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Biomedical subjects

H Katoh

Publications and source records attributed to H Katoh.

At least 433 records · Page 24Linked to original sources

[A case of prostate cancer with multiple pulmonary metastases].

A 65-year-old man was hospitalized with bloody sputum. His chest X-ray showed multiple nodules in both lung fields. Transbronchial lung biopsy demonstrated a poorly differentiated adenocarcinoma, which suggested that respiratory abnormalities might be metastatic cancer. Because he had noticed pollakisuria and dysuria, urologic consultation was sought. The findings of digital examination, urethrography, and ultrasonotomography suggested that he had an advanced prostate cancer. In addition, tumor markers of prostatic acid phosphatase (PAP), acid phosphatase (ACP), and prostate antigen (PA) showed abnormal titers; 120 ng/dl, 166 IU/l, and 15.4 ng/ml, respectively. The prostate tissue obtained by transperineal biopsy revealed histopathologically adenocarcinoma and positive findings in immunohistochemical staining for PAP and PA as well as the specimens from the lung. Bilateral orchiectomy and medication of 250 mg of DESD daily as an antiandrogen therapy improved respiratory symptoms. One week after the operation, the multiple shadows on the chest X-ray diminished dramatically. Moreover, serum values of PAP and PA also decreased to the normal range. He is alive in a stable condition 6 months after the operation.

Adenocarcinoma↗

Kinetic studies on turtle pancreatic ribonuclease: a comparative study of the base specificities of the B2 and P0 sites of bovine pancreatic ribonuclease A and turtle pancreatic ribonuclease.

Kinetic constants for the transesterification of eight dinucleoside phosphates CpX and UpX by bovine and turtle pancreatic ribonuclease were determined. Both ribonucleases have a preference for purine nucleotides at the position X. However, bovine ribonuclease, like other mammalian ribonucleases, prefers 6-amino bases at this site, while turtle ribonuclease prefers 6-keto bases. This difference in specificity at the B2 site may be explained by the substitution of glutamic acid at position 111 by valine in turtle ribonuclease. These results have been confirmed by inhibition studies with the four nucleoside triphosphates. Inhibition studies with pT and pTp showed that a cationic binding group (P0) for the 5'-phosphate of the pyrimidine nucleotides bound at the primary B1 site is present in turtle ribonuclease, although lysine at position 66 in bovine ribonuclease is absent in turtle ribonuclease. However, the side chain of lysine 122 in turtle ribonuclease is probably located in the correct position to take over the role as cationic P0 site.

Animals↗

Changes in conformation of spin-labeled calmodulin by phospholipids.

Spin-labeled calmodulin was synthesized and the effects of phospholipids on its conformation were examined by ESR spectroscopy. Phosphatidylserine (0.1-1.0 mM) increased the signal intensity of the ESR spectrum of spin-labeled calmodulin and decreased the apparent rotational correlation time in the presence of 0.1 mM CaCl2. This change was reversed by addition of excess calcium, and in the absence of calcium phosphatidylserine did not change the spectrum, suggesting that the change in spin-labeled calmodulin brought about by phosphatidylserine was not induced by a hydrophobic interaction of the two, but by inhibition of the binding of calcium to calmodulin. L-Serine and O-phospho-L-serine had no effect on the ESR signals of spin-labeled calmodulin. The effects of various other phospholipids were also examined. Their inhibitory activities were in the order phosphatidic acid greater than phosphatidylserine greater than phosphatidylglycerol = phosphatidylinositol; phosphatidylethanolamine and phosphatidylcholine had no effect on the spectra. The effects of these phospholipids were dependent on their binding activities toward calcium. Furthermore, phosphatidic acid and phosphatidylserine at 1 mM reduced the activity of calmodulin-dependent phosphodiesterase by 16.4 and 8.7%, respectively. These findings indicate that spin-labeled calmodulin did not interact with the phospholipids by a hydrophobic interaction, but that calcium binding to spin-labeled calmodulin interfered with phosphatidic acid, phosphatidylserine, phosphatidylglycerol and phosphatidylinositol, and some of these phospholipids inactivated calmodulin. Thus the activity of calmodulin may be regulated in part by some phospholipids.

Binding Sites↗

Chondroblastoma of temporal bone.

The case of a 55-year-old female with chondroblastoma arising from the left temporal bone is presented. Although 10 cases of temporal chondroblastoma have been reported, this is the first in which plain radiography, pluridirectional tomography, computed tomography (CT) and angiography were performed. We discuss the clinical and radiological aspects of this rare tumor.

Cerebral Angiography↗

Protection of liver cells from experimentally induced liver cell injuries by tritoqualine.

Liver cell damages were inducible, when isolated liver cells coated with specific antibody against the liver cell membrane were cultured with peripheral blood mononuclear cells. Although this antibody-dependent cell-mediated cytotoxicity (ADCC) was induced by the closed contact of effector cells to targets via the specific antibody, a cytotoxic factor or factors causing the inhibition of protein synthesis in the liver cells was detected in the culture supernatant of the ADCC reaction. Similarly, peritoneal exudate macrophages activated by endotoxin lipopolysaccharide also exerted cytotoxic effects on the isolated liver cells by producing a cytotoxic substance or substances. These liver cell injuries induced by either the ADCC or activated macrophage culture supernatant were significantly reduced, when the isolated liver cells were pretreated with tritoqualine before adding the cytotoxic culture supernatants. These results suggest that tritoqualine may protect liver cells from immunological injuries.

Animals↗

A new variant of the Es-1 locus in the rat.

A new prealbumin plasma esterase was demonstrated by the use of miniaturized polyacrylamide slab gel electrophoresis. Genetic analysis indicated that the new variant is controlled by the Es-1 locus and this gene was designated Es-1c. Among 11 rat strains only one strain, WJ, possessed the gene. Two random-bred stocks, Jcl:Wistar and Jcl:SD, also maintained it in their populations. Miniaturized polyacrylamide slab gel electrophoresis showed that the ES-1 band consisted of two close bands with the cathodal one staining darker.

Animals↗

Liver transplantation in dogs after 30 minutes of warm ischemia.

In order to investigate the applicability of liver transplantation after warm ischemia, a partial auxiliary auto-transplantation of the liver after 30 min of warm ischemia was carried out in 9 mongrel dogs. Among them, 6 dogs survived longer than 7 days. Liver functions, blood coagulability and histological changes were investigated before and after the transplantation. Serum GOT, LDH, and GPT levels were elevated immediately after transplantation, and returned to normal within a few days. Hemostatic tests also showed significant abnormalities after transplantation. Although PT and thrombotest became normal within a week, PTT and antithrombin III remained slightly abnormal for longer periods. Microscopically, vacuolization and degeneration of hepatocytes were observed after transplantation but they recovered completely within 4 weeks. Based on these results, it could be said that the livers subjected to warm ischemia for 30 min ischemia were still acceptable for auxiliary transplantation.

Animals↗

Maternal contamination of some NZB sublines and genetic profiles of NZ-strains.

Six sublines of NZB mice bred in Japan were collected and their mitochondrial DNA (mtDNA) was examined by restriction analysis. The phenotypes of at least three of these sublines (NZB/Nrs, NZB/Nga and NZB/KlJms) differed from a standard one (NZB/BlWehi). Since mtDNA is inherited maternally, all sublines of a single inbred strain should share the same mtDNA phenotype. Therefore, b-type of mtDNA should be observed in all NZB sublines. Nevertheless, the above-mentioned sublines showed d-type mtDNA. These results suggested a genetic contamination of these sublines. This was confirmed by the finding that six aberrant alleles were detected also in their nuclear genomes using biochemical markers. For elucidation of the cause of contamination, we characterized the genetic profiles of four standard NZ-strains, NZB/BlWehi NZO/BlWehi, NZC/BlWehi and NZX/BlWehi, and of common inbred strains with black coat color, C57BL/6J, C57BL/10Sn, C57BL/Ks, C58/J and AU/SsJ. We found that five of the six aberrant alleles most strongly corresponded with those of C57BL/Ks. These results suggest that this contamination was ascribable to cross of NZB mice with a certain C56BL strain. We also deduced that NAB/BlPt and NZB/Füll also probably were contaminated strains, suggesting that this contamination was not restricted to Japan.

Alleles↗

Effect of vitamin E on toxicity and antitumor activity of adriamycin in mice.

The use of vitamin E as a protective agent against adriamycin-induced toxicity in CDF1 and BDF1 mice resulted in potentiation of the chemotherapeutic index of adriamycin. A single dose of 15 mg of adriamycin per kg body weight produced a significantly reduced mean survival time. A dosage of adriamycin of 15 mg per kg body weight was employed in the following experiments. In P388 ascites tumor-bearing mice, four consecutive injections of several doses of vitamin E before injection of adriamycin produced a significant prolongation of the mean survival. In concomitant studies of serum tocopherol content, 7 to 10 micrograms/ml appeared to be an appropriate serum concentration, in accordance with the result of our previous report on its immunopotentiation effect. alpha-tocopherol seemed to have a two- to three-fold greater physiological activity than alpha-tocopheryl acetate. Dietary vitamin E treatments offered no protection against adriamycin toxicity, because the serum tocopherol content reached only 4.39 micrograms/ml in mice given the vitamin E-sufficient feed in this study. The results suggested that an increase of the serum tocopherol level to about two to three times the untreated control would be required before the adriamycin treatment to reduce its toxicity.

Animals↗

Actin-binding peptide obtained by the cyanogen bromide cleavage of the 20-kDa fragment of myosin subfragment-1.

The 20-kDa fragment of myosin subfragment-1 heavy chain was cleaved with cyanogen bromide. Gel electrophoresis of the fragmented peptides indicated the presence of 20-, 18-, 16-, 14-, 12-, and 10-kDa peptides in addition to two peptides smaller than 10 kDa. The renaturation procedure of Muhlrad and Morales (Muhlrad, A., and Morales, M. (1984) Proc. Natl. Acad. Sci. U. S. A. 81, 1003-1007) was applied to the mixture of these peptides. The peptides larger than 10 kDa, which contain both the reactive SH1 and SH2 groups, were precipitated with F-actin by ultracentrifugation. The 10-kDa peptide was purified and was identified as p10 of Elzinga and Collins (Elzinga, M., and Collins, J. H. (1977) Proc. Natl. Acad. Sci. U. S. A. 74, 4281-4284). The renaturation procedure was applied to the purified 10-kDa peptide. The 10-kDa peptide was also precipitated with F-actin by ultracentrifugation. Affinity of the 10-kDa peptide for F-actin was determined with an increase of turbidity, and the apparent dissociation constant was 0.94 microM. Results are consistent with our proposition that a binding site for F-actin exists around the SH1 and SH2 groups of subfragment-1 (Katoh, T., Imae, S., and Morita, F. (1984) J. Biochem. 95, 447-454; Katoh, T., and Morita, F. (1984) J. Biochem. 96, 1223-1230).

Actins↗

Effects of long-term administration of clofibric acid on peroxisomal beta-oxidation, fatty acid-binding protein and cytosolic long-chain acyl-CoA hydrolases in rat liver.

Long-term effects of rho-chlorophenoxyisobutyric acid (clofibric acid) on inductions of peroxisomal beta-oxidation, fatty acid-binding protein and cytosolic acyl-CoA hydrolases in rat liver were studied. Male rats were fed clofibric acid at a dietary concentration of 0.25% for 22 weeks. The induction of peroxisomal beta-oxidation activity lasted throughout the long-term treatment of rats, the activity being a half that of rats treated with clofibric acid for 2 weeks. cytosolic long-chain acyl-CoA hydrolase I and II were both induced by the long-term and the short-term treatment of age-matched rats with clofibric acid, although the ability to induce hydrolase I decreased greatly by aging of rats. There was little difference in the inducing effect on fatty acid-binding protein between the long-term treatment and the short-term treatment. These results suggest that the inductions of peroxisomal beta-oxidation, fatty acid-binding protein and two cytosolic long-chain acyl-CoA hydrolases are essential responses of rats to clofibric acid (but not the brief events which occur in only the first stage of the continuous treatment with clofibric acid).

Animals↗

Protection of liver cells from experimentally induced liver cell injury by glycyrrhizin.

Liver cell damage is induced when isolated liver cells coated with specific antibody against the liver cell membrane are cultured with peripheral blood mononuclear cells. Although this antibody-dependent cell-mediated cytotoxicity (ADCC) was induced by closed contact of effector cells with targets via specific antibody, a cytotoxic factor or factors causing inhibition of protein synthesis in liver cells was detected in the culture supernatant of the ADCC reaction. Similarly, peritoneal exudate macrophages activated by endotoxin lipopolysaccharide (LPS) also had cytotoxic effects on isolated liver cells by producing a cytotoxic substance or substances. These liver cell injuries caused by either ADCC or activated macrophage culture supernatants were significantly reduced by pretreatment of the isolated liver cells with glycyrrhizin before the addition of the cytotoxic culture supernatants. These results suggest that glycyrrhizin may protect liver cells from immunological injuries.

Animals↗

Effect of clofibric acid and tiadenol on peroxisomal beta-oxidation and fatty acid binding protein in intestinal mucosa of rats.

Rats were fed a diet containing clofibric acid or tiadenol. The treatment of rats with clofibric acid caused an increase in the activity of cyanide-insensitive palmitoyl-CoA oxidation and in the concentration of a polypeptide with a molecular weight of about 80,000 in the light mitochondrial fraction in intestinal mucosa. Treatment of rats with tiadenol increased the activity of cyanide-insensitive palmitoyl-CoA oxidation more markedly than with clofibric acid. The induced activity in intestinal mucosa was about 1/10th that in liver. Treatment of rats with either of the two peroxisome proliferators increased both [1-14C]oleic acid binding capacity and the concentration of FABP in intestinal mucosa of rats. The treatment of rats with clofibric acid did not seem to alter the properties of FABP found in intestinal mucosa.

Administration, Oral↗