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Introduction: Systemic lupus erythematosus (SLE) complicated by thrombotic microangiopathy (TMA) and non-cirrhotic portal hypertension (NCPH) is rare. We present a case of a female patient with SLE who developed TMA and NCPH and responded positively to rituximab and plasma exchange treatment.

Case Description: A 53-year-old woman was admitted with 6 h of confusion.

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Background And Objective: Previously, the novel small molecule ISFP10 has been shown to inhibit fungal phosphoglucomutase (PGM) activity in and spp. With 50-fold selectivity over the human PGM molecule due to the presence of a unique yet conserved cysteine residue present in a number pathogenic fungal PGMs, use of this compound may provide a novel broad-spectrum approach to treating fungal infections. Accordingly, we sought to determine the tolerability in test animals receiving this compound, as well as the potential antifungal activity of ISFP10 on cultures of the common fungal pathogens and .

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  • Amniotic epithelial stem cells (AEC) have regenerative potential, particularly through their conditioned medium (AEC-CM), which shows immunomodulatory and regenerative effects.
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Evolution of SARS-CoV-2 spike trimers towards optimized heparan sulfate cross-linking and inter-chain mobility.

Sci Rep

December 2024

Institute of Physiological Chemistry and Pathobiochemistry, University of Münster, Waldeyerstrasse 15, D-48149, Münster, Germany.

The heparan sulfate (HS)-rich extracellular matrix (ECM) serves as an initial interaction site for the homotrimeric spike (S) protein of SARS-CoV-2 to facilitate subsequent docking to angiotensin-converting enzyme 2 (ACE2) receptors and cellular infection. More recent variants, notably Omicron, have evolved by swapping several amino acids to positively charged residues to enhance the interaction of the S-protein trimer with the negatively charged HS. However, these enhanced interactions may reduce Omicron's ability to move through the HS-rich ECM to effectively find ACE2 receptors and infect cells, raising the question of how to mechanistically explain HS-associated viral movement.

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[Hereditary protein S deficiency in a patient with prominent mesenteric venous thrombosis: A case report].

Beijing Da Xue Xue Bao Yi Xue Ban

December 2024

Department of Rheumatology and Immunology, Peking University Third Hospital, Beijing 100191, China.

Hereditary protein S deficiency (PSD) is an autosomal dominant disorder caused by mutations in the 1 gene which can cause venous thrombosis. Individuals with PSD usually present with recurrent deep vein thrombosis and/or pulmonary embolism, but thrombosis may occur at unusual sites, such as the mesenteric and portal veins. Here we report a case of hereditary protein S deficiency patient with predominant mesenteric venous thrombosis.

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