CD36/Lyn kinase interactions within macrophages promotes pulmonary fibrosis in response to oxidized phospholipid.

Recent data from human studies and animal models have established roles for type II alveolar epithelial cell (AEC2) injury/apoptosis and monocyte/macrophage accumulation and activation in progressive lung fibrosis. Although the link between these processes is not well defined, we have previously shown that CD36-mediated uptake of apoptotic AEC2s by lung macrophages is sufficient to drive fibrosis. Importantly, apoptotic AEC2s are rich in oxidized phospholipids (oxPL), and amongst its multiple functions, CD36 serves as a scavenger receptor for oxPL.

Unexplained Fatal Hyperammonemia in a Patient With New Diagnosis of Acute Monoblastic Leukemia.

Idiopathic hyperammonemia is a serious condition that can arise after induction of chemotherapy and is characterized by plasma ammonia levels greater than two times the normal upper limit but within the context of normal liver function. While this dangerous complication usually appears several weeks after the start of chemotherapy, we report a fatal case of idiopathic hyperammonemia that was detected only nine days after induction chemotherapy in a 22-year-old man with no liver pathology or other risks for hyperammonemia. The patient's initial emergent presentation was altered mental status.

Cardiac sequelae of novel coronavirus disease 2019 (COVID-19): a clinical case series.

Background: COVID-19 caused by severe acute respiratory syndrome coronavirus 2 most commonly manifests with fever and respiratory illness. The cardiovascular manifestations have become more prevalent but can potentially go unrecognized. We look to describe cardiac manifestations in three patients with COVID-19 using cardiac enzymes, electrocardiograms, and echocardiography.

Efferocytosis of apoptotic alveolar epithelial cells is sufficient to initiate lung fibrosis.

Type II alveolar epithelial cell (AEC) apoptosis is a prominent feature of fibrotic lung diseases and animal models of pulmonary fibrosis. While there is growing recognition of the importance of AEC injury and apoptosis as a causal factor in fibrosis, the underlying mechanisms that link these processes remain unknown. We have previously shown that targeting the type II alveolar epithelium for injury by repetitively administering diphtheria toxin to transgenic mice expressing the diphtheria toxin receptor off of the surfactant protein C promoter (SPC-DTR) develop lung fibrosis, confirming that AEC injury is sufficient to cause fibrosis.

Human frataxin: iron and ferrochelatase binding surface.

The coordinated iron structure and ferrochelatase binding surface of human frataxin have been characterized to provide insight into the protein's ability to serve as the iron chaperone during heme biosynthesis.

Monomeric yeast frataxin is an iron-binding protein.

Friedreich's ataxia, an autosomal cardio- and neurodegenerative disorder that affects 1 in 50,000 humans, is caused by decreased levels of the protein frataxin. Although frataxin is nuclear-encoded, it is targeted to the mitochondrial matrix and necessary for proper regulation of cellular iron homeostasis. Frataxin is required for the cellular production of both heme and iron-sulfur (Fe-S) clusters.