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  1. Siar CH, Foo GC
    Med J Malaysia, 1984 Dec;39(4):306-10.
    PMID: 6544939
    Toxoplasmosis is a parasitic infection of worldwide distribution. It is caused by an obligate intracellular parasite, Toxoplasma gondii. The commonest form of this disease is the acquired simple lymphadenopathy. Such a case is described and the clinicopathological significance of the disease is discussed.
    Matched MeSH terms: Toxoplasmosis/pathology*
  2. Fong MY, Wong KT, Rohela M, Tan LH, Adeeba K, Lee YY, et al.
    Trop Biomed, 2010 Dec;27(3):447-50.
    PMID: 21399585 MyJurnal
    We report a case of unusual cutaneous toxoplasmosis manifestation in a HIV-positive patient. He presented with hard and painful nodular lesions on the arms, hands and chest. Serology tests for anti-Toxoplasma antibody were negative. However, histopathologic examination of the lesion revealed foci of macrophages containing crescent-shaped organisms resembling the zoites of the protozoan parasite Toxoplasma gondii. Ultrastructure examination under electron microscopy and PCR confirmed the organism as T. gondii.
    Matched MeSH terms: Toxoplasmosis/pathology*
  3. Harun MSR, Marsh V, Elsaied NA, Webb KF, Elsheikha HM
    Brain Res, 2020 11 01;1746:147002.
    PMID: 32592740 DOI: 10.1016/j.brainres.2020.147002
    Toxoplasma gondii can cause parasitic encephalitis, a life-threatening infection that predominately occurs in immunocompromised individuals. T. gondii has the ability to invade the brain, but the mechanisms by which this parasite crosses the blood-brain-barrier (BBB) remain incompletely understood. The present study reports the changes associated with infection and replication of T. gondii within human brain microvascular endothelial cells (BMECs) in vitro. Our results indicated that exposure to T. gondii had an adverse impact on the function and integrity of the BMECs - through induction of cell cycle arrest, disruption of the BMEC barrier integrity, reduction of cellular viability and vitality, depolarization of the mitochondrial membrane potential, increase of the DNA fragmentation, and alteration of the expression of immune response and tight junction genes. The calcium channel/P-glycoprotein transporter inhibitor verapamil was effective in inhibiting T. gondii crossing the BMECs in a dose-dependent manner. The present study showed that T. gondii can compromise several functions of BMECs and demonstrated the ability of verapamil to inhibit T. gondii crossing of the BMECs in vitro.
    Matched MeSH terms: Toxoplasmosis/pathology
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