[Nutrient requirement for a Japanese population--(the 4th revision].
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Activities of Daily Living↗
Biomedical subjects
K Kosaka
Publications and source records attributed to K Kosaka.
Cell membrane changes in brains manifesting senile plaques: an immunohistochemical study of GM1 membranous ganglioside.
To investigate structural changes in cell membranes of the Alzheimer-type dementia (ATD) brain, we immunostained for GM1 ganglioside which is a major component of the cell membrane. Our results have shown that astrocytic membranes and senile plaques (SPs) have the same immunoreactivity against the monoclonal anti-ganglioside GM1 antibody. Moreover, the astrocytic processes within the SPs were altered and their abnormal membranes seemed to contribute to the formation of SPs.
Aged↗
Localization of serotonin immunoreactivity in cephalopod visual system.
The distribution of 5-HT-like immunoreactivity in paraformaldehyde-fixed sections of retina, optic nerve and the optic lobe of Octopus vulgaris was studied by both immunofluorescence and avidin-biotin complex (ABC) immunohistochemical methods utilizing polyclonal antibodies to 5-HT. Some immunoreactive serotonin-containing cells were demonstrated in the retinal plexus, optic nerve, the ciliary body and the lens-generating tissue by both methods. An analysis of dissected retina and optic nerve of Octopus vulgaris by high pressure liquid chromatography (HPLC) with an electrochemical detector (ECD) also showed the presence of 5-HT. In the optic lobe, three 5-HT-immunoreactive bands in the plexiform layer of the cortex were clearly immunostained, and in the medulla both the cell islands and the neuropil contained some cells immunostained by both fluorescein isothiocyanate (FITC) and ABC methods. This is the first report on the systemic immunocytochemical visualization of 5-HT-containing cells and/or fibers in the cephalopod visual system.
Animals↗
Morphological characteristics of senile plaques in familial Alzheimer's disease.
The distribution and morphology of senile plaques (SPs) in the cerebral cortices and subcortical nuclei of six cases of familial Alzheimer's disease (AD) were examined using the Methenamine-Bodian method and compared with those of sporadic AD cases. SPs were grouped into three types according to their morphology. SP types were generally constant at each anatomical site in all of the cases. The SPs of familial cases, however, had a greater tendency to fuse together than those of sporadic cases, especially in the cingulate cortex, presubiculum and striatum. This tendency was more evident in cases with severe amyloid angiopathy. Here it appeared that a SP type corresponding to "diffuse plaques", at least in part, might be formed by transformation from another type. In the globus pallidus, all the familial cases had many compact-like plaques which appeared to be derived from "drusige Entartung" of the capillaries. Furthermore, the regional proportion of two types of SPs occurring in this nucleus varied along its anteroposterior axis. These findings may be the histological hallmarks of atypical AD rather than familial AD.
Alzheimer Disease↗
Distinctive, rapid, and easy labeling of diffuse plaques in the Alzheimer brains by a new methenamine silver stain.
We have developed a new methenamine silver (MS) stain for detecting diffuse plaques distinctively on paraffin-embedded tissue sections of Alzheimer-type dementia, Down's syndrome, and mentally normal aged brains. This rapid and easy method selectively labels amyloid-related component of senile plaques, but not of kuru plaques found in Gerstmann-Sträussler syndrome. Our MS stain shows almost the same staining pattern as that of the beta protein immunostaining with formic acid pretreatment. Therefore, new MS stain is appropriate to routine or screening studies for senile plaques including diffuse plaques.
Alzheimer Disease↗
Diffuse Lewy body disease in Japan.
Thirty-seven Japanese autopsy cases with diffuse Lewy body disease (DLBD) were reviewed from a clinicopathological viewpoint. Based on the neuropathological finding of whether or not many concomitant senile plaques (SPs) and/or neurofibrillary tangles (NFTs) are present. DLBD is divided into two forms: a common form and a pure form. In the common form not only numerous Lewy bodies but also many SPs and/or NFTs are found in the cerebral cortex, whereas in the pure form there are no or few senile changes. Of the 37 cases, 28 cases had the common form, and 9 had the pure form of DLBD. In the common form all cases had shown progressive cortical dementia in the presenile or senile period. About 60% of the cases began with memory disturbance, while 25% showed Parkinson's or Shy-Drager syndrome initially. Parkinson's syndrome, consisting mainly of muscular rigidity and akinesia, was usually marked in the later stage, although there were also 8 cases (28.6%) in which no parkinsonian symptoms were detected even in the terminal stage. On the other hand, almost all cases with the pure form of DLBD showed juvenile Parkinson's syndrome, followed by progressive cortical dementia, although there was one presenile case with mild dementia and Parkinson's syndrome. These Japanese cases are compared with cases reported in Western countries.
Adolescent↗
Light and electron microscopic examination of amyloid-rich primitive plaques: comparison with diffuse plaques.
In Alzheimer-type dementia brains, numerous "amyloid-rich primitive plaques (PPs)" were observed with beta-protein immunostaining and periodic-acid methenamine (PAM) staining. These amyloid-rich primitive plaques were accompanied by various degrees of small argyrophilic rod-like, granular or filamentous structures. Routine and modified-PAM electron microscopy revealed many bundles and flecks consisting of amyloid fibrils scattered widely throughout the plaques. Degenerate neurites, astrocytic processes and bundles of glial fibres also participated in the formation of the plaques. The similarities and differences between these amyloid-rich primitive plaques and diffuse plaques are described.
Alzheimer Disease↗
Selective loss of nigral neurons in Pick's disease: a morphometric study.
Loss of neurons from the substantia nigra (SN), which is often encountered in Pick's disease, was quantitatively analyzed in 13 cases of Pick's disease and 19 age-matched controls. On sections from the upper and lower portions of the SN, the pigmented zone (zona compacta) and the non-pigmented zone (zona reticulata) were delineated, and these zones were partitioned into quarters: medial, mid-medial, mid-lateral and lateral. Neuronal loss was fairly severe and more evident in the upper section of the SN (-40%), especially in the mid-medial and lateral quarters. In the lower section (neuronal loss: -28%), the medial quarter was most severely affected. Non-pigmented neurons were preserved. Fibrillary gliosis was denser in the zona reticulata, where neuronal loss was minimal. These findings revealed a selective vulnerability of nigral neurons according to their topography and pigmentation and suggests the primary involvement of some neuronal groups (especially the pigmented neurons) of the SN in Pick's disease.
Aged↗
Pancreatic cytokeratin: an antigen of pancreatic exocrine cell autoantibodies in type 1 (insulin-dependent) diabetes mellitus.
Autoantibodies reacting with human pancreatic exocrine cells were investigated by immunofluorescent techniques in 107 patients with Type 1 (insulin-dependent) diabetes mellitus, 20 first-degree relatives of the Type 1 diabetic patients, 347 patients with Type 2 (non-insulin-dependent) diabetes, 34 with alcoholic pancreatitis, 26 with rheumatoid arthritis and 107 normal control subjects. Both immunoblotting analysis and double-immunostaining methods were used to characterize the antigens targeted by the pancreatic exocrine cell autoantibodies. Sera positive for human pancreatic exocrine cell cytoplasm, producing a "fine fibrillar" pattern, were found in 21% (23/107) of the Type 1 diabetic patients. The autoantibodies were present in 39% (15/38) of Type 1 diabetic patients diagnosed within 3 months, and the prevalence decreased with duration of diabetes. The antibodies were of the IgM class in 87% (13/15) of recent-onset Type 1 diabetes cases, but IgG-autoantibodies became more prevalent with increasing duration of diabetes. Three out of 347 (0.9%) Type 2 diabetic patients and 4 of 20 (20%) first-degree relatives of Type 1 diabetic patients had autoantibodies targeted against pancreatic exocrine cells. None of the patients with alcoholic pancreatitis or rheumatoid arthritis and none of the control subjects had these antibodies. Immunoblotting analysis and double-immunostaining demonstrated that the autoantibodies reacted with 40 kilodalton cytokeratin in pancreatic exocrine cell cytoplasm. The antibody was absorbed by the Triton X-100-insoluble fraction of pancreatic extract. These results indicate the presence of distinct autoantibodies to pancreatic exocrine cells in Type 1 diabetes. This suggests the provocative concept that the cytoskeletal system of pancreatic exocrine cells is involved in the pathogenetic process of Type 1 diabetes.
Adolescent↗
Lectin-reactive profiles of alpha-fetoprotein characterizing hepatocellular carcinoma and related conditions.
Serum alpha-fetoprotein from 146 patients with hepatocellular carcinoma, other malignancies, and benign liver diseases, was fractionated by lectin-affinity electrophoresis coupled with our sensitive detection method of antibody-affinity blotting. Compared with chronic hepatitis and liver cirrhosis, hepatocellular carcinoma was characterized by the increase in proportions of lentil lectin A-reactive alpha-fetoprotein-L3 and erythroagglutinating phytohemagglutinin-reactive alpha-fetoprotein-P4; the yolk sac tumor was characterized by the increase of concanavalin A-nonreactive alpha-fetoprotein-C1, lentil lectin-A-weakly reactive alpha-fetoprotein-L2, erythroagglutinating phytohemagglutinin-strongly reactive alpha-fetoprotein-P5, and Allomyrina dichotoma lectin-nonreactive, slow-migrating alpha-fetoprotein-Als; and gastrointestinal tumors were characterized by alpha-fetoprotein-C1, alpha-fetoprotein-L2, alpha-fetoprotein-L3, alpha-fetoprotein-P5 and Allomyrina dichotoma-nonreactive alpha-fetoprotein-A1. By combined evaluation of alpha-fetoprotein-L3 and alpha-fetoprotein-P4, hepatocellular carcinoma was discriminated from chronic hepatitis and liver cirrhosis with a sensitivity of 97% at a specificity of 99.7%. Because the alpha-fetoprotein level of the studied cases ranged from 60-1,500,000 ng/mL (60-1,500,000 micrograms/L), mostly greater than 200 ng/mL (200 micrograms/L), additional patients with lower levels of alpha-fetoprotein [16-177 ng/mL (16-177 micrograms/L) for 16 cases of hepatocellular carcinoma with liver cirrhosis and 28-185 ng/mL (28-185 micrograms/L) for 17 cases of liver cirrhosis alone] were analyzed for alpha-fetoprotein-L3 and alpha-fetoprotein-P4. The resulting sensitivity for combined evaluation was still as high as 88% at the same high specificity of 99.7%, indicating that the simultaneous analysis of alpha-fetoprotein-L3 and alpha-fetoprotein-P4 is effective in monitoring the evolution of hepatocellular carcinoma in cirrhotic patients.
Adult↗
Neuropathological study of the amygdala in presenile Alzheimer's disease.
We studied neuropathological changes of the amygdala in 10 cases of presenile Alzheimer's disease. According to the anatomical classification of the amygdala, we subdivided the corticomedial group into 3 parts, and the basolateral group into 8 parts. We investigated qualitatively neuronal loss, and quantitatively the numbers of neurofibrillary tangles (NFTs) and senile plaques (SPs) in 11 parts. The degree of atrophy of the amygdala was also checked in relation to the clinical stages of the disease. Neuronal loss was more prominent in the later clinical stages. It was more intense in the corticomedial group than in the basolateral group. The density of NFTs tended also to be greater in the corticomedial group than in the basolateral group, although it did not always increase in parallel with the progress of dementia. The density of SPs was greater in the basolateral group than in the corticomedial group, and tended to increase in parallel with the progress of the disease. Atrophy of the amygdala was generally more prominent in the more advanced clinical stage. The distribution pattern of neuronal loss was similar to that of NFTs in the amygdala, whereas the distribution pattern of SPs was quite different.
Alzheimer Disease↗
Relationships among islet cell antibodies, residual beta-cell function, and metabolic control in patients with insulin-dependent diabetes mellitus of long duration: use of a sensitive C-peptide radioimmunoassay.
Relationships among islet cell antibodies (ICA), residual beta-cell function, and metabolic control were studied in 60 insulin-dependent diabetics (IDDs) of long duration (6 to 31 years). Sensitive C-peptide immunoreactivity (CPR) and ICA assays with limits of 0.017 nmol/L and 5 Juvenile Diabetes Foundation (JDF) U, respectively, demonstrated that baseline (0.16 +/- 0.02 nmol/L, mean +/- SE, n = 26), as well as maximum CPR values (0.34 +/- 0.05 nmol/L), during 100-g oral glucose tolerance tests (OGTT) in ICA-positive IDDs were significantly higher than corresponding values in ICA-negative ones (baseline values, 0.10 +/- 0.01 nmol/L, P less than .05; maximum values, 0.20 +/- 0.04 nmol/L, P less than .01, n = 34). Negative correlation was observed between increment of serum CPR and metabolic control indices, including fasting blood glucose (FBG) and HbA1c levels (P less than .05). In addition, ICA-positive insulin-dependent diabetes mellitus (IDDM) patients had lower values of FBG (8.2 +/- 0.4 mmol/L, P less than .01 v ICA-negative IDDs) and HbA1c (9.2% +/- 0.2%, P less than .05 v ICA-negative IDDs) than ICA-negative ones (FBG, 9.9 +/- 0.4 mmol/L; HbA1c, 9.8% +/- 0.2%). These results indicate that minute CPR responses to OGTT detected by sensitive methods may represent residual pancreatic beta cells, which may contribute to ICA generation and good metabolic control in IDDs of long duration.
Autoantibodies↗
[An autopsy case of complicated form of spastic paraplegia with amyotrophy, mental deficiency, sensory impairment, and parkinsonism].
An autopsied case of complicated form of spastic paraplegia with many unusual clinical and pathological features is reported. Present case: a 31-year-old male. His parents are first cousins. Pregnancy and delivery had been unremarkable. Though he was mentally retarded, his physical development was normal. He was considered normal until age 10. He suffered from progressive disturbance in gait at the age of 11. He could not walk without assistance at the age of 22. Neurological examination revealed the following findings. He was obese and mentally deteriorated. Spastic paraplegia with increased tendon reflexes and pathological reflexes was prominent. Though slight sensory disturbance was present in the lower extremities, neither involuntary movement nor cerebellar ataxia was observed. In the age of late 20's, dementia, general muscular atrophy, and Parkinsonism developed. At the age of 30, he could not move by himself. He was apathic and indifferent, and showed forced laughing. Muscle tonus was flaccid because of general muscular atrophy and peripheral neuropathy. He died of acute gastric enlargement. Neuropathological findings were characterized by mal-development of the central nervous system (CNS) and the multisystem degeneration. There existed cerebral white matter hypoplasia with hypogenesis of the corpus callosum and ectopia of neurons of the cerebral and cerebellar cortex. Hypoplasia of melanin pigment was also observed in the remaining neurons of the substantia nigra and the locus ceruleus. Many neurons in the CNS included lipofuscin granules of variable shapes. Some of them showed clusters of several block-like inclusions which were green with luxol fast blue and cresyl violet stain.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
[Recent concept and classification of diabetes mellitus].
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Diabetes Mellitus↗
[Diagnosis of diabetes mellitus].
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Adolescent↗
[A new automated renal biopsy technique under ultrasound guidance].
We evaluated a new automated biopsy device for percutaneous renal biopsies under ultrasound guidance, which was recently introduced in Japan for prostate biopsies. This device (Biopty-Gun: Bard Biopty Instrument Uppsala, Sweden) employs a Tru-Cut type smaller needle (18 gauge). We were able to obtain one or two renal tissues in all 57 cases with great ease and in little time. The length of specimen was sufficient (5-17 mm), but the width was thinner than the samples with the Vim-Silverman or Tru-Cut needles. We could achieve a definitive pathological diagnosis in 54 of 57 cases (94.7%), but now, we try to obtain two pieces of tissue for taking more adequate tissue. Only three patients had perirenal hematomas noted by computerized tomography or ultrasonography. We believe that this new automated technique offers a safer and more effective means of obtaining renal tissue.
Adolescent↗
Proposal of leukotoxin, 9,10-epoxy-12-octadecenoate, as a burn toxin.
It is postulated that toxic substances (burn toxin) synthesized in burned skin are transferred into general circulation and cause multiple organ failure. We found a highly cytotoxic substance, leukotoxin, a linoleate epoxide, exists in burned skin. Leukotoxin, as the name indicates, was synthesized by leukocytes from linoleate as a substrate. The aim of this study is to evaluate the possibility of leukotoxin as a burn toxin. We studied plasma leukotoxin level of four patients with extensive burns (over 50% of body surface area) and examined coagulation studies in these patients. We detected considerable amounts of leukotoxin (11.4 nmol/ml-37.0 nmol/ml) in all patients. Leukotoxin was not detected in the control subjects. Pulmonary edema, cardiac failure, and coagulation abnormalities were found in these patients. Exogeneously administered leukotoxin induced similar pathological conditions in experimental animals to those observed in patients with extensive burns. Hence, it is concluded that leukotoxin is a responsible substance as a burn toxin.
Adult↗
The formation of prostaglandins in the postmortem cerebral cortex of Alzheimer-type dementia patients.
The formation of arachidonic acid metabolites [prostaglandin (PG)D2, PGE2, PGF2 alpha, 6oxo-PGF1 alpha and thromboxane (TX)B2] has been examined in the frontal, temporal, and parieto-occipital regions of the cortex in the postmortem brains from five patients with a pathologically verified Alzheimer-type dementia (ATD) and in eight, age-matched controls. The study disclosed that the amount of PGD2 and TXB2 found in the ATD brains was greater than in controls, and that the formation of PGD2 was significantly increased in the frontal cortex of the ATD brains. Other PG metabolites, however, showed no significant changes in the ATD group. Since it is known that PGD2 is synthesized mainly in neurons, our results seem to suggest that the preserved cortical neurons in the ATD brain have an accelerated PGD2 production.
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