Endogenous secretory receptor for advanced glycation end-products inhibits amyloid-ß1-42 uptake into mouse brain.

The cell-surface receptor for advanced glycation end-products (RAGE) has been implicated in the development of diabetic vascular complications and Alzheimer's disease. RAGE has been considered to be involved in amyloid-ß1-42 (Aß1-42) uptake into brain. In the present study, we demonstrate that endogenous secretory RAGE (esRAGE), a decoy form of RAGE generated by alternative RNA processing, is able to inhibit Aß1-42 influx into mouse brain. Surface plasmon resonance and competitive binding assays revealed that human Aß1-42 interacted with human esRAGE within the immunoglobulin V type region. We next examined the uptake and distribution of 125I-labeled human Aß1-42 in various organs and body fluids of newly created mice overexpressing human esRAGE as well as RAGE-null and wild-type (WT) mice. The transition of the 125I-labeled Aß1-42 from circulation to brain parenchyma peaked at 30 min after the injection into WT mice, but this was significantly blunted in esRAGE-overexpressing and RAGE-null mice. Significant reduction in 125I-labeled Aß1-42-derived photo-stimulated luminescence were marked in ventricles, cerebral cortex, hippocampus, especially CA1 and CA3 regions, putamen, and thalamus. The results thus suggest the potential of esRAGE in protection against the development of Alzheimer's disease.

Development of a novel endoscopic manipulation system: The Endoscopic operation robot.

AIM: To develop and evaluate the endoscopic operation robot (EOR). The EOR is a robot system designed specifically for remote manipulation of the scope during gastrointestinal endoscopy by a seated endoscopist. METHODS: Total colonoscopy examinations using a colonoscopy training model were performed compared conventional insertion by manual manipulation and remote-controlled insertion, using the EOR. The author investigated the time taken for each of the 50 examinations. RESULTS: The median insertion time (in minutes) for each 10 examinations (EOR vs manual manipulation) was 73.70 ± 25.37 vs 3.77 ± 1.34 in the first group, 38.40 ± 6.24 vs 3.40 ± 0.97 in the second group, 27.6 ± 4.01 vs 2.70 ± 0.95 in the third group, 23.8 ± 3.65 vs 3.10 ± 0.88 in the fourth group, and 22.9 ± 5.02 vs 2.60 ± 1.08 in the fifth group. CONCLUSION: The study suggested the possibility of the clinical application of the EOR.

Coils coated with the cyclic peptide SEK-1005 accelerate intra-aneurysmal organization.

BACKGROUND: Although the treatment of intracranial aneurysms with detachable coils is now widely accepted, the problem of coil compaction and recanalization remains to be solved. OBJECTIVE: To prevent recanalization by inducing intra-aneurysmal organization through prepared platinum coils coated with a novel cyclic peptide, SEK-1005, which can accelerate wound healing. METHODS: Using a rat aneurysm model, we examined the tissue response to these coils. An SEK-1005-coated coil (SC) or unmodified coil was inserted into the ligated external carotid artery (ECA) sac of rats. The sacs were removed on day 14 or 42 after coil insertion and subjected to conventional and immunohistochemical examination. We evaluated the tissue response in the ECA sacs and compared the percentage of organized areas in the ECA sacs of rats with SCs and unmodified coils. RESULTS: In SC rats, tissue organization was accelerated and the proliferation of α-smooth muscle actin- and vimentin-positive cells was promoted. On days 14 and 42, tissue organization was significantly greater in the ECA sacs of rats with SCs. CONCLUSION: SCs accelerated intra-aneurysmal organization in our rat aneurysm model suggesting that platinum coils coated with the novel cyclic peptide SEK-1005 may prevent recanalization and improve the clinical outcome in patients treated by coil embolization.

Massive epistaxis from a thrombosed intracavernous internal carotid artery aneurysm 2 years after the initial diagnosis--case report.

A 77-year-old woman presented with a rare case of nontraumatic intracavernous internal carotid artery (ICA) aneurysm causing epistaxis. The thrombosed aneurysm was discovered incidentally, and was not treated. However, she suffered massive nasal bleeding 22 months after the initial diagnosis. The lesion was successfully treated by endovascular coil embolization. The present case shows that thrombosed intracavernous ICA aneurysm may still carry the risk of rupture. Radiological evidence of erosion of the sphenoid sinus wall and repeated minor bleeding may be important predicting signs for massive nasal bleeding. Parent artery occlusion including the aneurysm may be the best treatment for intracavernous ICA aneurysms if sufficient collateral blood flow to the territory of the affected ICA is expected.

Embolization of a wide-necked basilar bifurcation aneurysm by double-balloon remodeling using HyperForm compliant balloon catheters.

We report a patient with a wide-necked basilar bifurcation aneurysm that was difficult to address by standard coil embolization because the left and right posterior cerebral artery (PCA) branched from the base of the aneurysm. To preserve both PCAs, the aneurysm was endovascularly embolized using a double-balloon remodeling technique and HyperForm compliant balloon catheters (MicroTherapeutics, Irvine, CA, USA). The aneurysmal neck was not tightly embolized to avoid coil protrusion into the parent arteries. The present technique is an important adjunct to the embolization of wide-necked basilar bifurcation aneurysms.