YOUNG ADOLESCENT EFL LEARNERS’ PERSPECTIVES ON CRITICAL THINKING SKILLS

Critical Thinking Skills (CTs) are among the 21st century learning skills, and schools are expected to equip the students with these skills.  Turkey has been restructuring the educational system in order to improve the quality of education which enables students to acquire such learning skills as critical and creative thinking, problem solving, and collaboration. The present study based on the perspectives of Young Adolescent EFF learners presents findings on the students’ awareness of CTs, and whether or not they apply them to a given task, and if there is any conflict between knowledge and application of CTs. The findings showed that the students, despite their quiet well awareness, they did not effectively apply CTs. The problems they encountered were assumed to be resulted from lacking in metacognitive knowledge

Regio- and stereo-chemical ring-opening reactions of the 2,3-epoxy alcohol derivative with nucleophiles: Explanation of the structures and C-2 selectivity supported by theoretical computations

The ring-opening reactions of (1aS,2S,6bR)-5-ethyl-2-hydroxyhexahydro-4H-oxireno[2,3-e]isoindole-4,6(5H)-dione were investigated under very mild and nonchelated conditions. C-2 selective ring-opening products were obtained with nucleophilic additions such as Cl-, Br- and N-3(-). The exact configuration of (3aS,4R,5R,6S,7aS)-5-chloro-2-ethyl-4,6-dihydroxyhexahydro-1H-isoindole-1,3(2H)-dione was determined by X-Ray diffraction analysis which was obtained from the reaction of epoxy alcohol with HCl . On the other hand, theoretical computations were carried out to explain the regioselectivity in the ring opening reaction of epoxy alcohols. The results showed that the ring-opening reaction of both epoxy alcohols proceeds in a kinetically controlled manner and regioselectivity occurs depending on the transition state. (c) 2022 Published by Elsevier B.V

Expression of URG4/URGCP, Cyclin D1, Bcl-2, and Bax genes in retinoic acid treated SH-SY5Y human neuroblastoma cells

Retinoic acid (RA) plays important roles in development, growth, and differentiation by regulating the expression of its target genes. The pro-apoptotic Bax gene may form channels through oligomerization in the mitochondrial membrane and facilitate the cytosolic release of cytochrome c. The anti-apoptotic Bcl-2 gene can inhibit this process. Up-regulated gene 4/Upregulator of cell proliferation (URG4/URGCP) is a novel gene located on 7p13. URG4/ URGCP also stimulates cyclin D1 (CCND1) mRNA expression, and RNAi-mediated URG4/URGCP silencing diminishes CCND1mRNA expression in HepG2 cells. In this study, the effects of RA treatment on URG4/URGCP, CCND1, Bcl-2 and Bax gene expression changes in undifferentiated and differentiated SHSY5Y neuroblastoma cells was analyzed. SHSY5Y cells were cultured in the appropriate conditions. To induce differentiation, the cells were treated with 10micromolar RA in the dark for 3-10 days. SHSY5Y cells possess small processes in an undifferentiated state, and after treatment with RA, the cells developed long neurites, resembling a neuronal phenotype. Total RNA was isolated with Tri-Reagent. Expression profiles of the target genes were determined by semi-quantitative RT-PCR. According to the results, Bcl-2 and CCND1 gene expression levels were increased, while URG4/URGCP and Bax gene expression was decreased in RA treated cells compared to the control cells. Our preliminary results suggest that RA may induce cell proliferation and escape apoptosis using a novel pathway by the URG4/URGCP gene. Further investigations are needed to clarifymore direct transcriptional targets of RA signaling and the interaction of RA pathways with other pro-regenerative signals

Vitamin e treatment enhances erythrocyte deformability in aged rats

The harmful effects of aging on blood rheology have been well known. These effects in the aging have been found to be associated with an increase in oxidative stress. The aim of this study was to seek whether treatment of vitamin E as a potent antioxidant could improve the age-related haemorheological abnormalities. For this purpose, male Wistar rats at the age of 3 and 24 months were used. The following parameters were evaluated: red blood cell (RBC) deformability, aggregation, plasma viscosity, vitamin E level, total oxidant status (TOS), total antioxidant status (TAS) and oxidative stress index (OSI), and the following results were obtained. First, aging was associated with a decrease in RBC deformability and increase in RBC aggregation and plasma viscosity. Second, compared with the young group, while plasma TOS levels and OSI were found to be significantly increased in aged rats, there was no significant change in their plasma TAS level. Third, vitamin E administration produced significant improvement in RBC deformability and decrement in TOS and OSI values in aged rats with respect to young and aged control groups. We did not find any significant effect of vitamin E treatment on RBC aggregation in both young and aged rats and finally, we found a significantly lower plasma vitamin E level in aged rats than in young rats. In conclusion, these findings suggest that blood rheology impairs with age and vitamin E has ameliorating effects on age-induced haemorheological abnormalities especially in RBC deformability, probably by reducing the increased oxidative stress in old age

Regulation of URG4/URGCP and PPARα gene expressions after retinoic acid treatment in neuroblastoma cells

Neuroblastoma (NB), originating from neural crest cells, is the most common extracranial tumor of childhood. Retinoic acid (RA) which is the biological active form of vitamin A regulates differentiation of NB cells, and RA derivatives have been used for NB treatment. PPARα (peroxisome proliferator-activated receptor) plays an important role in the oxidation of fatty acids, carcinogenesis, and differentiation. URG4/URGCP gene is a proto-oncogene and that overexpression of URG4/URGCP is associated with metastasis and tumor recurrence in osteosarcoma. It has been known that URG4/URGCP gene is an overexpressed gene in hepatocellular carcinoma and gastric cancers. This study aims to detect gene expression patterns of PPARα and URG4/URGCP genes in SH-SY5Y NB cell line after RA treatment. Expressions levels of PPARα and URG4/URGCP genes were analyzed after RA treatment for reducing differentiation in SH-SY5Y NB cell line. To induce differentiation, the cells were treated with 10 μM RA in the dark for 3-10 days. Gene expression of URG4/URGCP and PPARα genes were presented as the yield of polymerase chain reaction (PCR) products from target genes compared with the yield of PCR products from the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) gene. SH-SY5Y cells possess small processes in an undifferentiated state, and after treatment with RA, the cells developed long neurites, resembling a neuronal phenotype. PPARα gene expression increased in RA-treated groups; URG4/URGCP gene expression decreased in SH-SY5Y cells after RA treatment compared with that in the control cells. NB cell differentiation might associate with PPARα and URG4/URGCP gene expression profile after RA treatment. © 2013 International Society of Oncology and BioMarkers (ISOBM)

Possible contribution of sulfide molecule on homocysteine toxicity and investigation of role of oxidative stress in neuroblastoma cell line

Homosistein, Metiyonin metabolizması sırasında oluşan kükürt içeren bir amino asittir. Sağlıklı kişilerde plazma homosistein düzeyi, remetilasyon ile metiyonine, transsülfürasyon yolu ile sistein aminoasidine dönüşümünü sağlayan yolaklar aracılığıyla yaklaşık 5-15 şmol/L gibi düşük bir düzeyde tutulur. Artmış plazma homosistein düzeyi başta nörolojik olmak üzere pek çok hastalık için risk faktörüdür. Nörodejeneratif hastalıklarda, homosisteine ilaveten plazma sistein düzeyi artmakta ve sülfat düzeyi azalmaktadır. Sülfat temel olarak güçlü bir nörotoksik molekül olan sülfit molekülünden sülfit oksidaz aracılığı ile oluşturulur. Sülfitin sülfit oksidaz enzimi ile sülfata çevrilerek detoksifiye edilmesi hayati önem taşır. Bu çalışmanın amacı, homosistein nörotoksisitesine sülfit molekülünün olası katkısı ve bu katkıda oksidatif stresin rolünü SH-SY5Y nöroblastoma hücreleri kullanarak araştırmaktır. Çalışmamızda, homosistein ve sülfitin oluşturduğu sitotoksisite XTT testi ile genototoksisite Comet yöntemi ile oksidatif stresin rolü TAS-TOS kiti ile incelendi. Sülfit ve homosisteinşin beraber uygulandığı hücre dizisinde tek başlarına oluşturdukları sitotoksisiteye göre toksik etkilerinin istatistiksel olarak daha da önemli olduğu bulunmuştur. Bu etkide oksidan stresin oynadığı önemli rol oksidatif stres indeksinin beraber uygulandıklarında, diğer gruplara göre anlamlı olarak yüksek bulunması ile ortaya konmuştur. Genotoksisite açısından ise en fazla hasarın yine homosistein+sülfit grubunda olduğu saptanmıştır. Sonuç olarak, nörodejeneratif hastalıkların ortaya çıkmasından çok önce izlenen homosistein artışına, benzerşekilde sülfit artışınında eşlik etmesi izlenen nörodejenerasyonun önemli bir bileşeni olabilir.Homocysteine is an amino acid, which is formed during methionine metabolism that contains sulfur. Plasma homocysteine level in healthy individuals is kept in a low level such as 5-15 ?mol/L by means of the pathways that ensure transformation to methionine via remethylation and to cystein amino acid through transsulfuration. An increased plasma homocysteine level is a risk factor for many diseases, particularly for neurological ones. In neurodegenerative diseases, the cystein level of plasma increases along with the homocystein, and the sulfate level decreases. Basically, Sulfate is formed from sulfite which is a strong neurotoxic molecule produced by sulfit oxidase enzyme. Transformation of sulfite to sulfate plays a vital role. The purpose of our study is to investigate the potential contribution of sulfite molecule to homocystein induced neurotoxicity and the role of oxidative stress in this process. In our study, the cytotoxicity caused by sulfide and homocysteine was investigated with XTT test in SH-SY5Y neuroblastoma cells. Genotoxicity and the role of oxidative stress was also investigated with comet method and TAS-TOS kit, respectively. According to statistical calculations, simultaneous administration of sulfite and homocystein on SH-Sy5Y cell line was found to be significantly more toxic than the individual administration of them in terms of sitotoxicity. In this effect, the significant role of the stress of oxidant was declared by statistically significant results of that administration with respect to other groups when both of them were administrated at the same time. The maximum damage in terms of genotoxicity was also found in the homocysteine + sulfite group. In conclusison, Consequently, an elevation of sulfite accompanying that of the homocysteine increase observed before the occurrence of disease symptoms characterized with neurodegeneration, may be an important component neurodegeneration

A new perspective on the relation between obesity and knee osteoarthritis: omentin.

OBJECTIVE: Knee osteoarthritis (KOA) is defined as a chronic degenerative joint disease. Obesity is a significant risk factor for KOA. Omentin is an adipose tissue-induced adipokine. The aim of the present study was to investigate the correlation between obesity and serum omentin levels in patients with KOA. METHODS: This study included 60 patients with KOA, 34 obese individuals (O-KOA) and 26 nonobese individuals (NO-KOA) and 40 controls, 17 obese individuals (OC) and 23 nonobese individuals (NOC) matched in terms of age, sex, and body mass index (BMI) who were recruited from the same polyclinic. Blood samples and knee radiographs were obtained from all the subjects, and clinical features, BMI, and laboratory parameters were recorded. The Kellgren-Lawrence (KL) grade and Western Ontario and McMaster Universities Osteoarthritis (WOMAC) index were used to classify the radiographic and clinical findings, respectively. Serum omentin levels were determined using an ELISA. RESULTS: Serum omentin levels in patients were significantly lower than those in the controls (p < 0.05). When the BMI values and KL scores were considered, serum omentin levels significantly decreased in severe O-KOA versus in mild-to-moderate O-KOA. There was no statistically significant decrease in severe NO-KOA versus mild-to-moderate NO-KOA. There was a significant negative correlation between the serum omentin level and BMI and WOMAC index. All findings were supported by a receiver operating characteristic curve analysis. CONCLUSION: Serum omentin levels were inversely related to obesity and the severity of KOA. The data indicate that omentin may be a new biomarker of KOA to our knowledge and may aid the diagnosis of early-stage O-KOA

Sulfite leads to neuron loss in the hippocampus of both normal and SOX-deficient rats

Sulfites are compounds commonly used as preservatives in foods, beverages and pharmaceuticals. Sulfite is also endogenously generated during the metabolism of sulfur-containing amino acids and drugs. It has been shown that sulfite is a highly toxic molecule. Many studies have examined the effects of sulfite toxicity, but the effect of ingested sulfite on the number of neurons in the hippocampus has not yet been reported. The present study was undertaken to investigate the effect of ingested sulfite on pyramidal neurons by counting cells in CA1 and CA3-2 subdivisions of the rat hippocampus. For this purpose, rats were assigned to one of four groups (6 rats per group): control (C), sulfite (S), deficient (D) and deficient + sulfite (DS). Sulfite oxidase deficiency was established by feeding rats a low molybdenum diet and adding 200 ppm tungsten (W) to their drinking water. Sulfite (70 mg/kg) was also administered to the animals via their drinking water. At the end of the experimental period, the rats were sacrificed by exsanguination under anesthesia, and their brains and livers quickly removed. The livers were used for a SOX activity assay, and the brains were used for neuronal counts in a known fraction of the CA1 and CA3-2 subdivisions of the left hippocampus using the optical fractionator method, which is a stereological method. The results showed that sulfite treatment caused a significant decrease in the total number of pyramidal neurons in three subdivisions of the hippocampus (CA1 and CA3-2) in the S, D and DS groups compared with the control group. It is concluded that exogenous administration of sulfite causes loss of pyramidal neurons in CA1 and CA3-2 subdivisions in both normal and SOX deficient rat hippocampus. This finding provides supporting evidence that sulfite is a neurotoxic molecule. © 2012 Elsevier Ltd. All rights reserved