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Biomedical subjects

Y Fukuda

Publications and source records attributed to Y Fukuda.

At least 937 records · Page 52Linked to original sources

Quantitative analysis of a cross-sectional area of the optic nerve: a comparison between albino and pigmented rats.

Comparative studies were made on albino and gray rats by measuring several morphological characteristics seen in cross-sections of the optic nerve. The total cross-sectional area of the optic nerve was about 30% smaller in the albino than in the gray rat, while the fiber density was 1.4 times higher in the albino than in the gray rat. The estimated total fiber count was about the same in the two strains: around 100,000 to 110,000 fibers. Except for a few unmyelinated fibers (less than 1%) all fibers were myelinated. Axon diameters of the optic nerve fibers were distributed in smaller values for the albino than for the gray rat, though the overall diameter range was similar (0.2-3.0 micron). The myelin sheath was also thinner in the albino than in the gray rat.

Animals↗

Cholinergic synaptic activation due to HCO-3 in the superior cervical ganglion of the rat.

Influence of acid-base change on synaptic transmission was studied in the isolated superior cervical ganglion of the rat. Effects of changes in PCO2, [HCO-3], or pH of the superfusing solution were studied, using as an index of synaptic excitation the amplitude of the initial negative deflection of surface potential induced by preganglionic stimulation. An increase or decrease in the extracellular fluid (ECF) pH by changing [HCO-3] at a normal PCO2 elicited respectively augmentation or suppression of the negative deflection. Similar shifts in the ECF pH with varying PCO2 at a normal [HCO-3] had small or almost negligible effects on the negative deflection. Simultaneous increase in both the PCO2 and [HCO-3], which compensated for the pH change in the ECF, induced a consistent increase in the amplitude of the negative deflection. The amplitude of negative deflection in various acid-base conditions was positively correlated with the ECF [HCO-3] but not with the ECF pH or PCO2. These results suggest that an increase in the ECF [HCO-3] activates cholinergic (nicotinic) synaptic transmission in the ganglion.

Acetylcholine↗

Second report of an experimental study of cerebrocardiopulmonary resuscitation (CCPR) in dogs with reference to a new continuous brain cooling method, using a Resusci Pump TM-1.

In our previous report, the effect of CCPR (an intracarotid hypothermic infusion combined with the existing CPR) has been described by the authors on dogs in which cardiac arrest had been induced by the inhalation of nitrous oxide. This report contains a new continuous brain cooling method, using a Resusci Pump TM-1 which has been newly devised by us and which has a carotid-carotid bypass in order to reduce oxygen consumption and cerebral metabolism while maintaining a continuous cerebral blood flow. Cardiac arrest was induced experimentally by electrical stimulation. The duration of cardiac arrest was 5 to 10 min duration. The continuous brain cooling was carried out during the period of 10-30 min. Through the experiment, we have investigated vital signs, acid base balance, cardiac output, carotid arterial blood flow, oxygen availability of the brain tissue, and regional cerebral blood flow in both groups of CPR and CCPR . As for the clinical signs and cardiac output, there were no significant differences between two groups. Oxygen availability of the brain tissue and regional blood flow were much more improved in CCPR group than in CPR group. The brain was selectively cooled by means of the continuous brain cooling. This resulted in the minimum effect on circulatory and respiratory system as compared to the effects caused by general hypothermia. Furthermore, the continuous brain cooling decreased cerebral metabolism and CMRO2, and prevented a progressive development of cerebral hypoxia Cerebral perfusion at a given constant pressure may protect the brain tissue from the disturbance of cerebral microcirculation. Therefore, we might expect the continuous brain cooling to have a beneficial effect on cerebral respiration, circulation and metabolism.

Acid-Base Equilibrium↗

Histamine metabolism in patients with histidinemia: determination of urinary levels of histamine, N tau-methylhistamine, imidazole acetic acid, and its conjugate(s).

Histamine metabolism in histidinemic patients was studied by measuring the urinary levels of histamine and its metabolites. The urinary excretions of histamine, N tau-methylhistamine, imidazole acetic acid, and its conjugate(s) were higher in patients with histidinemia than in controls, and these levels of excretion were correlated with the plasma histidine level. The urinary histamine levels of patients with eczema-like dermatitis were twice that of those without dermatitis. The urinary excretion of 3-methylhistidine showed a close correlation with the urinary histidine excretion. Thus, it was concluded that histamine metabolism is higher in histidinemic patients than in normal controls.

Amino Acid Metabolism, Inborn Errors↗

Relapsing polychondritis. Pathological and immunological findings in an autopsy case.

Relapsing polychondritis (RP) is a disorder of unknown etiology characterized by the destruction of cartilage. A case of RP in a 59-year-old male was autopsied, and systemic inflammation of various cartilages was confirmed. We demonstrated the circulating antibodies to Type II (cartilage) collagen. No antibodies to other collagen types were demonstrated. The presence of granular deposits of immunoglobulins, fibrinogen, and the C3 component of complement at the chondrofibrous junction was also demonstrated. From these findings, this case suggested that the pathogenesis of RP is related to an immune mechanism.

Adult↗

Purine-mediated growth inhibition caused by a pyrE mutation in Escherichia coli K-12.

A purine-sensitive phenotype results from a previously described mutation in the structural gene (pyrE) for orotate phosphoribosyltransferase (OPT) in Escherichia coli K-12. OPT from both the mutant and the wild-type was partially inhibited by adenine and adenosine, although other purine derivatives were not effective for this inhibition. The Km values of the mutant OPT were 580 and 760 microM for orotate and 5'-phosphoribosyl-1'-pyrophosphate (PRib-PP), respectively, whereas the corresponding values for the wild-type OPT were 40 and 60 microM. The intracellular level of PRib-PP was decreased to less than 15% of the normal level when purine derivatives were added to exponentially growing cultures of both the parent and mutant strains. However, this decrease of the PRib-PP level was not found in strains derived from the mutant, in which the purine-sensitive phenotype was suppressed by a secondary mutation. The purine-sensitive phenotype was caused by retardation of the pyrimidine de novo pathway, when the intracellular level of PRib-PP was diminished by exogenously supplied purine derivatives.

Adenine↗

Morphological correlates of physiologically identified Y-, X-, and W-cells in cat retina.

The action spike activities of single ganglion cells were recorded from the nasal retina of the intact eye of anesthetized and immobilized cats. Each ganglion cell was identified as a Y-, X-, or W-cell on the basis of its axonal conduction velocity, its receptive-field properties, and the level of maintained activity. Of about 100 ganglion cells physiologically identified and penetrated with horseradish peroxidase (HRP)-containing glass microelectrodes, 21 cells were subsequently identified in flat-mount preparations of the retinas and processed for detection of HRP. Of a total of nine Y-cells recovered, four had been penetrated at the soma and five at the axon. All had the morphology of the alpha-cell of Boycott and Wässle. Eight X-cells recovered. All had been penetrated at the soma and showed beta-cell morphology. Four W-cells were penetrated at the soma and recovered. Two off-tonic W-cells had small somas (15-16 micron in diam) and sparse dendritic fields, resembling gamma-cells of Boycott and Wässle. They are also similar to "G4" and "G18" of Kolb et al.'s classification. One on-tonic W-cell had somewhat larger soma (18 micron) with a relatively densely branched dendritic field. This corresponds to delta-cell of Boycott and Wässle or to "G15" of Kolb et al. One on-off phasic W-cell had a medium-sized soma (25.3 micron) with a fanlike dendritic expansion characteristic of the "unilateral horizontal broad range cell" of Shkolnik-Yarros or of "G22" of Kolb et al. Alternatively, all these W-cells can be called medium-sized gamma-cells. Among all three classes of ganglion cells, a positive correlation was found between the diameter of the receptive-field center and the dendritic field. Assuming that in the cat retina 1 degree of visual angle = 230 micron, dendritic fields of Y-cells seemed larger than their physiologically determined receptive-field centers. By contrast, the reverse relation was found between these two dimensions in X-cells. Axon diameters ranged from 4.0 to 5.6 micron (mean, 4.5 micron) in Y-cells and from 1.9 to 2.7 micron (mean, 2.2 micron) in X-cells. Three W-cells showed axon diameters of 0.6, 1.1, and 1.8 micron. The axon diameter distributions made from axons labeled by massive injections of HRP into the optic nerve fiber layer showed a pattern of distribution similar to that obtained from physiologically identified Y-, X-, and W-cell axons.

Animals↗

'Decubitus' of renal graft on psoas muscle. Local changes of cortical thickness and function in the graft.

Using computerized tomography (CT scan), it was demonstrated that the renal cortex of the graft was thinner in the contact area with the psoas muscle than in the rest of the kidney and that its function in the local area appeared somewhat decreased. These findings might be related to the importance of the perirenal fat in shielding the kidney from mechanical pressure.

Adipose Tissue↗

Paraquat-induced pulmonary fibrosis. Role of the alveolitis in modulating the development of fibrosis.

Paraquat, a widely used herbicide, can cause severe and often fatal pulmonary fibrosis in humans and in laboratory animals. Although paraquat is known to be directly cytotoxic to lung parenchymal cells, the mechanism by which this leads to pulmonary fibrosis is not completely understood. In a model of paraquat-induced pulmonary fibrosis using the cynomolgus monkey, the administration of paraquat (10 mg/kg/wk subcutaneously for 2 consecutive wk) was followed by an alveolitis comprised of neutrophils and macrophages in the exposed animals as evaluated by lung morphologic examination and bronchoalveolar lavage. The lungs of the exposed animals showed typical interstitial fibrosis within 4 to 8 wk. At 1 to 2 wk after paraquat exposure, bronchoalveolar lavage cells harvested from the paraquat-exposed animals were spontaneously releasing a chemotactic factor for neutrophils, thus providing a possible mechanism for the recruitment of neutrophils to the alveolar structures. Lavage fluid from paraquat-exposed animals contained increased amounts of the fibroblast chemoattractant fibronectin (paraquat, 3.1 +/- 0.3 ng/micrograms albumin; control, 1.6 +/- 0.7 ng/micrograms albumin; p less than 0.05), and alveolar macrophages from these animals showed increased fibronectin production suggesting that local production accounted for part of the increased amounts of this glycoprotein (paraquat, 6.1 +/- 2.5 ng/10(6) cell/h; control, 1.4 +/- 0.5 ng/10(6) cell/h; p less than 0.05). In addition, alveolar macrophages from the exposed animals were spontaneously releasing a growth factor for fibroblasts, and normal alveolar macrophages exposed to paraquat in vitro were induced to release this growth factor.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

The electron microscopic immunohistochemistry of elastase-treated aorta and nuchal ligament of fetal and postnatal sheep.

In conjunction with the immunoperoxidase and the immunoferritin methods, antielastin antibody was used to study the localization of elastin in untreated and elastase-treated elastic fibers of the nuchal ligament and the aorta of fetal and young adult sheep. In tissues not treated with elastase, the staining reaction for antielastin antibody was localized in the outer zones of the amorphous components and along the surfaces of the microfibrils ; the central zones of the amorphous components were unreactive. After mild elastase treatment, incompletely digested amorphous components showed staining both in their central and outer zones, and some of the microfibrils became unreactive. After extensive elastase treatment, small scattered amorphous components were still found in association with bundles of microfibrils. These components were stained diffusely by the antielastin antibody method but were not detectable by staining with uranyl acetate and lead citrate or with Kajikawa 's method for elastin; elastin was not detected on the surfaces of the microfibrils by any of the methods used. These findings were interpreted as indicating that the surfaces of the microfibrils are associated with small amounts of elastin, and that evenly stained amorphous components are composed of elastin, which is loosely arranged and allows the penetration of antielastin antibody. These observations support the concept that microfibrils serve an important role as a scaffold for elastin deposition in elastogenesis. Because of their high sensitivity, immunohistochemical methods for detecting elastin are useful to study partially degraded elastic fibers.

Age Factors↗

Mitochondrial encephalomyopathy with lactate-pyruvate elevation and brain infarctions.

We studied a patient with somatic growth failure with easy fatigability, myopathy with mitochondrial abnormality, increased lactate and pyruvate in blood and CSF, mental retardation, seizure, myoclonus, deafness, cerebellar ataxia, and blindness with macular degeneration and optic atrophy. Pathologic findings included multiple brain infarctions and massive calcification in the basal ganglia. Biochemical studies of isolated mitochondria revealed decreased oxygen consumption in skeletal muscle, diaphragm, and brain, suggesting an abnormality in the respiratory chain.

Adolescent↗

An autopsy case of rheumatoid arthritis with aortic steno-insufficiency, angina pectoris and severe heart failure.

Although nonspecific pericarditis, myocarditis, valvulitis, and coronary arteritis are known as cardiac lesions that accompany rheumatoid arthritis (RA), there have been few reports of the occurrence of clinically severe valvular disease. We report here the case of 69-year-old man with a 25-year history of RA who died of acute left-sided heart failure complicating to aortic steno-insufficiency and angina pectoris. Autopsy findings revealed the coincidence of a congenital bicuspid aortic valve with chronic inflammation, fibrosis and calcification; eccentric hypertrophy and myocardial fibrosis of the left ventricle; 75% luminal narrowing of the proximal portion of the coronary artery due to atherosclerosis, and narrowing of the small arteries of the cardiac muscle due to angitis. It is deduced that the coronary artery lesions, aortic valve lesions and myocardial lesions were aggravated by the bicuspid aortic valve, changes with ageing and corticosteroid therapy.

Aged↗

The incidence of thromboembolism and the hemocoagulative background in patients with rheumatic heart disease.

We discussed the existence of a thrombotic tendency and the relationship between the high incidence of thromboembolism and the thrombotic tendency in patients with rheumatic heart disease (RHD). The augmentation of platelet function was detected in all kinds of rheumatic valvular disease from the finding of high values of plasma beta-thromboglobulin (72 ng/ml, normal 29 ng/ml). The existence of hypercoagulation was also detected in patients with mitral stenosis by showing low levels of plasma antithrombin III (AT III), while fibrinolytic reaction remained normal. The degree of hypercoagulation became augmented in the order of cases of mitral stenosis (MS) complicated by both atrial fibrillation and chronic congestive heart failure, MS complicated only atrial fibrillation and MS with normal sinus rhythm (AT III: 19.6, 25.0, 26.7 mg/dl, respectively). On the contrary, hypercoagulation, the degree of which was almost the same as that in the respective MS groups, also existed in comparable controls of non-RHD, accompanied by the acceleration of fibrinolytic reaction as shown by the decrease in activity of plasma alpha 2-plasmin inhibitor. Therefore, it was concluded that thrombotic tendency certainly existed in patients with MS compared to those with non RHD and that it was one of the causes of the significantly high incidence of thromboembolism in comparison with non RHD.

Antithrombin III↗

High Ca content of pacemaker tissues in the frog heart.

Cation contents of various cardiac regions were determined in the isolated perfused bullfrog heart. The Ca content was much higher in the pacemaker tissues (sinus venosus and atrio-ventricular ring muscle) than in the atrial or ventricular muscles even with extracellular Ca deficiency. A possible relationship between stored Ca and spontaneous pacemaker activity is discussed.

Animals↗

Systemic vascular lesions and prognosis in systemic lupus erythematosus.

The purpose of this paper is to show the relationship of systemic vascular lesions to the clinical manifestations and prognosis in SLE. Thirty-four autopsied cases of SLE formed the subject material for this study. Histopathological tissue studies were made on vascular lesions from almost all organs. Vascular lesions were separated into three groups according to the size of the involved vessel: 1) medium-sized artery (9 cases), 2) small artery (12 cases) and 3) (13 cases) without systemic vascular lesions. Vascular lesions were also separated into five groups (a) fibrinoid degeneration (10 cases), b) intimal thickening (6 cases), c) thrombosis (6 cases), d) sclerosis (7 cases) and e) (13 cases) without systemic vascular lesions. Patients with involvement of medium-sized arteries had a low female incidence, photosensitivity, and positive LE cell incidence, and the cause of death in these patients was cerebral vascular involvement. The cause of death in patients with vascular fibrinoid degeneration and thrombosis was mainly uremia, whereas patients with sclerosis more often died from infection. Regarding systemic vascular lesions in SLE, the prognosis for the patients with thrombosis and vascular involvement of medium-sized arteries was the most grave.

Adult↗