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Kawasaki K.,Chiba Cardiovascular Center | Imazeki M.,Chiba Cardiovascular Center | Hasegawa R.,Chiba Cardiovascular Center | Shiba S.,Chiba Cardiovascular Center | And 11 more authors.
Radiological Physics and Technology | Year: 2013

In interventional radiology, dose estimation using the interventional reference point (IRP) is a practical method for obtaining the real-time skin dose of a patient. However, the IRP is defined in terms of adult cardiovascular radiology and is not suitable for dosimetry of the head. In the present study, we defined a new reference point (neuro-IRP) for neuro-interventional procedures. The neuro-IRP was located on the central ray of the X-ray beam, 9 cm from the isocenter, toward the focal spot. To verify whether the neuro-IRP was accurate in dose estimation, we compared calculated doses at the neuro-IRP and actual measured doses at the surface of the head phantom for various directions of the X-ray projection. The resulting calculated doses were fairly consistent with actual measured doses, with the error in this estimation within approximately 15 %. These data suggest that dose estimation using the neuro-IRP for the head is valid. © 2013 Japanese Society of Radiological Technology and Japan Society of Medical Physics. Source


Imamura S.,Chiba Prefectural Togane Hospital | Hirai K.,Chiba Prefectural Togane Hospital | Hirai A.,Chiba Prefectural Togane Hospital
Tohoku Journal of Experimental Medicine | Year: 2013

Diabetic nephropathy (DN) is the leading cause of end-stage renal disease. Glucagon-like peptide-1 (GLP-1) is one of the incretins, gut hormones released from the intestine in response to food intake. GLP-1 receptor (GLP-1R) agonists have been used to treat type 2 diabetes. Here, we studied the effect of the administration of a GLP-1R agonist, liraglutide, on proteinuria and the progression of overt DN in type 2 diabetic patients. Twenty-three type 2 diabetic patients with overt DN, who had already been treated with blockade of renin-angiotensin system under dietary sodium restriction, were given liraglutide for a period of 12 months. Treatment with liraglutide caused a significant decrease in HbA1c from 7.4 ± 0.2% to 6.9 ± 0.3% (p = 0.04), and in body mass index (BMI) from 27.6 ± 0.9 kg/m2 to 26.5 ± 0.8 kg/m2 after 12 months (p < 0.001), while systolic blood pressure did not change. The progression of DN was determined as the rate of decline in estimated glomerular filtration rate (eGFR). The 12-month administration of liraglutide caused a significant decrease in proteinuria from 2.53 ± 0.48 g/g creatinine to 1.47 ± 0.28 g/g creatinine (p = 0.002). The administration of liraglutide also substantially diminished the rate of decline in eGFR from 6.6 ± 1.5 mL/min/1.73 m2/year to 0.3 ± 1.9 mL/min/1.73 m2/year (p = 0.003). Liraglutide can be used not only for reducing HbA1c and BMI, but also for attenuating the progression of nephropathy in type 2 diabetic patients. © 2013 Tohoku University Medical Press. Source


Kawai Y.,RIKEN | Kimura Y.,RIKEN | Lezhava A.,RIKEN | Kanamori H.,RIKEN | And 31 more authors.
PLoS ONE | Year: 2012

Background: In 2009, a pandemic (pdm) influenza A(H1N1) virus infection quickly circulated globally resulting in about 18,000 deaths around the world. In Japan, infected patients accounted for 16% of the total population. The possibility of human-to-human transmission of highly pathogenic novel influenza viruses is becoming a fear for human health and society. Methodology: To address the clinical need for rapid diagnosis, we have developed a new method, the "RT-SmartAmp assay", to rapidly detect the 2009 pandemic influenza A(H1N1) virus from patient swab samples. The RT-SmartAmp assay comprises both reverse transcriptase (RT) and isothermal DNA amplification reactions in one step, where RNA extraction and PCR reaction are not required. We used an exciton-controlled hybridization-sensitive fluorescent primer to specifically detect the HA segment of the 2009 pdm influenza A(H1N1) virus within 40 minutes without cross-reacting with the seasonal A(H1N1), A(H3N2), or B-type (Victoria) viruses. Results and Conclusions: We evaluated the RT-SmartAmp method in clinical research carried out in Japan during a pandemic period of October 2009 to January 2010. A total of 255 swab samples were collected from outpatients with influenza-like illness at three hospitals and eleven clinics located in the Tokyo and Chiba areas in Japan. The 2009 pdm influenza A(H1N1) virus was detected by the RT-SmartAmp assay, and the detection results were subsequently compared with data of current influenza diagnostic tests (lateral flow immuno-chromatographic tests) and viral genome sequence analysis. In conclusion, by the RT-SmartAmp assay we could detect the 2009 pdm influenza A(H1N1) virus in patients' swab samples even in early stages after the initial onset of influenza symptoms. Thus, the RT-SmartAmp assay is considered to provide a simple and practical tool to rapidly detect the 2009 pdm influenza A(H1N1) virus. © 2012 Kawai et al. Source


Morlighem J.-E.,RIKEN | Aoki S.,RIKEN | Kishima M.,RIKEN | Hanami M.,RIKEN | And 25 more authors.
PLoS ONE | Year: 2011

Background: Pandemic influenza A(H1N1) virus infection quickly circulated worldwide in 2009. In Japan, the first case was reported in May 2009, one month after its outbreak in Mexico. Thereafter, A(H1N1) infection spread widely throughout the country. It is of great importance to profile and understand the situation regarding viral mutations and their circulation in Japan to accumulate a knowledge base and to prepare clinical response platforms before a second pandemic (pdm) wave emerges. Methodology: A total of 253 swab samples were collected from patients with influenza-like illness in the Osaka, Tokyo, and Chiba areas both in May 2009 and between October 2009 and January 2010. We analyzed partial sequences of the hemagglutinin (HA) and neuraminidase (NA) genes of the 2009 pdm influenza virus in the collected clinical samples. By phylogenetic analysis, we identified major variants of the 2009 pdm influenza virus and critical mutations associated with severe cases, including drug-resistance mutations. Results and Conclusions: Our sequence analysis has revealed that both HA-S220T and NA-N248D are major non-synonymous mutations that clearly discriminate the 2009 pdm influenza viruses identified in the very early phase (May 2009) from those found in the peak phase (October 2009 to January 2010) in Japan. By phylogenetic analysis, we found 14 micro-clades within the viruses collected during the peak phase. Among them, 12 were new micro-clades, while two were previously reported. Oseltamivir resistance-related mutations, i.e., NA-H275Y and NA-N295S, were also detected in sporadic cases in Osaka and Tokyo. © 2011 Morlighem et al. Source


Yamamoto T.,Chiba University | Kanahara N.,Chiba University | Hirai A.,Chiba Prefectural Togane Hospital | Watanabe H.,Chiba University | Iyo M.,Chiba University
Clinical Neuropharmacology | Year: 2013

BACKGROUND: Lamotrigine (LMG) is an anticonvulsant currently registered for the treatment of bipolar disorder (BP) depression. We report the case of a 61-year-old woman with comorbid binge-eating disorder (BED), BP depression, and treatment-resistant type 2 diabetes mellitus (T2DM), in which LMG showed significant efficacy against BED and BP depression and resulted in a drastic decrease in plasma glucose levels. CASE REPORT: The patient had had untreated BP depression, BED, and T2DM for more than 30 years. We prescribed LMG at 25 mg/d for BP depression and titrated it up to 50 mg/d over 4 weeks, then maintained this dose for the next 16 weeks. At follow-up after the first 4-week period, she reported a significant decrease in compulsive eating impulses and depressive mood, and her positive reports were consistent in the following months. Hemoglobin A1c levels at National Glycohemoglobin Standardization Program decreased drastically from 9.6% to 7.1% over the 20 weeks after initiating treatment. CONCLUSION: This case suggests that LMG might be beneficial for BED with concomitant BP depression, and potentially for treatment-resistant T2DM, if this refractoriness is identified to result from comorbidity of BED and BP. Copyright © 2013 by Lippincott Williams &Wilkins. Source

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