[Gallium scintigraphy in patients with adult T-cell leukemia-lymphoma].
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Biomedical subjects
Publications and source records attributed to K Harada.
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Various pharmacological properties of a new antiplatelet aggregating agent, 4-cyano-5,5-bis(4-methoxyphenyl)-4-pentenoic acid (E-5510), were examined in order to elucidate its mode of action, Firstly, the inhibitory effect on in vitro aggregation of platelets from humans and various experimental animals was studied. E-5510 inhibited human platelet aggregation induced by collagen, arachidonic acid, adenosine diphosphate (ADP), platelet activating factor (PAF) and epinephrine. Thrombin-induced platelet aggregation, which was not inhibited by acetylsalicylic acid (ASA) or the thiazole drug, 4,5-bis(4-methoxyphenyl)-2-(trifluoromethyl) thiazole, was inhibited by E-5510. E-5510 inhibited collagen-induced platelet aggregation in platelet-rich plasma (PRP) from guinea pigs, beagle dogs and monkey to the same degree as in human PRP, but its effect was weaker in rat PRP. Human platelet adhesion to a collagen-coated plastic disk and thrombin-induced adenosine triphosphate (ATP) release from human platelets were also inhibited by this compound. Next, the ex vivo anti-platelet effect of E-5510 was examined in guinea pigs and beagle dogs. E-5510 was the most potent among the tested drugs (ticlopidine, ASA, cilostazol and the thiazole drug. The anti-platelet effect of this compound appeared within 1 h and lasted more than 8 h after oral administration. The above results suggest that E-5510 may antagonize platelet activation by inhibiting phospholipase C and/or A2, which results in suppression of both phosphatidylinositol breakdown and arachidonic acid release from phospholipids, as well as by inhibiting cyclooxygenase. E-5510 exerted its anti-platelet action without affecting prostaglandin I2 production in the blood vessels. It is considered that E-5510 has a highly potent anti-platelet aggregating effect and a unique multi-site mode of action. This compound is a promising candidate as an antithrombotic drug for clinical use.
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An 82-year-old woman was admitted to the Department of Neurosurgery, Saiseikai Fukuoka General Hospital with complaints of persistent headache and left hemiparesis. Neurological examination on admission revealed mild left hemiparesis with hyperreflexia. However, no choked disc nor pathological reflexes were noted. Roentgenograms of the skull showed thickening of the bone in the right temporoparietal region with intracranial calcification. CT showed a large right frontoparietal mixed dense space-occupying lesion bordered by a high dense calcified rim. The right lateral ventricle was compressed while the left exhibited a deviation to the left. Furthermore, thickening of the right frontal and parietal bone around the margin of mass was noted. The patient was operated upon under the diagnosis of calcified chronic subdural hematoma. A large osteoplastic flap was turned down on the right front parietal area and hypertrophy of the skull, especially around the hematoma, was noticed. Over the dura just beneath the hypertrophic lesion of the calvaria, a soft, reddish granulation tissue was noted. The dura was stripped easily from the outer membrane. The capsule was opened and the content was found to be of compact consistency, screeching when cut, and it appeared to be filled with large clots, not all homogeneously organized and made out of a substance composed of reddish-yellow material. The inner membrane was removed except for the frontal lesion where remarkable adhesion to the arachnoid membrane was noted. The postoperative course was uneventful. At the time of the patient's dismissal, her symptoms had completely disappeared. Histologically, the granulation tissue to be the bone marrow consisted of three hematopoietic cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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The cell cycle of cultured human endometrial adenocarcinoma cells were observed with a SEM using the synchronous culture method and the following results were obtained. In the M phase, the cells changed morphologically to become a minimum size and rounded in shape. Filopodia became thin and straight and reached their maximum length. Moreover, blebs reaches their greatest number. In the G0+1 phase, the cells developed from a round shape to an oval shape, and finally became polymorphic. The ends of the filopodia degenerated and became shortened. The number of blebs was decreased only in this stage. During the S phase, the cells became slender and reached maximum size. Short filopodia reappeared. No blebs but the largest microvilli were found. When we compared the late G1 with the early G2 phase, we found polymorphism of the cells and coexistence of microvilli and blebs common to both phases. However, ruffles were observed only in the former phase, while in the latter phase renewal of short filopodia together with thick and bent filopodia was evident. When we compared the late G2 with the early G1 phase, we found that the cells were small in size and round shape, and that the existence of blebs was common to both phases. However, the tips of the filopodia were destroyed in the latter phase, while in the former phase thick and bent filopodia were observed.
A case of medullary venous malformation with azygos anterior cerebral artery aneurysm is reported, which was associated with the leptomenigeal angiomatosis on the cortex of the right frontal lobe. A 62-year-old female was admitted to the Kurume University Hospital on June 21, 1985, because of a convulsive seizure. On admission, neurological and general examinations, except for slightly liver function disorder, was no abnormality. Plain CT scan showed the cortical atrophy and two small high-density areas in the right frontal lobe. Enhanced CT scan showed a high-density area in the genu of the corpus callosum. MRI (magnetic resonance imaging), on T2 weighted image, showed a high signal intensity area in the right paraventricular deep white matter and the right frontal region. A right internal carotid angiogram in the venous phase showed numerous enlarged medullary veins in the deep frontal region, converging into a single large draining vein that empties into the basal vein of Rosenthal. An azygos anterior cerebral artery was visualized on the right and left carotid angiograms. The aneurysm was situated at the distal end of the azygos artery. Twenty eight days after admission, a right frontal cranioplastic craniotomy was performed. During operation, the surface of the right frontal lobe was covered by fine, vascular networks, which was reddish brown. A right frontal lobectomy, including venous malformation and vascular networks, was performed. The aneurysm was clipped via an interhemispheric approach. Histologically, the malformation vessels had spread into the subarachnoid space.(ABSTRACT TRUNCATED AT 250 WORDS)
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