We present a case of a woman with an ectopic pelvic kidney and symptomatic hydronephrosis who failed conservative treatment and required ureteric stent placement. Authors: Toepfer, Nicholas; Parikh, Ankur; Bhangdia, Darshan Corresponding Author: Toepfer, Nicholas J Introduction Hydronephrosis during pregnancy is common and has a reported occurrence between 43% and 100% (1). Both mechanical […]

Deficiency of DNA fragmentation factor 45 results in reduced oocyte apoptosis in response to doxorubicin

Although sonographic artifacts are common in sonography, they can create diagnostic challenges and even lead to critical diagnostic errors. The authors report a case of an echogenic artifact resembling an abdominal aortic thrombus. An awareness of the existence of this pseudothrombus and techniques to differentiate this artifact from an actual fibrinous clot may help avoid unnecessary anxiety and costly testing.

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Excitotoxicity is a process by which excitatory amino acids induce neuronal cell death. To what extent excitotoxicity is regulated by apoptotic molecules is currently unclear. We previously found that endonuclease G (EndoG) plays an important role in both normal apoptosis in vivo and in pre-implantation embryogenesis. To investigate whether EndoG participates in neuronal cell death, we compared EndoG expression and kainic acid (KA)-induced seizure behavior and excitotoxicity in EndoG+/− and wild-type mice. We found that EndoG expression in the hippocampus of EndoG+/− mice is reduced compared to that in the wild-type mice. The reduction of EndoG expression levels in the hippocampus did not result in altered KA-induced seizure severity in EndoG+/− mice compared to that in wild-type mice. However, both CA3 and CA1 pyramidal neurons in EndoG+/− mice are more resistant to KA-induced cell death than that in wild-type mice. These results indicate that reduced expression of EndoG in the hippocampi of EndoG+/− mice leads to resistance to excitotoxicity.