Biomedical subjects

H Nagatomo

Publications and source records attributed to H Nagatomo.

At least 37 records · Page 2Linked to original sources

PubMed1996

Liver cell adenoma in a young man with elevated serum PIVKA-II level.

A 21-year-old man was referred to our hospital because of a liver mass lesion detected by abdominal ultrasonography. He had received no hormonal treatment. Physical examinations revealed no abnormalities, and laboratory data, including hepatic function test results, were within normal ranges, with the exception of elevated levels of serum protein induced by vitamin K absence or antagonist (PIVKA)-II (2.2 AU/ml). Abdominal ultrasonography revealed a hyperechoic mass lesion measuring 10 x 10 cm, with hypoechoic areas located in the right posterior segment of the liver. A low-density area and a hypervascular area were detected in the right posterior segment of the liver by computed tomography and celiac angiography, respectively. As hepatocellular carcinoma could not be completely excluded, the tumor was resected. The tissue consisted of sheets of tumor cells with eosinophilic cytoplasm and round nuclei showing a thin trabecular pattern, and these histological findings indicated liver cell adenoma. After resection of the tumor, serum PIVKA-II returned to the normal level.

Adenoma, Liver Cell↗

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

Quantitative comparison between serum components and somatic cells in bovine quarter milk.

Quantitative comparisons between serum components and somatic cells in 202 bovine quarter milks collected at 3 dairy farms were conducted. Detection of serum components was carried out by an immunological technique, and cell counts were calculated by Breed's method. A high correlation (r = 0.77) between cell counts and gamma-globulin contents was demonstrated, while correlation between cell counts and serum albumin was not close (r = 0.45). In a comparison between cell counts and gamma-globulin contents, 19 (65.4%) out of 29 milks containing over 500,000 cells/ml had gamma-globulin less than 1.138 mg/ml, which was also seen in 97% of 172 milks having less than 500,000 cells/ml. From these results, it was suggested that the gamma-globulin content of milk might be of use for differentiating normal milk from abnormal ones.

Animals↗

PubMed1996

Antibody response to Mycoplasma bovis of calves introduced to a farm contaminated with the organism.

Antibody against Mycoplasma bovis in sera of 48 calves introduced to a farm, in which calf pneumonia associated with M. bovis had been occurring in the last 3 years, was detected by an indirect hemagglutination test. Significant rises of antibody titers in sera of calves belonging to the groups A (16 calves) and B (14 calves) were recorded by day 60 post-introduction. On the other hand, a significant increase of antibody titers of 18 calves in group C, which had been administered antibiotics as a preventive therapy, was demonstrated at day 248 after arrival. These results indicated that the spread of M. bovis infection occurred easily on the contaminated farm, and a preventive therapy could delay the outbreak of calf pneumonia associated with M. bovis.

Animals↗

PubMed1996

[A patient with parkinsonism presenting hyperintensity in the globus pallidus on T1-weighted MR images: the correlation with manganese poisoning].

We report a 55-year-old woman who developed symptoms resembling parkinsonism. Her psychiatric symptoms in the early stage, cervical dystonia and tremor increasing on movement were consistent with manganese poisoning. Manganese levels were elevated to 1.5 micrograms/l in the serum (normal; 0.3-1.1 micrograms/l) and to 1.4 micrograms/l in the urine (normal; less than 1.2 micrograms/l). Intravenous infusion of calcium disodium editate (CaEDTA; chelating agent) was followed by the marked excretion of manganese (27.3 micrograms/l) in the urine. These findings support manganese poisoning. Manganese poisoning is a disease which results from chronic exposure to manganese, but the source of manganese exposure remained obscure in this patient. T1-weighted MRI of the brain showed symmetric high signal intensity in the globus pallidus without any abnormality on T2-weighted images. There is a report that manganese induced brain lesions in Macaca fascicularis as revealed by MRI and the fascicularis developed signs of unsteady gait and hypoactivity. The patient responded to treatment with CaEDTA and the second MRI demonstrated regression of abnormal signal intensity. This may be due to enhanced manganese excretion. To our knowledge, this is the first case of probable manganese-induced human parkinsonism whom changes in MRI were noted after treatment with CaEDTA.

Edetic Acid↗

PubMed1995

Interaction of the hemolytic lectin CEL-III from the marine invertebrate Cucumaria echinata with the erythrocyte membrane.

CEL-III is one of four Ca(2+)-dependent galactose/N-acetylgalactosamine (GalNAc)-binding lectins from the marine invertebrate Cucumaria echinata which exhibits hemolytic activity, especially toward rabbit and human erythrocytes. The hemolytic activity of CEL-III was also Ca(2+)-dependent and was found to be inhibited by galactose or GalNAc-containing carbohydrates, suggesting that the hemolysis was caused by CEL-III binding to specific carbohydrates on the erythrocyte membrane by Ca(2+)-dependent lectin activity, followed by partial destruction of the membrane. The activity of CEL-III was highest at 10 degrees C and decreased markedly with increasing temperature, unlike usual enzymatic reactions. The hemolytic activity of CEL-III increased with increasing pH from neutral to 10, but almost no hemolysis was observed below pH 6.5. Immunoblotting analysis of proteins from the erythrocyte membrane after treatment with CEL-III indicated that CEL-III aggregates were irreversibly bound to the membrane. When erythrocytes were incubated with CEL-III in the presence of dextran with molecular masses greater than 4 kDa, lysis was impeded considerably, while a concomitant release of ATP was detected from these osmotically protected cells. It was found that CEL-III released carboxyfluorescein from artificial globoside-containing lipid vesicles, and it is suggested that CEL-III is a novel pore-forming protein with the characteristics of a Ca(2+)-dependent lectin, which may act as a toxic protein to foreign microorganisms.

Adenosine Triphosphate↗

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)

Aged↗

PubMed1995

Immunologic characteristics of anti-erythrocyte membrane antibody produced in dogs during Babesia gibsoni infection.

Serum anti-erythrocyte membrane (RBCm) antibodies and anti-RBCm antibodies eluted from erythrocytes of Babesia gibsoni-infected dogs were examined for immunologic characteristics by immunoblotting analysis. Serum anti-RBCm antibodies of the dogs before and after the experimental inoculation with parasitized erythrocytes reacted with cytoskeletal (bands 1, 2, 2.1, 4.1, 4.2 and 5) and transmembrane structural (band 3) proteins of either self or non-self RBCm. Anti-RBCm antibodies eluted from erythrocytes of B. gibsoni-infected dogs reacted with bands 3 and 4.2 of self and non-self RBCm.

Animals↗

PubMed1995

[Autotopagnosia ameliorated by looking at the image reflected in a mirror].

A 52-year-old right-handed man presented progressive dystonia and apraxia of his right hand of five years' duration. He also suffered from parkinsonian features such as rigidity or impaired postural reflexes. Serial investigation of brain MRI revealed progressive cerebral atrophy, which started in the left parietal lobe, and subsequently extended to both hemispheres. He was clinically diagnosed as corticobasal degeneration. He could not point at any part of his own body in response to verbal or visual commands. On the other hand, he could point at every part of the examiner's body or of the illustrated body image. Deep sensations and linguistic functions were not involved. This cognitive impairment was regarded as autotopagnosia. In contrast with inability to recognize any part of the own body in response to the commands, he could name every part of his body as soon as the examiner touched there. Moreover, his symptoms of autotopagnosia were ameliorated by looking at himself in a mirror; he could point at any part of his own body. Disconnection between primary proprioceptive sensory area and the center of body schema was thought to be the mechanism of autotopagnosia in this patient, because the impairment improved with the aid of visual or tactile informations. We speculated the lesion was the left parietal lobe.

Agnosia↗

PubMed1995

[Familial early onset cerebellar ataxia with hypoalbuminemia].

We describe two brothers with early onset cerebellar ataxia associated with hypoalbuminemia (EOCAH). Choreo-athetoid movements preceded the cerebellar ataxia, and serum pseudocholinesterase elevation preceded the hypoalbuminemia. The parents are first cousins. Patient 1, the 22-year-old elder brother, developed choreoathetoid movements of the neck and extremities at the age of eighteen months. He later developed slowly progressive cerebellar ataxia with decreased tendon reflexes. The choreoathetoid movements ceased at about 16 years of age. A recent examination revealed cerebellar ataxia, action myoclonus of the neck and upper limbs, diminished tendon reflexes, mild sensory disturbance in the lower extremities, and very slight amyotrophy of the feet. Patient 2, the 18-year-old younger brother, developed choreo-athetoid movements at the age of 6 years, followed by slowly progressive cerebellar ataxia with disminished tendon reflexes. No scoliosis, ECG abnormalities, or edema was detected. Serum biochemistry studies revealed elevated pseudocholinesterase (6,226 to 2,390 IU) in the patient's early teens. Serum albumin levels tended to be low (3.7 to 4.1 g/dl). Serum triglyceride and beta-lipoprotein levels were elevated in the patients' late teens. Genetic studies showed slight linkage of D9S15. The maximum lod score was 0.289 (recombination fraction rate was 0.14).

Adolescent↗

PubMed1995

[A case of sarcoidosis with advanced cystic and fibrotic changes in a young patient].

A 29-year-old man was referred to our hospital because of exertional dyspnea and progressive eruption on the buttocks and the lower extremities. Chest roentgenograms and computed tomograms taken at that time revealed diffuse fibrotic changes accompanied by multiple cavities and bullae in the lungs. There were no signs of mediastinal or hilar lymphadenopathy. A chest roentgenogram taken 7 years before admission showed no abnormalities. Serum ACE and lysozyme levels were high: 29.9 IU/l and 14.1 micrograms/ml, respectively. 67Ga scintigraphy showed diffuse uptake in both lung fields. The PPD skin test was negative, and repeated sputum smears and cultures were negative for pyogenic bacteria and acid-fast bacilli. Examination of transbronchial lung biopsy and skin biopsy specimens confirmed the diagnosis--they showed noncaseating epithelioid granulomas with giant cells and a negative reaction of the stain to acid-fast bacilli, which are compatible with sarcoidosis. The patient was given 30 mg/d of prednisone orally. The dyspnea and eruption were clearly alleviated, although there was little roentgenographic regression of cystic or fibrotic changes. There have been only a few reports of cystic and fibrotic changes early in the course of sarcoidosis. The cystic lesions in this case were probably secondary pulmonary cavities caused by the contracting and obstructive changes related to pulmonary fibrosis.

Adult↗

PubMed1995

[A case of Lissauer's general paresis with left hemisphere dominant brain atrophy and leuko-araiosis in the deep white matter on MRI].

A 38-year-old man presented with personality change, postural tremor of the right arm and leg, and right hemidysesthesia. MR imaging (MRI) revealed left hemisphere dominant brain atrophy and leuko-araiosis in the deep white matter. Serological test of serum and cerebrospinal fluid demonstrated high titers of antibodies to Treponema pallidum. He was diagnosed as Lissauer's general paresis based on the clinical symptoms and signs, and MRI findings. This disorder is characterized by focal cerebral atrophy, corresponding to focal neurologic signs. Neuropathological features in Lissauer's general paresis are spongiform atrophy of the cerebral cortex and demyelination of the white matter. Leuko-araiosis on MRI in our case may represent demyelination of the white matter. Although MRI findings in general paresis are usually nonspecific, this is, as far as we know the first case report of general paresis with MRI showing focal cerebral atrophy and leuko-araiosis.

Adult↗

PubMed1994

[A case of familial Mediterranean fever with obvious family history].

A 26-year-old female was admitted to our hospital on December 4, 1992, because of recurrent fever. She had experienced recurrent fever of over 38 degrees C, occurring at irregular intervals 4-6 times a year with chest or abdominal pain, since the age of 19. After delivery of a baby at the age of 25, her symptoms had increased to once a week. In the febrile phase, leukocytosis, an increased erythrocyte sedimentation rate and positive CRP were recognized. These symptoms and laboratory findings spontaneously disappeared within a few days. Despite systemic and careful examinations, no evidence of infectious diseases, collagen diseases or malignant diseases were found. There were no significant differences of serum and urine catecholamines, and urine etiocholanolone between the febrile phase and the afebrile phase. An intravenous infusion of metaraminol induced symptoms similar to a spontaneous attack, and the metaraminol rechallenge test became negative after she was treated with oral colchicine. Based on these findings, she was diagnosed as having familial Mediterranean fever. Since she was treated with colchicine, the febrile attacks have decreased. Significantly, her elder brother has had similar recurrent fever with abdominal pain. He was diagnosed as having familial Mediterranean fever due to a positive metaraminol provocative test, and his febrile attacks have also been suppressed by colchicine. This is the first case of familial Mediterranean fever with obvious family history in Japan.

Adult↗

PubMed1994

Purification and characterization of four Ca(2+)-dependent lectins from the marine invertebrate, Cucumaria echinata.

Four Ca(2+)-dependent, N-acetylgalactosamine/galactose-specific lectins were purified from the marine invertebrate, Cucumaria echinata (Holothuroidea), by column chromatography on lactosyl-Sepharose 4B, Sephacryl S-200, and Q-Sepharose. The molecular masses of these lectins were estimated to be 27 kDa (CEL-I), 35 kDa (CEL-II), 45 kDa (CEL-III), and 68 kDa (CEL-IV) on SDS-PAGE under nonreducing conditions. Among these lectins, CEL-I and CEL-IV strongly agglutinated rabbit and human erythrocytes, and were found to recognize N-acetylgalactosamine and galactose-containing carbohydrates from the results of a hemagglutination inhibition assay. In contrast, CEL-II failed to agglutinate any erythrocytes tested, although its carbohydrate-binding ability was confirmed by a carbohydrate-binding assay involving asialofetuin-horseradish peroxidase. Interestingly, CEL-III caused hemolysis of rabbit and human erythrocytes, while it showed only hemagglutination of chicken and horse erythrocytes at relatively high concentrations. The hemolytic activity of CEL-III was also dependent on the Ca(2+)-concentration, and inhibited by N-acetylgalactosamine and galactose-containing carbohydrates, suggesting that the hemolysis was caused by Ca(2+)-dependent binding of CEL-III to specific carbohydrate chains on the erythrocyte surface and the following partial destruction of the membrane.

Animals↗

PubMed1994

Quantitation of erythrocyte-bound IgG by competitive solid-phase enzyme immunoassay.

A competitive solid-phase enzyme immunoassay technique for the quantitation of erythrocyte (RBC)-bound IgG was devised. This method is highly sensitive, reproducible and can be performed more simply. Anemic dogs with a positive Coombs' test result were observed to have higher RBC-bound IgG values (IgG concentration, ng/ml) than healthy dogs.

Anemia↗

PubMed1994

Elevated erythrocyte-bound IgG value in dogs with clinical Babesia gibsoni infection.

Erythrocyte (RBC)-bound IgG values (IgG concentration, ng/ml) were examined in 8 Babesia gibsoni-infected and 10 healthy dogs by a competitive enzyme immunoassay. Five dogs with clinical B. gibsoni infection, manifesting severe anemia, were observed to have increased RBC-bound IgG values compared to dogs with subclinical B. gibsoni infection and healthy controls, this suggesting that anemia in B. gibsoni infection may be explained in part on the basis of a humoral immunologic mechanism.

Anemia↗

PubMed1994

Reactivity of serum anti-erythrocyte membrane antibody in Babesia gibsoni-infected dogs.

Reactivity of anti-erythrocyte membrane (RBCm) antibody in sera of B. gibosni-infected dogs on native RBCm and erythrocyte surface (RBCs) was examined using an enzyme linked immunosorbent assay. Anti-RBCm antibody attached to native RBCm and the surface of erythrocytes (RBC) treated with phenylhydrazine or neuraminidase, but not to the surface of non-treated RBC. Based on these results, anti-cytoskeletal protein antibody in sera of B. gibsoni-infected dogs is considered to attach to native RBCm, and furthermore free radical-induced oxidative stress imposed on RBC and sialic acid removal from glycoproteins of RBC are considered necessary for anti-transmembrane protein antibody in sera of B. gibsoni-infected dogs to be bound to RBCs. These are important to elucidating the mechanism of the marked increase in RBCs-bound IgG value and anemia in B. gibsoni infection.

Animals↗

PubMed1994

[A case of limited Wegener's granulomatosis with hemophilia A, complicated by empyema, bronchopleural fistula and herpes zoster during therapy].

A 36-year-old man with hemophilia A was admitted to hospital because of otalgia, hearing loss, nasal obstruction, nonproductive cough, and high fever. His laboratory data showed high-grade acute inflammatory reactions. His chest X-ray and CT films showed multiple cavitary masses in the right lower lung field. Bronchoscopy performed at our institution revealed bronchial nodules in the intermediate truncus, and BAL revealed increases in the neutrophils and an IgG index (BAL IgG/albumin divided by serum IgG/albumin). Biopsy specimens obtained from nasal mucosa showed epithelioid granulomas with Langerhans' giant cells and necrotizing vasculitis. Antineutrophil cytoplasmic antibodies were also positive, but no evidence of glomerulonephritis was observed. The diagnosis of limited Wegener's granulomatosis was thus made. He was treated with standard therapy (daily cyclophosphamide and glucocorticoids), but within 1 month he had complications of empyema with herpes zoster, and bronchopleural fistula. The complications resolved with appropriate treatment.

Adult↗