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N Aoki

Publications and source records attributed to N Aoki.

At least 685 records · Page 38Linked to original sources
PubMed1979

PPD-induced blastogenesis is auto-regulated by suppressor cells generated in vitro.

Suppressor cell induction can be demonstrated during antigen specific blastogenesis by using the same methods which have shown induction of suppressor cells by Con A. Since suppressor cells are rapidly generated during antigen specific blastogenesis, they must regulate the final level of blastogenesis induced during the seven day in vitro incubation.

Concanavalin A↗
PubMed1979

Localization of urinary procoagulant in the human kidney.

By the indirect immunofluorescent and immunoenzymatic techniques with monospecific antiserum against urinary procoagulant (a tissue factor which accelerates blood coagulation), we found the urinary procoagulant in the kidney distributed to the loop of Henle and distal convoluted tubules. In these areas urinary procoagulant was found in association with the luminal and intercellular borders as well as in the cytoplasm of epithelial cells. Both the descending and ascending limbs of Henle were equally stained. The cytoplasmic staining was patchy in distribution among cells of distal tubules and was predominantly localized in the supranuclear areas. Glomeruli, the proximal tubular cells, the vascular wall, and the interstitium were not stained. There was, however, fluorescent staining along the epithelial layers of the Bowman's capsule, which was observed only in the frozen sections. Casts in the distal tubules were also positively stained. These findings suggest that urinary procoagulant is synthesized in the epithelial cells of these particular parts of nephron and is secreted into urine, although its physiologic roles and pathologic significance are not entirely known.

Blood Coagulation Factors↗
PubMed1979

Inhibitory spectrum of alpha 2-plasmin inhibitor.

alpha 2-Plasmin inhibitor (alpha 2PI) has been recently characterized as a fast-reacting inhibitor of plasmin in human plasma and appears to play an important role in the regulation of fibrinolysis in vivo. We have studied the effect of purified alpha 2PI upon various proteases participating in human blood coagulation and kinin generation. At physiological concentration (50 microgram/ml), alpha 2PI inhibited the clot-promoting and prekallikrein-activating activity of Hageman factor fragments, the amidolytic, kininogenase, and clot-promoting activities of plasma kallikrein, and the clot-promoting properties of activated plasma thromboplastin antecedent (PTA, Factor XIa) and thrombin. alpha 2PI had minimal inhibitory effect on surface-bound activated PTA and activated Stuart factor (Factor Xa). alpha 2PI did not inhibit the activity of activated Christmas factor (Factor IXa) or urinary kallikrein. Heparin (1.5-2.0 units/ml) did not enhance the inhibitory function of alpha 2PI. These results suggest that, like other plasma protease inhibitors, alpha 2PI possesses a broad in vitro spectrum of inhibitory properties.

Blood Coagulation Factors↗
PubMed1979

A test of significance for geographic clusters of disease.

The geographic pattern of disease has been visually studied by depicting the categorized mortality or morbidity rates on a map. Visual study, however, by no means indicates the statistical significance of observed clusters, i.e., whether or not the geographic aggregations could occur by chance alone. In this paper, an approach for assessing the deviation from chance expectation of the geographic pattern actually observed on the map is described. A simple chi-square test is proposed, and its validity is substantiated by a Monte Carlo approach, which is derived analytically as a special case of Knox's test for space--time clustering. The parameters required for the test are (1) total number of areas, (2) numbers of subareas for each mortality of morbidity category, (3) total number of geographically adjacent areas, and (4) observed numbers of adjacent areas having concordant category pairs.

Adult↗
PubMed1979

Congenital deficiency of alpha 2-plasmin inhibitor associated with severe hemorrhagic tendency.

alpha(2)-Plasmin inhibitor (alpha(2)PI) is a recently characterized, fast-reacting plasmin inhibitor in human plasma that appears to play an important role in regulation of in vivo fibrinolysis. We report here a case of complete deficiency of alpha(2)PI in man. The patient, a 25-yr-old Japanese man, had a life-long severe bleeding tendency (hemarthrosis and excessive bleeding after trauma). The following tests were within normal limits: platelet count, bleeding time, thrombin time, prothrombin time, partial thromboplastin time, titers of known clotting factors, platelet glass bead retention, Factor VIII-related antigen, platelet aggregation by ADP, collagen and ristocetin, and clot retraction. Routine liver function tests were also normal. The only abnormal finding was that whole blood clot lysis was extemely rapid and was complete in 4-8 h. The concentration of plasma protease inhibitors, including alpha(2)-macro-globulin, antithrombin III, alpha(1)-antitrypsin, and C1INH, were all normal. The concentration of alpha(2)-PI in the patient's plasma, assayed by immunological methods, was <0.1 mg/100 ml (normal concentration, 6.1+/-0.88 mg/100 ml [mean+/-SE]) and functional assays showed a complete deficiency of alpha(2)PI. Addition of purified alpha(2)PI to the patient's whole blood completely corrected the accelerated fibrinolysis. The patient's parents, four siblings, and four other members of this family were asymptomatic, but the titers of alpha(2)PI in their plasmas were congruent with50% of normal pooled plasma. There were three consanguineous marriages in this family, and the alpha(2)PI deficiency appears to have been inherited as an autosomal recessive trait. We speculate that alpha(2)PI deficiency in this patient has led to uninhibited in vivo fibrinolysis that probably causes the severe hemorrhagic tendency. Thus, this study indicates the important role of alpha(2)PI in hemostasis.

Adult↗
PubMed1979

Studies on suppressor cell function in thyroid diseases.

Suppressor cell function of peripheral mononuclear cells has been examined in patients with Graves' disease, Hashimoto's thyroiditis, and thyroid cancer, as well as in healthy subjects. Suppressor cell function was assessed through two methods: 1) measurement of enhanced blastogenesis after 24-h preculture and 2) concanavalin A-inducible suppressor activity. The results from the two tests were coincident and indicate that suppressor cell function was significantly decreased in the Graves' disease population but not changed in either the Hashimoto's thyroiditis or the thyroid cancer groups compared to healthy controls. The impairment of suppressor cell function in the Graves' disease population was still observed when patients became euthyroid by treatment with antithyroid drugs, although the treated patients had improved suppressor cell function compared to untreated patients (P = NS). Low activity of suppressor cell function in the Graves' disease population might be a constitutional character based on an inherited abnormality specific for the disease population.

Adolescent↗