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Biomedical subjects

M Takatama

Publications and source records attributed to M Takatama.

At least 19 recordsLinked to original sources
PubMed2001

The pathogenesis of cerebrovascular lesions in hypertensive rats.

In this study we investigated the pathogenesis of hypertensive cerebrovascular lesions by light microscopy, immunohistochemistry, scanning electron microscopy, and transmission electron microscopy. The brains of rats with experimentally induced hypertension exhibited severe edema and intracerebral hemorrhage. Light microscopy of the arteries showed severe medial lesions and the deposition of fibrinoid substance in the intima. Immunohistochemistry showed that intercellular adhesion molecule (ICAM)-1, platelet-endothelial cell adhesion molecule (PECAM)-1, interleukin (IL)-1alpha, IL-6, IL-8, and tumor necrosis factor (TNF)-alpha endothelial cell expression was upregulated. Scanning electron microscopy of these arteries revealed the adhesion of neutrophils, monocytes, and a few platelets to endothelial cells, and their invasion of endothelial cell junctions and opened junctions. Transmission electron microscopy showed neutrophil and monocyte adhesion to the endothelial cells and neutrophil and monocyte invasion of endothelial cell junctions, intimal deposition of fibrinoid substance, and severe medial cell injury. Intravenously injected horseradish peroxidase insulated from endothelial cell junctions and, via pinocytotic vesicles, into the subendothelial space. These findings suggest that hypertension activates endothelial cells to increase the expression of adhesion molecules and cytokines, and induces neutrophil and monocyte adhesion and migration, resulting in endothelial cell injury and increased permeability of endothelial cells, which results in hypertensive arterial disease.

Animals↗
PubMed2001

Different roles of arteriosclerosis in the rupture of intracranial dissecting aneurysms.

AIMS: Although intracranial dissecting aneurysm (IDA) is a newly described variant of the brain aneurysms that affects mainly the vertebrobasilar arterial system, its pathogenesis remains obscure. We aimed to clarify the role of arteriosclerosis in the pathogenesis of IDA based on histopathological findings in seven autopsy cases of IDA. METHODS AND RESULTS: All cases exhibited systemic hypertension or left ventricular hypertrophy. Macroscopically, all cases exhibited subarachnoid haemorrhage. Two types of dissection were recognized in the vertebral artery. Six of seven IDA cases showed a widespread disruption of the entire thickness of the arterial wall with the formation of a dilated pseudoaneurysm, which consisted of thin adventitia (arterial wall disruption type). Medial disruption of the arterial wall and subadventitial dissecting haemorrhage were also found, resulting in the formation of a false lumen and stenosis of the 'true' lumen of the artery. However, these lesions were connected to the site of rupture of the entire arterial wall. Within 1 day after onset of IDA, the autopsy cases showed formation of fibrin thrombus, marked leucocyte infiltration and necrosis of the arterial wall at the site of the lesion. Cases that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration in the lesions. These cases showed no atherosclerotic plaque, but non-atherosclerotic fibrocellular intima. The thickness of intima and media was significantly less in the vertebral artery of IDA patients than that of non-IDA patients with systemic hypertension. On the other hand, the remaining case showed severe atherosclerosis with haemorrhage into the lipid core without connection to the arterial lumen (intra-atheromatous plaque haemorrhage type). However, unusual arterioles and neovascularization of the intra-and peri-arterial walls were observed. CONCLUSIONS: Our results suggest that disruption of the entire arterial wall may be a critical event in the development of IDA and result in the medial disruption and subadventitial haemorrhage. Non-atheromatous intima might function as a protective factor in arterial wall disruption. On the other hand, atherosclerosis may predispose to intra-atheromatous plaque haemorrhage type of IDA through intramural haemorrhage originating from the newly formed vessels.

Adult↗
PubMed2000

The involvement of the neuronal Golgi apparatus and trans-Golgi network in the human olivary hypertrophy.

We studied the Golgi apparatus (GA) and trans-Golgi network (TGN) in the human olivary hypertrophy by immunohistological methods with organelle specific antibodies against the medial cisternae of the organelle (MG160) and the trans-Golgi network (TGN46). The GA and TGN of enlarged neurons in the inferior olivary nuclei in the early stages after central tract lesions lost the normal network-like configuration, and they were reduced to numerous small disconnected granules (fragmentation). In chronic stages after lesions, the GA and TGN of vacuolated or enlarged neurons showed a variety of morphological profiles, such as normal-looking patterns, fragmentation, reduction in number, and aggregation around nuclei or at a distance in the cytoplasm. In patients with multiple system atrophy, the GA and TGN of the neurons in the inferior olivary nuclei showed almost similar findings to those seen in the chronic stages after brainstem lesions. These results suggest that the GA and TGN are affected in degenerating neurons by anterograde transneuronal mechanisms.

Aged↗
PubMed2000

Pathology of a dissecting intracranial aneurysm.

The pathological findings of six autopsy cases of dissecting intracranial aneurysm are studied. Clinically, all cases exhibited systemic hypertension or left ventricular hypertrophy. Macroscopically, all cases exhibited rupture of the vertebral artery and subarachnoid hemorrhage. Two types of lesion were present. First, all cases showed the formation of a dilatated pseudoaneurysm with widespread disruption of the entire arterial wall, which was composed of thin adventitia. Second, a medial disruption of the arterial wall and subadventitial dissecting hemorrhage, which formed a false lumen and stenosis of the 'true' lumen of the artery, was also found. However, these lesions were found to be connected to the site of rupture. The autopsy cases within 1 day of onset of intracranial dissecting aneurysm showed the formation of fibrin thrombus, a marked degree of leukocyte infiltration and necrosis of the arterial wall at the site of the lesion. The cases that survived more than 1 week showed smooth muscle cell proliferation, macrophage accumulation and lymphocytic infiltration. No arteriosclerosis was found in any lesion studied. These data suggest that the disruption of the entire arterial wall might initially occur and cause medial disruption and subadventitial hemorrhage. Hypertension and arteriosclerosis might function as causal and protective factors in the pathogenesis of dissecting intracranial aneurysms, respectively.

Adult↗
PubMed1996

An autopsy case of malignant lymphoma with a high serum CA 125 level occurring only in the brain and pericardium.

We report an autopsy case of a central nervous system (CNS) B-cell type lymphoma followed by cardiac tamponade. In this case, lymphoma cells which occurred primarily in the pericardium appear to metastasize to the brain and gradually increase in size in spite of control of the CNS lesion. The serum carbohydrate antigen 125 (CA 125) level was highly elevated and the autopsy findings showed the involvement of lymphoma only in the pericardium rather than the CNS, and the pericardium, not the tumor cells, was immunohistochemically positive for CA 125. Through this rare case, two things are suggested: first, the serum CA 125 level is elevated when B-cell type lymphoma infiltrates the coelomic epithelium; second, CA 125 is overproduced and secreted by the pericardium but not the lymphoma cells. Measurement of the serum CA 125 level may become a diagnostic marker for the infiltration of malignant lymphoma in the coelomic epithelium such as the pericardium, peritoneum or pleura.

Aged↗
PubMed1995

Extrahepatic portal-systemic encephalopathy without portal hypertension.

We report three cases of extrahepatic portal-systemic encephalopathy (EHPSE), two of which did not show portal hypertension (PH) and in the other of which precirrhotic state with chronic active hepatitis was detected at liver biopsy. Our review of the literature regarding EHPSE without PH leads us to conclude that a part of the shunts is congenitally or spontaneously formed, that PH is not always essential to shunt formation. Since the clinical symptoms most often do not manifest until middle age, cases with only mild disturbance of consciousness are not easily distinguished from dementia. Furthermore, all reported patients underwent shunt closure followed by marked improvement of clinical symptoms and uneventful postoperative course. EHPSE without PH which can be corrected by shunt closure should always be differentiated from EHPSE with PH.

Aged↗
PubMed1994

Localization of metallothionein in aged human brain.

The localization of metallothionein (MT), a small molecular weight heavy metal binding protein in aged human brain, was investigated by immunohistochemical techniques. The amount of MT and heavy metals (Zn, Cu) were also assayed by radioimmunoassay and atomic absorption spectrophotometry, respectively. Immunohistochemically, MT was found in the pia mater, ependymal cells, protoplasmic astrocytes nand glial processes neuropil of the gray matter and fibrous astrocytes of the white matter of the telencephalon, whereas oligodendroglia and microglia did not show any positive immunostaining for MT. Cytoplasm, glial processes and some nuclei of protoplasmic and fibrous astrocytes showed strong MT immunostaining. Vascular feet and adventitia were also positive for MT immunostaining. Moreover, the pia mater, astrocytes and ependyma in the diencephalon, mesencephalon, pons, medulla oblongata and spinal cord showed the same positive immunostaining for MT as the telencephalon. In the cerebellum, Bergmann's glia, protoplasmic astrocytes of the granular layer and fibrous astrocytes of the white matter showed strongly positive immunostaining for MT. According to the radioimmunoassay, the amount of MT in the brain was relatively high at about 39.3 +/- 9.5 micrograms/g wet weight; of the heavy metals in the brain, zinc and copper were detected.

Age Factors↗
PubMed1993

Oculomotor nuclear pathology in amyotrophic lateral sclerosis.

We examined the oculomotor and/or trochlear nuclei of 27 amyotrophic lateral sclerosis (ALS) patients and 10 controls by histological and immunohistological methods. Their neurons were relatively well preserved. In 7 of 22 sporadic ALS patients (including 3/3 ALS with ophthalmoplegia) and in 4 of 5 ALS patients with dementia, some morphological changes similar to those in anterior horns (Bunina bodies, ubiquitin-positive skein-like inclusions, Lewy body-like inclusions, conglomerate inclusions and spheroids) were rarely, but clearly seen. These changes were not observed in controls. Our results suggest that the oculomotor and trochlear nuclei in ALS patients are slightly affected in a manner similar to that in the anterior horns, but the degree is less than that necessary for development of ophthalmoplegia in the majority of ALS patients.

Adult↗
PubMed1993

[A case of pontine infarction with persistent primitive proatlantal artery].

A 61-year-old woman was admitted to the hospital on September 18, 1991 because of left hemiparesis, dysphagia, and dysarthria since five days before. She was formerly pointed out diabetes mellitus and hypertension, but she did not receive any treatment. The MRI showed a high signal area in the right paramedian portion of the upper pons on T2 weighted image and proton image. The angiography showed that persistent primitive proatlantal artery originated from the left internal carotid artery and joined to the horizontal portion of the left vertebral artery. The image of carotid-vertebrobasilar system and proatlantal artery showed so severely arteriosclerotic. This is the first report of brainstem infarction with persistent primitive proatlantal artery. In this case, the pontine infarction was thought to occur on the basis of the arteriosclerosis of blood vessels and change of blood flow of carotid-vertebrobasilar system due to persistent primitive proatlantal artery.

Basilar Artery↗
PubMed1991

Light and electron microscopic and immunohistochemical observations of the Onuf's nucleus of amyotrophic lateral sclerosis.

We examined the Onufrowicz nucleus (Onuf's nucleus) of ten sporadic amyotrophic lateral sclerosis (ALS) patients with light and electron microscopic and immunohistochemical methods. Neurons in the Onuf's nucleus of ALS patients were better preserved than those in anterior horn cells. However, some showed morphological changes in the nucleus, namely, central chromatolytic changes, Bunina bodies, ubiquitin-positive filaments and spheroids. The Onuf's neurons of ALS patients showed more argentophilia than those of non-ALS patients. Electron microscopic observations revealed that neurofilaments were relatively more numerous in the Onuf's neurons of ALS patients. Bunina bodies and degenerated neurites were also seen in the Onuf's nucleus. In conclusion, the Onuf's nucleus in sporadic ALS patients showed some morphological changes similar to those noted in anterior horn cells.

Aged↗
PubMed1991

Ultrastructure of diffuse plaques in senile dementia of the Alzheimer type: comparison with primitive plaques.

We compared the ultrastructure between diffuse and primitive plaques in the brains of senile dementia, using pairs of routine electron microscopic ultrathin sections and adjacent semithin sections, which were immunolabeled for beta protein. In the frontal cortex, amyloid fibrils were rarely seen in a minority of diffuse plaques, suggesting an initial stage of the diffuse plaques. A majority of the diffuse plaques had electron-dense material and/or amyloid fibrils between cell processes in part of but not the entire beta/A4-immunoreactive areas. Small degenerating neurites were often seen with apparent amyloid fibrils in the diffuse plaques, and these were considered to be in an advanced stage. The size and number of degenerating neurites were proportional to the amount of amyloid. Bundles of amyloid fibrils were occasionally surrounded by astroglial processes forming gap junctions. Neurons were found within some diffuse plaques, but capillaries were rarely seen. In contrast, in the temporal cortex, the diffuse plaques were smaller, and even these small ones had apparent amyloid fibrils. The amount of amyloid correlated significantly with plaque size in the temporal cortices, but not in the frontal cortices. Most of the diffuse plaques of the frontal lobe remained as advanced diffuse plaques (apparent amyloid with occasional astroglia and some degenerating neurites) for a long time, and did not transformed into primitive plaques, whereas the temporal diffuse plaques tended to transform into primitive plaques.

Alzheimer Disease↗
PubMed1989

A study of beta protein precursor using antiserum against a synthetic peptide (1-28).

We studied the presence of the beta protein precursor by immunocytochemistry and Western blot analysis using antiserum against a synthetic beta peptide (1-28). The brains of 4 patients with dementia of the Alzheimer type (DAT) were examined immunocytochemically. Frozen and formic acid pretreated paraffin sections were best for beta protein immunostaining. Both the senile plaque amyloid and cerebrovascular amyloid were immunostained with 28K1. In addition to primitive and typical plaques, amorphous granular or fibrous deposits of amyloid were observed in high numbers in various areas of the DAT brains. However, the beta protein precursor, which was suggested to be present in neuronal cells by in situ hybridization, was not stained. Neurofibrillary tangles were not stained, either. Sera and cerebrospinal fluid (CSF) from 6 patients with DAT were examined using Western blot analysis. A 52-kD band was detected with 28K1 in DAT patients as well as in normal controls. Further investigation revealed the 52-kD band to be the heavy chain of IgG. The staining pattern using the beta protein immunostain was quite different from the IgG immunostain. In this study there was no detection of the beta protein precursor, with the use of immunocytochemistry and Western blot analysis. Thus, further investigations are necessary using the antiserum against other residues of the beta protein precursor or using specimens without IgG.

Alzheimer Disease↗
PubMed1989

[Chemical durability of composite resins].

To evaluate their chemical durability, samples of posterior composite resins were stored in NaOH (0.1 mol, 1 mol), HCl (0.1 mol, 1 mol), acetone (99%), and distilled water at 37 degrees C for a week and subjected to the direct tensile test, measurement of surface roughness and SEM observation. NaOH caused the degradation of composite resins, decrease of tensile strength and increase of surface roughness. The SEM photograph of fractured surface of tensile specimens revealed the degradation zone under the surface. It was considered that NaOH caused the hydrolysis of silan coupling of composite resins. HCl also caused the degradation of composite resins, but some resins showed the durability in this condition. More examination is needed to clarify the mechanism of degradation. Acetone caused the degradation of matrix resin and some composite resins. It was considered to dissolve the low degree of polymerized matrix resin of composite resins. Immersion in chemicals of composite resins was thought to be useful to evaluate the chemical durability and to accelerate the degradation in water.

Composite Resins↗
PubMed1989

Immunocytochemical study of alpha 1-antichymotrypsin in the senescent cerebral amyloid.

We immunocytochemically examined the brains of patients with dementia of the Alzheimer type (DAT), to clarify the relation between alpha 1-antichymotrypsin and cerebral amyloid. Antiserum to synthetic beta protein (1-28 residue) was used to stain the senile plaque amyloid and cerebrovascular amyloid. Cryostat sections and paraffin embedded sections pretreated with formic acid were prepared for staining beta protein-like immunoreactivity. Fine, amorphous cerebral amyloid deposits were also positive. alpha 1-antichymotrypsin-like immunoreactivity was also found in senile plaques and cerebrovascular amyloid. Primitive plaque, typical plaque, core plaque and amorphous cerebral amyloid deposits had alpha 1-antichymotrypsin-like immunoreactivity. Eosinophilic extracellular tangles were also positive. Hirano bodies were weakly stained. Intracellular tangles and granulovacuolar degeneration were negative. Double immunoenzymatic staining revealed that alpha 1-antichymotrypsin-like immunoreactivity was very closely related to beta protein-positive senile plaques. About 99% of all plaques had both alpha 1-antichymotrypsin- and beta protein-like immunoreactivities. These results indicate that alpha 1-antichymotrypsin is one of the components of the senile plaque amyloid.

Alzheimer Disease↗
PubMed1989

Immunogold electron microscopic study of cerebrovascular and senile plaque amyloid using anti-beta protein antibody.

Both light and immunogold electron microscopy revealed that beta protein is closely associated with cerebrovascular and senile plaque amyloid. Diffuse (very primitive) plaques of the cerebral cortex and cerebellum in subjects with senile dementia of the Alzheimer type (SDAT) were seen as ill-defined areas of the fine fibrillar materials labeled by beta protein immunostain and silver impregnation. Electron and immunogold electron microscopic investigation revealed that cerebral diffuse plaques consist of accumulations of small bundles of amyloid fibrils scattered among the normal-looking neurites including a few altered neurites. The cell process membranes just adjacent to amyloid fibrils were frequently missing. Cerebellar diffuse plaques had structures similar to cerebral diffuse plaques, with two qualifications. First, the former had more altered neurites, and second, enlarged neurites contained mainly dense bodies and abnormally dense mitochondria lacking filamentous materials. In conclusion, cerebral diffuse plaques, which are the main plaques in SDAT, consist chiefly of amyloid fibrils interspersed among a majority of normal-looking neurites and a minority of altered neurites. This suggests the importance of amyloid deposition in the genesis of senile plaques.

Alzheimer Disease↗
PubMed1988

Role of lysosomes in mesenteric arterial lesions of renal hypertensive rats.

The acid phosphatase activities of arterial cells in the mesenteric arteries of renal hypertensive rats were investigated by both light and electron microscopy. Light microscopically, strongly positive acid phosphatase reactions were confirmed in endothelial cells, intimal cells, medial cells and adventitial cells of the mesenteric arteries, together with considerable deposition of fibrinoid substance in the intima and media in contrast to the appearance in control rats. Electron microscopically, lysosomes with acid phosphatase-positive reaction products were increased in number in endothelial cells, intimal smooth muscle cells, medial smooth muscle cells and adventitial neutrophils or macrophages. The lysosomes in intimal smooth muscle cells and those which were extracellularly discharged were responsible for lysis of the fibrinoid substance. In the media, acid phosphatase-positive lysosomes of medial cells and extracellularly discharged matrix lysosomes with acid phosphatase-positive reactions were also involved in the hydrolysis of necrotic substances and extracellular matrix. These acid phosphatase-positive reactions were diminished both light and electron microscopically in endothelial cells, intimal cells, medial muscle cells and adventitial cells in the regions of healing arteries where fibrinoid substance had been degradated and the intima showed cellulofibrous thickening. The possible role of this acid phosphatase activation for the clearance of cell debris as well as exudative substances in the healing of damaged arterial tissue was discussed.

Acid Phosphatase↗