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Nishimura H.,Osaka Saiseikai Nakatsu Hospital
Nippon rinsho. Japanese journal of clinical medicine | Year: 2011

In type 2 diabetes, macroangiopathy manifests as atherosclerosis like in nondiabetic patients, characterized by formation of plaques that follows in stages but with an accelerated course due to the several risk factors. Atherosclerosis in diabetes begins earlier, is more markedly pronounced and progresses more rapidly. It is still a debated question whether antidiabetic therapy to target normal glycated hemoglobin levels would reduce cardiovascular events in patients with advanced type 2 diabetes. New findings result from ACCORD Study reveal that microvascular and macrovascular effects of intensive glucose lowering have to be considered separately. On the other hand, our NICE Study yielded better cardiovascular outcomes for those patients with intensive glucose-lowering therapy using rapid-acting insulin analogue reducing postprandial glucose levels with less hypoglycemia.


Endo Y.,Translational Medical Center | Endo Y.,National Institute of Neuroscience | Endo Y.,Kyoto University | Noguchi S.,Translational Medical Center | And 19 more authors.
Human Molecular Genetics | Year: 2015

The store-operated Ca2+ release-activated Ca2+ (CRAC) channel is activated by diminished luminal Ca2+ levels in the endoplasmic reticulum and sarcoplasmic reticulum (SR), and constitutes one of the major Ca2+ entry pathways in various tissues. Tubular aggregates (TAs) are abnormal structures in the skeletal muscle, and although their mechanism of formation has not been clarified, altered Ca2+ homeostasis related to a disordered SR is suggested to be one of the main contributing factors. TA myopathy is a hereditary muscle disorder that is pathologically characterized by the presence of TAs. Recently, dominant mutations in the STIM1 gene, encoding a Ca2+ sensor that controls CRAC channels, have been identified to cause tubular aggregate myopathy (TAM). Here, we identified heterozygous missense mutations in the ORAI1 gene, encoding the CRAC channel itself, in three families affected by dominantly inherited TAM with hypocalcemia. Skeletal myotubes from an affected individual and HEK293 cells expressing mutated ORAI1 proteins displayed spontaneous extracellular Ca2+ entry into cells without diminishment of luminal Ca2+ or the association with STIM1. Our results indicate that STIM1-independent activation of CRAC channels induced by dominant mutations in ORAI1 cause altered Ca2+ homeostasis, resulting in TAM with hypocalcemia. © The Author 2014. Published by Oxford University Press. All rights reserved.


Fujita H.,Osaka Saiseikai Nakatsu Hospital
Journal of applied clinical medical physics / American College of Medical Physics | Year: 2011

The aim of the present study was to evaluate the clinical efficacy of the single-shot dual-energy subtraction technique for obtaining portal images. We prepared two storage phosphor plates for this study. A 1 mm thick tungsten sheet was placed between the two storage phosphor plates. A single use of the double-exposure technique provides two portal images simultaneously (i.e., a standard image and a low-contrast image), using the same patient position and with no additional radiation delivered to the patient. A bone-enhanced image is created by image subtraction between these two images. For evaluation of clinical efficacy, three treatment sites--the brain, lung, and pelvis--were imaged. Ten sets of images were obtained for each site, and five landmarks were selected for each treatment site. The visibility of each landmark and the ease of overall verification for the selected treatment sites were assessed separately for the standard and bone-enhanced images. Four observers consisting of one radiation oncologist and three radiation therapists participated in the present study. For most of the landmarks studied, the bone-enhanced images were significantly superior to the standard images. Regarding the ease of overall verification, the bone-enhanced images were significantly superior to the standard images at all sites. The p-values of mean rating for the brain, lung, and pelvis were 0.002, 0.012, and 0.003, respectively. The bone-enhanced images obtained using our technique increased the image quality in terms of bone visibility, and are considered useful for routine clinical practice.


In total hip arthroplasty (THA) for dysplastic hip osteoarthritis, bony deformity makes it difficult to identify the correct cup height and medialization. The authors developed a new technique for registration and navigation of cup position for dysplastic hips using an imageless navigation system. Eighty dysplastic hips (Crowe type I, n=58; type II, n=18; type III, n=4) underwent THA. Thirty-four hips were operated on while in the supine position and 46 hips were operated on while in the lateral position. Before capsulectomy, the anterior pelvic plane and the position of the femur were registered. After exposure of the acetabulum, the teardrop, posterior rim, and medial wall of the acetabulum were registered. Then the cup height, cup medialization, cup inclination, anteversion, and leg lengthening were navigated. The difference between the navigated and radiographic cup heights was 4.5 ± 4.0 mm, the difference in cup medialization was 3.0 ± 2.5 mm, the difference in cup inclination was 4.3° ± 3.1°, the difference in cup anteversion was 5.5° ± 3.8°, and the difference in leg lengthening was 3.7 ± 3.0 mm. Comparison of the first 20 cases with the last 20 cases showed that the accuracy of cup medialization was significantly improved. These differences were not affected by Crowe type or surgical position. Because the correct cup height and medialization are key issues in THA for dysplastic hip osteoarthritis, the accuracy of cup height and medialization in this imageless navigation system were acceptable for clinical application. Copyright 2012, SLACK Incorporated.


Maehara A.,Columbia University Medical Center | Maehara A.,Cardiovascular Research Foundation | Ben-Yehuda O.,Columbia University Medical Center | Ben-Yehuda O.,Cardiovascular Research Foundation | And 13 more authors.
JACC: Cardiovascular Interventions | Year: 2015

Objectives The present study sought to determine whether optical coherence tomography (OCT) guidance results in a degree of stent expansion comparable to that with intravascular ultrasound (IVUS) guidance. Background The most important predictor of adverse outcomes (thrombosis and restenosis) after stent implantation with IVUS guidance is the degree of stent expansion achieved. Methods We compared the relative degree of stent expansion (defined as the minimal stent area divided by the mean of the proximal and distal reference lumen areas) after OCT-guided stenting in patients in the ILUMIEN (Observational Study of Optical Coherence Tomography [OCT] in Patients Undergoing Fractional Flow Reserve [FFR] and Percutaneous Coronary Intervention) (N = 354) and IVUS-guided stenting in patients in the ADAPT-DES (Assessment of Dual Antiplatelet Therapy With Drug-Eluting Stents) study (N = 586). Stent expansion was examined in all 940 patients in a covariate-adjusted analysis as well as in 286 propensity-matched pairs (total N = 572). Results In the matched-pair analysis, the degree of stent expansion was not significantly different between OCT and IVUS guidance (median [first, third quartiles] = 72.8% [63.3, 81.3] vs. 70.6% [62.3, 78.8], respectively, p = 0.29). Similarly, after adjustment for baseline differences in the entire population, the degree of stent expansion was also not different between the 2 imaging modalities (p = 0.84). Although a higher prevalence of post-PCI stent malapposition, tissue protrusion, and edge dissections was detected by OCT, the rates of major malapposition, tissue protrusion, and dissections were similar after OCT- and IVUS-guided stenting. Conclusions In the present post-hoc analysis of 2 prospective studies, OCT and IVUS guidance resulted in a comparable degree of stent expansion. Randomized trials are warranted to compare the outcomes of OCT- and IVUS-guided coronary stent implantation. © 2015 American College of Cardiology Foundation

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