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  1. Article ; Online: Known drugs and small molecules in the battle for COVID-19 treatment

    Alexios A. Panoutsopoulos

    Genes and Diseases, Vol 7, Iss 4, Pp 528-

    2020  Volume 534

    Abstract: COVID-19 has been declared a pandemic by the World Health Organization on March 11th and since then more than 3 million cases and a quarter million deaths have occurred due to it. The urge to find a resultful treatment or cure is now pressing more than ... ...

    Abstract COVID-19 has been declared a pandemic by the World Health Organization on March 11th and since then more than 3 million cases and a quarter million deaths have occurred due to it. The urge to find a resultful treatment or cure is now pressing more than any other time since the outbreak of the pandemic. Researchers all over the world from different fields of expertise are trying to find the most suitable drugs, that are already known to treat other diseases, and could tackle the process of SARS-CoV2 through which it invades and replicates in human cells. Here, we discuss five of the most promising drugs that can potentially play a major role in the treatment of COVID-19. While nicotine and ivermectin may be blocking transport abilities of the virus or its components, famotidine, remdesivir and chloroquine in combination with zinc ions can deactivate important enzymes needed for the replication of the virus. While clinical trials for some of these drugs have already started, it is common knowledge that lack of organization between countries, institutes and hospitals might slow down the whole process for an official treatment based in wide, randomized, placebo controlled trials.
    Keywords Chloroquine ; Coronavirus ; COVID-19 ; Famotidine ; Ivermectin ; Nicotine ; Medicine (General) ; R5-920 ; Genetics ; QH426-470
    Language English
    Publishing date 2020-12-01T00:00:00Z
    Publisher Elsevier
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  2. Article ; Online: Pak1ip1 Loss-of-Function Leads to Cell Cycle Arrest, Loss of Neural Crest Cells, and Craniofacial Abnormalities

    Alexios A. Panoutsopoulos / Angelo Harlan De Crescenzo / Albert Lee / Amelia MacKenzie Lu / Adam P. Ross / Laura N. Borodinsky / Ralph Marcucio / Paul A. Trainor / Konstantinos S. Zarbalis

    Frontiers in Cell and Developmental Biology, Vol

    2020  Volume 8

    Abstract: Neural crest cells (NCCs) comprise a transient progenitor cell population of neuroepithelial origin that contributes to a variety of cell types throughout vertebrate embryos including most mesenchymal cells of the cranial and facial structures. ... ...

    Abstract Neural crest cells (NCCs) comprise a transient progenitor cell population of neuroepithelial origin that contributes to a variety of cell types throughout vertebrate embryos including most mesenchymal cells of the cranial and facial structures. Consequently, abnormal NCC development underlies a variety of craniofacial defects including orofacial clefts, which constitute some of the most common birth defects. We previously reported the generation of manta ray (mray) mice that carry a loss-of-function allele of the gene encoding the preribosomal factor Pak1ip1. Here we describe cranioskeletal abnormalities in homozygous mray mutants that arise from a loss of NCCs after their specification. Our results show that the localized loss of cranial NCCs in the developing frontonasal prominences is caused by cell cycle arrest and cell death. In addition, and consistent with deficits in ribosome biosynthesis, homozygous mray mutants display decreased protein biosynthesis, further linking Pak1ip1 to a role in ribosome biogenesis.
    Keywords neural crest ; development ; orofacial clefts ; mouse ; Pak1ip1 ; ribosomopathies ; Biology (General) ; QH301-705.5
    Subject code 571
    Language English
    Publishing date 2020-09-01T00:00:00Z
    Publisher Frontiers Media S.A.
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

    Full text online

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