Wos Açık Erişimli Yayınlar

Permanent URI for this collectionhttps://hdl.handle.net/11727/10754

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    Quantitative Data for Transcutaneous Electrical Nerve Stimulation and Acupuncture Effectiveness in Treatment of Fibromyalgia Syndrome
    (2019) Yueksel, Merve; Ayas, Sehri; Cabioglu, Mehmet Tugrul; Yilmaz, Derya; Cabioglu, Cagri; 0000-0002-1903-7132; 0000-0002-5078-6529; 30949223
    Aim. To evaluate the effects of acupuncture and transcutaneous electric nerve stimulation (TENS) applications on the quantitative electroencephalography (qEEG) changes and to evaluate their therapeutic effects in patients with fibromyalgia syndrome (FMS). The study included 42 patients with FMS and 21 healthy volunteers. The patients were randomly assigned to two groups (n=21 in each) to undergo either TENS or acupuncture application. In both acupuncture and TENS groups, baseline electroencephalography (EEG) recording was performed for 10min and, then, TENS or acupuncture was performed for 20min, followed by another 10min EEG recording. Baseline qEEG findings of FMS patients in the TENS and acupuncture groups were similar. Delta and theta powers over the frontal region of FMS patients were lower than controls. Theta powers of right posterior region were also lower than controls. In the TENS group, after the treatment, an increase was observed in the alpha power of the left anterior region as well as a decrease in pain scores. In the acupuncture group, an increase was determined in the alpha power of the right and left posterior regions as well as a decrease in pain score after the treatment. The power of low- and moderate-frequency waves on resting EEG was decreased in the patients with FMS. Decreased pain and increased inhibitor activity were found on qEEG after TENS and acupuncture applications. In conclusion, both TENS and acupuncture applications seem to be beneficial in FMS patients.
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    Therapeutic Potential of Apigenin, a Plant Flavonoid, for Imatinib-Sensitive and Resistant Chronic Myeloid Leukemia Cells
    (2014) Solmaz, Soner; Gokbulut, Aysun Adan; Cincin, Birsu; Ozdogu, Hakan; Boga, Can; Cakmakoglu, Bedia; Kozanoglu, Ilknur; Baran, Yusuf
    Despite the presence of many therapeutic regimens like imatinib and other tyrosine kinase inhibitors, the development of resistance, intolerance, and side effects makes chronic myeloid leukemia (CML) therapy challenging. Thus, there is a need to discover novel drugs for CML patients. In this study, we attempted to assess apigenin, a common plant dietary flavonoid, in terms of its cytotoxic, apoptotic, and cytostatic effects on imatinib-sensitive and resistant Philadelphia-positive CML cells. We analyzed apigenin's effects on cell proliferation, apoptosis, caspase-3 activity, loss of mitochondrial membrane potential, and cell cycle progression in K562 and K562/IMA3 cells. Furthermore, we described genes and gene networks that are modulated in CML in response to apigenin. Results of our study revealed that apigenin has cytotoxic and apoptotic effects on both cell types. We also displayed that apigenin induced G2/M arrest in K562 cells while arresting K562/IMA3 cells in S phase especially at the highest apigenin concentration. The expression analysis identified a set of genes that were regulated by apigenin in K652 and K562/IMA3 cells. Association of modulated genes with biological functional groups identified several networks affected by apigenin including cell survival, proliferation, cell death, cell cycle, and cell signalling pathways.
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    Biphasic ROS production, p53 and BIK dictate the mode of cell death in response to DNA damage in colon cancer cells
    (2017) Kutuk, Ozgur; Aytan, Nurgul; Karakas, Bahriye; Kurt, Asli Giray; Acikbas, Ufuk; Temel, Sehime Gulsun; Basaga, Huveyda; 0000-0001-9854-7220; 28796811; AAH-1671-2019
    Necrosis, apoptosis and autophagic cell death are the main cell death pathways in multicellular organisms, all with distinct and overlapping cellular and biochemical features. DNA damage may trigger different types of cell death in cancer cells but the molecular events governing the mode of cell death remain elusive. Here we showed that increased BH3-only protein BIK levels promoted cisplatin-and UV-induced mitochondrial apoptosis and biphasic ROS production in HCT-116 wild-type cells. Nonetheless, early single peak of ROS formation along with lysosomal membrane permeabilization and cathepsin activation regulated cisplatin-and UV-induced necrosis in p53-null HCT-116 cells. Of note, necrotic cell death in p53-null HCT-116 cells did not depend on BIK, mitochondrial outer membrane permeabilization or caspase activation. These data demonstrate how cancer cells with different p53 background respond to DNA-damaging agents by integrating distinct cell signaling pathways dictating the mode of cell death.