Proximal basilar artery hemorrhage after submaximal angioplasty for intracranial atherosclerotic disease presenting as a large vessel occlusion treated with pipeline embolization device.

Iatrogenic vessel perforation from endovascular intervention is a devastating complication that commonly is treated with vessel sacrifice. We present a unique case of an iatrogenic proximal basilar artery perforation after submaximal angioplasty in a 67-year-old male presenting with an acute basilar artery occlusion with underlying intracranial atherosclerotic disease. Telescoping flow-diverting stents were then deployed to reconstruct the vessel wall with resulting active hemorrhage resolution. Our case documents a successful deployment of flow-diverting stents with resolution of active hemorrhage after an iatrogenic basilar artery perforation.

Obstructive hydrocephalus treated with endoscopic third ventriculostomy in a patient with Hajdu-Cheney syndrome: case report.

Hajdu-Cheney syndrome (HCS) is a rare genetic disorder with autosomal dominant inheritance, although most cases result from de novo mutations. Progressive platybasia and basilar impression (BI) can potentiate obstructive hydrocephalus due to aqueductal stenosis. Limited literature exists on the surgical intervention for hydrocephalus in patients with this condition. The authors present (to their knowledge) the first case of obstructive hydrocephalus due to aqueductal stenosis from BI treated with an endoscopic third ventriculostomy in a patient with the complex anatomy of HCS.

Impact of renal function recovery utilizing left ventricular assist device support.

BACKGROUND: In heart failure (HF) patients with renal insufficiency (RI), we hypothesize that mechanical circulatory support (MCS) with the left ventricular assist device (LVAD) will promote renal function recovery (RR). We sought to quantify RR with LVAD support over 6 months of follow-up. METHODS: RR data at 30, 90, and 180 days were analyzed for all LVAD patients with RI at the time of surgery. RI was defined as either the use of hemodialysis (HD) or a glomerular filtration rate (GFR) less than 60 mL/min/1.73 m2 . RESULTS: Between January 2008 and December 2013, 47 of 127 (37%) LVAD recipients had RI at the time of surgery. The mean preoperative GFR was 48 ± 7. We observed RR at each follow-up, with 30-, 90-, and 180-day mean GFRs of 79 ± 33, 71 ± 31, and 63 ± 21, respectively. The absolute increase in GFR at 30, 90, and 180 days was 34 ± 31, 26 ± 29, and 19 ± 20, respectively (All with P < .001). Four patients (8.5%) with RI required HD preoperatively. Of these, three recovered renal function, the fourth patient died. An additional 13 patients (30.2%) that were previously non-HD-dependent required HD postoperatively. Six of these 13 (46%) recovered renal function during the study period, four (30.7%) remain on HD and three (23%) died. CONCLUSIONS: RI improves significantly with LVAD support. Improvements in GFR are marked in the first 30 days. Among those patients requiring either pre- or post-operative HD, a majority recovered renal function.

The Alternative Splicing of Cytoplasmic Polyadenylation Element Binding Protein 2 Drives Anoikis Resistance and the Metastasis of Triple Negative Breast Cancer.

Triple negative breast cancer (TNBC) represents an anomalous subset of breast cancer with a greatly reduced (30%) 5-year survival rate. The enhanced mortality and morbidity of TNBC arises from the high metastatic rate, which requires the acquisition of AnR, a process whereby anchorage-dependent cells become resistant to cell death induced by detachment. In this study TNBC cell lines were selected for AnR, and these cell lines demonstrated dramatic enhancement in the formation of lung metastases as compared with parental cells. Genetic analysis of the AnR subclones versus parental cells via next generation sequencing and analysis of global alternative RNA splicing identified that the mRNA splicing of cytoplasmic polyadenylation element binding 2 (CPEB2), a translational regulator, was altered in AnR TNBC cells. Specifically, increased inclusion of exon 4 into the mature mRNA to produce the CPEB2B isoform was observed in AnR cell lines. Molecular manipulations of CPEB2 splice variants demonstrated a key role for this RNA splicing event in the resistance of cells to anoikis. Specifically, down-regulation of the CPEB2B isoform using siRNA re-sensitized the AnR cell lines to detachment-induced cell death. The ectopic expression of CPEB2B in parental TNBC cell lines induced AnR and dramatically increased metastatic potential. Importantly, alterations in the alternative splicing of CPEB2 were also observed in human TNBC and additional subtypes of human breast cancer tumors linked to a high metastatic rate. Our findings demonstrate that the regulation of CPEB2 mRNA splicing is a key mechanism in AnR and a driving force in TNBC metastasis.