How Mobile Devices Affect Students According To Teachers' Beliefs

The purpose of this study is to examine teachers' beliefs concerning the effects on students using mobile devices, and to determine whether these beliefs vary according to the demographic characteristics and Internet usage purposes. For this purpose, a demographic information questionnaire and the scale developed by Diker Coskun & Kizilkaya Cumaoglu (2013) were revised with validity and reliability studies and utilized on teachers (N=200). In total, the scale has three dimensions (with a total of 15 items). These are social effects (9 items), psychological effects (3 items), and learning-related effects (3 items). According to the results of the study, teachers believe that students are affected by mobile devices on all three dimensions of the scale (social, psychological, and learning dimensions). The most striking finding of the study is related to the learning dimension of the beliefs concerning mobile devices scale. In every Internet usage purpose examined within the study, it was determined that the teachers' beliefs concerning the "learning" dimension are always more positive than those that do not use the Internet for any given purpose

On the role of 4-hydroxynonenal in health and disease

AbstractPolyunsaturated fatty acids are susceptible to peroxidation and they yield various degradation products, including the main α,β-unsaturated hydroxyalkenal, 4-hydroxy-2,3-trans-nonenal (HNE) in oxidative stress. Due to its high reactivity, HNE interacts with various macromolecules of the cell, and this general toxicity clearly contributes to a wide variety of pathological conditions. In addition, growing evidence suggests a more specific function of HNE in electrophilic signaling as a second messenger of oxidative/electrophilic stress. It can induce antioxidant defense mechanisms to restrain its own production and to enhance the cellular protection against oxidative stress. Moreover, HNE-mediated signaling can largely influence the fate of the cell through modulating major cellular processes, such as autophagy, proliferation and apoptosis. This review focuses on the molecular mechanisms underlying the signaling and regulatory functions of HNE. The role of HNE in the pathophysiology of cancer, cardiovascular and neurodegenerative diseases is also discussed

Polyphenolic Extracts from Olea europea L. Protect Against Cytokine-Induced beta-Cell Damage Through Maintenance of Redox Homeostasis

Various pancreatic beta-cell stressors, including cytokines, are known to induce oxidative stress, resulting in apoptotic/necrotic cell death and inhibition of insulin secretion. Traditionally, olive leaves or fruits are used for treating diabetes, but the cellular mechanism(s) of their effects are not known. We examined the effects of Olea europea L. (olive) leaf and fruit extracts and their component oleuropein on cytokine-induced beta-cell toxicity. INS-1, an insulin-producing beta-cell line, was preincubated with or without increasing concentrations of olive leaf or fruit extract or oleuropein for 24 hr followed by exposure to a cytokine cocktail containing 0.15 ng/mL interleukin-1 beta (IL-1 beta), 1 ng/mL interferon-gamma (IFN-gamma), and 1 ng/mL tumor necrosis factor-alpha (TNF-alpha) for 6 hr. The cytotoxicity was assessed by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) testing. Apoptosis was quantified by detecting acridine orange/ethidium bromide-stained condensed nuclei under a fluorescent microscope. The cells exposed to cytokines had a higher apoptotic rate, a decreased viability (MTT), and an increased caspase 3/7 activity. Both extracts and oleuropein partially increased the proportion of living cells and improved the viability of cells after cytokines. The protective effects of extracts on live cell viability were mediated through the suppression of caspase 3/7 activity. Oleuropein did not decrease the amount of both apoptotic and necrotic cells, whereas extracts significantly protected cells against cytokine-induced death. Cytokines led to an increase in reactive oxygen species (ROS) generation and inhibited glutathione level, superoxide dismutase activity, and insulin secretion in INS-1. Insulin secretion was almost completely protected by leaf extract, but was partially affected by fruit extract or oleuropein. Neither cytokines nor olive derivatives had a significant effect on cellular cytochrome c release and catalase activity. Moreover, the cells incubated with each extract or oleuropein showed a significant reduction in cytokine-induced ROS production and ameliorated abnormal antioxidant defense. The molecular mechanism by which olive polyphenols inhibit cytokine-mediated beta-cell toxicity appears to be involving the maintenance of redox homeostasis

Inhibition of ErbB2 by Herceptin reduces viability and survival, induces apoptosis and oxidative stress in Calu-3 cell line

Human epidermal growth factor receptor 2 (ErbB2) amplification and overexpression has been seen in many cancer types including non-small cell lung cancer (NSCLC). Thus, ErbB2 is an important target for cancer therapies. Increased ErbB2 expression has been associated with drug resistance in cancer cells. Herceptin is a humanized monoclonal antibody that targets the extracellular domain of ErbB2. In this study, we aimed to block ErbB2 signaling with Herceptin and assess cytotoxicity and effects on apoptosis, oxidative stress, nuclear factor kappa-B (NF-kB), and Survivin expression in Calu-3 cell line. 3-(4,5-dimethyl-2-thiazolyl)-2,5-diphenyl-2H-tetrazolium bromide (MTT) assay were used to assess cell viability as a marker of proliferation. Acridine orange/ethidium bromide (AO/EB) staining and caspase 3/7 activity were measured as the markers of apoptosis. The relative expressions of NF-kB-p50 and Survivin mRNAs were evaluated. Activities of antioxidant enzymes such as superoxide dismutase (SOD) and catalase (CAT), and the levels of glutathione (GSH) and reactive oxygen species (ROS) were determined in a time- and dose-dependent manner. Our results show that Herceptin treatment inhibits cell proliferation and activates apoptosis but without effects on Survivin and NF-kB expression in Calu-3 cell line. Intracellular glutathione levels and SOD and CAT activities were decreased in a time- and dose-dependent manner associated with oxidative stress. Also, ROS were increased at 24 h. These results provide evidence that Herceptin can be used as a cytotoxic and apoptotic agent in NSCLC

Effects of antioxidant stobadine on protein carbonylation, advanced oxidation protein products and reductive capacity of liver in streptozotocin-diabetic rats: Role of oxidative/nitrosative stress

Background: Increased oxidative/nitrosative stress is important in the pathogenesis of diabetic complications, and the protective effects of antioxidants are a topic of intense research. The purpose of this study was to investigate whether a pyridoindole antioxidant stobadine (STB) have a protective effect on tissue oxidative protein damage represented by the parameters such as protein carbonylation (PC), protein thiol (P-SH), total thiol (T-SH) and non-protein thiol (Np-SH), nitrotyrosine (3-NT), and advanced oxidation protein products (AOPP) in streptozotocin-diabetic rats

Goji Berry Fruit Extract Suppresses Cell Proliferation of Breast Cancer Cells by Inhibiting EGFR/ERK Signalling

Herbal medicines have been used in cancer treatment, with many exhibiting favorable side effect and toxicity profiles compared with conventional chemotherapeutic agents. The aim of this study was to verify whether Lycium barbarum fruit (red and black fruit) extracts inhibit proliferation of MDA-MB-231cells through EGFR/ERK pathway. Cytotoxicity with MTT reduction assay and phosphorylation of EGFR and ERK were analyzed by western blot. IC50 values were 87.0 and 79.4 µg/mL for goji berry black fruit extract (GBBFE) and goji berry red fruit extract (GBRFE) expectively. Pretreatment with both extract inhibited phosphorylation of EGFR/ERK in EGF-treated cells. Goji berry fruit extracts cause cellular death of MDA-MB-231 breast cancer cells by inhibiting EGFR/ERK signaling and this study suggests that Goji berry fruit extracts could be beneficial for treating breast cancer

Effects of olive leaf polyphenols against H2O2 toxicity in insulin secreting beta-cells

In pancreatic beta-cells, although H2O2 is a metabolic signal for glucose stimulated insulin secretion, it may induce injury in the presence of increased oxidative stress (OS) as in the case of diabetic chronic hyperglycemia. Olea europea L. (olive) leaves contain polyphenolic compounds that may protect insulin-secreting cells against OS. The major polyphenolic compound in ethanolic olive leaf extract (OLE) is oleuropein (about 20%), thus we compared the effects of OLE with the effects of standard oleuropein on INS-1 cells. The cells were incubated with increasing concentrations of OLE or oleuropein for 24 h followed by exposure to H2O2 (0.035 mM) for 45 min. H2O2 alone resulted in a significantly decreased viability (MTT assay), depressed glucose-stimulated insulin secretion, increased apoptotic and necrotic cell death (AO/EB staining), inhibited glutathione peroxidase activity (GPx) and stimulated catalase activity that were associated with increased intracellular generation of reactive oxygen species (ROS) (fluorescence DCF). OLE and oleuropein partly improved the viability, attenuated necrotic and apoptotic death, inhibited the ROS generation and improved insulin secretion in H2O2-exposed cells. The effects of oleuropein on insulin secretion were more pronounced than those of OLE, while OLE exerted a stronger anti-cytotoxic effect than oleuropein. Unlike OLE, oleuropein had no significant preserving effect on GPx; however, both compounds stimulated the activity of catalase in H2O2-exposed cells. These findings indicate different modulatory roles of polyphenolic constituents of olive leaves on redox homeostasis that may have a role in the maintenance of beta-cell physiology against OS

Oxidant/antioxidant status in premenstrual syndrome

To investigate oxidant/antioxidant status in premenstrual syndrome (PMS)