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Biomedical subjects

Y Uno

Publications and source records attributed to Y Uno.

At least 127 records · Page 7Linked to original sources
PubMed1992

Aging-associated deletions of human diaphragmatic mitochondrial DNA.

It is known that respiratory function deteriorates with age. Endogenous damage to DNA is thought to contribute to the aging process. The mitochondrial oxidative phosphorylation system, a bio-engine, consists of five complexes, and 13 subunits of those complexes are biosynthesized from information encoded in mitochondrial DNA. Mitochondrial DNA is shown to have a much higher mutation rate than nuclear DNA. We examined the diaphragms obtained at autopsy from 34 humans, 23 men and 11 women, ranging in age from 25 to 85 yr, for mitochondrial DNA deletions using the polymerase chain reaction method. Multiple mitochondrial DNA deletions were detected particularly among the elderly; the number of deletions in those over age 70 was significantly higher than in those under age 40. The occurrence of a 3.4-kbp deletion of mitochondrial DNA increased with age, i.e., 0% of those under age 30, 20.0% of those in their forties, 25.0% of those in their fifties, 28.6% of those in their sixties, 72.7% of those in their seventies, and in all of those over age 80. The mutation was based on the directly repeated sequence, 5'-TCACCCC-3', which exists in both the CO3 gene and the ND5 gene. Replication impairment occurred at that directly repeated sequence, which caused the elimination of a genome between the CO3 gene and the ND5 gene, and information for biosynthesis of four subunits in complex I (ND3, ND4L, ND4, and ND5), one in complex IV (CO3), and five transfer RNA genes was missing.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1992

[Two cases of familial pulmonary arteriovenous fistula].

Two cases of familial pulmonary arteriovenous fistula are reported. Case 1: A 54-year-old woman was admitted with exertional dyspnea. An abnormal shadow on chest X-ray had been noted since the age of 37 years. Pulmonary angiography demonstrated bilateral pulmonary arteriovenous fistulas. Case 2: A 25-year-old man, the son of Case 1, was admitted for operation for the same disease. The mother and son both suffered from repeated epistaxis due to Rendu-Osler-Weber disease. In order to reserve pulmonary function, fistulectomy was performed in both cases, and their subsequent clinical courses were good.

Adult↗
PubMed1992

[Prophylaxis of thrombosis in a pregnant woman with congenital antithrombin III deficiency: changes in hemostatic molecular markers before the onset of thrombosis].

A pregnant woman with congenital antithrombin III (AT III) deficiency was given AT III concentrate and warfarin at the first and after 36th week of gestation periods and at the other gestation period, respectively. The patient developed thrombosis in the left leg, but fibrinopeptide A (FPA) and thrombin-AT III complex (TAT) had already shown high values one week before, suggesting the possibility of their being forecast markers of thrombosis. The administration of AT III concentrate caused an improvement in thrombosis. Therefore, in case of high FPA and TAT values as determined one or two times a week, the administration of AT III concentrate was thought necessary. In case of warfarin, however, non-administration during the 6th-9th weeks of gestation for the purpose of avoiding teratogenicity and frequent blood coagulation tests taking heed of overdosage for the purpose of avoiding fetal central nervous system abnormalities were suggested necessary. Delivery was uneventful, both mother and child being doing very well; umbilical blood AT III activity was 18%. It is generally difficult for us to form the diagnosis as AT III deficiency only from AT III activity at neonatal stage, but in the present study, we analyzed the restriction fragment length polymorphism of the AT III gene using umbilical blood, and succeeded in diagnosing the neonatal child as AT III deficiency.

Adult↗
PubMed1991

Effects of atropine treatment on in vitro and in vivo binding of 4-[125I]-dexetimide to central and myocardial muscarinic receptors.

Upregulation of muscarinic cholinergic receptors (mAChR) after chronic atropine treatment has been described previously. The present study was designed to evaluate 4-iodine-125 dexetimide as an agent to determine changes in the number of mAChR. Rats were injected subcutaneously with atropine (500 mg/kg) either once or chronically, once daily for 10 days, and sacrificed 24 h later. In vitro binding assays with 4-[125I]-dexetimide showed significant increases in the number of mAChR in cerebra (21%) and ventricles (45%) after chronic atropine treatment but not after acute treatment. The affinity of binding to cerebral and ventricular mAChR declined after acute and chronic atropine treatment. In vivo studies were carried out involving intravenous injection of 4-[125I]-dexetimide 24 h after atropine treatment. Binding was markedly reduced in the brain and heart. Upregulation of mAChR, as seen in in vitro studies, could not be observed because of the remaining atropine. Occupancy of mAChR by atropine persisted as long as 7 days after one dose. The results of these studies indicate that 4-[125I]-dexetimide binding reflects the effects of atropine on central and peripheral muscarinic cholinergic receptors in vitro and in vivo.

Animals↗
PubMed1991

Serum lipoprotein lipid concentration and composition in homozygous and heterozygous patients with cholesteryl ester transfer protein deficiency.

Six homozygous, 10 heterozygous and 8 unaffected subjects in a CETP deficient family confirmed by CETP gene analysis were studied to characterize serum lipoproteins separated by ultracentrifugation, and to examine the relations between CETP levels and lipoprotein lipid concentration and composition. The serum CETP levels were measured by radioimmunoassay using 125I-labeled monoclonal antibodies (TP2). The serum CETP levels in the homozygotes were undetectable and those in the heterozygotes were significantly lower than those in the unaffected subjects (1.5 +/- 0.1 vs. 2.2 +/- 0.5 microgram/ml, P less than 0.01). In the HDL fraction, esterified cholesterol (EC) levels in the homozygotes were significantly increased (P less than 0.01), and those in the heterozygotes were slightly increased (n.s.), in comparison with those in the unaffected and the normolipidemic controls. The EC levels in the IDL fractions were lower in the homozygotes than in the normolipidemic controls. The EC/triglyceride (TG) molar ratios in IDL, the fraction obtained from the homo- and heterozygotes, were lower than those from the unaffected subjects (P less than 0.01 and less than 0.01, respectively), and the EC/TG ratios in the HDL fraction obtained from the homo- and heterozygotes were higher than those from the unaffected subjects (P less than 0.01 and n.s., respectively). Linear regression analysis showed that positive correlates of the serum CETP levels in all subjects were: IDL-EC (r = 0.463), HDL-TG (r = 0.603) and VLDL- and IDL-EC/TG ratio (r = 0.698 and 0.843).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1991

Necrotizing tubulointerstitial nephritis associated with adenovirus infection.

We report 10 autopsy cases of necrotizing tubulointerstitial nephritis induced by adenovirus (ADV). Hemorrhagic, necrotizing tubulitis with intranuclear inclusion bodies was observed in the kidneys of five bone marrow transplant recipients and five patients treated with intensive chemotherapy for malignancies (four cases of leukemia and one case of lung cancer). It was histopathologically demonstrated that necrobiotic tubular cells had inclusion-bearing cells of three types: "smudge cells," Cowdry A intranuclear inclusion cells, and full-type intranuclear-containing cells. Immunofluorescent examination with anti-ADV antibody demonstrated specific fluorescence on the affected tubular cells of all 10 kidneys. Specific antigens for ADV type 11 were also revealed in all but one case by an immunofluorescent test using type-specific antiserum and convalescent serum containing high titer antibody to this serotype. Electron microscopy revealed intranuclear crystalline arrays of viral particles, 75 to 80 nm in diameter, in each of the seven cases examined. Extrarenal involvement, indicated by ADV-induced cytopathologic change, was confined to bladder or prostate. Hemorrhagic cystitis was recorded in all the bone marrow transplant cases as well as in one leukemia case. Adenovirus type 11 was isolated from urine in all five cases tested during these episodes. Renal failure was ascribed to ADV infection in two of five patients who died from renal dysfunction. The presence of hemorrhagic cystitis and localization of invasive infection in urogenital organs suggested that renal infection might occur by ascending route from the bladder. We propose that ADV should be added as a viral agent to the pathogenetic list of tubulointerstitial nephritis.

Adenoviridae Infections↗
PubMed1991

Mutagenicity of 3-nitrodibenzofuran and 3-aminodibenzofuran.

Mutagenicities of 3-nitrodibenzofuran and 3-aminodibenzofuran were examined using Salmonella typhimurium TA98 and TA100. Strong mutagenicity was found in both compounds. The mutagenic potency of 3-nitrodibenzofuran was approximately 3.5-fold stronger in TA98 and twice stronger in TA100 than that of benzo[a]pyrene. Mutagenicity of 3-aminodibenzofuran was observed under metabolic activation and was 10 times stronger in TA98 and about 5 times stronger in TA100 than that of benzo[a]pyrene.

Benzofurans↗
PubMed1991

Effects of hydralazine and prostaglandin E1 on regional myocardial function in the ischemic canine heart.

The effects of hydralazine and prostaglandin E1 on regional myocardial function were studied in dogs. Sixteen dogs were randomly assigned to one of two drug treatment groups of eight dogs each. The first group (G1) was treated with 0.4 mg/kg hydralazine administered as a bolus. The second group (G2) received prostaglandin E1 given as an infusion for a total dose of 0.8 micrograms/kg. Regional myocardial function was assessed through the measurement of myocardial segment shortening during systole. We call this index percent systolic shortening (%SS). An ischemic heart preparation was created by partial occlusion of coronary blood flow. The degree of induced ischemia was determined by following the reduction in %SS. Hydralazine reduced %SS of the ischemic myocardium while increasing the cardiac index, stroke volume index, and coronary blood flow. Prostaglandin E1 increased %SS, cardiac index, and stroke volume index in the ischemic heart preparation. Hydralazine, therefore, induced dissociation between global ventricular function and regional myocardial function whereas prostaglandin E1 did not. The present findings emphasize that evaluation of vasoactive drugs should consider their effects on regional myocardial function as well as on global hemodynamics.

Alprostadil↗
PubMed1991

L-methionine uptake by human cerebral cortex: maturation from infancy to old age.

Age-associated changes in amino acid transport from blood to normal frontal cortex were studied using positron emission tomography (PET). Seventeen patients, 1.8-71 yr, were injected intravenously with tracer doses of [11C] L-methionine and a baseline PET scan was obtained. To assess competitive inhibition of [11C]L-methionine uptake, patients received either oral L-phenylalanine or an i.v. infusion of amino acids 1 hr before a second PET study. Uptake of [11C]L-methionine by frontal cortex decreased seven-fold between 1.8 and 71 yr (r = -0.71; p less than 0.05). Blood-to-brain transfer of [11C]L-methionine, at 4.5 yr, exceeded mean adult values by more than five-fold. Competitive inhibition reduced L-methionine uptake in all patients older than 4.6 yr. These developmental changes parallel findings in animals. The neutral amino acid transport system may modulate human brain amino acid levels to meet changing developmental metabolic needs.

Adult↗
PubMed1991

In vitro and in vivo characterization of 4-[125I]iododexetimide binding to muscarinic cholinergic receptors in the rat heart.

4-[125I]iododexetimide binding to muscarinic cholinergic receptors (mAChR) was evaluated in the rat heart. 4-[125I]iododexetimide displayed high in vitro affinity (Kd = 14.0 nM) for rat myocardial mAChR. In vivo, there was high accumulation of 4-[125I]iododexetimide in the rat atrium and ventricle which could be blocked by approximately 60% by preinjection of atropine. In contrast, accumulation of the radiolabeled stereoisomer, 4-[125I]iodolevetimide, was 63% lower than 4-[125I]iodolevetimide and was not blocked by atropine. The blood clearance of 4-[125I]iododexetimide was rapid, providing heart-to-blood ratios of up to 14:1; however, heart-to-lung and heart-to-liver ratios were below unity. The data indicate that 4-[125I]iododexetimide binds potently to rat mAChR. However, since nonspecific binding is relatively high, it is not clear whether iododexetimide labeled with 123I will be useful in SPECT imaging studies of myocardial mAChR. Further studies in humans are indicated.

Animals↗
PubMed1990

Trajectory formation of arm movement by cascade neural network model based on minimum torque-change criterion.

We proposed that the trajectory followed by human subject arms tended to minimize the time integral of the square of the rate of change of torque (Uno et al. 1987). This minimum torque-change model predicted and reproduced human multi-joint movement data quite well (Uno et al. 1989). Here, we propose a neural network model for trajectory formation based on the minimum torque-change criterion. Basic ideas of information representation and algorithm are (i) spatial representation of time, (ii) learning of forward dynamics and kinetics model and (iii) relaxation computation based on the acquired model. The model can resolve ill-posed inverse kinematics and inverse dynamics problems for redundant controlled object as well as ill-posed trajectory formation problems. By computer simulation, we show that the model can produce a multi-joint arm trajectory while avoiding obstacles or passing through viapoints.

Algorithms↗
PubMed1990

Undifferentiated carcinoma of the parotid gland in a 10-month-old child.

Malignant salivary gland tumors in children are very rare. This report describes the autopsy of a child with parotid gland cancer. The patient, a 10-month-old girl, was admitted to the Nagoya First Red Cross Hospital with facial nerve palsy. Incisional biopsy of a post-auricular tumor was performed, and undifferentiated carcinoma was diagnosed. The patient died 6 months later of respiratory failure due to pulmonary lymphangitis carcinomatosis. Light and electron microscopic and immunohistochemical examinations of the tumor tissue were performed. The tumor cells were arranged in a medullary, sheet-like manner. Keratinization or mucus lakes were not observed. PAS-alcian blue staining demonstrated intracytoplasmic mucus as granules, and also small intercellular droplets of mucus that might otherwise have been unnoticed. Ultrastructurally, some of the tumor cells had tonofilament-like keratin filaments, and also small hollow spaces bounded by microvilli and containing secretory particles. These were stained by antisera against CEA and keratin. These findings are suggestive of differentiation to mucoepidermoid carcinoma. We also review and discuss malignant salivary tumors of epithelial origin in children.

Carcinoma↗
PubMed1990

Vascular pattern of the guinea pig tympanic membrane.

The vascular organization of the guinea pig tympanic membrane was studied by light microscopy in India-ink-, colored-gelatin-, or horseradish peroxidase (HRP)-injected specimens. The ultrastructural localization of the vessels was examined by transmission electron microscopy in HRP-injected material. We found that the tympanic membrane is supplied by two arterial sources, the superior and inferior tympanic arteries, both of which arise from the posterior auricular artery. The superior tympanic artery gives off arterioles which, in the tympanic membrane, run centrifugally from the attachment of the manubrium, while the inferior tympanic artery emits arterioles which run centripetally from the tympanic annulus. Both sets of arterioles divide into capillaries and form a monolayered polygonal meshwork. The capillaries drain into venules which run between arterioles in the membrane and empty into either the superior tympanic vein located at the manubrium or the inferior tympanic vein at the annulus.

Animals↗
PubMed1990

[Changes in myocardial energy charge following cardiac arrest and subsequent resuscitation].

Cardiac resuscitation becomes more difficult as time of arrest is prolonged. This study was designed to investigate changes in energy charge (EC) during cardiac arrest and subsequent resuscitation periods. The experiment was divided into 2 parts. In the first part, 36 rats were divided into 6 groups. Control rats were anesthetized only with pentobarbital and the heart was extirpated. In other rats, an acute exsanguination was carried out until mean arterial pressure (MAP) fell to 0, and then the rats were divided into 5 groups according to the time of extirpation following the cardiac arrest: 1, 5, 10, 15 and 20 minutes, respectively. The extirpated hearts were rapidly frozen with liquid nitrogen. ATP, ADP and AMP were enzymatically measured and EC was calculated. ECG was monitored to ascertain complete electrical arrest. Disappearance of ECG activity was observed about 9 minutes after MAP reaching zero. In the second part; 36 rats were also divided into 6 groups. After the same manipulation as in the first part, the extirpated heart was perfused for 30 minutes using Langendorff method and both cardiac function (LVP, LV dp/dt and HR) and EC were investigated. Total adenine nucleotide (TAN) was already diminished at 1 minute and decreased progressively. On the contrary, EC was well maintained around control level until ECG activity disappeared completely, and an abrupt decrease in EC occurred after electrical arrest. When the heart was perfused about 30 minutes, EC recovered almost to the control level in the groups in which perfusion was started within 10 minutes, but its recovery was incomplete in the groups in which perfusion was begun after 10 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1990

[Congenital plasminogen deficiency in a Japanese family].

A Japanese family with congenital plasminogen deficiency was described. The propositus was a 43-year-old woman, who complained of the attack of tonic convulsion. Her maternal grandfather was died of myocardial infarction and grandmother died of cerebral infarction. Her mother had thrombosis of the left femoral artery at the age of 56 years. She was made a diagnosis of late onset epilepsy due to cerebral infarction or cerebral tumor by electroencephalography, brain CT, and brain MRI. Her plasma plasminogen activity determined using chromogenic substrate was 54%, and the plasma level of plasminogen antigen measured by single radial immunodiffusion was 4.8 mg/dl. Family studies revealed parallel decreases in plasminogen activity and antigen levels in her mother and second daughter. These data suggest that congenital plasminogen deficiency is inherited as an autosomal dominant defect in this family.

Adolescent↗
PubMed1989

Mechanism of potentiation by manganese ion of aggregation of porcine pancreatic elastase-treated human platelets.

The effect of manganese ion (Mn2+) on the aggregation of porcine pancreatic elastase-treated platelets (ETP) induced by fibrinogen (Fbg) was studied. Mn2+ enhanced the aggregation of ETP on addition of Fbg specifically and dose-dependently. This effect of Mn2+ was not associated with the formation of thromboxane A2, and was not affected by pretreatment of ETP with acetylsalicylic acid in the presence of Mn2+. Moreover, it was not dependent on extracellular adenosine diphosphate, as shown by removal of extracellular adenosine diphosphate by pretreatment of ETP with creatine phosphate/creatine phosphokinase. Studies on the binding of 125I-Fbg to ETP showed that Mn2+ increased the Kd value of binding but did not affect the number of Fbg binding sites. These results indicate that Mn2+ specifically and dose-dependently potentiated Fbg-induced aggregation of ETP and that this effect of Mn2+ may be due to an increase in the affinity of binding of Fbg to the glycoprotein IIb-IIIa complex on the membranes of ETP.

Aspirin↗
PubMed1989

Formation and control of optimal trajectory in human multijoint arm movement. Minimum torque-change model.

In this paper, we study trajectory planning and control in voluntary, human arm movements. When a hand is moved to a target, the central nervous system must select one specific trajectory among an infinite number of possible trajectories that lead to the target position. First, we discuss what criterion is adopted for trajectory determination. Several researchers measured the hand trajectories of skilled movements and found common invariant features. For example, when moving the hand between a pair of targets, subjects tended to generate roughly straight hand paths with bell-shaped speed profiles. On the basis of these observations and dynamic optimization theory, we propose a mathematical model which accounts for formation of hand trajectories. This model is formulated by defining an objective function, a measure of performance for any possible movement: square of the rate of change of torque integrated over the entire movement. That is, the objective function CT is defined as follows: (formula; see text) We overcome this difficult by developing an iterative scheme, with which the optimal trajectory and the associated motor command are simultaneously computed. To evaluate our model, human hand trajectories were experimentally measured under various behavioral situations. These results supported the idea that the human hand trajectory is planned and controlled in accordance with the minimum torque-change criterion.

Arm↗