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Nanotechnological Interventions for Neurodegenerative Disorders Using Phytoactives
Published in Bhupinder Singh, Om Prakash Katare, Eliana B. Souto, NanoAgroceuticals & NanoPhytoChemicals, 2018
Sumant Saini, Charan Singh, Shikha Lohan, Atul Jain, Eliana B. Souto, Bhupinder Singh
In this context, the mitochondrion serves as the pivotal organelle, with the ETC operating in the inner chamber. In mitochondrial physiology, fusion and fission processes occur simultaneously, and a disruption of this dynamic balance leads to erroneously working mitochondria, resulting in the symptoms of neurodegenerative disorders. Nicotinamide-Adenine Dinucleotide Phosphate (NADPH) oxidase is also responsible for increasing the ROS levels in the body. At the advent of neurodegeneration, there is an elevated level of NADPH oxidase. Excessive levels of ROS, as the result of an upregulated NADPH oxidase, causes the oxidation of various cell biomolecules, including DNA, via a redox-signal pathway. This leads to neuroinflammation, which has now been realized as the cardinal sign for the various neurodegenerative disorders (Hernandes and Britto, 2012). Another similar enzyme, xanthine oxidase (XO), is also considered as a key player in ROS-mediated mitochondrial neurodegeneration, as an enzyme associated with purine and pyrimidine metabolism. The enzyme catalyzes the conversion of hypoxanthine to uric acid, superoxide (O2−), and peroxide (O2−2) (Atlante et al., 1997; Obuobi et al., 2016).
Pulmonary infection induced by drugs
Published in Philippe Camus, Edward C Rosenow, Drug-induced and Iatrogenic Respiratory Disease, 2010
Marc B Feinstein, Dorothy A White
TNF-α antagonists inhibit the cytokine TNF, a key modulator of the inflammatory response. These drugs represent a family of monoclonal antibodies that blocks binding to the TNF receptor and has proven effective in a number of autoimmune diseases, such as rheumatoid arthritis and inflammatory bowel disease. Temozolomide is an oral compound metabolized into an active alkylating agent. Prolonged administration has been associated with lymphopenia, CD4 T-cells being preferentially affected, which can be persistent. In a majority of treated patients, lymphopenia was still present 2 months after drug discontinuation.9 Methotrexate (MTX) is an inhibitor of the enzyme dihydrofolate reductase. It indirectly impedes folinic acid-dependent metabolic pathways within the cell, including purine and pyrimidine metabolism and, at high doses, amino acid synthesis. Its mechanism of action as an anti-inflammatory agent at low doses is less well known, but may result from the clonal deletion or apoptosis of T-cells, decreased cytokine production, or effects on adenosine metabolism.10,11
COVID-19 pathogenesis and host immune response
Published in Sanjeeva Srivastava, Multi-Pronged Omics Technologies to Understand COVID-19, 2022
Surbhi Bihani, Shalini Aggarwal, Arup Acharjee
In COVID-19 affected patients, change in the immunological profile includes nutrient drop in blood profile and the rise in inflammatory molecules that diversify with disease progression (Shen et al. 2020). The inflammatory response alteration includes cytokine IL-6 and a rise in the T-cell population resulting in lymphocyte proliferation exhaustion (Zheng et al. 2020). Keratin-19 has been reported to be upregulated in damaged muscle tissues and is suspected to be a potential biomarker for tissue damage (Su et al. 2020). In the patient cohort transforming from moderately severe to severe, it is reported to find further alterations in the immune response–related cellular population such as lymphopenia (X. Cao 2020), robust HLA class II downregulation on monocytes (Wilk et al. 2020), spontaneous rise in inflammatory cytokines levels (Del Valle et al. 2020), altered mammalian target of rapamycin (mTOR) signaling in dendritic cells (Arunachalam et al. 2020), and altered levels of myeloid cells in severe COVID-19 (Schulte-Schrepping et al. 2020; Silvin et al. 2020). Virus infection inside a host requires various biomolecules for its various stages of survival and reproduction, such as invasion, replication, encapsulation, and reinfection of other host cells (Bley, Schöbel, and Herker 2020). This results in alteration of carbon metabolism (D. Wu et al. 2020), nitrogen metabolism (Thomas et al. 2020; D. Wu et al. 2020; Heer et al. 2020), pyrimidine metabolism (D. Wu et al. 2020), lipid metabolism (Shen et al. 2020; J.-W. Song et al. 2020; Maras et al. 2020), and amino acid metabolism (Shen et al. 2020; J.-W. Song et al. 2020; Maras et al. 2020; Thomas et al. 2020) pathways of the host system.
Re-Analysis of Non-Small Cell Lung Cancer and Drug Resistance Microarray Datasets with Machine Learning
Published in Cybernetics and Systems, 2023
Çiğdem Erol, Tchare Adnaane Bawa, Yalçın Özkan
All genes obtained as a result of the analyzes and their distribution according to frequencies are shared in the findings section (Tables 2 and 3). It is thought that genes with high frequency in the same data set should also be considered as potential candidates. As a result; ELOVL7, HMGA2, SAT1, RRM1, IER3, SLC7A11, and U2AF1 genes were found in at least 2 different datasets. Pathways for 7 genes obtained as a result of our research and their links are given in parentheses; ELOVL7 (Synthesis of very long-chain fatty acyl-CoAs), HMGA2 (Formation of Senescence-Associated Heterochromatin Foci), SAT1 (Interconversion of polyamines, Arginine and Proline metabolism), RRM1 (Glutathione metabolism, Pyrimidine metabolism, Purine metabolism, Mitochondrial DNA Depletion Syndrome-3), IER3 (PI5P, PP2A, and IER3 Regulate PI3K/AKT Signaling, Gastrin_CCK2R_240212), SLC7A11 (Amino acid transport across the plasma membrane, Basigin interactions, Transport of inorganic cations/anions and amino acids/oligopeptides), U2AF1 (Transport of Mature mRNA derived from an Intron-Containing Transcript, pre-mRNA splicing, RNA Polymerase II Transcription Termination, mRNA 3′-end processing).
Gene expression in human umbilical vein endothelial cells exposed to fine particulate matter: RNA sequencing analysis
Published in International Journal of Environmental Health Research, 2022
Zhixiang Zhou, Mengnan Qin, Sara Khodahemmati, Wenke Li, Bingyu Niu, Jiangshuai Li, Yanghua Liu, Jingfeng Gao
Consistent evidence from both epidemiological and experimental studies has demonstrated that exposure to particulate matter, in particular, PM2.5, is associated with CVDs (Liang et al. 2020; Hayes et al. 2020; Zhang et al. 2021). However, the cellular and molecular mechanisms underlying PM2.5 induced CVDs are largely unknown. Although several studies have investigated the molecular mechanisms of PM-induced CVDs in Beijing city (Huang et al. 2016; Hua et al. 2017; Feng et al. 2017; He et al. 2018), to our knowledge, this is the first RNA sequencing analysis conducted using Beijing winter samples. In this work, we used RNA-Seq to profile the gene expression pattern and analyze the pathways in HUVECs exposed to PM2.5. Exposure to PM2.5 led to concentration-dependent cytotoxicity and a broad and significant impact on gene expression in HUVECs. The levels of genes involved in the metabolic response, oxidative stress, inflammation, and vascular dysfunction changed significantly. In addition, the prominent significant pathways of PM2.5-induced toxicity included the p53 pathway, pyrimidine metabolism, the NF-κB signaling pathway, and the Cytokine-cytokine receptor interaction. This suggested that a systemic response was elicited by PM2.5 exposure in HUVECs.
Growth and genetic analysis of Pseudomonas BT1 in a high-thiourea environment reveals the mechanisms by which it restores the ability to remove ammonia nitrogen from wastewater
Published in Environmental Technology, 2022
Jingxuan Deng, Zhenxing Huang, Wenquan Ruan
The C, N, and S metabolic processes of BT1 were constructed based on gene annotation. In terms of C metabolism, BT1 has the complete starch and sucrose metabolism, pentose phosphate pathway, glycolysis/gluconeogenesis, and citrate cycle (TCA cycle). It can convert cellodextrin, cellobiose, and maltose into glucose or directly use glucose as the initial C source and then metabolise glucose into alpha-D-glucose-1P through the process of starch and sucrose metabolism. Alpha-D-glucose-1P enters the pentose phosphate pathway and is metabolised into pyruvate and PRPP, which can be further metabolised into energy, amino acids, purine, and pyrimidine metabolism. In addition, BT1 has a completed tricarboxylic acid (TCA) cycle, and it can convert oxaloacetate metabolised by the TCA cycle into pyruvate through glycolysis and gluconeogenesis (Figure 2).