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Biomedical subjects

T Yamashima

Publications and source records attributed to T Yamashima.

At least 109 records · Page 6Linked to original sources
PubMed1986

Ultrastructural study of the final cerebrospinal fluid pathway in human arachnoid villi.

Human arachnoid villi were studied ultrastructurally to clarify the mechanism of cerebrospinal fluid absorption. Arachnoid villi of humans showed quite different features from those of animals. The former were not always invested with endothelial linings as previously reported in the latter. Instead, there was a covering layer of arachnoid cells which consisted of both an electron-lucent outer zone and an electron-dense inner zone. The outer zone had less cytoplasmic filaments and desmosomes than the inner zone. The inner zone was basically indistinguishable from the arachnoid membrane and had numerous cytoplasmic filaments and a series of desmosomes. Often, the covering layer was further encompassed by the thin fibrous capsule which reflected from the dura mater or sinus wall. Both the outer and inner zones were characterized by numerous extracellular cisterns which appeared, electron-optically, to be empty or contain a little 'fuzzy' material. In the villi affected by subarachnoid hemorrhage, extracellular cisterns were distended by intact of disintegrating erythrocytes which appeared to be natural tracers of cerebrospinal fluid. The size of these cisterns measured approximately 10 microns in the maximum diameter. It is suggested that extracellular cisterns may contribute to the bulk outflow of cerebrospinal fluid.

Adolescent↗
PubMed1986

An electron microscopic study of cerebral vasospasm with resultant myonecrosis in cases of subarachnoid haemorrhage, meningitis and trans-sylvian surgery.

Electron microscopic data on the development of myonecrosis following cerebral vasospasm associated with subarachnoid haemorrhage, meningitis and trans-sylvian surgery are presented. The basic feature of myonecrosis was dissolution of myofilaments with resultant fine granular or filamentous material. The disintegrating cytoplasm often contained numerous glycogen granules, dense bodies, autophagic vacuoles and myelin-like membranous bodies. A well-developed sarcoplasmic reticulum was preserved despite myofilament dissolution, while mitochondria showed marked swelling. The nuclei showed either dilution of chromatin or pyknotic change. The basal lamina was remarkably thickened and maintained an irregular outline of the necrotic smooth muscle cells. Enlarged intercellular space contained abundant cellular debris, vesicular structures and connective tissue fibres. The pathogenesis of these changes is discussed.

Adult↗
PubMed1986

Formation of psammoma bodies in meningocytic whorls. Ultrastructural study and analysis of calcified material.

Psammoma bodies in meningocytic whorls were investigated by electron microscopy. In some whorls, connective tissue fibers were seen and membrane-bound vesicles were contiguous to degenerated cells. Some small vesicles, 0.1 to 0.5 micron in diameter, were outlined by plasma membrane (matrix vesicles), other larger ones, about 1 to several micron in diameter, were invested by a thick wall (matrix giant bodies). Mineralized deposits were frequent in these vesicles and occasionally large masses of mineralized connective tissue fibers (psammoma bodies) were seen. Analysis of the material in the mineralized vesicles and fibers, using an energy dispersive X-ray microanalyzer, showed that both calcium and phosphorous were evident and hydroxyapatite was substantiated using an X-ray diffractometer. Psammoma body formation in the meningocytic whorls may represent degeneration in some whorls of the central cells which contain connective tissue fibers, producing cell debris such as membrane invested vesicles. Subsequently, calcification occurs in these vesicles, and the mineralization process extends to neighboring connective tissue fibers. The calcified mass forms a psammoma body.

Calcinosis↗
PubMed1986

The origin of psammoma bodies in the human arachnoid villi.

The fine structure of the human arachnoid villi was studied to clarify the origin of psammoma bodies. Within the villous surface layer, collagen fibrils and fine granular material clustered forming microcores of variable caliber measuring up to 10 microns. An early stage of psammoma body formation was seen more frequently in these villous microcores than in the meningocytic whorls. The villous microcores contained a large number of membrane-free matrix granules as well as a small number of membrane-bound matrix vesicles and matrix minerals. The matrix granules were irregularly oval structures with electron-lucent halo, measuring 0.05-0.70 micron in diameter. Hydroxyapatite crystals were frequently precipitated within and around the matrix granules which aggregated with calcifying matrix vesicles and matrix minerals. Numerous calcifying matrix granules were present within and around enlarging psammoma bodies. The matrix granules may serve as the principal calcification nidi of psammoma bodies in the human arachnoid villi. The possible mechanisms of matrix granule biogenesis are extrusion of preformed arachnoid cell structures or secretion of fine granular material with its extracellular assemblage.

Adolescent↗
PubMed1986

Abnormal cilia in a malignant ependymoma.

Abnormal cilia were frequently exposed in a malignant ependymoma of the cerebellar vermis by an electron microscope study. Among these erratic cilia, compound cilia, huge axoneme with bizarre shapes, were repeatedly observed. These giant cilia commonly had random orientation of many microtubular doublets as well as complicated cavities in their granular ciliary matrix. Additionally, abnormal cilia of normal-sized axoneme showed diversified arrangement of peripheral doublets and central singlets. The formation process of these abnormal cilia is discussed.

Adult↗
PubMed1986

Amyloid formation in prolactinoma.

Amyloid deposits within a prolactin-secreting pituitary adenoma were investigated with light and electron microscopy. The appearance of amyloid with Congo red revealed amorphous and round green-yellow birefringence under polarized light. Spheroidal concretions disclosed prolactin-positive areas by immunohistochemistry. The amyloid commonly exhibited a structure of fine fibrils of 10 to 13 nm in width, with a hollow core. The fibrils were usually grouped in compact, stout bundles. Some bundles were present in extracellular space, others were obviously within the adenoma cells. Extracellular amyloid fibrils frequently gathered in a stellate arrangement to make a round body. The presence of intracellular amyloid fibrils in adenoma cells may represent that the source of the amyloid is neoplastic cells rather than mesenchymal cells. In addition, prolactin-positive parts in round bodies presumably exemplify that the amyloid fibrils are formed by hormone-relating proteins.

Adenoma↗
PubMed1985

The origin of inner membranes in chronic subdural hematomas.

Electron-microscopic findings of inner membranes of chronic subdural hematomas showed multilayered tiers of flattened cells. The basic characteristics of these cells were similar to dural border cells in the human dura-arachnoid interface layer. The cells covering the hematoma surface had indented nuclei with a prominent nucleolus and were abundant in enlarged rough ER, glycogen granules, lipid droplets, and caveolae. The cells in the intermediate layer had thin cytoplasmic extensions containing tonofilaments, which were oriented almost parallel to the long axis of inner membranes. The cells facing the arachnoid surface sometimes showed disintegration of cellular organelles and dissolution of nuclear chromatin. Between these cells and the tiers was an increased amount of extracellular substance, such as collagen fibrils, elastins, and finely granular material, which were often intermingled with blood pigments or fibrins, especially toward the arachnoid surface. In two of the ten cases studied, there was a syncytial mass of arachnoid cells which reinforced the arachnoid surface of inner membranes. Conceivably, a primary extravasation of blood within the dura-arachnoid interface layer may cleave a few tiers of dural border cells, which envelope the inner surface of the hematoma, proliferate, and later on form inner membranes.

Adult↗
PubMed1985

Meningothelial rosettes in the canine subarachnoid space.

A previously unrecognized type of rosette consisting of meningothelial cells is reported. Meningothelial clusters with a formation of numerous rosettes were incidentally observed in the canine subarachnoid space after single subarachnoid injection of 0.2 mg/kg of epinephrine. Light microscopy revealed that the cell clusters with distinct rosettes occurred in the extensive cords and nests, surrounding the small subarachnoid arteries or adhering to the arachnoid epithelium. There were scattered mast cells adjacent to the cell clusters. Electron microscopy revealed that the rosettes usually consisted of four to 12 tightly packed cells which were arranged like spokes and contained concentrations of tonofilaments. The rosette cells were knitted together by numerous junctional devices, such as desmosomes and desmosome-like junctions as well as a small number of interdigitations at the lateral surfaces toward the central core. The latter measured approximately 0.77-12.72 micron in long diameter, containing electron-dense, coarsely granular material. Both intracytoplasmic and extracellular inclusions with projecting microvilli were reminiscent of hyaline inclusions in certain meningiomas.

Animals↗
PubMed1985

Eosinophil degranulation in the capsule of chronic subdural hematomas.

A previously unrecognized role of eosinophils in chronic subdural hematomas is described. Outer membranes of hematomas with marked infiltration by eosinophils were studied ultrastructurally with particular attention to the degranulation of these cells. In all of the five cases studied, degranulation was observed. Disintegration of the cells contributed to the release of granules. The free granules, the matrix of which has been demonstrated to contain plasminogen, were often circulating in the vascular lumen and trapped among the aggregated platelets. They were also found within the fragile vascular wall surrounded by fibrinoid material and in the edematous perivascular interstitium. Some of the perivascular eosinophils showed frank solubilization of granule matrix contents in spite of unaltered crystalloids. These findings suggest a role of eosinophils in the development of local hyperfibrinolysis within the outer membranes, which might contribute to the fluidity of chronic subdural hematomas and the resultant leakage of blood from the vessels in the capsules.

Cell Membrane↗
PubMed1985

Clinicopathological classification of chronic subdural hematoma.

Clinicopathological classification of chronic subdural hematoma was made, based on a study of 135 cases; chronic subdural hematoma with a visible inner membrane (type I: 123 cases), acute subdural hematoma in chronic healing stage (type II: 8 cases), and chronic subdural effusion of hemorrhagic type (type III: 4 cases). Type I is an expanding lesion, due to repetitive hemorrhage from outer membrane. It is a traditional hematoma with a distinct inner membrane. Type II is a late healing stage of a previously unrecognized or unoperated acute subdural hematoma, and not an expanding lesion. It has a subdural granulation tissue of irregular thickness with little rebleeding tendency, but it lacks a visible inner membrane. Type III is a variant of chronic subdural effusion, in which a minimum amount of fresh blood is added to a maximum amount of xanthochromic fluids. The latter contains an extremely low level of LDH.

Adult↗
PubMed1985

Three phases of cerebral arteriopathy in meningitis: vasospasm and vasodilatation followed by organic stenosis.

A systematic radiological and pathological study of the cerebral arteries was made in an autopsy case of meningitis associated with three phases of cerebral arteriopathy. The latter consisted of vasospasm, vasodilatation, and organic stenosis. A marked change in the caliber of the cerebral arteries was demonstrated 3 times. Vasospasm, the stimulus phenomenon, was produced by the surrounding purulent material. Vasodilatation, the paralytic phenomenon, was presumably due to decreased contractile energy in association with myonecrosis. Organic stenosis, the repair process, was due to the organization of subendothelial edema with resultant intimal thickening. Evidence of increased endothelial permeability, subendothelial proliferation of smooth muscle cells, and necrosis of the latter in the media is presented in both light and electron micrographs.

Adult↗
PubMed1985

[Clinical manifestation of small thalamic hemorrhage].

CT scan is useful for the simultaneous evaluation of the relation between the thalamic lesions and the clinical manifestations. According to CT findings, twenty-three patients with thalamic hemorrhage measuring less than 2 cm in size could be classified into 4 groups: 1) anterior group--hematoma located in the anterior nuclear group, 2) medial group--hematoma located in the medial nuclear group, 3) lateral group--hematoma located in the lateral nuclear group close to the internal capsule, 4) posterior group--hematoma located in the pulvinar. The clinical manifestations of both the anterior and medial groups were characterized by the disturbance of consciousness followed by the mental impairment; the lateral group, by the hemiparesis or hemiplegia with the sensory disturbance, and the posterior group, especially with left thalamic lesions, by the speech disturbance. The motor palsy in cases of thalamic hemorrhage differed from that of putaminal hemorrhage: the patients with thalamic hemorrhage could move their fingers despite being unable to move their shoulders and elbows, or the motor weakness was more severe in their lower extremities than in their upper ones. As the sensory disturbance, the sensory impairment (hypesthesia) was frequently associated with the numbness (dysesthesia). The prognosis of motor palsy, ocular manifestations, and speech disturbance was good, whereas that of sensory and mental disturbance was not always good.

Adult↗
PubMed1984

Clinicopathological study of acute subdural haematoma in the chronic healing stage. Clinical, histological and ultrastructural comparisons with chronic subdural haematoma.

Seven cases of acute subdural haematoma in the chronic healing stage, were studied clinicopathologically. Operation was not performed until 17-30 days after major trauma, and revealed subdural granulation tissue of irregular thickness, but no visible inner membranes. Although this capsule contained blood pigment and numerous macrophages, new haemorrhagic foci or eosinophilic infiltrations were extremely rare. Capsular vessels generally had thick vascular walls, distinct basement membranes and tight endothelial junctions. Perivascular blood substance was presumably not secondary haemorrhage from these vessels, but residue from the acute subdural haematoma itself. The possibility of transition from this haematoma to chronic subdural haematoma is discussed.

Aged↗