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Biomedical subjects

N Yuki

Publications and source records attributed to N Yuki.

At least 181 records · Page 10Linked to original sources
PubMed1997

Early administration of Bifidobacterium breve to preterm infants: randomised controlled trial.

AIM: To investigate the colonisation with Bifidobacterium breve of the bowels of very low birthweight (VLBW) infants. METHODS: The adverse effects of B breve were examined in 66 VLBW infants (preliminary study). A prospective randomised clinical study of 91 VLBW infants was also completed and these infants were followed up for three years. Precise viable bacterial counts of serial stool specimens were examined for the first eight weeks after birth in 10 infants. The colonisation rates of administered bacteria were examined using immunohistochemical staining of stool specimens with a B breve specific monoclonal antibody. RESULTS: In the preliminary study there were no side effects attributable to the bacteria. Immunohistochemical staining of stool specimens showed that the colonisation rates of the administered bacteria were 73% at 2 weeks of age, but only 12% in the control group. Early administration of B breve significantly decreased aspirated air volume from the stomach and improved weight gain. CONCLUSIONS: B breve can colonise the immature bowel very effectively and is associated with fewer abnormal abdominal signs and better weight gain in VLBW infants, probably as a result of stabilisation of their intestinal flora and accelerated feeding schedules.

Bifidobacterium↗
PubMed1997

[A case of Guillain-Barré syndrome after the travel in southeast Asia--isolation of Campylobacter jejuni PEN 5 serotype].

A 57-year-old man, while on travel in Malaysia, suffered from diarrhea after he ate fruits. He developed limbs weakness without sensory disturbance after his return to Japan. Serum from the patient had high IgG anti-GM1 antibody titer. Campylobacter jejuni was isolated from his stool. The serotype belonged to PEN 5. The patient received double-filtration plasmapheresis 7 times during from days 6 to 17. Muscle strength began to recover gradually on day 10, and returned to normal 5 months after the onset of neurologic symptoms. Repeated neurophysiologic studies indicated that the axonal degeneration of motor nerves was predominant process. This case suggests that Guillain-Barré syndrome is a complication of traveler's diarrhea.

Campylobacter Infections↗
PubMed1997

[Guillain-Barré syndrome with high titers of anti-GM2 and anti-GalNAc-GD1a antibody following cytomegalovirus hepatitis].

A 28-year-old housewife developed motor and sensory neuropathy in both limbs with facial nerve paralysis and decreased taste sensation, two weeks after cough and sore throat with slight fever. On laboratory examination, mild increase of transaminases was found. Enzyme-linked immunosorbent assay showed that the serum had markedly high titers of IgG antibodies to GM2 (1:3,200) and Ga1NAc-GD1a (1:1,600). Serum IgM-EIA index and CF titer of cytomegalovirus were markedly high. In cerebrospinal fluid examination, protein was increased (110 mg/dl). Blink reflex indicated involvement of bilateral facial nerves. In limb motor and sensory nerves, conduction studies revealed the presence of both axonal degeneration and segmental demyelination. The diagnosis of Guillain-Barré syndrome (GBS) with facial nerve paralysis, relatively unique to CMV infection, was made. In the fourth week following the initial neurologic symptom, weakness in facial and limb muscles and sensory disturbances in both limbs were gradually improved. In about three months, conduction studies of limb nerves and CSF protein were normalized. During the clinical course above, the titers of antibodies to GM2 and Ga1NAc-GD1a, IgM-EIA index and the titer of CF of CMV were significantly decreased. Anti-GM2 antibody was reported to be found in the sera from the patient of GBS associated with CMV infection. However, there is no report of GBS patient with CMV infection whose serum showed the presence of both anti-GM2 and anti-Ga1NAc-GD1a antibodies. In this patient, antibodies to CMV, GM2 and Ga1NAc-GD1a epitopes and other unexamined or/and unknown epitopes may be related to the neuropathy. The studies of the specific antibody to react with facial nerve in the serum from GBS patients with facial nerve paralysis and the molecular mimicry between the specific ganglioside and the structure of CMV are warranted in future.

Acetylgalactosamine↗
PubMed1997

[Axonal Guillain-Barré syndrome associated with antibodies to Ga1NAc-GD1a and unidentified acidic glycolipids].

A 19-year-old male student with Guillain-Barré syndrome (GBS) was described. Neurologic examination revealed severe and moderate degrees of weakness in the distal and proximal muscles, respectively, in both upper and lower limbs. He was unable to walk even with support. Both superficial and deep sensations were normal. Serial electrophysiologic studies indicated that the predominant pathologic process of the peripheral nerve was axonal degeneration of motor nerves. Enzyme-linked immunosorbent assay showed that serum from the patient had markedly high titer of IgG antibody to Ga1NAc-GD1a (1:204,800). Thin-layer chromatography with immunostaining revealed that his serum IgG strongly reacted with Ga1NAc-GD1a prepared from both bovine brain and cauda equina, and additionally with unidentified acidic glycolipids prepared only from bovine cauda equina. Serum containing antibody to Ga1 NAc-GD1a and the unidentified acidic glycolipids may be responsible for axonal degeneration of motor nerves in this patient.

Acetylgalactosamine↗
PubMed1997

[A case of chronic inflammatory demyelinating neuropathy associated with antibodies to gangliosides GM1 and GalNAc-GD1a].

In January 1993, a 43-year-old man was admitted to our hospital for left wrist-drop. Neurological examinations revealed asymmetrical distal weakness in the upper limbs. Deep tendon reflexes were normal in all 4 limbs. Sensory and autonomic nervous functions were intact. CSF examinations were within normal limits. Thin-layer chromatography with immunostaining revealed serum antibodies that reacted with GM1 and GalNAc-GD1a. Motor nerve conduction studies revealed abnormal temporal dispersion, and a low amplitude of compound muscle action potential in the left radial nerve. Neurological symptoms gradually improved with prednisolone over one and a half years. He was hospitalized again in January 1995, because of right wrist-drop and slight sensory loss of the limbs. Those findings were improved by methylprednisolone (1,000 mg/day) for 3 days. The interval until maximal disability in this patient was more than one month for each admission. This case must belong to inflammatory demyelinating neuropathy.

Acetylgalactosamine↗
PubMed1997

[Removal ability of immunoglobulins in plasma exchange and double-filtration plasmapheresis].

The value of plasma exchange (PE) in Guillain-Barré syndrome (GBS) is well established. Although no controlled trial has reported on the effect of double-filtration plasmapheresis(DFPP), neurologist in Japan often treat the GBS patients using DFPP. The therapeutic effect probably relates to the removal of circulating factors, which are immunoglobulins. We compared removal ability of immunoglobulins between PE and DFPP. IgG was less effectively removed by DFPP than by PE. We suggest that PE is more beneficial treatment for GBS than DFPP.

Adult↗
PubMed1997

[Association of IgA anti-GM1 antibody with antecedent diarrhea in patients with Guillain-Barré syndrome].

IgA has an important role in the gastrointestinal immune system. We investigated IgA anti-GM1 antibodies in Guillain-Barré syndrome (GBS) subsequent to diarrhea. IgA anti-GM1 antibodies were detected more often in GBS patients with a history of antecedent diarrhea than in those without that. Between the GBS patients with a history of prior symptoms of upper respiratory tract infections and those without that, we found no difference of the frequency of increased IgA anti-GM1 antibody titers. Six GBS patients who had antecedent symptoms of upper respiratory tract infections had IgA anti-GM1 antibodies. However, 5 patients of them also had a history of antecedent diarrhea. Our findings show that IgA anti-GM1 antibodies are associated with GBS following diarrhea.

Autoantibodies↗
PubMed1997

[Removal ability of anti-ganglioside antibodies in immunoadsorption using a modified tryptophan-immobilized column].

Guillain-Barré syndrome (GBS) patients are often treated by immunoadsorption using a tryptophan-immobilized column (TR) in Japan. To reduce adsorption of fibrinogens, a modified TR (TR-S) was developed. In this study, we compared removal ability of antiganglioside antibodies among TR-S, TR and a phenylalanine-immobilized column (PH). We selected the plasma samples that had high antiganglioside antibody titers from 49 patients with GBS or related disorders. Before and after each immunoadsorption, samples were longitudinally taken from the inlet and outlet of the affinity column. Plasma anti-ganglioside antibody titers were tested by ELISA. TR-S adsorbed anti-ganglioside antibodies less effectively than the TR and PH. Despite of reduction in plasma fibrinogen, no significant bleeding was observed in the patients during each session. We therefore assumed that the TR-S should not be used for GBS and related disorders.

Autoantibodies↗
PubMed1997

[No association between IgG anti-GTla antibody and bulbar palsy in Guillain-Barré and Fisher's syndromes].

Pharyngeal-cervical-brachial weakness (PCB) is a rare variant of Guillain-Barré syndrome (GBS) and shows a regional muscle weakness, specially in oropharynx. Mizoguchi et al. (1994) reported a GBS patient with PCB-like symptoms who had serum IgG anti-GTla antibodies in the acute phase of illness. We therefore assumed that bulbar palsy was associated with anti-GTla antibodies and made serological study in patients with GBS or Fisher's syndrome. The frequency of positive IgG anti-GTla antibody was significantly higher in patients with bulbar palsy than those without bulbar palsy. Most of the patients with IgG anti-GTla antibodies, however, had also anti-GQlb antibodies in their sera and anti-GTla antibodies were more closely associated with ophthalmoplegia than with bulbar palsy. These findings do not support that IgG anti-GTla antibodies play an important role in the pathogenesis of bulbar palsy in GBS.

Autoantibodies↗
PubMed1996

Hepatitis C biochemical remission and viral replication in haemodialysis patients.

The natural course of non-A, non-B (type C) hepatitis was studied in 62 haemodialysis patients. From the onset of the disease, serum alanine aminotransferase levels were monitored monthly for 9-218 mon (median 115). After fluctuation of aminotransferase levels for 1-206 mon (median 39), 57 (92%) patients showed normalization of these levels lasting until the end of the follow-up, which was for > 2 yr in 31 (50%) cases and for > 5 yr in 15 (24%) cases. At the end of follow-up, hepatitis C viraemia was assessed by reverse transcription-polymerase chain reaction (RT-PCR) and branched DNA (bDNA) assay. Viraemic levels were significantly lower in the 15 patients with normal aminotransferase for > 5 yr (median RT-PCR + ve/bDNA-ve, range RT-PCR-ve to 10(6.7) Eq/mL) than in the 47 cases with normal levels for < 5 yr (median 10(6.6), range RT-PCR + ve/bDNA-ve to 10(7.6) Eq/mL) (P < 0.01). Moreover, a significant inverse relation was observed between viraemic levels and the duration of aminotransferase normalization (r = -0.46, P < 0.01). These findings indicate that biochemical remission of hepatitis C may be frequent in haemodialysis patients and may be related to viral attenuation.

Adult↗
PubMed1996

Acute paresis of extraocular muscles associated with IgG anti-GQ1b antibody.

There have been several case reports of acute ophthalmoparesis without ataxia subsequent to infection or immunization. The nosological position and therapy for acute ophthalmoparesis have yet to be established. Sera from patients are reported to have IgG anti-GQ1b antibody, which is frequently found in sera from patients with Fisher's syndrome. To establish the etiology of acute ophthalmoparesis, I tested sera from 8 patients with acute ophthalmoparesis for anti-GQ1b antibody. High IgG anti-GQ1b antibody titers were present in sera from patients in the acute phase of the illness. I describe the successful treatment with plasmapheresis and intravenous immunoglobulin. Some cases of acute ophthalmoparesis following infection or immunization may be categorized as an auto-immune disease related to Fisher's syndrome.

Acute Disease↗
PubMed1996

Persistent increased threshold of electrical stimulation selective to motor nerve in multifocal motor neuropathy.

In multifocal motor neuropathy (MMN) the threshold of electrical stimulation showed a persistent, marked increase for the motor nerve which decreased after treatment with intravenous immunoglobulin or oral cyclophosphamide; whereas, the threshold was normal for the sensory nerve. This discrepancy of the thresholds for motor and sensory nerves indicates that the increased threshold for motor nerve is not caused by change in perineural capacitance, such as subperi- and endoneural edema or perineural thickening. Inching studies showed that the site of the elevated motor nerve threshold was closely associated with conduction slowing and block. For the cause of the increased threshold, therefore, we suppose the presence of a factor which interferes with reorganization of the nodal property in the remyelinative process or which directly blocks sodium channels where the blood-nerve barrier is impaired in MMN.

Action Potentials↗
PubMed1996

Autoantibodies to peripheral nerve glycosphingolipids SPG, SLPG, and SGPG in Guillain-Barré syndrome and chronic inflammatory demyelinating polyneuropathy.

Unlike CNS myelin, human peripheral nerve myelin has the acidic glycosphingolipids sialosyl paragloboside (SPG), sialosyl lactosaminyl paragloboside (SLPG), and sulfated glucuronyl paragloboside (SGPG). To elucidate the pathogenesis of Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating neuropathy (CIDP), we investigated the autoantibodies to peripheral nerve molecules in patients with these diseases and compared the frequency of the autoantibodies with that of autoantibody to GM1 which is present in both the CNS and PNS. The report of Sheikh et al. (Ann. Neurol. 1995; 38: 350) that Campylobacter jejuni bears the SGPG epitope led us to study whether sera from patients with GBS subsequent to C. jejuni enteritis have anti-SGPG antibody; but, high anti-SGPG antibody titers were not found in the GBS patients from whom C. jejuni was isolated. Although the frequency of the anti-SPG, anti-SLPG and anti-SGPG antibodies were lower than that of the anti-GM1 antibody in GBS, 5 patients with demyelinating GBS had high IgG anti-SPG antibody titers. IgG anti-SPG antibody may function in the development of demyelinating GBS. We found that 6 CIDP patients had elevated IgM anti-SGPG antibody titers. Immunoelectrophoresis failed to detect IgM M-protein in 3 of the patients. IgM anti-SGPG antibody could be a diagnostic marker for a subgroup of CIDP with or without paraprotein.

Aged↗
PubMed1996

Antibody to GalNAc-GD1a and GalNAc-GM1b in Guillain-Barré syndrome subsequent to Campylobacter jejuni enteritis.

N-Acetylgalactosaminyl GD1a (GalNAc-GD1a) is a proposed target molecule for serum antibody in some patients with Guillain-Barré syndrome (GBS) (Kusunoki et al., 1994). We examined autoantibody to GalNAc-GD1a in sera from 58 GBS patients. Eight GBS patients had high IgG anti-GalNAc-GD1a antibody titers, 3 of whom also had high IgM anti-GalNAc-GD1a antibody titers. These 8 patients had experienced gastrointestinal infection before the onset of their neurological symptoms. Campylobacter jejuni was isolated from 4 of them. An absorption test indicated the presence of the GalNAc-GD1a epitope in lipopolysaccharides of C. jejuni. Sera that had anti-GalNAc-GD1a antibody reacted with several acidic glycolipids in bovine peripheral nerve, one of which was identified as N-acetylgalactosaminyl GM1b (GalNAc-GM1b). Serum binding to GalNAc-GM1b was decreased by absorption with GalNAc-GD1a. The presence of GalNAc-GM1b as well as GalNAc-GD1a has been reported in human peripheral nerves. We assume that C. jejuni, which bears the [GalNAc beta 1-4 (NeuAc alpha 2-3) Gal beta 1-3 GalNAc beta 1-] epitope, is the immunogen and that the glycoconjugates with the epitope are target molecules for the autoantibody in peripheral nerves of some GBS patients.

Animals↗
PubMed1996

Quantitative analysis of antibody to hepatitis C virus envelope 2 glycoprotein in patients with chronic hepatitis C virus infection.

The significance of circulating antibody to hepatitis C virus (HCV) envelope glycoprotein 2 (E2)/nonstructural protein 1 (NS1) glycoprotein was studied in 83 patients with chronic HCV infection diagnosed by polymerase chain reaction (PCR). E2/NS1 antibody was quantitatively examined by a passive hemagglutination test using recombinant E2/NS1 glycoprotein encompassing amino acids 388 to 664 of the HCV-H strain. The results were correlated with clinical and virological features such as genotypes and viremic levels assessed by a competitive reverse-transcription PCR assay. E2/NS1 antibody was found in 73 patients (88%), and its occurrence was related to viremic levels. E2/NS1 antibody titers were low in asymptomatic HCV carriers with low levels of viral replication; 9 of 17 such patients tested positive for E2/NS1 antibody (53%), compared with 64 of 66 chronic hepatitis C patients (97%) (P < .01). A significant direct relationship was observed between viremic levels and E2/NS1 antibody titers (r = .52, P < .01). Of the 13 patients with low viremic levels of < 10(6) copies/mL, only 5 tested positive for E2/NS1 antibody (38%), whereas 68 of the 70 patients with viremic levels of > or = 10(6) copies/mL had it (97%) (P < .01). As for the relation to HCV genotypes, no difference was seen in E2/NS1 antibody titers among genotypes examined (1b, 2a, and 2b). These findings suggest that the E2/NS1 antibody tested exhibits no neutralizing activity in chronic HCV infection but may serve as a serological indicator of active virus replication.

Adult↗