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Biomedical subjects

K Kamakura

Publications and source records attributed to K Kamakura.

At least 55 records · Page 3Linked to original sources
PubMed1998

Alzheimer's disease with asymmetric parietal lobe atrophy: a case report.

A 52-year-old, right-handed female presented with visuospatial dysfunction including left hemineglect, incomplete Balint's syndrome, and environmental agnosia, together with left-sided motor symptoms such as unskillful movement, dystonic postures, and myoclonus in the left hand, without significant dementia. Symptoms progressed to akinetic mutism prior to her death 10 years after onset of illness. Imaging studies such as MRI, SPECT, and PET studies showed severe, predominantly right-sided involvement of parietal and parieto-occipital areas. The motor signs might originate from the right parietal lesions such as area five or somatosensory area. Neuropathologic studies including immunocytochemistry showed tau-positive neurofibrillary tangles and abundant neuritic plaques with amyloid deposits, confirming the diagnosis of Alzheimer's disease. An analysis of serum apolipoprotein E revealed epsilon3/epsilon3 homozygosity. This case represents a variant of Alzheimer's disease conspicuous for progressive motor signs and visuospatial dysfunction with a striking laterality, reflecting asymmetric parietal involvement. Alzheimer's disease with asymmetric parietal atrophy is difficult to be clinically distinguished from corticobasal degeneration characterized by progressive unilateral motor signs and focal cortical signs.

Agnosia↗
PubMed1998

Lectin-gradient gel affinity electrophoresis of glycoproteins.

Lectin-gradient agarose gel affinity electrophoresis was developed for identification of glycoforms of glycoproteins in lectin affinity electrophoresis. Gradation of lectin was done by stacking agarose gel blocks with increasing concentrations of lectin (discontinuous system) and by keeping the plate in a moist chamber at 4 degrees C overnight (continuous system) before electrophoresis. On the visualization of separated glycoform lines, the antibody-affinity blotting was superior for low concentrations of alpha-fetoprotein. Fluoresceine isothiocyanate (FITC) labeling of whole serum proteins, enzyme activity staining for alkaline phosphatase, and prestaining for lipoproteins were also applicable for visualization of proteins at higher concentrations. The conventional Western blotting can not be recommended because of the competition between lectin and glycoproteins in binding to nitrocellulose membrane. Lectin-gradient affinity electrophoresis also had a wide application for optimization of the condition of lectin affinity electrophoresis.

Adult↗
PubMed1998

Lectin-dependent modulation of interaction between human alpha-fetoprotein and its monoclonal antibodies. Epitope mapping.

The effect of lentil lectin (LCA) on the binding of mouse monoclonal antibody (MoAb) against human alpha-fetoprotein (AFP) to LCA-nonreactive AFP-L1 and LCA-reactive AFP-L3 was studied on a panel of 30 MoAbs provided by the TD-2 Workshop of ISOBM for epitope mapping. LCA inhibited the binding of MoAbs 93 and 98 to AFP-L3 but not to AFP-L1, indicating that there was a competition between the MoAbs and LCA for the AFP sugar chain. With MoAbs 100, 109, 118, and 120, LCA rather increased the binding to AFP-L3 over that to AFP-L1. These modulating effects of LCA on the MoAb binding to AFP-L3 were abolished by periodate treatment of the AFP preparations without affecting the binding of MoAb to AFP. Concanavalin A had similar inhibiting and enhancing effects on MoAb binding, but equally to AFP-L1 and AFP-L3, both of which are fully reactive with concanavalin A. The results suggested that MoAbs 93 and 98 recognized epitopes closely related to sugar chain, and their binding to AFP-L3 was inhibited by the bound LCA due to steric hindrance. The enhanced binding of some MoAbs to AFP-L3 over AFP-L1 with LCA, or both glycoforms of AFP with concanavalin A, may be explained by postulating an allosteric mechanism mediated by the oligosaccharide-lectin interaction.

Animals↗
PubMed1998

Serum alpha-fetoprotein levels in healthy Japanese adults.

With advances in lectin affinity electrophoresis of alpha-fetoprotein (AFP), the detection of significant changes in serum AFP at low levels in cirrhotics has become important for early detection of hepatocellular carcinoma. Serum AFP levels of 616 healthy individuals without abnormal liver function tests or virus markers of hepatitis B and C were determined by enzyme immunoassay with IMx-AFP Dainapack using automated IMx apparatus set at twice the ordinary sensitivity and compared with those of 241 individuals with abnormal liver function tests and/or positive hepatitis virus markers. The coefficient of variation in this assay was less than 10% at AFP levels as low as 0.2 ng/ml with a lower detection limit of 0.1 ng/ml. The AFP level of healthy population showed a Gaussian distribution curve after logarithmic transformation with a median and 2.5-97.5 percentile reference range of 2.2 (0.6-5.6) ng/ml. There was no significant difference in the AFP level between males and females. Individuals with abnormal liver function tests alone showed no significant increase in serum AFP unless they were associated with positive hepatitis virus markers.

Adult↗
PubMed1998

[A qualitative analytical method for nonpermitted food colors by HPLC].

The Ministry of Health and Welfare has been proposed an analytical method for food colors by HPLC. Conditions in the method and modified conditions of the proposed method were applied for permitted and nonpermitted food colors, and relative retention times were obtained. The relative retention times would be a clue of the confirmation of these nonpermitted colors by other method.

Chromatography, High Pressure Liquid↗
PubMed1997

AMPA receptor-mediated slow neuronal death in the rat spinal cord induced by long-term blockade of glutamate transporters with THA.

Excitotoxicity secondary to the loss of glutamate transporters (GluT) has been proposed as a possible pathogenetic mechanism for neuronal degeneration in amyotrophic lateral sclerosis. We therefore investigated whether prolonged in vivo pharmacologic inhibition of GluT would result in neuronal damage in the rat. DL-Threo-beta-hydroxyaspartate (THA), a potent GluT inhibitor, and glutamate were continuously infused into the rat spinal subarachnoid space by using a mini-osmotic pump. Animals that received both THA and glutamate, but not those received either singly, displayed tail paralysis with or without hind-limb paralysis and urinary incontinence after the third postoperative day. Pathologically, symptomatic animals exhibited neuronal loss with a variable extent of gliosis preferentially involving the dorsal horn of the lumbosacral cord. In the rostral spinal segments adjacent to those regions of intense pathologic changes, small neurons in the dorsal horn were selectively destroyed, a pattern similar to the late-onset neuronal damage induced by continuous intrathecal administration of 1-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid (AMPA) [R. Nakamura et al., Brain Res. 654 (1994) 279-285]. These behavioral and pathologic changes were blocked by 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), suggesting that pharmacologic blockade of GluT causes selective neuronal damage in vivo by AMPA receptor activation.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1997

Painful small-fibre multifocal mononeuropathy and local myositis following influenza B infection.

A 47-year-old man experienced multifocal mononeuropathy and putative ganglionopathy associated with influenza B infection, characterized by aching and dysesthesia in the right arm and left leg with normal deep sense. He displayed muscle atrophy in the affected limbs, which might have resulted from local myositis or a disorder similar to neuralgic amyotrophy. Sural nerve biopsy revealed a severe loss of unmyelinated and thinly myelinated fibres, consistent with a small fibre neuropathy, without evidence of angiopathy or inflammation. We could not detect any other cause of the neuropathy except influenza B. In this case, it may be inferred that small-diameter neurons in the dorsal root ganglia and thinly- or nonmyelinated fibres were selectively involved through a post-infectious immune process. To our knowledge, small fibre neuropathy following influenza B has never been reported.

Humans↗
PubMed1997

Atypical MRI features of Wilson's disease: high signal in globus pallidus on T1-weighted images.

Most reports of MRI in Wilson's disease have been of abnormal low-signal lesions on T1-weighted images and high signal intensity on T2-weighted images. In contrast, we report three patients who had high-signal lesions in the globus pallidus on T1-weighted images, a finding seen in patients with portal-systemic encephalopathy. The possible causes include the paramagnetic effect of copper or iron and accumulation of Alzheimer type II glial cells.

Adult↗
PubMed1997

Concentration-dependent changes in motor behavior produced by continuous intrathecal infusion of excitatory amino acids in the rat spinal cord.

A growing body of evidence has suggested that glutamate receptors mediate selective degeneration of neurons in the central nervous system during the development of neurodegenerative diseases. Glutamate receptors are divided into N-methyl-D-aspartate (NMDA)-type and non-NMDA-type. Neurotoxicity mediated by the latter has attracted much interest as a possible causative mechanism underlying amyotrophic lateral sclerosis (ALS). As the clinical course of ALS is chronic and progressive, investigation of chronic effects of non-NMDA receptor agonists on neuronal function would be useful for evaluating the role of glutamate receptor-mediated neurotoxicity in ALS. However, chronic non-NMDA receptor-mediated neurotoxicity has been investigated less thoroughly than acute neurotoxicity. We infused an aqueous solution of R,S-alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) intrathecally and continuously by an osmotic minipump in rats. This method of continuous infusion enabled us to keep the drug concentration relatively constant in the cerebrospinal fluid surrounding the spinal cord. The present method of AMPA administration is more suitable for investigating ALS pathogenesis than acute injections, in view of the gradual progression of the disease and the selectivity of lesions produced.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1997

[A case of Sjögren's syndrome with a high titer of anticardiolipin antibody that developed as parkinsonism].

A 50-year-old-male consulted us, complaining of gait disturbance. He was diagnosed as having Parkinson syndrome, but had no benefit of drugs for Parkinson disease. On admission he showed symptoms of parkinsonism such as parkinsonian gait, bradykinesia and muscle rigidity, and recurrent aseptic meningitis. Additionally, his condition was complicated by Sjögren's syndrome, based on the preliminary criteria of Sjögren's syndrome established by the European Community. Because his parkinsonism and meningitis were considered to be caused by Sjögren's syndrome, he was administered corticosteroids, which improved his parkinsonism and aseptic meningitis. The brain MR images in our case did not match those typically reported in cases of central nervous system Sjögren's syndrome (CNS-SS). Although the most common abnormalities are small distinct areas of increased signal intensity on T2-weighted images, the MR images in our case revealed periventricular diffuse areas of increased signal intensity on T2-weighted images. Although his parkinsonism and aseptic meningitis are believed to the effects of vasculitis caused by Sjögren's syndrome, it is also possible that his parkinsonism is related to Binswanger's disease resulting from a high titer of anticardiolipin antibody. Our report proposes a possible relationship between anticardiolipin antibody and CNS-SS when MR images reveal diffuse high intensity areas on T2-weighted images.

Antibodies, Anticardiolipin↗
PubMed1997

[A Japanese family with paroxysmal dystonic choreoathetosis].

We present the first report of Japanese family with paroxysmal dystonic choreoathetosis (PDC). At least seventeen individuals of this family in six generations were affected by PDC by autosomal dominant inheritance. The affected individuals had attacks of choreoathetosis/dystonia-like involuntary movements without loss of consciousness. These attacks were precipitated by stress, caffeine, menstruation or ovulation, but not by sudden voluntary movements, which are common precipitating factors in paroxysmal kinesigenic choreoathetosis (PKC). MRI studies of the brain revealed no abnormalities. Some of the family members received clonazepam, or garlic with significant therapeutic effects, while one female case improved after hysterectomy. The pathogenesis of PDC remains unknown, but it could be attributed to a form of channelopathy. Recently, two linkage studies were reported and the PDC locus was identified on chromosome 2q, which may lead to clarify the PDC gene. The family described here may be important for the future biochemical and genetic analyses. We also suspect that PDC may relate to endocrinological abnormalities besides channelopathy.

Adolescent↗
PubMed1995

Magnetic resonance imaging of multiple brain abscesses of the bilateral basal ganglia.

A 64-year-old woman developed multiple brain abscesses of the basal ganglia associated with Klebsiella pneumoniae septicemia. Magnetic resonance (MR) images showed three different stages of the brain abscesses. The images of early cerebritis of this site mimicked lacunar infarctions or dilated Virchow-Robin spaces. The differentiation of the brain abscess from lacunae and dilated Virchow-Robin spaces is discussed, together with the evolution of the brain abscesses on MR images.

Basal Ganglia↗
PubMed1995

[Myotonin protein kinase].

The mutation underlying myotonic dystrophy is the expansion of polymorphic CTG repeat in the 3'-noncoding region of the myotonin protein kinase (MtPK) gene mapping to chromosome 19q13.3. A full-length cDNA of human MtPK was cloned and expressed in COS-1 cells. MtPK is recovered from the COS cell extract as a 70 kDa protein, which coincides with the size deduced from the predicted amino acid sequence. Biochemical characteristics of MtPK expressed in COS cells and its expression are investigated.

Chromosomes, Human, Pair 19↗
PubMed1994

Late-onset selective neuronal damage in the rat spinal cord induced by continuous intrathecal administration of AMPA.

Neurotoxicity mediated by 1-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) was investigated by infusing this agent continuously for 7 days intrathecally to adult rats using a mini-osmotic pump. Behavioral changes were apparent only after the second postoperative day, when the rats displayed hindlimb palsy or incontinence of urine. The behavioral deficits became progressively severe and the rats usually displayed both hindlimb paraplegia and incontinence of urine by the 7th postoperative day. These progressive behavioral deficits were induced in a dose-dependent manner in the rats that received AMPA at a dose of > 100 pmol/h (100 microM at 1 microliter/h, 17 nmol in total dose). The severity of behavioral deficits was in parallel with that of neuropathological changes in the lumbosacral cords. In spinal segments rostrally adjacent to those with severe pathological changes, only the neurons in the dorsal horns (Rexed's laminae II-IV) were destroyed with intense gliosis. These changes were not induced by infusing AMPA for 1 day. The concomitant administration of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), an antagonist for non-N-methyl-D-aspartate (NMDA) receptors, with AMPA, but not that of 2-amino-5-phosphonovalerate (APV), an antagonist for NMDA receptor, prevented induction of the behavioral and neuropathological changes. The findings of the present study suggest that this late-onset, selective neurotoxicity is mediated by AMPA-type glutamate receptors.

Animals↗
PubMed1994

Dystrophin-related protein is found in the central nervous system of mice at various developmental stages, especially at the postsynaptic membrane.

Dystrophin deficiency is known to be the cause of X-linked Duchenne muscular dystrophy (DMD). A recently cloned B3-cDNA shares 80% homology with the C-terminus and actin-binding portion of dystrophin. This autosome-derived gene product is called dystrophin-related protein (DRP). DRP is known to exist in fetal muscles even in mdx mice, an animal model for X-linked DMD, but not in mature mouse muscles. We raised a polyclonal antibody against a B3-unique amino acid sequence (Ab-LDP) and investigated the existence and distribution of DRP in the central nervous system (CNS) tissues of mdx and normal control B10 mice at various stages of development using immunoblotting and immunohistochemical methods. The former shows that DRP exists in the CNS of both B10 and mdx mice, regardless of the developmental stage, with the exception that the 420 kDa DRP band of the 15-day fetus is faint. In immunohistochemical studies, the choroid plexus, some neurons, glial cels, pia mater, and blood vessels were stained with Ab-LDP. Staining intensity did not differ between B10 and mdx mice or between developmental stages except that the 15-day fetus stained only faintly. This is in contrast to the results obtained for muscles in which DRP localized to muscle membrane in embryo decreases and is assembled at the neuromuscular junction in adults. In addition, an electron microscopic study on the cerebral cortex from adult B10 mice was also performed and revealed Ab-LDP staining of the postsynaptic membrane of dendrite and the rough endoplasmic reticulum of neurons.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗
PubMed1994

[Toxicity of AMPA, an excitatory amino acid, to rat spinal cord neurons under intrathecal administration].

The neurotoxicity mediated by alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA), an agonist for glutamate receptors, was investigated by infusing adult rats with this agent intrathecally for either a short term (2 hours) or a long term (7 days) using a mechanical pump or a mini-osmotic pump, respectively. In the short-term infusion group, spasticity of the hindlimbs developed during infusion at 0.5 nmol/h or more of AMPA, tremors at 50 nmol/h or more, and flaccidity at 65 nmol/h or more. One day later, flaccid paralysis of the hindlimbs and urinary incontinence were observed in the rats that received 50 nmol/h (total dose: 100 nmol) or more of AMPA. These symptoms were thought to be permanent. On the other hand, in the long-term infusion group, behavioral changes were apparent only after second postoperative day, when rats displayed hindlimb palsy or urinary incontinence. Behavioral deficits became progressively severe, and rats usually displayed both hindlimb paraplegia and urinary incontinence by the 7th postoperative day. These progressive behavioral deficits were induced in a dose-dependent manner in rats that received AMPA at doses greater than 0.1 nmol/h. Gliosis with neuronal loss involving the partial (lumbar segments) and whole (sacral segments) gray matter of the spinal cord was induced in rats that received AMPA at doses greater than 50 nmol/h in the short-term infusion group and greater than 0.1 nmol/h in the long-term infusion group.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

[A patient with Guillain-Barré syndrome in association with Campylobacter jejuni enteritis (PEN19:LIO7) in a patient with HLA-B52 antigen].

We report a 15-year-old boy with Guillain-Barré syndrome (GBS) in association with Campylobacter jejuni enteritis. A neurologic examination revealed distal-dominant weakness and areflexia. Compound muscle action potentials were markedly reduced in amplitude, but the decrease in motor conduction velocities was slight. C. jejuni was isolated from his stool culture and the serotype belonged to PEN19:LIO7. Thin-layer chromatography-immunostaining showed that his serum IgG reacted strongly with GM1 and weakly with GD1b. The patient had HLA-B52 antigen, whose epitope is very similar to that of B35 antigen.

Adolescent↗