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Biomedical subjects

N Aoki

Publications and source records attributed to N Aoki.

At least 739 records · Page 41Linked to original sources
PubMed1977

Potentiation by collagen or epinephrine of platelet responsiveness to aggregation. The possible role of substance(s) released from platelet membranes.

When human platelets in plasma were exposed to a small amount (nonaggregating concentration) of collagen, epinephrine, or arachidonic acid, their responsiveness to aggregating agents was potentiated and they were aggregated by a subsequent addition of nonaggregating concentrations of the stimulants. Otherwise the nonaggregating concentrations of the stimulants were incapable of inducing platelet aggregation. The potentiation of platelet responsiveness to aggregating agents was also caused by collagen- or epinephrine-treated platelet membranes. Furthermore, the soluble fraction of collagen- or epinephrine-treated membranes contained some material responsible for platelet potentiation, indicating that the responsible material was released from platelet membranes by collagen or epinephrine. It is suggested that the material may be arachidonic acid or its derivatives related to prostaglandins, since the soluble fraction of collagen- or epinephrine-treated membranes contained a larger amount of the precursor(s) of prostaglandin Falpha than the untreated membranes.

Arachidonic Acids↗
PubMed1977

[A case of posterior fossa acute subdural hematoma diagnosed through extravasated contrast media (author's transl)].

The authors report a case of posterior fossa acute subdural hematoma diagnosed preoperatively through extravasted contrast media from the hemispheric branch of the posterior inferior cerebellar artery along a linear fracture across the transverse sinus unto the pyramis. In a review of the literature it is to be noted that in acute cases, nystagmus and cerebellar signs are very rare and patients fall in coma within 24 hours after injury with promptly advancing severe brain stem compression signs in contrast to subacute or chronic cases. Therefore, whenever the diagnosis is suspected, time should not be lost for a burr hole opening and decompressive craniectomy. Vertebral angiography is sometimes very confirmative but it should be done only when time affording.

Acute Disease↗
PubMed1976

Isolation and characterization of alpha2-plasmin inhibitor from human plasma. A novel proteinase inhibitor which inhibits activator-induced clot lysis.

A procedure is presented for purifying a novel proteinase inhibitor in human plasma whose apparent unique biological property is to inhibit efficiently the lysis of fibrin clots induced by plasminogen activator. The final product is homogeneous as judged by disc gel electrophoresis, and immunoelectrophoresis. Its molecular weight estimated by sodium dodecyl sulfate gel electrophoresis or sedimentation equilibrium is 67,000 and 63,000, respectively. The inhibitor is a glycoprotein consisting polypeptide chain containing 11.7% carbohyrate. It migrates in the alpha2-globulin region in immunoelectrophoresis. The inhibitor is chemically and immunologically different from all the other known inhibitors in plasma. Inhibition of plasmin by the inhibitor is almost instantaneous even at 0 degrees, in contrast to the slow inhibition of urokinase (plasminogen activator in urine). Plasminogen activation by urokinase-induced clot lysis is inhibited by the inhibitor mainly through a mechanism of instantaneous inhibition of plasmin formed and not through the inhibition of urokinase. The inhibitor also inhibits trypsin. Consequently, it is suggested that this newly identified inhibitor is named alpha2-plasmin inhibitor or alpha2-proteinase inhibitor. A specific antibody directed against the inhibitor neutralizes virtually all inhibitory activity of plasma to activator-induced clot lysis. Immunochemical quantitation of the inhibitor was specific antiserum to the inhibitor and the purified inhibitor as a standard indicates that the concentration of the inhibitory in the serum of a healthy man is in or near the range of 5 to 7 mg/100 ml, which is the lowest concentration among the concentration of the proteinase inhibitors in plasma. The inhibitor and plasmin, trypsin, or urokinase form a complex which cannot be dissociated with denaturing and reducing agents. The formation of the enzyme-inhibitor complex occurs on a 1:1 molar basis and is associated with the cleavage of a unique peptide bone, which is most clearly demonstrated in the interaction of the inhibitor and beta-trypsin. In the complex formation between the inhibitor and plasmin, the inhibitor is cross-linked with the light chain which contains the active site of plasmin. It is suggested that, in a fashion analogous to complex formation between alpha1-antitrypsin and trypsin, the cross-links are formed between the active site serine of the enzyme and the newly formed COOH-terminal residue of the inhibitor, with cleavage of a peptide bond.

Amino Acids↗
PubMed1976

Effects of thyroxine on T-cell counts and tumour cell rejection in mice.

In an attempt to study the effect of thyroxine on peripheral T-cell (thymus derived lymphocyte) counts or immunological functions, inbred C3H/He mice (8-10 weeks old) were injected subcutaneously with thyroxine for more than 3 months. After treatment for 3 months the mice were examined for peripheral T-cell counts, thymic incorporation of tritiated thymidine and rejection of tumour transplants. The number of T-cells was counted by the indirect immunoflourescence method using anti-thetaC3H serum after separation of lymphocytes on "Ficoll-Conray". It was revealed that the peripheral counts of both lymphocytes and T-cells were increased in the thyroxine treated group as compared with the control group, as was reported in the patients with Graves' disease. Thymic incorporation of tritiated thymidine was also found to be significantly increased in the thyroxine treated group. In addition, in order to study T-cell activity of the host, thyroxine treated and control mice were challenged with Ehrlich carcinoma cells at several concentrations (10(2), 10(4) and 2 x 10(6) per mouse). It was found that rejection of tumour transplants was significantly enhanced in the T-cell rich mice. Thus, it is possible that throxine affects peripheral T-cell counts and enhances immunological functions of the host.

Animals↗
PubMed1976

[A case of the lateral ventricular tumor (subependymal glomerate astrocytoma) with preceding Parkinsonian symptoms due to normal pressure hydrocephalus (author's transl)].

Authors report a patient with a subependymal glomerate astrocytoma in the right lateral ventricle. He maifested parkinsonian symptoms and dementia related to the preceding normal pressure hydrocephalus which was proved by an infusion test, and then advanced an akinetic mutism. Soon after a shunting operation was carried out he showed a full recovery from the symptoms, which may suggest that an incomplete block of the ventricular system is one cause of the normal pressure hydrocephalus. From pathology it was revealed that the tumor is an intraventricular astrocytoma with a fibrous stalk and was totally removed with an ease. The findings seem to accord with "Subependymal glomerate astrocytoma" (Boykin.) Further corroboration would be necessary to establish this entity.

Aged↗
PubMed1976

[Treatment of acute subdural hematoma in infancy-tapping only method and a follow-up study (author's transl)].

Acute subdural hematoma in infants is characterized by convulsive seizure, disturbance of consciousness, vomiting and irritability soon after mild head injury. The majority of cases have tence or bulged anterior fontanel and preretinal hemorrhage. Eleven cases, all traumatic in etiology and male under the age of one year were reported. Nine of them were treated by percutaneous subdural tapping alone, i.e., "Tapping Only Method". For the first several days, tappings were carried out daily. The subdural content was liquefied old dark blood or liquefied fresh-appearing blood in most cases. After that taps were performed only in the presence of intracranial hypertension. Vomiting and irritability were fairly reliable indicaters of intracranial hypertension but the most consistent signs were the fontanel tension to palpation and the measurement of head circumference. As soon as it could be determined that increased pressure did not recur within ten days after the last tap or that dry tap was confirmed the infant was discharged and follow as an outpatient. Follow-up studies on this series by cerebral angiography, EEG, skull measurement and Denver developmental screening test revealed normal physical and mental development in nine cases, although three out of nine cases showed mild but persistent avascular area. The remaining two cases showed more or less physically and mentally retarded developments: the initial treatment for both of them was delayed more than ten days. Acute infantile subdural hematoma due to mild head injury should be divided into the following two types: "Fulminant type", which rapidly falls in coma and may be fatal. The another, "Mild type" manifests only signs and symptoms of mild intracranial hypertension. This mild type should be treated by tapping only method without delay. There is a possibility that some mild type cases are overlooked and later progress to chronic infantile subdural hematoma. For comparison, thirteen cases of acute infantile subdural hematoma treated by trephination and/or craniotomy were reviewed. Pathological study revealed that early formation of capsular membrane is one of the characteristic findings.

Brain Injuries↗