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N Amano

Publications and source records attributed to N Amano.

At least 37 records · Page 2Linked to original sources
PubMed1997

Morphologic difference of neuropil threads in Alzheimer's disease, corticobasal degeneration and progressive supranuclear palsy: a morphometric study.

Using Gallyas-Braak's silver stain, neuropil threads (NTs) in Alzheimer's disease (AD), corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP) were analyzed morphologically and morphometrically. The NT density was highest in the cerebral cortical layer V in AD and CBD, and in the subcortical white matter in PSP. An overlaid, two-dimensional, camera lucida drawing revealed differences in the fine profile of NTs among these three disease groups. The differences were confirmed by computerized feature analysis which revealed differences in maximum length, breadth, Feret's angle and orientation of the NTs. Unlike a previous assumption that all NTs have a similar appearance, our study revealed that NTs in AD, CBD and PSP were distinctively different with respect to their morphology.

Aged↗
PubMed1997

DNA recognition by beta-sheets.

The modes of DNA recognition by beta-sheets are analyzed by using the known crystal and solution three-dimensional structures of DNA-protein complexes. Close fitting of the protein surface and the DNA surface determines the binding geometry. Interaction takes place so that essentially the N-to-C direction of the beta-strands either follows or crosses the DNA groove. Upon following the major groove a two-stranded antiparallel beta-sheet dives into the groove and contacts DNA bases with its convex side facing the DNA, while upon following the minor groove, it binds around the sugar-phosphate backbones, with its opposite concave side shielding the DNA. In order for the beta-strands crossing the minor groove to interact with the DNA, the dinucleotide steps need to almost totally helically untwist and roll around major groove. The beta-sheet, on the other hand, needs to adopt a concave curvature on the binding surface in the direction that follows the DNA minor groove, and a convex surface in the direction that bridges the sugar-phosphate backbones across the groove. The result is to produce a hyperbolic paraboloidal DNA-binding surface.

Amino Acid Sequence↗
PubMed1997

The distribution and dynamic density of oligodendroglial cytoplasmic inclusions (GCIs) in multiple system atrophy: a correlation between the density of GCIs and the degree of involvement of striatonigral and olivopontocerebellar systems.

The distribution and dynamic density of oligodendroglial cytoplasmic inclusions (GCIs) were studied based on 30 cases of multiple system atrophy (MSA), including striatonigral degeneration (SND), olivopontocerebellar atrophy (OPCA) and Shy-Drager syndrome. GCIs were widely spread throughout the central nervous system, including the striatonigral and olivopontocerebellar systems. Inclusion-bearing cells appeared to be oligodendrocytes which usually had larger and lighter nuclei than those of normal-looking oligodendrocytes. The distribution of GCIs was similar in all cases, irrespective of the degrees of OPCA and SND, but the frequency of GCIs varied from case to case. We classified all the cases into two categories based on the degree of neuropathological changes of SND (mild and severe) and, independently, into three groups based on that of OPCA (minimal, moderate and severe), i.e., a total of six groups. An association between the frequency of GCIs and the severity of the lesions was obtained. For example, many GCIs were seen the cerebellar white matter in the cases in which OPCA was not histologically confirmed. More GCIs were seen in the cases with moderate OPCA. In the cases with severe OPCA, GCIs were rarer and smaller, in proportion to the devastation of fibers; no GCIs were seen in the cases with more severe OPCA. The incidence of GCIs showed a positive correlation to the severity of OPCA but not that of SND in the corticopontine tracts, of both OPCA and SND in the pyramidal tracts, and of SND but not of OPCA in the pencil fibers of the putamen. It is suggested that GCIs may represent either a change synchronous with neuronal degeneration or a phenomenon preceding neuronal changes, especially in the cerebellar white matter. Thus, they may represent the early changes in MSA and may be a useful neuropathological hallmark for diagnosis of MSA, even in cases with minimal OPCA and SND.

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PubMed1997

Scanning electron microscopical study of the neurofibrillary tangles of Alzheimer's disease.

Neurofibrillary tangles (NFTs) have been ultrastructurally studied by various methods, leading to several three-dimensional models of paired helical filaments (PHFs). In this study, we present the scanning electron microscopic findings of NFTs in an autopsy case of Alzheimer's disease and clarify the three-dimensional structures of NFTs. NFTs were clearly defined in freeze-cracked nerve cells and consisted of two types of filamentous structures, straight and helical filaments. Straight filaments measured from 20 to 25 nm in diameter and had a smooth surface. They were slightly bent but mostly straight with no constrictions. One type of straight filaments ran in a bundle in the same direction, another was intertwined to each other. Most of the helical profiles of filaments usually measured about 28 nm in diameter, with a distance of 100 nm between periodic constrictions. They seemed to consist of a pair of isodiametric filaments of 10 nm in diameter. In addition, two unusual types of helical filaments were occasionally observed. One comprised thick filaments of about 38 nm in diameter, with a distance of 100 nm between constrictions; these helical filaments appeared to consist of two or more strands. The other comprised thin helical filaments of about 20 nm in diameter and regularly constricted at an interval of 50 nm. All types of the helical filaments examined in this case were leotropic. This result supports a protofilament model of PHFs. Scanning electron microscopy using the freeze-cracked and maceration method is a useful and simple method for three-dimensional observation of the filamentous structures in NFTs.

Alzheimer Disease↗
PubMed1997

Amyotrophic lateral sclerosis with numerous axonal spheroids in the corticospinal tract and massive degeneration of the cortex.

A 53-year-old woman developed bulbar palsy, spastic quadriplegia, amyotrophy, and supranuclear ophthalmoplegia, and thereafter her condition was managed with mechanical ventilation for 1 year. Her total clinical course was 6 years. The autopsy examination revealed neuronal loss with reactive astrocytosis in the precentral cortex, thalamus, mammillary body, amygdala, putamen, globus pallidus, subthalamic nucleus, and the substantia nigra, in addition to degeneration of lower motor neurons, some of which contained Bunina bodies. Along the corticospinal tract, there were severe axonal loss and numerous axonal spheroids, which were positive for phosphorylated neurofilament, ubiquitin, and synaptophysin, and lipid-laden macrophages in the centrum semiovale to the crus cerebri. Ballooned neurons, which were positive for phosphorylated neurofilament, were occasionally seen in the frontal cortex. Although in the common form of amyotrophic lateral sclerosis (ALS) both upper and lower motor neurons are mainly involved, the corticospinal tract degeneration cannot be traced rostral to the pons. The noteworthy features in our patient were the precentral cortical degeneration and axonal spheroids in the corticospinal tract rostral to the pons. It remains unclear why axonal spheroids in the corticospinal tract and precentral cortical degeneration are not observed in most ALS cases. Whether their development depends on the clinical duration, mechanical ventilator management, or some other factors remains an open question.

Amyotrophic Lateral Sclerosis↗
PubMed1997

Aberrant expression of bcl-2 gene family in Down's syndrome brains.

Down's syndrome (DS) patient brains are known to develop prematurely the same degenerative changes as those seen in Alzheimer's disease (AD). On the assumption that the apoptotic mechanism is involved in the neuronal loss in DS, we have investigated the expression of the bcl-2 gene family in DS brains and found marked alterations. The most prominent changes were in the temporal lobes where neuronal loss was greatest. Our findings suggest that a apoptotic process is involved in the neuronal loss in DS.

Amyloid beta-Protein Precursor↗
PubMed1997

Apolipoprotein E in progressive supranuclear palsy in Japan.

Progressive supranuclear palsy (PSP) is a rare neurodegenerative disease which shows several psychiatric and neurologic symptoms: pseudobulbar palsy, supranuclear ocular palsy, extrapyramidal rigidity, gait ataxia, and dementia. Almost all cases seem to be sporadic; therefore, the elucidation of risk factors is important to clarify the pathological mechanism. Apolipoprotein E4 (ApoE4) is now well established as a risk factor of Alzheimer's disease (AD). Here we report the ApoE allele frequency in PSP, which shares pathological findings such as neurofibrillary tangle (NFT) with AD. NFT is an important sign for the derangement of normal cytoskeletons in degenerating neurons. Although there was no significant increase in epsilon 4 allele frequency in the present series of PSP cases compared with that in the Japanese controls, there was a significant increase in the epsilon 2 allele frequency in PSP compared to controls.

Aged↗
PubMed1997

Effects of dietary fructose or glucose on triglyceride production and lipogenic enzyme activities in the liver of Wistar fatty rats, an animal model of NIDDM.

Effects of dietary carbohydrates on triglyceride production and hepatic lipogenic enzyme activities were examined in Wistar fatty rats, an animal model of noninsulin dependent diabetes mellitus, fed fructose or glucose and were compared with those of Wistar lean rats. Carbohydrates were supplied in 10% drinking solutions for 21 days. As compared with lean rats, Wistar fatty rats were characterized by hyperglycemia, hyperinsulinemia and hypertriglyceridemia, the last of which was associated with an increased hepatic activity of fatty acid synthetase and an increased rate of triglyceride secretion from the liver to the circulation. Feeding fructose to genetically obese diabetic rats produced a threefold increase in the hepatic activity of fatty acid synthetase, a twofold increase in NADPH-generating enzymes (malic enzyme and glucose-6-phosphate dehydrogenase) and a 56% increase in the rate of triglyceride secretion, with a resultant 86% increase in plasma triglyceride concentrations. Feeding glucose produced a similar increase in the activity of NADPH-generating enzymes and triglyceride production in the fatty liver but it differed in producing no change in plasma triglyceride concentrations or hepatic fatty acid synthetase activity. Neither dietary fructose nor glucose changed glycemia or insulinemia. These results show that in genetically obese, diabetic rats feeding fructose and glucose is associated with an increase in hepatic lipogenic enzyme activities and triglyceride production, and suggest that fructose stimulates triglyceride production but impairs triglyceride removal, whereas glucose stimulates both of them.

Animals↗
PubMed1997

Genomes and DNA conformation.

Genomic DNA sequences code not only for protein sequences but also for their own physical characteristics. The composition of a genome for creating particular physical characteristics is reviewed by first summarizing the conformational characteristics of short DNA fragments, and second by summarizing the combination of fragments in a genome. In this analysis the pyrimidine (Y)/purine (R) classification of the four bases is important. In genomes, there is a tendency to create YY and RR combinations rather than YR and RY combinations, with a resulting minimization of the deviation of the local DNA structure from the standard B-conformation. Among the YY combinations, TT steps are positioned with a preference for the periodicity of approximately 10 bases, which is close to the helical periodicity of the DNA. The coding regions possess another periodicity of 3 bases in addition to the approximately 10 base periodicity, which differentiates these regions from the non-coding regions in terms of the physical characteristics. It is likely that the above characteristics of genomes are designed as part of their efficient transcription mechanisms.

DNA↗
PubMed1997

Three dimensional analysis of abnormal filaments of Pick's disease by scanning electron microscopy.

The three dimensional structure of filaments in Pick bodies and ballooned neurons in an autopsy case of Pick's disease was examined by scanning electron microscopy (SEM) and compared with the appearances on transmission electron microscopy (TEM). SEM revealed two types of filament in Pick bodies; one type was randomly orientated straight filaments of about 20 nm in width and the other was twisted helical filaments resembling paired helical filaments (PHFs). The maximum diameter of helical filaments was 44 nm with periodic constrictions of about 200 nm; the direction of the helix was left-handed. Ballooned neurons contained mainly randomly arranged filaments, 17-22 nm diameter. The three types of filament described here were greater in diameter in SEM images than in TEM; this may be due to the fixed increased thickness of 10 nm due to the platinum pallidium compound coating. However, SEM images are much more suitable than TEM profiles for three dimensional analysis of filamentous structures, especially those with helically twisted profiles; preparation for SEM did not change the periodicity of the twisted structures or the direction of the helix on these filaments even after metal coating. SEM has proved to be an effective and straightforward method for assessing the arrangement, direction and distribution of filaments and this technique could be applied to similar structures in other diseases.

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PubMed1996

Rattan bamboo blind (Japanese sudare)-like profiles of neurofibrillary tangles in Alzheimer's disease.

An unusual ultrastructure for neurofibrillary tangles, which has not been described so far, is presented in a case of Alzheimer's disease. This profile consists of parallelly arranged paired helical filaments and criss-cross tubular profiles that are arranged at regular interval of 300-500 nm, resembling rattan bamboo blind or Japanese sudare-like profiles. Coexistence of Hirano bodies in the same neuron is infrequently encountered.

Alzheimer Disease↗
PubMed1996

Coexistence of paired helical filaments and polyglucosan bodies in the same neuron in an autopsy case of Alzheimer's disease.

The coexistence of polyglucosan bodies (PBs) and paired helical filaments (PHFs) in the same neuron is reported in an autopsy case of Alzheimer's disease. The patient was a 56-year-old Japanese male with a typical clinical course and pathological findings of Alzheimer's disease. Electron microscopically, numerous neurofibrillary tangles, mainly composed of PHFs, were observed in the neuronal cytoplasm, axons and dendrites. Some of them coexisted with other filamentous structures, which comprised randomly oriented branching filaments with a diameter of 5-10 nm. These structures were compatible with PBs. Glial tangles could not be found. Coexistence of these two structures was thought to occur in neurites.

Alzheimer Disease↗
PubMed1996

Eosinophilic bodies in the cerebral cortex of Alzheimer's disease cases.

The light microscopical, immunohistochemical and ultrastructural aspects of eosinophilic bodies in the cerebral cortex from patients with Alzheimer's disease (AD) are described, based on a study of 16 cases of AD, 5 elderly non-demented controls and, as disease controls, 5 cases of Pick's disease, 9 with progressive supranuclear palsy, 5 with Creutzfeldt-Jakob disease and 1 with Binswanger's disease. At the light microscopy level, the bodies were clearly separated from the surrounding tissues and were mostly round or elliptic with a diameter of 5-30 microns and a central, intensely eosinophilic core. Ultrastructurally, they consisted of a central homogeneous electron-dense body (HDB), and filamentous structures (resembling either neurofilaments or paired helical filaments) or other small organelles in the periphery. Immunohistochemically, some of these bodies exhibited ring-shaped rims which were positive with antibodies against paired helical filaments, tau-2, phosphorylated neurofilaments and ubiquitin. The bodies were widely distributed throughout the cerebral cortex, but were not observed in the white matter. These bodies were thought to be compatible with one type of axonal dystrophy in the gracile nucleus (termed 'old' spheroid by Jellinger), and are here referred to as the HDB-type spheroid based on their ultrastructure. In this study HDB-type spheroids were found in high incidence in the AD cases, but only two HDB-type spheroids were seen in one case of Pick's disease, and none in any of the other cases of neurodegenerative diseases or in the elderly non-demented controls. It seems plausible that the incidence of HDB-type spheroids in the cerebral cortex might be related to a pathological process and not to a physiological ageing phenomenon, and might be characteristic of, but not unique to, AD.

Aged↗
PubMed1996

Corticobasal degeneration: widespread argentophilic threads and glia in addition to neurofibrillary tangles. Similarities of cytoskeletal abnormalities in corticobasal degeneration and progressive supranuclear palsy.

A 57-year-old man had exhibited cortical sensory disturbance, rigidity, spasticity, dementia, alien hand, grasp reflex, supranuclear ophthalmoplegia, pseudobulbar palsy, and neck dystonia for 4 years. Histological examination of autopsied specimens revealed neuronal loss in the cerebral cortex, with ballooned neurons, subthalamic nucleus, substantia nigra, basal ganglia, midbrain tegmentum, and the thalamus. There were neurofibrillary tangles in the subthalamic nucleus and the substantia nigra. Gallyas-Braak silver impregnation demonstrated numerous argentophilic tangles, threads, and a few argentophilic glia in the cerebral cortex, subcortical white matter, particularly in the precentral gyrus, subcortical nuclei, and the brainstem. These argentophilic structures were largely positive for tau, and negative for ubiquitin, paired helical filaments, and phosphorylated neurofilament. Ultrastructurally, 15-nm-wide straight tubules were observed in the neurons of the substantia nigra, globus pallidus, and the precentral cortex, coexisting with a few twisted tubules periodically constricted at 160- to 230-nm intervals. It was conclusively shown that Gallyas- and tau-positive cytoskeletal abnormalities occurred widely in brain of corticobasal degeneration. Both distribution and morphology of abnormal phosphorylated tau protein in corticobasal degeneration appear to resemble these features in progressive supranuclear palsy. These findings suggest a common cytoskeletal etiopathological significance in corticobasal degeneration and progressive supranuclear palsy.

Basal Ganglia↗
PubMed1996

VLDL triglyceride kinetics in Wistar fatty rats, an animal model of NIDDM: effects of dietary fructose alone or in combination with pioglitazone.

The effects of dietary fructose alone or in combination with a new oral agent, pioglitazone, on VLDL-triglyceride (TG) turnover were studied in genetically obese Wistar fatty rats characterized by hyperinsulinemia (7,488 +/- 954 pmol/l), hyperglycemia, (22.5 +/- 1.4 mmol/l), and hypertriglyceridemia (4.39 +/- 0.54 mmol/l). They had an increased hepatic TG production (16.2 +/- 0.1 micromol/min; lean rats, 5.4 +/- 0.3 micromol/min) as well as a longer half-life of VLDL-TG from lean donors (8.8 +/- 1.4 min, lean recipients; 2.3 +/- 0.9 min). In addition, in lean recipients, the half-life of VLDL-TG from fatty donors was longer than that from lean donors (4.80 +/- 0.56 vs. 3.14 +/- 0.23 min). Although feeding fructose into fatty rats did not change plasma glucose and insulin levels, it produced a twofold increase in TG levels (8.74 +/- 1.15 mmol/l). This was associated with a 1.7-fold increase in TG production to 27.5 +/- 1.2 micromol/min, while no significant change was found in the half-life of lean VLDL-TG in fructose-fed fatty recipients (10.9 +/- 2.4 min) or in that of VLDL-TG from fructose-fed fatty donors in lean recipients (4.46 +/- 0.76 min). Daily administration of pioglitazone (3 mg/kg body weight) in fructose-fed fatty rats ameliorated glycemia and triglyceridemia to the level of lean rats (8.1 +/- 0.7 and 1.18 +/- 0.05 mmol/l, respectively) and insulinemia to a lesser extent (2,712 +/- 78 pmol/l). A fall in TG levels was associated with improvement of an impairment in the ability of fructose-fed fatty rats to remove lean VLDL-TG (half-fife: 2.6 +/- 0.6 min). Pioglitazone, however, produced no change in TG production (25.9 +/- 2.7 micromol/min), the half-life of VLDL-TG from fructose-fed fatty donors in lean recipients (4.17 +/- 0.38 min), or the activity of lipoprotein lipase and hepatic lipase in postheparin plasma. We conclude that in Wistar fatty rats 1) hypertriglyceridemia is attributed to TG overproduction and impaired TG catabolism, and the latter is due to changes in both VLDL, such that they are less able to be removed, and changes in the nature of Wistar fatty rats, such that they are less able to remove VLDL-TG; 2) fructose further increases hepatic TG production with a resultant deterioration in hypertriglyceridemia; 3) pioglitazone normalizes TG levels by altering the physiology of the Wistar fatty rats in a manner that increases their ability to remove VLDL-TG from the circulation.

Animals↗
PubMed1996

Oesophageal carcinoma with humoral hypercalcaemia of malignancy and leucocytosis.

We report a case of oesophageal carcinoma with humoral hypercalcaemia of malignancy and leucocytosis in a 66-year-old man. We also demonstrate parathyroid hormone-related protein, by immunohistology. After admission, calcitonin was administered for the hypercalcaemia but the patient died of pneumonia on the 17th day of hospitalization. As oesophageal carcinoma with humoral hypercalcaemia of malignancy and leucocytosis is characterized by rapid progression and metastasis, earlier diagnosis and treatment is mandatory.

Aged↗
PubMed1995

Distribution of tangles and threads in the cerebral cortex in progressive supranuclear palsy.

Recent studies have described silver- and tau-positive glia and threads in the degenerating lesions of progressive supranuclear palsy. In this study, Gallyas-Braak silver impregnation and several immunohistochemical techniques were employed to examine the distribution of tangles, abnormal glia and threads in the cerebral cortex of nine cases of progressive supranuclear palsy. In addition to neurofibrillary tangles, argentophilic glia and threads were impregnated exclusively by Gallyas-Braak technique. This technique demonstrated two types of glia profiles: tightly coiled intra-cytoplasmic profiles surrounding nuclei (coiled profiles) and thorn-like profiles with radial ramifications (thorn-like profiles). Thorn-like profiles are possibly in astrocytes and were detected in the cerebral cortex, while coiled profiles are possibly in oligodendroglia and were detected both in the cerebral cortex and subcortical white matter. Topographically, many neurofibrillary tangles were constantly seen in the frontal cortex and in the pre-central gyrus. Numerous neurofibrillary tangles were detected in the entorhinal cortex of the two brains. Argentophilic glia and threads were also frequent both in the frontal cortex and the precentral gyrus; however, they were more frequent in the pre-central gyrus that in the frontal cortex in four of the eight cases examined. In two brains, argentophilic threads were distributed widely in the cerebral cortex and white matter except for the temporal cortex. In immunohistochemical studies, argentophilic glia and threads were mostly positive for Tau 2, and a small number of them were weakly positive for ubiquitin and paired helical filament protein. The immunoproperties of these abnormal glia and threads seemed to be virtually identical to those of neurofibrillary tangles.(ABSTRACT TRUNCATED AT 250 WORDS)

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