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Biomedical subjects

N Yuki

Publications and source records attributed to N Yuki.

At least 163 records · Page 9Linked to original sources
PubMed1998

[A case of polyneuropathy by microscopic polyarteritis nodosa].

We report a 59-year-old man with chronic sensorimotor polyneuropathy mimicking chronic inflammatory demyelinating polyneuropathy. Sural nerve biopsy revealed marked loss of myelinated fibers and myelin ovoid formation with vasculitis in the epineurium. Renal biopsy was performed subsequently because of the laboratory findings suspecting systemic vasculitis of which consisted CRP positivity, ESR elevation, perinuclear antineutrophil cytoplasmic antibodies (pANCA), and creatinine clearance reduction. The biopsy specimen revealed segmental necrotizing glomerulonephritis with frequent formation of a crescent. These findings confirmed the diagnosis of microscopic polyangitis. Oral administration of prednisolone with additional azathioprine following ethylprednisolone pulse therapy was effective, and pANCA was not detected anymore. We conclude that vasculitic neuropathy has to be considered as a possible cause of polyneuropathy.

Demyelinating Diseases↗
PubMed1997

Prominent sensory ataxia in Guillain-Barré syndrome associated with IgG anti-GD1b antibody.

Sensitization with GD1b has been shown to cause sensory neuropathy in rabbit. A patient with chronic sensory-dominant polyneuropathy who had IgM antibody specifically to GD1b has been reported previously. This report describes the first patient with acute demyelinating polyneuropathy with prominent sensory symptoms who had a high titer of serum IgG anti-GD1b antibody. The serum reacted with neither GM1 nor with other b-series gangliosides (GD2, GD3, GT1b and GQ1b). Improvement in symptoms was coincident with decrease in IgG anti-GD1b antibody titer after plasmapheresis. This case supports the experimental results in rabbit suggesting that anti-GD1b antibody functions in the development of sensory ataxia.

Ataxia↗
PubMed1997

Antibodies to fucogangliosides in neurological diseases.

We examined serum antibodies to 4 species of fucogangliosides: fucosyl-GM1, fucosyl-GD1b, alpha galactosyl (alpha fucosyl) GM1 and alpha galactosyl (alpha fucosyl) GD1b, in 329 patients with various neurologic diseases, 32 patients with non-neurologic autoimmune diseases and 50 healthy persons. Nine patients with Guillain-Barre syndrome, 2 with amyotrophic lateral sclerosis and 2 with cerebral infarction had IgG anti-fucosyl-GM1 antibody. Five patients with Guillain-Barre syndrome, 1 with cerebral infarction and 1 normal control subject had IgM anti-fucosyl-GM1 antibody, 3 of whom also had IgG anti-fucosyl-GM1 antibody. Sixteen of 17 patients who had IgG or IgM antibody to fucosyl-GM1 showed no sensory dysfunction. Yoshino et al. [J. Neurochem. 1993, 61: 658-663] speculated that anti-fucosyl-GM1 antibody functions in the development of sensory neuropathy, but our results do not support this. Two patients with sensory ataxic neuropathy had high IgM antibody titers to fucosyl-GD1b and alpha galactosyl (alpha fucosyl) GD1b. These fucogangliosides may be the target molecules for serum antibodies in some patients with sensory ataxic neuropathy.

Autoantibodies↗
PubMed1997

Association of Campylobacter jejuni serotype with antiganglioside antibody in Guillain-Barré syndrome and Fisher's syndrome.

Using Penner's method and Lior's scheme, we serotyped 31 isolates from patients with Guillain-Barré syndrome, 7 isolates from those with Fisher's syndrome, and isolates from patients with sporadic enteritis. PEN 19 of Campylobacter jejuni was isolated more frequently from the Guillain-Barré syndrome patients (16/31 isolates, 52%) than from the sporadic enteritis patients (5%). LIO 7 of C. jejuni also was isolated more frequently from the Gillain-Barré syndrome patients (14/31 isolates, 45%) than from the enteritis patients (3%). One reason why Guillain-Barré syndrome is rare, despite the high incidence of C. jejuni enteritis, may be the low frequencies of PEN 19 and LIO 7. The frequency of positive anti-GM1 antibody titers in the Guillain-Barré syndrome patients with PEN 19 isolates was higher than that in the Guillain-Barré syndrome and Fisher's syndrome patients without PEN 19 isolates. We speculate that the serotypic determinant of PEN 19 aids in the production of anti-GM1 antibody by a GM1-like lipopolysaccharide. In contrast, 5 of the 7 isolates from the Fisher's syndrome patients belonged to PEN 2:LIO 4. The IgG anti-GQ1b antibody was associated with PEN 2 and LIO 4. These serotypic determinants may aid in the production of IgG anti-GQ1b antibody by a GQ1b-like lipopolysaccharide.

Antibodies↗
PubMed1997

Disease stage of chronic hepatitis C assessed by both peritoneoscopic and histologic findings and its relationship with response to interferon therapy.

BACKGROUND: Disease stage in patients with chronic hepatitis C was assessed by both peritoneoscopy and histology and correlated with responses to interferon therapy. METHODS: The subjects were 105 patients with chronic hepatitis C treated with interferon who were classified into 28 sustained responders, 34 transient responders, and 43 nonresponders according to alanine aminotransferase normalization. The influence of various patient's characteristics on responses to interferon therapy was investigated by multivariate analysis. RESULTS: Patients were categorized into 21 patients who exhibited a "smooth liver" on peritoneoscopy and did not demonstrate histologic bridging fibrosis (group I) and 84 patients who exhibited a "granular" or "nodular liver" on peritoneoscopy and/or had histologic bridging fibrosis (group II). Multivariate analysis showed that genotype 2a/2b (p = .0002), low viremia (p = .0048), and early disease stage (group I) (p = .0290) were significant independent factors contributing to sustained response, and that early disease stage (group I) (p = .0010) and genotype 2a/2b (p = .0085) were those contributing to sustained or transient response. Neither peritoneoscopic nor histologic findings alone were a significant factor influencing responses to interferon therapy. CONCLUSION: Disease stage assessed by both peritoneoscopic and histologic findings may serve as a reliable marker for predicting responses to interferon therapy in chronic hepatitis C.

Adult↗
PubMed1997

Overlap of Guillain-Barre syndrome and Bickerstaff's brainstem encephalitis.

The nosological relationship between Bickerstaff s brainstem encephalitis (BBE) and Guillain-Barre syndrome (GBS) has yet to be clarified. We report results of the autopsy of a patient for whom overlapping BBE and GBS was diagnosed clinically. This and similar cases support the original authors' hypothesis that BBE is closely related to GBS.

Aged↗
PubMed1997

Pathogenesis of the neurotoxicity caused by anti-GD2 antibody therapy.

After treatment of melanomas with anti-GD2 monoclonal antibody (MAb) (14G2a), some patients develop sensorimotor demyelinating polyneuropathy with and without the syndrome of inappropriate antidiuretic hormone (SIADH). To clarify what causes the neurotoxicity of anti-GD2 MAb, we investigated the immunohistochemical localization of GD2 in the human nervous system. Anti-GD2 MAb (14G2a) reacted with the myelin sheaths in the peripheral nerves as well as with the pituicyte cytoplasm in the posterior lobe of the pituitary gland. We assume that the binding of anti-GD2 MAb to peripheral nerve myelin and the pituicytes in the posterior pituitary causes sensorimotor demyelinating neuropathy and SIADH.

Animals↗
PubMed1997

Close association of Guillain-Barré syndrome with antibodies to minor monosialogangliosides GM1b and GM1 alpha.

Cumulative evidence supports the theory that anti-ganglioside antibodies function in the development of Guillain-Barré syndrome (GBS). Some patients have developed GBS after the administration of monosialoganglioside extracted from bovine brain. To clarify the pathogenesis of GBS associated with and without administration of the monosialoganglioside fraction, we investigated serum antibodies to the minor monosialogangliosides GM1b and GM1 alpha in patients with GBS and in control patients. GM1b and GM1 alpha were recognized specifically by the IgG antibody from the GBS patients. Twelve of 20 GBS patients who had high IgG anti-GM1b antibody titers had a preceding gastrointestinal infection. To evaluate the hypothesis that GM1b could be an immunogen, we determined whether a GM1b epitope was present in Campylobacter jejuni isolated from a patient with GBS associated with anti-GM1b antibody. Immunostaining with the monoclonal anti-GM1b antibody indicated that the lipopolysaccharide of the C. jejuni strain has the GM1b epitope. We speculate that an injection of bovine GM1 fraction that contains GM1b, as well as infection by an agent that bears the GM1b epitope, induces production of the anti-GM1b antibody which functions in the development of GBS in some patients.

Animals↗
PubMed1997

Cholinergic neuron-specific ganglioside GQ1b alpha a possible target molecule for serum IgM antibodies in some patients with sensory ataxia.

In neurological diseases the presence of certain anti-glycosphingolipid antibody species is associated with the clinical features. We recently isolated the novel cholinergic neuron-specific gangliosides GQ1b alpha and GT1a alpha from bovine brain. A monoclonal antibody specific for GQ1b alpha and GT1a alpha reacted strongly with the dorsal born of human spinal cord but not with human motor neurons. We investigated the serum antibodies to these minor gangliosides in a number of neurologic diseases and found that 4 patients with sensory ataxic neuropathy had a remarkably high IgM anti-GQ1b alpha antibody titer. GQ1b alpha may be a target molecule for serum IgM antibodies in some patients with sensory ataxic neuropathy.

Animals↗
PubMed1997

Fc portion of intravenous immunoglobulin suppresses the induction of experimental allergic neuritis.

To clarify how intravenous immunoglobulin (IVIg) acts on Guillain-Barré syndrome, we investigated the effects of intact-type IVIg treatment on experimental allergic neuritis (EAN) induced by immunizing with synthetic peptide from bovine P2 protein. Treatment with intact-type IVIg (400 mg/kg/day) on days 0, 7, 14, 15 and 16 after immunization prevented the paralysis, whereas treatment with F(ab')2 failed to alter the clinical course. Intact-type IVIg treatment given on days 0 and 1 showed almost the same efficacy. These results suggest that intact-type IVIg is superior to F(ab')2 in ameliorating the clinical course of EAN and that the Fc portion might affect the immune system.

Animals↗
PubMed1997

Cleavage of viral RNA and inhibition of viral translation by hepatitis C virus RNA-specific hammerhead ribozyme in vitro.

BACKGROUND/AIMS: A hammerhead ribozyme has been used as a new way to suppress specific gene expression. We designed hammerhead ribozymes directed against hepatitis C virus RNA, and investigated their cleavage efficiency and inhibitory effect on viral translation in vitro. METHODS: Three hammerhead ribozymes bearing different cleavage sites in the core region of hepatitis C virus RNA (genotype 1b) were designed in this study. Ribozymes and the target hepatitis C virus RNA were synthesized by in vitro transcription. The cleavage efficiency was evaluated by the ribozyme cleavage assay. The inhibitory effect of the ribozyme on viral translation was further studied by the viral translation inhibition assay. RESULTS: All ribozymes specifically cleaved the target RNA of 1217 bases at a physiological temperature in a dose-dependent manner, with the specific cleavage increasing with a longer incubation period. The target RNA was cleaved most efficiently by the ribozyme with the cleavage site located nearest to the initiation codon. In the viral translation inhibition assay, all ribozymes showed a significant inhibitory effect on viral translation. The ribozyme with the cleavage site located farthest from the initiation codon blocked viral translation most efficiently, and demonstrated almost 70 to 80% inhibition. For ribozymes with the T7 transcription terminator sequence, both the target RNA cleavage and the inhibition of viral translation tended to be achieved less efficiently by ribozymes with T7 terminator than by those without it. CONCLUSIONS: These findings suggest that ribozyme-mediated hepatitis C virus RNA cleavage may serve as a new strategy in the treatment of hepatitis C virus infection.

Hepacivirus↗
PubMed1997

Relation of disease activity during chronic hepatitis C infection to complexity of hypervariable region 1 quasispecies.

We studied the heterogeneity in the E2/NS1 hypervariable region 1 of the hepatitis C virus (HCV) genome in relation to the natural course after infection. The subjects were composed of 38 chronic hepatitis C carriers who had been followed for 9 to 218 months after the onset of non-A, non-B (type C) hepatitis, being tested monthly for serum alanine aminotransferase levels. The complexity of the sequence heterogeneity was assessed by single-strand conformation polymorphism analysis. The quasispecies complexity had no relation to the route of infection, the time from infection and the duration of aminotransferase elevation after the onset. However, it had a significant relationship with the degree of aminotransferase elevation in the course of the disease. The quasispecies complexity was directly correlated with the first peak of serum aminotransferase at the onset (r = .48, P < .01) and the mean aminotransferase levels during the period of persistent aminotransferase elevation (r = .58, P < .01). Twenty-three of the 38 patients were further followed for 24 months with biweekly alanine transaminase (ALT) tests. Their aminotransferase levels remained within the normal range during follow-up, and no significant change was seen in the quasispecies complexity after this asymptomatic period. However among the 23 patients, the quasispecies complexity increased in six cases (26%) and decreased in five (22%). A significant direct relation was seen between changes in the quasispecies complexity and the mean aminotransferase levels during the asymptomatic period (r = .55, P = .01). These findings suggest that the development of the HCV quasispecies nature may be related to the severity of the hepatitis in the course of infection.

Adult↗
PubMed1997

Molecular mimicry between gangliosides and lipopolysaccharides of Campylobacter jejuni isolated from patients with Guillain-Barré syndrome and Miller Fisher syndrome.

Some patients developed Guillain-Barré syndrome (GBS) after being given bovine gangliosides. Patients with GBS subsequent to Campylobacter jejuni enteritis frequently have IgG antibody to GM1 ganglioside. Miller Fisher syndrome (MFS), a variant of GBS, is associated with IgG antibody to GQ1b ganglioside. The existence of molecular mimicry between GM1 and lipopolysaccharide of C. jejuni isolated from a GBS patient and that between GQ1b and C. jejuni lipopolysaccharides from patients with MFS are shown herein. The molecular mimicry between infectious agents and gangliosides may function in the production of anti-ganglioside antibodies and the development of GBS and MFS.

Antibodies, Bacterial↗
PubMed1997

Ability to remove immunoglobulins and antiganglioside antibodies by double filtration plasmapheresis in Guillain-Barré syndrome: is it equivalent to plasma exchange?

The value of plasma exchange (PE) in Guillain-Barré syndrome (GBS) is well established. In Japan, patients with GBS and related diseases often receive double filtration plasmapheresis (DFPP) as well as PE. No comparative trials between PE and DFPP, however, have been conducted. We compared their abilities to remove immunoglobulins and antiganglioside antibodies to find out whether DFPP is equivalent to PE. The ability to remove immunoglobulins and antiganglioside antibodies was compared between PE and DFPP using plasma samples from 41 patients with GBS and related diseases before and after each treatment session. The ability of DFPP to remove both IgGs and antiganglioside IgG antibodies were significantly inferior to those of PE. There is a less theoretical basis for selecting DFPP as the first choice of plasmapheresis for GBS and related disorders.

Aged↗
PubMed1997

Two patients with acute Guillain-Barré syndrome treated with different apheresis methods.

We treated 2 patients with severe acute Guillain-Barré syndrome (GBS) with different apheresis methods. Sera from these patients in the acute phase contained a high titer of immunoglobulin (Ig)G anti-GM1 ganglioside antibody. One was a 57-year-old female treated with immunoadsorption (IA). IgG anti-GM1 antibody titer was reduced from 1:102,400 to 1:6,400 measured by ELISA after 1 month. However, her residual deficit was severe. The other patient was a 43-year-old male treated with plasma exchange (PE). IgG anti-GM1 antibody was reduced from 1:3,200 to 1:400 after 1 session of PE. After 1 month, he could walk independently. The better prognosis of the latter was possibly because of the patient's younger age and the plasma exchange that might have reduced such pathogenic factors as antiganglioside antibodies at the early stage of GBS.

Acute Disease↗
PubMed1997

Comparison of the adsorption ability between tryptophan and modified tryptophan columns.

Immunoadsorption therapy (IAT) using the tryptophan column (TR:TR-350, Asahi Medical Co., Tokyo, Japan) is used for patients with Guillain-Barré syndrome or Fisher's syndrome. Recently, a modified tryptophan column (modified TR:TR-350S, Asahi) was developed to reduce adsorption of fibrinogens. However, it is not clear whether the new column can effectively adsorb the antiganglioside antibodies. We treated 2 patients with Guillain-Barré syndrome, 1 patient with Fisher's syndrome, and 1 patient with Bickerstaff's brainstem encephalitis by IAT using the TR and the modified TR. Samples were taken from the inlet and outlet of the affinity column. We compared the adsorption ability of antiganglioside antibodies between the TR and modified TR. The modified TR adsorbed antiganglioside antibodies less effectively than the TR. No significant bleeding was observed in the patients during each session. Furthermore, results of the clinical study were confirmed by batchwise adsorption test. We propose that the modified TR should not be used for treating patients with Guillain-Barré syndrome and related disorders.

Adsorption↗
PubMed1997

Hepatitis C virus replicative levels and efficiency of genotyping by specific PCR and antibody assay.

We studied factors which influence the detection of hepatitis C virus genotypes by the group-specific PCR of the sequence within the core region gene and by the newly developed genotype-specific NS4 antibody assay. Genotyping was performed on 75 hepatitis C virus carriers in Japan, where patients with hepatitis C viremia are exclusively infected with genotype 1b, 2a, and 2b. PCR failed to identify genotypes in 8 (11%) patients, whereas 12 (16%) patients, including the 8 patients mentioned above, could not be genotyped by the serological assay. Serological genotypes showed almost complete agreement with those found by the PCR except that double infection was revealed in only two of the eight patients serologically judged to be coinfected with genotypes 1 and 2. In each assay, disease activity and levels of viremia assessed by a competitive reverse transcription PCR assay were significantly lower in patients infected with untypeable isolates than in those infected with typeable ones (P < 0.01). The PCR could identify the genotypes of isolates from all 64 patients with levels of viremia of > or = 10(6) copies/ml, and the genotype-specific antibody responses were found in 60 (94%) patients. In contrast, isolates from only 3 (27%) of 11 patients with low levels of viremia (< 10(6) copies/ml) could be genotyped by the PCR (P < 0.00001), and these patients showed the genotype-specific antibody responses (P < 0.00001). These findings suggest that low levels of hepatitis C virus replication may reduce the efficiency of genotyping by serological assay as well as by PCR.

Adult↗