Sinus of Valsalva aneurysm in a Göttingen minipig.

A 26.6-kg, intact, 9-mo-old female Göttingen minipig was presented for a coronary stent study. Angiography revealed a sinus of Valsalva aneurysm (SVA) in the aortic root that involved both the left and noncoronary sinuses of the heart. Gross histologic examination of the heart revealed 2 regions of aneurysmal formation: one at the ostium to the left main coronary artery, with aortic sinus involvement, and the other at the dorsal aspect of the aortic root involving the noncoronary aortic sinus. With no history of any infectious diseases, and the microscopic findings showing no evidence of necrosis, degeneration, or infection, confirmed that the aneurysmal-like dilation of the sinuses was most likely a congenital anomaly. This case illustrates the diagnosis and comparative findings of a rare cardiac anomaly found in only a few species to date. To our knowledge, antemortem diagnosis of unruptured SVA involving both the left and noncoronary aortic sinuses of the minipig heart has not been reported previously.

Mxi1-0, an alternatively transcribed Mxi1 isoform, is overexpressed in glioblastomas.

The c-Myc transcription factor regulates expression of genes related to cell growth, division, and apoptosis. Mxi1, a member of the Mad family, represses transcription of c-Myc-regulated genes by mediating chromatin condensation via histone deacetylase and the Sin3 corepressor. Mxi1 is a c-Myc antagonist and suppresses cell proliferation in vitro. Here, we describe the identification of Mxi1-0, a novel Mxi1 isoform that is alternatively transcribed from an upstream exon. Mxi1-0 and Mxi1 have different amino-terminal sequences, but share identical Max- and DNA-binding domains. Both isoforms are able to bind Max, to recognize E-box binding sites, and to interact with Sin3. Despite these similarities and in contrast to Mxi1, Mxi1-0 is predominantly localized to the cytoplasm and fails to repress c-Myc-dependent transcription. Although Mxi1-0 and Mxi1 are coexpressed in both human and mouse cells, the relative levels of Mxi1-0 are higher in primary glioblastoma tumors than in normal brain tissue. This variation in the levels of Mxi1-0 and Mxi1 suggests that Mxi1-0 may modulate the Myc-inhibitory activity of Mxi1. The identification of Mxi1-0 as an alternatively transcribed Mxi1 isoform has significant implications for the interpretation of previous Mxi1 studies, particularly those related to the phenotype of the mxi1 knockout mouse.