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1.
Front Public Health ; 9: 642983, 2021.
Article in English | MEDLINE | ID: mdl-34277534

ABSTRACT

Infectious diseases exacerbated by Antimicrobial Resistance (AMR) are of increasing concern in Sweden, with multi-drug resistant strains associated with new resistance mechanisms that are emerging and spreading worldwide. Existing research has identified that sub-optimal living conditions and poor access to healthcare are significant factors in the spread and incubation of AMR strains. The article considers this linkage and the effort to control the spread of AMR in relation to migrants, highlighting deficiencies in public policy where such individuals are often increasingly exposed to those conditions that exacerbate AMR. In many of the richest countries, those conditions are not accidental, but often direct goals of policies designed with the goal of deterring migrants from staying within host countries. Without engaging with the politics around migration control, the article points to urgent need for more holistic assessment of all public policies that may, however unintentionally, undermine AMR control through worsening living conditions for vulnerable groups. The consequences of prioritizing policies meant to deliberately worsen the living conditions of migrants over avoiding those conditions that accelerate AMR spread, are today made ever apparent where new AMR strains have the potential to dwarf the societal effects of the current Covid-19 pandemic.


Subject(s)
COVID-19 , Transients and Migrants , Anti-Bacterial Agents/pharmacology , Drug Resistance, Bacterial , Humans , Pandemics , Public Health , Public Policy , Risk Factors , SARS-CoV-2 , Social Conditions , Sweden/epidemiology
2.
Front Public Health ; 8: 574334, 2020.
Article in English | MEDLINE | ID: mdl-33194974

ABSTRACT

Refugees are already a vulnerable group in society and are in a stressful situation due to their often uncertain legal status in seeking asylum and integration in the new society after migration. Refugees are, in general, at greater risk of poor health outcomes when contracting Covid-19, exacerbated by poor living conditions and difficulties in accessing healthcare. The longer-term social consequences of the pandemic also disproportionately impact refugees, including social isolation, unemployment, and difficulties to obtain correct health information. The aim of this paper is to review the social and health consequences that Covid-19 has brought to the refugees residing in Sweden. This needs to be emphasized in order to mitigate against these likely consequences and improve the overall well-being among such a highly vulnerable group in society. As Covid-19 demonstrates, human health needs to be understood holistically, meaning that the vulnerability of any individuals, or even nations, is a vulnerability for the whole population requiring urgent action.


Subject(s)
COVID-19 , Refugees , Humans , Pandemics/prevention & control , SARS-CoV-2 , Sweden/epidemiology
3.
Microb Pathog ; 41(4-5): 168-73, 2006.
Article in English | MEDLINE | ID: mdl-16949788

ABSTRACT

Group B streptococcus (GBS), the leading cause of neonatal meningitis, has been shown to invade human brain microvascular endothelial cells (HBMEC), which constitute the blood-brain barrier. GBS invasion of HBMEC has been shown to require the host cell actin cytoskeleton rearrangements. The present study examined the mechanisms underlying actin cytoskeleton rearrangements that are involved in type III GBS invasion of HBMEC. We showed that type III GBS invasion was inhibited by genistein, a general tyrosine kinase inhibitor (mean 54% invasion decrease at 100 microM), and LY294002, a phosphatidylinositol 3 (PI3) kinase inhibitor (mean 70% invasion decrease at 50 microM), but not by PP2, an inhibitor of the Src family tyrosine kinases. We subsequently showed that the focal adhesion kinase (FAK) was the one of the host proteins tyrosine phosphorylated by type III GBS. Over-expression of a dominant negative form of the FAK C-terminal domain significantly decreased type III GBS invasion of HBMEC (mean 51% invasion decrease). In addition, we showed that FAK phosphorylation correlated with its association of paxillin, an adapter protein of actin filament, and PI3-kinase subunit p85. This is the first demonstration that FAK phosphorylation and its association with paxillin and PI3 kinase play a key role in type III GBS invasion of HBMEC.


Subject(s)
Blood-Brain Barrier/enzymology , Blood-Brain Barrier/microbiology , Focal Adhesion Protein-Tyrosine Kinases/metabolism , Streptococcal Infections/enzymology , Streptococcal Infections/microbiology , Streptococcus agalactiae/pathogenicity , Actins/metabolism , Blood-Brain Barrier/drug effects , Blotting, Western , Chromones/pharmacology , Cytoskeleton/metabolism , Cytoskeleton/microbiology , Endothelial Cells/drug effects , Endothelial Cells/enzymology , Endothelial Cells/microbiology , Enzyme Activation , Focal Adhesion Protein-Tyrosine Kinases/antagonists & inhibitors , Genistein/pharmacology , Humans , Morpholines/pharmacology , Paxillin/pharmacology , Phosphatidylinositol 3-Kinases/metabolism , Phosphorylation , Protein Kinase Inhibitors/pharmacology , Pyrimidines/pharmacology
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