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Biomedical subjects

K Iida

Publications and source records attributed to K Iida.

At least 397 records · Page 22Linked to original sources

[A case of 17 alpha-hydroxylase deficiency with male pseudohermaphroditism (author's transl)].

A 17-year-old youth was admitted because of proteinuria noted during a routine examination at his high school. His parents and three siblings were living in good health and there was no familial tendency to hypertension and no consanguinity. On physical examination, he was 161cm in height and weighed 43Kg, and his facial expression was female-like. Neither webbed neck nor cubitus valgus was noticed. Severe hypertension ranging from 190/120 to 230/130 was noted. No axillary or pubic hair was present, and the breasts were prepubertal in size. A gynecological examination revealed the presence of labia and vagina. Laboratory findings on admission were summarized as follows: The urine gave a (-)--(+) test for protein, renal function was revealed as normal, serum potassium ranged from 3.2 to 4.2mEq/L, the specimen of arterial blood showed pH 7.421, and an electrocardiogram revealed left ventricular hypertrophy and U wave changes in leads V2, V3, V4. X-rays showed a bone age of 12 years, and chromosome analysis revealed a karyo type of 46,XY. Endocrinological studies confirming the presence of a 17 alpha-hydroxylase deficiency were summarized as follows: 1) Plasma ACTH was markedly elevated. 2) Plasma renin activity was markedly suppressed showing no response to exercise. 3) Plasma progesteron, plasma DOC and plasma-corticosteron were extremely high. In contrast, plasma aldosteron was extremely low. 4) Plasma 17 alpha-OH progesteron and plasma cortisol were markedly reduced. Urinary excretion of 17-OHCS was extremely low. 5) Plasma testosteron and urinary 17-KS were markedly reduced. The patient was treated with 2mg then 1mg dexamethasone daily for half a year. After one month of therapy, the blood pressure was down to 160/100mmHg, and the serum potassium had risen from 3.2mEq/liter to 5.6mEq/liter. Plasma progesteron, plasma DOC, plasma corticosteron and plasma ACTH decreased to a normal level. Subsequently suppressed plasma renin activity elevated to a normal value. After 6 weeks of this treatment, a laparotomy was performed. Ovaries and uterus were absent, but bilateral testes were found at the external inguinal ring. Microscopic examination of the testis showed Sertoli cell adenoma. We have reported here a case of 17 alpha-hydroxylase deficiency with male pseudohermaphoriditism and discussed the endocrinological data and histological findings of the testis.

Adolescent↗

Inhibition of cell division of Escherichia coli by a new synthetic penicillin, piperacillin.

The mechanism of the action of piperacillin against Escherichia coli was investigated. This drug converted cells to filaments, but did not show lytic action in a range of concentrations below 25 mug/ml. In some of the filaments, stretched constrictions with various diameters were observed. Addition of piperacillin to a synchronous culture inhibited cell division immediately at any stage of the cell cycle. The results of morphological examination of synchronous cultures show that the percentage of filaments with a stretched constriction corresponds to that of normally septated cells before addition of the drug. Furthermore, peptidoglycan synthesis and cross-linking were not inhibited by this drug. It is likely that this drug inhibits only septum formation, but not the growth of wall, and that stretched constrictions are a result of longitudinal growth of septation caused by the drug. Examination of affinity of the drug to penicillin-binding proteins shows that protein 3 is the most sensitive, proteins 2 and 7 are moderately so, and protein 1 is sensitive only to high concentrations of the drug.

Bacterial Proteins↗

Reaction mechanisms of beta1H globulin.

The reaction mechanisms of beta1H were studied. The generation of alternative pathway C3 and C5 convertases on the cell surface as well as in the fluid phase was inhibited by beta1H globulin. The cell preparation bearing the C3b site could bind beta1H with little effect on the C3b hemolytic activity. Bound beta1H was dissociated by the action of C3bINA and C3bINA-treated C3b bearing cell did not bind beta1H anymore. Cell-bound beta1H was also dissociated by the action of B (or Bb). From these and other results, the following conclusions were obtained. The C3b site-bearing cell could bind beta1H on the C3c region of C3b molecules facilitating the C3bINA action on C3b, and beta1H shared the same binding site with B (or Bb) inhibiting the generation of the alternative pathway convertases competitively.

Beta-Globulins↗

Interaction of S-sulfonated human IgG with human complement and its components.

S-sulfonated human IgG (S-sIgG) was prepared by treating IgG with sodium sulfite and sodium tetrathionate. The treatment resulted in the selective cleavage of interchain disulfide bonds of the IgG to give S-sulfonate groups. Complement fixing activities of aggregated S-sIgG and the immune complex formed with the S-sIgG antibody were very weak. S-sIgG at a high dose reduced the activity of the first complement component (C1) in normal human serum without any reduction of other complement components activites, but S-alkylated IgG at the same dose did not. Loss of C1 activity was not caused by either S-sulfonated myeloma proteins (IgA and IgE) or urea-treated S-sIgG, in which both inter- and intra-chain disulfide bonds were cleaved. These results suggest that the selective reduction of C1 by S-sIgG is due to a conformational change of the immunoglobulin.

Complement Fixation Tests↗

Effect of dihydroxymethyl furatrizine on cell division of Escherichia coli.

Antibacterial activities of 3-di(hydroxymethyl) amino-6[2-(5-nitro-2-furyl)vinyl]-1,2,4-triazine, (dihydroxymethyl furatrizine) were investigated using mutant strains of Escherichia coli lacking repair systems for DNA damage, i.e. polA, uvrA, uvrA, uvrC, recA, recB, recC and uvrArecA. All of the mutant strains were more sensitive to the drug than the parent sgrains, as was the case with the sensitivity to UV-irradiation. These results indicate that the drug acts lethally on sensitive bacteria by damaging their DNA, and parts of the damaged DNA are repaired by excision and recombinational repair systems. Filamentous cell formation was induced in all strains except the uvrArecA strain by sublethal concentration of the drug, as well as by UV-irradiation. It is possible that the occurrence of the short period of "unbalanced growth" induced by such DNA damaging agents leads to filament formation. In the cells of the double mutant, filament formation was induced by the drug but not by UV-irradiation, and the majority of the filamentous cells formed were multinucleated. This suggests that, in this double mutant, the drug directly reacts with the septation mechinery of the cell envelope, resulting in filament formation. This hypothesis is supported by the electron microscopic observations that septation is interrupted in the filamentous cells induced by the drug.

Anti-Bacterial Agents↗

The cold activation of the classical complement pathway: The cause of the differences between plasma and serum complement in liver cirrhosis.

The mechanism responsible for making the differences between plasma and serum complement (CH50) was studied on eight patients with hepatitis-B(s) antigen negative alcoholic liver cirrhosis. CH50 and C4 activities of the sera of all patients were equal to those of the corresponding EDTA-plasma, when sera wre separated after clotting the blood at 37 degrees C. CH50 and C4 activities of the sera, prepared at 21 degrees C or 4 degrees C, from four of eight patients were very low. When serum from one of these four patients was added to normal human serum, C4 activity of the serum mixture markedly decreased at 4 degrees C but not at 37 degrees C. The inactivation of C4 was prevented by adding EDTA or heparin to the serum mixture. These results indicated that very low complement in the sera, prepared at 21 degrees C or 4 degrees C, of the four cases were due to the cold activation of the classical complement pathway.

Cold Temperature↗