Biomedical subjects

M Kodaka

Publications and source records attributed to M Kodaka.

28 records · Page 2Linked to original sources

PubMed1998

Enhancement of type IV collagenases by highly metastatic variants of HT1080 fibrosarcoma cells established by a transendothelial invasion system in vitro.

A novel in vitro invasion assay system was established in this laboratory, in which the invasion of tumor cells after interaction with endothelial cells could be examined. Two variant cell lines (FP-10, FP-21) were established from parental HT1080 cells using this assay system. FP-10 and FP-21 cells had higher invasive and metastatic potential than the parental cells both in vitro and in vivo. The activity of anchorage-independent proliferation and the adhesion to the HUVEC monolayer of FP-10 and FP-21 was greater than the parental cells. The secretion of type IV collagenase (both MMP-2 and MMP-9) was also increased more significantly by the variant cells than by the parental cells, and the expression of uPA mRNA was higher in FP-10 and FP-21. Treatment of variant cells with human TIMP-2 remarkably suppressed the increment of the in vitro invasion to the same level as parental cells. These results suggest that this in vitro transendothelial invasion system accelerates multiple mechanisms of the metastasis by HT1080, especially the production of type IV collagenases. It can thus provide a useful model of tumor metastasis.

Animals↗

PubMed1997

Cytotoxicity of platinum (II) dinuclear complexes with 1-alkylthymine ligands against mouse sarcoma 180 cells.

We synthesized five platinum (II) dinuclear complexes containing 1-alkylated thymines. Two of the 1-alkylated thymine, 1-MeThy and 1-EtThy, complexes afforded good crystals. The X-ray structures of these complexes were determined. The 1-MeThy complexes has a head-to-head (H-H) arrangement, while the 1-EtThy complex has a head-to-tail (H-T) arrangement. The 1-MeThy complex (H-H) shows high electrophilicity against chloride anion (CI-) and high cytotoxicity against mouse sarcoma 180 (S-180) cells in vitro. The 1-EtThy complex (H-T) is inactive. The other 1-MeThy complex does not produce CDDP in the reaction with chloride ion and is inactive against the S-180 cell line. This complex is assumed to have an H-T arrangement. Similarly, two different 1-Pr(n)Thy complexes, one with high electrophilicity and cytotoxicity and the other without, must have an H-H and H-T arrangement, respectively. For comparison, we investigated six complexes, 1-methyluracil (1-MeUra) (H-H) dimer, alpha-pyridone (H-T) dimer, alpha-pyridone blue tetramer (PPB), 1-methylcytosine (1-MeCyt) (H-T) dimer, acetate dimer, and 1-MeUra monomer complexes. The alpha-pyridone (H-T), PPB, 1-MeCyt (H-T) dimer, and 1-MeUra monomer complexes are inert to chloride ion and inactive against mouse sarcoma S-180. The 1-MeUra (H-H) dimer and acetate dimer complexes show high electrophilicity and high cytotoxicity. Cellular accumulation of the platinum complexes phenomenally shows that all are incorporated to cancer cells to a lesser extent than CDDP. The relationships between the accumulation, the electrophilicity, and the interaction of these complexes with proteins are discussed.

Alkylation↗

PubMed1997

[The effects of premedication on induction doses of propofol and hemodynamic responses during induction].

We chose five sedatives for premedication and investigated the effect of these drugs on the induction doses of propofol. One hundred patients were allocated into one of five groups of 20. These groups consisted of control group (C) given only atropine 0.5 mg i.m.; CL group (plus clonidine 0.15 mg orally); H group (plus hydroxyzine 25 mg i.m.); M group (plus midazolam 3 mg i.m.) and D group (plus diazepam 10 mg orally). The induction dose was measured using loss of count technique. Arterial pressure and heart rate were measured, before and after propofol induction as well as after intubation. We also calculated rate pressure products (RPP) at each point. The induction doses were significantly lower in M-group than those in C-group. On the other hand, in hemodynamic responses, RPP was unchanged in any groups after propofol induction and after the intubation. Both propofol and midazolam have been known to have a depressive effect on the central nervous system via GABA-A receptor-mediated inhibition, although the exact receptor for propofol is unknown. We thought, therefore, that when the interaction occurred, both midazolam and propofol had the same effect on the GABA-A receptor and increased chloride ion flux through the channels. Hydroxyzine and clonidine, however, do not share a common receptor or exert effect on the GABA-A receptor. We consider that this was one of the reasons why induction doses of both H and CL group could not decrease significantly. We concluded that midazolam 3 mg decreased propofol induction dose significantly. Both midazolam 3 mg and clonidine 0.15 mg decreased RPP before induction and hemodynamic responses to induction and intubation were stable.

Adult↗

PubMed1992

[Effect of isoflurane, enflurane and halothane on hemodynamics during the induction of anesthesia].

The effects of isoflurane(I), halothane(H) and enflurane(E) on hemodynamics of 36 patients (12, 11 and 13, respectively) were studied during the inhalation of 1.5 MAC of each anesthetics before the surgery. Mean arterial pressure(MAP), heart rate(HR), cardiac index(CI), systemic vascular resistance index(SVRI), and stroke volume index (SVI) were measured noninvasively using the automatic blood pressure manometer and the ultrasonic Doppler method (Accucom). MAP decreased with I, E and H, but a larger decrement was observed with E than with H. CI and SVI with H were less than with E. SVRI decreased with I and E but a significant difference was observed between E and H. Each value with I was between those with H and E. These results indicate that isoflurane causes the depression of blood pressure mostly by its effect to decrease afterload during the induction of anesthesia, although its depressing effect is less than that of enflurane.

Adult↗

PubMed1992

[Anesthetic management of the patient with a permanent pacemaker].

Anesthetic management of two patients with a permanent pacemaker is reported; patient no. 1 had the VVI mode pacemaker and patient no. 2 had the DDD mode pacemaker. In patient no. 1, the hypotensive response of the 'pacemaker syndrome' occurred during general anesthesia. Patient no. 2 had no anesthetic problems but careful attention should be paid to the DDD mode pacemaker, because the newer widely used dual lead systems (DDD) are more susceptible to electromagnetic interference. Anesthetists often encounter patients with pacemakers. Knowledge of pacemakers available of the increasingly wide range is necessary to ensure safe management of these patients, many of whom are frail and elderly.

Aged↗

PubMed1983