Nanoparticles as potential clinical therapeutic agents in Alzheimer’s disease: focus on selenium nanoparticles

In etiology of Alzheimer’s disease (AD), involvement of amyloid β (Aβ) plaque accumulation and oxidative stress in the brain have important roles. Several nanoparticles such as titanium dioxide, silica dioxide, silver and zinc oxide have been experimentally using for treatment of neurological disease. In the last decade, there has been a great interest on combination of antioxidant bioactive compounds such as selenium (Se) and flavonoids with the oxidant nanoparticles in AD. We evaluated the most current data available on the physiological effects of oxidant and antioxidant nanoparticles.Areas covered: Oxidative nanoparticles decreased the activities of reactive oxygen species (ROS) scavenging enzymes such as glutathione peroxidase (GSH-Px), superoxide dismutase (SOD) and catalase in the brain of rats and mice. However, Se-rich nanoparticles in small size (5–15 nm) depleted Aβ formation through decreasing ROS production. Reports on low levels of Se in blood and tissue samples and the low activities of GSH-Px, catalase and SOD enzymes in AD patients and animal models support the proposed crucial role of oxidative stress in the pathogenesis of AD.In conclusion, present literature suggests that Se-rich nanoparticles appeared to be a potential therapeutic compound for the treatment of AD

A critical analysis of religious education in Turkey in the context of banking concept of education

Bu makalede geleneksel ve modern eğitim anlayışlarına karşı kuramsal bir eleştiri olarak 20. yüzyılda ortaya çıkmış olan eleştirel pedagojinin anahtar kavramı olan “bankacı eğitim” kavramı din eğitimi açısından yorumlanmış, Türkiye’deki örgün din eğitimi uygulamaları bağlamında bu kavram açısından anlamlı sayılabilecek konular ve sorunlar üzerine bir değerlendirme yapılmıştır. Nitel araştırma mantığıyla hazırlanmış çalışma; başta Freire olmak üzere eleştirel pedagoji alanyazınının incelenmesi ve Türkiye’deki örgün din eğitiminin durumuna ilişkin metin, doküman ve raporların “bankacı eğitim” kavramı bağlamında eleştirel bir yaklaşımla yorumlanmasına dayalıdır. Çalışmada öncelikli olarak eleştirel pedagojinin teorik temeline değinilmiş ve bu yaklaşımın din eğitimi bağlamındaki olası uzanımları tartışılmıştır. Daha sonra “bankacı eğitim” kavramı perspektifinden örgün din eğitiminin bazı güncel sorunları teşhis edilmeye çalışılmıştır. Bu bağlamda din eğitiminde bankacı eğitim olarak nitelenebilecek sorunlar; “nesnel bilgi kaygısı”, “rekabet ve sıralamaya dayalı ölçme-değerlendirme anlayışı” ve “teknik-meslekî bakış açısı” olarak üç başlık altında ele alınmış, sonuç bölümünde bu sorunların giderilmesine yönelik olarak eleştirel pedagojinin bakış açısından hareketle öneriler sunulmuştur.In this paper, we propose the banking concept of education of critical pedagogy as a useful tool for addressing the some current issues in religious education in Turkey. As a key concept of critical pedagogy that emerged in the 20th century as a theoretical criticism towards the traditional and modern approaches of education, banking concept of education deserves to be interpreted in terms of religious education. In accordance with the purpose, the theoretical grounds of the critica pedagogy has been problematized and discussed the possible contributions of this approach for optimizing the efficiency and effectiveness of the religious education. The article has been conducted in the frame of qualitative research design in order to determine a starting point for a critical pedagogical paradigm in religious education. In order to estimate the value of critical pedagogy for religious education, we firstly reviewed the literature of critical pedagogy –predominantly Paulo Freire’s works-. Secondly, we interpreted several related texts, documents and reports that subject the current situation in religious education practices in Turkey in a critical manner. As a result, we consider the problems of current religious education practices that are able to be debated within the scope of banking concept; “overemphasizing the objective knowledge”, “competition and grading-orientedness in measurement and evaluation” and “technical-career focuseness”. In the conclusion, we discussed how the critical pedagogy can offers conceptional and theoretical contribution for overcoming these problems

Toxic effects of Bisphenol S on the Gonad and Visceral Organs of Goldfish (Carassius auratus)

Bisfenol A (BPA), polikarbonat plastiklerin ve epoksi reçinelerinin üretiminde kullanılan çevresel bir kirleticidir. Bununla birlikte bisfenol S (BPS), son zamanlarda BPA ürünlerine alternatif olarak kullanılmaya başlanan bir bisfenol analoğudur. Bu çalışmada farklı BPS konsantrasyonlarına (0, 100 ve 500 μg/L) 21 gün maruz bırakılan japon balıklarının (Carassius auratus) karaciğer, böbrek, gonad ve solungaç dokularındaki bir dizi etki histopatolojik olarak belirlenmiştir. Solungaçlarda BPS’nin hiperemi, ödem, epitel hücrelerinde deskuamasyon ve nekroza neden olduğu dikkat çekmiştir. Böbreklerde nekroz ve melanomakrofaj infiltrasyonları sıklıkla gözlenmiştir. Karaciğerde BPS’nin hiperemi ve inflamatuar hücre infiltrasyonlarına neden olduğu saptanmıştır. Bu çalışma, BPS'nin Carassius auratus'un çeşitli viseral organlarında dejeneratif değişikliklere neden olduğu ve histopatolojik değişikliklerin şiddetinin doza bağlı olduğunu ortaya koymuştur.Bisphenol-A (BPA) is an environmental contaminant used in the manufacturing of polycarbonate plastics and epoxy resins. Whereas bisphenol S (BPS) is a bisphenol analogue which is recently used to replace BPA products. We demonstrated the effects of BPS on liver, kidney, gonad, and gills in goldfish (Carassius auratus) by a histopathological examination. Fishes treated with different concentrations (0, 100 and 500 μg/L) of BPS were tested for a duration of 21-days. In gills, BPS caused hyperemia, edema, epithelial desquamation and necrosis. Kidney lesions included necrosis and melanomacrophage infiltrations. BPS stress caused hyperemia and inflammatory cell infiltrations in livers. The present study revealed that BPS causes degenerative changes in various visceral organs of Carassius auratus and severity of histopathological changes were dose related

Albumin evokes Ca 2+ -induced cell oxidative stress and apoptosis through TRPM2 channel in renal collecting duct cells reduced by curcumin

In proteinuric nephropathies of chronic kidney disease, the epithelial cells of the nephron including the collecting duct are exposed to high concentrations of luminal albumin. Albumin is taken up from collecting duct cells by endocytosis causing excessive reactive oxygen species (ROS) production and a proinflammatory response. Curcumin used in the traditional medicine possesses anti-inflammatory and antioxidant effects. ROS and ADP-ribose (ADPR) activate the cation channel TRPM2. We hypothesize, that albumin-induced cell stress and proinflammatory response are mediated by Ca2+ and can be reduced by curcumin. The cortical collecting duct (CCD) cells mpkCCDc14 exhibit spontaneous and inducible Ca2+ oscillations, which can be blocked by pre-treatment with curcumin. Curcumin accumulates in plasma membrane and intracellular vesicles, where it interferes with TRPM2 and decreases the influx of Ca2+. Albumin reduces cell viability and increases apoptosis, NF-κB activation, and mitochondrial membrane depolarization via Ca2+-dependent signaling, which results in increased ROS production. Albumin-induced cell stress is diminished by the inhibition of TRPM2 after administration of curcumin and ADPR (PARP1) inhibitors. Curcumin did not reduce the Ca2+ elevation induced by thapsigargin in Ca2+-free medium, but it reduced the function of store-operated Ca2+ channels and ATP-evoked Ca2+ response. In conclusion, albumin-induced oxidative stress is mediated by Ca2+-dependent signaling via TRPM2 and leads to cell damage and a proinflammatory response, strengthening the role of CCD cells in the progression of chronic kidney disease

Menthol evokes Ca2+ signals and induces oxidative stress independently of the presence of TRPM8 (menthol) receptor in cancer cells

Menthol is a naturally occurring monoterpene alcohol possessing remarkable biological properties including antipruritic, analgesic, antiseptic, anti-inflammatory and cooling effects. Here, we examined the menthol-evoked Ca2+ signals in breast and prostate cancer cell lines. The effect of menthol (50–500µM) was predicted to be mediated by the transient receptor potential ion channel melastatin subtype 8 (TRPM8). However, the intensity of menthol-evoked Ca2+ signals did not correlate with the expression levels of TRPM8 in breast and prostate cancer cells indicating a TRPM8-independent signaling pathway. Menthol-evoked Ca2+ signals were analyzed in detail in Du 145 prostate cancer cells, as well as in CRISPR/Cas9 TRPM8-knockout Du 145 cells. Menthol (500µM) induced Ca2+ oscillations in both cell lines, thus independent of TRPM8, which were however dependent on the production of inositol trisphosphate. Results based on pharmacological tools point to an involvement of the purinergic pathway in menthol-evoked Ca2+ responses. Finally, menthol (50–500µM) decreased cell viability and induced oxidative stress independently of the presence of TRPM8 channels, despite that temperature-evoked TRPM8-mediated inward currents were significantly decreased in TRPM8-knockout Du 145 cells compared to wild type Du 145 cells

Antimicrobial activity of apple cider vinegar against Escherichia coli, Staphylococcus aureus and Candida albicans; downregulating cytokine and microbial protein expression

The global escalation in antibiotic resistance cases means alternative antimicrobials are essential. The aim of this study was to investigate the antimicrobial capacity of apple cider vinegar (ACV) against E. coli, S. aureus and C. albicans. The minimum dilution of ACV required for growth inhibition varied for each microbial species. For C. albicans, a 1/2 ACV had the strongest effect, S. aureus, a 1/25 dilution ACV was required, whereas for E-coli cultures, a 1/50 ACV dilution was required (p < 0.05). Monocyte co-culture with microbes alongside ACV resulted in dose dependent downregulation of inflammatory cytokines (TNFα, IL-6). Results are expressed as percentage decreases in cytokine secretion comparing ACV treated with non-ACV treated monocytes cultured with E-coli (TNFα, 99.2%; IL-6, 98%), S. aureus (TNFα, 90%; IL-6, 83%) and C. albicans (TNFα, 83.3%; IL-6, 90.1%) respectively. Proteomic analyses of microbes demonstrated that ACV impaired cell integrity, organelles and protein expression. ACV treatment resulted in an absence in expression of DNA starvation protein, citrate synthase, isocitrate and malate dehydrogenases in E-coli; chaperone protein DNak and ftsz in S. aureus and pyruvate kinase, 6-phosphogluconate dehydrogenase, fructose bisphosphate were among the enzymes absent in C.albican cultures. The results demonstrate ACV has multiple antimicrobial potential with clinical therapeutic implications

TRPM2 channel deficiency prevents delayed cytosolic Zn²⁺ accumulation and CA1 pyramidal neuronal death after transient global ischemia

Transient ischemia is a leading cause of cognitive dysfunction. Postischemic ROS generation and an increase in the cytosolic Zn²⁺ level ([Zn²⁺]c) are critical in delayed CA1 pyramidal neuronal death, but the underlying mechanisms are not fully understood. Here we investigated the role of ROS-sensitive TRPM2 (transient receptor potential melastatin-related 2) channel. Using in vivo and in vitro models of ischemia-reperfusion, we showed that genetic knockout of TRPM2 strongly prohibited the delayed increase in the [Zn²⁺]c, ROS generation, CA1 pyramidal neuronal death and postischemic memory impairment. Time-lapse imaging revealed that TRPM2 deficiency had no effect on the ischemia-induced increase in the [Zn²⁺]c but abolished the cytosolic Zn²⁺ accumulation during reperfusion as well as ROS-elicited increases in the [Zn²⁺]c. These results provide the first evidence to show a critical role for TRPM2 channel activation during reperfusion in the delayed increase in the [Zn²⁺]c and CA1 pyramidal neuronal death and identify TRPM2 as a key molecule signaling ROS generation to postischemic brain injury