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JaLCDOI 10.18926/AMO/48961
FullText URL 66_5_369.pdf
Author Akiyama, Mari| Kobayashi, Katsuhiro| Ohtsuka, Yoko|
Abstract Dravet syndrome (DS), or severe myoclonic epilepsy in infancy, is one of the most severe types of genetic epilepsy. It is characterized by the initial occurrence of febrile or afebrile seizures that often evolve into status epilepticus in infants with normal development, and by the subsequent appearance of myoclonic and/or atypical absence seizures as well as complex partial seizures. The key feature that characterizes DS is fever sensitivity, although photosensitivity and pattern-sensitivity are also often seen. The prognosis is unfavorable in most cases. Seizures become drug-resistant and persist, with many patients suffering from motor and cognitive impairment. Mutations of SCN1A, which encodes the voltage-gated sodium channel NaV1.1, are the most frequent genetic cause of this syndrome. SCN1A mutations and/or microchromosomal rearrangements involving SCN1A are detected in about 85% of patients. Mutations of PCDH19 have also been reported in female patients with clinical findings compatible with DS. PCDH19 mutations might account for 5% of overall DS cases. Thirty years after its first description, DS is considered as a model of channelopathy. This survey reviews recent developments in the research literature on DS, focusing on the clinical course, as well as its genetic causes.
Keywords Dravet syndrome long-term outcome SCN1A PCDH19
Amo Type Review
Publication Title Acta Medica Okayama
Published Date 2012-10
Volume volume66
Issue issue5
Publisher Okayama University Medical School
Start Page 369
End Page 376
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 23093055
Web of Science KeyUT 000310253900001
JaLCDOI 10.18926/AMO/48690
FullText URL 66_4_351.pdf
Author Ohara, Ichiyou| Ogata, Sho| Okusa, Yasushi| Ogawa, Tomomichi| Matsuzaki, Koji| Kaga, Hitoshi| Niihara, Naoko| Tominaga, Susumu| Hase, Kazuo|
Abstract In the duodenum, mixed exocrine-endocrine tumors exhibiting both neuroendocrine and glandular differentiations [cf. appendiceal goblet cell carcinoids (GCCs)] are rare. We present a Japanese case with a duodenal GCC that was found during pathologic examination of a gastrectomy specimen removed for gastric mucosal cancer. The tumor was widely distributed within both the first portion of the duodenum and the gastric antrum, although mucosal involvement was observed only in the duodenum. The tumor cells formed solid nests, trabeculae, or tubules, and some displayed a goblet cell appearance. They were immunoreactive against antibodies for both serotonin and somatostatin, and showed an argentaffin reaction (similar to a “midgut” enterochromaffin cell carcinoid). Ultra-structurally, the tumor cells had an amphicrine nature. Physicians encounter GCC in the duodenum only rarely, and its discovery may be incidental. Its diagnosis will be challenging and will require careful clinical and pathologic examinations.
Keywords amphicrine tumor duodenum goblet cell carcinoid serotonin somatostatin
Amo Type Case Report
Publication Title Acta Medica Okayama
Published Date 2012-08
Volume volume66
Issue issue4
Publisher Okayama University Medical School
Start Page 351
End Page 356
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22918208
Web of Science KeyUT 000307918900008
Author Mizukami, Shusaku|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Ma, Shaobo|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Hayashi, Keiichiro| Ohmori, Iori| Matsui, Hideki|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
Author Fujimura, Atsushi| Tomizawa, Kazuhito| Matsui, Hideki|
Published Date 2012-08-01
Publication Title 岡山医学会雑誌
Volume volume124
Issue issue2
Content Type Journal Article
JaLCDOI 10.18926/AMO/48569
FullText URL 66_3_285.pdf
Author Mizobuchi, Satoshi| Matsuoka, Yoshikazu| Obata, Norihiko| Kaku, Ryuji| Itano, Yoshitaro| Tomotsuka, Naoto| Taniguchi, Arata| Nishie, Hiroyuki| Kanzaki, Hirotaka| Ouchida, Mamoru| Morita, Kiyoshi|
Abstract Perioperative beta-blocker administration has recently been recommended for patients undergoing cardiac or other surgery due to the beneficial cardiovascular effects of these agents. In addition, some studies have reported that perioperatively administered beta-blockers also have analgesic effects. In this study, to investigate the antinociceptive effects and the analgesic profile of landiolol, we examined the effects of intrathecal landiolol administration on nociceptive pain behavior and c-fos mRNA expression (a neural marker of pain) in the spinal cord using a rat formalin model. We found that pain-related behavior was inhibited by intrathecal landiolol administration. Moreover, the increase in c-fos mRNA expression on the formalin-injected side was less pronounced in rats administered landiolol than in saline administered controls. Thus, intrathecal administration of landiolol exhibited antinociceptive effects. Further investigation of the antinociceptive mechanism of landiolol is required.
Keywords beta-blocker landiolol formalin pain behavior c-fos
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-06
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 285
End Page 289
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22729110
Web of Science KeyUT 000305669700013
JaLCDOI 10.18926/AMO/48565
FullText URL 66_3_253.pdf
Author Zhang, Kai| Yamamoto, Yumiko| Suzuki, Tomonori| Yokota, Kenji| Ma, Shaobo| Nengah Dwi Fatmawati, Ni| Oguma, Keiji|
Abstract Cultured Clostridium botulinum strains produce progenitor toxins designated as 12S, 16S, and 19S toxins. The 12S toxin consists of a neurotoxin (NTX, 7S) and a non-toxic non-hemagglutinin (NTNH). The 16S and 19S toxins are formed by conjugation of the 12S toxin with hemagglutinin (HA), and the 19S toxin is a dimer of the 16S toxin. Type A cultures produce all 3 of these progenitor toxins, while type E produces only the 12S toxin. The 7S toxin is cleaved into heavy (H) and light (L) chains by a protease(s) in some strains, and the H chain has 2 domains, the N-terminus (Hn) and C-terminus (Hc). It has been reported that type A toxins bind to the intestinal cells or cultured cells via either HA or Hc. In this study, we investigated the binding of type A and E toxins to Caco-2 cells using Western blot analysis. Both the type E 7S and 12S toxins bound to the cells, with the 7S toxin binding more strongly, whereas, in the type A strain, only the 16S/19S toxins showed obvious binding. Pre-incubation of the type E 7S toxin with IgG against recombinant type E Hc significantly inhibited the 7S toxin binding, indicating that Hc might be a main binding domain of the type E toxin.
Keywords Clostridum botulinum neurotoxins Caco-2 binding Hc
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-06
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 253
End Page 261
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22729106
Web of Science KeyUT 000305669700009
Related Url http://ousar.lib.okayama-u.ac.jp/metadata/48451
JaLCDOI 10.18926/AMO/48562
FullText URL 66_3_231.pdf
Author Takahashi, Kingo| Hayashi, Masamichi| Fujii, Toshihiro| Kawamura, Kenji| Ozaki, Toshifumi|
Abstract The objective of early rehabilitation after anterior cruciate ligament (ACL) reconstruction is to increase the muscle strength of the lower extremities. Closed kinetic chain (CKC) exercise induces co-contraction of the agonist and antagonist muscles. The purpose of this study was to compare the postoperative muscle strength/mass of subjects who performed our new CKC exercise (new rehabilitation group:group N) from week 4, and subjects who received traditional rehabilitation alone (traditional rehabilitation group:group T). The subjects stood on the device and maintained balance. Then, low-frequency stimulation waves were applied to 2 points each in the anterior and posterior region of the injured thigh 3 times a week for 3 months. Measurement of muscle strength was performed 4 times (before the start, and then once a month). Muscle mass was evaluated in CT images of the extensor and flexor muscles of 10 knees (10 subjects) in each group. The injured legs of group N showed significant improvement after one month compared to group T. The cross-sectional area of the extensor muscles of the injured legs tended to a show a greater increase at 3 months in group N. This rehabilitation method makes it possible to contract fast-twitch muscles, which may be a useful for improving extensor muscle strength after ACL reconstruction.
Keywords anterior cruciate ligament reconstruction closed kinetic chain electrical muscle stimulation standing-shaking-board exercise
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-06
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 231
End Page 237
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22729103
Web of Science KeyUT 000305669700006
JaLCDOI 10.18926/AMO/48557
FullText URL 66_3_183.pdf
Author Tanabe, Kenji| Takei, Kohji|
Abstract Charcot-Marie-Tooth disease (CMT) is an inherited neuronal disorder, and is induced by mutations of various genes associated with intracellular membrane traffic and cytoskeleton. A large GTPase, dynamin, which is known as a fission protein for endocytic vesicles, was identified as a gene responsible for dominant-intermediate CMT type 2B (DI-CMT2B). Of these mutants, the PH domain, which is required for interaction with phosphoinositides, was mutated in several families. Interestingly, the expression of a deletion mutant, 551Δ3, did not impair endocytosis, but induced abnormal accumulation of microtubules. Recent evidence has shown that dynamin 2 regulates the dynamic instability of microtubules, and 551Δ3 lacks this function. We propose a model for the regulation of the dynamic instability of microtubules by dynamin 2 and discuss the relationship between dynamin 2 and CMT.
Keywords neuropathy Charcot-Marie-Tooth disease membrane traffic dynamin microtubules
Amo Type Review
Publication Title Acta Medica Okayama
Published Date 2012-06
Volume volume66
Issue issue3
Publisher Okayama University Medical School
Start Page 183
End Page 190
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22729098
Web of Science KeyUT 000305669700001
Author Yoshimoto, Masaaki| Kataoka, Takahiro| Toyota, Teruaki| Taguchi, Takehito| Yamaoka, Kiyonori|
Published Date 2012-02-01
Publication Title Inflammation
Volume volume35
Issue issue1
Content Type Journal Article
Author Watanabe, Makiko|
Published Date 2012-03-23
Publication Title
Content Type Thesis or Dissertation
Author Li, Xiujun|
Published Date 2012-03-23
Publication Title
Content Type Thesis or Dissertation
Author Yamaguchi, Daisuke|
Published Date 2012-03-23
Publication Title
Content Type Thesis or Dissertation
FullText URL K0004501.pdf K004501_honbun.pdf
Author Zhang, Kai|
Published Date 2012-03-23
Content Type Thesis or Dissertation
Grant Number 甲第4501号
Granted Date 2012-03-23
Thesis Type Doctor of Philosophy in Medical Science
Grantor 岡山大学
language Japanese English
Author Miyazaki, Kazunori|
Published Date 2012-03-23
Publication Title
Content Type Thesis or Dissertation
JaLCDOI 10.18926/AMO/48264
FullText URL 66_2_143.pdf.pdf
Author Watanabe, Makiko| Ueno, Hiroshi| Suemitsu, Shunsuke| Yokobayashi, Eriko| Matsumoto, Yosuke| Usui, Shinichi| Sujiura, Hiroko| Okamoto, Motoi|
Abstract Recent studies have demonstrated the important role of immune molecules in the development of neuronal circuitry and synaptic plasticity. We have detected the presence of FcγRllB protein in parvalbumin- containing inhibitory interneurons (PV neurons). In the present study, we examined the appearance of PV neurons in the barrel cortex and the effect of sensory deprivation in FcγRllB-deficient mice (FcγRllB-/-) and wild-type mice. There was no substantial difference in the appearance of PV neurons in the developing barrel cortex between FcγRllB-/- and wild-type mice. Sensory deprivation from immediately after birth (P0) or P7 to P12-P14 induced an increase in PV neurons. In contrast, sensory deprivation from P7 or P14 to P28, but not from P21 to P28, decreased PV neurons in wild-type mice. However, sensory deprivation from P0 or P7 to P12-P14 did not increase PV neurons and sensory deprivation from P7 or P14 to P28 did not decrease or only modestly decreased PV neurons in FcγRllB-/- mice. The results indicate that expression of PV is regulated by sensory experience and the second and third postnatal weeks are a sensitive period for sensory deprivation, and suggest that FcγRllB contributes to sensory experience-regulated expression of PV.
Keywords parvalbumin fast-spiking interneurons FcγRllB barrel cortex sensory deprivation
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-04
Volume volume66
Issue issue2
Publisher Okayama University Medical School
Start Page 143
End Page 154
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22525472
Web of Science KeyUT 000303175300007
JaLCDOI 10.18926/AMO/48261
FullText URL 66_2_111.pdf.pdf
Author Shinomiya, Misae| Kawamura, Kenji| Tanida, Emiko| Nagoshi, Megumi| Motoda, Hirotoshi| Kasanami, Yoshiko| Hiragami, Fukumi| Kano, Yoshio|
Abstract We studied the effects of natural essential oil on neurite outgrowth in PC12m3 neuronal cells to elucidate the mechanism underlying the action of the oils used in aromatherapy. Neurite outgrowth can be induced by nerve growth factor (NGF), where ERK and p38 MAPK among MAPK pathways play important roles in activating intracellular signal transduction. In this study, we investigated whether d-limonene, the major component of essential oils from oranges, can promote neurite outgrowth in PC12m3 cells, in which neurite outgrowth can be induced by various physical stimulations. We also examined by which pathways, the ERK, p38 MAPK or JNK pathway, d-limonene acts on PC12m3 cells. Our results showed that neurite outgrowth can be induced when the cells are treated with d-limonene. After treatment with d-limonene, we observed that p38 MAPK is strongly activated in PC12m3 cells, while ERK is weakly activated. In contrast, JNK shows little activity. A study using an inhibitor of p38 MAPK revealed that neurite outgrowth in PC12m3 cells is induced via the activation of p38 MAPK by d-limonene. The results thus indicate that d-limonene may promote neural cell differentiation mainly via activation of the p38 MAPK pathway.
Keywords essential oil d-limonene p38 MAP kinase PC12 mutant cells
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-04
Volume volume66
Issue issue2
Publisher Okayama University Medical School
Start Page 111
End Page 118
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22525469
Web of Science KeyUT 000303175300004
JaLCDOI 10.18926/AMO/48079
FullText URL 66_1_31.pdf
Author Utsumi, Hiroya| Terashi, Hiroo| Ishimura, Yohei| Takazawa, Tomoko| Hayashi, Akito| Mochizuki, Hideki| Okuma, Yasuyuki| Orimo, Satoshi| Takahashi, Kazushi| Yoneyama, Mitsuru| Mitoma, Hiroshi|
Abstract To quantify gait bradykinesia during daily activity in patients with Parkinson's disease (PD), we measured movement-induced accelerations over more than 24h in 50 patients with PD and 17 age-matched normal controls, using a new device, the portable gait rhythmogram. Acceleration values induced by various movements, averaged each 10 min, exhibited a gamma distribution. The mean value of the distribution curve was used as an index of the "amount of overall movement per 24h". Characteristic changes were observed in both the gait cycle and gait acceleration. During hypokinesia, the gait cycle became either faster or slower. A number of patients with marked akinesia/bradykinesia showed a reduced and narrow range of gait acceleration, i.e., a range of floor reaction forces. The results suggest that assessment of the combination of changes in gait cycle and gait acceleration can quantitatively define the severity of gait bradykinesia.
Keywords Parkinson's disease gait disorders portable gait rhythmogram
Amo Type Original Article
Publication Title Acta Medica Okayama
Published Date 2012-02
Volume volume66
Issue issue1
Publisher Okayama University Medical School
Start Page 31
End Page 40
ISSN 0386-300X
NCID AA00508441
Content Type Journal Article
language English
Copyright Holders CopyrightⒸ 2012 by Okayama University Medical School
File Version publisher
Refereed True
PubMed ID 22358137
Web of Science KeyUT 000300800700005
Author Sakamoto, Tomoaki| Tomioka, Kenji|
Published Date 2007-06
Publication Title Zoological Science
Volume volume24
Issue issue6
Content Type Journal Article