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Biomedical subjects

M Odaka

Publications and source records attributed to M Odaka.

At least 19 recordsLinked to original sources
PubMed2006

Relationship of bacterial strains to clinical syndromes of Campylobacter-associated neuropathies.

BACKGROUND: Clinical and serologic studies suggest that Guillain-Barré syndrome (GBS) and atypical GBS with preserved muscle stretch reflexes (MSRs) form a continuous spectrum as well as do Fisher syndrome (FS), FS/GBS overlap, Bickerstaff brainstem encephalitis (BBE), BBE/GBS overlap, acute ophthalmoparesis (AO), ataxic GBS, and acute oropharyngeal palsy. OBJECTIVE: To clarify the spectrum of neurologic disorders that occur subsequent to Campylobacter jejuni enteritis. METHODS: We recruited patients with various neurologic conditions and from whom C jejuni was isolated. Bacterial features were investigated. RESULTS: Diagnoses for the patients from whom C jejuni was isolated were GBS (n = 90), FS (n = 22), MSR-preserved GBS (n = 10), FS/GBS (n = 6), BBE (n = 1), BBE/GBS (n = 2), AO (n = 3), ataxic GBS (n = 1), and acute oropharyngeal palsy (n = 3). Isolates from MSR-preserved GBS were similar to those of GBS in serotype (HS:19), genotype (lipo-oligosaccharide [LOS] locus class A or B, cst-II genotype [Thr51]), and GM1 or GD1a epitope expression on LOS. FS/GBS overlap, BBE, BBE/GBS overlap, AO, ataxic GBS, and acute oropharyngeal palsy isolates were similar to those of FS in serotype (HS:2 or HS:4-complex), genotype (LOS locus class A or B, cst-II genotype [Asn51]), and GQ1b epitope expression on LOS. CONCLUSIONS: The bacterial findings support the proposal that Guillain-Barré syndrome (GBS) and muscle stretch reflex-preserved GBS comprise a continuous spectrum as well as do Fisher syndrome (FS), FS/GBS overlap, Bickerstaff brainstem encephalitis (BBE), BBE/GBS overlap, acute ophthalmoparesis, ataxic GBS, and acute oropharyngeal palsy.

Adolescent↗
PubMed2006

Spectrum of neurological diseases associated with antibodies to minor gangliosides GM1b and GalNAc-GD1a.

The authors reported the neurological disease spectrum associated with autoantibodies against minor gangliosides GM1b and GalNAc-GD1a. IgG and IgM antibody reactivity against gangliosides GM1, GM2, GM1b, GD1a, GalNAc-GD1a and GQ1b was investigated in sera from 7000 consecutive patients who had various neurological conditions. The clinical diagnoses for 456 anti-GM1b-positive patients were Guillain-Barré syndrome (GBS, 71%), atypical GBS with preserved deep tendon reflexes (12%), Fisher syndrome (10%), Bickerstaff's brainstem encephalitis (2%), ataxic GBS (2%) and acute ophthalmoparesis (1%). For 193 anti-GalNAc-GD1a-positive patients, the diagnoses were GBS (70%), atypical GBS (16%), Fisher syndrome (10%) and Bickerstaff's brainstem encephalitis (3%). Of the patients with GBS or atypical GBS, 28% of 381 anti-GM1b-positive and 31% of 166 anti-GalNAc-GD1a-positive patients had neither anti-GM1 nor anti-GD1a antibodies. Of those patients with Fisher syndrome, Bickerstaff's brainstem encephalitis, ataxic GBS or acute ophthalmoparesis, 33% of 67 anti-GM1b-positive, and 52% of 25 anti-GalNAc-GD1a-positive patients had no anti-GQ1b antibodies. Autoantibodies against GM1b and GalNAc-GD1a are associated with GBS, Fisher syndrome and related conditions. These antibodies should provide useful serological markers for identifying patients who have atypical GBS with preserved deep tendon reflexes, ataxic GBS, Bickerstaff's brainstem encephalitis or acute ophthalmoparesis, especially for those who have no antibodies to GM1, GD1a or GQ1b. A method to prepare GM1b was developed.

Adolescent↗
PubMed2006

Synthetic double-stranded RNA induces multiple genes related to inflammation through Toll-like receptor 3 depending on NF-kappaB and/or IRF-3 in airway epithelial cells.

BACKGROUND: We hypothesized that synthetic double-stranded (ds)RNA may mimic viral infection and induce expression of genes related to inflammation in airway epithelial cells. OBJECTIVE: We analysed what gene was up-regulated by synthetic dsRNA poly I : C and then focused this study on the role of Toll-like receptor 3 (TLR3), a receptor of dsRNA and its transcriptional pathway. METHODS: Airway epithelial cell BEAS-2B and normal human bronchial epithelial cells were cultured in vitro. Expression of targets RNA and protein were analysed by PCR and ELISA. Localization of TLR3 expression in the cells was analysed with flow cytometry. To analyse the role of TLR3 and transcription factors, knockdown of these genes was performed with short interfering RNA (siRNA). RESULTS: Real-time PCR revealed that poly I : C significantly increased the expression of mRNAs for chemokines IP-10, RANTES, LARC, MIP-1alpha, IL-8, GRO-alpha and ENA-78 and cytokines IL-1beta, GM-CSF, IL-6 and the cell adhesion molecule ICAM-1 in both cell types. Increases in protein levels were also observed. Expression of these genes was significantly inhibited in BEAS-2B cells in which TLR3 expression was knocked down. However, pre-treatment with anti-TLR3 mAb, which interferes with the function of TLR3 expressed on the cell surface, did not inhibit the genes expression and these data were concordant with the results that TLR3 was expressed inside airway epithelial cells. The study of siRNA for NF-kappaB and IRF3 showed that they transduce the signal of poly I : C, but their roles were different in each target gene. CONCLUSION: TLR3 is expressed inside airway epithelial cells and transduces synthetic dsRNA signals. These signals may increase expression of inflammatory cytokines, chemokines and ICAM-1 through activation of transcription factors NF-kappaB and/or IRF3 in airway epithelial cells.

Antibodies, Monoclonal↗
PubMed2005

Side effects of combined therapy of methylprednisolone and intravenous immunoglobulin in Guillain-Barré syndrome.

Side effects were compared in 9 patients with Guillain-Barré syndrome treated with standard intravenous immunoglobulin (IVIg) only and in 9 treated with combined methylprednisolone and IVIg therapy. Headache occurred in 2 in both groups, indicative that pre-infusion with steroids does not prevent headache. Transient liver function disturbances were present in 2 patients of the former group and in 6 of the latter.

Adult↗
PubMed2005

Intractable chronic inflammatory demyelinating polyneuropathy treated successfully with ciclosporin.

BACKGROUND: Chronic inflammatory demyelinating polyneuropathy (CIDP) is a heterogeneous disorder and both clinical course and response to treatment vary widely. Because of the propensity for relapse, CIDP requires maintenance therapy after the initial response to treatment. There is no consensus regarding this in the published literature. PRESENT REPORT: A patient with CIDP was treated with oral prednisolone and cyclophosphamide pulse therapy but required repeated plasma exchange and intravenous immunoglobulin (IVIg). Treatment with ciclosporin freed the patient from repeated IVIg administration. Therapeutic responses in 14 subsequent cases including three patients who showed improvement with ciclosporin are also presented along with an algorithm of the authors' suggested protocol for treatment. CONCLUSION: Ciclosporin should be considered for patients with intractable CIDP who require repeated IVIg.

Administration, Oral↗
PubMed2004

Acute motor axonal neuropathy after Mycoplasma infection: Evidence of molecular mimicry.

BACKGROUND: Patients with Guillain-Barré syndrome (GBS) after Mycoplasma pneumoniae infection often have antibodies to galactocerebroside (GalC). Electrodiagnosis may show acute inflammatory demyelinating polyneuropathy (AIDP). METHODS: The authors report a patient with acute motor axonal neuropathy (AMAN) after Mycoplasma infection and review seven cases of Mycoplasma-associated GBS. They investigated anti-GalC serology under various conditions associated with Mycoplasma infection. RESULTS: The patient had immunoglobulin (Ig)G and IgM antibodies against GM1 and GalC, which cross-reacted. During the acute phase, IgM selectively immunostained axons. The cholera toxin B-subunit and rabbit anti-GM1 IgG stained a band in the lipid extract from M pneumoniae, indicative of the presence of a GM1 epitope. Six Mycoplasma-associated GBS patients with anti-GalC antibodies had non-AIDP electrodiagnoses, whereas one with Mycoplasma-associated AIDP had no anti-GalC antibodies. Anti-GalC antibodies were positive in two of five patients who had neurologic diseases other than GBS after Mycoplasma infection and in one of 12 who had acute respiratory disease caused by M pneumoniae not followed by a neurologic disease. CONCLUSIONS: Anti-GalC antibodies in Mycoplasma-associated GBS may be an epiphenomenon. In certain cases, anti-GM1 antibodies induced by molecular mimicry with M pneumoniae may cause acute motor axonal neuropathy.

Acute Disease↗
PubMed2004

Usefulness of anti-GQ1b IgG antibody testing in Fisher syndrome compared with cerebrospinal fluid examination.

Fisher syndrome (FS), a variant of Guillain-Barré syndrome (GBS), is a rare disorder, and there are few reported studies of a large number of patients with FS. Cerebrospinal fluid (CSF) albuminocytological dissociation was found in 59% of 123 FS patients during the first 3 weeks of illness, while serum anti-GQ1b IgG antibody was positive in 85%. Whereas the incidence of CSF albuminocytological dissociation increased from the first to second weeks in FS, anti-GQ1b IgG antibody peaked in the first week, but there was no CSF albuminocytological dissociation. Statistically, anti-GQ1b antibody testing was superior to a CSF examination in supporting a diagnosis of FS during the first 3 weeks of illness, especially in the first week.

Adolescent↗
PubMed2004

Double-stranded RNA activates RANTES gene transcription through co-operation of nuclear factor-kappaB and interferon regulatory factors in human airway epithelial cells.

BACKGROUND: Regulated on activation, normal T cells expressed and secreted (RANTES) is a member of the CC chemokine family and contributes to viral-induced airway inflammation including exacerbations of asthma. Double-stranded RNA (dsRNA) is known to be synthesized during replication of many viruses and a ligand of Toll-like receptor 3. We hypothesized that dsRNA may mimic viral infection and induce RANTES expression in airway epithelial cells. OBJECTIVE: We first confirmed that dsRNA up-regulated RANTES mRNA and protein synthesis in the airway epithelial cells. We next focused our studies on the transcriptional regulation of RANTES. METHODS: Airway epithelial cell line BEAS-2B and normal human bronchial epithelial cells were used in vitro study. Levels of RANTES mRNA and protein expression were determined with RT-PCR and ELISA. Mechanisms of transcriptional regulation were assessed by electrophoretic mobility shift assay and dual luciferase assay using RANTES promoter-luciferase reporter plasmids. RESULTS: Activation of nuclear factor-kappaB (NF-kappaB) was confirmed by nuclear protein binding to a DNA probe derived from the RANTES promoter. Activity of the RANTES promoter was increased by dsRNA. The stimulation with dsRNA was partially inhibited in plasmids mutated at either of the binding sites for NF-kappaB or IFN regulatory factors (IRFs). When both sites were mutated, the activation was totally abrogated. CONCLUSION: These results imply that dsRNA activates NF-kappaB and IRFs and these transcription factors activate transcription of the RANTES promoter and its protein expression in airway epithelial cells.

Bronchi↗
PubMed2001

Eradication of intraperitoneal and distant tumor by adenovirus-mediated interferon-beta gene therapy is attributable to induction of systemic immunity.

Malignant mesothelioma remains an incurable disease for which immune-modulatory therapies, such as exogenous cytokines, have shown some promise. One such cytokine, IFN-beta, has potent antiproliferative and immunostimulatory activity in vitro, but its in vivo use has been limited by toxicity. We thus conducted studies evaluating intracavitary delivery of a replication-deficient adenoviral (Ad) vector encoding for the murine IFN-beta gene (Ad.muIFN-beta) in mouse models of malignant mesothelioma. In contrast to multiple injections of recombinant protein, a single i.p. injection of Ad.muIFN-beta into animals with established tumors elicited remarkable antitumor activity leading to long-term survival in >90% of animals bearing either AB12 or AC29 i.p. mesotheliomas. A control adenovirus vector had minimal antitumor effect in vivo. Significant therapeutic effects were also seen in animals treated with large tumor burdens. Importantly, treatment of i.p. tumor also led to reduction of growth in tumors established at a distant site (flank). A number of experiments suggested that these effects were attributable to an acquired CD8(+) T-cell-mediated response including: (a) the induction of long-lasting antitumor immunity; (b) loss of efficacy of Ad.muIFN-beta in tumor-bearing, immune-deficient (SCID, SCID/beige) mice; (c) detection of high levels of specific antitumor cytolytic activity from unstimulated splenocytes harvested from Ad.muIFN-beta-treated animals that was abolished by CD8(+) T-cell depletion; and (d) abrogation of antitumor effects of Ad.muIFN-beta in tumor-bearing CD8(+) T-cell-depleted animals. These data show that intracavitary IFN-beta gene therapy using an adenoviral vector provides strong CD8(+) T-cell-mediated antitumor effects in murine models of mesothelioma and suggest that this may be a promising strategy for the treatment of localized tumors such as mesothelioma or ovarian cancer in humans.

Adenoviridae↗
PubMed2001

Acute ophthalmoparesis (without ataxia) associated with anti-GQ1b IgG antibody: clinical features.

OBJECTIVE: To examine the clinical features of acute ophthalmoparesis (AO) (without ataxia) associated with anti-GQ1b immunoglobulin G (IgG) antibody. DESIGN: Retrospective observational case series. PARTICIPANTS: Twenty-one subjects with AO (without ataxia) who had anti-GQ1b IgG. METHODS: Clinical features of 21 subjects with AO were analyzed. RESULTS: Seventeen had symptoms of antecedent infection. Gaze limitation was bilateral in 16 subjects and unilateral in five, indicative that laterality does not always negate AO. Nine subjects showed abducens paresis, and two limitation of abduction and adduction. Eight, who initially had bilateral abducens palsy, subsequently had impairment of adduction and vertical movement. These showed that bilateral abducens palsy followed by oculomotor nerve involvement is characteristic of AO. Muscle stretch reflexes were normal in nine subjects, hypoactive in eight, absent in three, and brisk in one. Distal paresthesias were present in seven subjects. Acellular cerebrospinal fluid (CSF) associated with raised protein concentration was detected in three. CONCLUSIONS: Antecedent infectious symptoms, characteristic limitation of ocular movement, areflexia, distal paresthesias, and CSF albuminocytologic dissociation are useful markers for diagnosing AO as well as anti-GQ1b IgG. AO can be considered a mild form of Miller Fisher syndrome or a regional variant of Guillain-Barré syndrome.

Abducens Nerve Diseases↗
PubMed2001

Fe-type nitrile hydratase.

The characteristic features of Fe-type nitrile hydratase (NHase) from Rhodococcus sp. N-771 are described. Through the biochemical analyses, we have found that nitric oxide (NO) regulates the photoreactivity of this enzyme by association with the non-heme iron center and photoinduced dissociation from it. The regulation is realized by a unique structure of the catalytic non-heme iron center composed of post-translationally modified cysteine-sulfinic (Cys-SO2H) and -sulfenic acids (Cys-SOH). To understand the biogenic mechanism and the functional role of these modifications, we constructed an over-expression system of whole NHase and individual subunits in Escherichia coli. The results of the studies on several recombinant NHases have shown that the Cys-SO2H oxidation of alphaC112 is indispensable for the catalytic activity of Fe-type NHase.

Binding Sites↗
PubMed2001

Overlapping Guillain-Barré syndrome and Bickerstaff's brainstem encephalitis associated with anti-GQ1b IgG antibody after herpes simplex virus infection.

Herpes simplex virus (HSV) is a rare, antecedent infectious agent in Guillain-Barré syndrome (GBS). We report a patient with overlapping GBS and Bickerstaff's brainstem encephalitis (BBE). The patient had a vesicular lesion on her nose. Antecedent HSV type 1 (HSV-1) infection was confirmed by isolation of the virus and detection of the presence of serum anti-HSV-1 IgM antibody during the acute phase. Her serum IgG had high anti-GQ1b antibody titer. External ophthalmoplegia has been noted in 2 of 4 reported cases of HSV-associated GBS. Herpetic brainstem encephalitis cases of poor prognosis are known, but only 2 cases of benign brainstem encephalitis secondary to HSV infection, in which there was acute ophthalmoplegia and clinical features consistent with those of BBE have been reported.

Autoantibodies↗
PubMed2001

Anti-GQ1b IgG antibody syndrome: clinical and immunological range.

OBJECTIVES: To clarify the nosological relation among Miller Fisher syndrome (MFS), Guillain-Barré syndrome (GBS) with ophthalmoplegia, Bickerstaff's brain stem encephalitis (BBE), and acute ophthalmoparesis without ataxia. Serum samples from patients with each condition often have anti-GQ1b IgG antibody. METHODS: Information on antecedent illness, initial symptoms, neurological signs during the illness, and CSF findings were reviewed in 194 patients with anti-GQ1b IgG. It was determined whether overlapping MFS and GBS (MFS/GBS), as well as overlapping BBE and GBS (BBE/GBS), is explained by the combined action of anti-GQ1b IgG and anti-GM1 or anti-GD1a IgG, serological markers of GBS. RESULTS: Based on the diagnostic criteria, all the patients with acute ophthalmoparesis, MFS, MFS/GBS, BBE/GBS, and BBE had external ophthalmoplegia; all the patients with MFS, MFS/GBS, or GBS had hyporeflexia or areflexia; and all those with MFS and BBE showed ataxia. Tendon reflexes were decreased or absent in 91% of those with BBE/GBS, 67% of those with BBE, and 53% of those with acute ophthalmoparesis. Ataxia was present in 68% of the patients with MFS/GBS and 45% of those with BBE/GBS. Antecedent illness caused by upper respiratory tract infection had occurred in 60% to 80% of these patients, and CSF albuminocytological dissociation in 25% to 75%. Anti-GM1 or anti-GD1a IgG was present in 50% of those with GBS, 35% of those with MFS/GBS, 27% of those with BBE/GBS, 16% of those with MFS, and 8% of those with BBE. CONCLUSIONS: These findings together with the common autoantibody (anti-GQ1b IgG) suggest that a common autoimmune mechanism functions in the pathogenesis of these illnesses. In a larger study, it was confirmed clinically that MFS, GBS, BBE, and acute ophthalmoparesis are closely related, forming a continuous range. This is supported by the immunological findings. The term "anti-GQ1b IgG antibody syndrome" is not intended to be used as a clinical diagnosis, but recognition of this syndrome is useful for understanding the aetiological relation among the various illnesses and for introducing the established treatments of GBS for use with other conditions.

Adolescent↗
PubMed2001

Animal model of axonal Guillain-Barré syndrome induced by sensitization with GM1 ganglioside.

Some humans develop the axonal form of Guillain-Barré syndrome after receiving bovine brain ganglioside. On sensitization with the ganglioside mixture, all of a group of rabbits injected developed high anti-GM1 IgG antibody titers, flaccid limb weakness of acute onset, and a monophasic illness course. Pathological findings for the peripheral nerves showed predominant Wallerian-like degeneration, with neither lymphocytic infiltration nor demyelination. IgG was deposited on the axons of the anterior roots, and GM1 was proved to be present on the axons of peripheral nerves. Sensitization with purified GM1 also induced axonal neuropathy, indicating that GM1 was the immunogen in the mixture. A model of human axonal Guillain-Barré syndrome has been established that uses inoculation with a bovine brain ganglioside mixture or isolated GM1. This model may help to clarify the molecular pathogenesis of the syndrome and to develop new treatments for it.

Animals↗
PubMed2001

[Pure dysarthria due to pontine infarction].

A 60-year-old man developed dysarthria in the morning. Neurological examination revealed no abnormality except for dysarthria. We diagnosed the patient as having a lacunar infarction. T2-weighted brain MRI revealed hyperintense lesion in the ventrolateral portion of the left upper pontine base. The clinical symptom completely disappeared on day 20. This is the first report on the MRI findings of the patient who showed pure dysarthria, which responsible lesion is in the pontine base. Involvement of corticopontine and corticobulbar tracts were considered to be responsible for the dysarthria in this case. This case may be useful for the somatotopy of corticopontine and corticobulbar tracts with articulation in the pontine base.

Cerebral Infarction↗
PubMed2000

Arginine 56 mutation in the beta subunit of nitrile hydratase: importance of hydrogen bonding to the non-heme iron center.

Arginine 56 in the beta subunit (betaArg56) of the iron-containing nitrile hydratase (NHase), one of the strongly conserved residues within the NHase family, is known to form hydrogen bonds to the sulfinyl (-SO2H) and sulfenyl (-SOH) groups of the post-translationally modified cysteine residues in the catalytic center. BetaArg56 was substituted by tyrosine, glutamate or lysine, respectively, and the respective mutant enzymes generated by reconstitution were characterized. The betaR56K mutant complex exhibited about 1% of the enzymatic activity of native NHase, while the others were totally inactive. The kinetic analysis of the betaR56K mutant complex exhibited a drastic decrease in turnover number and decreases in kinetic constants for substrate and inhibitors as compared to the native NHase. Changes in UV-visible absorption and light-induced Fourier transform infrared difference spectra suggest that betaArg56 is involved in the positioning of the -SO2H and -SOH groups of the modified Cys residues in the catalytic center so as to fine tune the electronic state of the iron center suitable for catalysis. Thus, betaArg56 is essential for catalysis.

Arginine↗