Bilateral common iliac vein stent migration

Venous stent migration to the heart is considered to be a rare complication of a common procedure. Therefore, many physicians do not include this complication in their differential diagnosis. We explain why this complication is likely more common than currently thought and why it should be considered as a potential diagnosis. This case describes migration of bilateral iliac vein stents into the right ventricular outflow tract and right interlobar pulmonary artery. We provide multiple imaging modalities demonstrating the migrated stents. We believe radiologists should be cognizant of this complication and consider it as a potential diagnosis. Hopefully, this will create a greater awareness of this life-threatening complication of venous stent placement

ABCE1 Regulates RNase L-Induced Autophagy during Viral Infections

Host response to a viral infection includes the production of type I interferon (IFN) and the induction of interferon-stimulated genes that have broad antiviral effects. One of the key antiviral effectors is the IFN-inducible oligoadenylate synthetase/ribonuclease L (OAS/RNase L) pathway, which is activated by double-stranded RNA to synthesize unique oligoadenylates, 2-5A, to activate RNase L. RNase L exerts an antiviral effect by cleaving diverse RNA substrates, limiting viral replication; many viruses have evolved mechanisms to counteract the OAS/RNase L pathway. Here, we show that the ATP-binding cassette E1 (ABCE1) transporter, identified as an inhibitor of RNase L, regulates RNase L activity and RNase L-induced autophagy during viral infections. ABCE1 knockdown cells show increased RNase L activity when activated by 2-5A. Compared to parental cells, the autophagy-inducing activity of RNase L in ABCE1-depleted cells is enhanced with early onset. RNase L activation in ABCE1-depleted cells inhibits cellular proliferation and sensitizes cells to apoptosis. Increased activity of caspase-3 causes premature cleavage of autophagy protein, Beclin-1, promoting a switch from autophagy to apoptosis. ABCE1 regulates autophagy during EMCV infection, and enhanced autophagy in ABCE1 knockdown cells promotes EMCV replication. We identify ABCE1 as a host protein that inhibits the OAS/RNase L pathway by regulating RNase L activity, potentially affecting antiviral effects

Disseminated mycobacterium avium complex spinal osteomyelitis in a patient with interferon gamma receptor deficiency: A case report

Disseminated mycobacterium avium complex (MAC) infection is rare and is classically associated with immunodeficient states. Osteomyelitis is a rare manifestation of disseminated MAC infection. The overwhelming majority of MAC infections occur in patients with human immunodeficiency virus (HIV). Disseminated MAC infection has been described in interferon gamma receptor deficiency, an immunodeficiency mechanistically linked to mycobacterial infection. We present a case of disseminated MAC vertebral osteomyelitis in a patient with interferon gamma receptor deficiency