Ruptured vertebral artery dissecting aneurysm associated with parent artery occlusion

A 63-year-old hypertensive man presented with vertebral artery (VA) dissection manifesting as subarachnoid hemorrhage located mainly in the posterior fossa. Left vertebral angiography on the day of hemorrhage showed complete occlusion of the left VA. Right vertebral angiography showed retrograde filling of the distal portion of the left VA and the left posterior inferior cerebellar artery, and a “double lumen”-like finding in the left VA. He was managed conservatively. Follow-up angiography on Day 29 showed spontaneous recanalization of the occlusive lesion and an almost normal arterial configuration. T2-weighted magnetic resonance (MR) imaging on Day 45 revealed multiple infarctions in the brainstem. T1-weighted MR imaging showed a high intensity area, suggestive of intramural hematoma, in the left VA. He was transferred to another hospital in a persistent vegetative state

Genome-wide analysis of target genes regulated by HoxB4 in hematopoietic stem and progenitor cells developing from embryonic stem cells

Forced expression of the transcription factor HoxB4 has been shown to enhance the self-renewal capacity of mouse bone marrow hematopoietic stem cells (HSCs) and confer a long-term repopulating capacity to yolk sac and embryonic stem (ES) cell–derived hematopoietic precursors. The fact that ES cell–derived precursors do not repopulate bone marrow without HoxB4 underscores an important role for HoxB4 in the maturation of ES-derived hematopoietic precursors into long-term repopulating HSCs. However, the precise molecular mechanism underlying this process is barely understood. In this study, we performed a genome-wide analysis of HoxB4 using ES cell–derived hematopoietic stem/progenitor cells. The results revealed many of the genes essential for HSC development to be direct targets of HoxB4, such as Runx1, Scl/Tal1, Gata2, and Gfi1. The expression profiling also showed that HoxB4 indirectly affects the expression of several important genes, such as Lmo2, Erg, Meis1, Pbx1, Nov, AhR, and Hemgn. HoxB4 tended to activate the transcription, but the down-regulation of a significant portion of direct targets suggested its function to be context-dependent. These findings indicate that HoxB4 reprograms a set of key regulator genes to facilitate the maturation of developing HSCs into repopulating cells. Our list of HoxB4 targets also provides novel candidate regulators for HSCs