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    Role of folic acid induced oxidative stress in acute kidney injury and kidney fibrosis

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    Kidneys are vital organs that filter and purify metabolic waste and maintain homeostasis of body fluids for normal physiological function. Kidney disease may affect any age of people, and an estimated 10 % of people worldwide are affected by chronic kidney disease. The only available options for kidney patients with end-stage renal disease are hemodialysis and renal replacement. These options are too costly, and because of that, it is not accessible to all socioeconomic groups. There are no approved therapeutics for reversing kidney injury and kidney fibrosis. One of the common mechanisms proposed in kidney fibrosis and kidney injury involves oxidative damage to cellular molecules by reactive oxygen species (ROS). Reports show that oxidative stress-induced molecular pathways are induced during the initiation and progression of fibrosis. The folic acid-induced kidney fibrosis mouse model is an established model to study the mechanism of kidney injury and kidney fibrosis. In this study, we uncover how a high dose of folic acid-induced oxidative stress leads to acute kidney injury and the long-term development of kidney fibrosis. C57BL/6 mice were used as an in vivo model, and Caki-1, HK-2 and NRK cells as in vitro models to study high concentrations of folic acid-mediated kidney injury and kidney fibrosis. We assessed in vitro toxicity using the MTT cell viability assay and ROS generation using the DCF assay. The consequences of ROS on the cell cycle were analyzed by Flow cytometry. Further analysis of transcript abundance by qRT - PCR was performed on samples from in vivo exposed mouse kidneys and from in vitro exposed cell lines to confirm the effect of an increased level of ROS on a molecular level. In this study, we have reported the toxicity of the high concentration of Folic Acid on Kidney epithelial cells via the generation of ROS. Further molecular analysis confirms that the generation of ROS-mediated downstream effects proceeds fibrogenesis via epithelial to mesenchymal transition (EMT) of Renal tubular Epithelial cells.Restricted until 06/2027. To request the author grant access, click on the PDF link to the left

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed

    Role of Nephrotoxicant - Induced Oxidative Stress in Acute Kidney Injury and Kidney Fibrosis

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    The kidney is an essential organ that filters metabolic waste from the body and maintains the balance of body fluids necessary for normal functioning. Kidney disease can affect individuals of any age, with an estimated 10% of the global population impacted by chronic kidney disease. Due to the kidney's filtration function, it is exposed to various xenobiotics, including nephrotoxins. Kidney epithelial cells, which play a significant role in filtration and active transport, are particularly vulnerable to exposure to nephrotoxins. For patients with end-stage renal disease, renal replacement therapies such as hemodialysis are often the only available options. However, these treatments can be invasive and costly, making them inaccessible to individuals across different socioeconomic backgrounds. Unfortunately, there are currently no approved therapeutics for reversing kidney injury or kidney fibrosis. Reactive oxygen species (ROS) are often observed during kidney injury caused by nephrotoxins, and several studies indicate that oxidative stress-induced molecular pathways contribute to the initiation and progression of fibrosis. The folic acid-induced kidney fibrosis mouse model is a well-established model for studying the mechanisms of kidney injury and fibrosis. In this study, we investigate how exposure to nephrotoxins—specifically high doses of folic acid and arsenic—leads to oxidative stress, resulting in acute kidney injury and the long-term development of kidney fibrosis. We utilized C57BL/6 mice as our in vivo model and Caki-1 and HK-2 epithelial cell lines as our in vitro models to evaluate nephrotoxin-induced kidney injury and fibrosis. The generation of ROS in kidney epithelial cells due to arsenic exposure was measured using the DCF assay. The impact of ROS on DNA damage was assessed through RAPD PCR in kidney epithelial cells. We evaluated the effects of a high dose (125 mg/kg) of folic acid injection on mouse health and kidney function by measuring body weight, serum albumin levels, and creatinine levels. Kidney injury and fibrosis were assessed using histopathological examination and immunofluorescence analysis. We examined the molecular consequences of ROS by analyzing transcript and protein expression through qRT-PCR and Western blotting of RNA and protein isolated from both in vivo mouse kidneys and in vitro cell lines. The results of this study revealed that nephrotoxins induce ROS production, leading to DNA damage and cytotoxicity in vitro, as well as reduced kidney function in the in vivo mouse model. This response was associated with changes in antioxidant levels, as well as alterations in genes and proteins related to DNA damage. Consequently, fibrogenic genes were activated through specific signaling pathways, including TGF-Beta/Smad, Notch, and Wnt/B-catenin signaling. The underlying molecular mechanisms for these alterations were linked to oxidative stress-induced changes in epigenetic regulatory mechanisms, such as histone modification and DNA methylation. In summary, our findings indicate that the activation of fibrogenic signaling is reversible by antioxidants, which restore epigenetic regulatory proteins, suggesting that oxidative stress plays a crucial role in fibrogenesis

    Variations on the Author

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    “Variations on the Author” discusses two of Eduardo Coutinho’s recent films (Um Dia na Vida, from 2010, and Últimas Conversas, posthumously released in 2015) and their contribution to the general question of documentary authorship. The director’s filmography is characterized by a consistent yet self-effacing form of authorial self-inscription: Coutinho often features as an interviewer that rather than express opinions propels discourses; an interviewer that is good at listening. This mode of self-inscription characterizes him as an author who is not expressive but who is nonetheless markedly present on the screen. In Um Dia na Vida, however, Coutinho is completely absent form the image, while Últimas Conversas, on the contrary, includes a confessional prologue that moves the director from the margins to the center of his films. This article examines the ways in which these works stand out in the filmography of a director who offers new insights into the notion of cinematic authorship

    Appropriate Similarity Measures for Author Cocitation Analysis

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    We provide a number of new insights into the methodological discussion about author cocitation analysis. We first argue that the use of the Pearson correlation for measuring the similarity between authors’ cocitation profiles is not very satisfactory. We then discuss what kind of similarity measures may be used as an alternative to the Pearson correlation. We consider three similarity measures in particular. One is the well-known cosine. The other two similarity measures have not been used before in the bibliometric literature. Finally, we show by means of an example that our findings have a high practical relevance.information science;Pearson correlation;cosine;similarity measure;author cocitation analysis

    Dispelling the Myths Behind First-author Citation Counts

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    We conducted a full-scale evaluative citation analysis study of scholars in the XML research field to explore just how different from each other author rankings resulting from different citation counting methods actually are, and to demonstrate the capability of emerging data and tools on the Web in supporting more realistic citation counting methods. Our results contest some common arguments for the continued use of first-author citation counts in the evaluation of scholars, such as high correlations between author rankings by first-author citation counts and other citation counting methods, and high costs of using more realistic citation counting methods that are not well-supported by the ISI databases. It is argued that increasingly available digital full text research papers make it possible for citation analysis studies to go beyond what the ISI databases have directly supported and to employ more sophisticated methods

    Author Index

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    koamabayili/VECTRON-author-checklist: VECTRON author checklist

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    We have done our best to complete the author checklist relating to the use of animals in the hut study. Note that the objective for the hut study was to evaluate the IRS treatment applications for residual efficacy against Anopheles mosquitoes, including the local An. coluzzii mosquito population. Cows were only used to attract mosquitoes into the huts and no tests were carried out directly on the cows. The author checklist is intended for use with studies where experiments are carried out on animals, which is why we have had such difficulty in completing this for the hut study, as many of the questions do not relate to how the cows were used
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