The Tohoku Journal of Experimental Medicine
Online ISSN : 1349-3329
Print ISSN : 0040-8727
ISSN-L : 0040-8727
Volume 187, Issue 4
April
Displaying 1-8 of 8 articles from this issue
Regular Contributions
  • Mika Watanabe, Takashi Sawai
    1999 Volume 187 Issue 4 Pages 291-303
    Published: 1999
    Released on J-STAGE: September 27, 2005
    JOURNAL FREE ACCESS
    Elastic fiber is one of the major component of the extracellular matrix, which provides the resilience to many tissues. Elasticity is an important property of human aorta, and this elastic property decreases in various pathological conditions such as dissecting aneurysm (DA). Since the cross-linking structures in elastin are responsible for this elasticity, we studied the alteration of various cross-linking amino acids in human aorta associated with DA by a new method using high-performance liquid chromatography (HPLC). Materials were obtained from non-atherosclerotic areas of thoracic aorta of 27 autopsy cases which had no particular aortic disease and 19 cases of DA at replacement operation. After acid hydrolysis, SEP-PAK™ silica-gel column and Fe3+/activated charcoal column pretreatment were carried out for analysis of desmosine (DES), isodesmosine (ISDES), neodesmosine (NEO), oxodesmosine (OXO) and isooxodesmosine (ISOXO), and for analysis of aldosine (ALD), respectively. These prepared samples were applied to the reversed-phase HPLC column. We also analyzed pyridinoline (PYR), a major cross-linking amino acid of collagen as an index of fibrosis. All crosslinks of elastin were decreased in DA as compared to the age-matched control. The decrease of ISOXO was marked. The increase of PYR and PYR/(DES+ISDES) were not statistically significant. It is suggested oxidative degradation on elastin crosslinks occur in DA, and the ratio of collagen to elastin didn't contribute to the pathogenesis of DA.
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  • Shoji Tsutaya, Masaru Shoji, Yuka Saito, Hitomi Kitaya, Shinichi Nakat ...
    1999 Volume 187 Issue 4 Pages 305-310
    Published: 1999
    Released on J-STAGE: September 27, 2005
    JOURNAL FREE ACCESS
    To assess clinical availability of the aldehyde dehydrogenase (ALDH) 2 gene polymorphism to detect alcohol sensitivity among a Japanese population, we determined the ALDH 2 genotypes and also compared to an ethanol patch test in 119 young Japanese. Their alcohol sensitivity was evaluated by a questionnaire on the frequency of alcohol-associated symptoms when they drink. Genomic DNA was extracted from blood samples and amplified by polymerase chain reaction (PCR). PCR primers were flanking the polymorphic region in exon 12 of the ALDH 2 gene. The distribution of the typical homozygote, the heterozygote and the atypical homozygote was 63.9, 31.9 and 4.2%, respectively. Gene frequencies of the typical and atypical alleles calculated from the genotype frequencies were 0.80 and 0.20. The atypical genotypic homozygotes were positively associated with facial flushing symptom, but not with positive response for ethanol patch test. These results indicate that ALDH 2 genotypes determination is essential to detect alcohol sensitivity whereas the ethanol patch test has some limitations.
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  • Takafumi Seki, Hiroshi Okayama, Shogen Isoyama, Yutaka Kagaya, Kunio S ...
    1999 Volume 187 Issue 4 Pages 311-322
    Published: 1999
    Released on J-STAGE: September 27, 2005
    JOURNAL FREE ACCESS
    Alcohol ingestion often provokes attacks in patients with vasospastic angina. Type 2 aldehyde dehydrogenase (ALDH2) deficiency, which is based on a single point mutation (Glu487Lys) of the ALDH2 gene, is common in the Japanese population, but rare among the Caucasian population. We investigated how the genotype of ALDH2 affects the characteristics of alcohol-induced vasospastic angina. Ninety-one patients with vasospastic angina who had ingested alcohol daily or occasionally were studied. Patients had been diagnosed as vasospastic angina by a provocation test with an intracoronary injection of ergonovine or acetylcholine during coronary angiography. The Glu487Lys mutation was detected by allele specific PCR. We interviewed the patients to obtain information concerning the relationship between alcohol ingestion and anginal attacks. Alcohol ingestion induced attacks in 16 of 66 patients without the Glu487Lys mutation, 8 of 22 in heterozygotes, and 1 of 3 in mutant homozygotes. The intervals between alcohol ingestion and the onset of anginal attacks were shorter in homozygotes (0.17 hours) and heterozygotes (1.5±0.6 hours) for ALDH2*2 than in normal homozygotes for ALDH2*1 (5.4±0.6 hours). The amount of ethanol which induced attacks was significantly greater in normal homozygotes than in homozygotes (11 ml) and heterozygotes (42.5±7.1 ml) for ALDH2*2 (96.1±13.4 ml in normal patients). The frequency of anginal attacks induced by alcohol ingestion did not differ between ALDH deficient and normal homozygotes. In ALDH deficient patients, however, anginal attacks were induced by a smaller amount of alcohol immediately after its ingestion. Thus, the ALDH2 genotype modifies the characteristics of the anginal attacks as a co-factor for the induction of vasospastic angina after alcohol ingestion.
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  • Kimihira Seki, Wataru Abo, Yoshiki Yamamoto, Akihiro Matsuura
    1999 Volume 187 Issue 4 Pages 323-328
    Published: 1999
    Released on J-STAGE: September 27, 2005
    JOURNAL FREE ACCESS
    Cystic fibrosis (CF) is an inheritable disorder characterized by defective epithelial chloride transport and progressive lung disease, caused by mutations in the CF transmembrane conductance regulator (CFTR) gene. The subject of this study was an 8-year old Japanese boy, who developed typical CF symptoms including meconium ileus, pancreatic insufficiency, an elevated sweat chloride concentration and pulmonary disease. Analysis of the CFTR gene of this patient revealed compound heterozygous mutations in exon 11 (1742 delAC) and intron 9 (1525-18 GtoA) of the CFTR gene.
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  • Junichi Kameyama, Yasunobu Handa, Nozomu Hoshimiya, Minoru Sakurai
    1999 Volume 187 Issue 4 Pages 329-337
    Published: 1999
    Released on J-STAGE: September 27, 2005
    JOURNAL FREE ACCESS
    The purpose of this study is to restore the motion of the paralyzed shoulder caused by upper motor neuron disorders using functional electrical stimulation (FES). Percutaneous wire electrodes were implanted into twelve muscles of the shoulder in six patients with stroke or cervical spinal cord injury. The motion of the paralyzed shoulder was controlled by a portable FES computer system, with the three standard stimulation patterns for restoring motion of 90° flexion to 90° horizontal abduction, 90° flexion to 20° horizontal adduction, and 90° abduction to 90° horizontal adduction. Shoulder movements were repeatedly controlled according to the created stimulation patterns in five of the patients. The two dimensional motion analyzer also confirmed shoulder control over a satisfactorily broad range of excursion. One hemiplegic patient, who was a signboard painter, had his paretic left upper extremity improved by FES, and he drew a large picture on a board with his normal right hand and, with his affected left arm against the wall, to support his trunk. This may be a world first case of producing shoulder motion through FES.
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  • Junichi Kameyama, Yasunobu Handa, Nozomu Hoshimiya, Minoru Sakurai
    1999 Volume 187 Issue 4 Pages 339-351
    Published: 1999
    Released on J-STAGE: September 27, 2005
    JOURNAL FREE ACCESS
    The purpose of this study is to create the standard stimulation patterns of shoulder motion from electromyographic (EMG) data in 13 healthy human volunteers in order to control the movement of the paralyzed shoulder in quadriplegic and hemiplegic patients by functional electrical stimulation (FES). Simultaneous EMG measurement was made at 24 points of 17 major muscles relating to shoulder motion. Since the number of the output channels in the portable FES apparatus is limited, 12 major muscles were selected from statistically processing these EMG data and stimulation patterns were created based on the EMG data of these muscles. Thus three standard stimulation patterns were created to move the shoulder, i.e., (i) 90° flexion to 90° horizontal abduction, (ii) 90° flexion to 20° horizontal adduction, and (iii) 90° abduction to 90° horizontal adduction. With the created stimulation patterns, the restoration of the shoulder motion in plegic patients was successful and it will be reported in the next paper.
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  • Junko Kuboki, Sei-ichi Ishiguro, Makoto Tamai
    1999 Volume 187 Issue 4 Pages 353-361
    Published: 1999
    Released on J-STAGE: September 27, 2005
    JOURNAL FREE ACCESS
    It is possible that Na, K-ATPase may play some roles in ischemic damage of nervous tissue. To determine whether Na, K-ATPase is affected in ischemic and reperfused retina, we measured enzyme activities. Retinal ischemia was induced by clamping the optic nerve of female adult Sprague-Dawley (SD) rats for 90 minutes. At 0.5, 2 and 24 hours after reperfusion, rat eyes were enucleated, and the retinas were removed. In addition to unseparated, total ouabain-sensitive Na, K-ATPase activity, we measured weakly ouabain-sensitive (α) and highly ouabain-sensitive (α[+]) isoform activities separately by ATP hydrolysis. Total ouabain-sensitive Na, K-ATPase activity, α and α(+) isoform activities showed no significant difference from sham-operated contralateral eyes at 0.5 and 2 hours of reperfusion. After 24 hours of reperfusion, total ouabain-sensitive Na, K-ATPase activity decreased to 63% of the control. The activities of α and α(+) isoforms were 47% and 72%, respectively. The ratios of the α and α(+) isoform activities (α/α[+]) significantly decreased at 2 and 24 hours of reperfusion. Activity in α isoform decreased markedly in reperfused rat retinas. This response may be beneficial for reducting the oxidative stress in reperfused retinas.
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Special Report
  • Tatsuya Takahashi, Steven L. Simon, Klaus R. Trott, Keisei Fujimori, N ...
    1999 Volume 187 Issue 4 Pages 363-375
    Published: 1999
    Released on J-STAGE: September 27, 2005
    JOURNAL FREE ACCESS
    The objective of this report is to present a summary of progress of the Marshall Islands Nationwide Thyroid Study. As well known, the US atomic weapons testing program in the Pacific was conducted primarily between 1946 and 1958 in the Marshall Islands. The nuclear tests resulted in radioactive contamination of a number of atolls and resulted in exposure of Marshallese to undefined levels before our study. Little information has been paid to health consequences among residents of the nearly twenty inhibited atolls except for some information about nodular thyroid disease which was reported on by an US group. In a cooperative agreement with the Government of the Marshall Islands, between 1993 and 1997 we studied the prevalence of both thyroid nodules and thyroid cancer among 4766 Marshallese potentially exposed to radioiodines from bomb test fallout. That group represents more than 65% of the population at risk. We diagnosed 45 thyroid cancers and 1398 benign thyroid nodules. In addition, 23 study participants had been operated on prior to our study for thyroid cancer. Presently, we are developing a database of information to estimate radiation doses and planning a statistical analysis to determine if a dose-response relationship exists. These data will be important for the health promotion of exposed people all over the world including Hiroshima, Nagasaki, Semipalatinsk, Chernobyl and other locations. A timely completion is important for purpose of assisting Marshallese as well as to add the global understanding of radiation induced thyroid cancer.
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