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Biomedical subjects

K Kohda

Publications and source records attributed to K Kohda.

At least 109 records · Page 6Linked to original sources
PubMed1990

Digoxin-like immunoreactivity in Chinese medicine.

Immunoreactive digoxin-like activity was observed in Chinese medicine, KYUSHIN tablet, taken popularly in Japan without prescription. The antibodies used in the assays of digoxin reacted with Chan-su, the major effective component of KYUSHIN, which contained cardiotonic steroids with similar chemical structure as digoxin. One tablet of KYUSHIN had digoxin-like immunoreactivity equivalent to 1.9, 1.5, and 72 micrograms of digoxin measured by three different commercial kits. These different equivalences may be attributed to differences in cross-reactivity of the antibody used in the immunoassays. Two healthy volunteers took two KYUSHIN tablets three times a day, a typical dose, and digoxin-like immunoreactivity reached almost 0.4 micrograms/L in 0.5 day. Therapeutic drug monitoring should be interpreted carefully in patients taking Chinese medicines, many of which contain the Chan-su component.

Cross Reactions↗
PubMed1990

Singlet oxygen takes part in 8-hydroxydeoxyguanosine formation in deoxyribonucleic acid treated with the horseradish peroxidase-H2O2 system.

Treatment of calf thymus deoxyribonucleic acid (DNA) with the horseradish peroxidase-H2O2 system resulted in efficient formation of 8-hydroxydeoxyguanosine (8-OH-dG) residues. It was concluded that singlet oxygen was the reactive species involved, based on experiments using active oxygen scavengers and D2O. For 8-OH-dG formation, a higher-ordered polynucleotide structure seems to be required: double stranded DNA was a better substrate for the reactive species than single stranded DNA, and monomeric deoxyguanosine underwent C8-hydroxylation to a lesser extent.

8-Hydroxy-2'-Deoxyguanosine↗
PubMed1989

Danazol stimulates the release of follicle-stimulating hormone and inhibits the release of prolactin in vitro studies on rat pituitary cell cultures.

The actions of danazol on the release of gonadotropins and prolactin (PRL) were investigated by using a culture of rat anterior pituitary gland cells. The addition of danazol in the range between 10(-9) M and 10(-5) M elevated the levels of follicle-stimulating hormone (FSH) in a dose-dependent manner. Danazol at 10(-5) M caused a 70% increase in FSH levels over the control. The intracellular contents of FSH was also increased by danazol, suggesting its stimulatory effect on both the synthesis and release of FSH. Danazol had no effect on the release of luteinizing hormone (LH). Danazol diminished the sensitivity of gonadotrophs to luteinizing hormone-releasing hormone (LHRH) in that the LHRH-induced release of both FSH and LH was suppressed. The amount of PRL released into medium was decreased by danazol in a dose-dependent way.

Animals↗
PubMed1989

Deoxyribonucleic acid (DNA) damage induced by bleomycin-Fe(II) in vitro: formation of 8-hydroxyguanine residues in DNA.

Treatment of calf thymus deoxyribonucleic acid (DNA) with bleomycin-Fe(II) at 0 degree C for 5 min resulted in the formation of 8-hydroxyguanine (8-OH-Gua) residues in DNA in a dose dependent manner, in addition to the formation of base propenal, a DNA-degradation product. The amount of 8-OH-Gua was about one-hundredth of that of base propenal. Treatment of cellular DNA with bleomycin did not result in any increase of 8-OH-Gua even under conditions of 100% cell killing.

Bleomycin↗
PubMed1989

Enhanced cytotoxicity in simultaneous and sequential drug-heat treatments of cultured Chinese hamster V79 cells.

Under hyperthermal conditions, some genotoxic drugs such as bleomycin, paraquat, and N-alkyl-N-nitrosoureas exhibit increased cytotoxicity toward cultured Chinese hamster V79 cells. Sequential combinations of heat and drug treatments, regardless of whether drug-exposure precedes or follows hyperthermia, also induce synergistic cytotoxicity to some extent. This may be attributed not only to the relationship of temperature and chemical injury as defined by the Arrhenius law, but also to a lethal interaction between the biological consequences of chemical injury and thermal damage. Ethanol, dimethylsulfoxide (DMSO), ethylenediaminetetraacetic acid (EDTA), and urea, which are known to affect cell membrane and protein, also exert synergistic cytotoxicity at 43 degrees C at a dose range that is nontoxic at 37 degrees C. When used sequentially with thermal treatment, they also proved to be synergistic. Glycerol, however, protected cells against thermal damage when used in a simultaneous chemical-thermal combination. But when treatments were carried out sequentially, glycerol proved destructive.

Animals↗
PubMed1989

[A case of chronic myelogenous leukemia complicated with nephrotic syndrome].

An 81-year-old woman was admitted, complained general malaise, and edema on face and lower extremities. In the peripheral blood, leucocytosis (17,220/mm3), microcytic hypochromic anemia (RBC 348 x 10(4)/mm3, Hb 9.6 g/dl, Ht 29.2%), and thrombocytosis (130 x 10(4)/mm3) were present, and many myeloid cells containing of myeloblasts, promyelocytes and so on were observed. Bone marrow aspiration revealed increment of the myeloid series without hiatus leukemia . The Neutrophil Alkaline Phosphatase score and rate was low, and on bone marrow scintigram using indium chloride, liver and extremities were shown. On admission, proteinuria (21.5 g/dl) and hypoalbuminemia (2.5 g/day) were pointed out, and the renal biopsy specimen showed membraneous proliferative glomerulonephritis (MPGN), so we diagnosed this case that chronic myelogenous leukemia (CML) complicated with nephrotic syndrome. At first, she was treated with prednisolone, but proteinuria was not entirely improved, then busulfan was given, myeloid cells in peripheral blood were disappeared and proteinuria was gradually decreased. From this coarse, the causality between CML and nephrotic syndrome was verified.

Aged↗
PubMed1988

Structural studies of O6-methyldeoxyguanosine and related compounds: a promutagenic DNA lesion by methylating carcinogens.

O6-Methylation of guanine residues in DNA can induce mutations by formation of base mispairing due to the deprotonation of N(1). The electronic, geometric and conformational properties of three N(9)-Substituted O6-methylguanine derivatives, O6-methyldeoxyguanosine (O6mdGuo), O6-methylguanosine (O6mGuo) and O6, 9-dimethylguanine (O6mdGua), were investigated by X-ray and/or NMR studies. O6mdGuo crystallizes in the monoclinic space group P2(1) with cell parameters a = 5.267(1), b = 19.109(2), c = 12.330(2) A, beta = 92.45(1) degrees, V = 1239.8(3) A3, z = 4 (two nucleosides per asymmetric unit), and O6mGua in the monoclinic space group P2(1)/n with cell parameters a = 10.729(2), b = 7.640(1) c = 10.216(1) A, beta = 92.17(2) degrees, V = 836.7(2) A3, z = 4. The geometry and conformation of O6-methylguanine moieties observed in both crystals and are very similar. Furthermore, the molecular dimensions of the O6methylguanine residue resemble more closely those of adenine than those of guanine. The methoxy group is coplanar with the purine ring, the methyl group being cis to N(1). The conformation of O6-methylguanine nucleosides is variable. The glycosidic conformation of O6mdGuo is anti for molecule (a) and high-anti for molecule (b) in the crystal, while that of O6mGuo is syn [Parthasarathy, R & Fridey, S. M. (1986) Carcinogenesis 7, 221-227]. The sugar ring pucker of O6mdGuo is C(2')-endo for molecule (a) and C(1')-exo for molecule (b). The C(4')-C(5') exocyclic bond conformation in O6mdGuo is gauche- for molecule (a) but trans for molecule (b), in contrast with gauche+ for O6mGuo. The hydrogen bonds exhibited by O6-methylguanine derivatives differ from those in guanine derivatives; the amino N(2) and ring N(3) and N(7) atoms of O6-methylguanine residues are involved in hydrogen bonding. 1H-NMR data for O6mdGuo and O6mdGuo reveal the predominance of a C(2')-endo type sugar puckering. In O6mdGuo, however, a contribution of a C(1')-exo sugar puckering is significant. The NOE data also indicate that O6mdGuo molecules exist with nearly equal population for anti (including high anti) and syn glycosidic conformations. These observations and their biological implications are discussed.

Alkylating Agents↗
PubMed1988

Structural requirement for the induction of the adaptive response in Escherichia coli among N-(substituted alkyl)-N-nitrosoureas.

Using E. coli CSH26 transformed with a plasmid carrying an alkA'-lacZ' fused gene, a series of N-(substituted alkyl)-N-nitrosoureas were subjected to a colorimetric assay to evaluate their capacity to induce the adaptive response, an inducible DNA-repair network in E. coli. Some of these derivatives induced the response in greater or lesser degrees, while others did not. Several structural requirements for the induction were disclosed. The capacity of these derivatives to induce the SOS response, which is another inducible DNA-repair network, was also evaluated using E. coli transformed with a plasmid carrying a umuC'-lacZ' fused gene. Since all the derivatives induced the SOS response, the structural requirements for the adaptive response disclosed in this study are substantially related to the molecular mechanism involved in the adaptive response.

Alkylating Agents↗
PubMed1988

Immunohistochemical identification of type I procollagen in tumour cells of scirrhous adenocarcinoma of the stomach.

Human gastric carcinomas were tested for their immunohistochemical reactivity with anti-type I procollagen antiserum. In all specimens of scirrhous carcinomas, staining of the tumour cells was strongly positive, while in medullary carcinomas staining of the tumour cells was generally poor. These results suggest that the tumour cells in scirrhous carcinomas produce collagen in their stroma.

Adenocarcinoma, Scirrhous↗
PubMed1988

Antitumor activity and neutrophil-selective hematopoietic toxicity of busulfan analogs in mice.

The antitumor activity and hematopoietic toxicity of two busulfan analogs were evaluated in comparison with those of busulfan. Although a program of five daily ip treatments with busulfan was not effective in treating sarcoma 180-bearing mice, a fluorine-containing busulfan analog, 1,4-butanediol di-2,2,2-trifluoroethanesulfonate (BFS), and a water-soluble analog, 1,4-butanediol diisethionate (BIT), were significantly effective when given on the same schedule. Busulfan did not appreciably prolong the life span of either P388- or Meth A-bearing mice, whereas BFS and BIT produced significant increases in the life span. It is worth noting that both the analogs were definitely less toxic to the host mice than busulfan. All the drugs examined exhibited suppressive effects on the counts of total WBCs, neutrophils, and lymphocytes. Relative toxicity toward neutrophils versus lymphocytes was increased significantly in the BFS and BIT treatments compared with busulfan treatment. It seems that the toxicity of busulfan in host mice might be due to unidentified side effects other than bone marrow suppression. These results suggest that BFS and BIT could be improved substitutes for busulfan.

Alkanesulfonates↗