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Biomedical subjects

N Aoki

Publications and source records attributed to N Aoki.

At least 721 records · Page 40Linked to original sources
PubMed1978

Abnormal plasminogen. A hereditary molecular abnormality found in a patient with recurrent thrombosis.

A patient who suffered a recurring thrombosis over the last 15 yr has been investigated. The only abnormality found in this patient was a significantly depressed level of plasminogen activity in plasma. In spite of the depressed plasminogen activity, the patient was found to have a normal level of plasminogen antigen concentration. It was calculated that the activity per milligram of plasminogen of the patient was approximately one-half the values of normal subjects. The same discrepancy between biological activity and antigen concentration was found in the other members of the kindred. A niece was found to have practically no plasminogen activity but possessed a normal concentration of plasminogen antigen. Both her parents were found to have approximately half the normal plasminogen activity and normal antigen levels. These studies suggested that the molecular abnormality was inherited as an autosomal characteristic, and the family members who had half the normal levels of activity with normal plasminogen antigen were heterozygotes whereas the one with practically no plasminogen activity was homozygote. Subsequent studies showed that the pattern of gel electrofocusing of purified plasminogen of the heterozygotes consisted of 10 normal bands and 10 additional abnormal bands, each of which had a slightly higher isoelectric point than each corresponding normal component. This indicates that plasminogen of the heterozygote is a mixture of normal and abnormal molecules in an approximately equal amount, which was substantiated by active site titration of purified plasminogen preparations obtained from the propositus and a normal individual. The gel electrofocusing pattern of the homozygote consisted of abnormal bands only. The defect is a hereditary abnormality of plasminogen.

Adult↗
PubMed1978

[Intrathecal gentamicin in the treatment of meningitis--clinical case study (author's transl)].

The authors report 33 cases of meningitis treated with intrathecally administered gentamicin (GM) and examine it's effectiveness for meningitis side effects and optimum dose. Of 33 cases 15 cases (group I1 were treated with GM alone 7 cases (group IIa) with GM combined with SB--PC or CP. In 8 cases of the other 11 cases (group IIb) GM was changed for SB--PC or CP because of it's inefficiency and side effects (6 cases) and other reasons (2 cases). In the remaining three cases of group IIb SB--PC or CP was changed for GM due to their inefficiecy. Maximum intrathecal dose is shown below : 4 mg--7 cases, 8 mg--5 cases, 10 mg--15 cases, 20 mg--4cases, 40 mg--2 cases. In all cases GM was not administered systemically, but each of CP, CB--PC, SB--PC and TC was administereed systemically. In group I, only one case did not G--I tract bleeding but the others were cured. In group IIa all but one case was cured. In group IIb one case of cyptococcosis was dead. Total effective cases of intrathecal GM were 17 of 24 cases excluding group IIa (7 cases) and 3 cases of group IIb. There was no side effect in cases of which maximum dose was 4--20 mg, but in one of 40 mg administered cases in which GM was injected from cisternal puncture hearing, vestibular and visual function were disturbed permanently. Therefore GM should not be injected into the cistern. In our conclusion intrathecal GM is thought to be effective in the treatment of meningitis without systemic GM. Effective optimum dose in 4--8 mg/day day in adult and if ineffective after 7--10 days GM should be changed for other antibiotics.

Adolescent↗
PubMed1978

Inhibition of platelet aggregation by protease inhibitors. Possible involvement of proteases in platelet aggregation.

The possible participation of proteases in human platelet aggregation was explored using various protease inhibitors and substrates. Protease inhibitors used included naturally occurring inhibitors of serine proteases and synthetic inhibitors that modify the active site of protease. Substrates used were synthetic substrates for the trypsin type as well as for the chymotrypsin type of protease. All these inhibitors and substrates inhibited platelet aggregation and serotonin release induced by ADP, collagen, epinephrine, or thrombin. In ADP- and epinephrine-induced platelet aggregation the second phase of aggregation was most efficiently inhibited. The inhibitors suppressed the formation of malondialdehyde during platelet aggregation. Release by aggregating agents of arachidonate and its metabolites from indomethacin-treated platelets as well as nontreated platelets was also inhibited. The inhibitors apperar to interact with stimulated platelets but not with unstimulated platelets. These observations suggest that the interaction of an aggregating agent with its platelet receptor activates a unique precursor serine protease that in turn activates platelet phospholipase to liberate arachidonic acid (the precursor of the potent platelet aggregating agent thromboxane A2) from platelet phospholipids.

Arachidonic Acids↗
PubMed1978

[A case of colloid cyst of the third ventricle (author's transl)].

The authors report a case of colloid cyst of the third ventricle diagnosed preoperatively through CT scan, pneumoencephalography and carotid angiography. The patient was a twenty-six year old housewife with a history of two repeated episodic headaches followed by gait disturbance, vomiting and cold sweating. At operation, the colloid cyst which completely occluded the right foramen of Monro, was reached by anterior transcallosal approach and was partially removed with subsequent cure of her symptoms. The cyst fluid contained cholesterin crystals, cholesterol, protein (12.8 g/dl), and sugar (16 mg/dl). Histologically, the cyst wall consisted of a single layered cuboidal or columnar epithelium with many cilias internally and loose connective tissue rich in vascluar channels externally. Cytoplasm and cellular surface was partly positive at mucicarmine, PAS and alusian blue staining. The fact would confirm that there is mucin secreting function among the epithelial cells of the cyst.

Adult↗
PubMed1978

Release of arachidonic acid from human platelets. A key role for the potentiation of platelet aggregability in normal subjects as well as in those with nephrotic syndrome.

Low (nonaggregating) concentrations of collagen that potentiate platelet aggregation did not induce the formation of measurable amount of malondialdehyde (MDA) but released small but significant amounts of radioactivity from 14C-arachidonic acid-labeled platelets. A major portion of the radioactive compounds released by nonaggregating concentrations of collagen existed as arachidonic acid and a minor part as thromboxane B2. The nephrotic syndrome enhances platelet aggregability, and this effect is abolished by correcting hypoalbuminemia in vitro and in vivo by the addition of albumin, which is the main carrier for free fatty acids, including arachidonic acid. Human albumin (fatty acid free) inhibited collagen-induced aggregation, MDA formation, and release of the radioactivity from 14C-arachidonic acid-labeled platelets in normals as well as in those with nephrotic syndrome. These data support our hypothesis that the main mechanism responsible for the potentiation of platelet aggregation is the release of arachidonic acid from platelet membrane phospholipids via the activation of phospholipase A2. Furthermore, enhanced platelet aggregation in the nephrotic syndrome was at least partly attributable to an increased availability of arachidonic acid released secondary to hypoalbuminemia. Albumin inhibits aggregation probably by binding to released arachidonic acid preventing arachidonic acid from being metabolized to potent aggregating substances, endoperoxides and thromboxane A2. The mechanism of release of arachidonic acid may play a key role in the potentiation of platelet aggregability in normals as well as in pathologic conditions such as the nephrotic syndrome.

Albumins↗
PubMed1978

A novel vascular relaxing agent, N-(6--aminohexyl)-5-chloro-1-naphthalensulfonamide which affects vascular smooth muscle actomyosin.

The relaxing effect and possible mechanism of N-(6-aminohexyl)-5-chloro-1-naphthalenesulfonamide (W-7) on isolated rabbit artery were investigated. The addition of W-7 in concentrations ranging from 1 X 10(-6) to 3 X 10(-4) M caused a significant relaxation of isolated rabbit vascular strips contracted by KCl, prostaglandin F2alpha, norepinephrine, histamine, CaCl2, serotonin or angiotensin II. W-7 also caused a shift to the right of the dose-response curves for all agonists tested. Propranolol and atropine did not affect W-7 induced relaxation, suggesting that this drug does not act through beta adrenergic or cholinergic receptors. Superprecipitation of actomyosin from bovine aorta smooth muscle was inhibited by the addition of W-7 in a dose-dependent fashion. The concentration of W-7 which inhibited superprecipitation of bovine aorta smooth muscle actomyosin was in good agreement with the dose producing relaxation of isolated vascular strips. These facts suggest that W-7 produces relaxation of isolated vascular strips by inhibiting actin and myosin interaction.

Actomyosin↗
PubMed1977

On the interaction of alpha2-plasmin inhibitor and proteases. Evidence for the formation of a covalent crosslinkage and non-covalent weak bondings between the inhibitor and proteases.

alpha2-plasmin inhibitor is a proteinase inhibitor in plasma which efficiently inhibits the lysis of fibrin clots induced by plasminogen activator. The nature of the binding of the inhibitor to trypsin or plasmin was studied by the chemical treatment of the enzyme-inhibitor complex with 7.5 M hydrazine at pH 10.0. With the hydrazine treatment, the complexes were degraded to proteins corresponding to the respective enzyme and inhibitor moieties. These results indicate that the covalent bond between the inhibitor and the enzymes is a carboxylic ester. The binding reaction of the inhibitor to active site-modified trypsin was also studied. The inhibitor formed complexes with anhydrotrypsin and carboxyamidomethylated trypsin. The complexes were dissociated in the presence of 1% sodium dodecyl sulfate, to the individual components: the respective enzyme and inhibitor moieties. The inhibitor, however, did not form a complex with diisopropylphosphorylated trypsin regardless of the presence or absence of the denaturing reagent. These results suggest the contribution of non-covalent interactions to the complex formation between the inhibitor and native enzymes.

Binding Sites↗
PubMed1977

Inhibition of proteases in coagulation, kinin-forming and complement systems by alpha2-plasmin inhibitor.

Inhibitory activities of alpha2-plasmin inhibitor against various proteases were investigated. The inhibitor promptly inhibited the esterolytic activity of alpha-chymotrypsin and progressively inhibited the esterolytic or amidolytic activities of bovine plasma kallikrein, bovine thrombin and bovine activated factor X. Heparin had no effect on the reaction of the inhibitor with thrombin or activated factor X. However, the inhibitor had no effect on the activities of human C-1-esterase, papain and snake venom kininogenase. On the basis of its rapid inhibition of kallikrein, alpha2-plasmin inhibitor is considered to exert some regulating effect on kallikrein activity in plasma.

Animals↗
PubMed1977

The behavior of alpha2-plasmin inhibitor in fibrinolytic states.

Human plasma alpha2-plasmin inhibitor in fibrinolytic states was studied using immunochemical methods and radioiodinated plasminogen. The concentration and activity of plasma alpha2-plasmin inhibitor decreased when urokinase was added to plasma in vitro or infused intravenously in man. The decrease was associated with the appearance of plasmin-alpha2-plasmin inhibitor complex which subsequently disappeared from the circulation in a short time. A decrease of other major inhibitors, such as alpha2-macroglobulin and alpha1-antitrypsin, was not observed when the amount of urokinase added or infused was relatively small, and conversion of plasminogen to plasmin was not extensive. The formation of plasmin-alpha2-macroglobulin complex was observed only when plasma plasminogen was activated with a larger amount of urokinase, and after most of the alpha2-plasmin inhibitor was consumed by forming complexes with plasmin. The formation of plasmin-alpha1-antitrypsin complex was not observed even in the highly activated plasma unless exogenous plasmin was added to the plasma. alpha2-Plasmin inhibitor was the only inhibitor of which the concentration in plasma was significantly decreased in patients with disseminated intravascular coagulation and fibrinolysis among the major plasmin inhibitors in plasma. The most reactive inhibitor for regulating plasma fibrinolysis very likely is alpha2-plasmin inhibitor.

Alpha-Globulins↗
PubMed1977

Epidemiological evaluation of funduscopic findings in cerebrovascular diseases. III. Observer variability and reproducibility for funduscopic findings.

In order to evaluate observer variability and reproducibility for the funduscopic findings, the color slides of one hundred cases in Akabane and Asahi town in Japan were investigated and the following were revealed: 1. Observer variability for Keith-Wagener's classification was the least in the grade 3 and the most in grade 0. The variability of diagnosis between observers was the least for retinal bleeding and the most for anteriolar reflex and remarkable for lateral displacement and arteriolar narrowing. In general, the observe variability was one grade at most. 2. Reproducibility for Scheie's hypertensive classification was 73 per cent and that for Scheie's arteriosclerotic and Keith-Wagner's classifications was 66 per cent. Fairly good reproducibility was observed in retinal bleeding and poor reproducibility in arteriolar reflex and vertical and lateral displacements, In general, the intra-observer variability for the funduscopic findings was one grade at most. 3. Observer variability and reproducibility for the funduscopic findings would be improved by establishment of the detailed diagnostic criteria of various funduscopic findings, taking color pictures in focus and systematic training for the fresh doctors or technicians without enough experience. 4. The cases with definite narrowing of arteriole revealed smaller A/V ratio than 0.70.

Adult↗