研究者詳細 - 小野寺　理

論文 - 小野寺　理

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The detection of anti-Purkinje cell antibody (anti-Yo antibody) by ELISA using recombinant Yo fusion protein 査読

K. Tanaka, M. Tanaka, O. Onodera, S. Igarashi, S. Tsuji

Brain and Nerve 46 ( 1 ) 47 - 51 1994年

USE OF A RADIATION-REDUCED HYBRID PANEL FOR THE LOCALIZATION OF 7 MARKERS IN THE XQ28 REGION OF THE HUMAN GENOME 査読

A SMAHI, B PETERLIN, O ONODERA, S TSUJI, MC FULCHIGNONILATAUD

ANNALES DE GENETIQUE 37 ( 1 ) 11 - 13 1994年

Correlation between degrees of the CTG repeat expansion and clinical features of myotonic dystrophy 査読

I. Eguchi, R. Koike, O. Onodera, K. Tanaka, H. Kondo, S. Tsuji

Clinical Neurology 34 ( 2 ) 118 - 123 1994年

MRI findings of posterior spinal artery syndrome - Report of a case 査読

K. Okuizumi, M. Wakasugi, O. Onodera, H. Okumura, S. Tsuji

Clinical Neurology 34 ( 11 ) 1116 - 1120 1994年

CHROMOSOMAL LOCALIZATION OF THE EPSILON-1, EPSILON-3, AND ZETA-1 SUBUNIT GENES OF THE HUMAN NMDA RECEPTOR-CHANNEL 査読

H TAKANO, O ONODERA, H TANAKA, H MORI, K SAKIMURA, T HORI, H KOBAYASHI, M MISHINA, S TSUJI

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS 197 ( 2 ) 922 - 926 1993年12月

ABSENCE OF LINKAGE DISEQUILIBRIUM AT AMYLOID PRECURSOR PROTEIN GENE LOCUS IN JAPANESE FAMILIAL ALZHEIMERS-DISEASE WITH 717VAL-]ILE MUTATION 査読

H TANAKA, S NARUSE, K SEKI, O ONODERA, H KOBAYASHI, T MIYATAKE, A SHIBATA, Y SAKAKI, K KAMINO, T MIKI, N NUKINA, M IMAGAWA, NAKANO, I, T SHIMIZU, T KOJIMA, J HARDY, S TSUJI

NEUROSCIENCE LETTERS 162 ( 1-2 ) 63 - 66 1993年11月

Positional cloning--current status and future directions 査読

Onodera, O., Tsuji, S.

Nippon rinsho. Japanese journal of clinical medicine 51 ( 9 ) 2225 - 2233 1993年9月

Molecular genetic approach for positional cloning of X-chromosome-linked diseases 査読

Onodera, O., Tanabe, H., Tuji, S., Kaneko, K., Kobayashi, H.

Tanpakushitsu kakusan koso. Protein, nucleic acid, enzyme 38 ( 3 ) 354 - 360 1993年2月

HTRA1 Disorder 査読

Osamu Onodera, Hiroaki Nozaki, Toshio Fukutake

1993年

記述言語：英語出版者・発行元：University of Washington, Seattle

CLINICAL CHARACTERISTICS: HTRA1 disorder is a phenotypic spectrum in which some individuals have few to no symptoms and others manifest with the more severe CARASIL (cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy) phenotype. Those who have a heterozygous HTRA1 pathogenic variant may have mild neurologic findings (sometimes identified only on neuroimaging) or mild-to-moderate neurologic signs and symptoms of CARASIL. In this chapter, the term "classic CARASIL" refers to the more severe phenotype associated with biallelic pathogenic variants, and "HTRA1 cerebral small vessel disease" (HTRA1-CSVD) refers to the milder phenotype associated with a heterozygous HTRA1 pathogenic variant. Classic CARASIL is characterized by early-onset changes in the deep white matter of the brain observed on MRI, and associated neurologic findings. The most frequent initial symptom is gait disturbance from spasticity beginning between ages 20 and 40 years. Forty-four percent of affected individuals have stroke-like episodes before age 40 years. Mood changes (apathy and irritability), pseudobulbar palsy, and cognitive dysfunction begin between ages 20 and 50 years. The disease progresses slowly following the onset of neurologic symptoms. Scalp alopecia and acute mid- to lower-back pain (lumbago) before age 30 years are characteristic. The most frequent initial symptom in individuals with HTRA1-CSVD is slowly progressive gait disturbance after age 40 years, which may be followed by the development of mood changes and cognitive dysfunction. A majority of affected individuals have a stroke-like episode after age 40 years. Spondylosis and alopecia are seen in a minority of individuals with HTRA1-CSVD. DIAGNOSIS/TESTING: The diagnosis of HTRA1 disorder is established in a proband by identification of either a heterozygous or biallelic pathogenic variant(s) in HTRA1 on molecular genetic testing. MANAGEMENT: Treatment of manifestations: Consideration of anti-platelet therapy and anti-hypertensive therapy for those with cerebral microbleeds; physical therapy, walking aids, and home adaptations for those with gait disturbance; consideration of medication (baclofen or tizanidine) for spasticity; wig or hairpiece for those with alopecia; standard treatment for spinal spondylosis and mood disorder; supportive care including emotional support and counseling for affected individuals and their families. Surveillance: Follow-up intervals are based on the severity and type of symptoms and the needs of the individuals and their caregivers. Agents/circumstances to avoid: Smoking and a high-salt diet, which may hasten the progression of arteriosclerosis. GENETIC COUNSELING: HTRA1 disorder caused by biallelic pathogenic variants (i.e., the classic CARASIL phenotype) is inherited in an autosomal recessive manner. HTRA1 disorder caused by heterozygous pathogenic variants is inherited in an autosomal dominant manner. Autosomal recessive inheritance. At conception, each sib of an affected individual has a 25% chance of inheriting both HTRA1 pathogenic variants and being affected, a 50% chance of inheriting one pathogenic variant and being heterozygous, and a 25% chance of inheriting neither pathogenic variant and not being at risk for HTRA1 disorder. Autosomal dominant inheritance. Each sib of an affected individual has a 50% risk of inheriting the pathogenic variant from their affected parent. Once the HTRA1 pathogenic variant(s) have been identified in an affected family member, prenatal testing for a pregnancy at increased risk and preimplantation genetic testing for HTRA1 disorder are possible.

PubMed

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CARASIL 査読

Onodera O, Nozaki H, Fukutake T, Adam MP, Ardinger HH, Pagon RA, Wallace SE, Bean LJH, Stephens K, Amemiya A

1993年

MRI findings of olivopontocerebellar atrophy and Machado-Joseph disease - Diagnostic value of transverse pontine fibers 査読

J. Idezuka, O. Onodera, T. Yuasa, S. Tsuji, J. Ito

Clinical Neurology 33 ( 3 ) 289 - 293 1993年

Spinocerebellar Ataxia Type 17 査読

Yasuko Toyoshima, Osamu Onodera, Mitsunori Yamada, Shoji Tsuji, Hitoshi Takahashi

1993年

記述言語：英語出版者・発行元：University of Washington, Seattle

CLINICAL CHARACTERISTICS: Spinocerebellar ataxia type 17 (SCA17) is characterized by ataxia, dementia, and involuntary movements, including chorea and dystonia. Psychiatric symptoms, pyramidal signs, and rigidity are common. The age of onset ranges from three to 55 years. Individuals with full-penetrance alleles develop neurologic and/or psychiatric symptoms by age 50 years. Ataxia and psychiatric abnormalities are frequently the initial findings, followed by involuntary movement, parkinsonism, dementia, and pyramidal signs. Brain MRI shows variable atrophy of the cerebrum, brain stem, and cerebellum. The clinical features correlate with the length of the polyglutamine expansion but are not absolutely predictive of the clinical course. DIAGNOSIS/TESTING: The diagnosis of SCA17 is established in a proband by identification of an abnormal CAG/CAA repeat expansion in TBP. Affected individuals usually have more than 41 repeats. The CAA and CAG codons both encode glutamine residues resulting in a pathogenic polyglutamine expansion. MANAGEMENT: Treatment of manifestations: Psychotropic medications for psychiatric problems, antiepileptic drugs for seizures (AEDs); botulinum toxin injections for dystonia; adaptation of the environment to accommodate dementia. Prevention of secondary complications: Side effects of psychotropic medications and AEDs may require total or intermittent discontinuation of the treatment or reduction in dose. Surveillance: Annual or semiannual evaluation by a neurologist or more frequently if symptoms are progressing rapidly. Agents/circumstances to avoid: Sedative/hypnotic agents, such as ethanol or certain medications, may exacerbate incoordination. GENETIC COUNSELING: SCA17 is inherited in an autosomal dominant manner. Offspring of affected individuals are at a 50% risk of inheriting the expanded TBP allele. The age of onset, severity, specific symptoms, and progression of the disease are variable and cannot be precisely predicted by family history or size of expansion. Prenatal testing for pregnancies at increased risk is possible if the diagnosis has been established in an affected family member by molecular genetic testing.

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STRONG CORRELATION BETWEEN THE NUMBER OF CAG REPEATS IN ANDROGEN RECEPTOR GENES AND THE CLINICAL ONSET OF FEATURES OF SPINAL AND BULBAR MUSCULAR-ATROPHY 査読

S IGARASHI, Y TANNO, O ONODERA, M YAMAZAKI, S SATO, A ISHIKAWA, N MIYATANI, M NAGASHIMA, Y ISHIKAWA, K SAHASHI, T IBI, T MIYATAKE, S TSUJI

NEUROLOGY 42 ( 12 ) 2300 - 2302 1992年12月

GENOMIC ORGANIZATION OF A CDNA (QM) DEMONSTRATING AN ALTERED MESSENGER-RNA LEVEL IN NONTUMORIGENIC WILMS MICROCELL HYBRID-CELLS AND ITS LOCALIZATION TO XQ28 査読

K KANEKO, H KOBAYASHI, O ONODERA, T MIYATAKE, S TSUJI

HUMAN MOLECULAR GENETICS 1 ( 7 ) 529 - 533 1992年10月

RAPID DIAGNOSIS OF TUBERCULOUS MENINGITIS BY POLYMERASE CHAIN-REACTION (PCR) 査読

K KANEKO, O ONODERA, T MIYATAKE, S TSUJI

NEUROLOGY 40 ( 10 ) 1617 - 1618 1990年10月

ATRIAL STANDSTILL AFTER TREADMILL EXERCISE TEST AND UNIQUE RESPONSE TO ISOPROTERENOL INFUSION IN RECURRENT POSTEXERCISE SYNCOPE 査読

Y TAMURA, O ONODERA, K KODERA, Y IGARASHI, T MIIDA, Y AIZAWA, T IZUMI, A SHIBATA, S TAKANO

AMERICAN JOURNAL OF CARDIOLOGY 65 ( 7 ) 533 - 535 1990年2月

A case of rigid spine syndrome with rimmed vacuole 査読

O. Onodera, M. Yamazaki, T. Atsumi, T. Miyatake, T. Izumi

Clinical Neurology 30 ( 5 ) 516 - 519 1990年

[Research into actual conditions and preventive care in periodontal disease. Relationship between questionnaire results and periodontal disease in youth]. 査読

Nakashima K, Kurihara C, Kawanaga T, Kurihashi Y, Ohsawa K, Onodera O, Shimoyama M, Watanabe Y, Ikeda K

Nihon Shishubyo Gakkai kaishi 31 ( 4 ) 1220 - 1241 1989年12月

記述言語：日本語出版者・発行元：特定非営利活動法人日本歯周病学会

川越市下の若年者3,886名を対象に,口腔清掃の習慣や歯周疾患に関する自覚症状等についての問診表による意識調査と,プラークの付着,歯石の沈着,歯肉の炎症,う蝕,歯列不正およびプロービングデプスについての口腔内診査を行い,両者の関連性について検討した。1.意識調査の結果,歯磨きの回数については,83.1%の者が毎日複数回歯を磨く等,口腔清掃の習慣は向上してきている。2.歯周疾患に関連する自覚症状については,歯磨き時の出血と答えた者が18.4%で最も高い割合を示した。3.歯周疾患の進行と年齢の関連性については,13歳で最高値を示した。また,歯周疾患が進行するにしたがい,男子の占める割合が高くなった(χ^2-test: α<0.01)。4.口腔内診査の結果,歯磨きの回数の減少と歯周疾患の進行の間には有意な関連性が認められた(χ^2-test: α<0.001)。5.歯磨き時わ出血と歯肉の腫脹の自覚症状と歯周疾患の進行との間に強い関連性が認められた(χ^2-test: α<0.001)。6.プラークの付着,歯石の沈着,う蝕および歯列不正の状態の悪化と歯周疾患の進行との間に関連性が認められた(χ^2-test: α<0.001)。

DOI： 10.2329/perio.31.1220

その他リンク： http://search.jamas.or.jp/link/ui/1991208106

[A method of protection on out-flow of hydroxyapatite]. 査読

Watanabe Y, Kurihara N, Nakashima K, Onodera O, Ousawa K, Mashima T, Kurihashi Y, Miyata T, Ikeda K

Nihon Shishubyo Gakkai kaishi 30 ( 4 ) 1108 - 1115 1988年12月

記述言語：日本語出版者・発行元：特定非営利活動法人日本歯周病学会

コラーゲンをペプシン処理して得られたアテロコラーゲンは,抗原性が少なく生体組織においては細胞成長の足場となり,種々の形状に変えることが出来るなどの特徴を持っている。この報告は,アテロコラーゲンインプラント^[○!R]の1%溶液を歯槽骨欠損部に填塞したハイドロキシアパタイトの初期流出の防止を目的として使用した結果についてである。アテロコラーゲンインプラント^[○!R]は,低温では液状を呈し,37℃付近になるとゲル化する性質を持っている。すなわち,ハイドロキシアパタイト填塞面に滴下してゲル化する性質を利用するのである。実験法は術後1週,2週および4週目に半規格X線写真を撮影し,ハイドロキシアパタイト残存量を画像解析装置を用いて比較する。その結果は,術後4週目でのハイドロキシアパタイト残存量からみて,アテロコラーゲンの滴下群が,ハイドロキシアパタイトの流出を有意(p<0.01)に抑制することがわかった。また,肉眼的所見においても炎症症状の早期消退と創面の閉鎖が早期に起こり治癒する傾向を示した。

[The study of dentifrice containing Phellodendron amurense extract on periodontal disease (II). The clinical effects of dentifrice containing Phellodendron amurense extract and anti-inflammatory agents]. 査読

Sato I, Watanabe Y, Shimojima T, Onodera O, Ohsawa K, Nakajima K, Kurihashi Y, Mashima T, Kusunoki K, Ikeda K

Nihon Shishubyo Gakkai kaishi 30 ( 3 ) 887 - 900 1988年9月

記述言語：日本語出版者・発行元：特定非営利活動法人日本歯周病学会

抗プラスミン作用を有するトラネキサム酸,血流改善作用を有する酢酸トコフェロール,抗炎症,抗アレルギー作用を有するβ-グリチルレチン酸に加えた従来の歯磨剤の歯周疾患予防効果を一層高める目的で,さらに収斂性抗炎症作用を有するオウバクエキスを主成分として配合した歯磨剤(K歯磨剤)の検討をするため,K歯磨剤よりオウバクエキスを除いたアクティブプラセボである歯磨剤(A歯磨剤)を対照に2重盲検法により臨床試験を行った。その結果,両歯磨剤群間にはPMA index及び発赤に有意差が認められ,K歯磨剤に高い改善効果が認められた。また,初回検診値に対する各検診値の平均減少率で比較しても,PMA indexではK歯磨剤群は37.1%,A歯磨剤群は30.4%,発赤ではK歯磨剤群39.6%,A歯磨剤群28.6%で,いずれもK歯磨剤群のほうが高い平均減少率を示した。

DOI： 10.2329/perio.30.887

その他リンク： http://search.jamas.or.jp/link/ui/1990140203

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