Search PubMed⌕ Search

Biomedical subjects

K Sudo

Publications and source records attributed to K Sudo.

At least 217 records · Page 12Linked to original sources

[A case report of pulmonary arterio-venous fistula complicated with hereditary hemorrhagic telangiectasis].

A 5-year-old girl with multiple pulmonary arterio-venous fistulae was reported. Both her mother and grandmother have been diagnosed as the same disease previously. Her grandmother was treated with resection of the right basal segment for arterio-venous fistulae. Her mother is well with fistulae for more than 20 years. The patient was operated upon to enucleate two larger fistulae in segments 3 and 6 of right lung. Her postoperative course was uneventful. She was discharged from the hospital on the 22nd postoperative day. Pulmonary arteriovenous fistulae are thought to be a part of the hereditary hemorrhagic telangiectasis. Enucleation of the larger fistulae of the lung are preferable even for multiple lesions.

Arteriovenous Fistula↗

[Pacemaker implantation in 7 days or less old of early neonates].

We have implanted cardiac pacemaker (PM) in 3 early neonates ranging from 5 hours old to 7 days old of age with congenital complete or incomplete AV block. They were in advanced stage of rapidly developed cardiac failure with resistance to drug therapy and with ventricular tachycardia or fibrillation. Cardiac failure was improved immediately in the 3 cases after the operation and the effectiveness by the pacing was recognized for a long term observation (4 months to 2 years). There appeared PM implantation in-14 neonates, including our cases, in Japanese literatures. In review of the 14 neonates, we discussed the autoimmune disease, indication of the pacing, implantation site of the PM generator and prognosis. An immediate PM implantation after birth in neonate with cardiac failure complicated by congenital AV block is treatment of choice. The generator as well as the electrode design for neonates are still yet to be developed.

Age Factors↗

High-performance liquid chromatographic determination of a new nootropic, N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl)acetamide, in human serum and urine.

A high-performance liquid chromatographic method for the determination of a novel nootropic agent, N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl)acetamide (DM-9384, I), in human serum and urine has been developed. Compound I and the internal standard were extracted with chloroform from alkalinized serum and urine, and the organic layer was evaporated to dryness. The residue was chromatographed on a Nucleosil 7C18 reversed-phase column using 1/15 M potassium dihydrogen-phosphate-acetonitrile (7:3, v/v) as a mobile phase. Quantitation was achieved by monitoring the ultraviolet absorbance at 210 nm. The response was linear (0-2114.0 ng/ml) and the detection limits were 30 ng/ml for serum samples and 50 ng/ml for urine samples. The utility of the assay was demonstrated by determining compound I in serum and urine samples from three healthy male subjects receiving an oral dose of 30 mg of the drug. This method is satisfactorily sensitive and accurate, and is applicable for pharmacokinetic studies of I in humans.

Central Nervous System Agents↗

Lactate dehydrogenase M-subunit deficiency: a new type of hereditary exertional myopathy.

Three families with a complete deficiency of the lactate dehydrogenase M subunit show exertional myoglobinuria. The response to ischemic forearm work is characteristic in these three families: an increase of venous lactate concentration after ischemic work was not observed and a marked increase of venous pyruvate was found. Glycolysis was markedly retarded in the patient's muscle in the glyceraldehyde 3-phosphate dehydrogenase (GA3PD) step. A significant increases in glyceraldehyde 3-phosphate, dihydroxyacetone phosphate and fructose 1,6-diphosphate were observed. The glycolysis retardation may be attributed to the impaired reoxidation of NADH produced by GA3PD action. The cytosolic fraction of skeletal muscle is rich in alpha-glycerophosphate dehydrogenase. This enzyme reoxidizes the excess NADH and drains triose phosphates from the glycolytic pathway under anaerobic conditions. For this reason, ATP production was significantly impaired and muscle cells were damaged in these patients. Consequently, the cytosolic enzymes and proteins such as creatine kinase and myoglobin were released into the blood stream. Otherwise, patients with a lactate dehydrogenase M-subunit deficiency do not show muscle stiffness and myoglobinuria under ordinary circumstances. They complain of muscle rigidity and sudden myoglobinuria after strenous exercise under anaerobic conditions. Thus, the lactate dehydrogenase M-subunit deficiency does not show any symptoms under ordinary circumstances, but is a latent hereditary disorder, now recognized as a new type of hereditary exertional myoglobinuria.

Adolescent↗

Stabilizing basic fibroblast growth factor using protein engineering.

Using site directed mutagenesis, each of the four cysteines present at amino acid residues 26, 70, 88, and 93 of the mature protein of human basic fibroblast growth factor (bFGF) was individually changed to serine. The biological activity and heparin binding ability was retained when the serine was substituted for the cysteine residue at either 70 or 88 of the bFGF protein. This finding indicates that the cysteines at these positions are not essential for expressing biological activity. The substitution of the residues at these positions, especially at position 88, reduced the heterogeneity recognized as several peaks of bFGF eluted from a heparin affinity column, even after oxidation with hydrogen peroxide, suggesting that the cysteines at these positions are exposed to the surface of the molecule to form disulfide bonds that induce heterologous conformations. Furthermore, under acidic conditions, these modified bFGFs are revealed to be more stable in maintaining their activity. These facts suggest that this protein has been successfully modified by protein engineering.

Base Sequence↗

Study of the effect of an anti-androgen (oxendolone) on experimentally induced canine prostatic hyperplasia. I. Morphological analysis.

To investigate the effect of anti-androgens on BPH, Oxendolone (OXD), a pure anti-androgen, was tested in experimentally induced BPH in 17 beagle dogs, alone or in combination with medroxyprogesterone acetate (MPA) which displays both anti-androgenic and anti-estrogenic activity. The relatively early stage of canine BPH was induced by administration of 3 alpha-androstanediol (3 alpha-A) plus estradiol (E2) for 6 months and followed by testosterone propionate (TP) plus E2 for another 6 months during the anti-androgenic treatment. By the manipulation with T, a decrease in volume of glandular component associated with a relative increase in stromal tissue was achieved, which mimics human BPH histology. The prostate substituted with T and E2, however, gradually decreased in size. Therefore the effect of OXD or OXD + MPA was not significant against the untreated controls (T-E control). The weight of the prostate in these OXD +/- MPA groups was however significantly reduced as compared to that of BPH controls which received 3 alpha-A and E2 throughout the experimental period. On histological examination, atrophic changes were observed in the hormone-treated groups compared to the T-E control. The finding was the most striking in the OXD + MPA group with small non-involuted acini scattered in the abundant stomal tissue. This was almost identical to the appearances of castrated control groups. Atrophy may be due not only to the anti-androgenic but also to the anti-estrogenic property of MPA. A report on the hormonal background of this experiment will appear in the second article.

Androstane-3,17-diol↗

Study of the effect of an anti-androgen (oxendolone) on experimentally induced canine prostatic hyperplasia. II. Endocrinological analysis.

The results of hormonal investigation of effects of an antiandrogen, Oxendolone (OXD), alone or in combination with medroxyprogesterone acetate (MPA), on experimentally induced canine BPH are reported. Seventeen beagle dogs were divided into 5 groups: 2 castrate controls for Group 0, 3 BPH controls for Group 1 which received 3 alpha-androstanediol (3 alpha-A) and estradiol (E2) for one year, and 12 dogs consisting of 3 groups which received 3 alpha-A and E2 for 6 months followed by testosterone propionate (TP) and E2 for another 6 months. The last 3 groups were treated with either 200 mg/week of OXD (Group 3) or OXD + 30 mg/week of MPA (Group 4), and otherwise untreated with these hormones (Group 2, T-E controls). On the blood hormone analysis, both T and 5 alpha-dihydrotestosterone (DHT) were generally lowered in the T-E administered groups (Group 2, 3 and 4) compared to those in Group 1. While MPA significantly decreased these androgen levels, OXD did not influence at all. The concentrations of E2 were similar. Although T content in the prostate did not differ significantly within the experimental groups, DHT was the highest in Group 1 and the lowest in Group 4 and was nearly the same level to Group 0. MPA reduced tissue DHT content but OXD did not. In the receptor assay study, nuclear androgen receptor (AR) content in Group 3 and 4 was significantly lower than that in Group 1. No obvious decrease in nuclear AR content could be seen among the other groups.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

[Effects of TJ-41 (Tsumura Hochu-ekki-to) on spermatogenic disorders in mice under current treatment with adriamycin].

Experiments were performed to investigate the effects of TJ-41 on spermatogenic disorders under current treatment with adriamycin (ADR). Male ICR mice were intraperitoneally injected with ADR at the dose of 0.15 mg/kg, twice a week for 5 weeks. Simultaneously, these mice were orally administered TJ-41 at the dose of 1, 2 or 4 g/kg for 12 weeks. The effects of TJ-41 were evaluated by histological analysis of germ cells in the testis at 7 weeks after the last injection of ADR. TJ-41 at a dose of 4 g/kg significantly inhibited the decrease of testis weight in mice treated with ADR. TJ-41 at doses of 1 and 4 g/kg significantly decreased the proportion of seminiferous tubules without germ cells as compared with the ADR-treated group. On the other hand, TJ-41 at doses of 1 and 4 g/kg significantly increased the proportion of normal seminiferous tubules and the Sertoli cell ratio of spermatocytes as compared with the ADR-treated group. These results indicate that TJ-41 may qualitatively and quantitatively protect against the decrease of germ cells in the testis of mice treated with ADR.

Animals↗

[The inhibitory effects of chicken ovomacroglobulin on collagenolytic activity in Bacteroides gingivalis culture supernatant, human PMN and human gingival crevicular fluid].

We examined in vitro the inhibitory effects of ovomacroglobulin on collagenolytic activity in Bacteroides gingivalis (B. gingivalis) culture supernatant, in human peripheral blood polymorphonuclear leucocytes (PMN), and in gingival crevicular fluid (GCF) from periodontitis patients. Measurement of collagenolytic activity was conducted with a CollagenoKit CLN-100 using FITC-conjugated type I collagen. The FITC-conjugated collagen was reacted with the sample in solution, and the residue was selectively degenerated at 35 degrees C and removed with ethanol. The fluorescence of the removed residue was then measured. The collagenolytic activity from B. gingivalis displayed dose dependent inhibition as high as 81.4% following addition of ovomacroglobulin at 224 micrograms/ml. The collagenolytic activity from human peripheral blood PMN showed, as a result of addition of 1,600 micrograms/ml of ovomacroglobulin, inhibition as high as 62.4%. The collagenolytic activity from human GCF, which was obtained from patients with different degrees of periodontal disease, exhibited as high as 71.0% inhibition after addition of 1,600 micrograms/ml ovomacroglobulin. Ovomacroglobulin showed almost the same level of inhibition obtained from alpha 2-macroglobulin, which was measured as a positive control. It was also recognized by SDS-PAGE that collagenolytic activity was inhibited after preincubation with added ovomacroglobulin. This collagenolytic activity, which dissolved the collagen substrate, was derived from B. gingivalis and human GCF. The above results demonstrate that ovomacroglobulin inhibits collagenolytic activity from B. gingivalis, human PMN, and human GCF.

Animals↗