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Carbon Nanomaterials for Biomedical Applications
Published in Kun Zhou, Carbon Nanomaterials, 2020
Hong Wu, Qianli Huang, Yanni Tan
Gene delivery is to import a gene into cells and then let these cells produce the therapeutic materials they need. Actually, gene therapy technology has two main sorts: viral gene delivery and nonviral gene delivery. For viral gene delivery, the foreign gene is attached to the virus body, which has been modified by removing the harmful parts and then introduced into the cell to realize gene delivery. All viruses can be developed as a tool for gene transfer through a series of treatments. However, because of the difference in the life cycle and molecular pathology of different viruses, four kinds of virus carriers are mainly used: retrovirus vector (including lentivirus vector), adenovirus vector, adeno-associated virus carrier, and herpes simplex virus carrier. Nonviral transmission is carried through DNA or attached to lipids or polymers and then inserted into different cells. Nonviral vectors are favored by many researchers and clinicians because of their advantages such as no infectivity, no restriction on carrier capacity, and mass product ability. There are four kinds of nonviral DNA transfer methods: bare DNA, liposomes, polymers, and molecular conjugates. In the way of gene delivery, carbon nanomaterials, especially CNTs and GR, are extensively researched as well as applied for gene-delivery applications.
Droplet-Based Digital Microfluidics for Single-Cell Genetic Analysis
Published in Eric Lagally, Krzysztof Iniewski, Microfluidics and Nanotechnology, 2017
To address the fundamental technical challenge of single-genome extraction, we have adapted our SCGA methodology and the emulsion generator array technology to facilitate a novel agarose droplet-based method. In this method, individual cells are confined in gelled agarose droplets for integration with a standard DNA extraction protocol consisting of detergent membrane solubilization and enzymatic protein digestion to release and protect genomic DNA within the droplet. We explored multilocus single-cell sequencing of the control gene β-actin and the chromosomal translocation t(14;18) to validate this technology. The BCL-2/IgH translocation t(14;18) is highly prevalent in many blood cancers, including ~80% of follicular lymphoma (FL) cases and ~25% of large-cell B-cell lymphoma cases.59 This trans-location brings the B-cell lymphoma-2 (BCL-2) gene from 18q21 under the control of the strong enhancers of the IgH locus, ultimately disrupting BCL-2’s normal pattern of expression in B cells.60BCL-2 is an antiapoptotic protein and its overexpression can be intimately involved in the pathogenesis of B-cell neoplasms.61 t(14;18) is also found in healthy individuals at very low levels and may be an early biomarker for lymphoma.62–64 A high-throughput technique that can sequence and quantify t(14;18) could provide insight into the molecular pathology and clinical importance of t(14;18).
Ethics of Medical Product Development
Published in Howard Winet, Ethics for Bioengineering Scientists, 2021
Since its establishment in 1790, the patent office has not changed as much as, say, the NIH. Two recent patent decisions that have had major impacts on bioengineering are as follows:Legislation to change patent rights eligibility from “first to invent” to “first to file” was passed by Congress in 2011 and activated in 2013.The Superior Court held in Molecular Pathology v. Myriad Genetics Inc., 2013 that genetic material that differs from a naturally occurring DNA sequence simply by having been isolated from it is a not eligible for patent protection.
The New Zealand Genetic Frontotemporal Dementia Study (FTDGeNZ): a longitudinal study of pre-symptomatic biomarkers
Published in Journal of the Royal Society of New Zealand, 2023
Brigid Ryan, Ashleigh O’Mara Baker, Christina Ilse, Kiri L. Brickell, Hannah M. Kersten, Joanna M. Williams, Donna Rose Addis, Lynette J. Tippett, Maurice A. Curtis
FTD is highly heritable: 30-50% of FTD cases have an autosomal dominant family history (Rohrer and Warren 2011). Of these cases, 60% have causative mutations in one of three genes (Olszewska et al. 2016): Chromosome 9 open reading frame 72 (C9orf72) (DeJesus-Hernandez et al. 2011); progranulin (GRN) (Baker et al. 2006); or microtubule-associated protein tau (MAPT) (Hutton et al. 1998). MAPT mutations cause FTLD-Tau; GRN and C9orf72 mutations cause FTLD-TDP. In sporadic FTD cases, particularly sporadic bvFTD, there is poor correlation between phenotype and pathology, hence it is often not possible to determine the underlying molecular pathology using clinical criteria (Josephs et al. 2011). MAPT mutations most commonly cause bvFTD; however, they can also cause PSP, PPA and CBS (Takada 2015). Rarely, patients with MAPT mutations present with an AD phenotype; however, the neuropathological diagnosis was not AD in any of these cases (Takada 2015). In New Zealand it is not common clinical practise for all FTD cases to be genetically screened. In general, FTD cases will not be genetically screened unless a family history is reported or suspected based on questioning.
Application of constrained coefficient fuzzy linear programming in medical electrical impedance tomography
Published in Applied Mathematics in Science and Engineering, 2022
Mingliang Ding, Xiaotong Li, Shuaibo Zhao
According to the development mechanism of molecular pathology, the course of lung tissue development from normal to cancerous is a gradually changing process. Previous studies by our group have also shown that the lesion process of lung cancer tissues is positively correlated with tissue conductivity [21]. That is, when lung tissues become cancerous, their conductivity usually increases [22].
Influence of quartz exposure on lung cancer types in cases of lymph node–only silicosis and lung silicosis in German uranium miners
Published in Archives of Environmental & Occupational Health, 2018
Stefan Mielke, Dirk Taeger, Kerstin Weitmann, Thomas Brüning, Wolfgang Hoffmann
Four main biological pathways are discussed as the molecular pathology of silicosis. First, crystalline quartz dust contact causes an inflammation reaction in lung parenchyma communicated by alveolar macrophages.49,50 Second, quartz dust directly increases the concentration of reactive oxygen species (ROS)51 or nitrogen species in mice.52 Third, while the role of direct cytotoxicity is still unclear, inflammation and ROS are not only able to manipulate gene expression and gene integrity53 but also signal transduction.54 Fourth, silica contact can cause a higher lysosomal permeability through the insufficient process of internalization with consecutive cell death and proinflammatory cytokine release.52 The scavenger receptor macrophage receptor with collagenous structure (MARCO) expressed on alveolar macrophages may play an important role in internalization of silica particles.55 Building a NALP3 (NACHT, LRR, and PYD domains containing protein 3) inflammasome,10,56 releasing proinflammatory cytokines such as interleukin 1 beta (IL-1β)10,57 or tumor necrosis factor alpha (TNF-α),10,56,58,59 and stimulating transcription factor NF-κB (nuclear factor–kappa-light-chain-enhancer of activated B-cells)60,61 can be the leading ways of chronic inflammation. In the mice model, a disturbed balance between the more suppressive alveolar macrophages and the more stimulatory dendritic cells with a higher lung parenchyma emigration of dendritic cells is the consequence.62 In the absence of lymphocytes, silica-induced inflammation can prosper through NALP3 inflammasome modulation as a lymphopenic mice model has shown.63 Moreover, cyclooxygenase activity and prostaglandin synthesis are affected by silica particles.64 Furthermore, it was shown that cytokines TGF-β1 (transforming growth factor beta 1) can induce epithelial to mesenchymal transition,65 maybe also as a first step of cell degeneration as an inflammation consequence. Immunology in silicosis is a complex mixture of more pro- but also anti-inflammatory interactions.66 There is some evidence that quartz dust causes chronic inflammation as the main pathogenic process,51,67,68 especially since silica-induced apoptosis stimulates inflammation by releasing former ingested silica particles.66,69