Spike Protein of SARS-CoV-2 Activates Cardiac Fibrogenesis through NLRP3 Inflammasomes and NF-κB Signaling.

Background: The spike protein of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is crucial to viral entry and can cause cardiac injuries. Toll-like receptor 4 (TLR4) and NOD-, LPR-, and pyrin-domain-containing 3 (NLRP3) inflammasome are critical immune system components implicated in cardiac fibrosis. The spike protein activates NLRP3 inflammasome through TLR4 or angiotensin-converting enzyme 2 (ACE2) receptors, damaging various organs.

[Long-term results of isolated chemoperfusion of the lung with melphalan and cisplatin in combination with metastasectomy in treatment for resectable metastatic lung lesion].

For treatment of metastatic lung lesions there was used the method isolated chemoperfusion of the lung in combination with metastasectomy. The study includes 74 patients with metastases in the lungs who underwent 101 normothermal isolated chemoperfusion of the lung: of these 38 (37,6%) with melphalan and 63 (62,4%) with cisplatin without lethality. In the early postoperative period 1 (1,4%) patient died due to postperfusion lung edema.

Pathological study of archival lung tissues from five fatal cases of avian H5N1 influenza in Vietnam.

Highly pathogenic avian H5N1 influenza virus (H5N1) infection in humans causes acute respiratory distress syndrome, leading to multiple organ failure. Five fatal cases of H5N1 infection in Vietnam were analyzed pathologically to reveal virus distribution, and local proinflammatory cytokine and chemokine expression profiles in formalin-fixed, paraffin-embedded lung tissues. Our main histopathological findings showed diffuse alveolar damage in the lungs.