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T Maki

Publications and source records attributed to T Maki.

At least 163 records · Page 9Linked to original sources
PubMed1989

Effect of gamma-irradiation on mouse pancreatic islet-allograft survival.

Elimination or inactivation of lymphoid tissue in the pancreatic islet preparation achieves prolongation of islet-allograft survival. In this study we examined the effect of gamma-irradiation on mouse islet-allograft survival. In a B6AF1 isograft model, irradiation up to 2400 rad did not induce deterioration of islet function over 200 days, but greater doses caused cessation of graft function between 83 and 186 days. When DBA/2 crude islets were transplanted into B6AF1 recipients, all nonirradiated allografts were acutely rejected. Marked prolongation of allograft survival was achieved by islet irradiation with doses between 800 and 12,000 rad. With higher doses, significant numbers of allografts survived beyond the controls, but many lost function between 78 and 180 days, with none surviving greater than 200 days. Irradiation with 16,000 rad caused acute radiation damage. Because most secondary islet allografts in recipient mice that lost primary islet-graft function between 84 and 195 days survived greater than 100 days, late functional loss was probably due to the radiation injury. Combined use of recipient treatment with cyclosporin A and graft irradiation (2400 rad) achieved prolongation of DBA/2 islets in B6AF1 mice.

Animals↗
PubMed1989

[A case of rapidly progressive pulmonary pulmonary hypertension in a 14-year-old girl].

A 14-year-old girl was admitted with chief complaints of edema and chest pain. She had hepatomegaly, but did not have heart murmur and accentuation of the pulmonary component of the second heart sound. The electrocardiogram showed right axis deviation, negative T wave in V3,4 and ST depression in III, aVF. But right ventricular hypertrophy was not dominant. Chest radiography showed a cardiothoracic ratio of 54% and a slight prominence of proximal pulmonary arteries. The edema was soon diminished only by the diuretics, but it appeared again without the diuretics. At the cardiac catheterization 3 months after the onset of symptoms, the pulmonary arterial pressure was 150/85 mmHg and the pulmonary resistance was 3,232 dyn/sec/cm5. The right atrial pressure was 9.5 mmHg and oxygen saturation at the pulmonary artery was 31.0%. Prostaglandin E1 reduced the pulmonary artery pressure only a little, but raised the systemic pressure. The patient was treated with several vasodilators, but her condition deteriorated rapidly and she developed severe right ventricular failure. She died only 8 months after the onset of symptoms and 5 months after the catheterization. At autopsy, histological examination demonstrated intimal fibrotic thickening of the small-sized pulmonary arteries and organizing thrombus. But there was not plexiform lesion. Heart failure was easily improved when she was first admitted. But after 3 months the cardiac catheterization revealed that her condition was already severe. Several vasodilators was not effective to such a rapidly progressive primary pulmonary hypertension.

Adolescent↗
PubMed1989

[A case of multiple sclerosis with pure alexia].

We report here a case of multiple sclerosis (MS) showing pure alexia. The patient was a 28 year-old, right-handed male student of medicine. He had been healthy prior to college, but when he tried to read the newspaper one morning in January of 1983, he suddenly became aware that he could not. He could speak fluently and had no disturbances of auditory comprehension. No signs of abnormality were noted in his writing ability. Thereafter, the patient occasionally experienced difficulty in reading, together with right homonymous hemianopsia. These symptoms, however, usually vanished following sleep. In April, 1984, the patient experienced headache and ataxia when walking, followed by repeated remission and exacerbation of the symptoms. Corticosteroid therapy produced complete disappearance of the headache and ataxia. In September of 1985, he was hospitalized at our department due to the clouding of consciousness accompanied by convulsions. Neurologically, no abnormalities of the ocular fundus were noted and Babinski's sign was negative, but left hemiplegia was observed. Neuropsychologically, his intelligence was normal and he had no difficulty in writing, but paralexia was noted. There were no disorders of spontaneous speech or auditory comprehension. Examination by CT scan and magnetic resonance imaging revealed a number of lesions in the white substance of the cerebrum, including the left occipital lobe. The abnormal signs seen radiographically vanished when cortical hormones were administered. It has been thought that the symptoms of multiple sclerosis are due mainly to disorders of the white substance, and that MS seldom produces symptoms of aphasia, due to the fact that the lesions in this disease are generally small.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1989

[Antemortem diagnosis of Marchiafava-Bignami disease].

Marchiafava-Bignami disease (M-B disease) is a peculiar disease, observed in hardened drinkers and resulting in demyelinization and necrosis of the corpus callosum. The clinical symptoms are diverse, and it is difficult to diagnose accurately while the patient is alive. Almost all reports in the past have been based on necropsy. Only three cases of M-B disease have been reported in Japan so far, none of which was based on a diagnosis while the patient was alive. We have been able to perform diagnosis of M-B disease while the patients were still alive by means of X-ray computed tomography (CT) and magnetic resonance imaging (MRI), and to study the clinical symptoms from the acute stage. In addition to the study on our own patients, we also conducted a neurosymptomatic study on the clinical symptoms of 6 cases, for which details of the symptomatology have been described-out of about 150 cases reported in the past. In the acute stage of M-B disease, we observed psychic symptoms, such as clouding of consciousness, mnemonic disorders and disorders and disorientation, or various frontal lobe symptoms, such as change in personality, raptus nervorum, dysphemia, pyramidal signs and astasia-abasia. These are non-specific symptoms and it is necessary to differentiate from encephalitis and other encephalopathy. In the chronic stage, dysphemia becomes sustained and, in addition, symptoms of transection of the corpus callosum are noted among the disorders of higher cerebral functions. If M-B disease is suggested from clinical symptoms, it is advisable to confirm the lesions in the corpus callosum by X-ray CT and MRI.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1988

Movement of water in conjunction with plant movement visualized by NMR imaging.

The water distribution in the pulvinus of Mimosa can be visualized by an NMR imaging technique. After stimulation of a Mimosa plant, water in the lower half of the main pulvinus disappeared, the water previously contained in this area seeming to be transferred to the upper half of the main pulvinus. Movement of the water in conjunction with Mimosa movement was visualized sequentially by a non-invasive NMR imaging procedure.

Magnetic Resonance Spectroscopy↗
PubMed1988

Induction of antigen-specific unresponsiveness to pancreatic islet allografts by antilymphocyte serum.

The mechanism (or mechanisms) underlying the indefinite survival of DBA/2 islet allografts in strongly histoincompatible (C57BL/6xA)F1 (B6AF1) mice, induced either by the combined use of Ficoll-prepared crude islets and treatment of recipients with antilymphocyte serum (ALS), or by the use of handpicked, purified islets in nonimmunosuppressed recipients, was examined. B6AF1 mice bearing DBA/2 crude islet allografts for more than 100 days following ALS treatment accepted secondary DBA/2 crude islet allografts, but acutely rejected third-party A.SW crude islet allografts. This antigen-specific unresponsiveness to islet allografts can be successfully transferred into syngeneic B6AF1 mice by spleen cells. However, the state of unresponsiveness to donor antigen observed in these animals appears to be relatively weak, since transplantation of DBA/2 skin allografts or injection of DBA/2 spleen cells (5 x 10(7] caused acute rejection of long-term-accepted islet allografts. In contrast, B6AF1 mice bearing DBA/2 purified islet allografts over 100 days without immunosuppression rejected the secondary DBA/2 crude islet allografts acutely. Transfer of spleen cells obtained from these animals to syngeneic B6AF1 mice failed to induce prolongation of DBA/2 crude islet allografts. Thus, the mechanism (or mechanisms) involved in the long-term acceptance of islet allografts induced by the use of ALS and crude islets appears to be different from that involved in the long-term acceptance of purified islet allografts. The possible roles played by ALS in the induction of specific unresponsiveness to islet allografts are discussed.

Animals↗