Publications by authors named "S Briedenhann"

The resistance of HIV strains to the available antiretroviral medication has become a major problem in the world today. This has forced researchers to investigate the possible use of alternative drugs such as homeopathic medicine (e.g.

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In normal pregnancy there is an increase in procoagulant activity. Furthermore, the fibrinolytic activity is impaired and remains low during labor and delivery, but returns rapidly to normal, following delivery. Here, we show ultrastructural changes in fibrin networks found in pregnant individuals and nonpregnant individuals.

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Several hematological abnormalities associated with HIV have been documented, but the mechanisms responsible for the cytopenias in AIDS patients are complex and not always completely understood. Thrombocytopenia, which occurs in about 40% of patients with HIV infection, may be caused by increased peripheral platelet destruction, a defect in platelet production due to the impaired formation of platelets by HIV-infected magakaryocytes, or a combination of these. The aim of this study was to compare the morphology of the platelet aggregates in platelet-rich plasma (PRP) clots prepared from HIV patients with those of controls without HIV.

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The aim of the current study was to investigate the ultrastructural morphology of three different sources of fibrin networks and platelets, namely, lyophilized human platelet-rich plasma (LPRP), freshly prepared human platelet-rich plasma (FPRP), and human platelet concentrate (HPC). The ultrastructural morphology of the three different fibrin networks was studied using the scanning electron microscope (SEM). Turbidity curves were drawn at 405 nm at room temperature and fibrinogen concentrations were measured.

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Article Synopsis
  • Inborn errors in fibrinogen structure lead to congenital dysfibrinogenemias, specifically in a Pretoria family with a defect at amino acid position 139 on the gamma chain.
  • Scanning electron microscopy showed a tighter fibrin network with a "stellate" appearance and an absence of platelets, indicating structural issues that affect clot formation.
  • Clinical symptoms varied, with some family members experiencing thrombosis and bleeding tendencies, potentially linked to the impaired connection of fibrin to activated platelets.
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