[Localized callosal infarctions and dementia].
Explore the source record for details and available documents.
Aged↗
Biomedical subjects
M Tomonaga
Publications and source records attributed to M Tomonaga.
Immunocytochemical identification of beta-protein precursor in cultured vascular cells.
The immunocytochemical and immunochemical identification of beta-protein precursor in cultured vascular cells was undertaken using three types of antibodies to the synthetic predictive peptides (extracellular portion; 275-286, beta-protein portion; 597-620, C-terminal portion; 681-695) of beta-protein precursor. Monoclonal antibody directed toward the beta-protein portion stained the surface membrane of the cultured endothelial cells as well as cytoplasmic organelles. Immunoblotting of the subcellular fractions of the cell homogenate with three antibodies revealed that the plasma membrane associated beta-protein precursor consists of 105-130 kDa protein complexes and that the mitochondria-microsome-associated beta-protein consists of related 30-67 kDa protein complexes. The immunoreactivity of the protein bands was blocked by pretreating the monoclonal antibody with bovine serum albumin-conjugated beta-protein. These results indicate that the form of the beta-protein precursor or beta-protein-related components in cultured vascular cells is heterogeneous in terms of molecular size and subcellular localization.
Amyloid↗
[An autopsy case of postencephalitic parkinsonism: investigation on neurofibrillary tangles in comparison with those in progressive supranuclear palsy].
We report an autopsy case of postencephalitic parkinsonism (PEP). The distribution, histochemical, and immunohistochemical characteristics of neurofibrillary tangles (NFTs) in the case were studied and compared with NFTs in progressive supranuclear palsy (PSP). The patient was a 78-year-old woman who had suffered from "sleeping sickness" at age 27 and parkinsonism developed 13 years later. NFTs were found in the brainstem, basal ganglia, subthalamus, hypothalamus, thalamus and hippocampus in addition to marked degeneration of the substantia nigra. In the brainstem, NFTs were found not only in the amine-containing neurons but also in the pedunculopontine nucleus, which was recently reported to have cholinergic neurons. NFTs were immunostained by antibodies against tau and ubiquitin, both of which have been identified as antigenic components of NFTs in Alzheimer's disease and also those in PSP. Ultrastracturally, NFTs were composed of paired helical filaments. In serial sections with stained with Congo red and Bodian stains, all NFTs visible with Bodian stain in the brainstem of the case seemed to have Congo red birefringence which is produced by beta-sheet conformation of protein. In contrast, in three cases of PSP, less than half of NFTs seemed to have birefringence. These findings suggest that the protein components of NFTs in PEP and PSP are common to each other, but the conformation of the protein of some NFTs in PSP may be different from those in PPE.
Aged↗
[Neuronal death and neurotrophic factors in Alzheimer's disease].
Progressive neuronal death in cerebral cortex and subcortical regions may lead to dementia in Alzheimer's disease (AD). The neuronal death is accompanied by accumulation of senile plaques, neurofibrillary tangles and curly fibers. Recent immunocytochemical studies have suggested that abnormal sprouting responses, occurring in AD brain, may be involved in the formation of these lesions. The hypothesis concerning the lack of neurotrophic factors cannot explain abnormal sprouting responses in AD brain. We have investigated the mechanism of abnormal sprouting responses in AD brain, using primary culture of rat cerebral cortical neurons. In AD brain, loss of growth-inhibitory factors led to an apparently higher level of neurotrophic activity. One of the growth-inhibitory factors in normal aged brain was a 5 kDa heat-stable acidic protein. These results suggest that loss of inhibitory factors may induce abnormal sprouting responses in AD brain. In consequence, neurons might be exhausted and die.
Alzheimer Disease↗
Detection of preleukemic state of adult T-cell leukemia (pre-ATL) in HTLV-1 carriers.
The prevalence of the preleukemic state of adult T-cell leukemia (pre-ATL) was studied in Nagasaki prefecture, one of the endemic human T-lymphotropic virus type 1 (HTLV-1) areas in Japan. Pre-ATL cases have the monoclonal proliferation of abnormal lymphocytes, without signs of malignant proliferation or clinical signs and symptoms related to leukemia. HTLV-1 carriers who have monoclonal integration of HTLV-1 proviral DNA may be at high risk of developing ATL. Abnormal lymphocytes with either bilobular or large and chromatin-rich nuclei were found in 63/356 (17.7%) of HTLV-1 carriers among inhabitants. We analyzed DNA of peripheral lymphocytes from 108 carries with abnormal lymphocytes by Southern blot technique. Monoclonal integration of HTLV-1 has been detected in 12 cases (11.1%). These results lead to the conclusion that the prevalence rate of pre-ATL among all HTLV-1 carriers is about 2%. Pre-ATL is presumed to be the clinical stage which precedes ATL, although the possibility remains that the HTLV-1 carrier may develop symptoms of ATL directly, without going through the pre-ATL stage.
Adult↗
Elevation of the petrous bone caused by hyperplasia of the occipital bone presenting as hemifacial spasm: diagnostic values of magnetic resonance imaging and three-dimensional computed tomographic images in a bone anomaly.
A case of elevation of the petrous bone due to hyperplasia of the occipital bone presenting as hemifacial spasm is reported. A 44-year-old man sought treatment for twitching of the buccal muscles on the right side that progressed rapidly in severity within 2 weeks of the onset. The anatomical details of the petrous and occipital bones were delineated clearly by computed tomographic scans of a bone window level. Details of the brain stem were shown by magnetic resonance images. The bone anomaly was displayed more realistically by three-dimensional computed tomographic reconstructions. The faithful representation of structures with these radiological studies should be mandatory, to prepare the surgical planning of such a complicated bone anomaly.
Adult↗
Molecular cloning and characterization of a chromosomal gene for human eosinophil peroxidase.
Using human myeloperoxidase cDNA as a probe, a chromosomal gene related to myeloperoxidase was isolated from a human gene library. Comparison of the amino acid sequence deduced from the nucleotide sequence of the cloned gene with that of human eosinophil peroxidase purified from buffy coats has indicated that the isolated gene is the chromosomal gene for human eosinophil peroxidase. Like human myeloperoxidase gene, human eosinophil peroxidase gene consists of 12 exons and 11 introns spanning about 12 kilobases. The gene can code for a protein of 715 amino acids with a calculated Mr of 81,036. The heavy chain and the light chain of eosinophil peroxidase were located on the COOH and NH2 terminus of the protein, respectively. The coding sequences of eosinophil peroxidase and myeloperoxidase show homologies of 72.4% at the nucleotide and 69.8% at the amino acid level, while little homology was found in the 5'-flanking region. Northern hybridization and S1 mapping analysis of RNA from human leukemic cells have indicated that the eosinophil peroxidase gene is expressed in the eosinophilic subline of human HL-60 cells but not in the neutrophilic subline or in parental HL-60 cells.
Amino Acid Sequence↗
Neurotrophic action of Alzheimer's disease brain extract is due to the loss of inhibitory factors for survival and neurite formation of cerebral cortical neurons.
Cell cultures of neonatal rat cerebral cortex in a serum-free medium were used to investigate whether specific neurotrophic factors are accumulated or inhibitory factors for neuronal survival and neurite formation decrease in AD brain extract. Neurotrophic activity in brain extract was quantified by using the ELISA for microtubule-associated protein 2 (MAP2). Inhibitory factors, which blocked neurotrophic activity, were present in normal brain extract. In AD brain extract, loss of the inhibitory factors resulted in a relative increase in neurotrophic activity. The inhibitory factors in normal brain extract were retained on the ultrafiltration membrane with molecular weight cutoff of 10 kDa.
Aged↗
Decrease in nerve fibres in cerebral white matter in progressive subcortical vascular encephalopathy of Binswanger type. An electron microscopic study.
To study white matter changes in the frontal lobes and to investigate the histopathological basis for the dementia in progressive subcortical vascular encephalopathy (PSVE), the frontal white matter was examined by electron microscopy in seven cases with PSVE, and compared with that in a control group and in cases with senile dementia of Alzheimer's type (SDAT). The number of nerve fibres per unit selected area of the white matter was significantly less in PSVE compared with that in the control group or in SDAT. Nerve fibres in PSVE had a tendency to have thinner myelin sheaths than in the control group or in SDAT, but the difference was not significant. The pallor of the frontal white matter in PSVE is mainly based on the loss of nerve fibres, and may be in part based on the thin myelin sheaths. The dementia in PSVE is probably related to the loss of nerve fibres in the cerebral white matter.
Aged↗
Acute necrotizing encephalopathy with widespread edematous lesions of symmetrical distribution.
A 67-year-old Japanese woman with liver cirrhosis was affected by an unusual acute progressive encephalopathy, presenting mental confusion and slurred speech as its initial symptoms. She died in profound coma, following the entire course of 17 days. Autopsy disclosed bilateral symmetrical, widespread, edematous and necrotic lesions, their centers being located in the basal ganglia, diencephalon and midbrain, and their peripheries expanding into the cerebral white matter, cerebellum, pons and medulla. Diapedesis of erythrocytes and serum plasma was conspicuous, in contrast to paucity of capillary proliferation. Although the lesions were somewhat similar to those of Wernicke's and Leigh's encephalopathies, they were considered to be representative of a more acute metabolic disorder distinct from the latter conditions.
Acute Disease↗
Immunocytochemical and ultrastructural study of Lewy body-like hyaline inclusions in familial amyotrophic lateral sclerosis.
Lewy body-like hyaline inclusion (LI) in the neuronal soma and swollen cord-like processes is a characteristic feature in the anterior horn cells and neurons in thoracic nucleus (Clarke) of familial amyotrophic lateral sclerosis (ALS) with posterior column involvement. We have studied the LI in the case of two sisters with this disorders. Microscopically the LI consists of an eosinophilic "core" surrounded by a basophilic "halo". Ultrastructurally the core consists of granule-associated filaments, while the halo consists of normal-looking neurofilament. Immunocytochemistry with anti-ubiquitin antibody shows that these granule-associated filaments in the core are highly ubiquitinated, while the normal-looking neurofilaments in the halo are not recognized by anti-ubiquitin antibody. Our study proves that LI consists of an aggregation of ubiquitinated filaments among a neurofilamentous accumulation, possibly representing a form of neuronal cytoskeletal disorganization in familial ALS.
Amyotrophic Lateral Sclerosis↗
Calcified chronic subdural hematoma with intracerebral rupture forming a subcortical hematoma. A case report.
We report a calcified chronic subdural hematoma which ruptured intracerebrally forming an acute subcortical hematoma in the frontal lobe in a 59-year-old woman with long-standing liver cirrhosis. Both hematoma cavities communicated each other through a small defect within the inner membrane of the subdural hematoma. The content of both hematomas was identical and was of a clay-like clot. The inner membrane around this communication consisted of thick, very vascular granulation tissue with many hemosiderin deposits and was tightly adherent to the cortex. We speculated that a fresh bleeding into the granulation tissue resulted in formation of a subcortical hematoma through a rupture of the inner membrane. Disseminated intravascular coagulation likely played an important role in this unusual condition.
Brain Diseases↗
Primary calvarial meningiomas.
Two cases of primary calvarial meningioma developing epidurally and protruding extracranially without subdural involvement are reported. The relevant literature on calvarial meningioma is reviewed.
Aged↗
Antibodies against p40tax gene product of human T-lymphotropic virus type-I (HTLV-I) under various conditions of HTLV-I infection.
We investigated antibodies against pX gene product, p40tax, by ELISA using recombinant p40tax protein in HTLV-I seropositive carriers as well as patients with adult T cell leukemia (ATL) and HTLV-I-associated myelopathy (HAM). Seventy (49.0%) out of 143 HTLV-I healthy carriers were found to be positive for antibody against p40tax antigen and the follow-up samples at two-year intervals revealed constant reactivity by ELISA in each carrier. The onset of antibody production was delayed 4 to 12 weeks as compared with anti-HTLV-I in primary infection cases. The anti-p40tax-positive rate (90%) in HAM patients was significantly higher than that of healthy carriers, acute and chronic ATL patients and their family members. Furthermore, HAM patients and a few healthy carriers showed high reactivities by ELISA. Children from mothers with anti-p40tax showed a higher anti-HTLV-I-positive rate than that of children from mothers without anti-p40tax (54.5% versus 12.5%). Two men without anti-p40tax and one female with low anti-p40tax developed ATL during follow-up studies. These results suggest that HTLV-I carriers could be divided into 2 or 3 sub-populations according to antibody response to p40tax. A smaller population with anti-p40tax, especially a high antibody reactivity, could have a high risk of developing HAM and of transmission from mother to child. In addition, ATL may occur in a population with low or absent anti-p40tax.
Carrier State↗
Recurrence of embolic stroke in non-valvular atrial fibrillation (NVAF). An autopsy study.
From 3434 consecutive autopsied cases over 60 years of age, we performed retrospective, clinicopathological examinations on 81 patients with symptomatic embolic stroke and non-valvular atrial fibrillation (NVAF) who had not received anticoagulant therapy during their lives. Twenty-one had recurrent embolic strokes (recurrence rate: 25.9%). In the thrombotic infarction without NVAF, the recurrence rate was 21.4%. Recurrent strokes occurred earlier in the embolic infarction of NVAF than in the thrombotic infarction. Most of the lesions of initial embolic strokes were present in the territory of one middle cerebral artery (MCA), while many lesions of recurrent strokes were found in the territory of the contralateral MCA. Between the NVAF cases with and without recurrent embolic stroke, there was no significant difference in the background condition such as history of hypertension, duration of NVAF, severity of cerebral arterial atherosclerosis, heart weight, intracardiac thrombi, myocardial infarctions and infarctions in other systemic organs.
Aged↗
[Empiric therapy with aztreonam for febrile neutropenic patients with hematological malignancies].
Combination of aztreonam/amikacin/ticarcillin (AAT) and latamoxef/amikacin/ticarcillin (LAT) were compared in a prospective randomized trial of empiric therapy for febrile neutropenic patients with hematological malignancies. Low dose amphotericin B was also added to each regimen from the beginning. Of 45 evaluable episodes, 23 were treated with AAT and 22 with LAT. The response rates were 61 percent for AAT and 50 percent for LAT, statistically not significant. There was one infection-related death among patients assigned to AAT therapy and also one among those assigned to LAT therapy. Dose escalation of amphotericin B seemed to be effective for those patients who did not improve with initial therapy.
Aztreonam↗
Nonvalvular atrial fibrillation as a cause of fatal massive cerebral infarction in the elderly.
By studying 3,408 consecutive autopsied elderly patients, we found that two thirds of the 132 massive cerebral infarctions (86) were embolic, of cardiac origin. Embolic infarction associated with nonvalvular atrial fibrillation was seen in 48 cases (36%), half due to the first stroke. Embolic infarction associated with heart disease other than nonvalvular atrial fibrillation was seen in 23 cases (17%), and that from nonbacterial thrombotic endocarditis was seen in 15 cases (11%). Thrombotic infarction or infarction of nonembolic cardiac origin was found in only 39 cases (30%). Of 56 patients with fatal massive cerebral infarction who died less than or equal to 2 weeks after their stroke, 25 (45%) had embolic strokes associated with nonvalvular atrial fibrillation. Our study shows that nonvalvular atrial fibrillation is a very important cause of fatal massive cerebral infarction in the elderly.
Aged↗