Calcium (Ca2+) release from the endoplasmic reticulum (ER) controls numerous cellular functions including proliferation, and is regulated in part by inositol 1,4,5-trisphosphate receptors (IP3Rs). IP3Rs are ubiquitously expressed intracellular Ca2+-release channels found in many cell types. Although IP3R-mediated Ca2+ release has been implicated in cellular proliferation, the biochemical pathways that modulate intracellular Ca2+ release during cell cycle progression are not known. Sequence analysis of IP3R1 reveals the presence of two putative phosphorylation sites for cyclin-dependent kinases (cdks). In the present study, we show that cdc2/CyB, a critical regulator of eukaryotic cell cycle progression, phosphorylates IP3R1 in vitro and in vivo at both Ser(421) and Thr(799) and that this phosphorylation increases IP3 binding. Taken together, these results indicate that IP3R1 may be a specific target for cdc2/CyB during cell cycle progression.

Most cases with chronic subdural hematoma (CSDH) are treated by simple irrigation and drainage, then more than eighty percent of them result in good recovery. But we sometimes encounter intractable cases with hematoma re-collection, which is considered of repeated bleeding from macrocapillary in the hematoma capsule. Embolization of the middle meningeal artery (MMA) is considered to be useful to eliminate the blood supply to this structure. The authors experienced seven cases of intractable CSDH treated by MMA embolization and no recurrence took place in all cases for up to 15 months. Endovascular treatment may be a good alternative modality for recurrent CSDH.

Increase in intracellular Ca2+ [Ca2+]i regulates many biological functions including apoptosis, but the protein(s) linking [Ca2+]i and apoptosis are not completely understood. We have previously shown that IP3R-deficient cells are resistant to T-cell receptor (TCR)-induced apoptosis due to lack of Ca2+ release from endoplasmic reticulum (ER) and calcineurin activation. Here we show that caspase-9 and -3 are not activated in IP3R-deficient cells after TCR stimulation, consistent with the resistance of these cells to apoptosis. However, we also demonstrate that Bcl-2 expression in IP3R-deficient cells is comparable to control cells. Taken together, these results strongly suggest that IP3R-mediated Ca2+ release plays a critical role in regulating the activity of caspases-3 and -9 independent of Bcl-2.

Objective Advances in vascular reconstruction devices and coil technologies have made coil embolization a popular and effective strategy for treatment of relatively wide-neck cerebral aneurysms. However, coil protrusion occurs occasionally, and little is known about the frequency, the risk factors and the risk of thrombo-embolic complications. Method We assessed the frequency and the risk factors for coil protrusion in 330 unruptured aneurysm embolization cases, and examined the occurrence of cerebral infarction by diffusion-weighted magnetic resonance imaging (DW-MRI). Result Forty-four instances of coil protrusion were encountered during coil embolization (13.3% of cases), but incidence was reduced to 33 (10% of cases) by balloon press or insertion of the next coil. Coil protrusion occurred more frequently during the last phase of the procedure, and both a wide neck (large fundus to neck ratio) (OR = 1.84, P = 0.03) and an inadequately stable neck frame (OR = 5.49, P = 0.0007) increased protrusion risk. Coil protrusions did not increase the incidence of high-intensity lesions (infarcts) on DW-MRI (33.3% vs 29% of cases with no coil protrusion). However, longer operation time did increase infarct risk ( P = 0.0003). Thus, tail or loop type coil protrusion did not increase the risk of thrombo-embolic complications, if adequate blood flow was maintained. Conclusion Coil protrusion tended to occur more frequently in cases of wide-neck aneurysms with loose neck framing. Moderate and less coil protrusion carries no additional thrombo-embolic risk, if blood flow is maintained, which can be aided by additional post-operative antiplatelet therapy.

A 68-year-old male presented with a syncopal attack subsequent to acute myocardial infarction. His ultrasonographic and radiological examination revealed severe left internal carotid artery (ICA) stenosis and the presence of a persistent primitive hypoglossal artery (PPHA) immediately distal to the stenosis. The bilateral anterior and left middle cerebral arteries, and the vertebrobasilar system were opacified via the stenotic ICA. Carotid arterial stenting was selected as the treatment method because the lesion was high and a shunt placement during carotid endarterectomy was considered to be technically difficult. A self-expanding stent was successfully deployed with flow control, and the patient was discharged six days after surgery without any neurological deficit. There are sixteen reported cases including ours of PPHA associated with ICA stenosis presenting with ischemic attacks of the vertebrobasilar system. To the best of our knowledge, the current case is the first report of a cervical ICA stenosis with ipsilateral carotid-basilar anastomosis treated with carotid arterial stenting.