An Unusual Case of Combined Thrombosis and Amegakaryocytopenia Resembling Thrombosis With Thrombocytopenia Syndrome Following COVID-19 Infection in an Unvaccinated Patient.

As a global community, we have learned that the manifestations of severe acute respiratory syndrome coronavirus 2 (SAR-CoV-2), infection, or coronavirus disease 2019 (COVID-19), extends far beyond respiratory compromise. Thrombocytopenia is thought to occur secondary to increased platelet consumption. Platelet activation and platelet-mediated immune inflammation contribute towards the thromboembolic complications seen in COVID-19 patients. In this report, the authors present the unusual case of a 75-year-old female with a history of COVID-19 infection who presented with a transient ischemic attack, thrombocytopenia, and amegakaryocytopenia.

IL-26 mediated human cell activation and antimicrobial activity against Borrelia burgdorferi.

Lyme disease is an inflammatory disease caused by infection with Borrelia burgdorferi (Bb). Inflammatory sequelae of Bb infection appear to be refractory to antibiotics. An antimicrobial peptide with the ability to bind the DNA in the tissue could serve as a viable option of treatment for chronic complications of Lyme borreliosis. DNA of Bb can remain in tissues causing a prolonged inflammatory response that lead to chronic joint pain. Here we examined the effect of IL-26, a newly reported antimicrobial protein, against Bb DNA. An antimicrobial effect of IL-26 on the spirochete was observed. In human macrophages, IL-26 treated cells showed an increase in IRF activation upon Bb stimulation. Moreover, IL-26 treated macrophages showed an increased in phagocytic activity compared to untreated cells. Although no Bb DNA degradation was observed using a TUNEL assay run in an agarose gel, a Comet assay on whole bacteria showed cellular and Bb DNA degradation by IL-26. Our results showed that IL-26 (monomer and dimer) has not only the potential to control Bb growth in vitro, but it also enhances the anti-borrelial response of human macrophages. Further research aiming to characterize the role of IL-26 in controlling other aspects of the inflammatory response that could provide insight of its potential therapeutic applications are needed.

Manipulating the Excited States of Cyclometalated Iridium Complexes with ß-Ketoiminate and ß-Diketiminate Ligands.

A series of cyclometalated iridium complexes with ß-ketoiminate and ß-diketiminate ligands are described. Two different cyclometalating (C^N) ligands-2-phenylpridine (ppy) and 2-phenylbenzothiazole (bt)-are used in concert with three different ancillary (LX) ligands-a phenyl-substituted ß-ketoiminate (acNac(Me)), a phenyl-substituted ß-diketiminate (NacNac(Me)), and a fluorinated version of the ß-diketiminate (NacNac(CF3))-to furnish a suite of six complexes. The complexes are prepared by metathesis reactions of chloro-bridged dimers [Ir(C^N)2(µ-Cl)]2 with potassium or lithium salts of the ancillary LX ligand. Four of the complexes are characterized by X-ray crystallography, and all six were subjected to in-depth optical and electrochemical interrogation. Cyclic voltammetry shows both reduction and oxidation waves, with the latter strongly dependent on the identity of the LX ligand. The complexes are all luminescent, with the nature of the emissive excited state and the quantum yield (Φ) dependent on the identity of both the C^N and LX ligands. Whereas the complexes Ir(ppy)2(NacNac(Me)) and Ir(ppy)2(acNac(Me)) are weakly luminescent (Φ ≈ 0.01), the complexes Ir(bt)2(NacNac(Me)) and Ir(bt)2(acNac(Me)) are strongly luminescent, with the latter's quantum efficiency (Φ = 0.82) among the highest ever observed for cyclometalated iridium complexes. Fluorination of the NacNac ligand gives rise to completely disparate emission behavior suggestive of a NacNac-centered emissive state. The results described here, in comparison with previous groups' studies on acetylacetonate (acac) analogues, suggest that the weaker-field NacNac and acNac ligands raise the energy of the metal-centered HOMO, with energy of the HOMO increasing in the order NacNac(CF3) < acNac(Me) < NacNac(Me).