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BACKGROUND Although dissecting aneurysm of vertebral artery is known as one of the causes of subarachnoid hemorrhage (SAH) in the posterior circulation, the best surgical treatment method remains controversial. METHOD AND RESULT This 64-year-old woman was admitted to our service with headache due to SAH caused by a ruptured vertebral dissecting aneurysm in the distal portion of the posterior inferior cerebellar artery. After confirming tolerance of parent artery occlusion by temporary balloon occlusion, both the dissection site and the proximal portion of the parent artery were occluded completely by interlocking detachable coils (IDCs) without any ischemic complications. The patient was discharged without any neurologic deficit on the 25th day after the therapy. CONCLUSION The goal of treatment for the ruptured dissecting aneurysm is isolation of the dissection site from the circulation to prevent rerupture. In our case, endovascular occlusion with IDCs was sufficient to reach the goal. In cases with difficulties in the surgical approach, embolization of the dissection site with IDCs should be considered.

✓ The authors describe the histopathological findings in a case involving rerupture of a recanalized aneurysm of the internal carotid artery 8 months after partial (95%) embolization with interlocking detachable coils. The aneurysm was filled with poorly organized thrombus, and its orifice was devoid of endothelial cells. It appears likely that a long period of observation may be required to confirm the complete thrombotic organization of coil-embolized aneurysms. This indicates that caution is needed because rupture may follow recanalization of the aneurysm.

Background Bronchoscopy has been the gold standard for diagnosing blunt laryngo-cervical-tracheal injury (BLCTI); however, BLCTI is often undetected. Ultrasonography (US) is an indispensable tool in the field of critical care and traumatology, but has not been considered useful for evaluation of the airway. The aim of this study was to determine the usefulness of US in the diagnosis of BLCTI. Methods To determine the detectability of BLCTI by US, we use a model of cylindrical plastic with a protruding mass made of paste. The model was placed in a water bath and US (3.5-MHz probe) was used to try to detect the mass. Results We could detect the existence of the mass as a high echoic mass with strongly high echoic tail. We used four patients with BLCTIs whose sites of injury were confirmed by computed tomography (CT) and bronchoscopy. We evaluated the larynx and the cervical trachea as their outline of air in the cranial section near the sternal notch using a 3.5-MHz convex probe. The following US findings were compared with CT and bronchoscopic images as specific findings of BLCTI: discontinuity of the laryngo-cervical-tracheal wall and an abnormal mass protruding into the laryngo-cervical-tracheal lumen. Specific findings of BLCTI were detected in three of the four patients, whose sites of injury were the anterior or lateral side of the larynx or the cervical trachea. The site of injury of the remaining patient, where we detected no specific BLCTI findings, was the posterior wall of the larynx. Conclusions US is useful for the diagnosis of BLCTI because it is capable of presenting specific images showing BLCTI features such as discontinuity of the laryngo-cervical-tracheal wall and abnormal masses protruding into the lumen; not only as a single diagnostic tool but one tool with many uses.

The Wilms' tumor gene WT1 is overexpressed in various kinds of solid cancers. However, it remains unclear whether WT1 is expressed in esophageal squamous cell carcinoma.Expression of the WT1 gene was examined by real-time RT-PCR in 12 esophageal squamous cell carcinoma (ESCC) and by immunohistochemistry in 9 of these 12 and another 29.Real-time RT-PCR showed that the WT1 mRNA was overexpressed in all of the 12 ESCC examined Immunohistochemical analysis showed that the WT1 protein was overexpressed in ESCC cells in 36 (95%) of the 38 examined Furthermore, expression of the WT1 protein was examined in 20 esophageal squamous dysplasia. The WT1 protein was overexpressed in 5 (45%) out of 11 mild dysplasia and in 8 (89%) out of 9 moderate to severe dysplasia.These results may indicate an important role of the WT1 gene in the tumorigenesis of ESCC.

Serial changes of anti-platelet-aggregating activity in the endothelial cells after experimental subarachnoid hemorrhage were studied in 30 feline two-hemorrhage models. One hour or 2, 4, 7, or 14 days after mimic subarachnoid hemorrhage, ADP (40 mg/kg) was infused into the basilar artery via the right vertebral artery to activate circulating platelets. Immediately after ADP infusion, the basilar artery was fixed by intra-arterial perfusion with 1.5% glutaraldehyde in 0.1 mol/L phosphate buffer and was removed. The luminal surface was examined under a scanning electron microscope. One hour after subarachnoid hemorrhage, no platelets adhered or aggregated on the luminal surface. However, 4 to 7 days after subarachnoid hemorrhage, many platelets were observed adhering or aggregating on the luminal surface. These findings suggest the impairment of anti-platelet-aggregating activity of endothelial cells after subarachnoid hemorrhage. This impairment may be involved in inducing cerebral ischemia during cerebral vasospasm by causing platelet adhesion and aggregation.

El mice were given the pitching stimulation at 25 days of postnatal age, showing the initial appearance of convulsive seizures at about 75 days. The regional and developmental heterogeneities of the central muscarinic receptor and its deviation in El from dd-Y, as a normal control, were elucidated by the binding assays using [3H]-1-quinuclidinyl benzilate. In the hippocampus and the septal area, the receptor densities (Bmax) of El were down regulated. In the cerebral cortex they were up regulated. In the striatum they showed the crossing change from the down regulation at 25 days to the up regulation at 75 days. These deviations of El were not the response of the El convulsion and did not directly correlate with the pitching stimulation. As the convulsive seizures increased the pitching stimulation significantly decreased the Kd value of dd-Y(st), but it, conversely, increased that of El except in the septal area where there was no effect. These deviations of the receptor densities and affinities in El may reflect the dysfunction of the receptor regulation and may be related to the biochemical basis of epileptogenesis in the genetic model of epilepsy.

The biochemical characteristics of the muscarinic acetylcholine receptors were studied on the E1 strain mouse brain by the binding assay using [3H]1- quinuclidinyl benzylate. Scatchard analyses showed that the receptor density (Bmax) of the hippocampus significantly decreased by 26.4% and the affinity (Kd) increased by 18.8% in E1(+) compared to dd-Y. It is suggested that this hippocampal subsensitivity found in E1(+) mouse might be strain-specific, because repeated megimide convulsions failed to produce the same down regulation.