, alteration in structure of target proteins, decreased drug uptake and increased detoxification are well-known mechanisms of resistance. On the other hand, in some cases, even if anticancer drugs reach their sites of action, bypassing drug efflux system of the cells, some cells still may survive via the dysregulation of apoptotic signalling. In this study, mechanisms of resistance to imatinib-induced apoptosis in human Meg-01 CML cells were examined. Continuous exposure of cells to step-wise increasing concentrations of imatinib resulted in the selection of 200- and 1000 nM imatinib-resistant sub-lines referred to as Meg-01/IMA-0,2 and Meg-01/1MA-1, respectively. MTT cell proliferation, cell cycle analyses and trypan blue dye exclusion analyses showed that Meg-0l/IMA-1 cells were resistant to imatinib-induced apoptosis as compared to parental sensitive cells. There was an increased expression of BCR/ABL, Bcl-2 and an increase in mitochondrial membrane potential (MMP) detected in resistant cells comparing to parental sensitive cells. There was no mutation detected in imatinib binding site of ABL kinase region. Various diverse mechanisms have been reported for their involvement in the multidrug resistance. In this study, it has been shown that the degree of BCR/ABL expression appears to be directly proportional to the levels of imatinib resistance. In addition, there have been BCR/ABL-independent mechanisms reported for deriving resistance against imatinib. Our results revealed that besides BCR/ABL overexpression, imatinib resistance also depends on the inhibition of apoptosis as a result of up-regulation of anti-apoptotic stimuli and down-regulation of pro-apoptotic stimuli through MMP but does not depend on any mutation on imatinib binding site of ABL kinase.