PubMed İndeksli Yayınlar Koleksiyonu / PubMed Indexed Publications Collection
Permanent URI for this collectionhttps://hdl.handle.net/11147/7645
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Article Citation - WoS: 5Citation - Scopus: 10Removal of Pesticide Residues From Apple and Tomato Cuticle(Springer, 2023) Tari, Vinaya; Yalçın, Melis; Turgut, Nalan; Gökbulut, Cengiz; Mermer, Serhan; Sofuoğlu, Sait Cemil; Turgut, CaferPesticide residues are always an unsolved problem in the world despite all kinds of prevention measures. The present research work is based on a scientific hypothesis, i.e., The removal of average pesticide residue is inversely proportional to the thickness of cuticle. The effects of boron-containing products and plant-based surfactants were tested for the removal of five pesticides (lambda-cyhalothrin, chlorpyrifos, diflubenzuron, metaflumizone, acetamiprid) on tomatoes and apples. Boron-containing products were able to remove the pesticide residues on average between 58.0 and 72.6% in tomatoes and 33.2-58.8% in an apple. While plant-based surfactants removed residues on average between 58.5 and 66.6% in tomatoes and 41.0-53.2% in an apple. The highest removal rate was 72% with etidot at 1%. The solution of 1% C8-C10 provided 66.6% average removal for tomatoes. Less removal was achieved in apples. For an apple, Log K-ow and molecular mass (independent variables) were significant with p < 0.01, and the coefficient of determination (R-2) was > 0.87. However, the multiple linear regression analysis for ground colemanite was significant with R-2 of 0.96. In tomatoes, neither Log K-ow nor molecular mass as significant. The correlation was found between the physical and chemical properties of pesticides, but it is estimated that the thickness of the cuticle is effective in removing pesticides.Article Citation - WoS: 37Citation - Scopus: 40Gm2 Ganglioside Accumulation Causes Neuroinflammation and Behavioral Alterations in a Mouse Model of Early Onset Tay-Sachs Disease(BioMed Central Ltd., 2020) Akyıldız Demir, Seçil; Timur, Zehra Kevser; Ateş, Nurselin; Martinez, Luis Alarcon; Seyrantepe, VolkanBackground Tay-Sachs disease (TSD), a type of GM2-gangliosidosis, is a progressive neurodegenerative lysosomal storage disorder caused by mutations in the alpha subunit of the lysosomal beta-hexosaminidase enzyme. This disease is characterized by excessive accumulation of GM2 ganglioside, predominantly in the central nervous system. Although Tay-Sachs patients appear normal at birth, the progressive accumulation of undegraded GM2 gangliosides in neurons leads to death. Recently, an early onset Tay-Sachs disease mouse model, with genotypeHexa-/-Neu3-/-, was generated. Progressive accumulation of GM2 led to premature death of the double KO mice. Importantly, this double-deficient mouse model displays typical features of Tay-Sachs patients, such as cytoplasmic vacuolization of nerve cells, deterioration of Purkinje cells, neuronal death, deceleration in movement, ataxia, and tremors. GM2-gangliosidosis is characterized by acute neurodegeneration preceded by activated microglia expansion, macrophage, and astrocyte activation, along with the production of inflammatory mediators. However, the mechanism of disease progression inHexa-/-Neu3-/-mice, relevant to neuroinflammation is poorly understood. Method In this study, we investigated the onset and progression of neuroinflammatory changes in the cortex, cerebellum, and retina ofHexa-/-Neu3-/-mice and control littermates by using a combination of molecular genetics and immunochemical procedures. Results We found elevated levels of pro-inflammatory cytokine and chemokine transcripts, such as Ccl2, Ccl3, Ccl4, and Cxcl10 and also extensive microglial and astrocyte activation and proliferation, accompanied by peripheral blood mononuclear cell infiltration in the vicinity of neurons and oligodendrocytes. Behavioral tests demonstrated a high level of anxiety, and age-dependent loss in both spatial learning and fear memory inHexa-/-Neu3-/-mice compared with that in the controls. Conclusion Altogether, our data suggest thatHexa-/-Neu3-/-mice display a phenotype similar to Tay-Sachs patients suffering from chronic neuroinflammation triggered by GM2 accumulation. Furthermore, our work contributes to better understanding of the neuropathology in a mouse model of early onset Tay-Sachs disease.