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Biomedical subjects

M Katori

Publications and source records attributed to M Katori.

At least 181 records · Page 10Linked to original sources
PubMed1979

Enzyme immunoassay of bradykinin.

An enzyme immunoassay of bradykinin was developed by using beta-D-galactosidase as a labeling enzyme. Bradykinin was conjugated to beta-D-galactosidase with a new coupling agent of a hetero bis-functional type, N-(m-maleimidobenzoyloxy)-succinimide (MBS). Antisera were obtained from rabbits immunized with bradykinin linked to albumins (ovalbumin or bovine serum albumin) with toluene-2,4-diisocyanate. Double antibody method was employed to separate the antibody-bound antigen from free. The enzyme activity in the precipitate was measured with a fluorogenic substrate, 4-methyl-umbelliferyl-beta-D-galactoside. This assay is based on heterogeneous competitive binding between unlabeled and labeled antigens, so that unlabeled bradykinin reduces binding of bradykinin-enzyme conjugates to the antibody. A standard inhibition curve was linear between 3 and 300 ng bradykinin/assay tube.

Bradykinin↗
PubMed1979

Non-specific antagonism against thromboxane A2 of 7-ethoxycarbonyl-6,8-dimethyl-4-hydroxymethyl-1(2H)-phthalazinone (EG-626) in contraction of isolated smooth muscles.

7-Ethoxycarbonyl-6,8-dimethyl-4-hydroxymethyl-1(2H)-phthalazinone (EG-626) was reported as an antagonist of thromboxane (Tx) A2 in the contraction of rabbit aorta. It was, however, observed that EG-626 did inhibit the contraction of superfused rabbit aorta, but also did inhibit that of rabbit coeliac artery, rat stomach strip and rat colon induced by TxA2, PG endoperoxides, angiotensin II and PGF2 alpha in non-specific manner. EG-626 had no effect on the biosynthesis of PG endoperoxides as well as TxA2. These results indicate that EG-626 is not a TxA2 antagonist, but has a general inhibitory effect on the smooth muscles. This inhibitory effect of EG-626 may be explained by the inhibition of phosphodiesterase.

Angiotensin II↗
PubMed1979

The significant reduction of high molecular weight-kininogen in synovial fluid of patients with active rheumatoid arthritis.

It has been proposed that kinin system was implicated in inflammatory joint diseases such as rheumatoid arthritis. Our present work provides further support on the involvement of the kinin system. In osteoarthritis patients, the total, high molecular weight (HMW)-, and low molecular weight (LMW)-kininogen levels in synovial fluid were not different from those in plasma. On the contrary, in rheumatoid patients, HMW-kininogen level in synovial fluid was significantly lower than that in plasma, whereas LMW-kininogen level in synovial fluid was not different from that in plasma. The reduction of HMW-kininogen level in synovial fluid was much more marked in active cases of those who showed high blood sedimentation rate and high C-reactive protein value. Furthermore, the reduction was closely related to the clinical severity. In active rheumatoid patients, HMW-kininogen level was further reduced in the synovial fluid after withdrawal of indomethacin.

Adult↗
PubMed1979

Fujiwara trait: the first case of kininogen deficiency in Japan.

Asymptomatic identical twins were found to show the prolonged activated partial thromboplastin time, which was corrected by addition of normal, Hageman factor deficient or Fletcher trait plasma but not corrected by Fitzgerald or Williams plasma. The prolonged activated partial thromboplastin time was also corrected by addition of highly purified bovine high molecular weight kininogen but not by low molecular weight kininogen. When total kininogen was measured as the amount of bradykinin released by trypsin on acid treated plasma, only trace amount was detected in Fujiwara and Williams plasmas, although Fitzgerald plasma showed approximately 50% of the total kininogen of normal plasma level. Acetone-kaolin activated amidase activity of plasma kallikrein was not generated by Fujiwara plasma. Substitution with normal plasma in various ratios showed plasma kallikrein activity proportionally to the normal plasma contents. Extrapolation with the values at 120 min after activation gave the prekallikrein content of Fujiwara plasma as 30% of the normal value.

Diseases in Twins↗