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18. Estimation with Tc-99m tetrofosmin SPECT of salvaged myocardial mass after emergent reperfusion therapy in acute myocardial infarction

Author

Shuke, N, Fujita, T, Koshiyama, H, Enomoto, M, Yamazaki, S, Nigo, T, and Kurihara, T

Abstract

The original publication is available at www.springerlink.com author, OBJECTIVES: The purpose of this study was to validate a new quantitative index of salvaged myocardial mass calculated from Tc-99m tetrofosmin SPECT for evaluating the therapeutic effect of emergent reperfusion therapy in acute myocardial infarction (AMI). METHODS: Tc-99m tetrofosmin SPECT was performed before and after emergent percutaneous transluminal coronary angioplasty (PTCA) in eight patients with AMI. In the pre-PTCA study, Tc-99m tetrofosmin was injected before emergent PTCA. Two weeks after the PTCA, post-PTCA study was performed. As a quantitative index of salvaged myocardial mass, salvaged myocardial volume (SMV) was defined as the difference of myocardial functional volume between the SPECT studies before and after the PTCA. To investigate the clinical significance of SMV, SMV was compared with the grade of therapeutic efficacy determined visually from pre- and post-PTCA SPECT images and clinical parameters, namely peak creatine phosphokinase level (pCK) and the time from the onset of the AMI to reperfusion (RPT). RESULTS: SMV showed a significant correlation with the visual grade of therapeutic efficacy (r = 0.737, p < 0.037) and a trend toward significant correlation with pCK (r = -0.622, p < 0.1). SMVs in early- and late-reperfusion groups (RPT < or = 6 hr and RPT > 6 hr) were 30.0 +/- 14.0 and -6.2 +/- 25.5 ml, showing a greater mean SMV value in the early-reperfusion group (p < 0.07). CONCLUSION: SMV could be used as a quantitative index of salvaged myocardial mass for evaluating the therapeutic effect of emergent reperfusion therapy.

Published
2003

20. PO244 INVESTIGATION OF UPPER GASTROINTESTINAL SYMPTOMS IN JAPANESE PATIENTS WITH DIABETES

Author

Honjo, S., primary, Hamamoto, Y., additional, Matsuoka, A., additional, Tatsuoka, H., additional, Fujimoto, K., additional, Shibayama, Y., additional, Tokumoto, S., additional, Yamaguchi, E., additional, Okamura, E., additional, Wada, Y., additional, Ikeda, H., additional, Kawasaki-Ogita, Y., additional, Fujikawa, J., additional, Koshiyama, H., additional, and Hamasaki, A., additional

Published
2014
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21. Autosomal dominant pseudohypoparathyroidism type Ib is associated with a heterozygous microdeletion that likely disrupts a putative imprinting control element of GNAS

Author

Bastepe, M., Frohlich, L. F., Hendy, G. N., Indridason, O. S., Josse, R. G., Koshiyama, H., Korkko, J., Nakamoto, J. M., Rosenbloom, A. L., Slyper, A. H., Sugimoto, T., Tsatsoulis, A., Crawford, J. D., and Juppner, H.

Subjects
Adult, Adolescent, Genomic Imprinting, DNA Methylation, Humans, Exons, GTP-Binding Protein alpha Subunits, Gs/*genetics, Child, Gene Deletion, Pseudohypoparathyroidism/*genetics, Pedigree
Abstract

Patients with pseudohypoparathyroidism type Ib (PHP-Ib) have hypocalcemia and hyperphosphatemia due to renal parathyroid hormone (PTH) resistance, but lack physical features of Albright hereditary osteodystrophy. PHP-Ib is thus distinct from PHP-Ia, which is caused by mutations in the GNAS exons encoding the G protein alpha subunit. However, an imprinted autosomal dominant form of PHP-Ib (AD-PHP-Ib) has been mapped to a region of chromosome 20q13.3 containing GNAS. Furthermore, loss of methylation at a differentially methylated region (DMR) of this locus, exon A/B, has been observed thus far in all investigated sporadic PHP-Ib cases and the affected members of multiple AD-PHP-Ib kindreds. We now report that affected members and obligate gene carriers of 12 unrelated AD-PHP-Ib kindreds and four apparently sporadic PHP-Ib patients, but not healthy controls, have a heterozygous approximately 3-kb microdeletion located approximately 220 kb centromeric of GNAS exon A/B. The deleted region, which is flanked by two direct repeats, includes three exons of STX16, the gene encoding syntaxin-16, for which no evidence of imprinting could be found. Affected individuals carrying the microdeletion show loss of exon A/B methylation but no epigenetic abnormalities at other GNAS DMRs. We therefore postulate that this microdeletion disrupts a putative cis-acting element required for methylation at exon A/B, and that this genetic defect underlies the renal PTH resistance in AD-PHP-Ib. J Clin Invest

Published
2003

22. Rapid progress of acute suppurative cholangitis to secondary sclerosing cholangitis sequentially followed-up by endoscopic retrograde cholangiography

Author

Yuji Tanaka, Koshiyama H, Kimura M, Nakao K, Yukihiko Adachi, Makita Y, Kobayashi Y, and Yoshida Y

Subjects
Male, medicine.medical_specialty, Cholagogues and Choleretics, Cholangitis, Cholangitis, Sclerosing, Intrahepatic bile ducts, Colonic polypectomy, Gastroenterology, Cholangiography, Internal medicine, Chronic cholestasis, medicine, Humans, Aged, Cholangiopancreatography, Endoscopic Retrograde, medicine.diagnostic_test, business.industry, Ursodeoxycholic Acid, Suppurative cholangitis, medicine.disease, Surgery, Major duodenal papilla, Bile Ducts, Intrahepatic, Acute Disease, Disease Progression, Endoscopic retrograde cholangiography, Secondary sclerosing cholangitis, business, Dilatation, Pathologic
Abstract

A 66-year-old man was admitted to our hospital because of right hypochondralgia and fever after colonic polypectomy. Endoscopic examination revealed purulent bile excretion from the duodenal papilla orifice; based on this finding, acute suppurative cholangitis was diagnosed. An endoscopic retrograde cholangiography revealed no abnormality in the biliary tree. However, chronic cholestasis persisted, and endoscopic cholangiography performed 4 months later disclosed a beaded appearance of the intrahepatic bile ducts; this sign is a characteristic finding of sclerosing cholangitis. This is the first report of rapid progression of acute suppurative cholangitis to secondary sclerosing cholangitis sequentially followed-up by endoscopic retrograde cholangiography.

Published
2001

23. Efficacy and safety of live varicella zoster vaccine in diabetes: a randomized, double-blind, placebo-controlled trial.

Author

Hata, A., Inoue, F., Hamamoto, Y., Yamasaki, M., Fujikawa, J., Kawahara, H., Kawasaki, Y., Honjo, S., Koshiyama, H., Moriishi, E., Mori, Y., and Ohkubo, T.

Subjects
AUTOANTIBODIES, CONFIDENCE intervals, DIABETES, CLINICAL drug trials, GLYCOSYLATED hemoglobin, IMMUNITY, PATIENT safety, PLACEBOS, PNEUMOCOCCAL vaccines, RESEARCH funding, SAFETY, SKIN tests, DATA analysis, RANDOMIZED controlled trials, CONTROL groups, CHICKENPOX vaccines, PATIENT selection, HERPES zoster vaccines, DESCRIPTIVE statistics
Abstract

Aims To elucidate varicella zoster virus ( VZV)-specific cell-mediated immunity and humoral immunogenicity against live attenuated Oka varicella zoster vaccine concurrently vaccinated with 23-valent pneumococcal polysaccharide vaccine ( PPSV23) in elderly people with diabetes mellitus. Methods This double-blind randomized controlled single-centre study of 60-70-year-old people with diabetes compared immunity and safety profiles 3 months after one dose of varicella zoster vaccine or placebo. PPSV23 was immunized simultaneously. Primary analysis evaluated cell-mediated immunity using the VZV skin test. Secondary analyses were a VZV interferon-γ enzyme-linked immunospot ( ELISPOT) assay and immunoadherence haemagglutination test. Adverse experiences were recorded using diary questionnaires. Results By intent-to-treat analysis, 27 participants with diabetes who had been administered the vaccine were compared with 27 participants who were given a placebo. Changes in skin test scores were 0.41 ± 0.80 and 0.11 ± 0.93 ( P = 0.2155), and geometric mean fold rises of the ELISPOT counts were 1.2 [95% confidence interval ( CI) 0.2, 7.9] and 1.2 (95% CI 0.2, 7.3) ( P = 0.989) in the vaccine and placebo groups, respectively. The geometric mean titre did not increase 3 months after vaccination in either group. No vaccination-related severe adverse experience was reported and no participant developed herpes zoster. Discussion Our previous results demonstrated that varicella zoster vaccine safely enhanced VZV-specific immunity in elderly people with or without diabetes. The results of this study showed that varicella zoster vaccine can be used safely, but it cannot boost virus-specific immunity in elderly people with diabetes when administered with concurrent PPSV23. Alternative strategies are needed to prevent VZV-associated diseases in this population. [ABSTRACT FROM AUTHOR]

Published
2016
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26. Fibroblast growth factor 23 in oncogenic osteomalacia and X-linkedhypophosphatemia.

Author

Jonsson, KB, Zahradnik, R, Larsson, T, White, KE, Sugimoto, T, Imanishi, Y, Yamamoto, T, Hampson, G, Koshiyama, H, Ljunggren, O, Oba, K, Yang, IM, Miyauchi, A, Econs, MJ, Lavigne, J, Juppner, H, Jonsson, KB, Zahradnik, R, Larsson, T, White, KE, Sugimoto, T, Imanishi, Y, Yamamoto, T, Hampson, G, Koshiyama, H, Ljunggren, O, Oba, K, Yang, IM, Miyauchi, A, Econs, MJ, Lavigne, J, and Juppner, H

Published
2003

28. MS41 PITAVASTATIN REDUCES HIGH-SENSITIVITY C-REACTIVE PROTEIN AND IMPROVES LIPID PROFILES IRRESPECTIVELY OF BODY MASS INDICES – SUBANALYSIS OF KISHIMEN MULTI-CENTER PROSPECTIVE STUDY

Author

Kume, N., primary, Fujioka, Y., additional, Taniguchi, A., additional, Tanaka, K., additional, Kagimoto, S., additional, Hirata, K., additional, Nakamura, Y., additional, Yamamoto, T., additional, Fujimoto, S., additional, Hamamoto, Y., additional, Tsuda, K., additional, Inagaki, N., additional, Seino, Y., additional, and Koshiyama, H., additional

Published
2010
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30. Abstract: P962 PITAVASTATIN IMPROVES LIPID PROFILES AND REDUCES INFLAMMATION - KISHIMEN MULTI-CENTER PROSPECTIVE STUDY

Author

Kume, N, primary, Fujioka, Y, additional, Taniguchi, A, additional, Tanaka, K, additional, Kagimoto, S, additional, Hirata, K, additional, Nakamura, Y, additional, Yamamoto, T, additional, Fujimoto, S, additional, Hamamoto, Y, additional, Tsuda, K, additional, Inagaki, N, additional, Seino, Y, additional, and Koshiyama, H, additional

Published
2009
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31. P-60 Pitavastatin improves lipid profiles and reduces high-sensitivity CRP in Japanese diabetic subjects with hypercholesterolemia (KISHIMEN multi-center prospective study)-subanalysis of diabetic subjects

Author

Koshiyama, H., primary, Taniguchi, A., additional, Fujioka, Y., additional, Tanaka, K., additional, Kagimoto, S., additional, Hirata, K., additional, Nakamura, Y., additional, Iwakura, A., additional, Hara, K., additional, Yamamoto, T., additional, Kuroe, A., additional, Ohya, M., additional, Fujimoto, S., additional, Hamamoto, Y., additional, Honjo, S., additional, Ikeda, H., additional, Nabe, K., additional, Tsuda, K., additional, Inagaki, N., additional, Seino, Y., additional, and Kume, N., additional

Published
2008
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35. The gene responsible for pseudohypoparathyroidism type Ib is paternally imprinted and maps in four unrelated kindreds to chromosome 20q13.3.

Author

UCL - SSS/DDUV - Institut de Duve, Jüppner, H, Schipani, E, Bastepe, M, Cole, D E, Lawson, M L, Mannstadt, M, Hendy, G N, Plotkin, H, Koshiyama, H, Koh, T, Crawford, J D, Olsen, B R, Vikkula, Miikka, UCL - SSS/DDUV - Institut de Duve, Jüppner, H, Schipani, E, Bastepe, M, Cole, D E, Lawson, M L, Mannstadt, M, Hendy, G N, Plotkin, H, Koshiyama, H, Koh, T, Crawford, J D, Olsen, B R, and Vikkula, Miikka

Abstract

Hypocalcemia and hyperphosphatemia caused by parathyroid hormone (PTH)-resistance are the only discernible abnormalities in pseudohypoparathyroidism type Ib (PHP-Ib). Because mutations in the PTH/PTH-related peptide receptor, a plausible candidate gene, had been excluded previously, we conducted a genome-wide search with four PHP-Ib kindreds and established linkage to a small telomeric region on chromosome 20q, which contains the stimulatory G protein gene. We, furthermore, showed that the genetic defect is imprinted paternally and thus is inherited in the same mode as the PTH-resistant hypocalcemia in kindreds with PHP-Ia and/or pseudo-pseudohypoparathyroidism, two related disorders caused by different stimulatory G protein mutations.

Published
1998

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