[Evaluation of the assay for fibrin derivatives using monoclonal antibodies to D-dimer].
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Biomedical subjects
Publications and source records attributed to M Fujimaki.
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A multi-institutional cooperative phase II study of Cisplatin for esophageal carcinoma was conducted. Cisplatin was administered by i.v. infusion at 10-20 mg/m2 body surface area daily for 5 days and repeated every 3-4 weeks (method A) or at 50-100 mg/m2 body surface area once every 3-4 weeks (method B). Out of 78 cases entered, 47 were evaluable. No complete response (CR) was obtained and partial responses (PR) were observed in 10 cases, the overall response rate being 21.3%. Response rates by administration methods A and B were 12.5% and 25.8%, respectively. Responders to treatment exhibited significantly longer survival periods compared to non-responders (p less than 0.05, generalized Wilcoxon test). Major adverse reactions were gastrointestinal symptoms, generalized malaise, bone marrow suppression and renal disorders. One case of leukopenia leading to eventual death from pneumonia was observed.
A 50-year-old man was admitted with a diagnosis of acute appendicitis on January, 5, 1984 and an appendectomy was performed on the same day. The acutely inflamed appendix measured 7 cm in length, and a gross tumor, was seen at the apex. Histologic examination of the gross tumor, which was 1.7 cm in diameter, revealed a neoplasm representing a goblet cell carcinoid. Silver impregnation by both the Grimelius and Masson-Fontana methods disclosed a positive reaction in some neoplastic cells. Electron microscopically, endocrine granules with both limiting membranes and ahlos, 100-210 nm in diameter, were present in the neoplastic cells, Because of the relatively large size of the tumor and neoplastic invasion to the mesoappedix in this case and, in addition, the possible malignant nature of carcinoid tumor, ileoascendocolectomy was performed as an additional operation.
Captopril (SQ14,225), an orally administered angiotensin converting enzyme inhibitor, was given to 8 patients with idiopathic edema, in order to study the role of the renin-angiotensin-aldosterone system in orthostatic sodium and water retention. Compared to 5 normal subjects, patients with idiopathic edema showed significantly greater reduction in water and sodium excretion, and greater increment in plasma aldosterone and plasma renin activity, in the upright posture. Captopril significantly restored water and sodium excretion, attenuated the increment in plasma aldosterone, and enhanced the rise in plasma renin activity in patients with idiopathic edema. The effects of captopril on these variables were not remarkable in normal subjects. These results suggest that an enhanced response of the renin-angiotensin-aldosterone system to standing plays an important role in the pathophysiology of idiopathic edema.
The vascular bed in a murine dermal tissue responded to inoculated tumor cells by two-phased changes in the vascular permeability. The initial increase in the vascular permeability was seen in an early stage (1 to 3 day post tumor cells inoculation), and the inflammation was sensitive to glutathione (GSH). Glucocorticoids reduced the increased vascular permeability, but neither acetylsalicylic acid nor indomethacin did. The later vascular response was produced by a growing solid tumor in a continuous mode beginning at 5th to 10th day post inoculation. The degree of the increased vascular permeability in this chronic phase was in direct proportion to the wet weight of the solid tumor, and the inflammation was insensitive to glutathione. Glucocorticoids reduced the increased vascular permeability, but neither acetylsalicylic acid nor indomethacin did. The action of glucocorticoids on the tumor-induced vascular hyper-permeability was discussed in connection with a tumor factor possibly responsible for the vasoexudation.
It is well known that surgical treatment is a major therapy on esophageal carcinoma. But the prognosis of the operated patients has not been yet satisfactory due to high frequency of recurrence. Therefore effective adjuvant therapy is necessary pre and/or post operatively such as radiation therapy, chemotherapy, immunotherapy and hyperthermia, etc. However, there is no general method of combination therapy with operation, since each patient shows different sensitivity to adjuvant therapy. This paper summarized that an appropriate multidisciplinary therapy had been carried on each case.
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A new sensitive, reproducible and simple assay for factor XIII activity was developed, in which fluorescent dansylcadaverine (DC) is incorporated into casein and DC-casein is separated from free DC by gel filtration. A good correlation was found between our method and Lorand's. The main advantages of our method are: (1) our assay technique is simple with good reproducibility and takes only a couple of hours; (2) the detectable limit of factor XIII activity is about 1% of normal pool plasma, but, if necessary, can be lowered by increasing the sample amount and lengthening the reaction time.
To study the effect of hypokalaemia in the regulation of aldosterone secretion, repeated injections of frusemide (3 mg/kg) plus saline with or without simultaneous infusion of potassium chloride (1 mEq/kg/h) were performed in 24 conscious female rabbits for 7 h. Without potassium supplementation, the plasma renin activity (PRA) remained elevated throughout the study, while an initial increase (1 h to 3 h) in plasma aldosterone (PA) gradually returned to normal with reduction of the serum potassium. In rabbits on potassium supplements to prevent the development of hypokalaemia, both PRA and PA remained elevated. The incremental aldosterone response to administration of potassium chloride, angiotensin II or ACTH, was considerably smaller in potassium-depleted rabbits than in potassium-repleted rabbits. These results suggest that serum potassium modulates the effects of angiotensin II or ACTH on aldosterone secretion, and that a certain level of potassium is necessary to maintain the aldosterone secretory capacity of the adrenal gland.
A comparison between forelimb amputations through the radius-ulna and the humerus was made in the adult newt, Cynops pyrrhogaster pyrrhogaster and the young toad, Xenopus laevis. Newts regenerated their forelimbs after the amputations and the new parts resembled the old in structure and function. Toads regenerated their forelimbs incompletely after the amputations. The new parts lacked joints and fingers showing a simply elongate pattern. The effect of re-amputation of exposed bone on the regeneration was evaluated in the adult newt. A left forelimb was amputated through the humerus and the exposed bone which protruded from the cut surface due to the relationships of the soft tissues, was then re-amputated a few minutes later. A right forelimb of the same individual was simply amputated without re-amputation of the exposed bone. Newts regenerated both forelimbs simultaneously. The new parts resembled the old in structure and function.
Plasma levels of aldosterone and other mineralocorticoids were determined in six patients with Bartter's syndrome. In spite of a remarkable elevation of plasma renin activity, the plasma aldosterone and 18-hydroxycorticosterone levels varied in each patient. These levels were slightly increased in three of the six patients, almost normal in two patients, and slightly reduced in one patient. The plasma deoxycorticosterone and corticosterone levels were within the normal range in all patients. The responses of plasma aldosterone to infusion of angiotensin II were reduced in all patients. Plasma aldosterone and 18-hydroxycorticosterone significantly increased with supplement of potassium, and the responses of plasma aldosterone to infusion of angiotensin II were also improved after supplement of potassium. Our results suggest that plasma aldosterone in Bartter's syndrome is dependent on potassium balance, even though plasma renin activity is remarkably increased, and that hyperaldosteronism is not an inevitable finding in Bartter's syndrome.
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