Death during surgery in Japan.
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Forensic Medicine↗
Biomedical subjects
Ken-ichi Yoshida
Publications and source records attributed to Ken-ichi Yoshida.
Production of gamma-hydroxybutyric acid in postmortem liver increases with time after death.
Gamma-hydroxybutyric (GHB) acid, which is becoming popular as a drug of abuse, was shown by means of gas chromatography-mass spectrometry (GC-MS) to increase in mouse liver with time after death. The amount detected was 0.8 +/- 1.0 microg/g at 3 h after death, 4.7 +/- 1.5 microg/g at 24 h, and 8.8 +/- 0.8 microg/g at 72 h. Furthermore, GHB was detected in samples from deceased persons, at concentrations of 2.6-12.0 microg/g in liver, 0.4-7.3 microg/ml in blood, and 0-2.6 microg/ml in urine, but was not detected in the blood and urine of living persons. Although 1,4-butanediol has been suggested to be a precursor of GHB produced after death, 1,4-butanediol was not detected in any of our samples. Additionally, succinate semialdehyde arising from gamma-aminobutyric acid (GABA) transamination to GHB was also barely detectable in any of our samples. This study supports previous reports that GHB is a product of postmortem decomposition. Production of GHB increases with time after death in postmortem liver; since we were unable to identify endogenous 1,4-butanediol and succinate semialdehyde in our samples, the pathway of GHB production after death remains unclear.
Animals↗
Phosphoinositide 3-kinase accelerates calpain-dependent proteolysis of fodrin during hypoxic cell death.
We have shown recently that phosphoinositide 3-kinase (PI 3-kinase) accelerates the hypoxia-induced necrotic cell death of H9c2, derived from rat cardiomyocytes, by enhancing metabolic acidosis. Here we show the downstream events of acidosis that cause hypoxic cell death. Hypoxia induces the proteolysis of fodrin, a substrate of calpain. Intracellular Ca(2+) chelation by BAPTA, and the addition of SJA6017, a specific peptide inhibitor of calpain, also reduces cell death and fodrin proteolysis, indicating that Ca(2+) influx and calpain activation might be involved in these events. The overexpression of wild type PI 3-kinase accelerates fodrin proteolysis, while dominant-negative PI 3-kinase reduces it. Both (N-ethyl-N-isopropyl)amiloride (EIPA), an inhibitor of the Na(+)/H(+) exchanger, and KB-R7943, an inhibitor of the Na(+)/Ca(2+) exchanger, reduce hypoxic cell death and fodrin proteolysis. The depletion of intracellular Ca(2+ )stores by thapsigargin, an inhibitor of endoplasmic reticulum Ca(2+)-ATPase, also reduces cell death and fodrin proteolysis, indicating that Ca(2+ )release from intracellular Ca(2+ )stores might be also involved. These results indicate that PI 3-kinase might accelerate hypoxic cell death by enhancing the calpain-dependent proteolysis of fodrin.
Acidosis↗
Screening of indigenous plants from Japan for modulating effects on transformation of the aryl hydrocarbon receptor.
The aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor with which halogenated and polycyclic aromatic hydrocarbons such as dioxins and benzo[a]pyrene interact as ligands. Since such compounds cause various toxicological effects, including cancer, through the transformation of AhR, it is important to determine influence of modulating factors. It has been reported that certain plant components such as flavonoids and indoles can affect AhR transformation. In this study, to obtain clues to novel ligands of AhR, 191 species of indigenous plants were collected in Japan, and their 50% methanolic extracts (total 368 plant parts) were tested for modulating effects on AhR transformation in a cell-free system using a rat hepatic cytosolic fraction. Among tested extracts at a concentration of 1 mg dry weight of plant/mL, 174 of 368 extracts suppressed 1 nM 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD)-induced AhR transformation to 50% or less, while 9 extracts per se induced AhR transformation equivalent to more than 20% of that induced by 1 nM TCDD. Mallotus japonicus (Thunb.) Muell. (leaf) and Trichosanthes rostrata Kitamura (fruit and fruit skin) strongly suppressed 1 nM TCDD-induced AhR transformation, while Phellodendron amurense Ruprecht (seed) per se strongly induced AhR transformation. These results suggest that a large variety of plants in Japan contain various compounds modulating, mainly suppressing, AhR transformation.
Animals↗