Biomedical subjects
Publications and source records attributed to M Tagami.
A case of parathyroid carcinoma is reported. The histology of the parathyroid glands disclosed carcinoma in 1 gland and chief cell hyperplasia in another. Therefore, we recommend careful exploration of all parathyroid glands. An electron microscopic feature of parathyroid carcinoma is presented.
Parasystole is an arrhythmia resulting from simultaneous activity of two independent impulse-forming foci, one of which is protected by the other. Ventricular parasystole which arises from an ectopic focus situated in ventricule is relatively common. On the contrary, supraventricular parasystole which is centered in the atria or atrioventricular junction, is extremely rare. Kaufmann and Rothberger studied first parasystole as an entity, and they reported the first case of atrial parasystole. However, the first correctly mentioned example of atrial parasystole was described by Jervell. In the previous paper, we described one observation on atrial parasystole and discussed on its consisting-mechanism. The occurrence of ventricular parasystole is not a rarity, since it has been estimated to be present once in every 1,200 electrocardiograms taken in a general hospital. In contrast, well-documented cases of atrial parasystole are exceedingly rare, and since the first case of it was reported by Kaufmann and Rothberger, only 25 cases have hitherto been reported. In the present paper is described and discussed a case of the extremely rare combination of atrial and ventricular parasystole with exit block and fusion phenomenon...
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Histopathological and immunohistochemical examinations were made on four female horses aged 9-12 years with pulmonary granular cell tumours (GCTs). The tumours, which were multiple, of varying size, firm and off-white in colour, surrounded the bronchi and bronchioles. Metastatic lesions were not detected. The tumour cells had abundant eosinophilic cytoplasm filled with prominent coarse eosinophilic granules. Immunohistochemically, these tumour cells reacted uniformly with vimentin and S100 antibodies. Most were immunolabelled by antibodies against glial fibrillary acidic protein (GFAP), myelin basic protein (MBP) and protein gene product 9.5 (PGP9.5), and a few cells were positive with Leu7 antibody. However, the tumour cells did not react with antibodies against neurofilament protein (NF), cytokeratin (CK), chromogranin, alpha1 antichymotrypsin (AACT), myoglobin, desmin, alpha-actin or alpha-smooth muscle actin (alpha-SMA). These immunohistochemical properties of tumour cells support the hypothesis that equine pulmonary GCTs are derived from Schwann cells of the peripheral nervous system in peribronchial and peribronchiolar tissues. GFAP, MBP, Leu7 and PGP9.5 antibodies should help to distinguish equine granular cell tumours from other tumours.
1. It has been suggested that astrocytes prompt the induction of blood-brain barrier (BBB) functions in cerebrovascular endothelial cells. 2. In the present study we have tried to elucidate the genetic differences between astrocytes isolated from Wistar-Kyoto (WKY) control rats and astrocytes isolated from stroke-prone spontaneously hypertensive rats (SHRSP). 3. We show that endothelial cells develop tight junction-like structures, a reduction in vesicular transport and high electrical resistance when they are co-cultured with astrocytes isolated from WKY rats. In contrast, SHRSP astrocytes have less of an ability to induce BBB functions than do WKY astrocytes. 4. In addition, we demonstrate that SHRSP astrocytes produce enormous quantities of lactic acid when cerebral ischaemia develops. The decrease in pH causes astrocyte swelling and damages BBB functions. 5. Consequently, we reason that genetically weak functions in astrocytes cause disruptions of BBB function and result in widespread cerebral lesions in SHRSP.
1. We evaluated the induction of endothelial barrier functions by the type 1 astrocyte-derived supernatant in culture using horseradish peroxidase (HRP) as a parameter. 2. A gel filtration fraction (molecular weight 16-20 kDa) of type 1 astrocyte-derived supernatant reduced plasmalemmal vesicles and induced tight junctions in endothelial cells. 3. In addition, this fraction promoted the uptake of [3H]-glucosamine by endothelial cells. This cell activity disappeared after heating at 95 degrees C for 10 min and was sensitive to trypsin. 4. These results suggest that a type 1 astrocyte-derived protein factor(s) promotes proteoglycan synthesis with a resultant increase in charge selectivity in endothelial cells and plays an important role in the induction of blood-brain barrier functions.
Mechanisms of vascular hypertrophy induced by hypertension were studied in cultured aortic smooth muscle cells from spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) and compared with those from normotensive Wistar-Kyoto (WKY) rats. Fetal calf serum-stimulated ornithine decarboxylase (ODC) activity of cultured smooth muscle cells was greater in SHR and SHRSP than in WKY. Beta- but not alpha-adrenergic agonist stimulated ODC activity acutely in cultured smooth muscle cells from WKY, and isoprenaline-induced activation was blocked by the beta-blocker, propranolol, and enhanced by the phosphodiesterase inhibitor, 1-methyl-3-isobutylxanthine. These results indicate that cultured vascular smooth muscle cells from SHR and SHRSP are more prone to increase the protein synthesis than those from WKY through the trophic induction of ODC activity and that the regulation of ODC activity by catecholamines is mediated through beta-agonistic effect in cultured smooth muscle cells.
Since the early development of structural cardiovascular change in spontaneously hypertensive rats (SHR) and stroke-prone SHR (SHRSP) indicated the involvement of non-pressure-dependent factors in this process in hypertension, smooth muscle cells (SMC) from the aorta of SHR, SHRSP, and normotensive Wistar-Kyoto rats (WKY) were investigated under tissue culture conditions free from blood pressure and humoral factors in vivo. By the observation of such factors as growth rate and DNA or protein synthesis vascular SMC from these rats with genetic hypertension were proved to have intrinsically greater growth activity independently of blood pressure. Although serum from SHR and SHRSP had no specific stimulative effect on SMC growth, circulating epinephrine may accelerate cardiovascular structural changes because isoproterenol added to the culture media enhanced ornithine decarboxylase (ODC) activity. Moreover, SMC from SHR and SHRSP showed greater thymidine incorporation than those from WKY even in response to lower extracellular Na+ concentration. Local nutritional conditions of SMC, which were proved to have a great effect on the morphology and structure of cultured SMC, may be a basic determinant of the development of hypertension-induced structural vascular changes or lesions.
Permeability of intracranial extracerebral arteries of stroke-prone spontaneously hypertensive rats (SHRSP) was studied using labeling techniques (ferritin and horseradish peroxidase), at the cellular level. In the arterial endothelial cells, the tracer molecules were slowly but constantly transported by the plasmalemmal vesicles to the subendothelial space. This endothelial transportation of the tracers into these cerebral arteries did not seem to be significantly influenced by aging, increased blood pressure, hyperlipidemia or the existence of cerebral bleeding and infarction. Around the adventitia, there were a great number of periadventitial capillaries, especially near bifurcations. In the periadventitial capillaries, the tracer molecules were readily trapped by endothelial cells and were quickly transported to pericapillary spaces. The tracer molecules were then detected in the phagocytes adjacent to the deeper layers of the media, and further in the medial smooth muscle cells. The possibility that large amounts of plasma components are supplied to the media from periadventitial capillaries in the intracranial extracerebral arteries has to be considered in the pathogenic mechanisms of cerebrovascular lesions.
Permeability of brain capillaries of stroke-prone spontaneously hypertensive rats (SHRSP) was studied using labelling (horseradish peroxidase) and cytochemical techniques at the cellular level. In the cerebral capillary endothelium the tracer molecules were quickly transported by abundant transendothelial channels which directly connected the capillary lumen to the subendothelial space. Transendothelial channels are abundant and should be postulated as structural formations engaged in the increased transport of proteins across the capillary endothelium. Ultracytochemical studies revealed that the channels, bounded by indistinct delimiting membranes, initially had no acid phosphatase activity. With the passage of time, however, the channels showed acid phosphatase activity and were lined with distinct membranes. These observations suggested that the lysosomes might fuse with the transendothelial channels and might play an important part in the transport of macromolecules.
We studied ultrastructurally cerebral perforating arteries in 60 stroke-prone spontaneously hypertensive rats (SHRSP), which were sequentially killed at 4-52 weeks of age before showing symptoms of stroke. Another 24 SHRSP were killed soon after they showed symptoms of cerebral infarction. The initial vascular lesions observed in the asymptomatic group included focal cytoplasmic necrosis in the outer layers of the media. This change progressed to widespread medial necrosis with time. In the infarction group, numerous monocytes were seen adhering to the endothelium of the arteries having advanced medial damage. Following the adherence of monocytes to the endothelium, large amounts of plasma components were visible in the arterial wall. The accumulation of the plasma components (especially fibrin) thickened the wall, narrowed the lumen, and resulted in occlusion. These results suggest that monocytes may affect the endothelium, perhaps disturbing the so-called blood-brain barrier to proteins. The monocytes may therefore be closely related to the occurrence of arterial occlusion with resultant cerebral infarction.