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Biomedical subjects

C Fukuda

Publications and source records attributed to C Fukuda.

At least 19 recordsLinked to original sources

Frontal N30 of median nerve SSEPs for evaluation of movement disorders with destructive basal ganglia deficits.

This study was performed to show the usefulness of N30 and N20 of median nerve SSEPs for evaluating the pathogenesis of central nervous system movement disorders. The subjects were 14 patients, consisting of 7 patients with an extrapyramidal lesion, 3 patients with suspicion of hypoxic-ischemic cerebral injury before birth period (H-I group), 3 patients with kernicterus during the neonatal period (kernicterus group), and 1 patient having Wilson's disease. Seven patients had spastic hemiplegia. Patients with athetotic CP had the ability to handle an electric wheelchair alone, and those with spastic hemiplegia could walk alone. Thirty control subjects were included in this study for clinical investigation. The characteristic finding of a predominant absence or amplitude reduction of frontal N30 compared with that of parietal N20 (4 and 1, respectively, out of 6 examinations) was obtained in athetotic CP patients of the H-I group. The predominant absence of N30 compared with N20 did not appear in the kernicterus group, hemiplegic patients or a patient with Wilson's disease. Therefore, frontal N30 might sensitively reflect destructive damage in the frontal basal ganglia in children.

Adolescent↗

Effects of human recombinant calcitonin on a rat osteopenia model induced by TPTX and arotinoid.

Recombinant human calcitonin (rh-CT) has been developed as an agent for patients with excessive bone resorption to replace calcitonins from animal species, which are associated with tolerance problems. In this study, inhibitory effects of rh-CT against bone resorption were examined in thyroparathyroidectomized (TPTX) rats, the animal model of accelerated bone resorption induced by administering a synthetic retinoid (arotinoid). The arotinoid-treated TPTX rats exhibited signs of stimulated bone resorption, such as hypercalcemia, reduced bone mineral density, and inferior bone strength. Significant improvements were seen in all of these changes after a daily treatment with rh-CT (30, 300 U/kg s.c.) for 1 week. A histomorphometrical analysis showed that the treatment with rh-CT markedly suppressed the reduction of trabecular bone volume and that of cortical thickness in the femur of arotinoid-treated TPTX rats. These results suggest that rh-CT may prevent osteopenia caused by accelerated bone resorption.

Animals↗

Effectiveness of systematized hepatectomy with Glisson's pedicle transection at the hepatic hilus for small nodular hepatocellular carcinoma: retrospective analysis.

BACKGROUND: The effectiveness of systematized hepatectomy with transection of Glisson's pedicle at the hepatic hilus in patients with small nodular hepatocellular carcinoma (HCC) has not been confirmed. METHODS: Surgical outcomes were reviewed in 204 patients with single nodular HCCs less than 5 cm in greatest diameter, including 68 patients with tumors that showed extranodular growth and 136 patients with tumors that did not, who had undergone curative hepatectomy (partial hepatic resection, n = 114; systematized hepatectomy, n = 90) from 1990 through 1994. RESULTS: The rates of microscopic vascular invasion and intrahepatic metastasis were significantly higher in patients who had single nodular HCCs with extranodular growth (34% and 49%) than in patients who had single nodular HCCs without extranodular growth (13%, P =.001, and 4%, P <.001). The 5-year survival rate in patients who had single nodular HCCs with extranodular growth was significantly greater after systematized hepatectomy (67%) than after partial hepatic resection (21%, P =.0002). Multivariate analysis showed that the type of operation was an independent prognostic factor in patients with single nodular HCCs with extranodular growth (P =.0008). CONCLUSIONS: Systematized hepatectomy with Glisson's pedicle transection at the hepatic hilus should be performed in patients who have single small nodular HCCs with extranodular growth because these tumors often invade within the liver sector containing the tumor.

Aged↗

Hydra biological detection of biologically active peptides in rat cerebrospinal fluid.

The Hydra bioassay system utilizes a tentacle ball formation (TBF), a component of the feeding response of hydra, elicited by S-methyl-glutathione. TBF is modulated by many biologically active peptides in a specific way to individual peptides, and is useful in investigating biologically active peptides in a complex biological sample. We applied the hydra bioassay to explore a possible biologically active substance responsible for the decrease in the motor activity of the mice. The suppression of the CSF obtained from rats after exhaustive exercise was marked lower than that of sedentary rats. Addition of transforming growth factor-beta (TGF-beta), which is the only substance known to nullify TBF, to CSF of the sedentary rat reproduced this change in the suppression of the TBF. This system is useful to screen active peptides in small amounts of biological samples containing very low concentrations of peptides.

Animals↗

Suppression of S-methylglutathione-induced tentacle ball formation by peptides and nullification of the suppression by TGF-beta in Hydra.

Tentacle ball formation (TBF) in Hydra elicited by S-methylglutathione (GSM) was modulated by a number of biologically active peptides. Hydra fed on Artemia, which had been hatched in a common salt solution supplemented with LiCl and ZnCl(2), easily induced TBF in response to GSM after pretreatment with trypsin. After Hydra were treated with 100 pg/ml trypsin for 10 min, the response to GSM (TBF) was sensitively suppressed by acidic fibroblast growth factor and other biologically active peptides for >10 h. Various peptides, but not transforming growth factor beta (TGF-beta), suppressed GSM-induced TBF in a specific pattern for each peptide. However, TGF-beta was unique in that it did not suppress the response to GSM, but nullified the suppressive effect of other peptides. Only active TGF-beta nullified the suppressive effect of the peptides, and the latent form of TGF-beta neither suppressed GSM-induced TBF nor nullified the suppressive effect of other peptides. Members of the TGF-beta family suppressed GSM-induced TBF. These results indicate that all peptides examined, except for TGF-beta suppressed the response to GSM in a manner specific to each peptide. This assay system would be useful in identification of biologically active peptides.

Animals↗

Transforming growth factor-beta activated during exercise in brain depresses spontaneous motor activity of animals. Relevance To central fatigue.

Intracerebroventricular administration into sedentary mice of the high molecular mass fraction of cerebrospinal fluid (CSF) from exercise-exhausted rats produced a decrease in spontaneous motor activity [K. Inoue, H. Yamazaki, Y. Manabe, C. Fukuda, T. Fushiki, Release of a substance that suppresses spontaneous motor activity in the brain by physical exercise, Physiol. Behav. 64 (1998) 185-190]. CSF from sedentary rats had no such effect. This suggests the presence of a substance regulating the urge for motion as a response to fatigue. A bioassay system using hydra, a freshwater coelenterate, showed an activity indistinguishable from transforming growth factor-beta (TGF-beta) in the CSF from exercise-fatigued rats, while not in that from sedentary rats. The increase in the concentration of active TGF-beta in the CSF from exercise-fatigued rat was also ascertained by another bioassay system using mink lung epithelial cells (Mv1Lu). Injection of TGF-beta into the brains of sedentary mice elicited a similar decrease in spontaneous motor activity in a dose-dependent manner. Increasing the exercise load on rats raised both the levels of active TGF-beta and the activity of depression on spontaneous motor activity of mice in the CSF of rats. Taken together, these results suggest that exercise increases active TGF-beta in the brain and it creates the feeling of fatigue and thus suppresses spontaneous motor activity.

Animals↗

Interstitial accumulation of Na+ and K+ during flush-out and cold storage of rat livers: implications for graft survival.

Intracellular-type electrolyte solutions were introduced into organ preservation to prevent K+ efflux and Na+ and Cl- influx into cells and cell swelling during cold ischemia. We studied cation accumulation in the interstitial space by microdialysis, during rat liver cold storage and after flush-out with high-K+ and low-K+ solutions. The effect of Na+ and K+ on graft function and survival was studied in an isolated perfused liver model and an orthotopic transplantation model after rat liver storage in iso-osmolar high-K+ and low-K+ solutions. After 24 hours of cold ischemia [Na+]o dropped from 136 +/- 2 mmol/L to 91.8 +/- 1.1 mmol/L, and [K+]o increased from 5.9 +/- 0.1 mmol/L to 12.2 +/- 1.6 mmol/L (P < .001 vs. control). [Na+]o and [K+]o after flush-out did not equilibrate with [Na+]sol and [K+]sol after 24 hours of cold storage. Rat livers preserved in low-K+ solutions produced significantly more bile during isolated reperfusion and released less alanine transaminase, aspartate transaminase, and lactate dehydrogenase into the reperfusion medium than high-K+ solutions. Rat liver survival after 14 hours of preservation was higher in low-K+ solutions (13 of 13) than in high-K+ solutions (7 of 13). Those studies indicate that during cold storage of rat livers, transmembraneous Na+-K+ sodium-potassium exchange might not follow the 3:2 stochiometry of a sole sodium-potassium exchange via Na+-K+ sodium-potassium adenosine triphosphatase (ATPase), and that low-K+ solutions might improve graft function and survival after rat liver preservation.

Animals↗

Release of a substance that suppresses spontaneous motor activity in the brain by physical exercise.

Injection of the cerebrospinal fluid (CSF) collected from rats fatigued by obligatory swimming into the cisterna magna of mice suppressed the spontaneous motor activity of the mice. The suppressive activity was abolished by heat denaturation of the CSF and was found in the CSF fraction with a molecular weight above 10,000 after ultrafiltration. These findings suggest the presence of a substance(s) released in a fatigued animal's brain that suppresses its spontaneous motor activity and generates the sensation of fatigue.

Animals↗

Prenylflavonoids: a new class of non-steroidal phytoestrogen (Part 2). Estrogenic effects of 8-isopentenylnaringenin on bone metabolism.

In order to examine whether 8-isopentenylnaringenin (1), which has been proven to possess estrogen agonist activity in in vitro tests, also produces in vivo estrogenic properties, the effects of 1 on uterus and on bone metabolism were determined in ovariectomized rats. Rats were ovariectomized and treated with 1 at 30 mg/kg/day subcutaneously for two weeks or 17 beta-estradiol at 0.01 mg/kg/day subcutaneously for two weeks. Ovariectomy resulted in an increase in urinary excretion of bone resorption markers (hydroxyproline, pyridinoline and deoxypyridinoline) and a decrease in bone mineral density of the proximal tibia as well as reduced uterine weight. Treatment with 1 or 17 beta-estradiol completely suppressed these ovariectomy-induced bone and uterine changes in a qualitatively similar manner. These results demonstrate that 1 acts as an estrogen agonist in the uterus as well as in bone in vivo.

Amino Acids↗

[Clinical usefulness of the measurements of plasmin-alpha 2-plasmin inhibitor complex and plasma tissue factor activity in patients with disseminated intravascular coagulation].

The early stage of the state in which coagulation or fibrinolytic pathway is activated has been difficult to estimate. It has become possible to detect disseminated intravascular coagulation (DIC) at an early stage due to the development of highly sensitive methods which quantitate so called "molecular markers". Herein, to evaluate the clinical usefulness of plasmin-alpha 2-plasmin inhibitor complex (PIC) and tissue factor activity in plasma were examined. The first time, monitoring the plasma levels of PIC might be useful for the diagnosis of a pre-DIC condition and for effective control of therapy. We believed that combination assay for both PIC and D dimer will be adequate to differentiate whether the hemostatic abnormalities are induced mainly by DIC or hepatic insufficiency. Recently, new clinical usefulness of PIC has been reported. The PIC/thrombin-antithrombin III complex ratio was lower in patients with poor prognosis than in those with good prognosis, and it was also lower in those with organ failure than in those without it. The tissue factor is a major activator of the coagulation cascade and may play a role in initiating thrombosis. A simple chromogenic substrate assay for the quantitation of tissue factor activity in plasma samples was developed. Abnormally high levels were found in 80% of the patients with DIC, predominantly in patients with non-hematological solid tumors and acute leukemia. Serial determinations of plasma tissue factor demonstrated that plasma tissue factor changes immediately with the course of DIC. Plasma tissue factor did not correlate with hemostatic markers of DIC such as thrombin-antithrombin III complex, PIC, FDP D-dimer. Tissue factor activity correlated well with membrane anchoring region of tissue factor protein levels. Tissue factor activity correlate with tumor necrosis factor alpha levels in patients with non-hematological solid tumors without hepatocellular carcinoma. These findings suggest that the plasma tissue factor is potentially valuable for monitoring the progress of DIC in a limited population of patients.

Antifibrinolytic Agents↗

[An improved assay for plasma tissue factor activity].

We developed an improved assay for measuring tissue factor activity in plasma with chromogenic substrate (S-2765) which is highly sensitive to factor Xa. In the ordinary assay with S-2222, it was required to prepare the euglobulin fraction of plasma and to heat it, while the improved assay required 20-fold-diluted plasma with Owren's barbital buffer (pH 7.35). The absorbance at 405nm on a colorimeter and human placental tissue thromboplastin preparation (HPT; Thromborel S, Behringwerke AG) was regressed on a semilogarithmic curve. The mean value obtained by this assay for normal subjects was 15.8 +/- 16.4 micrograms/ml HPT (mean +/- 2SD). A correlation of tissue factor activities assayed by the present method and the ordinary method was 0.62. Our data suggest that this improved assay is a useful method for measuring the plasma tissue factor activity.

Adult↗

[Blood coagulation-fibrinolysis tests by a biochemical method].

Blood coagulation-fibrinolysis factors are conventionally measured using fibrinogen or fibrin as a natural substrate. With recent advances in the technology to biochemically separate and purify, individual coagulation-fibrinolysis factors were isolated and purified, and their biochemical properties, function, and primary structure were clarified. Measurement techniques for blood coagulation-fibrinolysis factors were also developed. At present, enzyme activity for each factor is measured by the synthetic substrate method, on the other hand trace proteins and complex proteins are measured using monoclonal antibody. We present an outline of blood coagulation-fibrinolysis factors and synthetic substrates, and describe the characteristics of the synthetic substrate method using measurement of plasma tissue factor and protein C activity as examples.

Antithrombin III↗

A new hereditary abnormal protein C (protein C Yonago) with a dysfunctional Gla-domain.

A familial abnormal protein C most probably with the dysfunctional Gla domain was found in a 60-year-old man with recurrent thrombosis. Namely, the anticoagulant activity as measured by the APTT method and the antigen level by an ELISA utilizing a calcium-dependent antibody were reduced to nearly half of normal, 43.5% and 2.1 micrograms/ml (normal range: 2.8-5.0 micrograms/ml), respectively. On the other hand, the amidolytic activity determined on a synthetic chromogenic substrate, S-2366, and the total antigen measured by an ELISA utilizing a polyclonal antibody were both in the normal range, 74.1% and 83% of normal, respectively. Crossed immunoelectrophoresis showed more anodal migration than the normal control in the presence of calcium ions, and adsorption of protein C to barium citrate was insufficient. These data altogether indicated that a half population of protein C in the patient's plasma was dysfunctional in the Gla domain or its related structures. Four other members of his immediate family were found to have the same abnormality of protein C, although they had been all asymptomatic. We thus conclude that the dysfunctional protein C is hereditary, and that the abnormalities noted in several tests are most likely due to a structural defect residing in the Gla or its related regions. We hereby designate this abnormal protein C as protein C Yonago.

Blood Coagulation Tests↗

Measurements of tissue factor-like activity in plasma of patients with DIC.

Tissue factor-like activity was measured in the plasma of 30 patients with disseminated intravascular coagulation(DIC) and 22 patients without DIC using a chromogenic substrate. Twenty-three of the 30 patients with DIC (77%) exhibited tissue factor-like activity levels above normal range (greater than 3.0 U/L), and in eleven of these patients, the levels were more than 10 U/L. Of the 22 patients without DIC, seven patients had elevated levels (3-10 U/L), and had a possibility to be developing DIC. So, we considered them to be in a pre-DIC state. No correlation was found between tissue factor-like activity and alpha 2 plasmin inhibitor-plasmin complex or FDP-D dimer. In a patient with acute monocytic leukemia, the elevated tissue factor-like activity (84.4 U/L) rapidly decreased after the initiation of chemotherapy, whereas in a patient with pancreatic cancer, the level remained elevated (67.4-79.2 U/L). These results suggested that the plasma tissue factor-like activity is differ from the other parameters reflecting the process of DIC and is a useful indicator of the presence of an initiating factor of blood coagulation in some selected patients with DIC or pre-DIC.

Adult↗

Adrenocorticotropic hormone unresponsiveness associated with hypertrophic cardiomyopathy.

The clinical and autopsy findings in a case of adrenocorticotropic hormone unresponsiveness associated with hypertrophic cardiomyopathy are reported. A four-month-old female with feeding difficulties and skin hyperpigmentation from two months of age was admitted with convulsions. She was hypoglycemic with normal serum electrolytes and the presence of hypertrophic cardiomyopathy was indicated by electrocardiogram and echocardiogram. Cardiac arrest occurred on the second hospital day. Low serum cortisol, high plasma adrenocorticotropic hormone, low urinary 17-ketosteroids, and normal urinary aldosterone excretion were documented after her death. Hypoplasia of the adrenal cortex with a persistent fetal zone and concentric hypertrophy of the heart were found at autopsy. We propose that the pathogenesis of this disease lies in impaired remodelling of the fetal adrenal cortex into the permanent cortex, and postulate an effect of adrenocorticotropic hormone on the myocardium as the cause of hypertrophic cardiomyopathy.

17-Ketosteroids↗