[Anti-centromere antibody positive case of malignant lymphoma].
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Aged↗
Biomedical subjects
T Inagaki
Publications and source records attributed to T Inagaki.
Ultrastructural identification of light microscopic giant mitochondria in alcoholic liver disease.
Ultrastructural identification of light microscopic giant mitochondria was performed on the same specimens for light and electron microscopic observations. The liver tissue specimens were fixed in OsO4, embedded in epoxy resin, cut 4 microns thick and stained with polychrome. At the beginning of the study a light microscopic observation was made, and a microphotograph was taken. The identification of light microscopic giant mitochondria by conventional microscopy was identified by the occupation rate in liver cells, the negative findings of stainability and the morphological consistency (round, cigar-shaped and granular). The specimens were subsequently embedded again in epoxy resin and cut into ultrathin sections of 400 A. A transillumination electron microscope was used for the observation, and ultrastructural images of light microscopic giant mitochondria revealed that they were crystalloid bodies with a crystalline latticelike structure. The occupation rates within liver cells and the morphological shapes of the crystalloid bodies corresponded with those of light microscopic giant mitochondria. The light microscopic giant mitochondria obviously had different features from those of electron microscopic giant mitochondria and Mallory bodies (Yokoo's type II), although Mallory bodies showed the same staining properties as light microscopic giant mitochondria.
Cytoplasm↗
Granulovacuolar degeneration in the hippocampal cortex of aging and demented patients--a quantitative study.
The occurrence and topographic analysis of granulovacuolar degeneration (GVD) in the hippocampal cortex of mentally normal controls (75 cases) and patients with Alzheimer's dementia (AD; 17 cases which included Alzheimer's disease and senile dementia of Alzheimer type), multi-infarct dementia (MID; 16 cases), Pick's disease (PD; 5 cases) and atypical dementia [5 cases; non-Alzheimer, non-Pick dementia with Fahr's syndrome (NANPDF)] were investigated. GVD was rarely found in control cases below the age of 60 years. In elderly normal brains, the statistically most representative ranking order of predilection for GVD (in decreasing severity) was: in the 60 s, CA1 > prosubiculum > CA2 (no GVD was found in the CA3 and CA4); in the 70 s, CA1 > prosubiculum > CA2 > CA3 > CA4; in the 80 s, CA1 > prosubiculum > CA2 > CA3 > CA4; in the 90 s, CA1 > prosubiculum > CA2 > CA3 > CA4. In the brains of demented patients, the rank order for GVD was: for AD, CA1 > CA2 > CA3 > prosubiculum > CA4; for MID, CA1 > prosubiculum > CA2 > CA3 > CA4; for PD, CA1 > CA2 > CA3 > prosubiculum > CA4; and for atypical dementia (NANPDF), CA1 > CA2 > prosubiculum > CA3 > CA4. The similarity of the predilection to ranking order was noted both in normal aged subjects and in MID as well as both in AD and in PD.(ABSTRACT TRUNCATED AT 250 WORDS)
Adolescent↗
Relationship between superoxide dismutase (SOD) and viral liver diseases.
Immunohistochemical evaluation of Cu, Zn- and Mn-superoxide dismutase (SOD) activity in various viral liver diseases was performed by the peroxidase-conjugated antibody indirect method. Anti-human Cu, Zn-SOD (rabbit) and anti-human Mn-SOD (guinea-pig) derived and purified from SOD of human erythrocytes and placentas were used to determine SOD distribution in liver tissues. SOD in the liver tissues was detected in 68 inpatients of our unit. They consisted of 23 cases with chronic hepatitis caused by hepatitis B virus (13) and hepatitis C virus (10), 24 with liver cirrhosis caused by hepatitis B virus (5) and hepatitis C virus (19) (15: compensatory, 9: decompensatory) and 21 with hepatocellular carcinoma caused by hepatitis B virus (2) and hepatitis C virus (18) complicated of liver cirrhosis. In viral liver diseases, SODs in the liver tissues were distributed to hepatocytes mainly in the pattern of cytoplasmic diffusion. The incidence of immunohistochemical Cu, Zn-SOD and Mn-SOD were 47.8% and 56.5% in chronic hepatitis, 93.3% and 86.7% in compensated liver cirrhosis, 11.1% and 22.2% in decompensated liver cirrhosis, respectively. The aggression of viral liver disease was accompanied with the decrease of SOD concentration in the liver tissues. Hepatocellular carcinoma cells were negative for Mn-SOD in all cases, and weakly positive for Cu, Zn-SOD in 2 out of 21 cases. Comparatively strongly positive SOD findings were obtained from normal regions neighboring carcinomas. A close relationship between the depletion of SOD in liver tissues and carcinogenesis in viral liver diseases was observed.
Carcinoma, Hepatocellular↗
Immunoreactive parvalbumin concentrations in parahippocampal gyrus decrease in patients with Alzheimer's disease.
By using a sensitive enzyme immunoassay system for rat parvalbumin, we determined parvalbumin contents in the 4 cerebrocortical regions (superior frontal gyrus of frontal lobe, parahippocampal gyrus of temporal lobe, superior parietal lobule of parietal lobe, and calcarine area of occipital lobe) of patients with Alzheimer's disease and age-matched controls. Among the 4 regions, concentrations of parvalbumin were the highest in calcarine area (68.6 +/- 6.7 ng/mg protein, rat parvalbumin equivalents, mean +/- SE) and the lowest in the parahippocampal gyrus (11.0 +/- 1.7 ng/mg protein) in the controls. A similar regional difference of the concentration was observed also in the patients with Alzheimer's disease. When compared with the controls, however, concentrations of parvalbumin in parahippocampal gyrus of patients with Alzheimer's disease (4.0 +/- 0.9 ng/mg protein) were significantly low (P less than 0.01), showing less than a half of the control values. In contrast, the concentrations in the 3 other regions showed little difference between Alzheimer's disease and the controls.
Alzheimer Disease↗
Developmental and age-dependent changes of 28-kDa calbindin-D in the central nervous tissue determined with a sensitive immunoassay method.
For the quantitative analysis of vitamin D-dependent 28-kDa calcium-binding protein (calbindin-D) in the CNS, we have established a highly sensitive immunoassay method. The antisera were raised in rabbits with purified calbindin-D from rat kidneys, and the antibodies were purified with a calbindin-D-coupled Sepharose column. The purified antibodies were specific for calbindin-D, showing a single band on the immunoblot with the extract of rat kidney or cerebellum. The sandwich-type immunoassay system was prepared by the use of purified monospecific antibodies, and the minimum detection limit of the assay was 0.1 pg or 3.6 amol of calbindin-D, which was sufficiently sensitive for the measurement of calbindin-D content in isolated Purkinje cell bodies at the level of single cells. The average content of calbindin-D in a single Purkinje cell was 0.05 pg. Calbindin-D was detected in most of the rat tissues examined, but it was present predominantly in the kidney and CNS, especially in the cerebellum. Calbindin-D was detected at a similarly low level in the cerebral cortex, cerebellum, and brainstem of rat embryos of 15 gestational days, and it increased gradually but differently in these regions, reaching the respective adult levels by 4-5 weeks of postnatal age. In contrast, kidney calbindin-D increased sharply between 15 gestational days and 3 postnatal days, reaching the adult level by 6 days of age. Calbindin-D levels in the adult rat CNS were affected little by age, whereas the concentrations in human cerebral cortices were significantly low in the aged brain as compared with those in the young brain.(ABSTRACT TRUNCATED AT 250 WORDS)
Aging↗
[Bedridden elderly and dementia].
The purpose of this study is to clarify possible correlations between dementia and long term bedridden elderly patients in our special nursing home and geriatric hospital. At the time of our study, 42.6% of all our patients were bedridden, and the ratio increased in those groups of advanced age. The percentage of bedridden female patients was higher than that of males. Most bedridden patients, suffered disorders of the nervous system particularly disorders caused by cerebrovascular disease. Among the bedridden patients, the incidence of dementia was 82.8%. In most these cases, the degree of dementia was severe. The types and respective percentages of dementia were as follows: Vascular type 45.1%, Alzheimer's type 23.2%, mixed type 19.5% and others 12.2%. We think that Alzheimer's type dementia may cause a patient to become bedridden. On the other hand, vascular type dementia may be promoted by a patient's being bedridden for a long time. Tube-fed patients comprised 20% of all bedridden patients and all of these patients showed dementia. We believe that a patient's getting out of bed and receiving rehabilitation as soon as possible is vital to the prevention of becoming permanently bedridden. In respect to the present study of bedridden dementia patients, we would like to further study tube feeding and terminal care.
Aged↗
[Immunohistochemical studies on S-100 beta positive structures in the human hippocampus in regard to age and morphological change of dementia].
The histological localization of S-100 beta protein in the hippocampus of human autopsy brains of 47 males (71-103 years old) and 90 females (56-104 years old) was studied immunohistochemically. Astrocytes and their processes were positively stained, but neuronal cells were not stained. However, Alzheimer's neurofibrillary tangle-like, senile plaque-like and fibrillary spindle figures were stained positively. S-100 beta positive structures increased in grade with age, but not always equally on Alzheimer's neurofibrillary tangles or senile plaques stained by Bodian method. Astrocytes decreased in number with age, and showed marked compensatory hypertrophy of their processes. S-100 beta positive structures seemed to be related to astroglial changes in terms of degeneration or loss of synapses.
Aged↗
[Five year follow-up study on dementia in institutions for the elderly].
The purpose of this study was to clarify the prognosis of senile dementia based on a 5-year follow-up study in institutions for the elderly. The subjects consisted of 747 cases over 60 years of age. Of these 316 cases showed clinical dementia but 431 cases had no intellectual disturbance in July, 1987. The mortality rate (56.3%) of the demented group was significantly higher than that (31.8%) of the non-demented group. The mortality rate of patients increased with aging. However, the mortality rate of the demented group did not correlate with the severity of dementia. An autopsy study revealed that the direct causes of death in 51.1% of demented patients were pneumonia and cardiovascular diseases. Among the demented patients followed up for 5 years, 22.5% showed severe worsening of dementia, 25.8% showed slight or moderate degree of worsening and 51.7% showed no change. Factors causing exacerbation of dementia included cerebrovascular disease and bone fracture.
Aged↗
[Intellectual ability and activity of daily living of centenarians in institutions for the elderly].
The purpose of this study was to assess the intellectual ability and activity of daily living (ADL) of 12 centenarians in institutions for the elderly and to compare them with individuals in the 62-99 age group. At the time of our study, 66.7% of the centenarians were severely demented, three quarters of them suffering from Alzheimer's type dementia and the other one quarter the mixed type. There were qualitative differences between non-demented centenarians and the demented elderly in general, particularly in regard to understanding of surrounding objects and the presence or absence of mental symptoms indicating intellectual deterioration. A total of 50% of the centenarians were bedridden, but 41.7% of them could eat without assistance. Intellectual ability and ADL directly decreased with aging. We think centenarians do not present a special case and our clinical observations suggest a continuous process of aging. Five of the centenarians recently died and were autopsied. The agreement rate between clinical diagnoses and pathological findings with respect to dementia was 80%.
Activities of Daily Living↗
[A case of an aged patient suspected of craniopharyngioma with a chief symptom of eunuchoidism accompanied with panhypopituitarism].
A 78-year-old man with developmental disturbance of the genital organs and eunuchoidism was reported. He also had a high pitched voice, thickness of the lower lip and kyphosis of the thorax. He seemed to be fretful, but his intelligence was normal. Neurological tests revealed bilateral hemianopsia and decreased tendon reflexes. A plain skull radiograph clearly showed an egg shaped calcified mass extending upward from the sella turcica which resembled a ballooning shape. Brain CTs showed a high density round mass which expanded the sella turcica and raised the floor of the third ventricle. The inner part of the tumor showed irregular high density. T1-weighted MR imaging revealed an iso signal intensity, and T2 showed low signal intensity in the mass. These findings strongly supported the diagnosis of calcificated craniopharyngioma. Endocrinological study showed panhypopituitarism caused by the tumor compressing the pituitary gland and the hypothalamus. The main reasons why there were no apparent symptoms of hypopituitarism were because the receptors were up-regulated and secondarily because the thyroid and the adrenal cortical functions decreased while struggling to maintain balance with each other. There was also a possibility that these symptoms might have been masked by normal aging. Benign monoclonal hypergammopathy was also indicated, although we could not find a clear correlation between this finding and others.
Adrenocorticotropic Hormone↗
[A case of brain dead patient with a spinal pathology of preserved marginal white matter and pencil-shaped softening--a theory for pathogenesis of pencil-shaped softening].
We reported a case of brain death which had been caused by massive cerebral hemorrhage. The spinal pathology showed preserved marginal parts of spinal white matter in the segments of C7 to T5 and S1 to S3, and the other parts showed necrosis. We found pencil-shaped softening (PS)-like lesion in the segment C8 to T2, but the lesion was more preserved than the surrounding tissue. The intraspinal structure of C5 was distorted by the necrotic cerebellar tissue in the subarachnoid space of the segment and the posterior column area was decreased. The posterior column in C5 and PS showed the same severe pathology. Because the pia mater of the spinal cord is not so easily torn, and has some elasticity, swollen spinal necrotic tissue has no place to move but in a longitudinal direction; that circumstance may cause the PS. In this case the subarachnoid cerebellar tissue restricted the expansion of the spinal cord in C5, which might have helped cause PS. So we suggest that the subarachnoidal cerebellar tissue and changes of antero-posterior diameter in the spinal column, when the spine is flexed or extended, may contribute to the pathogenesis of PS. In this case the pathology of the PS was reversed as compared to the usual PS, because the PS was relatively preserved while the surrounding tissue was necrotic. There have been only a few reports which show preserved marginal white matter of the spinal cord.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗
[An autopsy case of ataxic form of Creutzfeldt-Jakob disease].
An autopsy case of ataxic form of Creutzfeldt-Jakob disease (Brownell and Oppenheimer, 1965) was reported. The patient, a 71-year-old male, noticed ataxic gait at the beginning of June in 1988, and was admitted to the Hiroshima City Hospital for the neurological examination at the end of June. He showed ataxia of the left arm and legs and diplopia. Gradually he became delirious at night. On July 16, tremor-like involuntary movement of the left hand was noticed. On July 20, he became somnolent and doubly incontinent. Myoclonus and paratonic rigidity were also observed. The EEG showed periodic synchronous discharge on July 25. The brain CT and MRI were normal. He became apallic gradually and died on October 28. The duration of illness was 5 months. At autopsy, brain weighed 1000gr. Cerebral atrophy and slight enlargement of the ventricles were observed. The cerebellum was also slightly atrophic. Histologically, the destruction of the cerebral cortical layer, slight sieve-like spongy state of the neuropil, slight neuronal loss of the thalamus and sieve-like spongy state of the striatum were observed. The cerebellar lesion was the most severe, where granular cell loss and gliosis of the cortex were observed.
Aged↗
[A case of aneurysm of the gastroduodenal artery diagnosed by endoscopic ultrasonography--review of literatures in Japan].
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Aneurysm↗
[A case of retrovesical fibrosarcoma with severe hypoglycemia].
We report a case of retrovesical fibrosarcoma with severe hypoglycemia. A 67-year-old man was admitted to our hospital with second recurrence of the retrovesical tumor with hypoglycemia. The episodes of hypoglycemia were accompanied by the advance of tumor size. Complete tumor resection with total cystectomy was performed on December 21, 1989, and the tumor was diagnosed histopathologically as fibrosarcoma. Soon after removal of the tumor, hypoglycemia disappeared and the patient has been well without local recurrence or distant metastasis for more than 20 months.
Aged↗
Structurally different rat liver medium-chain acyl CoA dehydrogenases directed by complementary DNAs differing in their 5'-region.
Different forms of rat liver medium-chain acyl CoA dehydrogenase (MCAD) (EC 1.3.99.3) were produced in Escherichia coli carrying expression plasmids (pRMCADm-1 approximately 9) differing at the 5'-region of the cDNA. The proteins expressed could be readily extracted from the cells. The protein (approximately 44 kDa) directed by pRMCADm-3 showed the highest activity and was readily purified to homogeneity. The purified enzyme contained non-covalently bound FAD and was similar to rat liver mitochondrial enzyme in all respects examined. The purified protein (approximately 45 kDa) directed by pRMCADm-1 did not contain FAD and showed no enzymatic activity. Therefore, the leader peptide disturbs the binding of FAD to the apoprotein. The purified protein (approximately 40 kDa) directed by pRMCADm-6 did not contain FAD. Thus, the deletion of the NH2-terminal portion of the apoprotein to some extent results in its inability to combine with FAD.
Acyl-CoA Dehydrogenase↗
Concentrations of several proteins characteristic of nervous tissue in cerebral cortex of patients with Alzheimer's disease.
Concentrations of nervous tissue-related proteins, including S-100 proteins (alpha and beta), enolase isozymes (alpha and gamma), superoxide dismutase (SOD) isozymes (Cu/Zn SOD and Mn SOD), and GTP-binding proteins (alpha subunits of GO and Gi2) were determined in the four cerebrocortical regions (superior frontal gyrus of frontal lobe, parahippocampal gyrus of temporal lobe, superior parietal lobule of parietal lobe, and calcarine area of occipital lobe) of patients with Alzheimer's disease, and age-matched control and young control patients by means of enzyme immunoassay methods. Although the temporal cortex of some patients with Alzheimer's disease (4/7) showed apparently enhanced S-100 beta with decreased gamma-enolase, concentrations of neuronal (neuron-specific gamma-enolase and the alpha subunit of GO) and glial (S-100 beta, S-100 alpha, and alpha-enolase) marker proteins, and both SODs in each region were not significantly different between patients with Alzheimer's disease and the age-matched controls. Concentrations of Gi2 alpha also showed similar values in the cerebral cortices of young and aged controls and patients with Alzheimer's disease. However, when compared with young controls, S-100 beta in the four regions of patients with Alzheimer's disease and aged controls, and Cu/Zn SOD in frontal cortex of patients with Alzheimer's disease were significantly enhanced (P less than 0.01).
Adult↗
[Clinical and pathological study of cerebrovascular disease in the 60-101 age group].
The purpose of this study is to clarify the clinical and pathological characteristics of cerebrovascular disease in nonagenarians and centenarians. In all autopsied cases from 1981 to 1986 (60-101 years old, 138 men and 157 women), cerebrovascular disease was observed in 32 cases (90-101 years old, 8 men and 24 women) and 174 cases (60-89 years old, 95 men and 79 women) in our hospital. The incidence of cerebrovascular disease was 58.3%, 68.8%, 75.1% and 64%, pathologically, in their sixties (60's), seventies (70's), eighties (80's) and over nineties (90's) respectively. In those who had cerebrovascular disease, cerebral infarctions were found in 79.9% of the cases of the under-90 group and 81.2% of cases of the over-90 group. In both groups, infarction was mainly found in over 2 regions, in the putamen, caudate, thalamus and in the white matter and cortex of the frontal lobe. In the over-90 group, the medium-sized infarctions decreased and small-sized infarctions increased. Cerebral hemorrhages were found in 16.1% of cases in the under-90 group and 12.6% of cases in the over-90 group. In the over-90 group, large-sized hemorrhages were found in 75%, and the incidence of hemorrhages was 50%, 50% in the lentiform nucleus and the subcortex respectively. The frequency of mental symptoms, frontal signs and oral dyskinesia in the over-90 group was significantly higher than in the under-90 group. The onset of cerebrovascular attacks was unknown in 43.8% cases.(ABSTRACT TRUNCATED AT 250 WORDS)
Aged↗